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                    <title><![CDATA[Pericarditis]]></title>

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

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                    <pubDate>Sun, 07 Jun 2026 07:50:17 +0000</pubDate>

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                    <title><![CDATA[Pericarditis]]></title>

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

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

                    </image><item><title><![CDATA[Hydralazine Induced Vasculitis: A Case Report]]></title><link>https://www.benthamscience.comarticle/136008</link><description><![CDATA[<p>Background: Hydralazine has been used in the treatment of hypertension and heart failure for a long time. It has been associated with the development of Vasculitis and Drug induced lupus. This is a male patient in his sixties who was admitted at the hospital and prescribed hydralazine. He developed Hydralazine-induced lupus with Pancytopenia and renal failure. This case report has been written to raise awareness about the hydralazine side effects. <p> Case Presentation: This case report describes a 68-year-old male, transferred to our hospital for rehabilitation. He was tracheostomized. He is hypertensive with a history of CVA. BP was elevated during the admission. He has no family history of immunological diseases or any allergies. 6 months after hydralazine, the patient started to have a purpuric rash over the lower limbs and an elevated renal profile. Only Direct Coomb’s test was positive. He had hematuria and pancytopenia also. He was started on steroids and he became edematous. On March 2021, the hydralazine was stopped and the patient's blood tests improved, the rash disappeared and hematuria stopped. Unfortunately, he got fungemia and septicemia with pneumonia. He became hypotensive and anuric. The patient kept deteriorating and passed away. <p> Discussion: Hydralazine is not a first line choice for the treatment of hypertension. Common side effects include tachycardia and headache. It can also cause drug-induced lupus. <p> Conclusion: Hydralazine has been used in the treatment of hypertension and heart failure for a long time. It has been associated with the development of Vasculitis and Drug induced lupus.</p>]]></description> </item><item><title><![CDATA[Multiple, Extensive Cardiac and Pulmonary Hydatid Cysts Managed by a
Single-stage Surgical Removal: A Case Report]]></title><link>https://www.benthamscience.comarticle/133360</link><description><![CDATA[<P>Background: Echinococcosis is a zoonotic infection that is characterised clinically by the development of hydatid cysts in different organs, mainly the liver and lungs. Cardiac involvement is rare but can lead to serious and fatal complications. <P> Case Report: We report a rare challenging case of multiple, extensive cardiac and pulmonary Echinococcal cysts that were treated by successful single-stage surgical resection via median sternotomy without additional thoracic incisions. <P> Conclusion: This article highlights the rare presentation of multiple, extensive cardiac and pulmonary Echinococcal cysts and how to overcome diagnostic challenges in the era of modern diagnostic imaging. Surgical removal remains the mainstay treatment, and a single-stage surgical approach is feasible in capable centres. Perioperative chemotherapy with Albendazole and the intraoperative use of scolicidal agents improved immediate surgical outcomes, although long-term effects could not be established in this case due to loss of follow-up.</P>]]></description> </item><item><title><![CDATA[A Review of the Dual Role of MicroRNA-21 in Cardiovascular Diseases: Risk
Factor or a Potential Therapeutic Target]]></title><link>https://www.benthamscience.comarticle/138046</link><description><![CDATA[Cardiovascular diseases (CVD) are the number one reason for morbidity and mortality in the modern world, and their incidence is increasing at an incredible pace. Increasing evidence has shown the significant functions of microRNAs in the cardiovascular system and has highlighted their potential application as a new era of diagnostic and therapeutic targets for CVD that can improve the prognosis and life expectancy of patients. Among more than 2,000 microRNAs, microRNA-21 (miR-21) is highly expressed in human hearts and has earned the interest of researchers as a potential biomarker in a wide range of common heart conditions. Here, we summarized recent research progress regarding the significant role of miR-21 in CVD, focusing on cardiotoxicity, heart arrhythmias, cardiomyopathies, and hypertension. Several signaling pathways (TGF-&#946;1/Smad2 signaling, FGFR1/FGF21/PPAR&#947;, NF-&#954;B/miR-21/SMAD7, miR-21/SPRY1/ERK/mTOR …) and molecular targets (BTG2, PDCD4, PTEN, STAT3…) were reported to be controlled, at least partially, by miR-21 and are linked to CVD pathogenesis. Most investigations highlighted miR-21 cardioprotective functions in heart injury, while some other studies showed that this miR is elevated in the serum/tissue of patients, promoting fibrosis and cardiac dysfunction. This dual role can be explained by the fact that miR-21 has multiple regulatory functions depending on the microenvironment, downstream signaling, and target genes, which indicates that cell-type-specific investigations should receive more attention. With further investigations, miR-21 can be considered a novel tailored therapy with favorable outcomes.]]></description> </item><item><title><![CDATA[Early Prognostic Instrumental and Laboratory Biomarkers in Post-MI]]></title><link>https://www.benthamscience.comarticle/138078</link><description><![CDATA[<p>Background: Post-myocardial infarction (MI) changes have been frequently reported in the literature and are associated with determining the prognosis. </p> <p> Aims: The aim of this study is to find a prognosis marker for the favorability of determination of the medium-term outcomes in patients with acute MI. </p> <p> Objectives: MI patients’ prognosis is poorly understood and requires further elaboration. </p> <p> Materials and Methods: A single center, cross-sectional cohort study involved 211 patients’ medical history with acute MI, for the period 2014-2019, had been evaluated retrospectively for 76 parameters. The data was collected from the Republic Rehabilitation Mordovian Hospital. The described measurement units were used in the local laboratories to describe the values. The descriptive values were expressed in the mean average and standard deviation. For statistical analysis, descriptive statistics, t-test independent by groups and dependent by numerical variables for repeated analysis for the same patients, multinomial logistic regression, Pearson’s correlation coefficient, ROC analysis, and for clarification purposes, diagrams and bar figures were used. For performing the statistical analysis, the SPSS program, version 28 was used. </p> <p> Results: Descriptive statistics showed a proportion of men to females 7:3. The mean age of the MI patients was 61.50 years (Std. Dev. ± 10.68), and the mean height of the sample was 171.00 cm (Std. Dev. ± 7.20). The mean body weight of the sample is 83.62 kg (Std. Dev. ± 12.35), and the body mass index (BMI) is 29.02 kg/m2 (Std. Dev. ± 5.07). The total hospitalization days are 14.79 (Std. Dev. ± 3.41). The mean heart rate (HR) beat per minute (bpm) was 79.03 (Std. Dev. ± 15.63), and the mean blood pressure was 138.53/84.09 mmHg (Std. Dev. ± 28.66/12.79). On the complete blood count (CBC), the mean level of the hemoglobin (Hb) 136.33 g/l (Std. Dev. ± 15.29), the mean level of the leukocytes (WBC) 8.76 /μl (Std. Dev. ± 2.77), the mean level of the red blood cells (RBC) 4.55 /μl (Std. Dev. ± 0.52), the mean level of the relative value of the lymphocytes 24.46 % (Std. Dev. ± 9.015), and the mean level of the thrombocytes 207.87 /μl (Std. Dev. ± 64.035). The mean erythrocytes segmentation rate (ESR) is 18.99 mm/hr (Std. Dev. ± 12.16). The regression analysis demonstrated that the dependent variable, complication, in particular, pericarditis, and the independent factor, concomitant disease, in particular, chronic heart failure, has a significant regression coefficient of 29.101 at p &#60;0.05. Furthermore, the dependent variable, complication, in particular, pneumonitis, and the independent factor, concomitant disease, particularly, arrhythmia, have a significant regression coefficient of 21.937 at p &#60;0.05. </p> <p> Conclusion: An elevated level of CPK-MB/LDH/Troponin I is linked to the development of arrhythmia. Patients with other medical conditions experience high diastolic blood pressure and an enlargement of the right ventricle. The early complication observed after MI is the formation of a left ventricular aneurysm. Complications arise due to low levels of potassium and calcium. Chronic Kidney Disease (CKD) contributes to the End-Diastolic Size (EDS) of the Left Ventricle (LV), Troponin I, and creatine phosphokinase-MB (CPK-MB). Advanced CKD patients have a hypertrophic left ventricle and persistently elevated post-myocardial Infarction (MI) cardiac biomarkers (CPKMB/ LDH/Troponin I) due to impaired kidney detoxification. Therefore, prolonged elevation of MI biomarkers can be an indicative of severe MI or kidney function impairment due to the chronic mild elevation in the MI biomarkers. Pericarditis development is related to the pre-existence of chronic heart failure. Moreover, pneumonitis development is related to the pre-existence of arrhythmia. </p> <p> Others: Hypertensive patients do not exhibit a significant increase in calcium levels, indicating that it is not a reliable biomarker in this patient population. Additionally, gender plays a crucial role in the development of ischemic heart disease, including myocardial infarction.</p>]]></description> </item><item><title><![CDATA[Assessment of Interleukin 17 in Egyptian Systemic Lupus Erythematosus
Patients as a Biomarker in Disease Activity]]></title><link>https://www.benthamscience.comarticle/138205</link><description><![CDATA[<p>Introduction: Systemic lupus erythematosus (SLE) is a chronic idiopathic systemic autoimmune disorder with dysregulation of adaptive and innate immune systems. Interleukin (IL)-17 is the prototypical pro-inflammatory cytokine of T helper 17 (Th17) cells. Therefore, it contributes to the pathogenesis of human SLE. <p> Aim: The aim of the research paper was the evaluation of IL-17 level as a biomarker in the SLE cohort and its relation to disease activity and analysis of IL-17 concentration in patients with lupus nephritis and non-lupus nephritis. <p> Methods: The research enrolled 45 SLE patients according to Systemic Lupus International Collaborating Clinics Classification Criteria (SLICC), and age and sex-matched. The patients underwent full history, clinical examination, laboratory investigation, and Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) calculation. <p> Results: The mean age ± SD of the participants equaled 32 ± 11 years, and serum IL-17 in SLE cases was statistically significantly high (p < 0.001). No statistically significant correlations were reported between disease activity according to SLEDAI and IL-17. In addition, a statistically significant positive correlation was reported between IL-17 and ESR, and a high statistically significant negative correlation was reported between IL-17 and C3 and C4 (P < 0.001). A statistically significant positive correlation was reported between IL-17 and 24-hour urinary proteins with a Pvalue of 0.01. <p> Conclusion: SLE cases demonstrated higher levels of serum IL-17, contributing to SLE pathogenesis. However, no statistically significant difference was reported between IL-17 and Lupus nephritis. IL-17 and SLE activity (SLEDAI) did not correlate. <p> A statistically significant positive relation was reported between IL-17 and 24-hour urinary proteins. Additionally, a high statistically significant negative correlation was reported between IL-17 and C3 and C4.</p>]]></description> </item><item><title><![CDATA[Zamzam Water Mitigates Cardiac Toxicity Risk through Modulation of GUT
