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                    <title><![CDATA[Spinal Cord Injuries]]></title>

                    <link>https://www.benthamscience.com</link>

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                    RSS Feed for Disease Wise Article | BenthamScience

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                    <pubDate>Thu, 16 Apr 2026 14:40:21 +0000</pubDate>

                    <image>

                    <title><![CDATA[Spinal Cord Injuries]]></title>

                    <url>https://www.benthamscience.com</url>

                    <link>https://www.benthamscience.com</link>

                    </image><item><title><![CDATA[Spinal Cord Image Denoising Using Dncnn Algorithm]]></title><link>https://www.benthamscience.comarticle/146944</link><description><![CDATA[<p>Background: Spinal image denoising plays a vital role in the accurate diagnosis of disc herniation (DH). </p> <p> Objective: Traditional denoising algorithms perform less due Limited Directional Selectivity problem and do not adequately capture directional information in pixels. Traditional algorithms' edge representation and texture details are insufficient for the earlier detection of DH. Limited Directional Selectivity leads to inaccurate diagnosis and classification of Disc Herniation (DH) stages. The DH stages are (i) Degeneration (ii) Prolapse (iii) Extrusion and (iv) Sequestration. Moreover, detection of DH size below 2mm using MR image is the major problem. </p> <p> Methods: To solve the above problem, spinal cord MR images fed to the proposed Parrot optimization tuned Denoising Convolutional Neural Network (Po- DnCNN) algorithm for perspective enhancement of nucleus pulposus region in the spinal cord, vertebrae. The perspective enhancement of Spinal cord image led to the accurate classification of stages and earlier detection of DH by using the proposed Hippopotamus optimization- Fast Hybrid Vision Transformer (Ho–FastViT) algorithm. For this study, spinal cord MR images are obtained from the Grand Challenge website – SPIDER dataset. </p> <p> Results: The proposed Po-DnCNN method and Ho-FastViT results are analysed quantitatively and qualitatively based on the edge, contrast, classification of the stage, and enhancement of the projected nucleus pulposus region in the spinal cord and vertebrae. The predicted DH results using the proposed method are compared with the manual Pfirrman Grade value of the spinal card method. </p> <p> Conclusion: Proposed method is better than traditional methods for earlier detection of DH. Po-DnCNN and Ho-FastViat methods give high accuracy of about 98% and 97% compared to traditional methods.</p>]]></description> </item><item><title><![CDATA[Cell Physiological Behavior in the Context of Local Hypothermia]]></title><link>https://www.benthamscience.comarticle/132813</link><description><![CDATA[Local hypothermia has protective effects on injured endothelial cells, cardiomyocytes, and neurocytes. Unfortunately, the underlying mechanism of local hypothermia is still unknown. The overall effect of local hypothermia involves changes in cellular and extracellular homeostasis. Reduction in cellular metabolism is the hallmark effect of local hypothermia, resulting in a reduction in energy expenditure already impaired by starvation conditions, such as ischemia. However, on a molecular basis, local hypothermia modifies cell physiology according to the type and the vitality of the cells (brain cells are more important than skin cells; therefore, local hypothermia of the brain tissue is more critical than skin tissue, and the overall reaction of the organism is to prevent the brain from dying). This involves activating survival mechanisms, such as autophagy of brain tissue and apoptosis. The activated signaling pathways are not identical in various tissues. However, the whole machinery signaling axes have not yet been elucidated. Local hypothermia promotes the healing of the injury and improves the proliferation of regenerative tissue, but not differentiation. Hypothermia prevents the transdifferentiation of endothelial cells, neurons, and myocardiocytes. Finally, the therapeutic effects of hypothermia involve activating the nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1).]]></description> </item><item><title><![CDATA[Anabolic Androgenic Steroids: A Review]]></title><link>https://www.benthamscience.comarticle/138822</link><description><![CDATA[A lot of athletes, bodybuilders, and those who want to look better in general use AAS (anabolic androgenic steroids) to achieve their goals. These steroids can be found in nature or synthesised in a lab. These substances are attempts to mimic the anabolic (muscle-building) and androgenic (masculinizing) properties of testosterone. Steroids like testosterone, methandienone, Nandrolone Decanoate (ND), and methenolone are only a few examples of AAS that are commonly abused. Initially exclusive to professional bodybuilders, these substances are increasingly being tried out by amateur and professional athletes alike. The anabolic properties of AAS have led to their usage in medicine for the treatment of conditions like chronic renal disease and osteoporosis in postmenopausal women. Despite being banned by the World Anti-Doping Agency, anabolic steroid (AAS) use is estimated to be between 1% and 3% among the general population of the United States (WADA). Their negative effects on several organs, including the cardiovascular and reproductive systems, have aroused concerns. Therefore, there are serious health risks linked with the inappropriate use of AAS. More education is needed for both the general public and medical professionals on how to recognise symptoms, administer effective care, and prevent AAS-related disorders. The goal of this study is to examine the current state of our understanding regarding the functioning of AAS and their associated deleterious consequences.]]></description> </item><item><title><![CDATA[Molecular Pathways and Treatment Updates on Huntington’s Disease with
Special Preference to Juvenile Phase: A Comprehensive Review]]></title><link>https://www.benthamscience.comarticle/139800</link><description><![CDATA[A degenerative brain ailment called Huntington's disease (HTD) causes irritable behavior, emotional distress, cognition, etc. It is also known as Huntington's chorea. Compared to men, women are more likely to get HTD. However, in India, if 3 to 5% of Europeans are affected, it is difficult to estimate the disease's prevalence. The full pathophysiological status, several molecular pathways, and pharmaceutical and non-pharmacological treatments for Huntington's disease are covered in this article. Google, PubMed, Scopus, Bentham, Elsevier, and other significant web resources were used to gather the scientific data. Moreover, this review article may serve as the foundation for future study, particularly on Huntington's illness.]]></description> </item><item><title><![CDATA[Posterior Longitudinal Ligament Calcification with Myelopathy - A Case Report]]></title><link>https://www.benthamscience.comarticle/138995</link><description><![CDATA[<P>Background: Ossification of the posterior longitudinal ligament (OPLL) constitutes a significant etiology of cervical myelopathy. The most common clinical presentations are myelopathy and radiculopathy, which result from a decrease in the spinal canal's volume and the spinal cord's subsequent compression by the ossified posterior longitudinal ligament. This results in motor and sensory deficits, especially in the extremities. <P> Case Presentation: A 48-year-old male presented with a complaint of neck pain that radiated to both upper limbs and was associated with numbness, tingling, and paranesthesia. He also had a history of lower back pain that radiated to the right leg, which was also associated with numbness and limited mobility to his cervical spine. Lhermitte's sign was positive. Sensory deficit to pinprick and touch was noted in the right upper limb and lower limbs. Flexion deformities of the right hand and elbow extension fingers were noted. Neuroimaging of the cervical spine showed cervical canal stenosis, OPLL, and myelopathy. Surgical management included internal fixation using plates and transpedicular screws, lateral mass fixation, and laminectomy of the third to sixth cervical vertebrae (C3-C6). <P> Conclusion: OPLL should be considered an integral component of the differential diagnosis when evaluating a patient with neck pain and consequent motor and sensory deficits of the extremities. OPLL with mild and/or non-progressive symptoms can be addressed with non-operative measures. Assessing preoperative neuroimaging is crucial before surgery to determine the degree of spinal cord compression and the presence of OPLL in all patients with cervical myelopathy. Surgical treatment options for posterior longitudinal ligament calcification include laminectomy and fusion, anterior decompression including transpedicular and costo-transversectomy, laminoplasty, and circumferential decompression via staged posterior and anterior approaches. Determining the most effective surgical approach for managing OPLL is still controversial, and selecting the appropriate procedure should be based on the patient's clinical presentation and level of pathological involvement.</P>]]></description> </item><item><title><![CDATA[RBM3 Accelerates Wound Healing of Skin in Diabetes through ERK1/2
Signaling]]></title><link>https://www.benthamscience.comarticle/135223</link><description><![CDATA[<p>Background: With the increasing risk of infections and other serious complications, the underlying molecular mechanism of wound healing impairment in diabetes deserves attention. Cold shock proteins (CSPs), including CIRP and RBM3 are highly expressed in the skin; however, it is unknown whether CSPs are involved in the wound-healing impairment of diabetic skin. <p> Objectives: The objective of this study is to investigate the effects of RBM3 on skin wound healing in diabetes. <p> Methods: In vitro experiments, western blot assay was used to test the levels of proteins in HaCaT cells treated with different concentrations of glucose. RBM3 was over-expressed in HaCaT cells using lentivirus particles. Cell viability was analyzed by Cell-Counting Kit-8 assay and colony formation assay. The migration of HaCaT cells at different concentrations of glucose was evaluated by wound healing assay. In vivo experiments, the mouse model of diabetes was established by intraperitoneal injection of streptozotocin. Four weeks later, the mice were anesthetized by intraperitoneal injection of pentobarbital sodium for skin tissue collection or wound healing experiments. RBM3 knockout mice were established by removing exons 2–6 using the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 technique and then used in skin wound healing experiments with or without diabetic stress. <p> Results: In this study, the expression of RBM3, rather than CIRP, was altered in the skin of diabetic specimens, and the RBM3’s overexpression accelerated the cell viability and proliferation of HaCaT cells under high glucose conditions. RBM3 deficiency caused delayed wound healing in RBM3 knockout in diabetic conditions. Moreover. RBM3 enhanced the ERK1/2 signaling pathway, and its inhibitor FR180204 blocked the beneficial effect of RBM3 overexpression on skin wound healing in diabetes. <p> Conclusion: RBM3 activated the ERK1/2 signal to facilitate skin wound healing in diabetes, offering a novel therapeutic target for its treatment.</p>]]></description> </item><item><title><![CDATA[A Detailed Review of Molecular Pathways and Mechanisms Responsible for the
Development and Aggravation of Neuropathy and Nephropathy in Diabetes]]></title><link>https://www.benthamscience.comarticle/130383</link><description><![CDATA[<P>Background: Diabetic mellitus is responsible for triggering many conditions, such as neuropathy, nephropathy, and retinopathy. Hyperglycemia leads to the development of oxidative stress conditions, activation of pathways, and generation of metabolites, leading to complications like neuropathy and nephropathy. <P> Objective: This paper aims to discuss the mechanism of actions, pathways, and metabolites triggered due to the development of neuropathy and nephropathy post-long-haul diabetes in patients. The therapeutic targets are also highlighted, proving to be a potential cure for such conditions. <P> Methods: Research works were searched from international and national databases with keywords like “diabetes,” “diabetic nephropathy,” “NADPH,” “oxidative stress,” “PKC,” “Molecular mechanisms,” “ cellular mechanisms,” “complications of diabetes,” and “factors.” The databases searched were PubMed, Scopus, Directory of open access journals, Semantic Scholar, Core, Europe PMC, EMBASE, Nutrition, FSTA- Food Science and Technology, Merck Index, Google Scholar, PubMed, Science Open, MedlinePlus, Indian citation index, World Wide Science, and Shodhganga. <P> Results: Pathways causing protein kinase C (PKC) activation, free radical injury, oxidative stress, and aggravating the conditions of neuropathy and nephropathy were discussed. In diabetic neuropathy and nephropathy, neurons and nephrons are affected to the extent that their normal physiology is disturbed, thus leading to further complications and conditions of loss of nerve sensation in diabetic neuropathy and kidney failure in diabetic nephropathy. <P> Current treatment options available for the management of diabetic neuropathy are anticonvulsants, antidepressants, and topical medications, including capsaicin. According to AAN guidelines, pregabalin is recommended as the first line of therapy, whereas other drugs currently used for treatment are gabapentin, venlafaxine, opioids, amitriptyline, and valproate. <P> Drug targets for treating diabetic neuropathy must suppress the activated polyol pathways, kinase C, hexosamine, and other pathways, which amplify neuroinflammation. Targeted therapy must focus on the reduction of oxidative stress and proinflammatory cytokines and suppression of neuroinflammation, NF-&#954;B, AP-1, etc. <P> Conclusion: Potential drug targets must be considered for new research on the treatment of neuropathy and nephropathy conditions.]]></description> </item><item><title><![CDATA[Review of the Role of Metabolic Factors in Determining the Post-surgical
Adhesion and its Therapeutic Implications, with a Focus on Extracellular
Matrix and Oxidative Stress]]></title><link>https://www.benthamscience.comarticle/135619</link><description><![CDATA[The potential role of metabolic reprogramming in fibrogenesis has recently attracted interest. Extracellular matrix stiffness, inflammation, and subsequent oxidative stress are essential mediators in the causation of fibrosis. The prevention of post-surgical adhesion is a challenge in medicine. It is defined as a fibrotic disorder in which adhesive bands develop after abdominal or pelvic surgery. Despite many studies related to the pathogenesis of post-surgical adhesion (PSA), many unknowns exist. Therefore, evaluating different pathways may help characterize and identify the cause of fibrotic scar formation post-operation. Glucose and lipid metabolism are crucial metabolic pathways in the cell’s energy production that may be targeted by hypoxia-induced factor alpha and profibrotic cytokines such as TGF-β to mediate fibrogenesis. Inhibition of upregulated metabolic pathways may be a viable strategy for ameliorating post-surgical adhesion. In this review, we have discussed the potential role of altered glucose and lipid metabolism in extracellular matrix (ECM) stiffness and oxidative stress as crucial mediators in fibrosis.]]></description> </item><item><title><![CDATA[Apelin Receptor Dimerization and Oligomerization]]></title><link>https://www.benthamscience.comarticle/133810</link><description><![CDATA[Apelin and its receptor are expressed in many tissues and play an important role in maintaining the homeostasis of the cardiovascular system and body fluids. Also, the association of this system with many diseases, such as diabetes, hypertension, obesity, cancer, diabetic retinopathy, etc., has been determined. This system is considered a therapeutic goal in many mentioned diseases. G protein-coupled receptors (GPCRs) have the ability to form oligomers and dimers with themselves and other receptors. The formation of these oligomers is associated with a change in the signaling pathways of the receptors. Research on the oligo and dimers of these receptors can revolutionize the principles of pharmacology. The apelin receptor (APJ) is also a GPCR and has been shown to have the ability to form dimers and oligomers. This article discusses the dimerization and oligomerization of this receptor with its own receptor and other receptors, as well as the signaling pathways.]]></description> </item><item><title><![CDATA[Nrf2 Mediates Effect of Resveratrol in Ischemia-reperfusion Injury]]></title><link>https://www.benthamscience.comarticle/138158</link><description><![CDATA[Ischemia-Reperfusion Injury (IRI) is a paradoxical phenomenon where removing the source of injury can cause additional damage. Ischemia reduces ATP production and intracellular pH, reducing oxidative reactions, increasing lactic acid release, and activating anaerobic metabolism. Reperfusion restores aerobic respiration and increases ROS production, leading to malfunction of transmembrane transport, activation of proteases, DNA dissolution, and protein denaturation, leading to apoptotic cell death. Nrf2 is a transcription factor that regulates cellular inflammation and oxidative responses. It is activated by oxidants and electrophiles and enhances detoxifying enzyme expression, maintaining redox homeostasis. It also activates ARE, which activates several ARE-regulated genes that favor cell survival by exhibiting resistance to oxidants and electrophiles. Nrf2 regulates the antioxidant defense system by producing phase II and antioxidant defense enzymes, including HO-1, NQO-1, gglutamylcysteine synthetase, and rate-limiting enzymes for glutathione synthesis. Nrf2 protects mitochondria from damage and supports mitochondrial function in stress conditions. Resveratrol is a stilbene-based compound with a wide variety of health benefits for humans, including antioxidant, anticarcinogenic, antitumor, and estrogenic/antiestrogenic. Resveratrol protects against IRI through several signaling pathways, including the Nrf2/ARE pathway. Here, we review the studies that investigated the mechanisms of resveratrol protection against IRI through modulation of the Nrf2 signaling pathway.]]></description> </item><item><title><![CDATA[Conditioned Medium Treatment for the Improvement of Functional Recovery after Spinal Cord Injury: A Meta-Analysis Study]]></title><link>https://www.benthamscience.comarticle/138852</link><description><![CDATA[<p>Background: While there is no certain treatment for spinal cord injury (SCI), stem cellbased therapy may be an attractive alternative, but the survival and differentiation of cells in the host tissue are poor. Conditioned medium (CM) has several beneficial effects on cells. </p> <p> Objective: In this meta-analysis study, we examined the effect of CM on SCI treatment. </p> <p> Methods: After searching on MEDLINE, SCOPUS, EMBASE, and Web of Science, first and secondary screening were performed based on title, abstract, and full text. The data were extracted from the included studies, and meta-analysis was performed using STATA.14 software. A standardized mean difference (SMD) with a 95% confidence interval was used to report findings. Quality control and subgroup analysis were also performed. </p> <p> Results: The results from 52 articles and 61 separate experiments showed that CM had a significantly strong effect on improving motor function after SCI (SMD = 2.58; 95% CI: 2.17 to 2.98; p &#60; 0.001) and also analysis of data from 12 articles demonstrated that CM reduced the expression of GFAP marker (SMD = -4.16; p &#60; 0.0001) compared to SCI group without any treatment. Subgroup analysis showed that treatment with CM of neural stem cells was better than CM of mesenchymal stem cells. It was more effective after a mild lesion than a moderate or severe one. The improvement was more pronounced with &#60;4 weeks than >4 weeks follow-up. </p> <p> Conclusion: CM had a significant effect in improving motor function after SCI, especially in cases of mild lesions. It has been observed that if CM originates from the neural stem cells, it has a more significant effect than mesenchymal cells.</p>]]></description> </item><item><title><![CDATA[Nrf2 Inhibits GAPDH/Siah1 Axis to Reduce Inflammatory Reactions and Proliferation of Microglia After Simulating Spinal Cord Injury]]></title><link>https://www.benthamscience.comarticle/137199</link><description><![CDATA[<p>Objective: To explore the effect of nuclear factor erythroid 2-related factor 2 (Nrf 2) on microglial inflammatory response and proliferation after spinal cord injury (SCI) through the glyceraldehyde phosphate dehydrogenase (GAPDH) / Seven in absentia homolog 1 (Siah 1) signaling pathway. </p> <p> Methods: Human microglia HMC3 was induced by lipopolysaccharide (LPS) to establish a SCI cell model. Microglia morphology after LPS stimulation was observed by transmission electron microscope (TEM), and cellular Nrf2, GAPDH/Siah1 pathway expression and cell viability were determined. Subsequently, the Nrf2 overexpression plasmid was transfected into microglia to observe changes in cell viability and GAPDH/Siah1 pathway expression. </p> <p> Results: Microglia, mostly amoeba-like, were found to have enlarged cell bodies after LPS stimulation, with an increased number of cell branches, highly expressed Nrf2, GAPDH and Siah1, and decreased cell viability (P<0.05). Up-regulating Nrf2 inhibited the GAPDH/Siah1 axis, decreased inflammatory responses, and enhanced activity in post-SCI microglia (P&#60;0.05). </p> <p> Conclusion: Up-regulating Nrf2 expression can reverse the inflammatory reaction of microglia after LPS stimulation and enhance their activity by inhibiting the GAPDH/ Siah1 axis.</p>]]></description> </item><item><title><![CDATA[T2 Black Synovitis in Musculoskeletal MRI: Disease Spectrum and Imaging