Microbiota and the Renin-angiotensin System]]></title><link>https://www.benthamscience.comarticle/139447</link><description><![CDATA[<p>Background: Cardiovascular diseases (CVDs) continue to exert a substantial global influence in specific areas due to population growth, aging, microbiota, and genetic/environmental factors. Drinking water has a strong impact on the health of an individual. Further, emerging evidence has highlighted the therapeutic potential and benefits of Zamzam water (Zam). <p> Objective: We investigated the influence of Zam on doxorubicin-induced cardiac toxicity, elucidating its consequential effects on GUT microbiota dysbiosis and hepatic and renal functions. <p> Methods: Male rats were categorized into four groups: Group 1 as Normal control (NC), Group 2 as Zamzam control (ZC), Group 3 Disease control (DC) and Group 4 as Therapeutic control (DZ) treated with Zam against doxorubicin-induced disease at a dose of 1mg/kg boy weight) intraperitoneally (i.p). <p> Results: Significant dysbiosis in the composition of GM was observed in the DC group along with a significant decrease (p &#60; 0.05) in serum levels of Zinc, interleukin-10 (IL-10), IL-6 and Angiotensin II (Ang II), while C-reactive protein (CRP), fibrinogen, and CKMB increased significantly (restoration of Zinc ions (0.72 ± 0.07 mcg/mL) compared to NC. Treatment with Zamzam exhibited a marked abundance of 18-times to 72% in Romboutsia, a genus of firmicutes, along with lowering of Proteobacteria in DZ followed by significant restoration of Zinc ions (0.72 ± 0.07 mcg/mL), significant (p ˂ 0.05) reduction in CRP (7.22 ± 0.39 mg/dL), CKMB (118.8 ± 1.02 U/L) and Fibrinogen (3.18 ± 0.16 mg/dL), significant (p &#60; 0.05) increase in IL-10 (7.22 ± 0.84 pg/mL) and IL-6 (7.18 ± 0.40 pg/ml), restoration of Ang II (18.62 ± 0.50 nmol/mL/min), marked increase in renin with normal myocyte architecture and tissue orientation of kidney, and restoration of histological architecture of hepatocyte. <p> Conclusion: Zam treatment mitigated cardiac toxicity risk through the modulation of GUT microbiota and the renin-angiotensin system and tissue histology effectively.</p>]]></description> </item><item><title><![CDATA[Cardiovascular Manifestations in Inflammatory Bowel Disease]]></title><link>https://www.benthamscience.comarticle/136288</link><description><![CDATA[<p>Inflammatory bowel disease is a group of long-term systemic inflammatory disorders affecting the gastrointestinal tract, including Crohn's disease and ulcerative colitis, which may be associated with an increased risk of developing extraintestinal manifestations, including cardiovascular disease, thereby decreasing the quality of life. Pathophysiological changes associated with inflammatory bowel disease include alterations of the microbiome, endotoxemia, and changes to glucose and lipid metabolism. Inflammatory bowel disease patients have higher carotid intima-media thickness, lower flow-mediated dilatation, and increased carotid-femoral pulse wave velocity, which are markers of elevated cardiovascular risk. In addition, inflammatory bowel disease patients are at an increased risk for developing venous and arterial thrombotic events due to a hypercoagulable state caused by thrombocytosis and coagulation system activation. To reduce the risk of developing cardiovascular disease, lifestyle modifications, such as smoking cessation, dietary changes, and increased physical activity alongside management with appropriate medication, should be considered. This paper examines how inflammatory bowel disease can influence the risk of cardiovascular complications and the involvement of drug therapy. <p> Methods: PubMed was searched using keywords, such as inflammatory bowel disease, Crohn's disease, ulcerative colitis, cardiovascular disease, pericarditis, thromboembolism, and many more. Relevant literature up to March 2023 has been examined and summarized, which consisted of data from various clinical trials, meta-analyses, retrospective/prospective cohort studies, and current guidelines.</p>]]></description> </item><item><title><![CDATA[Myocarditis and Pericarditis Related to mRNA COVID-19 Vaccination: A
Case Report]]></title><link>https://www.benthamscience.comarticle/130461</link><description><![CDATA[<p>Introduction: Reported cases after the post-commercialization phase of mRNA vaccines against COVID-19 have revealed that myocarditis and pericarditis may occur predominantly in male adolescents after the second dose of the vaccine. <p> Case Presentation: We report two cases of cardiac disorders associated with mRNA COVID-19 vaccination, both of them in 15 year-old males. One of the patients presented acute pericarditis and the second one presented acute myocarditis with left ventricular dysfunction at hospital discharge. <p> Discussion and Conclusion: Physicians should be aware with the typical manifestations of these cardiovascular events after the vaccination and report suspicious cases to pharmacovigilance agencies as soon as possible. The population should rely on the pharmacovigilance system that continues to recommend vaccination as the most effective strategy to reduce the negative consequences of the pandemic.</p>]]></description> </item><item><title><![CDATA[Advances in the Treatment of Chronic Myeloid Leukemia]]></title><link>https://www.benthamscience.comarticle/128752</link><description><![CDATA[<p>Background: The treatment of chronic myeloid leukemia has progressed in recent decades, becoming a model for a disease whose pathogenesis is primarily based on a genetic mutation and has led to survivals comparable to those of the general population. <p> Objectives: This review aims to present recent therapeutic advances in this area. <p> Methods: A mini-review was achieved using the articles published in Web of Science and Pub- Med between January 2021 - May 2022, and new patents were made in this field. <p> Results: The three generations of tyrosine kinase inhibitors have transformed chronic myeloid leukemia into a manageable disorder and greatly improved the treatment results of the chronic phase, the prognosis, survival, and quality of life of patients. The therapeutic goals today include achieving a deep and lasting molecular response as soon as possible, successful treatment-free remission, and discovering and applying new therapeutic strategies to act on impaired immune modulation and dormant leukemic stem cells. The allosteric inhibitor asciminib targets the ABL myristoyl pocket, reduces Abl kinase activity, and is effective against most cells that have mutations in the ABL1 kinase domain. Progress and recommendations for achieving long-term treatment- free remission are set out. Nearly 50% of the patients who received first-line tyrosine kinase inhibitors required a change of treatment by 10 years due to intolerance or resistance to treatment. Their main side effects are presented. <p> Conclusion: Obtaining a deep and persistent molecular response contributes to achieving longterm treatment-free remission.</p>]]></description> </item><item><title><![CDATA[High-sensitive Cardiospecific Troponins: The Role of Sex-specific Concentration
in the Diagnosis of Acute Coronary Syndrome (Mini-Review)]]></title><link>https://www.benthamscience.comarticle/131339</link><description><![CDATA[Cardiospecific troponins are specifically localized in the troponin-tropomyosin complex and the cytoplasm of cardiac myocytes. Cardiospecific troponin molecules are released from cardiac myocytes upon their death (irreversible damage in acute coronary syndrome) or reversible damage to cardiac myocytes, for example, during physical exertion or the influence of stress factors. Modern high-sensitive immunochemical methods for detecting cardiospecific troponins T and I are extremely sensitive to minimal reversible damage to cardiac myocytes. This makes it possible to detect damage to cardiac myocytes in the early stages of the pathogenesis of many extra-cardiac and cardiovascular diseases, including acute coronary syndrome. So, in 2021, the European Society of Cardiology approved diagnostic algorithms for the acute coronary syndrome, which allow the diagnosis of acute coronary syndrome in the first 1-2 hours from the moment of admission of the patient to the emergency department. However, high-sensitive immunochemical methods for detecting cardiospecific troponins T and I may also be sensitive to physiological and biological factors, which are important to consider in order to establish a diagnostic threshold (99 percentile). One of the important biological factors that affect the 99 percentile levels of cardiospecific troponins T and I are sex characteristics. This article examines the mechanisms underlying the development of sex-specific serum levels of cardiospecific troponins T and I and the importance of sexspecific cardiospecific troponin concentrations in diagnosing acute coronary syndrome.]]></description> </item><item><title><![CDATA[COVID-19 and Anti-COVID-19 Vaccination: Potential Damages to the
Thyroid Gland]]></title><link>https://www.benthamscience.comarticle/131640</link><description><![CDATA[]]></description> </item><item><title><![CDATA[Long COVID-19 Syndrome and Sudden Cardiac Death: The Phantom
Menace]]></title><link>https://www.benthamscience.comarticle/131792</link><description><![CDATA[]]></description> </item><item><title><![CDATA[Multisystemic Inflammatory Syndrome Post COVID-19 Infection in an Arab
Female: A Case Report of a Rare Manifestation]]></title><link>https://www.benthamscience.comarticle/130363</link><description><![CDATA[<P>Background: Multisystemic inflammatory syndrome is a rare but severe complication in children and adolescents infected with SARS-CoV-2. <P> Case Report: This report describes a four-year-old Arab descent female presenting with a history of high-grade fever of 7 days duration with erythematous rash and family history of COVID infection suggestive of atypical Kawasaki disease, which turned out to be multisystemic inflammatory syndrome (MIS-C) post COVID infection. Based on the available published evidence, the World Health Organization has provided a preliminary definition of MIS-C as “children and adolescents 0–19 years of age with fever > 3 days presenting with two of five clinical criteria, such as 1. skin rash or mucocutaneous inflammation or non-purulent conjunctivitis, 2. hypotensive shock, 3. signs of myocardial dysfunction, 4. coagulopathy, and 5. the acute gastrointestinal problem, elevated inflammatory markers, no evidence of other microbial infections, and evidence of COVID-19 (RT-PCR, antigen test or serology positive), or likely contact with patients with COVID-19”. <P> Some criteria are similar, and others are different from Kawasaki disease and toxic shock syndrome, such as the presence of rash, conjunctivitis, mucocutaneous inflammation, and coronaries involvement are shared criteria between Kawasaki and MIS-C, whereas hypotensive shock and coagulopathy are shared criteria between MIS-C and toxic shock syndrome. The positive testing for COVID-19 in the absence of microbiological isolation confirms MIS-C. <P> Conclusion: Among the complications of COVID-19 infection, MIS-C is rare. Owing to the management differences among Kawasaki, toxic shock syndrome, and MIS-C, timely diagnosis of MIS-C saves the children from a poor outcome.</P>]]></description> </item><item><title><![CDATA[Why do Athletes Develop Very Severe or Fatal Forms of COVID after
Intense Exercise Following SARS-CoV-2 Infection or Anti-COVID
Vaccination?]]></title><link>https://www.benthamscience.comarticle/128739</link><description><![CDATA[]]></description> </item><item><title><![CDATA[Significance of Beta-Blocker in Patients with Hypertensive Left Ventricular
Hypertrophy and Myocardial Ischemia]]></title><link>https://www.benthamscience.comarticle/129214</link><description><![CDATA[<p> Background: Arterial Hypertension (HTN) is a key risk factor for left ventricular hypertrophy (LVH) and a cause of ischemic heart disease (IHD). The association between myocardial ischemia and HTN LVH is strong because myocardial ischemia can occur in HTN LVH even in the absence of significant stenoses of epicardial coronary arteries. </p><p> Objective: To analyze pathophysiological characteristics/co-morbidities precipitating myocardial ischemia in patients with HTN LVH and provide a rationale for recommending beta-blockers (BBs) to prevent/treat ischemia in LVH. </p><p> Methods: We searched PubMed, SCOPUS, PubMed, Elsevier, Springer Verlag, and Google Scholar for review articles and guidelines on hypertension from 01/01/2000 until 01/05/2022. The search was limited to publications written in English. </p><p> Results: HTN LVH worsens ischemia in coronary artery disease (CAD) patients. Even without obstructive CAD, several pathophysiological mechanisms in HTN LVH can lead to myocardial ischemia. In the same guidelines that recommend BBs for patients with HTN and CAD, we could not find a single recommendation for BBs in patients with HTN LVH but without proven CAD. There are several reasons for the proposal of using some BBs to control ischemia in patients with HTN and LVH (even in the absence of obstructive CAD). </p><p> Conclusion: Some BBs ought to be considered to prevent/treat ischemia in patients with HTN LVH (even in the absence of obstructive CAD). Furthermore, LVH and ischemic events are important causes of ventricular tachycardia, ventricular fibrillation, and sudden cardiac death; these events are another reason for recommending certain BBs for HTN LVH.</p>]]></description> </item><item><title><![CDATA[Cardiac Injury Following Chemo/Radiation Therapy: An Updated Review
on Mechanisms and Therapeutic Approaches]]></title><link>https://www.benthamscience.comarticle/129495</link><description><![CDATA[Cardiovascular disorders are among the critical side effects of cancer therapy. Damage to the function and normal structure of the heart can cause serious threats to patients that are being treated for cancer. Cardiovascular complications may be induced by various types of chemotherapy drugs and also radiation therapy. The severity of cardiovascular toxicity depends on several factors, such as types of drugs, tumor location for radiotherapy, the presence of cardiac disease history, the dose of drugs or ionizing radiation, etc. Radiotherapy and chemotherapy can cause heart diseases through various mechanisms, such as oxidative stress, inflammation, cell death, fibrosis, endothelial to mesenchymal transition (EndMT), etc. Chronic inflammation following damage to a huge number of cells can trigger more accumulation of inflammatory cells and chronic release of reactive oxygen species (ROS) and nitric oxide (NO). Oxidative stress can induce more cell death and cardiac remodeling through damage to vessels and valvular and disruption of the normal structure of the extracellular matrix. These changes may lead to cardiomyopathy, myocarditis, pericarditis, and vascular disorders that may lead to heart attack and death. This review provides basic information on cellular and molecular mechanisms of different types of cardiovascular disorders following cancer therapy by radiation or chemotherapy. We also recommend some adjuvants and targets to reduce the risk of heart toxicity by radiation/chemotherapy.]]></description> </item><item><title><![CDATA[Effect of Statins on the Blood Lipid Profile in Patients with Different
Cardiovascular Diseases: A Systematic Review with Meta-analysis of
Randomized Clinical Trials]]></title><link>https://www.benthamscience.comarticle/127895</link><description><![CDATA[<P>Background: Statins are the main lipid-lowering drugs and are used in the prevention of cardiovascular diseases (CVDs). Since the results have been, to some extent, inconsistent in the clinical trials concerning different types of CVDs, a systematic review and meta-analysis was performed to prove the effect of statins on decreasing elevated levels of total cholesterol, triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) in patients with CVDs. <P> Methods: Literature search was performed on major electronic databases (MEDLINE/ PubMed, Scopus, and ISI Web of Science) from inception up to July 2021 to find randomized controlled trials (RCTs) evaluating the effect of different statins on different types of CVDs. The effect size was determined using weighted mean difference (WMD) and corresponding 95% confidence interval (CI). <P> Results: Statin therapy significantly decreased levels of total cholesterol (WMD = -33.37 mg/dl, 95% CI: -45.98 to -20.76, P<0.001), LDL-C (WMD = -29.42 mg/dl, 95% CI: -36.81 to -22.03, P<0.001), and TG (WMD = -15.19 mg/dl, 95% CI = -26.41 to -3.97, P<0.001), and increased levels of HDL-C (WMD = 1.55 mg/dl, 95% CI: 0.20, to 2.90, P=0.02) in patients with different CVDs. <P> Conclusion: Statin therapy was found effective in lowering levels of total cholesterol, LDL-C, and TG, and increasing levels of HDL-C in patients with different CVDs.</P>]]></description> </item><item><title><![CDATA[Organoid Models of Heart Diseases: Find a New Channel in Improvements
of Cardiac Regenerative Medicine]]></title><link>https://www.benthamscience.comarticle/127139</link><description><![CDATA[We are experiencing a revolution in regenerative medicine. Recent developments in organoid technology have provided unique opportunities for studying human biology and diseases. Indeed, organoid models have revolutionized the in vitro culture tools for biomedical research by creating robust three-dimensional (3D) architecture to recapitulate the primary tissues&#039; cellular heterogeneity, structure, and functions. Such organoid technology enables researchers to re-create human organs and diseases model in a culture dish. It thus holds excellent promises for many translational applications such as regenerative medicine, drug discovery, and precision medicine. This review summarizes the current knowledge on the progression and promotion of organoid models, particularly with the heart disease approach. We discuss the usefulness of clinical applications of cardiac organoids and ultimately highlight the currently advanced therapeutic strategies in vitro model of organoids aimed at personalizing heart disease treatment.]]></description> </item><item><title><![CDATA[Clinical and Laboratory Evaluation of Acute Pericarditis Associated with
Antinuclear Antibodies Positivity]]></title><link>https://www.benthamscience.comarticle/129180</link><description><![CDATA[<p>Background: Up to 30% of patients with acute pericarditis develop recurrent pericarditis. Acute pericarditis may be a manifestation of an underlying systemic autoimmune disease. Therefore, we evaluated the characteristics of patients with acute pericarditis according to antinuclear antibodies (ANA) positivity/negativity. <p> Methods: Participants with acute pericarditis and negative ANA (n=29), recurrent pericarditis with positive ANA (n=30) and healthy controls (n=11) were examined. The groups were compared using serum parameters (ANA, C-reactive protein, leucocyte count, erythrocyte sedimentation rate, total antioxidant status, nitric oxide (NO), and oxidative stress index (OSI)) and imaging techniques (electrocardiogram, echocardiography, cardiovascular magnetic resonance, and venous Doppler ultrasound). <p> Results: In females, acute pericarditis associated with ANA occurred more frequently (p<0.001). ANApositive acute pericarditis had significantly lower NO and OSI (p<0.05 and p<0.001, respectively) and pericardial inflammation on magnetic resonance. We found a pulmonary embolism in one patient with positive ANA. Slow venous flow (SVF) occurred more often in acute pericarditis associated with ANA than in the ANA-negative group on venous ultrasound (p<0.05). The prevalence of positive ANAs was 1.6 times higher among SVF patients than in controls. <p> Conclusion: This study suggests that acute pericarditis associated with ANA is more common in middle- aged females. SVF and lower oxidative stress tests were more common in patients with ANAassociated acute pericarditis. Acute pericarditis associated with ANA could be considered as a hypercoagulable state. Therefore, all newly diagnosed pericarditis patients (especially females) should be checked for ANA positivity. Awareness of this coexistence should be promptly addressed to establish management strategies.</p>]]></description> </item><item><title><![CDATA[Multilevel Pharmacological Effects of Antipsychotics in Potential Glioblastoma
Treatment]]></title><link>https://www.benthamscience.comarticle/128553</link><description><![CDATA[Glioblastoma Multiforme (GBM) is a debilitating type of brain cancer with a high mortality rate. Despite current treatment options such as surgery, radiotherapy, and the use of temozolomide and bevacizumab, it is considered incurable. Various methods, such as drug repositioning, have been used to increase the number of available treatments. Drug repositioning is the use of FDA-approved drugs to treat other diseases. This is possible because the drugs used for this purpose have polypharmacological effects. This means that these medications can bind to multiple targets, resulting in multiple mechanisms of action. Antipsychotics are one type of drug used to treat GBM. Antipsychotics are a broad class of drugs that can be further subdivided into typical and atypical classes. Typical antipsychotics include chlorpromazine, trifluoperazine, and pimozide. This class of antipsychotics was developed early on and primarily works on dopamine D2 receptors, though it can also work on others. Olanzapine and Quetiapine are examples of atypical antipsychotics, a category that was created later. These medications have a high affinity for serotonin receptors such as 5- HT2, but they can also act on dopamine and H1 receptors. Antipsychotic medications, in the case of GBM, also have other effects that can affect multiple pathways due to their polypharmacological effects. These include NF-B suppression, cyclin deregulation, and -catenin phosphorylation, among others. This review will delve deeper into the polypharmacological, the multiple effects of antipsychotics in the treatment of GBM, and an outlook for the field's future progression.]]></description> </item><item><title><![CDATA[Kikuchi-Fujimoto Disease: A Distinct Pathological Entity but also an
"Overlap" Autoimmune Syndrome: A Systematic Review]]></title><link>https://www.benthamscience.comarticle/126139</link><description><![CDATA[<p>Background: The association between KFD and autoimmune diseases, not only with systemic lupus erythematosus, has been repeatedly described. <p> Objective: The aim of this review is to evaluate whether an overlap syndrome is present between KFD and autoimmune diseases, whether there is a chronological and a casual relationship between the pathologies. <p> Methods: The databases used for the overlap case search were Medline and Embase from which we extrapolated the studies of interest. The search queries used were: Kikuchi-Fujimoto Syndrome and juvenile idiopathic arthritis or systemic lupus erythematosus or Systemic Sclerosis or Antiphospholipid Syndrome or Sjogren's Syndrome. All study types were considered (n = 103). <p> Results: Total number of included studies are 43. We have shown that there is an \"overlap\" syndrome between KFD and other autoimmune diseases. The chronology of disease onset was variable; autoimmune disease may be \"preceding\" (n = 11 cases) or \"simultaneous\" (n = 20 cases) or \"post\" (n = 8 cases). Kikuchi-Fujimoto Syndrome. Also, the autoimmune disease can present with a complete clinical picture or only with the presence of autoantibodies. <p> Conclusion: the different pathologies associated with KFD with different chronologies would suggest that there is an alteration of the immune system that allows the pathologies to occur in different temporal relationships.</p>]]></description> </item><item><title><![CDATA[Atypical Debut of Granulomatosis with Polyangiitis as Acute Tonsilitis and Strawberry Gum: A Case Report]]></title><link>https://www.benthamscience.comarticle/122538</link><description><![CDATA[Abstract: Background: Granulomatosis with polyangiitis (GPA) is a systemic necrotizing vasculitis characterized by necrosis, granulomatous inflammation, and vasculitis. It is characterized by the triad of the upper and lower respiratory system, lung, and kidney disease. Although it is usually a multisystemic disease, limited forms have also been described, and otolaryngological involvement is the first manifestation in up to 80-95% of the cases. <p> Case Presentation: In this report, we describe the case of an ANCA negative patient with a limited form of GPA that presented a necrotic lesion confined to the right tonsil compatible with granulomatosis with polyangiitis, which later presented positive ANCA antibodies. Oral lesions may be the initial manifestation of GPA, and systemic involvement can be presented within weeks or months. Although the oral manifestations have been well described, the initial presentation with oral lesions is very rare, and presentation with oropharyngeal manifestation is even rarer. This disease is generally characterized by anti-neutrophil cytoplasmic antibodies (ANCA); however, there are rare cases with negative ANCA. <p> Conclusion: The diagnosis was established based on the clinical presentation and the histopathological findings of the characteristic inflammatory pattern.]]></description> </item><item><title><![CDATA[Interleukin-1 in Coronary Artery Disease]]></title><link>https://www.benthamscience.comarticle/127032</link><description><![CDATA[Cardiovascular disease is the leading cause of mortality worldwide. Inflammation has long been established as a key component in the pathophysiology of coronary artery disease. The interleukin-1 family consists of 11 members that regulate the inflammatory response through both pro- and anti-inflammatory properties with the Nod-like receptor (NLR) family pyrin domain containing 3 inflammasome having a pivotal role in the process of converting interleukin-1 beta and interleukin- 18, two key inflammatory mediators, into their mature forms. Interleukin-1 affects various cell types that participate in the pathogenesis of atherosclerosis as it enhances the expression of leukocyte adhesion molecules on the surface of endothelial cells and augments the permeability of the endothelial cell barrier, attracting monocytes and macrophages into the vessel wall and aids the migration of smooth muscle cells toward atheroma. It also enhances the aggregation of low-density lipoprotein particles in endothelium and smooth muscle cells and exhibits procoagulant activity by inducing synthesis, cell-surface expression and release of tissue factor in endothelial cells, promoting platelet adhesion. The value of interleukin-1 as a diagnostic biomarker is currently limited, but interleukin-1 beta, interleukin-18 and interleukin-37 have shown promising data regarding their prognostic value in coronary artery disease. Importantly, target anti-inflammatory treatments have shown promising results regarding atherosclerosis progression and cardiovascular events. In this review article, we focus on the immense role of interleukin-1 in atherosclerosis progression, inflammation cascade and in the clinical application of target anti-inflammatory treatments.]]></description> </item><item><title><![CDATA[Oncostatin M: Risks and Benefits of a Novel Therapeutic Target for