Characteristics of Joint Diseases]]></title><link>https://www.benthamscience.comarticle/132211</link><description><![CDATA[The synovium may be affected by a wide spectrum of disorders, including inflammatory, infectious, degenerative, traumatic, hemorrhagic, and tumorous conditions. Magnetic resonance imaging (MRI) is a valuable imaging modality to characterize synovial disorders. Most abnormal lesions appear as areas of nonspecific high signal intensity on T2-weighted images (T2-WI) due to high water content or increased perfusion. However, T2 hypointensity can be attributed to blood components of varying ages, calcification, inorganic crystals, fibrosis, caseous necrosis and/or amyloid deposition. Hypointense lesions on T2-WI are infrequent and additional clinical and imaging characteristics can help to limit the list of differential diagnoses, which may include tenosynovial giant cell tumor, synovial chondromatosis, rheumatoid arthritis, tuberculous arthritis, chronic tophaceous gout, amyloid arthropathy, synovial hemangioma, lipoma arborescens and hemosiderotic synovitis. Recently, susceptibility weighted imaging has been developed and may contribute to more accurate diagnosis for deoxygenated blood and calcium. We review the MRI features of hypointense synovial lesions on MRI and emphasize the characteristic findings that suggest a correct diagnosis.]]></description> </item><item><title><![CDATA[Multimodal Medical Image Fusion Utilizing Two-scale Image Decomposition via
Saliency Detection]]></title><link>https://www.benthamscience.comarticle/135266</link><description><![CDATA[<p>Background: Modern medical imaging modalities used by clinicians have many applications in the diagnosis of complicated diseases. These imaging technologies reveal the internal anatomy and physiology of the body. The fundamental idea behind medical image fusion is to increase the image's global and local contrast, enhance the visual impact, and change its format so that it is better suited for computer processing or human viewing while preventing noise magnification and accomplishing excellent real-time performance. Objective: The top goal is to combine data from various modal images (CT/MRI and MR-T1/MR-T2) into a solitary image that, to the greatest degree possible, retains the key characteristics (prominent features) of the source images. <p> Methods: The clinical accuracy of medical issues is compromised because innumerable classical fusion methods struggle to conserve all the prominent features of the original images. Furthermore, complex implementation, high computation time, and more memory requirements are key problems of transform domain methods. With the purpose of solving these problems, this research suggests a fusion framework for multimodal medical images that makes use of a multi-scale edge-preserving filter and visual saliency detection. The source images are decomposed using a two-scale edge-preserving filter into base and detail layers. Base layers are combined using the addition fusion rule, while detail layers are fused using weight maps constructed using the maximum symmetric surround saliency detection algorithm. <p> Results: The resultant image constructed by the presumed method has improved objective evaluation metrics than other classical methods, as well as unhindered edge contour, more global contrast, and no ringing effect or artifacts. <p> Conclusion: The methodology offers a dominant and symbiotic arsenal of clinical symptomatic, therapeutic, and biomedical research competencies that have the prospective to considerably strengthen medical practice and biological understanding.</p>]]></description> </item><item><title><![CDATA[PET/CT Examination of Teratomas after Stem Cell Transplantation for a
Spinal Cord Injury: A Case Report]]></title><link>https://www.benthamscience.comarticle/137021</link><description><![CDATA[<p>Background: In clinical practice, stem cell transplantation has become an effective method for treating spinal cord nerve injury. Up to now, there has been no report on teratoma caused by transplanted stem cell’s abnormal differentiation in the clinic, especially in the analysis of imaging manifestations. Therefore, this article aims to analyze the PET/CT imaging manifestations of teratoma caused by stem cell transplantation to improve the imaging diagnosing capability. <p> Case Presentation: A patient with a spinal cord injury who had received a stem cell transplant was examined by PET/CT on September 10th, 2020. The PET/CT images of the lesion showed irregular mixed low density on the right side of the erector spinae muscle area at the level of the cervical 3-5 vertebral body, with a maximum cross-section of 9.1×3.9 cm. The 18F-FDG metabolism of the lesion was increased, and the maximum standard uptake value (SUVmax) was 10.7. The boundary was unclear with the third cervical vertebra and cervical 3 and 4-level vertebral plates. Based on the patient’s medical history, the lesion was diagnosed as an abnormal proliferative tumor, which was consistent with the pathological examination results. <p> Conclusion: To date, there have been no clinical reports on teratomas caused by stem cell transplantation for spinal cord injury at home or abroad. This case report enhances the knowledge of the diagnosis and treatment methods of this type of disease and confirms the diagnostic value of PET/CT examination.</p>]]></description> </item><item><title><![CDATA[A Case Report of Wire-localised Excision of Impalpable Recurrent Papillary
Thyroid Carcinoma and Discussion of Wire-guided Excision in the Head and
Neck Pathology]]></title><link>https://www.benthamscience.comarticle/133463</link><description><![CDATA[<p>Introduction/Background: Wire localisation techniques are used widely for precision surgery in many specialities. This convenient technique has not yet become mainstream in the field of head and neck surgery. With limited space and many vital structures coursing through the head and neck region, pathological nodes that are difficult to palpate can be a challenge for clinicians. <p> Case Presentation: A patient with a history of papillary thyroid cancer treated with surgery and radioactive iodine had a single pathological node detected on ultrasound surveillance. An isolated recurrence of papillary thyroid carcinoma was confirmed. An excisional biopsy was performed using ultrasound wire guidance to successfully remove the diseased node with minimal morbidity. <p> Conclusion: Wire-guided lymph node excision biopsy is a safe and effective method that can be applied to multiple pathologies. As of yet, it is not routine practice to employ this technique. Larger studies would increase the generalisability and safety profile of this technique in the head and neck region.</p>]]></description> </item><item><title><![CDATA[Establishment and Comparison of Piecewise Linear Regression Models to
Measure Thyroid Volume by 2D and 3D Ultrasound]]></title><link>https://www.benthamscience.comarticle/134366</link><description><![CDATA[<p>Objective: Compared thyroid volumes measured by 2-D and 3-D US with those of resected specimens and proposed new models to improve measurement accuracy. <p> Methods: This study included 80 patients who underwent total thyroidectomy. One 2D_model and one 3D_model were developed using piecewise linear regression analysis. The accuracy of these models was compared using an ellipsoid model (2-D_US value × 0.5), 3-D_US value, and Ying’s model [1.76 + (2-D_US value × 0.38)]. <p> Results: The new 2D_model was: V=2.66 + (0.71 * X1) - (1.51 * X2). In this model, if 2-D_US value <= 228.39, X1 = 2-D_US value and X2 = 0; otherwise, X1 = 2-D_US value and X2 = 2-D_US value - 228.39. The 3D_model was: V= 2.90 + (1.08 * X1) + (2.43 * X2). In this model, if 3- D_US value <= 102.06, X1 = 3-D_US value and X2 = 0; otherwise, X1 = 3-D_US value and X2 = 3-D_US value - 102.06. The accuracy of the new models was higher than that of the 3-D_US value, the ellipsoid model, and Ying’s model (P&#60;0.05). <p> Conclusion: The models established are more accurate than the traditional ones and can accurately measure thyroid volume.</p>]]></description> </item><item><title><![CDATA[Multidisciplinary Management of Aneurysmal Bone Cyst in Paediatric Patients:
A Case Report]]></title><link>https://www.benthamscience.comarticle/135518</link><description><![CDATA[<p>Background: The aneurysmal bone cyst is a benign neoplasm that tends to form the appearance of a mass with a bony septum that forms cavities with blood inside. It is estimated to represent 1% of bone tumours and has an incidence of 0.14 per 100,000 people worldwide. Current publications have not shown a multidisciplinary approach that can benefit patients, mainly in the functionality and quality of the management approach. <p> Objective: Describe the multidisciplinary approach and the benefits of quality of life and functionality in this diagnosis. <p> Case presentation: A paediatric patient was diagnosed with an aneurysmal bone cyst located in the cervical spine, which initially manifested with muscle pain, enlargement of the posterior cervical region, and difficulty in performing arcs of movement. He was treated with multidisciplinary management with surgery, embolisation, radiation, and bisphosphonate support. <p> Conclusion: The purpose of approaching multidisciplinary management helped to improve the accompanying symptoms that prevented our patient from having an active and quality life. However, more successful cases have not been reported to establish the best therapeutic protocol.</p>]]></description> </item><item><title><![CDATA[Secondary Degeneration of White Matter Tract following Basal Ganglia
Infarction: A Longitudinal Diffusion Tensor Imaging Study]]></title><link>https://www.benthamscience.comarticle/136384</link><description><![CDATA[<p>Introduction: We explored the relationship between secondary degeneration of white matter (WM) tracts and motor outcomes after left basal ganglia infarction and investigated alterations in the diffusion indices of WM tracts in distal areas. <p> Methods: Clinical neurological evaluations were accomplished using the Fugl–Meyer scale (FMS). Then, the fractional anisotropy (FA) of the bilateral superior corona radiata (SCR), cerebral peduncle (CP), corticospinal tracts (CST), and corpus callosum (CC) were measured in all patients and control subjects. <p> Results: Regional-based analysis revealed decreased FA values in the ipsilesional SCR, CP, and CST of the patients, compared to the control subjects at 5- time points. The relative FA (rFA) values of the SCR, CP, and CST decreased progressively with time, the lowest values recorded at 90 days before increasing slightly at 180 days after stroke. Compared to the contralateral areas, the FA values of the ipsilesional SCR and CST areas were significantly decreased (P=0.023), while those of the CP decreased at 180 days (P=0.008). Compared with the values at 7 days, the rFA values of the ipsilesional SCR and CP areas were significantly reduced at 14, 30, and 90 days, while those in the CST area were significantly reduced at 14, 90, and 180 days. The CP rFA value at 7 days correlated positively with the FM scores at 180 days (r=0.469, P=0.037). <p> Conclusion: This study provides an objective, comprehensive, and automated protocol for detecting secondary degeneration of WM, which is important in understanding rehabilitation mechanisms after stroke.</p>]]></description> </item><item><title><![CDATA[A New Method Used to Enhance the SPAIR Image of the Spine MRI]]></title><link>https://www.benthamscience.comarticle/138286</link><description><![CDATA[<P>Background: Magnetic resonance imaging (MRI) is a handy diagnostic tool for orthopedic disorders, particularly spinal and joint diseases. <P> Methods: The lumbar intervertebral disc is visible in the T1 and T2 weight sequences of the spine MRI, which aids in diagnosing lumbar disc herniation, lumbar spine tuberculosis, lumbar spine tumors, and other conditions. The lumbar intervertebral disc cannot be seen accurately in the Spectral Attenuated Inversion Recovery (SPAIR) due to weaknesses in the fat and frequency offset parameters, which is not conducive to developing the intelligence diagnosis model of medical image. <P> Results: In order to solve this problem, we propose a composite framework, which is first to use the contrast limited adaptive histogram equalization (CLAHE) method to enhance the SPAIR image contrast of the spine MRI and then use the non-local means method to remove the noise of the image to ensure that the image contrast is uniform without losing details. We employ the Information Entropy (IE), Peak signal-to-noise ratio (PSNR), and feature similarity index measure (FSIM) to quantify image quality after enhancement by the composite framework. <P> Conclusion: The outcomes of the experiments’ output images and quantitative data indicate that our composite framework is better than others.</P>]]></description> </item><item><title><![CDATA[Application of Magnetic Resonance Diffusion Tensor Imaging in Diagnosis of
Lumbosacral Nerve Root Compression]]></title><link>https://www.benthamscience.comarticle/132469</link><description><![CDATA[<P>Objective: The aim of this study was to assess the value of 3.0T magnetic resonance (MR) Diffusion tensor imaging (DTI) in the diagnosis of lumbosacral nerve root compression. <P> Methods: The radiology reports, and clinical records of 34 patients with nerve root compression caused by lumbar disc herniation or bulging and 21 healthy volunteers who had undergone magnetic resonance imaging (MRI) and DTI scan were retrospectively reviewed. The differences in fractional anisotropy (FA) and apparent diffusion coefficient (ADC) between compressed and non-compressed nerve roots from patients and the normal nerve roots from healthy volunteers were compared. Meanwhile, the nerve root fiber bundles were observed and analyzed. <P> Results: The average FA and ADC values of the compressed nerve roots were 0.254 ± 0.307 and 1.892 ± 0.346 10^-3mm<sup>2</sup>/s, respectively. The average FA and ADC values of the non-compressed nerve roots were 0.377 ± 0.659 and 1.353 ± 0.344 10^-3mm<sup>2</sup>/s, respectively. The FA value of compressed nerve roots was significantly lower than that of non-compressed nerve roots (P < 0.01). The ADC value of compressed nerve roots was significantly higher than that of non-compressed nerve roots. There were no significant differences between the left and right nerve roots of normal volunteers in FA and ADC values (P > 0.05). The nerve roots at different levels of L3-S1 had significantly different FA and ADC values (P < 0.01). Incomplete fiber bundles with extrusion deformation, displacement or partial defect were observed in the compressed nerve root fiber bundles. The real diagnosis of the clinical situation of the nerve can provide neuroscientists with an important computer tool to help them infer and understand the possible working mechanism from the experimental data of behavior and electrophysiology. <P> Conclusion: The compressed lumbosacral nerve roots can be accurately localized through 3.0T magnetic resonance DTI, which is instructive for accurate clinical diagnosis and preoperative localization.</P>]]></description> </item><item><title><![CDATA[Current Concepts of Pain Pathways: A Brief Review of Anatomy, Physiology,
and Medical Imaging]]></title><link>https://www.benthamscience.comarticle/131942</link><description><![CDATA[<p>Background: Although the essential components of pain pathways have been identified, a thorough comprehension of the interactions necessary for creating focused treatments is still lacking. Such include more standardised methods for measuring pain in clinical and preclinical studies and more representative study populations. <p> Objective: This review describes the essential neuroanatomy and neurophysiology of pain nociception and its relation with currently available neuroimaging methods focused on health professionals responsible for treating pain. <p> Methods: Conduct a PubMed search of pain pathways using pain-related search terms, selecting the most relevant and updated information. <p> Results: Current reviews of pain highlight the importance of their study in different areas from the cellular level, pain types, neuronal plasticity, ascending, descending, and integration pathways to their clinical evaluation and neuroimaging. Advanced neuroimaging techniques such as fMRI, PET, and MEG are used to better understand the neural mechanisms underlying pain processing and identify potential targets for pain therapy. <p> Conclusion: The study of pain pathways and neuroimaging methods allows physicians to evaluate and facilitate decision-making related to the pathologies that cause chronic pain. Some identifiable issues include a better understanding of the relationship between pain and mental health, developing more effective interventions for chronic pain's psychological and emotional aspects, and better integrating data from different neuroimaging modalities for the clinical efficacy of new pain therapies.</p>]]></description> </item><item><title><![CDATA[Single-cell Technology in Stem Cell Research]]></title><link>https://www.benthamscience.comarticle/137519</link><description><![CDATA[Single-cell technology (SCT), which enables the examination of the fundamental units comprising biological organs, tissues, and cells, has emerged as a powerful tool, particularly in the field of biology, with a profound impact on stem cell research. This innovative technology opens new pathways for acquiring cell-specific data and gaining insights into the molecular pathways governing organ function and biology. SCT is not only frequently used to explore rare and diverse cell types, including stem cells, but it also unveils the intricacies of cellular diversity and dynamics. This perspective, crucial for advancing stem cell research, facilitates non-invasive analyses of molecular dynamics and cellular functions over time. Despite numerous investigations into potential stem cell therapies for genetic disorders, degenerative conditions, and severe injuries, the number of approved stem cell-based treatments remains limited. This limitation is attributed to the various heterogeneities present among stem cell sources, hindering their widespread clinical utilization. Furthermore, stem cell research is intimately connected with cutting-edge technologies, such as microfluidic organoids, CRISPR technology, and cell/tissue engineering. Each strategy developed to overcome the constraints of stem cell research has the potential to significantly impact advanced stem cell therapies. Drawing on the advantages and progress achieved through SCT-based approaches, this study aims to provide an overview of the advancements and concepts associated with the utilization of SCT in stem cell research and its related fields.]]></description> </item><item><title><![CDATA[Efficacy and Mechanism of Highly Active Umbilical Cord Mesenchymal Stem Cells in the Treatment of Osteoporosis in Rats]]></title><link>https://www.benthamscience.comarticle/138338</link><description><![CDATA[<p>Background: Osteoporosis increases bone brittleness and the risk of fracture. Umbilical cord mesenchymal stem cell (UCMSC) treatment is effective, but how to improve the biological activity and clinical efficacy of UCMSCs has not been determined. </p> <p> Methods: A rat model of osteoporosis was induced with dexamethasone sodium phosphate. Highly active umbilical cord mesenchymal stem cells (HA-UCMSCs) and UCMSCs were isolated, cultured, identified, and infused intravenously once at a dose of 2.29 × 10<sup>6</sup> cells/kg. In the 4th week of treatment, bone mineral density (BMD) was evaluated via cross-micro-CT, tibial structure was observed via HE staining, osteogenic differentiation of bone marrow mesenchymal stem cells (BMMSCs) was examined via alizarin red staining, and carboxy-terminal cross-linked telopeptide (CTX), nuclear factor-κβ ligand (RANKL), procollagen type 1 N-terminal propeptide (PINP) and osteoprotegerin (OPG) levels were investigated via enzyme-linked immunosorbent assays (ELISAs). BMMSCs were treated with 10<sup>-6</sup> mol/L dexamethasone and cocultured with HA-UCMSCs and UCMSCs in transwells. The osteogenic and adipogenic differentiation of BMMSCs was subsequently examined through directional induction culture. The protein expression levels of WNT, &#946;-catenin, RUNX2, IFN-&#947; and IL-17 in the bone tissue were measured via Western blotting. </p> <p> Results: The BMD in the healthy group was higher than that in the model group. Both UCMSCs and HA-UCMSCs exhibited a fusiform morphology; swirling growth; high expression of CD73, CD90 and CD105; and low expression of CD34 and CD45 and could differentiate into adipocytes, osteoblasts and chondrocytes, while HA-UCMSCs were smaller in size; had a higher nuclear percentage; and higher differentiation efficiency. Compared with those in the model group, the BMD increased, the bone structure improved, the trabecular area, number, and perimeter increased, the osteogenic differentiation of BMMSCs increased, RANKL expression decreased, and PINP expression increased after UCMSC and HA-UCMSC treatment for 4 weeks. Furthermore, the BMD, trabecular area, number and perimeter, calcareous nodule counts, and OPG/RANKL ratio were higher in the HA-UCMSC treatment group than in the UCMSC treatment group. The osteogenic and adipogenic differentiation of dexamethasone-treated BMMSCs was enhanced after the coculture of UCMSCs and HA-UCMSCs, and the HA-UCMSC group exhibited better effects than the UCMSC coculture group. The protein expression of WNT, &#946;-catenin, and runx2 was upregulated, and IFN-&#947; and IL-17 expression was downregulated after UCMSC and HA-UCMSC treatment. </p> <p> Conclusion: HA-UCMSCs have a stronger therapeutic effect on osteoporosis compared with that of UCMSCs. These effects include an improved bone structure, increased BMD, an increased number and perimeter of trabeculae, and enhanced osteogenic differentiation of BMMSCs via activation of the WNT/&#946;-catenin pathway and inhibition of inflammation.