Atherosclerosis]]></title><link>https://www.benthamscience.comarticle/125420</link><description><![CDATA[<P>Background: Cardiovascular disease (CVD) is a leading cause of death worldwide. It is predicted that approximately 23.6 million people will die from CVDs annually by 2030. Therefore, there is a great need for an effective therapeutic approach to combat this disease. The European Cardiovascular Target Discovery (CarTarDis) consortium identified Oncostatin M (OSM) as a potential therapeutic target for atherosclerosis. The benefits of modulating OSM - an interleukin (IL)-6 family cytokine - have since been studied for multiple indications. However, as decades of high attrition rates have stressed, the success of a drug target is determined by the fine balance between benefits and the risk of adverse events. Safety issues should therefore not be overlooked. <P> Objective: In this review, a risk/benefit analysis is performed on OSM inhibition in the context of atherosclerosis treatment. First, OSM signaling characteristics and its role in atherosclerosis are described. Next, an overview of in vitro, in vivo, and clinical findings relating to both the benefits and risks of modulating OSM in major organ systems is provided. Based on OSM’s biological function and expression profile as well as drug intervention studies, safety concerns of inhibiting this target have been identified, assessed, and ranked for the target population. <P> Conclusion: While OSM may be of therapeutic value in atherosclerosis, drug development should also focus on de-risking the herein identified major safety concerns: tissue remodeling, angiogenesis, bleeding, anemia, and NMDA- and glutamate-induced neurotoxicity. Close monitoring and/or exclusion of patients with various comorbidities may be required for optimal therapeutic benefit.</P>]]></description> </item><item><title><![CDATA[The Role of NF-&#954;B in Myocardial Ischemia/Reperfusion Injury]]></title><link>https://www.benthamscience.comarticle/125515</link><description><![CDATA[Acute myocardial infarction (AMI) is a threat to human life and physical health worldwide. Timely reperfusion is very important to limit infarct size and protect ischemic myocardium. Unfortunately, it has also caused severer myocardial damage, which is called “myocardial ischemia/ reperfusion injury (MIRI)”. There is no effective clinical treatment for it. Over the past two decades, biological studies of NF-&#954;B have improved the understanding of MIRI. Nuclear Factor-&#954;B (NF-&#954;B) is a major transcription factor associated with cardiovascular health and disease. It is involved in the release of pro-inflammatory factors and apoptosis of cardiomyocytes. Recent studies have shown that inhibition of NF-&#954;B plays a protective role in acute hypoxia and reperfusion injury. Here we review the molecular regulation of NF-&#954;B in MIRI, better understanding of NF-&#954;B signaling mechanisms related to inflammation and crosstalk with endogenous small molecules. We hope this review will aid in improving therapeutic approaches to clinical diagnosing. This review provides evidence for the role of NF-&#954;B in MIRI and supports its use as a therapeutic target.]]></description> </item><item><title><![CDATA[ALKBH5 Expression could Affect the Function of T Cells in Systemic Lupus Erythematosus
Patients: A Case-control Study]]></title><link>https://www.benthamscience.comarticle/124603</link><description><![CDATA[<P>Background: N6-methyladenosine (m6A) modification is widespread in eukaryotic mRNA, regulated by m6A demethylase, AlkB homolog 5 (ALKBH5). However, the role of m6A in systemic lupus erythematosus (SLE) is still obscure. We explored ALKBH5 expression in SLE patients and its effects on T cells. <P> Methods: 100 SLE patients and 110 healthy controls were recruited to investigate the expression of ALKBH5 in peripheral blood mononuclear cells (PBMCs). An additional 32 SLE patients and 32 health controls were enrolled to explore the expression of ALKBH5 in T cells. Then we explored the function of ALKBH5 in T cells by lentivirus. <P> Results: The expressions of ALKBH5 were downregulated in both PBMCs and T cells in SLE patients (all P<0.05). In PBMCs: ALKBH5 mRNA levels were associated with a complement C4 level in plasma (P<0.05). In T cells: ALKBH5 mRNA levels were downregulated in SLE patients with low complement levels, high antidsDNA, anti-Sm, anti-RNP, and proteinuria compared with those without, respectively (all P<0.05); ALKBH5 mRNA levels were negatively related with SLE disease activity index score, erythrocyte sedimentation rate, and anti-dsDNA levels (all P<0.05), and positively correlated with complement C3 and C4 level (all P<0.05). Functionally, the overexpression of ALKBH5 promoted apoptosis and inhibited the proliferation of T cells (all P<0.05). <P> Conclusion: ALKBH5 expression is downregulated in SLE patients and could affect the apoptosis and proliferation of T cells, but the exact mechanism still needs to be further explored.</P>]]></description> </item><item><title><![CDATA[A Review on the Drug Delivery Strategies for Parasitic Infections: Scope
and Assertion]]></title><link>https://www.benthamscience.comarticle/121993</link><description><![CDATA[Parasitic infections are prime causes of morbidity and mortality worldwide. Significant progress has been made to cure these infections, such as discovering antiparasitic drugs, developing new formulation strategies, site-directed drug delivery, chemotherapy, etc. Synthetic drugs are perilous and have various side effects, leading to the development of drug resistance and loss of health. Herbal medicines are economical and generally free from potential side effects; therefore, they are acclaiming recognition. However, it is difficult to produce antiparasitic vaccines; major efforts have been made and still, there are no licensed vaccines currently available to control human parasitic ailments. This systematic review assesses various techniques for the treatment of parasitic infections. Moreover, the advancements and challenges involved in establishing novel trends in the development of more effective drug delivery systems are also investigated. Over the years, the incidences of several infectious ailments in humans have enhanced and it is estimated to further increase in the future. Over thirty new infective agents have been identified globally in the last 30 years; approximately 60 % of them are from zoonotic sources. Efficient drug delivery plays a key role in treating parasitic infections. The main goal of the modern antiparasitic drug delivery system is to minimize the potential side effects and deliver the drug directly to the target pathogens. Therefore, more sophisticated drug formulations than a simple tablet or solution are necessary for the treatment of many human parasitic diseases.]]></description> </item><item><title><![CDATA[Bisphenol A as a Factor in the Mosaic of Autoimmunity]]></title><link>https://www.benthamscience.comarticle/115636</link><description><![CDATA[<p>The population worldwide is largely exposed to bisphenol A (BPA), a commonly used plasticizer, that has a similar molecular structure to endogenous estrogens. Therefore, it is able to influence physiological processes in the human body, taking part in pathophysiology of various endocrinopathies, as well as, cardiovascular, neurological and oncological diseases. BPA has been found to affect the immune system, leading to the development of autoimmunity and allergies, too. <p> In the last few decades, the prevalence of autoimmune diseases has significantly increased that could be explained by a rising exposure of the population to environmental factors, such as BPA. BPA has been found to play a role in the pathogenesis of systemic autoimmune diseases and also organ-specific autoimmunity (thyroid autoimmunity, diabetes mellitus type 1, myocarditis, inflammatory bowel disease, multiple sclerosis, encephalomyelitis etc), but the results of some studies still remain controversial, so further research is needed.</p>]]></description> </item><item><title><![CDATA[Lesson from the Pandemic: People should Always Stay Physically Active]]></title><link>https://www.benthamscience.comarticle/119651</link><description><![CDATA[]]></description> </item><item><title><![CDATA[Plant Based Natural Products as Quorum Sensing Inhibitors in <i>E. Coli</i>: A
Critical Review]]></title><link>https://www.benthamscience.comarticle/118637</link><description><![CDATA[The existence of multidrug–resistant (MDR) E. coli (superbugs) is a global health issue confronting humans, livestock, food processing units, and pharmaceutical industries. The quorum sensing (QS) controlling ability of the E. coli to form biofilms has become one of the important reasons for the emergence of multidrug-resistant pathogens. Quorum signaling activation and formation of biofilm lead to the emergence of antimicrobial resistance of the pathogens increasing the therapy difficult for treating bacterial diseases. There is a crucial need, therefore, to reinforce newer therapeutic designs to overcome this resistance. As the infections caused by E. coli are attributed via the QSregulated biofilm formation, easing this system by QS inhibitors is a possible strategy for treating bacterial diseases. Plant based natural products have been reported to bind to QS receptors and interrupt the QS systems of pathogens by inhibiting biofilm formation and disrupting the formed biofilms, thus minimizing the chances to develop a resistance mechanism. The present report reviews critically the QS capability of E. coli to form biofilms leading to multidrug resistant pathogens and the investigations that have been carried out so far on plant acquired natural products as QS inhibitors.]]></description> </item><item><title><![CDATA[Neuropsychiatric Systemic Lupus Erythematosus: A Remaining Challenge]]></title><link>https://www.benthamscience.comarticle/123419</link><description><![CDATA[Systemic Lupus Erythematosus (SLE) is an autoimmune disease, which affects a wide range of organs with variable clinical features. Involvement of the nervous system is a challenging and multifaceted manifestation of the disease, presenting with a broad range of symptoms. Neuropsychiatric lupus (NPSLE) encompasses seven syndromes of the peripheral and 12 of the central nervous system, associated with a high disease burden. Despite advances in the management of SLE, NP manifestations still pose a challenge to clinicians. First, diagnosis and attribution of SLE are difficult due to the lack of specific biomarkers or imaging modalities. Second, therapeutic options are limited, and evidence is mainly based on case reports and expert consensus, as clinical trials are sparse. Moreover, no validated outcome measure on disease activity exists. Current recommendations for treatment include supportive as well as immunosuppressive medication, depending on the type and severity of manifestations. As NPSLE manifestations are increasingly recognized, a broader spectrum of therapeutic options can be expected.]]></description> </item><item><title><![CDATA[COVID-19 Vaccination in Children: An Open Question]]></title><link>https://www.benthamscience.comarticle/119505</link><description><![CDATA[<p>Background: A safe and effective vaccine represents the best way to control the COVID-19 pandemic, which has caused more than 4 million deaths to date. Several vaccines have now been approved worldwide, depending on the country. Being administered to healthy people, anti-SARS-CoV-2 vaccines must meet high safety standards, and this is even more important among the pediatric population in which the risk of developing severe disease is significantly lower than adults. However, vaccination of the pediatric population could help in reducing viral spread in the whole population. <p> Objective: Our narrative review analyzes and discusses the currently available literature on the advantages and disadvantages of COVID-19 vaccination in the pediatric population. <p> Methods: A bibliographic research was conducted through Pubmed, Read, and Scopus using COVID-19, SARS-CoV-2, immunization, antibody, COVID-19 vaccine efficacy, COVID-19 vaccine safety, children, adolescents, MIS-C, adverse effects as keywords. <p> Results: Although children are less susceptible to COVID-19 infection, they can develop serious consequences, including multi-inflammatory syndrome. However, any vaccine-related side effects should be evaluated before administering vaccination to children while ensuring complete safety. To date, adverse effects are reported in adolescents and young adults following vaccination; however, these are mostly isolated reports. <p> Conclusion: Further investigation is needed to establish whether there is indeed a cause-and-effect relationship in the development of vaccine-related adverse effects. However, to date, COVID-19 vaccination is recommended for children and adolescents older than 12 years of age. However, this question is still under debate and involves ethical, political, and social issues.</p>]]></description> </item><item><title><![CDATA[A Clinical Perspective of Soluble Epoxide Hydrolase Inhibitors in
Metabolic and Related Cardiovascular Diseases]]></title><link>https://www.benthamscience.comarticle/118046</link><description><![CDATA[Epoxide hydrolase (EH) is a crucial enzyme responsible for catabolism, detoxification, and regulation of signaling molecules in various organisms including human beings. In mammals, EHs are classified according to their DNA sequence, sub-cellular location, and activity into eight major classes: soluble EH (sEH), microsomal EH (mEH), leukotriene A4 hydrolase (LTA4H), cholesterol EH (ChEH), hepoxilin EH, paternally expressed gene 1 (peg1/MEST), EH3, and EH4. The sEH, an &#945;/&#946;-hydrolase fold family enzyme, is an emerging pharmacological target in multiple diseases namely, cardiovascular disease, neurodegenerative disease, chronic pain, fibrosis, diabetes, pulmonary diseases, and immunological disease. It exhibits prominent physiological effects including anti-inflammatory, anti-migratory, and vasodilatory effects. Its efficacy has been documented in various clinical trials and observational studies. This review specifically highlights the development of soluble epoxide hydrolase inhibitors (sEHIs) in the clinical setting for the management of metabolic syndrome and related disorders, such as cardiovascular effects, endothelial dysfunction, arterial disease, hypertension, diabetes, obesity, heart failure, and dyslipidemia. In addition, limitations and future aspects of sEHIs have also been highlighted which will help the investigators to bring the sEHI to the clinics.]]></description> </item><item><title><![CDATA[Using Colchicine in Pregnant Women with Pericarditis: Recommended or
Not?]]></title><link>https://www.benthamscience.comarticle/118361</link><description><![CDATA[]]></description> </item><item><title><![CDATA[Pharmacological Interventions for the Prevention and Treatment of Kidney