</p>]]></description> </item><item><title><![CDATA[Beneficial Effects of Spirulina on Brain Health: A Systematic Review]]></title><link>https://www.benthamscience.comarticle/137347</link><description><![CDATA[<p>Background: This review provides a concise overview of existing scientific research concerning the potential advantages of incorporating spirulina, a blue-green algae, into one's diet to promote brain health. The substantial nutritional composition and associated health benefits of algae have drawn significant interest. </p> <p> Methods: Numerous studies have illuminated the neuroprotective characteristics of spirulina, contributing to its positive influence on brain functionality. Primarily, spirulina boasts antioxidants, like phycocyanin and beta-carotene, that effectively counter oxidative stress and curb inflammation within the brain. This is particularly significant as these factors play roles in the advancement of neurodegenerative conditions like Parkinson's and Alzheimer's disease. Additionally, spirulina has demonstrated the capacity to enhance cognitive capabilities and enrich memory and learning aptitudes. </p> <p> Results: Animal-based investigations have revealed that introducing spirulina can bolster spatial learning and memory, as well as guard against cognitive decline linked to aging. Research has indicated its potential in shielding against neurotoxins, encompassing heavy metals and specific environmental pollutants. Its potential to neutralize heavy metals and counteract free radicals contributes to these protective effects, potentially thwarting neuronal harm. </p> <p> Conclusion: In conclusion, the extant scientific literature proposes that spirulina integration can elicit advantageous outcomes for brain health. Its antioxidative, neuroprotective, cognitiveenhancing, and mood-regulating properties present a promising avenue for bolstering brain health and potentially diminishing the susceptibility to neurodegenerative ailments. Nonetheless, further research, notably well-designed human clinical trials, is imperative to ascertain the optimal dosing, duration, and enduring consequences of spirulina supplementation concerning brain health.</p>]]></description> </item><item><title><![CDATA[Human Umbilical Cord Mesenchymal Stem Cells Alleviate Chronic Salpingitis by Modulating Macrophage-Associated Inflammatory Factors]]></title><link>https://www.benthamscience.comarticle/136948</link><description><![CDATA[<p>Introduction: Mesenchymal stem cells (MSCs) have been widely studied because of their established anti-inflammatory properties. During chronic salpingitis (CS), infiltrated macrophages have vital roles in inflammation and tissue remodeling. </p> <p> Methods: We employed the type of MSCs, human umbilical cord (huc) MSCs in an experimental CS model and therapeutic efficacy was assessed. hucMSCs exerted this therapeutic effect by regulating macrophage function. To verify the regulatory effects of hucMSCs on the macrophage, macrophage line RAW264.7 markers were analyzed under LPS stimulation with or without co-culturing with hucMSCs for 12h and 24h. In addition, flow cytometry analysis was applied to reveal the interaction of co-culture. For animal studies, CS was induced by the MoPn strain Chlamydia trachomatis (CT), hucMSCs were intravaginally injected in the CS, and we analyzed the infiltrated macrophage by immunofluorescence. </p> <p> Results: We found the markers IL-10 was markedly increased and IL-1&#946;, caspase-1 was notably downregulated after co-culturing with hucMSCs by RT-PCR. hucMSCs promote macrophage line RAW264.7 apoptosis. We also found that hucMSCs treatment can alleviate CS by decreasing the mRNA expression of IL-1&#946;, caspase-1 and MCP-1 in the tubal tissue by RT-PCR and decreasing the protein expression of IL-1&#946;, caspase-1 and TGF-β by western blotting. </p> <p> Conclusion: These results suggest that macrophage function may be related to the immune-modulating characteristics of hucMSCs that contribute to CS.</p>]]></description> </item><item><title><![CDATA[Fucoxanthin Enhances the Antifibrotic Potential of Placenta-derived Mesenchymal Stem Cells in a CCl4-induced Mouse Model of Liver]]></title><link>https://www.benthamscience.comarticle/137096</link><description><![CDATA[<p>Background: The effectiveness of fucoxanthin (Fx) in liver diseases has been reported due to its anti-inflammatory and antifibrotic effects. Mesenchymal stem cells (MSCs)-based therapy has also been proposed as a promising strategy for liver fibrosis treatment. Recent studies have shown that the co-administration of MSCs and drugs demonstrates a pronounced effect on liver fibrosis. </p> <p> Aim: This study aimed to determine the therapeutic potential of placenta-derived MSCs (PD-MSCs) in combination with Fx to treat liver fibrosis and evaluate their impact on the main links of liver fibrosis pathogenesis. </p> <p> Methods: After PD-MSCs isolation and identification, outbred ICR/CD1 mice were divided into five groups: Control group, CCl<sub>4</sub> group (CCl<sub>4</sub>), Fx group (CCl<sub>4</sub>+Fx), PD-MSCs group (CCl<sub>4</sub>+MSCs) and cotreatment group (CCl<sub>4</sub>+MSCs+Fx). Biochemical histopathological investigations were performed. Semiquantitative analysis of the alpha-smooth muscle actin (α-SMA+), matrix metalloproteinases (MMP-9+, MMP-13+), tissue inhibitor of matrix metalloproteinases-1 (TIMP-1+) areas, and the number of positive cells in them were studied by immunohistochemical staining. Transforming growth factor-beta (TGF-&#946;), hepatic growth factor (HGF), procollagen-1 (COL1&#945;1) in liver homogenate and proinflammatory cytokines in blood serum were determined using an enzyme immunoassay. </p> <p> Results: Compared to the single treatment with PD-MSCs or Fx, their combined administration significantly reduced liver enzyme activity, the severity of liver fibrosis, the proinflammatory cytokine levels, TGF-&#946; level, &#945;-SMA+, TIMP-1+ areas and the number of positive cells in them, and increased HGF level, MMP-13+, and MMP-9+ areas. </p> <p> Conclusion: Fx enhanced the therapeutic potential of PD-MSCs in CCl4-induced liver fibrosis, but more investigations are necessary to understand the mutual impact of PD-MSCs and Fx.</p>]]></description> </item><item><title><![CDATA[Mechanisms of Stem Cells and Their Secreted Exosomes in the Treatment of Autoimmune Diseases]]></title><link>https://www.benthamscience.comarticle/137044</link><description><![CDATA[Stem cells play a therapeutic role in many diseases by virtue of their strong self-renewal and differentiation abilities, especially in the treatment of autoimmune diseases. At present, the mechanism of the stem cell treatment of autoimmune diseases mainly relies on their immune regulation ability, regulating the number and function of auxiliary cells, anti-inflammatory factors and proinflammatory factors in patients to reduce inflammation. On the other hand, the stem cell- derived secretory body has weak immunogenicity and low molecular weight, can target the site of injury, and can extend the length of its active time in the patient after combining it with the composite material. Therefore, the role of secretory bodies in the stem cell treatment of autoimmune diseases is increasingly important.]]></description> </item><item><title><![CDATA[Enhancing Spermatogenesis in Non-obstructive Azoospermia Through Mesenchymal Stem Cell Therapy22]]></title><link>https://www.benthamscience.comarticle/137341</link><description><![CDATA[Stem cells hold great promise as novel and encouraging therapeutic tools in the treatment of degenerative disorders due to their differentiation potential while maintaining the capability to self-renewal and their unlimited ability to divide and regenerate tissue. A variety of different types of stem cells can be used in cell therapy. Among these, mesenchymal stem cell (MSC) therapy has gradually established itself as a novel method for treating damaged tissues that need restoration and renewal. Male infertility is an important health challenge affecting approximately 8-12% of people around the world. This abnormality can be caused by primary, congenital, acquired, or idiopathic reasons. Men with no sperm in their semen have a condition called azoospermia, caused by non-obstructive (NOA) causes and post-testicular obstructive causes. Accumulating evidence has shown that various types of MSCs can differentiate into germ cells and improve spermatogenesis in the seminiferous tubules of animal models. In addition, recent studies in animal models have exhibited that extracellular vesicles derived from MSCs can stimulate the progression of spermatogenesis and germ cell regeneration in the recipient testes. In spite of the fact that various improvements have been made in the treatment of azoospermia disorder in animal models by MSC or their extracellular vesicles, no clinical trials have been carried out to test their therapeutic effect on the NOA. In this review, we summarize the potential of MSC transplantation for treating infertility caused by NOA.]]></description> </item><item><title><![CDATA[The Role of Resveratrol in Alzheimer's Disease: A Comprehensive Review
of Current Research]]></title><link>https://www.benthamscience.comarticle/136645</link><description><![CDATA[Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, memory loss, and impaired daily functioning. The etiology of AD is complex and multifactorial, involving various pathological mechanisms such as the accumulation of amyloid-beta plaques, neurofibrillary tangles, neuroinflammation, and oxidative stress. As the global prevalence of AD continues to rise, there is a growing interest in identifying potential therapeutic interventions to prevent or slow down the progression of the disease. Resveratrol, a natural polyphenolic compound found in various plant sources such as grapes, berries, and peanuts, has gained considerable attention due to its potential neuroprotective effects. Numerous preclinical studies utilizing <i>in vitro</i> and animal models have investigated the impact of resveratrol on AD pathology and associated cognitive impairments. This review aims to provide a comprehensive summary of the current research on the role of resveratrol in AD. In conclusion, resveratrol holds promise as a potential therapeutic agent for AD due to its ability to target multiple pathological processes involved in the disease. Further research, including well-designed clinical trials with larger sample sizes, is needed to fully elucidate the efficacy, optimal dosage, and long-term effects of resveratrol in AD patients. Nevertheless, resveratrol remains an intriguing compound with neuroprotective properties and may contribute to the development of novel therapeutic approaches for AD in the future.]]></description> </item><item><title><![CDATA[Opportunities and Regulatory Challenges of Functional Foods and
Nutraceuticals During COVID-19 Pandemic]]></title><link>https://www.benthamscience.comarticle/138829</link><description><![CDATA[The novel Coronavirus has brought global mortality, disruption, and a significant loss of life. A compromised immune system is a known risk factor for all viral influenza infections. Due to the perceived “immune-boosting” properties of nutraceutical products, sales of dietary supplements have grown globally. In recent years, consumers have increasingly demanded nutraceutical products rather than curative synthetic medicines for preventive therapies for the coronavirus disease outbreak of 2019 (COVID-19). Healthy foods and nutraceuticals have become daily diet plans for consumers. Although there has been an increase in demand, there is no such regulation and harmonized process, which stands as a barrier to the approval of these products. Therefore, many misbranded and spurious products are entering the market, which may harm consumers. This article focuses on the role of functional foods and nutraceutical in the management of COVID-19 also focuses on the different nutraceutical regulations in each country and compare the similarities and differences of the following countries: India, the USA (United States of America), the EU (European Union), and China. The comparative study of nutraceutical regulations in India, the USA, Europe, and China shows that there is a difference regarding the nutraceutical regulations; however, despite the differences, it is observed that it has the same underlying objective, i.e., ensuring the safety of the consumers by maintaining the product quality.]]></description> </item><item><title><![CDATA[A Systematic Review on the Potential Applications of Theranostic
Nanoparticles in Diabetes and its Associated Complication Diabetic
Neuropathy]]></title><link>https://www.benthamscience.comarticle/137581</link><description><![CDATA[<p>Background: Diabetes neuropathy is a frequent ailment that has a substantial impact on patients by increasing the risk of falls and causing discomfort. The lower extremities are where diabetic neuropathy patients first feel pain. This discomfort could seem like a pinprick, an electric shock, or something else. </p> <p> Objective: Here, we give a comprehensive overview of this quickly developing theranostic application that includes all relevant imaging, diagnostic, therapeutic, and monitoring elements for the management of diabetes and diabetes neuropathy. </p> <p> Methods: The data for the current study was gathered by searching PubMed and Google Scholar. Several research and review publications from various publishers, including Springer Nature, Bentham Science, PLOS one, MDPI, and ACS Publishing Centre, were evaluated to compile the data. </p> <p> Result: Recent developments in theranostics have shown promise as alternate management approaches for diabetes and ailments linked to diabetes. Numerous nanotechnology-built biosensors, including multiwalled carbon nanotubes, copper nanowires, zinc oxide tetrapods, and nanoparticle- embedded contact lenses, offer benefits in monitoring diabetic neuropathy. </p> <p> Conclusion: The potency, usability, and dependability of insulin substitutes have been demonstrated by a variety of innovative methods for the management of diabetes, which includes nanotechnology approaches using Gene-Based Nanoparticles (siRNA), Liposomes, Exosomes/ Extracellular Vesicles, Neuromodulation, and Inhalable Nanoparticles. Over the past few years, the development of various theranostic nanoparticles for Diabetic neuropathy has experienced an unprecedented expansion. Even though much work needs to be done to precisely evaluate the genuine benefits provided by these particles, such as issues with nanotoxicity, theranostic nanoparticles will have a significant impact on the field of nanomedicine.</p>]]></description> </item><item><title><![CDATA[Mesenchymal Stem Cell Transplantation in Type 1 Diabetes Treatment:
Current Advances and Future Opportunity]]></title><link>https://www.benthamscience.comarticle/135081</link><description><![CDATA[Type 1 Diabetes (T1D) is characterized by hyperglycemia, and caused by a lack of insulin secretion. At present there is no cure for T1D and patients are dependent on exogenous insulin for lifelong, which seriously affects their lives. Mesenchymal stem cells (MSCs) can be differentiated to β cell-like cells to rescue the secretion of insulin and reconstruct immunotolerance to preserve the function of islet β cells. Due to the higher proportion of children and adolescents in T1D patients, the efficacy and safety issue of the application of MSC’s transplant in T1D was primarily demonstrated and identified by human clinical trials in this review. Then we clarified the mechanism of MSCs to relieve the symptom of T1D and found out that UC-MSCs have no obvious advantage over the other types of MSCs, the autologous MSCs from BM or menstrual blood with less expanded ex vivo could be the better choice for clinical application to treat with T1D through documentary analysis. Finally, we summarized the advances of MSCs with different interventions such as genetic engineering in the treatment of T1D, and demonstrated the advantages and shortage of MSCs intervened by different treatments in the transplantation, which may enhance the clinical efficacy and overcome the shortcomings in the application of MSCs to T1D in future.]]></description> </item><item><title><![CDATA[<i>In-silico, in-vitro</i> and <i>in-vivo</i> Biological Activities of Flavonoids for the
Management of Type 2 Diabetes]]></title><link>https://www.benthamscience.comarticle/137280</link><description><![CDATA[In spite of the fact that many medicinal plants have been truly utilized for the management of diabetes all through the world, very few of them have been reported scientifically. Recently, a diverse variety of animal models have been established to better understand the pathophysiology of diabetes mellitus, and new medications to treat the condition have been introduced in the market. Flavonoids are naturally occurring substances that can be found in plants and various foods and may have health benefits in the treatment of neuropathic pain. Flavonoids have also been shown to have an anti-inflammatory impact that is significant to neuropathic pain, as indicated by a decrease in several pro-inflammatory mediators such TNF-, NF-B IL-6, and IL-1. Flavonoids appear to be a viable novel therapy option for macrovasular complications in preclinical models; however, human clinical data is still inadequate. Recently, several <i>in silico, in-vitro</i> and <i>in-vivo</i> aproaches were made to evaluate mechanisms associated with the pathogenesis of diabetes in a better way. Screening of natural antidiabetic agents from plant sources can be analysed by utilizing advanced <i>in-vitro</i> techniques and animal models. Natural compounds, mostly derived from plants, have been studied in diabetes models generated by chemical agents in the majority of research. The aim of this work was to review the available <i>in silico, in-vitro</i> and animal models of diabetes for screening of natural antidiabetic agents. This review contributes to the scientist's design of new methodologies for the development of novel therapeutic agents having potential antihyperglycemic activity.]]></description> </item><item><title><![CDATA[Melatonin Alleviates High Glucose-induced Oxidative Stress and
Mitochondrial Dysfunction in Chondrocytes]]></title><link>https://www.benthamscience.comarticle/135907</link><description><![CDATA[<p>Background: Hyperglycemia triggers mitochondrial dysfunction in chondrocytes, potentially contributing to cell damage and the onset of osteoarthritis. </p> <p> Objective: This study is undertaken with the objective of examining the protective properties of melatonin against toxicity induced by high glucose in C28I2 human chondrocytes. </p> <p> Methods: To determine non-cytotoxic concentrations of melatonin, various concentrations (10, 25, 50, 75, 100, 500, and 1000 μM) were assessed over different time periods (24, 48, and 72 hours) for their impact on C28I2 cell viability. Following this, cells underwent a pretreatment with melatonin (10 and 100 μM) for 6 hours. This was followed by subjecting the cells to a high concentration of glucose (75 mM) for 48 hours. Oxidative stress markers, including reactive oxygen species (ROS) and malondialdehyde (MDA), alongside the enzymatic activities of glutathione peroxidase, superoxide dismutase, and catalase were quantitatively assessed. To assess mitochondrial function, we evaluated the adenosine diphosphate (ADP)/adenosine triphosphate (ATP) ratio and measured the mitochondrial membrane potential (MMP). </p> <p> Results: Elevated glucose levels significantly increased ROS and MDA levels, accompanied by reduced MMP, an elevated ADP/ATP ratio, and altered antioxidant enzyme activity. Pretreatment with melatonin effectively reversed the mitochondrial toxicity induced by high glucose (75 mM). </p> <p> Conclusion: These results indicate that melatonin exhibits a protective influence against hyperglycemia- induced toxicity in chondrocyte mitochondria.</p>]]></description> </item><item><title><![CDATA[N-Methyl-D-Aspartate (NMDA) Receptor Antagonists and their
Pharmacological Implication: A Medicinal Chemistry-oriented
Perspective Outline]]></title><link>https://www.benthamscience.comarticle/139809</link><description><![CDATA[N-methyl-D-aspartate (NMDA) receptors, i.e., inotropic glutamate receptors, are important in synaptic plasticity, brain growth, memory, and learning. The activation of NMDA is done by neurotransmitter glutamate and co-agonist (glycine or D-serine) binding. However, the over-activation of NMDA elevates the intracellular calcium influx, which causes various neurological diseases and disorders. Therefore, to prevent excitotoxicity and neuronal death, inhibition of NMDA must be done using its antagonist. This review delineates the structure of subunits of NMDA and the conformational changes induced after the binding of agonists (glycine and D-serine) and antagonists (ifenprodil, etc.). Additionally, reported NMDA antagonists from different sources, such as synthetic, semisynthetic, and natural resources, are explained by their mechanism of action and pharmacological role. The comprehensive report also addresses the chemical spacing of NMDA inhibitors and <i>in-vivo</i> and <i>in-vitro</i> models to test NMDA antagonists. Since the Blood-Brain Barrier (BBB) is the primary membrane that prevents the penetration of a wide variety of drug molecules, we also elaborate on the medicinal chemistry approach to improve the effectiveness of their antagonists.]]></description> </item><item><title><![CDATA[The Limping Child: A Guide for the Trainees]]></title><link>https://www.benthamscience.comarticle/130725</link><description><![CDATA[Limping is a common presenting complaint in children. Despite this, it remains to be a diagnostic challenge for treating physicians due to an expanded list of etiologies. It arises from a spectrum of disorders, ranging from physiological variations of gait at different stages of development to systemic causes, such as inflammatory diseases or musculoskeletal infections. On rare occasions, non-musculoskeletal causes could result in limping. The diagnostic challenge increases in younger age children where a detailed physical examination that helps identify the exact source of pathology may not be possible. In older patients who have a well-developed gait cycle, the physical assessment might be easier. Clinical assessment in a child presenting with a limp includes gait analysis, which is essential to guide the appropriate request of diagnostic laboratory tests and imaging studies. In this paper, we provide a practical guide for a trainee in General Pediatric and Pediatric Rheumatology on an approach to a limping child, aiming to identify the common causes of limping and to describe normal and abnormal gait cycles. We also discuss other diagnostic considerations in the assessment of these children.]]></description> </item><item><title><![CDATA[Revolutionizing Neurological Disorder Treatment: Integrating Innovations in
Pharmaceutical Interventions and Advanced Therapeutic Technologies]]></title><link>https://www.benthamscience.comarticle/139669</link><description><![CDATA[Neurological disorders impose a significant burden on individuals, leading to disabilities and a reduced quality of life. However, recent years have witnessed remarkable advancements in pharmaceutical interventions aimed at treating these disorders. This review article aims to provide an overview of the latest innovations and breakthroughs in neurological disorder treatment, with a specific focus on key therapeutic areas such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, and stroke. This review explores emerging trends in drug development, including the identification of novel therapeutic targets, the development of innovative drug delivery systems, and the application of personalized medicine approaches. Furthermore, it highlights the integration of advanced therapeutic technologies such as gene therapy, optogenetics, and neurostimulation techniques. These technologies hold promise for precise modulation of neural circuits, restoration of neuronal function, and even disease modification. While these advancements offer hopeful prospects for more effective and tailored treatments, challenges such as the need for improved diagnostic tools, identification of new targets for intervention, and optimization of drug delivery methods will remain. By addressing these challenges and continuing to invest in research and collaboration, we can revolutionize the treatment of neurological disorders and significantly enhance the lives of those affected by these conditions.]]></description> </item><item><title><![CDATA[Anti-gout and Urate-lowering Potentials of Curcumin: A Review from
Bench to Beside]]></title><link>https://www.benthamscience.comarticle/133079</link><description><![CDATA[<p>Background: Gouty arthritis is a complex form of inflammatory arthritis, triggered by the sedimentation of monosodium urate crystals in periarticular tissues, synovial joints, and other sites in the body. Curcumin is a natural polyphenol compound, isolated from the rhizome of the plant <i>Curcuma longa</i>, possessing countless physiological features, including antioxidant, anti-inflammatory, and anti-rheumatic qualities. <p> Objective: This study aimed to discuss the beneficial impacts of curcumin and its mechanism in treating gout disease. <p> Methods: Ten English and Persian databases were used to conduct a thorough literature search. Studies examining the anti-gouty arthritis effects of curcumin and meeting the inclusion criteria were included. <p> Results: According to the studies, curcumin has shown xanthine oxidase and urate transporter- 1 inhibitory properties, uric acid inhibitory characteristics, and antioxidant and anti- inflammatory effects. However, some articles found no prominent reduction in uric acid levels. <p> Conclusion: In this review, we emphasized the potency of curcumin and its compounds against gouty arthritis. Despite the potency, we suggest an additional well-designed evaluation of curcumin, before its therapeutic effectiveness is completely approved as an antigouty arthritis agent.</p>]]></description> </item><item><title><![CDATA[Involvement of Nrf2 Signaling in Lead-induced Toxicity]]></title><link>https://www.benthamscience.comarticle/131984</link><description><![CDATA[Nuclear factor erythroid 2-related factor 2 (Nrf2) is used as one of the main protective factors against various pathological processes, as it regulates cells resistant to oxidation. Several studies have extensively explored the relationship between environmental exposure to heavy metals, particularly lead (Pb), and the development of various human diseases. These metals have been reported to be able to, directly and indirectly, induce the production of reactive oxygen species (ROS) and cause oxidative stress in various organs. Since Nrf2 signaling is important in maintaining redox status, it has a dual role depending on the specific biological context. On the one hand, Nrf2 provides a protective mechanism against metal-induced toxicity; on the other hand, it can induce metalinduced carcinogenesis upon prolonged exposure and activation. Therefore, the aim of this review was to summarize the latest knowledge on the functional interrelation between toxic metals, such as Pb and Nrf2 signaling.]]></description> </item><item><title><![CDATA[An Updated Review on the Significance of DNA and Protein
Methyltransferases and De-methylases in Human Diseases: From
Molecular Mechanism to Novel Therapeutic Approaches]]></title><link>https://www.benthamscience.comarticle/132369</link><description><![CDATA[Epigenetic mechanisms are crucial in regulating gene expression. These mechanisms include DNA methylation and histone modifications, like methylation, acetylation, and phosphorylation. DNA methylation is associated with gene expression suppression; however, histone methylation can stimulate or repress gene expression depending on the methylation pattern of lysine or arginine residues on histones. These modifications are key factors in mediating the environmental effect on gene expression regulation. Therefore, their aberrant activity is associated with the development of various diseases. The current study aimed to review the significance of DNA and histone methyltransferases and demethylases in developing various conditions, like cardiovascular diseases, myopathies, diabetes, obesity, osteoporosis, cancer, aging, and central nervous system conditions. A better understanding of the epigenetic roles in developing diseases can pave the way for developing novel therapeutic approaches for affected patients.]]></description> </item><item><title><![CDATA[Neuroprotective Properties of Antiepileptics: What are the Implications
for Psychiatric Disorders?]]></title><link>https://www.benthamscience.comarticle/132022</link><description><![CDATA[Since the discovery of the first antiepileptic compound, increasing attention has been paid to antiepileptic drugs (AEDs), and recently, with the understanding of the molecular mechanism underlying cells death, a new interest has revolved around a potential neuroprotective effect of AEDs. While many neurobiological studies in this field have focused on the protection of neurons, growing data are reporting how exposure to AEDs can also affect glial cells and the plastic response underlying recovery; however, demonstrating the neuroprotective abilities of AEDs remains a changeling task. The present work aims to summarize and review the literature available on the neuroprotective properties of the most commonly used AEDs. Results highlighted how further studies should investigate the link between AEDs and neuroprotective properties; while many studies are available on valproate, results for other AEDs are very limited and the majority of the research has been carried out on animal models. Moreover, a better understanding of the biological basis underlying neuro-regenerative defects may pave the way for the investigation of further therapeutic targets and eventually lead to an improvement in the actual treatment strategies.]]></description> </item><item><title><![CDATA[Current Progress on Central Cholinergic Receptors as Therapeutic
Targets for Alzheimer's Disease]]></title><link>https://www.benthamscience.comarticle/139353</link><description><![CDATA[Acetylcholine (ACh) is ubiquitously present in the nervous system and has been involved in the regulation of various brain functions. By modulating synaptic transmission and promoting synaptic plasticity, particularly in the hippocampus and cortex, ACh plays a pivotal role in the regulation of learning and memory. These procognitive actions of ACh are mediated by the neuronal muscarinic and nicotinic cholinergic receptors. The impairment of cholinergic transmission leads to cognitive decline associated with aging and dementia. Therefore, the cholinergic system has been of prime focus when concerned with Alzheimer’s disease (AD), the most common cause of dementia. In AD, the extensive destruction of cholinergic neurons occurs by amyloid-β plaques and tau protein-rich neurofibrillary tangles. Amyloid-&#946; also blocks cholinergic receptors and obstructs neuronal signaling. This makes the central cholinergic system an important target for the development of drugs for AD. In fact, centrally acting cholinesterase inhibitors like donepezil and rivastigmine are approved for the treatment of AD, although the outcome is not satisfactory. Therefore, identification of specific subtypes of cholinergic receptors involved in the pathogenesis of AD is essential to develop future drugs. Also, the identification of endogenous rescue mechanisms to the cholinergic system can pave the way for new drug development. In this article, we discussed the neuroanatomy of the central cholinergic system. Further, various subtypes of muscarinic and nicotinic receptors involved in the cognition and pathophysiology of AD are described in detail. The article also reviewed primary neurotransmitters that regulate cognitive processes by modulating basal forebrain cholinergic projection neurons.]]></description> </item><item><title><![CDATA[Adaptive Autonomic and Neuroplastic Control in Diabetic Neuropathy:
A Narrative Review]]></title><link>https://www.benthamscience.comarticle/136289</link><description><![CDATA[<P>Background: Type 2 diabetes mellitus (T2DM) is a worldwide socioeconomic burden, and is accompanied by a variety of metabolic disorders, as well as nerve dysfunction referred to as diabetic neuropathy (DN). Despite a tremendous body of research, the pathogenesis of DN remains largely elusive. Currently, two schools of thought exist regarding the pathogenesis of diabetic neuropathy: a) mitochondrial-induced toxicity, and b) microvascular damage. Both mechanisms signify DN as an intractable disease and, as a consequence, therapeutic approaches treat symptoms with limited efficacy and risk of side effects. <P> Objective: Here, we propose that the human body exclusively employs mechanisms of adaptation to protect itself during an adverse event. For this purpose, two control systems are defined, namely the autonomic and the neural control systems. The autonomic control system responds via inflammatory and immune responses, while the neural control system regulates neural signaling, via plastic adaptation. Both systems are proposed to regulate a network of temporal and causative connections which unravel the complex nature of diabetic complications. <P> Results: A significant result of this approach infers that both systems make DN reversible, thus opening the door to novel therapeutic applications.</P>]]></description> </item><item><title><![CDATA[The Functions and Application Prospects of Hepatocyte Growth Factor in
Reproduction]]></title><link>https://www.benthamscience.comarticle/138754</link><description><![CDATA[Hepatocyte growth factor (HGF) is expressed in multiple systems and mediates a variety of biological activities, such as mitosis, motility, and morphogenesis. A growing number of studies have revealed the expression patterns and functions of HGF in ovarian and testicular physiology from the prenatal to the adult stage. HGF regulates folliculogenesis and steroidogenesis by modulating the functions of theca cells and granulosa cells in the ovary. It also mediates somatic cell proliferation and steroidogenesis, thereby affecting spermatogenesis in males. In addition to its physiological effects on the reproductive system, HGF has shown advantages in preclinical studies over recent years for the treatment of male and female infertility, particularly in women with premature ovarian insufficiency. This review aims to summarize the pleiotropic functions of HGF in the reproductive system and to provide prospects for its clinical application.]]></description> </item><item><title><![CDATA[Current Landscape of Gene Therapy for the Treatment of Cardiovascular
Disorders]]></title><link>https://www.benthamscience.comarticle/138068</link><description><![CDATA[Cardiovascular disorders (CVD) are the primary cause of death worldwide. Multiple factors have been accepted to cause cardiovascular diseases; among them, smoking, physical inactivity, unhealthy eating habits, age, and family history are flag-bearers. Individuals at risk of developing CVD are suggested to make drastic habitual changes as the primary intervention to prevent CVD; however, over time, the disease is bound to worsen. This is when secondary interventions come into play, including antihypertensive, anti-lipidemic, anti-anginal, and inotropic drugs. These drugs usually undergo surgical intervention in patients with a much higher risk of heart failure. These therapeutic agents increase the survival rate, decrease the severity of symptoms and the discomfort that comes with them, and increase the overall quality of life. However, most individuals succumb to this disease. None of these treatments address the molecular mechanism of the disease and hence are unable to halt the pathological worsening of the disease. Gene therapy offers a more efficient, potent, and important novel approach to counter the disease, as it has the potential to permanently eradicate the disease from the patients and even in the upcoming generations. However, this therapy is associated with significant risks and ethical considerations that pose noteworthy resistance. In this review, we discuss various methods of gene therapy for cardiovascular disorders and address the ethical conundrum surrounding it.]]></description> </item><item><title><![CDATA[Exosome and Other Extracellular Vesicles in Gene Therapy and
Personalized Care]]></title><link>https://www.benthamscience.comarticle/137616</link><description><![CDATA[Exosomes and other extracellular vesicles (EVs) have emerged as versatile agents facilitating cell-to-cell communication, assuming pivotal roles in both physiological and pathological contexts. This manuscript presents an extensive overview of the existing knowledge concerning the utilization of exosomes and EVs in gene therapy and personalized healthcare. It delves into their inherent capacity for transferring genetic material, their limited immunogenicity, and their potential for precise and targeted delivery. Furthermore, the paper investigates the ever-evolving domain of biomarker discovery, where exosomes and EVs hold substantial promise for the early detection of diseases and the monitoring of treatment responses. As ongoing research advances, the manuscript explores the potential for refining protocols related to standardization and quality control, along with the optimization of scalable manufacturing methods. Additionally, the manuscript sheds light on the burgeoning potential for individualized treatments driven by genomic profiling. By examining these facets, we foresee that exosomes and EVs will play a pioneering role in ushering in a new era of precision medicine, offering safer, more efficacious, and highly customized therapeutic interventions across a spectrum of medical conditions.]]></description> </item><item><title><![CDATA[The Therapeutic Application of Hydrogen in Cancer: The Potential and
Challenges]]></title><link>https://www.benthamscience.comarticle/139804</link><description><![CDATA[Hydrogen therapy has emerged as a possible approach for both preventing and treating cancer. Cancers are often associated with oxidative stress and chronic inflammation. Hydrogen, with its unique physiological functions and characteristics, exhibits antioxidant, anti-inflammatory, and anti-apoptotic properties, making it an attractive candidate for cancer treatment. Through its ability to mitigate oxidative damage, modulate inflammatory responses, and sustain cellular viability, hydrogen demonstrates significant potential in preventing cancer recurrence and improving treatment outcomes. Preclinical studies have shown the efficacy of hydrogen therapy in several cancer types, highlighting its ability to enhance the effectiveness of conventional treatments while reducing associated side effects. Furthermore, hydrogen therapy has been found to be safe and well-tolerated in clinical settings. Nonetheless, additional investigations are necessary to improve a comprehensive understanding of the mechanisms underlying hydrogen's therapeutic potential and refine the administration and dosage protocols. However, further clinical trials are still needed to explore its safety profile and capacity. In aggregate, hydrogen therapy represents an innovative and promising treatment for several malignancies.]]></description> </item><item><title><![CDATA[Exploring the Theranostic Applications and Prospects of Nanobubbles]]></title><link>https://www.benthamscience.comarticle/135194</link><description><![CDATA[Anticancer medications as well as additional therapeutic compounds, have poor clinical effectiveness due to their diverse distribution, non-selectivity for malignant cells, and undesirable off-target side effects. As a result, ultrasound-based targeted delivery of therapeutic compounds carried in sophisticated nanocarriers has grown in favor of cancer therapy and control. Nanobubbles are nanoscale bubbles that exhibit unique physiochemical properties in both their inner core and outer shell. Manufacturing nanobubbles primarily aims to enhance therapeutic agents' bioavailability, stability, and targeted delivery. The small size of nanobubbles allows for their extravasation from blood vessels into surrounding tissues and site-specific release through ultrasound targeting. Ultrasound technology is widely utilized for therapy due to its speed, safety, and cost-effectiveness, and micro/nanobubbles, as ultrasound contrast agents, have numerous potential applications in disease treatment. Thus, combining ultrasound applications with NBs has recently demonstrated increased localization of anticancer molecules in tumor tissues with triggered release behavior. Consequently, an effective therapeutic concentration of drugs/genes is achieved in target tumor tissues with ultimately increased therapeutic efficacy and minimal side effects on other non-cancerous tissues. This paper provides a brief overview of the production processes for nanobubbles, along with their key characteristics and potential therapeutic uses.]]></description> </item><item><title><![CDATA[Molecular Mechanisms of Medicinal Plant <i>Securinega suffruticosa</i>-derived
Compound Securinine against Spinal Muscular Atrophy based on Network