Injury Induced by Radiotherapy: Molecular Mechanisms and Clinical
Perspectives]]></title><link>https://www.benthamscience.comarticle/117459</link><description><![CDATA[More than half of cancer patients need radiotherapy during the course of their treatment. Despite the beneficial aspects, the destructive effects of radiation beams on normal tissues lead to oxidative stress, inflammation, and cell injury. Kidneys are affected during radiotherapy of abdominal malignancies. Radiation nephropathy eventually leads to the release of factors triggering systemic inflammation. Currently, there is no proven prophylactic or therapeutic intervention for the management of radiation-induced nephropathy. This article reviews the biomarkers involved in the pathophysiology of radiation-induced nephropathy and its underlying molecular mechanisms. The efficacy of compounds with potential radioprotective properties on amelioration of inflammation and oxidative stress is also discussed. By outlining the approaches for preventing and treating this critical side effect, we evaluate the potential treatment of radiation-induced nephropathy. Available preclinical and clinical studies on these compounds are also scrutinized.]]></description> </item><item><title><![CDATA[Molecular and Biochemical Pathways Encompassing Diabetes Mellitus
and Dementia]]></title><link>https://www.benthamscience.comarticle/118796</link><description><![CDATA[Diabetes mellitus is a major metabolic disorder that has now emerged as an epidemic, and it affects the brain through an array of pathways. Patients with diabetes mellitus can develop pathological changes in the brain, which eventually take the shape of mild cognitive impairment, which later progresses to Alzheimer’s disease. A number of preclinical and clinical studies have demonstrated this fact, and molecular pathways, such as amyloidogenesis, oxidative stress, inflammation, and impaired insulin signaling, are found to be identical in diabetes mellitus and dementia. However, the critical player involved in the vicious cycle of diabetes mellitus and dementia is insulin, whose signaling, when impaired in diabetes mellitus (both type 1 and 2), leads to a decline in cognition, although other pathways are also essential contributors. Moreover, it is not only the case that patients with diabetes mellitus indicate cognitive decline at a later stage, but many patients with Alzheimer’s disease also reflect symptoms of diabetes mellitus, thus creating a vicious cycle inculcating a web of complex molecular mechanisms and hence categorizing Alzheimer’s disease as ‘brain diabetes.’ Thus, it is practical to suggest that anti-diabetic drugs are beneficial in Alzheimer’s disease. However, only smaller trials have showcased positive outcomes mainly because of the late onset of therapy. Therefore, it is extremely important to develop more of such molecules that target insulin in patients with dementia along with such methods that diagnose impaired insulin signaling and the associated cognitive decline so that early therapy may be initiated and the progression of the disease can be prevented.]]></description> </item><item><title><![CDATA[Gemcitabine-Related Atrial Fibrillation: A Case Report and Review of the
Literature]]></title><link>https://www.benthamscience.comarticle/117289</link><description><![CDATA[<p>Introduction: Gemcitabine is a commonly used antimetabolite that has been effective in a broad spec- trum of tumors so far. The main grade three and four known toxicity of this drug is myelosuppres- sion. Cardiac adverse events have been rarely reported and gemcitabine-induced Atrial-Fibrillation (AF) has been described in only five previous cases so far. Here we report the 6th case of gemc- itabine-related AF. <p> Case Presentation: A 68-year-old man diagnosed with metastatic nasopharyngeal cancer was referred to our oncology department. He started first-line chemotherapy with gemcitabine and cisplatin. He presented poorly tolerated atrial fibrillation related to gemcitabine infusion that lasted for six days. The treatment was then withdrawn, and the patient received the best supportive care. <p> Conclusion: We conclude that medical oncologists and cardiologists should be aware of such toxicities of gemc- itabine, especially in the elderly who seem to be at a higher risk of such adverse events and which may dictate discontinuation of the drug.</p>]]></description> </item><item><title><![CDATA[Empirical Antimicrobial Therapy and QTc Interval Prolongation in Emergency
Medicine]]></title><link>https://www.benthamscience.comarticle/116396</link><description><![CDATA[<P>Background: QTc prolongation is common in dangerous clinical conditions, associated with an increased risk of life-threatening arrhythmia torsades de pointes. The goal of this short communication is to evaluate the principal causes of risk of QTc prolongation that are observed in an emergency department and discuss the differences between drug- and non-drug-associated factors. <P> Methods: The retrospective analysis was carried out on 130 patients that presented a QTc prolongation (>480 ms for man and >470 for female, respectively), admitted to the emergency department of a single Italian hospital. Patients with pace-maker (22) were excluded from this study. For each patient, a minimum of 3 ECGs (12 leads) were recorded. Attention was paid on electrolytes disturbances and to the pharmacotherapy, with a particular emphasis to the use of antibiotics. <P> Results: Mean age of the patients was 79.6 years (SD=11.3) and females and males were almost equally present (46.6% F, 53.7% M). The average QTc value was 492.2 ms (493.3 ms F, 492.8 M). The patients were divided in those with electrolytes disturbances (24.0%), antimicrobial therapy (35.2%), both antimicrobial therapy and electrolytes disturbances (24.1%), and other causes of QTc prolongation (16.7%). <P> Conclusion: This analysis shows the relevance of the empirical therapy established at the admission, in particular for infective diseases, as an important risk factor for the prolongation of QTc. Other factors that can increase the risk are electrolytes alterations, advanced age, cardiovascular diseases, and drug-drug interaction.</P>]]></description> </item><item><title><![CDATA[Do We Have Good Activity Indices in Systemic Sclerosis?]]></title><link>https://www.benthamscience.comarticle/117888</link><description><![CDATA[Background: No fully validated index is available for assessing overall disease activity in systemic sclerosis (SSc). <P> Objectives: To estimate the effect of disease activity as measured by different disease activity indices on the risk of subsequent organ damage. <P> Methods: The European Systemic sclerosis study group activity index (EScSG AI), the European Scleroderma Trials and Research Group Activity Index (r-EUSTAR AI), 12 point activity index proposed by Minier (12point AI) were calculated for 91 patients; the CRISS (The Composite Response Index for Systemic Sclerosis) for patients included after 2016. Data were analysed by parametric and non-parametric tests and logistic regression. <P> Results: EscSG AI, r-EUSTAR AI and 12point AI correlated with lung involvement. EScSG AI and r-EUSTAR AI correlated with diffuse skin involvement. EscSG AI correlated with digital ulcers and diffuse cutaneous involvement and r-EUSTAR AI with a renal crisis. Bivariate analysis showed an inverse correlation between the three disease activity scores and forced vital capacity (FVC) (<i>p</i><0.001) and diffusing capacity for carbon monoxide (DLCO) (<i>p</i><0.001) and positive correlation with pulmonary fibrosis (<i>p</i><0.001), modified Rodnan skin score (mRSS) (<i>p</i><0.001), health assessment questionnaire (HAQ) (<i>p</i><0.001), systolic pulmonary pressure (sPAP) (<i>p</i><0.001), C-reactive protein (CRP) (<i>p</i><0.001) and capillaroscopy scoring (<i>p</i><0.001) at both baseline visit and the 3-year follow-up visit. Logistic regression revealed that baseline EScSG AI adjusted for gender and age and that baseline 12-point AI both adjusted and unadjusted predicted worse skin involvement at 3-year follow-up; while adjusted EScSG AI predicted decreasing DLCO. Also, 12-point AI predicted a decline of FVC and higher HAQ scores at 3-year follow up; while baseline r-EUSTAR AI was able to predict muscular deterioration, decline of FVC and the increase of HAQ score during 3 years of following. An active disease according to EScSG AI at first visit predicted progression of joint involvement while an active disease at baseline showed by r- EUSTAR AI predicted muscular deterioration, FVC and DLCO worsening, as well as an increase in HAQ score during the follow-up period. r-EUSTAR AI was the only score to predict the decrease of FVC in a multiple regression prediction model (OR= 1.306 (1.025, 1.665), <i>p</i>=0.31) while baseline EScSG AI best predicted worsening of DLCO (OR=1.749 (1.104, 2.772), <i>p</i>=0.017). <P> Conclusion: Our study could not establish a gold standard to assess disease activity in SSc; especially EscSG AI and r-EUSTAR AI could quantify and predict major organ involvement in daily practice. CRISS can be useful as an outcome measure for patients with short disease duration included in clinical studies.]]></description> </item><item><title><![CDATA[Surgical Treatment of Pulmonary Embolism and Chronic Thromboembolic
Pulmonary Hypertension]]></title><link>https://www.benthamscience.comarticle/117644</link><description><![CDATA[Venous thromboembolism clinically presents as deep venous thrombosis or acute pulmonary embolism and is globally recognized as the third most frequent acute cardiovascular syndrome after myocardial infarction and stroke. Although pulmonary embolism does not typically cause severe pulmonary hypertension in the acute setting, thrombus organization and fibrosis can lead to stenosis or obliteration of pulmonary arteries in a minority of patients, which in turn result in severe pulmonary hypertension and right heart failure. This disease is labeled chronic thromboembolic pulmonary hypertension and can occur after a single episode or multiple ones of pulmonary embolism. The cornerstone of pulmonary embolism treatment is medical therapy, whereas systemic thrombolytic therapy has to be considered for patients with hemodynamic instability. Given the current acceptable short-term surgical mortality, the potential of first-line surgical embolectomy as an alternative to medical thrombolysis has gained momentum as far as pulmonary embolism treatment is concerned. In contrast to pulmonary embolism, bilateral complete pulmonary endarterectomy under short deep hypothermic circulatory arrest intervals is the treatment of choice against chronic thromboembolic pulmonary hypertension, given patients’ operability. Pulmonary endarterectomy is suggested in every operable patient when the operation is offered by an experienced multidisciplinary team, including at least one experienced surgeon. Surgical embolectomy should also be limited to large institutions since it also requires an experienced heart team. This review concerns a thorough discussion regarding surgical treatment of pulmonary embolism and chronic thromboembolic pulmonary hypertension. Eligibility criteria, operation-related complications and postoperative outcomes are discussed in detail.]]></description> </item><item><title><![CDATA[Constrictive Pericarditis Associated with Coronavirus Disease 2019 (COVID-19): A Case Report]]></title><link>https://www.benthamscience.comarticle/112239</link><description><![CDATA[Background: Since December 2019, there has been an increasing number of patients infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) around the world. As of March 2020, the World Health Organization declared a global pandemic. <p> Case Presentation: To our best knowledge, this is the first report of a patient with SARS-CoV-2 infection presenting with constrictive pericarditis, possibly from the COVID infection. She was presented after a week of fever, persistent dry cough, and diarrhea. She received a single dose of hydroxychloroquine 400 mg, Oseltamivir 75 mg every 12 hours, lopinavir/ritonavir (Kaletra) 400/100 mg every 12 hours, and levofloxacin 750 mg daily. After 24 hours, she was immediately transferred to the Intensive Care Unit (ICU) because of dyspnea and progressive respiratory failure with a drop of the O2 saturation to 70%. <p> Conclusion: After a week of progress, her respiratory condition deteriorated again. She was re-admitted to the ICU and she expired. She died due to constrictive pericarditis, most probably caused by SARS-CoV-2.]]