Pharmacology and Experimental Verification]]></title><link>https://www.benthamscience.comarticle/139441</link><description><![CDATA[<p>Background: Spinal Muscular Atrophy (SMA) is a severe motor neuronal disorder with high morbidity and mortality. Securinine has shown the potential to treat SMA; however, its anti-SMA role remains unclear. <p> Objective: This study aims to reveal the anti-SMA mechanisms of securinine. <p> Methods: Securinine-associated targets were acquired from Herbal Ingredients' Targets (HIT), Similarity Ensemble Approach (SEA), and SuperPred. SMA-associated targets were obtained from GeneCards and Dis- GeNET. Protein-protein Interaction (PPI) network was constructed using GeneMANIA, and hug targets were screened using cytoHubba. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed using ClusterProfifiler. Molecular docking was conducted using Pymol and Auto- Dock. In vitro assays were used to verify the anti-SMA effects of securinine. <p> Results: Twenty-six intersection targets of securinine and SMA were obtained. HDAC1, HDAC2, TOP2A, PIK3R1, PRMT5, JAK2, HSP90AB1, TERT, PTGS2, and PAX8 were the core targets in PPI network. GO analysis demonstrated that the intersecting targets were implicated in the regulation of proteins, steroid hormones, histone deacetylases, and DNA transcription. KEGG analysis, pathway-pathway, and hub target-pathway networks revealed that securinine might treat SMA through TNF, JAK-STAT, Ras, and PI3K-Akt pathways. Securinine had a favorable binding affinity with HDAC1, HSP90AB, JAK2, PRMT5, PTGS2, and TERT. Securinine rescued viability suppression, mitochondria damage, and SMN loss in the SMA cell model. Furthermore, securinine increased HDAC1 and PRMT5 expression, decreased PTGS2 expression, suppressed the JAK2-STAT3 pathway, and promoted the PI3K-Akt pathway. <p> Conclusion: Securinine might alleviate SMA by elevating HDAC1 and PRMT5 expression and reducing PTGS2 via JAK2-STAT3 suppression and PI3K-Akt activation.</p>]]></description> </item><item><title><![CDATA[Tabersonine Induces the Apoptosis of Human Hepatocellular Carcinoma <i>In vitro</i> and
<i>In vivo</i>]]></title><link>https://www.benthamscience.comarticle/139018</link><description><![CDATA[<p> Background: Tabersonine, a natural indole alkaloid derived from Apocynaceae plants, exhibits antiinflammatory and acetylcholinesterase inhibitory activities, among other pharmacological effects. However, its anti-tumor properties and the underlying molecular mechanisms remain underexplored. <p> Objective: The present study aims to investigate the anti-tumor effects of tabersonine and its mechanisms in inducing apoptosis in hepatocellular carcinoma. <p> Methods: The inhibitory effects of tabersonine on the viability and proliferation of liver cancer cells were evaluated using MTT assay and colony formation assay. AO/EB, Hoechst, and Annexin V-FITC/ PI staining techniques were employed to observe cell damage and apoptosis. JC-1 staining was used to detect changes in mitochondrial membrane potential. Western blot analysis was conducted to study the anti-tumor mechanism of tabersonine on liver cancer cells. Additionally, a xenograft model using mice hepatoma HepG2 cells was established to assess the anti-tumor potency of tabersonine <i>in vivo</i>. <p> Results and Discussion: Our findings revealed that tabersonine significantly inhibited cell viability and proliferation, inducing apoptosis in liver cancer cells. Treatment with tabersonine inhibited Akt phosphorylation, reduced mitochondrial membrane potential, promoted cytochrome c release from mitochondria to the cytoplasm, and increased the ratio of Bax to Bcl-2. These findings suggested that tabersonine induces apoptosis in liver cancer cells through the mitochondrial pathway. Furthermore, tabersonine treatment activated the death receptor pathway of apoptosis. <i>In vivo</i> studies demonstrated that tabersonine significantly inhibited xenograft tumor growth. <p> Conclusion: Our study is the first to demonstrate that tabersonine induces apoptosis in HepG2 cells through both mitochondrial and death receptor apoptotic pathways, suggesting its potential as a therapeutic agent candidate for hepatic cancer.</p>]]></description> </item><item><title><![CDATA[An Investigation into the Effects of Chemical, Pharmaceutical, and
Herbal Compounds on Neuroglobin: A Literature Review]]></title><link>https://www.benthamscience.comarticle/130913</link><description><![CDATA[Neuroglobin (Ngb) is an oxygen-binding globin protein that is mainly expressed in the neurons of the central and peripheral nervous system. However, moderate levels of Ngb have also been detected in non-neural tissues. Ngb and Ngb modulating factors have been increasingly studied over the last decade due to their neuroprotective role in neurological disorders and hypoxia. Studies have shown that a number of chemicals, pharmaceuticals, and herbal compounds can modulate the expression of Ngb at different dose levels, indicating a protective role against neurodegenerative diseases. Iron chelators, hormones, antidiabetic drugs, anticoagulants, antidepressants, plant derivatives and short-chain fatty acids are among these compounds. Therefore, this study aimed to review the literature focused on the possible effects and mechanisms of chemical, pharmaceutical, and herbal compounds on Ngbs.]]></description> </item><item><title><![CDATA[Biology of Tenascin C and its Role in Physiology and Pathology]]></title><link>https://www.benthamscience.comarticle/130686</link><description><![CDATA[Tenascin-C (TNC) is a multimodular extracellular matrix (ECM) protein hexameric with several molecular forms (180-250 kDa) produced by alternative splicing at the pre-mRNA level and protein modifications. The molecular phylogeny indicates that the amino acid sequence of TNC is a well-conserved protein among vertebrates. TNC has binding partners, including fibronectin, collagen, fibrillin-2, periostin, proteoglycans, and pathogens. Various transcription factors and intracellular regulators tightly regulate TNC expression. TNC plays an essential role in cell proliferation and migration. Unlike embryonic tissues, TNC protein is distributed over a few tissues in adults. However, higher TNC expression is observed in inflammation, wound healing, cancer, and other pathological conditions. It is widely expressed in a variety of human malignancies and is recognized as a pivotal factor in cancer progression and metastasis. Moreover, TNC increases both pro-and anti-inflammatory signaling pathways. It has been identified as an essential factor in tissue injuries such as damaged skeletal muscle, heart disease, and kidney fibrosis. This multimodular hexameric glycoprotein modulates both innate and adaptive immune responses regulating the expression of numerous cytokines. Moreover, TNC is an important regulatory molecule that affects the onset and progression of neuronal disorders through many signaling pathways. We provide a comprehensive overview of the structural and expression properties of TNC and its potential functions in physiological and pathological conditions.]]></description> </item><item><title><![CDATA[Novel Biomaterials Based Strategies for Neurodegeneration: Recent
Advancements and Future Prospects]]></title><link>https://www.benthamscience.comarticle/137565</link><description><![CDATA[Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, pose significant challenges for effective treatment due to the complex nature of the central nervous system and the limited delivery of therapeutic agents to the brain. Biomaterial-based drug delivery systems offer promising strategies to overcome these challenges and improve therapeutic outcomes. These systems utilize various biomaterials, such as nanoparticles, hydrogels, and implants, to deliver drugs, genes, or cells to the affected regions of the brain. They provide advantages such as targeted delivery, controlled release, and protection of therapeutic agents. This review examines the role of biomaterials in drug delivery for neurodegeneration, discussing different biomaterialbased approaches, including surface modification, encapsulation, and functionalization techniques. Furthermore, it explores the challenges, future perspectives, and potential impact of biomaterialbased drug delivery systems in the field of neurodegenerative diseases.]]></description> </item><item><title><![CDATA[Purinergic Signaling and its Role in the Stem Cell Differentiation]]></title><link>https://www.benthamscience.comarticle/135145</link><description><![CDATA[Purinergic signaling is a mechanism in which extracellular purines and pyrimidines interact with specialized cell surface receptors known as purinergic receptors. These receptors are divided into two families of P1 and P2 receptors, each responding to different nucleosides and nucleotides. P1 receptors are activated by adenosine, while P2 receptors are activated by pyrimidine and purines. P2X receptors are ligand-gated ion channels, including seven subunits (P2X1-7). However, P2Y receptors are the G-protein coupled receptors comprising eight subtypes (P2Y1/2/4/6/11/12/13/14). The disorder in purinergic signaling leads to various health-related issues and diseases. In various aspects, it influences the activity of non-neuronal cells and neurons. The molecular mechanism of purinergic signaling provides insight into treating various human diseases. On the contrary, stem cells have been investigated for therapeutic applications. Purinergic signaling has shown promising effect in stem cell engraftment. The immune system promotes the autocrine and paracrine mechanisms and releases the significant factors essential for successful stem cell therapy. Each subtype of purinergic receptor exerts a beneficial effect on the damaged tissue. The most common effect caused by purinergic signaling is the proliferation and differentiation that treat different health-related conditions.]]></description> </item><item><title><![CDATA[Advances in the Treatment of Kidney Disorders using Mesenchymal Stem Cells]]></title><link>https://www.benthamscience.comarticle/139152</link><description><![CDATA[Renal disease is a medical condition that poses a potential threat to the life of an individual and is related to substantial morbidity and mortality rates in clinical environments. The aetiology of this condition is influenced by multiple factors, and its incidence tends to increase with progressive aging. Although supportive therapy and kidney transplantation have potential advantages, they also have limitations in terms of mitigating the progression of KD. Despite significant advancements in the domain of supportive therapy, mortality rates in patients continue to increase. Due to their ability to self-renew and multidirectionally differentiate, stem cell therapy has been shown to have tremendous potential in the repair of the diseased kidney. MSCs (Mesenchymal stem cells) are a cell population that is extensively distributed and can be located in various niches throughout an individual's lifespan. The cells in question are characterised by their potential for indefinite replication and their aptitude for undergoing differentiation into fully developed cells of mesodermal origin under laboratory conditions. It is essential to emphasize that MSCs have demonstrated a favorable safety profile and efficacy as a therapeutic intervention for renal diseases in both preclinical as well as clinical investigations. MSCs have been found to slow the advancement of kidney disease, and this impact is thought to be due to their control over a number of physiological processes, including immunological response, tubular epithelial- mesenchymal transition, oxidative stress, renal tubular cell death, and angiogenesis. In addition, MSCs demonstrate recognised effectiveness in managing both acute and chronic kidney diseases via paracrine pathways. The proposal to utilise a therapy that is based on stem-cells as an effective treatment has been put forward in search of discovering novel therapies to promote renal regeneration. Preclinical researchers have demonstrated that various types of stem cells can provide advantages in acute and chronic kidney disease. Moreover, preliminary results from clinical trials have suggested that these interventions are both safe and well-tolerated. This manuscript provides a brief overview of the potential renoprotective effects of stem cell-based treatments in acute as well as chronic renal dysfunction. Furthermore, the mechanisms that govern the process of kidney regeneration induced by stem cells are investigated. This article will examine the therapeutic approaches that make use of stem cells for the treatment of kidney disorders. The analysis will cover various cellular sources that have been utilised, potential mechanisms involved, and the outcomes that have been achieved so far.]]></description> </item><item><title><![CDATA[Design Aspects of Lower Limb Exoskeleton]]></title><link>https://www.benthamscience.comarticle/136517</link><description><![CDATA[<p>Aim: This research work aimed at the design, simulation, and validation of a lower limb exoskeleton for rehabilitation. The device can provide regressive gait training for patients suffering from lower limb mobility disorders. <p> Background: People suffering from mobility disorders, such as spinal cord injuries, and other related diseases are in high proportion. Exoskeletons play a vital role in enhancing the lifestyle of people with disorders. Devices that provide locomotion assistance and help in reducing the burden of therapists through effective and repetitive gait training are in high demand. Exoskeletons have further extended to the fields of the military to enhance the performance of physically abled persons. Prototype development of lower limb exoskeletons is too expensive and many of them are patented. The requirement for this system to perform human trials is subjective to several medical and ethical norms. Thus, there exists a need to evaluate and validate the exoskeleton designs. <p> Methods: In this work, the design has been made inclusive of different body shapes and sizes. The device has been modeled in SOLIDWORKS and its structural integrity has been analyzed using the ANSYS software. Later, the model has been subjected to environmental assessment and then motion analysis using the ADAMS software. <p> Results: The structural integrity analysis has revealed the design to be adequate to carry the applied load as the stresses induced were less than the yield strength of the material. The sustainability analysis showed that LLE made of aluminium alloy had less impact on the environment relative to the other two materials. <p> Conclusion: The kinematic simulation revealed that the angular amplitudes, the reaction force of the right hip and knee joint, and the contact force between the shoe and the ground of the exoskeleton agreed well with the experimental findings of the literature.</p>]]></description> </item><item><title><![CDATA[The Effect of Transcranial Photobiomodulation for Motor Performance
Improvement in Patients with Brain Disorders]]></title><link>https://www.benthamscience.comarticle/136467</link><description><![CDATA[<p>Background: Transcranial photobiomodulation (PBM) therapy has emerged as a promising alternative therapeutic option for the management of neurological and psychiatric disorders. However, the underlying mechanisms of PBM therapy and its effects on motor performance in brain disorders are not yet fully understood. The aim of this literature review is to provide a more detailed and evidence-based explanation of the rationale and intent behind the correlation between PBM therapy and its effects on motor performance in brain disorders. <p> Methods: A literature search was performed in the databases \"PubMed/Medline\", \"Scopus,\" and \"Google Scholar\" for all relevant English language papers. A combination of different keywords was used for the database search. Video articles, patents, review articles, book chapters, articles using other transcranial methods, non-transcranial PBM, and case reports were excluded. <p> Results: Out of the 2174 papers, 18 addressed the effect of PBM on motor performance. Among these, four studies were on ischemic stroke models and individuals with stroke, six studies on models associated with traumatic brain injury (TBI), five studies on models associated with neurodegenerative diseases and Parkinson's disease, and four studies related to models and patients with central nervous system inflammation. All studies have shown that motor parameters improve with PBM. In two studies on healthy individuals, 65 showed improvement in motor function and 16 showed improvement in motor evoked potential. In most studies (n=10), the wavelength used was between 800 and 900 nm. Near-infrared or LED continuous light was used in most studies. However, two studies compared the effects of pulsed and continuous waves and found the superiority of pulsed over continuous waves. <p> Conclusions: PBM therapy appears to be useful in brain injury, inducing changes at the behavioral, motor, cellular, and chemical levels. Recent studies suggest that PBM therapy may have potential benefits in improving motor performance in brain disorders, including stroke, traumatic brain injury, Parkinson's disease, and demyelination. However, further research is needed to determine the optimal parameters for PBM therapy and to investigate its effects on motor function in different brain disorders. Overall, PBM therapy appears to be a promising therapeutic option for brain injury and warrants further investigation.</p>]]></description> </item><item><title><![CDATA[Undiagnosed Intra-articular Synovial Hemangioma: A Rare Cause of
Knee Pain and Swelling]]></title><link>https://www.benthamscience.comarticle/136914</link><description><![CDATA[<p>Introduction: Synovial hemangioma is a benign soft-tissue tumor of vascular origin. Hemangioma only accounts for 1% of all bone lesions and is mostly an incidental finding among the primary skeleton tumors. A delay in diagnosis results in joint degeneration and osteoarthritic damage because of infiltrating tumor growth. <p> Case Presentation: We presented a rare case of an intra-articular synovial hemangioma in a 13- year-old pediatric patient who was asymptomatic for 5 years. She attended orthopedics OPD at AIIMS, Mangalagiri. Surgical excision of the mass and partial synovectomy was done. Synovial hemangioma came out to be the diagnosis following a histologic study. <p> Conclusion: As radiography has limited diagnostic ability, synovial hemangiomas are difficult and challenging to identify on an outpatient basis. Histological examination and magnetic resonance imaging are extremely helpful. To minimize the hemarthrosis risks, early complete excision can be used as the best treatment modality.</p>]]></description> </item><item><title><![CDATA[P-coumaric Acid: Advances in Pharmacological Research Based on
Oxidative Stress]]></title><link>https://www.benthamscience.comarticle/137935</link><description><![CDATA[P-coumaric acid is an important phenolic compound that is mainly found in fruits, vegetables, grains, and fungi and is also abundant in Chinese herbal medicines. In this review, the pharmacological research progress of p-coumaric acid in recent years was reviewed, with emphasis on its role and mechanism in oxidative stress-related diseases, such as inflammation, cardiovascular diseases, diabetes, and nervous system diseases. Studies have shown that p-coumaric acid has a positive effect on the prevention and treatment of these diseases by inhibiting oxidative stress. In addition, p-coumaric acid also has anti-tumor, antibacterial, anti-aging skin and other pharmacological effects. This review will provide reference and inspiration for further research on the pharmacological effects of p-coumaric acid.]]></description> </item><item><title><![CDATA[Exosome-mediated Repair of Intervertebral Disc Degeneration: The
Potential Role of miRNAs]]></title><link>https://www.benthamscience.comarticle/131458</link><description><![CDATA[Intervertebral disc degeneration (IVDD) is a serious condition that manifests as low back pain, intervertebral disc protrusion, and spinal canal stenosis. At present, the main treatment methods for IVDD are surgical interventions such as discectomy, total disc replacement, and spinal fusion. However, these interventions have shown limitations, such as recurrent lumbar disc herniation after discectomy, lesions in adjacent segments, and failure of fixation. To overcome these shortcomings, researchers have been exploring stem cell transplantation therapy, such as mesenchymal stem cell (MSC) transplantation, but the treatment results are still controversial. Therefore, researchers are in search of new methods that are more efficient and have better outcomes. The exosomes from stem cells contain a variety of bioactive molecules that mediate cell interactions, and these components have been investigated for their potential therapeutic role in the repair of various tissue injuries. Recent studies have shown that MSC-derived miRNAs in exosomes and vesicles have therapeutic effects on nucleus pulposus cells, annulus fibrosus, and cartilage endplate. miRNAs play a role in many cell activities, such as cell proliferation, apoptosis, and cytokine release, by acting on mRNA translation, and they may have immense therapeutic potential, especially when combined with stem cell therapy. This article reviews the current status of research on intervertebral disc repair, especially with regard to the latest research findings on the molecular biological mechanisms of miRNAs in MSC-derived exosomes in intervertebral disc repair.]]></description> </item><item><title><![CDATA[Identification and Validation of Synapse-related Hub Genes after Spinal