></description> </item><item><title><![CDATA[Radioprotective Effects of Plants from the Lamiaceae Family]]></title><link>https://www.benthamscience.comarticle/111012</link><description><![CDATA[Background: Edible and medicinal plants are still an interesting source of promising biologically active substances for drug discovery and development. At a time of increasing cancer incidence in the world, alleviating the bothersome side effects of radiotherapy in debilitated cancer patients is becoming an important challenge. <p> Objective: The aim of the study was to overview the literature data concerning the radioprotective activity of extracts, essential oils, and some chemical compounds obtained from 12 species belonging to the Lamiaceae family, gathering of numerous spice and medicinal plants rich in valuable phytochemicals. <p> Results: The analysis of available publications showed radioprotective effectiveness of essential oils and complex extracts containing phenolic acids and flavonoids in various <i>in vitro</i> and <i>in vivo</i> models. Relatively welldocumented preventive properties exhibited the following species: <i>Mentha × piperita, Ocimum tenuiflorum, Origanum vulgare</i>, and <i>Rosmarinus officinalis</i>. However, few plants such as <i>Lavandula angustifolia, Mentha arvensis, M. spicata, Plectranthus amboinicus, Salvia miltiorrhiza, S. officinalis, Scutellaria baicalensis</i>, and <i>Zataria multiflora</i> should be more investigated in the future. Among the mechanisms of radioprotective effects of well-studied extracts and phytochemicals, it can be mentioned mainly the protection against chromosomal damage, scavenging free radicals, decreasing of lipid peroxidation and elevating of glutathione, superoxide dismutase, catalase, and alkaline phosphatase enzyme levels as well as the reduction of the cell death. The plant substances protected the gastrointestinal tract, bone marrow and lung fibroblasts. <p> Conclusion: The studied species of Lamiaceae family and their active chemical compounds are potent in alleviating the side effects of radiotherapy and should be considered as a complementary therapy.]]></description> </item><item><title><![CDATA[Natural Bioactive as a Potential Therapeutic Approach for the Management of Cyclophosphamide-induced Cardiotoxicity]]></title><link>https://www.benthamscience.comarticle/117336</link><description><![CDATA[Cyclophosphamide (CP) is an extensively used anticancer drug, but its cardiotoxic manifestation is a major concern for its widespread clinical use. The observed cardiotoxic attributes have been reported at the therapeutic dose and often result into a high mortality rate and poor clinical outcome. Fall in the level of antioxidant enzymes catalase (CAT), reduced glutathione (GSH), superoxide dismutase (SOD) generation of reactive oxygen species (ROS), inflammatory cytokines nuclear factor kappa-light-chain enhancer of activated B cells (NF-kB), tumor necrosis factor-alpha (TNF-&#945;), interleukin 1 beta (IL- 1&#946;), apoptotic proteins (caspases) and direct damage to myocardial tissue (histological and ultrastructural damage) are some of the reported manifestations of cardiotoxicity. The observed clinical attributes of CP-induced cardiotoxicity are myocarditis, hemorrhage, thrombosis, myocardial infarction (MI), reduced ejection fraction, altered electrocardiogram (ECG) reading and heart failure. However, unlike Daxarazasone (an adjuvant to reduce doxorubicin-induced cardiotoxicity), no approved adjuvant is available to mitigate CPinduced cardiotoxicity. Thus, various natural bioactives have been explored for the possible cardioprotective effect against CP-induced cardiotoxicity. In the current manuscript, we have discussed the clinical and preclinical aspects of CP-induced cardiotoxicity, its clinically used combination with other anticancer drugs, and the available therapeutic regimen to mitigate this cardiotoxicity. Further, we discussed the limitations of available synthetic drugs used as an adjuvant and discussed various natural bioactive and their experimental details. This manuscript's overall goal is to throw light on CP-induced cardiotoxicity and summarize all the experimental data so that researchers working in this field may scientifically get up-to-date information in one place.]]></description> </item><item><title><![CDATA[Comparison of Granulomatosis with Polyangiitis Clinical Features in Patients Depending on Involvement or Absence of Kidney Involvement]]></title><link>https://www.benthamscience.comarticle/116854</link><description><![CDATA[<P>Background: GPA is necrotizing inflammation of the small vessels with granulomas. Kidney involvement deteriorated its prognosis. <P> Objective: Comparison of GPA patients with Kidney (KI) and without Kidney Involvement (nKI). <P> Materials and Methods: We conducted a cross-sectional study of 50 consecutive adult GPA patients, 25 KI from Nephrology and 25 nKI from the Rheumatology Department of Central Clinical Hospital Ministry of Interior in Warsaw. We analyzed clinical features, organ involvement, laboratory, serological, imaging, histopathological data, BVAS and treatment. <P> Results: The mean age of KI patients was statistically older than nKI (67.3±9.5 vs. 55.1±15.9, p=0.002). Generalized, severe, disease resistance was observed respectively in 92% vs. 44%, p<0.001. The number of red blood cells (3.47 vs. 4.41T/l, p<0.001), hemoglobin (10.0 vs. 12.9 g/dl, p<0.001) was lower in KI, higher mean serum creatinine (3.95 vs. 0.89 mg/dl, p<0.001), lower GFR (20.1 vs. 79.3, p<0.001), higher CRP (median: 43.4 vs. 2.0 mg/l, p<0.001), BVAS (16.6±4.4 vs. 10.1±6.2, p<0.001), c-ANCA (median: 119.0 vs. 15.2CU, p=0.017). Nodules in 28% KI, in 4% nKI (p=0.048) in chest X-ray, infiltration in 43.5% KI, in 15% nKI (p=0.042) in HRCT were observed. Skin granulomas were found in 61.5% nKI vs. 18.2% KI, (p=0.047). Renal biopsy revealed in KI patients focal segmental glomerulonephritis in 11.8%, crescentic glomerulonephritis in 17.6%, and pauci-immune crescentic glomerulonephritis in 70.6%. <P> Conclusion: In patients with KI we found generalized, severe, resistant GPA, higher BVAS more frequently than inpatients without KI. The results of laboratory parameters were worse in patients with KI. Aggressive immunosuppressive treatment is often used in the KI group.</P>]]></description> </item><item><title><![CDATA[Medicinal Herbs with Anti-Inflammatory Activities for Natural and Organic Healing]]></title><link>https://www.benthamscience.comarticle/118797</link><description><![CDATA[One of the principal causes of different disorders is an uncontrolled inflammatory response. Alkaloids, flavonoids, polyphenolic, proanthocyanidin, terpenoid, and steroid compounds are the main reasons for the anti-inflammatory activities of medicinal herbs and plants. The current manuscript introduces a series of potential anti-inflammatory plants, particularly those which are routines in Iranian and Chinese traditional herbal medicine, and simplifies the function and mechanisms of natural constituents for the prevention and treatment of inflammatory disorders. PubMed, Science Direct, Google Scholar, Wiley Online Library, Springer, Taylor, Francis, etc., have been used to search for collecting of scientific publications for a full evaluation of current documentation in the literature showing the importance of medicinal plants with anti-inflammatory characteristics and natural medicines. The most notable medicinal plants with anti-inflammatory activities are Baccharis dracunculifolia, Aconitum bulleyanum, Crateya adansonii, Alliums spp., Centella asiatica, Flos lonicerae, Corydalis dubia, Syringae folium, Coptis chinensis, Casearia decandra, Nigella sativa, Cannabis sativa, Tamarindus indica L., Glycyrrhiza glabra, Panax ginseng, Panax notoginseng, Pistacia vera, Smilax china, Scutellaria baicalensis, Rosemarinus officinalis, Moringa olifera, Pulsatilla radix, Pistacia atlantica, Rullia tuberose, Canarium album, Dodonaea polyandra, Forsythia suspense, Polygala tenuifolia, Radiz Isatidis, Hypericum sampsonii, Geranium koreanum, Typha capensis, Isatidis folium, Ginkgo biloba, Houttuynia cordata, snow lotus, etc. Herbal medicine mainly uses numerous parts of plants or combinations of them to prevent and remedy diseases and promote health. More investigations and clinical experiments are needed to provide more information on the importance of medicinal plants as well as their roles in the treatment and prevention of inflammatory diseases.]]></description> </item><item><title><![CDATA[Atypical Manifestations of Severe Acute Respiratory Syndrome Coronavirus 2 Infection in Children: A Systematic Review]]></title><link>https://www.benthamscience.comarticle/115225</link><description><![CDATA[<P>Background: In December 2019, a local outbreak of pneumonia was presented in Wuhan (China) and quickly identified to be caused by a novel coronavirus, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). The disease caused by SARS-CoV-2 was named COVID-19 and was soon declared a pandemic because of the millions of infections and thousands of deaths worldwide. Children infected with SARS-CoV-2 usually develop the asymptomatic or mild type of disease compared to adults. They are also more likely to have atypical and non-specific clinical manifestations than adults. </P><P> Methods: A literature search was performed through PubMed and Scopus to summarize the extrapulmonary manifestations of SARS-CoV-2 infection in children since the beginning of the pandemic. Peer-reviewed papers in English were retrieved using the following keywords and combinations: ‘pediatric,’ ‘child,’ ‘infant,’ ‘neonate,’ ‘novel coronavirus,’ ‘SARS-CoV-2,’ ‘COVID 19’ and ‘gastrointestinal,’ ‘renal,’ ‘cardiac,’ ‘dermatologic’ or ‘ophthalmologic’. We included published case series and case reports providing clinical symptoms and signs in SARS-CoV2 pediatric patients. </P><P> Results: Although fever and symptoms of upper respiratory infection are the most frequently presented, a variety of other atypical presentations has also been reported. The clinical spectrum includes dermatological, ophthalmological, neurological, cardiovascular, renal, reproductive, and gastrointestinal presentations. In addition, a rare multi-inflammatory syndrome associated with SARS-- CoV-2 infection has been reported in children, often leading to shock and requiring inotropic support and mechanical ventilation. </P><P> Conclusion: Clinicians need to be aware of the wider range of extrapulmonary atypical manifestations of SARS-CoV-2 infection in children, so that appropriate testing, treatment, and public health measures can be implemented rapidly.</P>]]></description> </item><item><title><![CDATA[Adverse Reactions Induced by Minocycline: A Review of Literature]]></title><link>https://www.benthamscience.comarticle/113447</link><description><![CDATA[<P>Background: Minocycline is a tetracycline antibiotic that is widely used to treat infections and is a first-line oral antibiotic in the treatment of moderate to severe inflammatory acne. Although it has high efficacy, several adverse reactions, including life-threatening ones, have been reported in association with its use. </P><P> Objective: To identify all the potential adverse reactions due to minocycline and analyze them in terms of the number of cases reported so far, salient features, severity and clinical outcome. </P><P> Methods: Comprehensive PubMed search of English and non-English literature for case reports of adverse reactions to minocycline was conducted. </P><P> Results: A total of 550 cases were identified from over 200 publications. The major reported adverse events caused by minocycline are drug reaction with eosinophilia and systemic symptoms syndrome, autoimmune syndromes like hepatitis, lupus and vasculitis, acute eosinophilic pneumonia, pseudotumor cerebri, hyperpigmentation, serum sickness-like reaction, Sweet’s syndrome and drug fever. Several other reactions involving multiple organ systems have also been reported. These show an overlap of clinical features and may be associated with multiple events causing considerable morbidity. Eight of these cases resulted in the death of the patients. </P><P> Conclusion: In view of the evident potential of minocycline to cause long-lasting and severe adverse effects, significant morbidity and even mortality, it should be prescribed with caution in the first-line treatment for moderate to severe acne.</P>]]></description> </item><item><title><![CDATA[Relationship between Augmentation Index and Wall Thickening Fraction during Hypotension in an Animal Model of Myocardial Ischemia-Reperfusion and Heart Failure]]></title><link>https://www.benthamscience.comarticle/115016</link><description><![CDATA[<p>Aims: Non-invasive indices to evaluate left ventricular changes during ischemic heart failure are needed to quantify the myocardial impairment and the effectiveness of therapeutic manoeuvres. The aims of this work were to calculate the Wall Thickening Fraction (WTF) and the Augmentation Index (AIx) and to assess the relationship between WTF and AIx using data obtained from an animal model with heart failure followed by a myocardial ischemia stage and a reperfusion stage. </P><P> Methods: Nine Corriedale sheep that had been monitored for 10 minutes during a basal stage underwent 5-minute myocardial ischemia, followed by 60-minute reperfusion. Seven of them were subjected to an induced heart failure through an overdose of halothane, two of which were treated with intra-aortic counterpulsation during the reperfusion stage. The remaining two animals were monitored during their ischemia-reperfusion stage. </P><P> Results: Data obtained in the 5 animals suffering from heart failure followed by myocardial ischemia showed that: a) heart failure induction determined decrease in cardiac output, cardiac index and systolic and diastolic aortic pressure (AoP) with respect to their basal values (p<0.05), b) myocardial ischemia decreased the WTF compared with basal and induced heart failure values (p<0.05), c) during the reperfusion stage accompanied by induced heart failure, WTF increased with respect to values observed during the ischemia induction stage (p<0.05); nevertheless, basal values were not recovered after reperfusion (p<0.05). During this 60-minute stage, systolic and diastolic AoP values were lower (p<0.05) than those at the basal stage. </P><P> Conclusion: AIx and WTF values calculated from synchronically recorded values of aortic pressure and left ventricular wall thickness during the reperfusion stage in all animals (n = 9) showed a negative correlation (p<0.05). Analysed data provided evidence of a negative relationship between a left ventricular index of myocardial function and an arterial index obtained from AoP waves.