Cord Injury by Bioinformatics Analysis]]></title><link>https://www.benthamscience.comarticle/131223</link><description><![CDATA[<p>Background: Spinal cord injury (SCI) is a neurological disease with high morbidity and mortality. Previous studies have shown that abnormally expressed synapse-related genes are closely related to the occurrence and development of SCI. However, little is known about the interaction of these aberrantly expressed genes and the molecular mechanisms that play a role in the injury response. Therefore, deeply exploring the correlation between synapse-related genes and functional recovery after spinal cord injury and the molecular regulation mechanism is of great significance. <p> Methods: First, we selected the function GSE45006 dataset to construct three clinically meaningful gene modules by hierarchical clustering analysis in 4 normal samples and 20 SCI samples. Subsequently, we performed functional and pathway enrichment analyses of key modules. <p> Results: The results showed that related module genes were significantly enriched in synaptic structures and functions, such as the regulation of synaptic membranes and membrane potential. A protein-protein interaction network (PPI) was constructed to identify 10 hub genes of SCI, and the results showed that Snap25, Cplx1, Stxbp1, Syt1, Rims1, Rab3a, Syn2, Syn1, Cask, Lin7b were most associated with SCI. Finally, these hub genes were further verified by quantitative real-time fluorescence polymerase chain reaction (qRT-PCR) in the spinal cord tissues of the blank group and SCI rats, and it was found that the expression of these hub genes was significantly decreased in the spinal cord injury compared with the blank group (P ≤ 0.05). <p> Conclusion: These results suggest that the structure and function of synapses play an important role after spinal cord injury. Our study helps to understand the underlying pathogenesis of SCI patients further and identify new targets for SCI treatment.</p>]]></description> </item><item><title><![CDATA[Unlocking the Benefits of Fasting: A Review of its Impact on Various
Biological Systems and Human Health]]></title><link>https://www.benthamscience.comarticle/136295</link><description><![CDATA[Fasting has gained significant attention in recent years for its potential health benefits in various body systems. This review aims to comprehensively examine the effects of fasting on human health, specifically focusing on its impact on different body’s physiological systems. The cardiovascular system plays a vital role in maintaining overall health, and fasting has shown promising effects in improving cardiovascular health markers such as blood pressure, cholesterol levels, and triglyceride levels. Additionally, fasting has been suggested to enhance insulin sensitivity, promote weight loss, and improve metabolic health, thus offering potential benefits to individuals with diabetes and metabolic disorders. Furthermore, fasting can boost immune function, reduce inflammation, enhance autophagy, and support the body's defense against infections, cancer, and autoimmune diseases. Fasting has also demonstrated a positive effect on the brain and nervous system. It has been associated with neuroprotective properties, improving cognitive function, and reducing the risk of neurodegenerative diseases, besides the ability of increasing the lifespan. Hence, understanding the potential advantages of fasting can provide valuable insights for individuals and healthcare professionals alike in promoting health and wellbeing. The data presented here may have significant implications for the development of therapeutic approaches and interventions using fasting as a potential preventive and therapeutic strategy.]]></description> </item><item><title><![CDATA[Drugs to Treat Neuroinflammation in Neurodegenerative Disorders]]></title><link>https://www.benthamscience.comarticle/130673</link><description><![CDATA[Neuroinflammation is associated with disorders of the nervous system, and it is induced in response to many factors, including pathogen infection, brain injury, toxic substances, and autoimmune diseases. Astrocytes and microglia have critical roles in neuroinflammation. Microglia are innate immune cells in the central nervous system (CNS), which are activated in reaction to neuroinflammation-inducing factors. Astrocytes can have pro- or anti-inflammatory responses, which depend on the type of stimuli presented by the inflamed milieu. Microglia respond and propagate peripheral inflammatory signals within the CNS that cause low-grade inflammation in the brain. The resulting alteration in neuronal activities leads to physiological and behavioral impairment. Consequently, activation, synthesis, and discharge of various pro-inflammatory cytokines and growth factors occur. These events lead to many neurodegenerative conditions, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis discussed in this study. After understanding neuroinflammation mechanisms and the involvement of neurotransmitters, this study covers various drugs used to treat and manage these neurodegenerative illnesses. The study can be helpful in discovering new drug molecules for treating neurodegenerative disorders.]]></description> </item><item><title><![CDATA[Triazolopyrimidine Derivatives: An Updated Review on Recent
Advances in Synthesis, Biological Activities and Drug Delivery Aspects]]></title><link>https://www.benthamscience.comarticle/129883</link><description><![CDATA[Molecules containing triazolopyrimidine core showed diverse biological activities, including anti-Alzheimer's, anti-diabetes, anti-cancer, anti-microbial, anti-tuberculosis, anti-viral, anti-malarial, anti-inflammatory, anti-parkinsonism, and anti-glaucoma activities. Triazolopyrimidines have 8 isomeric structures, including the most stable 1,2,4-triazolo[1,5- a] pyrimidine ones. Triazolopyrimidines were obtained by using various chemical reactions, including a) 1,2,4-triazole nucleus annulation to pyrimidine, b) pyrimidines annulation to 1,2,4-triazole structure, c) 1,2,4-triazolo[l,5-a] pyrimidines rearrangement, and d) pyrimidotetrazine rearrangement. This review discusses synthetic methods, recent pharmacological actions and drug delivery perspectives of triazolopyrimidines.]]></description> </item><item><title><![CDATA[Advances in the Treatment of Autism Spectrum Disorder: Current
and Promising Strategies]]></title><link>https://www.benthamscience.comarticle/134856</link><description><![CDATA[Autism spectrum disorder (ASD) is an umbrella term for developmental disorders characterized by social and communication impairments, language difficulties, restricted interests, and repetitive behaviors. Current management approaches for ASD aim to resolve its clinical manifestations based on the type and severity of the disability. Although some medications like risperidone show potential in regulating ASD-associated symptoms, a comprehensive treatment strategy for ASD is yet to be discovered. To date, identifying appropriate therapeutic targets and treatment strategies remains challenging due to the complex pathogenesis associated with ASD. Therefore, a comprehensive approach must be tailored to target the numerous pathogenetic pathways of ASD. From currently viable and basic treatment strategies, this review explores the entire field of advancements in ASD management up to cutting-edge modern scientific research. A novel systematic and personalized treatment approach is suggested, combining the available medications and targeting each symptom accordingly. Herein, summarize and categorize the most appropriate ways of modern ASD management into three distinct categories: current, promising, and prospective strategies.]]></description> </item><item><title><![CDATA[Spinal Muscular Atrophy Treatment: The MTOR Regulatory
Intervention]]></title><link>https://www.benthamscience.comarticle/129454</link><description><![CDATA[Spinal muscular atrophy (SMA) is a hereditary disorder affecting neurons and muscles, resulting in muscle weakness and atrophy. Most SMA cases are diagnosed during infancy or early childhood, the most common inherited cause of infant mortality without treatment. Still, SMA might appear at older ages with milder symptoms. SMA patients demonstrate progressive muscle waste, movement problems, tremors, dysphagia, bone and joint deformations, and breathing difficulties. The mammalian target of rapamycin (mTOR), the mechanistic target of rapamycin, is a member of the phosphatidylinositol 3-kinase-related kinase family of protein kinases encoded by the mTOR gene in humans. The mTOR phosphorylation, deregulation, and autophagy have shown dissimilarity amongst SMA cell types. Therefore, exploring the underlying molecular process in SMA therapy could provide novel insights and pave the way for finding new treatment options. This paper provides new insight into the possible modulatory effect of mTOR/ autophagy in SMA management.]]></description> </item><item><title><![CDATA[A New Paradigm in Spinal Cord Injury Therapy: from Cell-free
Treatment to Engineering Modifications]]></title><link>https://www.benthamscience.comarticle/131045</link><description><![CDATA[Spinal cord injury (SCI) is an intractable and poorly prognostic neurological disease, and current treatments are still unable to cure it completely and avoid sequelae. Extracellular vesicles (EVs), as important carriers of intercellular communication and pharmacological effects, are considered to be the most promising candidates for SCI therapy because of their low toxicity and immunogenicity, their ability to encapsulate endogenous bioactive molecules (e.g., proteins, lipids, and nucleic acids), and their ability to cross the blood-brain/cerebrospinal barriers. However, poor targeting, low retention rate, and limited therapeutic efficacy of natural EVs have bottlenecked EVs-based SCI therapy. A new paradigm for SCI treatment will be provided by engineering modified EVs. Furthermore, our limited understanding of the role of EVs in SCI pathology hinders the rational design of novel EVbased therapeutic approaches. In this study, we review the pathophysiology after SCI, especially the multicellular EVs-mediated crosstalk; briefly describe the shift from cellular to cell-free therapies for SCI treatment; discuss and analyze the issues related to the route and dose of EVs administration; summarize and present the common strategies for EVs drug loading in the treatment of SCI and point out the shortcomings of these drug loading methods; finally, we analyze and highlight the feasibility and advantages of bio-scaffold-encapsulated EVs for SCI treatment, providing scalable insights into cell-free therapy for SCI.]]></description> </item><item><title><![CDATA[Soluble Factors Associated with Denervation-induced Skeletal Muscle
Atrophy]]></title><link>https://www.benthamscience.comarticle/136298</link><description><![CDATA[Skeletal muscle tissue has the critical function of mechanical support protecting the body. In addition, its functions are strongly influenced by the balanced synthesis and degradation processes of structural and regulatory proteins. The inhibition of protein synthesis and/or the activation of catabolism generally determines a pathological state or condition called muscle atrophy, a reduction in muscle mass that results in partial or total loss of function. It has been established that many pathophysiological conditions can cause a decrease in muscle mass. Skeletal muscle innervation involves stable and functional neural interactions with muscles <i>via</i> neuromuscular junctions and is essential for maintaining normal muscle structure and function. Loss of motor innervation induces rapid skeletal muscle fiber degeneration with activation of atrophy-related signaling and subsequent disassembly of sarcomeres, altering normal muscle function. After denervation, an inflammation stage is characterized by the increased expression of pro-inflammatory cytokines that determine muscle atrophy. In this review, we highlighted the impact of some soluble factors on the development of muscle atrophy by denervation.]]></description> </item><item><title><![CDATA[A State-of-the-Art Review on Opioids Induced Constipation and its
Management]]></title><link>https://www.benthamscience.comarticle/126110</link><description><![CDATA[<p>Background: Pain is a complex physiological and psychological response to a noxious stimulus, sometimes deteriorating a patient’s quality of life. Opioids remain the mainstay treatment modality for chronic pain. Several concerns are raised regarding the long-term use of opioids and the risks associated with their usage. Findings advocate that the longstanding practice of opioid consumption manifests in adverse effects. Objective: Due to the physiological changes opioids instigate in the gastrointestinal tract, opioid-induced constipation remains a common complication pragmatic in patients undergoing opioid medications. Several therapeutic interventions are made available, and the review describes the overall medications with practical examples, aiding in selecting a treatment plan. <p> Methods: The method comprises data collection from various search engines like PubMed, ScienceDirect, and SciFinder to get coverage of relevant literature for accumulating appropriate information regarding pain management, opioids, opioid-induced constipation, and its pharmacological interventions. <p> Results: The thoughtful custom of exploring several options to manage opioid-induced constipation must allow patients to benefit from opioid analgesia. <p> Conclusion: This paper reviews the role of opioids in pain management, the underlying mechanisms of their action, opioid-induced constipation, and pharmacological therapies, with experimental studies aiding clinicians to optimise treatment plans.</p>]]></description> </item><item><title><![CDATA[Unfolded Protein Response Signaling in Hepatic Stem Cell Activation in
Liver Fibrosis]]></title><link>https://www.benthamscience.comarticle/133898</link><description><![CDATA[Frequent exposure to various external and internal adverse forces (stresses) disrupts cell protein homeostasis through endoplasmic reticulum (ER) capacity saturation. This process leads to the unfolded protein response (UPR), which aims to re-establish/maintain optimal cellular equilibrium. This complex mechanism is involved in the pathogenesis of various disorders, such as metabolic syndrome, fibrotic diseases, neurodegeneration, and cancer, by altering cellular metabolic changes integral to activating the hepatic stellate cells (HSCs). The development of hepatic fibrosis is one of the consequences of UPR activation. Therefore, novel therapies that target the UPR pathway effectively and specifically are being studied. This article covers the involvement of the UPR signaling pathway in cellular damage in liver fibrosis. Investigating the pathogenic pathways related to the ER/UPR stress axis that contribute to liver fibrosis can help to guide future drug therapy approaches.]]></description> </item><item><title><![CDATA[The Effect of Statins on the Differentiation and Function of Central
Nervous System Cells]]></title><link>https://www.benthamscience.comarticle/130056</link><description><![CDATA[Statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) reduce plasma cholesterol and improve endothelium-dependent vasodilation, inflammation, and oxidative stress. The effect of statins on the central nervous system (CNS), particularly on cognition and neurological disorders such as cerebral ischemic stroke, multiple sclerosis (MS), and Alzheimer’s disease (AD), has received increasing attention in recent years, both within the scientific community and in the media. This review aims to provide an updated discussion on the effects of statins on the differentiation and function of various nervous system cells, including neurons and glial cells. Additionally, the mechanisms of action and how different types of statins enter the CNS will be discussed.]]></description> </item><item><title><![CDATA[Structure-Activity Relationships and Therapeutic Potential of
Purinergic P2X7 Receptor Antagonists]]></title><link>https://www.benthamscience.comarticle/130650</link><description><![CDATA[The purinergic P2X7 receptor (P2X7R), an ATP-gated non-selective cation channel, has emerged as a gatekeeper of inflammation that controls the release of proinflammatory cytokines. As a key player in initiating the inflammatory signaling cascade, the P2X7 receptor is currently under intense scrutiny as a target for the treatment of different pathologies, including chronic inflammatory disorders (rheumatoid arthritis and osteoarthritis), chronic neuropathic pain, mood disorders (depression and anxiety), neurodegenerative diseases, ischemia, cancer (leukemia), and many others. For these reasons, pharmaceutical companies have invested in discovering compounds able to modulate the P2X7R and filed many patent applications. This review article presents an account of P2X7R structure, function, and tissue distribution, emphasizing its role in inflammation. Next, we illustrate the different chemical classes of non-competitive P2X7R antagonists reported by highlighting their properties and qualities as clinical candidates for treating inflammatory disorders and neurodegenerative diseases. We also discuss the efforts to develop effective Positron Emission Tomography (PET) radioligands to progress the understanding of the pathomechanisms of neurodegenerative disorders, to provide evidence of drug-target engagement, and to assist clinical dose selection for novel drug therapies.]]></description> </item><item><title><![CDATA[Mechanically Activated Adipose Tissue as a Source for Novel Therapies in
Neurological Disease/Injury]]></title><link>https://www.benthamscience.comarticle/132288</link><description><![CDATA[In this review, we describe a new avenue that involves the therapeutic use of human adipose tissue. In the past two decades, thousands of papers have described the potential clinical use of human fat and adipose tissue. Moreover, mesenchymal stem cells have been a source of great enthusiasm in clinical studies, and these have generated curiosity at academic levels. On the other hand, they have created considerable commercial business opportunities. High expectations have emerged for curing some recalcitrant diseases or reconstructing anatomically defective human body parts, but several concerns have been raised by generating criticism on the clinical practice that have not been substantiated by rigorous scientific evidence. However, in general, the consensus is that human adipose-derived mesenchymal stem cells inhibit the production of inflammatory cytokines and stimulate the production of anti-inflammatory cytokines. Here, we show that the application of a mechanical elliptical force for several minutes to human abdominal fat activates anti-inflammatory properties and gene-related expression. This may pave the way for new unexpected clinical developments.]]></description> </item><item><title><![CDATA[Neuropathy, its Profile and Experimental Nerve Injury Neuropathic Pain Models:
A Review]]></title><link>https://www.benthamscience.comarticle/136534</link><description><![CDATA[Neuropathy is a terrible disorder that has a wide range of etiologies. Drug-induced neuropathy, which happens whenever a chemical agent damages the peripheral nerve system, has been linked here to the iatrogenic creation of some drugs. It is potentially permanent and causes sensory impairments and paresthesia that typically affects the hands, feet, and stockings; motor participation is uncommon. It might appear suddenly or over time, and the long-term outlook varies. The wide range of chronic pain conditions experienced by people has been one of the main obstacles to developing new, more effective medications for the treatment of neuropathic pain. Animal models can be used to examine various neuropathic pain etiologies and symptoms. Several models investigate the peripheral processes of neuropathic pain, whereas some even investigate the central mechanisms, such as drug induce models like vincristine, cisplatin, bortezomib, or thalidomide, etc., and surgical models like sciatic nerve chronic constriction injury (CCI), sciatic nerve ligation through spinal nerve ligation (SNL), sciatic nerve damage caused by a laser, SNI (spared nerve injury), etc. The more popular animal models relying on peripheral nerve ligatures are explained. In contrast to chronic sciatic nerve contraction, which results in behavioral symptoms of less reliable stressful neuropathies, (SNI) spared nerve injury generates behavioral irregularities that are more feasible over a longer period. This review summarizes the latest methods models as well as clinical ideas concerning this mechanism. Every strongest current information on neuropathy is discussed, along with several popular laboratory models for causing neuropathy.]]></description> </item><item><title><![CDATA[Biosensor Detection of COVID-19 in Lung Cancer: Hedgehog and Mucin
Signaling Insights]]></title><link>https://www.benthamscience.comarticle/136678</link><description><![CDATA[Coronavirus disease 2019 is a global pandemic, particularly affecting individuals with pre-existing lung conditions and potentially leading to pulmonary fibrosis. Age and healthcare system limitations further amplify susceptibility to both diseases, especially in low- and middle-income countries. The intricate relationship between Coronavirus disease 2019 and lung cancer highlights their clinical implications and the potential for early detection through biosensor techniques involving hedgehog and mucin signaling. This study highlights the connection between Coronavirus disease 2019 and lung cancer, focusing on the mucosa, angiotensin- altering enzyme 2 receptors, and their impact on the immune system. It details the inflammatory mechanisms triggered by Coronavirus disease 2019, which can result in pulmonary fibrosis and influence the cancer microenvironment. Various cytokines like Interleukins-6 and Tumor Necrosis Factor-alpha are examined for their roles in both diseases. Moreover, the review delves into the Hedgehog signaling pathways and their significance in lung cancer, particularly their influence on embryonic cell proliferation and tissue integrity. Mucin signaling is another vital aspect, highlighting the diverse mucin expression patterns in respiratory epithelial tissues and their potential as biomarkers. The review concludes with insights into diagnostic imaging techniques like chest computed tomography, Positron Emission Tomography and Computed Tomography, and Magnetic Resonance Imaging for early lung cancer detection, emphasizing the crucial role of biosensors in identifying specific biomarkers for early disease detection. This review provides a comprehensive overview of the clinical impact of Coronavirus disease 2019 on lung cancer patients and the potential for biosensors utilizing hedgehog and mucin signaling for early detection. It underscores the ongoing need for research and innovation to address these critical healthcare challenges.]]></description> </item><item><title><![CDATA[Understanding the Therapeutic Approaches for Neuroprotection]]></title><link>https://www.benthamscience.comarticle/136805</link><description><![CDATA[The term “neurodegenerative disorders” refers to a group of illnesses in which deterioration of nerve structure and function is a prominent feature. Cognitive capacities such as memory and decision-making deteriorate as a result of neuronal damage. The primary difficulty that remains is safeguarding neurons since they do not proliferate or regenerate spontaneously and are therefore not substituted by the body after they have been damaged. Millions of individuals throughout the world suffer from neurodegenerative diseases. Various pathways lead to neurodegeneration, including endoplasmic reticulum stress, calcium ion overload, mitochondrial dysfunction, reactive oxygen species generation, and apoptosis. Although different treatments and therapies are available for neuroprotection after a brain injury or damage, the obstacles are inextricably connected. Several studies have revealed the pathogenic effects of hypothermia, different breathed gases, stem cell treatments, mitochondrial transplantation, multi-pharmacological therapy, and other therapies that have improved neurological recovery and survival outcomes after brain damage. The present review highlights the use of therapeutic approaches that can be targeted to develop and understand significant therapies for treating neurodegenerative diseases.]]></description> </item><item><title><![CDATA[The Protective Effect of SLNP on Hepatic Fibrosis Induced by Thioacetamide
in Rats]]></title><link>https://www.benthamscience.comarticle/135830</link><description><![CDATA[<P> Introduction: The incidence of non-alcoholic fatty liver disease (NAFLD) has increased in recent years. Hepatic fibrosis (HF) is an important step in the progression of NAFLD to cirrhosis and even carcinoma and is also recognized as a possible reversal phase. <P> Aims: We previously found that the aqueous extract of Sedum Lineare Thunb. has hepatoprotective effects. This study investigated the hepatoprotective effect and mechanism of the Sedum Lineare Thunb. n-butanol phase (SLNP) on HF in rats. <P> Methods: Animals were intraperitoneally injected with thioacetamide solution twice a week for 8 weeks to prepare an HF model and were administered the corresponding drugs or an equal volume of normal saline by intragastric administration once a day for 8 weeks. Liver function, hydroxyproline and malondialdehyde (MDA) content, superoxide dismutase (SOD), Na<sup>+</sup>-K<sup>+-</sup>ATPase, and Ca<sup>2+</sup>-Mg<sup>2+</sup>-ATPase were analyzed using colorimetric methods. Moreover, mRNA expression and protein levels in the liver tissue were detected via quantitative polymerase chain reaction and western blotting, respectively. <P> Results: The results showed that SLNP could effectively improve the liver function of rats with HF and significantly reduce the content of hydroxyproline; the mRNA expression and protein levels of alpha-smooth muscle actin (α-SMA), collagen I, III, and IV, transforming growth factor beta 1 (TGF-&#946;1), Smad2/3, and Smad4 were also significantly reduced. Simultaneously, SLNP significantly increased the activities of SOD, Na<sup>+</sup>-K<sup>+-</sup> ATPase, and Ca<sup>2+</sup>-Mg<sup>2+</sup>-ATPase in the rat liver tissues, whereas it reduced the levels of MDA and SOD in the serum and liver tissues. <P> Conclusion: This study revealed that SLNP elicits an anti-fibrotic effect by inhibiting oxidative stress and stellate cell activation, thereby reducing the formation and deposition of the extracellular matrix. The TGF-β1/Smads signaling pathway may be involved in this process.</P>]]></description> </item><item><title><![CDATA[Role of Cerium Oxide Nanoparticles and Doxorubicin in Improving Cancer
Management: A Mini Review]]></title><link>https://www.benthamscience.comarticle/135960</link><description><![CDATA[Cancer is one of the significant issues with public health and the second leading cause of death worldwide. The three most lethal cancers in the general population are stomach, lung, and liver cancers, in which lung and breast cancers cause the majority of cancer-associated deaths among men and women, respectively. CeO<sub>2</sub> nanoparticles have a cytoprotectant effect in normal cells and a cytotoxic effect in cancer cells that enables them to induce the reactive oxygen species (ROS) production within cancer cells, which in turn develops reactive nitrogen species (RNS) that interfere with intracellular activities, and this property makes them an excellent anticancer agent. Because of its biofilm suppression, free radical scavenging ability, redox activity, and other unique properties, attention has been bestowed on cerium oxide nanoparticles as a potential alternative to solve many biomedical issues in the future. This review mainly focuses on the combinatorial effect of cerium dioxide nanoparticles and Doxorubicin in cancer management.]]></description> </item><item><title><![CDATA[Insight into Early Diagnosis of Multiple Sclerosis by Targeting Prognostic
Biomarkers]]></title><link>https://www.benthamscience.comarticle/135638</link><description><![CDATA[Multiple sclerosis (MS) is a central nervous system (CNS) immune-mediated disease that mainly strikes young adults and leaves them disabled. MS is an autoimmune illness that causes the immune system to attack the brain and spinal cord. The myelin sheaths, which insulate the nerve fibers, are harmed by our own immune cells, and this interferes with brain signal transmission. Numbness, tingling, mood swings, memory problems, exhaustion, agony, vision problems, and/or paralysis are just a few of the symptoms. Despite technological advancements and significant research efforts in recent years, diagnosing MS can still be difficult. Each patient's MS is distinct due to a heterogeneous and complex pathophysiology with diverse types of disease courses. There is a pressing need to identify markers that will allow for more rapid and accurate diagnosis and prognosis assessments to choose the best course of treatment for each MS patient. The cerebrospinal fluid (CSF) is an excellent source of particular indicators associated with MS pathology. CSF contains molecules that represent pathological processes such as inflammation, cellular damage, and loss of blood-brain barrier integrity. Oligoclonal bands, neurofilaments, MS-specific miRNA, lncRNA, IgG-index, and anti-aquaporin 4 antibodies are all clinically utilised indicators for CSF in MS diagnosis. In recent years, a slew of new possible biomarkers have been presented. In this review, we look at what we know about CSF molecular markers and how they can aid in the diagnosis and differentiation of different MS forms and treatment options, and monitoring and predicting disease progression, therapy response, and consequences during such opportunistic infections.]]></description> </item><item><title><![CDATA[Berberine: Pharmacological Features in Health, Disease and Aging]]></title><link>https://www.benthamscience.comarticle/129343</link><description><![CDATA[<P>Background: Berberine is the main active compound of different herbs and is defined as an isoquinoline quaternary botanical alkaloid found in barks and roots of numerous plants. It exhibits a wide range of pharmacological effects, such as anti-obesity and antidiabetic effects. Berberine has antibacterial activity against a variety of microbiota, including many bacterial species, protozoa, plasmodia, fungi, and trypanosomes. <P> Objective: This review describes the role of berberine and its metabolic effects. It also discusses how it plays a role in glucose metabolism, fat metabolism, weight loss, how it modulates the gut microbiota, and what are its antimicrobial properties along with its potential side effects with maximal tolerable dosage. <P> Methods: Representative studies were considered and analyzed from different scientific databases, including PubMed and Web of Science, for the years 1982-2022. <P> Results: Literature analysis shows that berberine affects many biochemical and pharmacological pathways that theoretically yield a positive effect on health and disease. Berberine exhibits neuroprotective properties in various neurodegenerative and neuropsychological ailments. Despite its low bioavailability after oral administration, berberine is a promising tool for several disorders. A possible hypothesis would be the modulation of the gut microbiome. While the evidence concerning the aging process in humans is more limited, preliminary studies have shown positive effects in several models. <P> Conclusion: Berberine could serve as a potential candidate for the treatment of several diseases. Previous literature has provided a basis for scientists to establish clinical trials in humans. However, for obesity, the evidence appears to be sufficient for hands-on use.</P>]]></description> </item><item><title><![CDATA[Interleukin-17: A Putative Novel Pharmacological Target for Pathological
Pain]]></title><link>https://www.benthamscience.comarticle/133565</link><description><![CDATA[Pathological pain imposes a huge burden on the economy and the lives of patients. At present, drugs used for the treatment of pathological pain have only modest efficacy and are also plagued by adverse effects and risk for misuse and abuse. Therefore, understanding the mechanisms of pathological pain is essential for the development of novel analgesics. Several lines of evidence indicate that interleukin-17 (IL-17) is upregulated in rodent models of pathological pain in the periphery and central nervous system. Besides, the administration of IL-17 antibody alleviated pathological pain. Moreover, IL-17 administration led to mechanical allodynia which was alleviated by the IL-17 antibody. In this review, we summarized and discussed the therapeutic potential of targeting IL-17 for pathological pain. The upregulation of IL-17 promoted the development of pathological pain by promoting neuroinflammation, enhancing the excitability of dorsal root ganglion neurons, and promoting the communication of glial cells and neurons in the spinal cord. In general, the existing research shows that IL-17 is an attractive therapeutic target for pathologic pain, but the underlying mechanisms still need to be investigated.]]></description> </item><item><title><![CDATA[Synthesis and Medicinal Applications of Fenamic Acid Derivatives]]></title><link>https://www.benthamscience.comarticle/134543</link><description><![CDATA[Fenamic acid-derived NSAIDs contain N-phenyl anthranilic acid as a pharmacophore with pKa ~ 4, which is completely ionized at the physiological pH and is mainly excreted in the urine by hydroxylation or glucuronidation. The acid (-COOH) functionality in fenamic acid provides a template for their fenamate derivatization for the development of analogues based on amidation, esterification, and etherification. Besides the repurposing of fenamates as neuroprotective agents in unmodified form, several of their derivatives have been reported for the management of disease pathogenesis by regulating the responsible pathways. In this review, we discuss the chemical modification of fenamic acid and its medicinal chemistry thereof.]]></description> </item><item><title><![CDATA[Central Sensitization and Pain: Pathophysiologic and Clinical Insights]]></title><link>https://www.benthamscience.comarticle/126937</link><description><![CDATA[<p>Central sensitization is an increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input. <p> Aim: To explain how the notion of central sensitization has changed our understanding of pain conditions, discuss how this knowledge can be used to improve the management of pain, and highlight knowledge gaps that future research needs to address. <p> Methods: Overview of definitions, assessment methods, and clinical implications. <p> Results: Human pain models, and functional and molecular imaging have provided converging evidence that central sensitization occurs and is clinically relevant. Measures to assess central sensitization in patients are available; however, their ability to discriminate sensitization of central from peripheral neurons is unclear. Treatments that attenuate central sensitization are available, but the limited understanding of molecular and functional mechanisms hampers the development of target-specific treatments. The origin of central sensitization in human pain conditions that are not associated with tissue damage remains unclear. <p> Conclusion: The knowledge of central sensitization has revolutionized our neurobiological understanding of pain. Despite the limitations of clinical assessment in identifying central sensitization, it is appropriate to use the available tools to guide clinical decisions towards treatments that attenuate central sensitization. Future research that elucidates the causes, molecular and functional mechanisms of central sensitization would provide crucial progress towards the development of treatments that target specific mechanisms of central sensitization.</p>]]></description> </item><item><title><![CDATA[<i>Zingiber officinale</i> Roscoe (Ginger) and its Bioactive Compounds in Diabetes:
A Systematic Review of Clinical Studies and Insight of Mechanism
of Action]]></title><link>https://www.benthamscience.comarticle/132031</link><description><![CDATA[<p>Background: <i>Zingiber officinale Roscoe</i> (Ginger) belongs to the Zingiberaceae family, which is renowned for its rich nutritional and phytochemical composition, and has been validated for its anti-diabetic and anti-inflammatory properties via in vitro, in vivo, and clinical studies. Nonetheless, a comprehensive review of these pharmacological studies, especially clinical studies, together with an analysis of the mechanism of action of the bioactive compounds is still lacking. This review provided a comprehensive and updated analysis of the anti-diabetic efficacy of <i>Z. officinale</i> and its compounds ginger enone, gingerol, paradol, shogaol, and zingerone. </p><p> Methods: The present systematic review was conducted using the PRISMA guidelines. Scopus, ScienceDirect, Google Scholar, and PubMed were the main databases used for retrieving information from inception to March 2022. </p><p> Results: From the findings obtained, <i>Z. officinale</i> can be regarded as a therapeutic species showing significant improvement in clinical studies on glycemic parameters (Fasting blood glucose (FBG), hemoglobin A1C (HbA1c), and insulin resistance). In addition, the bioactive compounds of <i>Z. officinale</i> act <i>via</i> several mechanisms as revealed by <i>in vitro</i> and <i>in vivo</i> studies. Overall, these mechanisms were by increasing glucose-stimulated insulin secretion, sensitising insulin receptors and raising glucose uptake, translocation of GLUT4, inhibition of advanced glycation end product-induced increase of reactive oxygen species, regulation of hepatic gene expression of enzymes associated with glucose metabolism, regulation of the level of pro-inflammatory cytokines, amelioration of the pathological injuries of kidneys, protective effect on the morphology of β-cells as well as its antioxidant mechanisms, among others. </p><p> Conclusion: <i>Z. officinale</i> and its bioactive compounds displayed promising results in <i>in vitro</i> and <i>in vivo</i> systems, nevertheless, it is highly recommended that human trials be conducted on these compounds since clinical studies are the core of medical research and considered the final stages of the drug development process.</p>]]></description> </item><item><title><![CDATA[Perinatal Management of Pregnancies with Fetal Congenital Anomalies:
A Guide to Obstetricians and Pediatricians]]></title><link>https://www.benthamscience.comarticle/126790</link><description><![CDATA[<p>Background: Congenital anomalies are responsible for approximately 20% of all neonatal deaths worldwide. Improvements in antenatal screening and diagnosis have significantly improved the prenatal detection of birth defects; however, these improvements have not translated into the improved neonatal prognosis of babies born with congenital anomalies. <p> Objectives: An attempt has been made to summarise the prenatal interventions, if available, the optimal route, mode and time of delivery and discuss the minimum delivery room preparations that should be made if expecting to deliver a fetus with a congenital anomaly. <p> Methods: The recent literature related to the perinatal management of the fetus with prenatally detected common congenital anomalies was searched in English peer-reviewed journals from the PubMed database to work out an evidence-based approach for their management. <p> Results: Fetuses with prenatally detected congenital anomalies should be delivered at a tertiary care centre with facilities for neonatal surgery and paediatric intensive care if needed. There is no indication for preterm delivery in the majority of cases. Only a few congenital malformations, like highrisk sacrococcygeal teratoma, congenital lung masses with significant fetal compromise, fetal cerebral lesions or neural tube defects with Head circumference >40 cm or the biparietal diameter is ≥12 cm, gastroschisis with extracorporeal liver, or giant omphaloceles in the fetus warrant caesarean section as the primary mode of delivery. <p> Conclusion: The prognosis of a fetus with congenital anomalies can be significantly improved if planning for delivery, including the place and time of delivery, is done optimally. A multidisciplinary team should be available for the fetus to optimize conditions right from when it is born.</p>]]></description> </item><item><title><![CDATA[Therapeutic Potential of Ascorbic Acid in the Management of Alzheimer's
Disease: An Update]]></title><link>https://www.benthamscience.comarticle/133388</link><description><![CDATA[<p>Background: Ascorbic acid is a potent natural antioxidant that protects against oxidative stress and performs various bodily functions. It is commonly found in fruits and vegetables. <p> Objective: The manuscript has been written to provide valuable insights into ascorbic acid in managing Alzheimer's disease. <p> Methods: The data has been gathered from web sources, including PubMed, Science Direct, Publons, Web of Science, and Scopus from 2000-2022 using AA, ascorbic acid, Alzheimer’s diseases, memory, dementia, and antioxidant keywords. <p> Results: In the present manuscript, we have summarized the impact of ascorbic acid and its possible mechanism in Alzheimer's disease by, outlining the information currently available on the behavioral and biochemical effects of ascorbic acid in animal models of Alzheimer's disease as well as its usage as a therapeutic agent to slow down the progression of Alzheimer disease in human beings. Oxidative stress plays a significant role in the advancement of AD. AA is a wellknown antioxidant that primarily reduces oxidative stress and produces protein aggregates, which may help decrease cognitive deficits in Alzheimer's disease. The current paper analyses of ascorbic acid revealed that deficiency of ascorbic acid adversely affects the central nervous system and leads to cognitive defects. However, the results of clinical studies are conflicting, but some of the studies suggested that supplementation of ascorbic acid improved cognitive deficits and decreased disease progression. <p> Conclusion: Based on clinical and preclinical studies, it is observed that ascorbic acid supplementation improves cognitive deficits and protects the neurons from oxidative stress injury.</p>]]></description> </item><item><title><![CDATA[Probiotic Influences on Motor Skills: A Review]]></title><link>https://www.benthamscience.comarticle/133420</link><description><![CDATA[The effects of probiotics have mostly been shown to be favorable on measures of anxiety and stress. More recent experiments indicate single- and multi-strain probiotics in treating motorrelated diseases. Initial studies in patients with Parkinson’s disease and Prader-Willi syndrome are concordant with this hypothesis. In addition, probiotics improved motor coordination in normal animals and models of Parkinson’s disease, multiple sclerosis, and spinal cord injury as well as grip strength in hepatic encephalopathy. Further studies should delineate the most optimal bacterial profile under each condition.]]></description> </item><item><title><![CDATA[Neuroprotective Role of MiRNA-9 in Neurological Diseases:
A Mini Review]]></title><link>https://www.benthamscience.comarticle/127188</link><description><![CDATA[MicroRNAs (miRNAs) are a class of non-coding small RNAs with about 22 nucleotides in eukaryotes. They regulate gene expression at the post-transcriptional level and play a key role in physiological and pathological processes. As one of the most abundant miRNAs in the human brain, miRNA-9 (miR-9) has attracted extensive attention due to its important role in the maintenance of normal function of the nervous system and the occurrence and development of nervous system diseases. Hence, we reviewed the neuroprotective effect of miR-9 in neurological diseases. MiR-9 may be a potential target of nervous system diseases.]]></description> </item><item><title><![CDATA[Functional Roles of Mesenchymal Stem Cell-derived Exosomes in Ischemic Stroke
Treatment]]></title><link>https://www.benthamscience.comarticle/128386</link><description><![CDATA[Stroke is a life-threatening disease and one of the leading causes of death and physical disability worldwide. Currently, no drugs on the market promote neural recovery after stroke insult, and spontaneous remodeling processes are limited to induce recovery in the ischemic regions. Therefore, promoting a cell-based therapy has been needed to elevate the endogenous recovery process. Mesenchymal stem cells (MSCs) have been regarded as candidate cell sources for therapeutic purposes of ischemic stroke, and their therapeutic effects are mediated by exosomes. The microRNA cargo in these extracellular vesicles is mostly responsible for the positive effects. When it comes to the therapeutic viewpoint, MSCsderived exosomes could be a promising therapeutic strategy against ischemic stroke. The aim of this review is to discuss the current knowledge around the potential of MSCs-derived exosomes in the treatment of ischemic stroke.]]></description> </item><item><title><![CDATA[Differential Expression of microRNAs and Target Genes Analysis in Olfactory
Ensheathing Cell-derived Extracellular Vesicles <i>Versus</i> Olfactory
Ensheathing Cells]]></title><link>https://www.benthamscience.comarticle/131043</link><description><![CDATA[<p>Introduction: Olfactory ensheathing cells (OECs) are important transplantable cells for the treatment of spinal cord injury. However, information on the mechanism of OEC-derived extracellular vesicles (EVs) in nerve repair is scarce. <p> Methods: We cultured OECs and extracted the OEC-derived EVs, which were identified using a transmission electron microscope, nanoparticle flow cytometry, and western blotting. High throughput RNA sequencing of OECs and OEC-EVs was performed, and the differentially expressed microRNAs (miRNAs) (DERs) were analyzed by bioinformatics. The target genes of DERs were identified using miRWalk, miRDB, miRTarBase, and TargetScan databases. Gene ontology and KEGG mapper tools were used to analyze the predicted target genes. Subsequently, the STRING database and Cytoscape software platform were used to analyze and construct miRNA target genes' protein-protein interaction (PPI) network. <p> Results: Overall, 206 miRNAs (105 upregulated and 101 downregulated) were differentially expressed in OEC-EVs (p &#60; 0.05;|log2 (fold change)|>2). Six DERs (rno-miR-7a-5p, rno-miR-143-3p, rno-miR-182, rno-miR-214-3p, rno-miR-434-5p, rno-miR-543-3p) were significantly up-regulated , and a total of 974 miRNAs target genes were obtained. The target genes were mainly involved in biological processes such as regulation of cell size, positive regulation of cellular catabolic process and small GTPase-mediated signal transduction; positive regulation of genes involved in cellular components such as growth cone, site of polarized growth, and distal axon; and molecular functions such as small GTPase binding and Ras GTPase binding. In pathway analysis, target genes regulated by six DERs were mainly enriched in axon guidance, endocytosis, and Ras and cGMP-dependent protein kinase G signaling pathways. Finally, 19 hub genes were identified via the PPI network. <p> Conclusion: Our study provides a theoretical basis for treating nerve repair by OEC-derived EVs.</p>]]></description> </item><item><title><![CDATA[Novel Concepts in the Management of Angina in Coronary Artery Disease]]></title><link>https://www.benthamscience.comarticle/131759</link><description><![CDATA[Coronary artery disease remains a condition with high prevalence and detrimental effects on the quality of life of affected individuals. Its most frequent manifestation, stable angina pectoris, may be challenging to manage despite the available antianginal pharmacotherapy and adequate risk factor control, especially in subjects not amenable to revascularization. In the direction of refractory angina pectoris, several approaches have been developed over the years with varying degrees of success. Among the most recognized techniques in managing angina is enhanced external counterpulsation, which utilizes mechanical compression of the lower extremities to increase blood flow to the heart. Moving to coronary sinus reduction, it leads to an increase in coronary sinus backward pressure, ultimately augmenting myocardial blood flow redistribution to ischemic regions and ameliorating chronic angina. Clinical trial results of the above-mentioned techniques have been encouraging but are based on small sample sizes to justify their widespread application. Other interventional approaches, such as transmyocardial laser revascularization, extracorporeal shockwave myocardial revascularization, and spinal cord stimulation, have been met with either controversial or negative results, and their use is not recommended. Lastly, angiogenic therapy with targeted intramyocardial vascular endothelial growth factor injection or CD34+ cell therapy may be beneficial and warrants further investigation. In this review, we summarize the current knowledge in the field of angina management, highlighting the potential and the gaps in the existing evidence that ought to be addressed in future larger-scale, randomized studies before these techniques can be safely adapted in the clinical practice of patients with refractory angina pectoris]]></description> </item><item><title><![CDATA[The Fulcrum of Demyelination in Multiple Sclerosis]]></title><link>https://www.benthamscience.comarticle/132942</link><description><![CDATA[Multiple sclerosis (MS) is an autoimmune disorder that affects the central nervous system (CNS), including the brain, spinal cord, and optic nerves. The symptoms can vary from muscle weakness to vision loss. In the case of MS, the immune system attacks the myelin sheath, which protects the nerve fiber and causes inflammation resulting in demyelination. The myelin sheath has the composition of various proteins including membrane proteins and glycoproteins. The four main proteins namely Myelin Basic Protein (MBP), Myelin associated Oligodendrocyte Basic protein (MOBP), Myelin Proteolipid Protein (PLP) and Myelin Associated Glycoprotein (MAG) are known to be critical auto-antigens in causing demyelination in CNS leading to MS. Three out of these four proteins are intrinsically disordered proteins and in this review, we attempted to understand how these proteins play a crucial role in maintaining the integrity of myelin, by exploring its structural and functional aspects and also their auto-antigenicity leading to multiple sclerosis.]]></description> </item><item><title><![CDATA[Imbalance of Th1 and Th2 Cytokines and Stem Cell Therapy in
Pathological Pain]]></title><link>https://www.benthamscience.comarticle/128450</link><description><![CDATA[The pathophysiological importance of T helper 1 (Th1) and Th2 cell cytokines in pathological pain has been highly debated in recent decades. However, the analgesic strategy targeting individual cytokines still has a long way to go for clinical application. In this review, we focus on the contributions of Th1 cytokines (TNF-&#945;, IFN-&#947;, and IL-2) and Th2 cytokines (IL-4, IL-5, IL-10, and IL-13) in rodent pain models and human pain-related diseases. A large number of studies have shown that Th1 and Th2 cytokines have opposing effects on pain modulation. The imbalance of Th1 and Th2 cytokines might determine the final effect of pain generation or inhibition. However, increasing evidence indicates that targeting the individual cytokine is not sufficient for the treatment of pathological pain. It is practical to suggest a promising therapeutic strategy against the combined effects of Th1 and Th2 cytokines. We summarize the current advances in stem cell therapy for pain-related diseases. Preclinical and clinical studies show that stem cells inhibit proinflammatory cytokines and release enormous Th2 cytokines that exhibit a strong analgesic effect. Therefore, a shift of the imbalance of Th1 and Th2 cytokines induced by stem cells will provide a novel therapeutic strategy against intractable pain. It is extremely important to reveal the cellular and molecular mechanisms of stem cell-mediated analgesia. The efficiency and safety of stem cell therapy should be carefully evaluated in animal models and patients with pathological pain.]]></description> </item><item><title><![CDATA[Regulatory Effect of Electroacupuncture on Hypothalamic Serotonin and
its Receptor in Rats with Cerebral Ischemia]]></title><link>https://www.benthamscience.comarticle/132460</link><description><![CDATA[<p>Background: Previous studies have shown that the neurological damage caused by middle cerebral artery occlusion (MCAO) is not only limited to local infarction but can also cause secondary damage in distant sites, such as the hypothalamus. 5-hydroxytryptamine (5-HT)/ 5-HT transporter (5-HTT) and 5-HT receptor 2A (5-HT2A) are important in the treatment of cerebrovascular diseases. <p> Objective: This study aimed to study the effect of electroacupuncture (EA) on the expression of 5- HT, 5-HTT, and 5-HT2A in the hypothalamus of rats with ischemic brain injury and to explore the protective effect and potential mechanism of EA on the secondary injury of cerebral ischemia. <p> Methods: Sprague-Dawley (SD) rats were randomly divided into three groups: sham group, model group, and EA group. The permanent middle cerebral artery occlusion (pMCAO) method was used to induce ischemic stroke in rats. In the EA group, the Baihui (GV20) and Zusanli (ST36) points were selected for treatment, which was administered once per day for two consecutive weeks. The neuroprotective effect of EA was evaluated by nerve defect function scores and Nissl staining. The content of 5-HT in hypothalamus was detected by enzyme linked immunosorbent assay (ELISA), and the expression of 5-HTT and 5-HT2A were detected by Western blot. <p> Results: Compared with that in the sham group, the nerve defect function score in the model group rats was significantly increased, the hypothalamus tissue showed obvious nerve damage, the levels of 5-HT and the expression of 5-HTT were significantly reduced, and the expression of 5-HT2A was significantly increased. After 2 weeks of EA treatment, the nerve defect function scores of pMCAO rats were significantly reduced, the hypothalamic nerve injury was significantly reduced, the levels of 5-HT and the expression of 5-HTT were significantly increased, and the expression of 5-HT2A was significantly decreased. <p> Conclusion: EA has a certain therapeutic effect on hypothalamic injury secondary to permanent cerebral ischemia, and its potential mechanism may be closely related to the upregulation of 5-HT and 5-HTT expression and the downregulation of 5-HT2A expression.</p>]]></description> </item><item><title><![CDATA[Endocrine, Metabolic, and Immune Pathogenesis of Postmenopausal
Osteoporosis. Is there a Therapeutic Role in Natural Products?]]></title><link>https://www.benthamscience.comarticle/130541</link><description><![CDATA[<p>Background: Bone health relies on the equilibrium between resorption and new bone generation. Postmenopausal osteoporosis depends on estrogen deficiency which favorite bone resorption and elevated risk of fractures. Moreover, osteoporosis is characterized by a high release of proinflammatory cytokines suggesting the role of the immune system in the pathogenesis of this complex disease (immunoporosis). </p><p> Aims: To review the pathophysiology of osteoporosis from an endocrinological and immunological viewpoint and treatments with a specific focus on nutraceuticals. </p><p> Methods: PubMed/MEDLINE, Scopus, Google Scholar, and institutional web site were searched. Original articles and reviews were screened and selected by September 2022. </p><p> Results: The activation of the Gut Microbiota-Bone Axis contributes to bone health by releasing several metabolites, including short-chain fatty acids (SCFAs), that facilitate bone mineralization directly and indirectly by the induction of T regulatory cells, triggering anti-inflammatory pathways. </p><p> Conclusion: Treatments of postmenopausal osteoporosis are based on lifestyle changes, calcium and vitamin D supplementation, and anti-resorptive and anabolic agents, such as bisphosphonates, Denosumab, Teriparatide, Romosozumab. However, phytoestrogens, polyphenols, probiotics, and polyunsaturated fatty acids may improve bone health by several mechanisms, including anti-inflammatory properties. Specific clinical trials are needed to assess the efficacy/effectiveness of the possible anti-osteoporotic activity of natural products as add on to background treatment.</p>]]></description> </item><item><title><![CDATA[Riboflavin and Histidine Metabolisms Are Two Key Pathways Related
to the Clinically Isolated Syndrome (CIS): A WGCNA-based <i>In silico</i>
Analysis]]></title><link>https://www.benthamscience.comarticle/131479</link><description><![CDATA[<p>Background: As an inflammatory disorder, Multiple Sclerosis (MS) causes demyelination, as well as axonal and neuronal injury in the central nervous system (CNS). Several clinical signs may be the indicators of MS among which, Clinically Isolated Syndrome (CIS) is the first symptom caused by the inflammation and demyelination of CNS. CIS is characterized by symptoms such as optic neuritis, brain stem or cerebellar syndrome, spinal cord syndrome, or sometimes cerebral hemispheric dysfunction. <p> Objective: So far, metabolic pathways involved in the development of CIS are not fully understood. Therefore, in this study, weighted gene co-expression network analysis (WGCNA) has been used to identify differentially expressed genes in CIS disease and the main pathways associated with it. <p> Methods: We grouped differentially expressed genes along with the functionally related genes into large modules to obtain their direct and indirect relationships. <p> Results: The results have identified two new pathways associated with CIS, including riboflavin and histidine metabolism-involved pathways. <p> Conclusion: Riboflavin and histidine metabolism-involved pathways may be considered potential therapeutic goals for CIS management in the future.</p>]]></description> </item><item><title><![CDATA[Cerium Oxide Nanoparticles Ameliorate Oxidative Stress, Inflammation,
and Pain Behavior in Neuropathic Rats]]></title><link>https://www.benthamscience.comarticle/129073</link><description><![CDATA[<p> Background: Neuropathic pain originating from a dysfunction in the nervous system is often intractable and chronic. Recently, several studies using nanoparticles suggested a new way to control neuropathic pain. This study intended to explore the potential neuroprotective effect of Cerium Oxide Nanoparticles (CNPs) synthesized by pullulan in neuropathic pain in rats. </p><p> Methods: On the right common sciatic nerve of male Wistar rats, the chronic constriction injury (CCI) procedure was used to establish a neuropathic pain model. CNPs were injected into the caudal vein of the rat. Behavioral methods were used to detect mechanical allodynia, cold allodynia, and thermal hyperalgesia in rats. Besides, inflammation factors, including tumor necrosis factor (TNF)-&#945;, interleukin (IL)-1&#946;, nitric oxide (NO), and markers of oxidative stress, including Malondialdehyde (MDA) and total thiol, were measured in the spinal cord segment of rats. </p><p> Results: In rats with CCI, mechanical allodynia, cold allodynia, and thermal hyperalgesia developed, which improved when the rats were administered CNPs. Spinal cord specimens of CCI rats had elevated inflammation and oxidative stress status (↑IL-1&#946;, ↑TNF-&#945;, ↑NO, ↑MDA) and decreased antioxidative levels (↓total thiol). As a result of CNPs treatment, these changes were reversed in the spinal cord specimens. </p><p> Conclusion: CNPs alleviate neuropathic pain by exhibiting antioxidative and anti-inflammatory activities.</p>]]></description> </item><item><title><![CDATA[The Use of Surface Plasmon Resonance to Study the Interactions of
Proteins Involved in Conformational Diseases: Experimental
Approaches for New Therapeutical Perspectives]]></title><link>https://www.benthamscience.comarticle/128876</link><description><![CDATA[In recent years, the scientific community has been trying to tackle different diseases by using unifying and holistic approaches based on the concept that it is possible to target apparently very different diseases under a comprehensive general scheme. In other words, various different diseases have been grouped together under the label of “conformational diseases”, because the triggering cause for each malady is the misfolding of a specific protein, whose dyshomeostasis and accumulation cause all the other downhill biomolecular events characteristic of each different disease. In a parallel manner, analytical techniques have developed to investigate protein misfolding and accumulation, so as to give a valid technical support to the investigation of conformational diseases. In this scenario, surface plasmon resonance (SPR) has widely contributed to study many different aspects correlated to conformational diseases, offering the advantages of real time investigations, use of small amounts of biological materials and possibility to mimic the cellular environments without recurring to the use of fluorescent tags. In this review, after a brief introduction about conformational diseases and the SPR technique, a thorough description of the various uses of SPR to investigate the biomolecular mechanisms involved in these diseases is given in order to provide the reader with an exhaustive list as well as a critical perspective of the use of SPR for such topic. The case of Alzheimer’s disease is discussed at a deeper level. We hope that this work will make the reader aware of all the possible SPR experimental approaches, which can be used to develop new possible therapeutic strategies to tackle conformational diseases.]]></description> </item><item><title><![CDATA[Identification of Differentially Expressed Proteins in Rats with Early Subacute
Spinal Cord Injury using an iTRAQ-based Quantitative Analysis]]></title><link>https://www.benthamscience.comarticle/128854</link><description><![CDATA[<p>Background: Injuries to the central nervous system (CNS), such as spinal cord injury (SCI), may devastate families and society. Subacute SCI may majorly impact secondary damage during the transitional period between the acute and subacute phases. A range of CNS illnesses has been linked to changes in the level of protein expression. However, the importance of proteins during the early subacute stage of SCI remains unknown. The role of proteins in the early subacute phase of SCI has not been established yet. </p><p> Methods: SCI-induced damage in rats was studied using isobaric tagging for relative and absolute protein quantification (iTRAQ) to identify proteins that differed in expression 3 days after the injury, as well as proteins that did not alter in expression. Differentially expressed proteins (DEPs) were analyzed employing Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis to discover the biological processes, cell components, and molecular functions of the proteins. We also performed Gene Set Enrichment Analysis (GSEA) software BP pathway and KEGG analysis on all proteins to further identify their functions. In addition, the first 15 key nodes of a protein-protein interaction (PPI) system were found. </p><p> Results: During the early subacute stage of SCI, we identified 176 DEPs in total between the control and damage groups, with 114 (64.77%) being up-regulated and 62 (35.23%) being downregulated. As a result of this study, we discovered the most important cellular components and molecular activities, as well as biological processes and pathways, in the early subacute phase of SCI. The top 15 high-degree core nodes were Alb, Plg, F2, Serpina1, Fgg, Apoa1, Vim, Hpx, Apoe, Agt, Ambp, Pcna, Gc, F12, and Gfap. </p><p> Conclusion: Our study could provide new views on regulating the pathogenesis of proteins in the early subacute phase after SCI, which provides a theoretical basis for exploring more effective therapeutic targets for SCI in the future.</p>]]></description> </item></channel></rss>