</p>]]></description> </item><item><title><![CDATA[Pathophysiology of Cardiovascular Diseases and the Role of Vitamins, and Herbal Extracts in the Reduction of Cardiovascular Risks]]></title><link>https://www.benthamscience.comarticle/112488</link><description><![CDATA[<P>Background: Heart disease (cardiovascular disease: CVD) is considered the leading cause of worldwide death. These diseases are recognized as group of disorders which are related to heart and blood vessels. Generally, heart diseases are considered life style associated diseases but many other factors are also found associated with cardiovascular diseases. </P><P> Objective: The aim of this review is to provide the till date information regarding local and circulatory disorders, role of different vitamins and herbs on heart diseases. </P><P> Methods: This review article contains a detailed survey of literature about cardiovascular diseases, which was available in different online databases such as; PubMed, Web of Science, Science Direct, Elsevier, and Google Scholar, etc. In this review, the authors have focused on the description of cardiovascular disorders, their pathophysiological properties and importance of micronutrients, vitamins and herbs in the management of cardiovascular diseases. </P><P> Results: Cardiovascular diseases are considered responsible for approximately 17.9 million deaths annually at the global level. Surprisingly, low- and middle-income countries count for 75% of CVD deaths. These diseases represent disorders related to circulatory systems specially heart and coronary arteries. Many lifestyle associated factors such as; high cholesterol consumption, smoking, alcohol consumption, tobacco use, metabolic disorders, stress, and other factors such as; family history, age, gender and genetic factors, etc. have been found involved in occurrence of CVDs. That’s why management of diet, management of tobacco and alcohol consumption, management of stress, increased physical activities are considered population-wide strategies for control cardiovascular diseases. On the basis of pathophysiology, heart diseases are of many types and out of them, Acute Myocardial Infarction (AMI) and Sudden Cardiac Death (SCD) are considered serious and catastrophic cardiac disorders. Intake of vitamins, micronutrients, lycopene, omega 3 fatty acid and many herbs like Crataegus oxyacantha (Hawthron), Allium sativum (garlic), Salvia miltiorrhiza (Danshen), Ganoderma lucidum (lingzhi), Ginkgo biloba have been identified good for cardiovascular diseases management and treatment. </P><P> Conclusion: Cardiovascular diseases are considered one of the fatal clinical conditions, as many of them are asymptomatic. The regulation of diet, increased physical activities, and healthy lifestyle are recommended to control the development of cardiovascular problems. Including this, scientific studies have supported the role of many vitamins, nutrients and herbs as beneficial in cardiovascular diseases, but many of them could not demonstrate their role at clinical level but it is suggested that their role as nutrients can not be ignored and their consumption may reduce the cardiovascular risks.</P>]]></description> </item><item><title><![CDATA[Association of Viruses in the Development of Cardiovascular Diseases]]></title><link>https://www.benthamscience.comarticle/115463</link><description><![CDATA[Cardiovascular diseases (CVD), primarily inflammatory cardiomyopathy, are characterized by the infiltration of inflammatory cells into the myocardium. It has a relatively high risk of deteriorating heart function and has heterogeneous etiologies. Inflammatory cardiomyopathy is mainly mediated by viral infections but can also be mediated by protozoa, fungal or bacterial infections. Besides that, there are a wide variety of drugs, toxic substances, and systemic immune-mediated diseases that result in the development of cardiovascular diseases (CVDs). Despite broad research, inflammatory cardiomyopathy has a poor prognosis. The roles of the pathogens, host genomic counterparts and environmental triggers in the progression of disease are still under consideration, including the role of some viruses as active inducers and others as bystanders. In this review article, we review the available evidence on the types, pathogenesis and treatment of myocarditis, inflammatory cardiomyopathy, and atherosclerosis with a particular focus on virus-associated cardiac diseases.]]></description> </item><item><title><![CDATA[New Viral Infection COVID-19: Current Status, Challenges and Possible Treatments]]></title><link>https://www.benthamscience.comarticle/112682</link><description><![CDATA[Since December 2019, the prevalence of novel coronavirus infection (named as COVID- 19 by WHO on Feb 11, 2020) has become a growing healthcare concern worldwide. On March 11, 2020, the WHO declared COVID-19 a global pandemic. As no specific approved treatment options are available for the COVID-19 infection, several existing antiviral drugs in combination with others have become the mainstay therapy. The targets for the treatment of the infection include viral targets such as polymerases, spike glycoproteins, membrane proteins, and viral envelope and host targets such as host proteases and host receptors. Antiviral agents, immunomodulatory agents, and empiric broad-spectrum antibiotics can be used as treatment therapies for the infection. Convalescent plasma therapy has also been proposed as an effective treatment for COVID-19. Additionally, many studies are ongoing to develop a potent and effective vaccine that completely blocks SARS-CoV-2. Nevertheless, prevention of spread of the virus remains the first and foremost step towards controlling and managing the coronavirus infection.]]></description> </item><item><title><![CDATA[Myocardial Infarction in Systemic Lupus Erythematosus – the Sex-Specific Risk Profile]]></title><link>https://www.benthamscience.comarticle/112284</link><description><![CDATA[<p>Background: Accelerated atherosclerosis is widely present in patients with systemic lupus erythematosus. </P><P> Objective: The aim of this review was to analyze the relationship between systemic lupus erythematosus and cardiovascular diseases, with the emphasis on acute myocardial infarction. </P><P> Methods: We conducted a literature review through PubMed and Cochrane, using keywords: SLE, atherosclerosis, atherothrombosis, coronary artery disease, myocardial infarction, prognosis, sex specifics. </P><P> Results: Various molecular mechanisms triggered by infection/inflammation are responsible for endothelial dysfunction and the development of atherosclerosis at an earlier age. A contributing factor is the cumulative effect of traditional cardiovascular risk factors interaction with disease-related characteristics. Myocardial infarction rates are 2- to 10-fold higher compared to the general population. Young women have the highest relative risk, however, men carry at least 3-fold higher risk than women. Coronary involvement varies from normal coronary artery with thrombosis, coronary microartery vasculitis, coronary arteritis, and coronary atherosclerosis. Typical clinical presentation is observed in men and older women, while atypical is more frequent in young women. Treatment is guided by the underlying mechanism, engaging invasive procedures alone, or accompanied with immunosuppressive and/or anti-inflammatory therapy. There are significant gender differences in pathophysiology and clinical presentation. However, they receive the same therapeutic treatments. </P><P> Conclusion: Systemic lupus erythematosus is a major contributor to atherosclerotic and non-atherosclerotic mechanisms involved in the development of myocardial infarction, which should be taken into account during therapeutic treatment. Although systemic lupus erythematosus per se is a “female” disease, males are at increased cardiovascular risk and worse outcomes.</p>]]></description> </item><item><title><![CDATA[Inhibition of Interleukin-1 in the Treatment of Selected Cardiovascular Complications]]></title><link>https://www.benthamscience.comarticle/108206</link><description><![CDATA[<p>Background: Interleukin-1 (IL-1) is a pro-inflammatory cytokine that is produced by endothelial cells, smooth muscle cells, and macrophages. It is an important regulator of a complex humoral and cellular inflammatory response. IL-1&#946; is known to be implicated in the development of chronic inflammatory disorders such as rheumatoid arthritis. We aimed to review the effects of IL-1&#946; antagonists in various cardiovascular disorders and to discuss their effectiveness in such diseases. </P><P> Methods: Major biomedical databases, including PubMed and Scopus, were searched for clinical studies regarding the treatment of cardiovascular diseases (CVD) using IL-1&#946; antagonists. Results: The drugs currently used in clinical trials are anakinra, the monoclonal antibodies canakinumab and gevokizumab, and the soluble decoy receptor rilonacept. There are clinical trials and case reports of patients with CVD in which anakinra administration, at the standard dose, has caused rapid clinical improvement and recovery in a few months. Our comprehensive search revealed that IL-1&#946; antagonists have beneficial effects in the treatment of various cardiovascular disorders such as myocarditis, pericarditis, heart failure, acute coronary syndrome, myocardial infarction, atherosclerosis, and Kawasaki disease. </P><P> Conclusion: The present review article shows that IL-1&#946; has a major role in the pathophysiology of cardiovascular disorders, its antagonists have beneficial effects in these conditions, and their use should be considered in future studies.</p>]]></description> </item><item><title><![CDATA[COVID-19 Treatment Success After Repeat Courses of Azithromycin: A Report of Three Cases]]></title><link>https://www.benthamscience.comarticle/111888</link><description><![CDATA[Background: Azithromycin has been considered as a possible therapeutic agent for COVID-19 patients. However, there is limited data on its efficacy. <p> Case Presentation: We describe three patients diagnosed with COVID-19 who did not respond to the initial treatment but improved dramatically upon adding azithromycin with a successful outcome. <p> Conclusion: We have presented evidence of the potential beneficial effect of the azithromycin in the treatment of patients with COVID-19 in three different clinical settings. More evidence is needed regarding the microbiological data, safety, and efficacy of this medication in the management of COVID-19.]]></description> </item><item><title><![CDATA[Colchicine: An Ancient Drug with Multiple Benefits]]></title><link>https://www.benthamscience.comarticle/110880</link><description><![CDATA[The history of colchicine dates to ancient Egyptians when it was used for alleviation of swelling and pain. Although its popularity varied throughout the years, colchicine has been a mainstay for the treatment of several diseases, mainly rheumatic and cardiac ones. The mechanism of action of the drug involves several intracellular and extracellular targets, although interaction with tubulin is the most described. Based on several clinical trials and meta-analyses, colchicine is safely recommended as a monotherapy or as an add-on for the treatment and prevention of recurrent pericarditis, post-pericardiotomy syndrome, gout, pseudogout, familial Mediterranean fever (FMF), and Behçet’s disease (BD). Notably, drug safety has been noted during pregnancy and lactation. Besides its major indications, colchicine has shown efficacy and safety in the treatment of various conditions. Because the indications for using colchicine in the prevention of certain conditions such as acute coronary syndrome, stroke, and hepatic cirrhosis and treatment of others such as pneumonia and psoriasis are still debatable, further research works are needed.]]></description> </item><item><title><![CDATA[Genotyping and Drug Susceptibility Patterns of <i>M. Tuberculosis</i> Isolated from HIV Seropositive Patients in Tehran Iran]]></title><link>https://www.benthamscience.comarticle/114578</link><description><![CDATA[<p>Aim: This study aims to investigate the prevalence and drug-resistance M. tuberculosis isolated from HIV seropositive individuals in Tehran, Iran. </P><P> Background: Human immunodeficiency virus (HIV) is one of the most important risk factors for developing active tuberculosis (TB). </P><P> Objective: The objective is to determine the rate of transmission and drug-resistant M. tuberculosis (MTB) strains isolated from HIV seropositive patients in Tehran province, Iran. </P><P> Methods: This study consecutively enrolled 217 TB/HIV coinfected patients from April 2018 to August 2019 at Emam Khomeini referral hospital and 5 other health centers in Tehran province. The isolates were genotyped using 15 loci Mycobacterial interspersed repetitive unit-variable number tandem repeats (MIRU-VNTR). Minimum inhibitory concentration (MIC) was determined for 6 drugs. In addition, mutations were assessed in rpoB, katG, inhA, and ahpC genes using Reverse Blot Hybridization Assay System. </P><P> Results: A 20 (9.2%) patients were culture-positive for M. tuberculosis and typed by MIRU-VNTR, 13 (65%) strains formed 5 clusters, but 6 (30%) isolates had a unique pattern. The total Hunter– Gaston discrimination index (HGDI) for all 15 loci was 0.846, and the cluster size was 2 to 4 patients. The estimated proportion of recent transmission was 45%. The mutation was identified in 1 isolate, lost inhAW1 and mutation in MT1 loci, which was resistant to isoniazid (INH). Moreover, 1 (5%) and 3 (15%) isolates were resistant to INH and ethambutol (EMB), respectively, of which 1 was resistant to INH and EMB. </P><P> Conclusion: The transmission rate of TB in HIV patients was relatively high; however, the prevalence of drug-resistant strains and TB infection in females was insignificant in this study (p < 0.05); none of the isolates was MDR strains.</p>]]></description> </item><item><title><![CDATA[Cutaneous Lupus Erythematosus in Children]]></title><link>https://www.benthamscience.comarticle/114524</link><description><![CDATA[<p>Background: The skin is commonly involved in autoimmune diseases, such as lupus erythematous. The cutaneous lupus erythematosus (CLE) can manifest with or without systemic symptoms. It is advantageous from a patient and healthcare system standpoint for early diagnosis and intervention. Prevention of complications is especially important in the pediatric population. </P><P> Objective: To familiarize physicians with the clinical presentation, diagnosis, evaluation, and management of pediatric cutaneous lupus. </P><P> Methods: The search term “cutaneous lupus” was entered into a Pubmed search. A narrow scope was applied to the categories of “epidemiology”, “clinical diagnosis”, “investigations”, “comorbidities”, and “treatment”. Meta-analyses, randomized controlled trials, clinical trials, observational studies, and reviews were included. The search was restricted to English literature and children. A descriptive, narrative synthesis of the retrieved articles was provided. </P><P> Results: A variety of innate and adaptive immune responses are being investigated to explain the pathogenesis of CLE. There are a number of variations of cutaneous manifestations varying from localized malar rash as in the case of ACLE lesions and papulosquamous psoriasiform lesions as in the case of SCLE to the multiple subtypes within chronic CLE. First-line pharmacological treatments include topicals, such as typical calcineurin inhibitors and corticosteroids, or oral agents, such as glucocorticoids, antimalarial drugs, and hydroxychloroquine. </P><P> Conclusion: CLE is inclusive of a number of subtypes that have varying dermatological manifestations in adult and pediatric populations. The current treatment modalities will change based on the newly understood molecular targets. Ongoing research on the mechanisms underlying CLE is necessary to derive new interventions for pediatric patients.</p>]]></description> </item><item><title><![CDATA[New Therapies to Modulate Post-Infarction Inflammatory Alterations in the Myocardium: State of the Art and Forthcoming Applications]]></title><link>https://www.benthamscience.comarticle/112299</link><description><![CDATA[Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. AMI causes necrosis of cardiac cells and triggers a complex inflammatory response, affecting infarct size, cardiac function and clinical outcomes. This inflammatory response can be divided into 3 phases: 1) the pro-inflammatory phase, in which the release of damage-associated molecular patterns from necrotic cells triggers the secretion of pro-inflammatory mediators and attracts immune cells to clean the debris, further damaging viable myocardium, 2) the reparative phase, in which anti-inflammatory signals activate immune-modulating cells and trigger the production of a stable scar, 3) the maturation phase, in which inflammatory and fibrotic signals are suppressed, but may persist, leading to left ventricular adverse remodelling. Thus, the inflammatory response is an appealing therapeutic target to improve the outcomes of patients with AMI. Numerous anti-inflammatory therapies have shown potential in animal models, but the translation to human trials exhibited limited benefit. Glucocorticoids and non-steroidal anti-inflammatory drugs showed signals of harm due to their non-specific effects. Other broad inhibitors, e.g., methotrexate, cyclosporine, or colchicine, did not improve clinical outcomes as acute therapies for MI. Specific inhibitors of the complement cascade, adhesion molecules, or inflammatory mediators were mostly disappointing in humans. However, an interleukin-1 inhibitor (anakinra) and a matrix metalloproteinase inhibitor (doxycycline) improved clinical outcomes in patients with AMI. Promising RNAse1, anti-toll-like receptor 2 antibodies, and inflammasome inhibitors still need to be tested in humans. Finally, positive results should be replicated in large clinical trials before they can be implemented into the standard AMI therapy.]]></description> </item><item><title><![CDATA[Single Photon Emission Tomography in the Diagnostic Assessment of Cardiac and Vascular Infectious Diseases]]></title><link>https://www.benthamscience.comarticle/107527</link><description><![CDATA[Cardiac and vascular infection is an arising cause of mortality and morbidity in the adult population. Diagnosis based on culture and anatomic imaging are frequently inconclusive. Radiolabeled leucocyte scintigraphy plays a useful role in the diagnosis and management of these serious infectious conditions. In this paper, we present an update on the diagnostic performance of single- photon emission tomographic (SPECT) techniques using different radionuclides in the management of patients with cardiac and vascular infections. We performed a thorough search of recent literature on the topic. We present a discussion on the clinical utility of different SPECT tracers in cardiac and vascular infections, including infective endocarditis, cardiac implantable electronic device (CIED) infections, left ventricular assist device infection, and vascular graft infection. Radionuclide technique using SPECT tracers is a useful imaging modality in the diagnosis of cardiac infection. Among the different SPECT tracers for infection imaging, radiolabeled leucocyte scintigraphy is currently the most useful tool in the diagnosis and management of patients with suspected cardiac and vascular infection. Radiolabeled leucocyte scintigraphy has a high specificity, a result of the ability of the leucocytes to accumulate as sites of pyogenic infection but not at sites of sterile inflammation such as seen in the early post-operative period or in response to the presence of a prosthetic cardiac or vascular material. Limited experience with radiotracers for in vivo labelling of leucocytes such as <sup>99m</sup>Tc-sulesomab and <sup>99m</sup>Tc-besilesomab show acceptable diagnostic performance without the need for the tedious process of ex-vivo labeling. <sup>67</sup>Ga scintigraphy used to be popular for cardiac and vascular infection imaging. Its use has run out of favor following the availability of more effective molecular imaging methods. SPECT techniques with radiolabeled leucocyte scintigraphy has a high diagnostic performance in the evaluation of patients with suspected cardiac or vascular infection. It is able to confirm or reject the presence of infection when results of anatomic imaging or culture remain inconclusive. Its diagnostic performance is not compromised by sterile inflammation occurring in the early post-operative period or in response to implanted prosthetic materials.]]></description> </item><item><title><![CDATA[Novel PET Tracers in the Management of Cardiac Sarcoidosis]]></title><link>https://www.benthamscience.comarticle/107047</link><description><![CDATA[Sarcoidosis is a systemic inflammatory disease of unknown etiology, pathologically characterized by non-caseating granulomas involving several organs and tissues. This pathological process can eventually affect the heart during his course leading to fibrosis associated with systolic dysfunction, conduction disturbance, and even sudden cardiac death. Due to this prognostic impact, diagnosis is crucial to optimize clinical management. The low sensitivity of endomyocardial biopsy and its invasive nature prevents its application as a first-line diagnostic approach. Thus, several efforts have been dedicated to the identification of advanced imaging tools for the diagnosis and monitoring of cardiac involvement in systemic sarcoidosis, including Positron Emission Tomography (PET). Starting from strengths and disadvantages of 18F-Fluorodeoxyglucose (18F-FDG) PET imaging, the present narrative review will summarize state of the art and future perspectives about radiotracers other than 18F-FDG of potential interest in the field of CS, including somatostatin receptor- ligands, proliferation markers and hypoxia displaying agents.]]></description> </item><item><title><![CDATA[The Role of 18FDG PET/CT in the Assessment of Endocarditis, Myocarditis and Pericarditis]]></title><link>https://www.benthamscience.comarticle/106001</link><description><![CDATA[Endocarditis, myocarditis and pericarditis are a heterogeneous group of phenotypic syndromes where the culprit area of inflammation is the heart. Inflammation may be determined by an infective agent, toxins, drugs or an activated immune system. Clinical manifestations can be subtle and diagnosis remains a challenge for cardiologists, requiring high level of suspicion and advanced multimodal cardiac imaging to avoid life-threatening consequences. The purpose of this review is to report the recent advances of PET/CT imaging with 18FDG in helping the management of patients affected by inflammatory heart disease. Two independent reviewers searched in PubMed articles published before or in June 2019 and final decisions on the inclusion of references were done in consensus with a third reviewer. At the end of the selection process 23/206 articles on “cardiac inflammation”; 26/235 articles on “endocarditis”, “prosthetic heart valve”, “pacemaker”, “implantable cardiac device”; 7/103 articles on “myocarditis”; 13/330 articles on sarcoidosis” and 2/19 articles on “pericarditis” were included. Compared with the conventional methods, molecular imaging has the advantage to non-invasively and directly trace the inflammatory process, and to identify earlier the presence and the extent of intra-cardiac and extra-cardiac involvement, to enable quantification of disease activity, guide therapeutic interventions, and monitor treatment success.]]></description> </item><item><title><![CDATA[Cardiovascular Manifestations of COVID-19]]></title><link>https://www.benthamscience.comarticle/111118</link><description><![CDATA[Coronavirus disease 2019 (COVID-19) first emerged in a group of patients who presented with severe pneumonia in Wuhan, China, in December 2019. A novel virus, now called SARSCoV- 2 (Severe Acute Respiratory Syndrome Coronavirus-2), was isolated from lower respiratory tract samples. The current outbreak of infection has spread to over 100 countries and killed more than 340,000 people as of 25th May, 2020. </p> The predominant clinical manifestation of COVID-19 is a respiratory disease- ranging from mild flu-like symptoms to fulminant pneumonia and Acute Respiratory Distress Syndrome (ARDS). Patients with pre-existing cardiovascular risk factors are considered more susceptible to the virus, and these conditions are often worsened by the infection. Furthermore, COVID-19 infection has led to de novo cardiac complications, like acute myocardial injury and arrhythmias. </p> In this review, we have focused on the cardiovascular manifestations of COVID-19 infection that have been reported in the literature so far. We have also outlined the effect of pre-existing cardiovascular disease as well as risk factors on the clinical course and outcomes of COVID-19 infection.]]></description> </item><item><title><![CDATA[Aortic Dissection: A Review of the Pathophysiology, Management and Prospective Advances]]></title><link>https://www.benthamscience.comarticle/110662</link><description><![CDATA[Aortic dissection is an emergent medical condition, generally affecting the elderly, characterized by a separation of the aortic wall layers and subsequent creation of a pseudolumen that may compress the true aortic lumen. Predisposing factors mediate their risk by either increasing tension on the wall or by causing structural degeneration. They include hypertension, atherosclerosis, and a number of connective tissue diseases. If it goes undetected, aortic dissection carries a significant mortality risk; therefore, a high degree of clinical suspicion and a prompt diagnosis are required to maximize survival chances. Imaging methods, most commonly a CT scan, are essential for diagnosis; however, several studies have also investigated the effect of several biomarkers to aid in the detection of the condition. The choice of intervention varies depending on the type of dissection, with open surgical repair remaining of choice in those with type. In dissections, however, the role of conventional open surgery has considerably diminished in complicated type B dissections, with endovascular repair, a much less invasive technique, proving to be more effective. In uncomplicated type B dissections, where medical choice reigned supreme as the optimal intervention, endovascular repair is being explored as a viable option which may reduce long- term mortality outcomes, although the ideal intervention in this situation is far from settled.]]></description> </item><item><title><![CDATA[HMG-CoA Reductase Inhibitors (Statins) and their Drug Interactions Involving CYP Enzymes, P-glycoprotein and OATP Transporters-An Overview]]></title><link>https://www.benthamscience.comarticle/113319</link><description><![CDATA[<P>Background: Hydroxymethyl glutaryl-CoA (HMG-CoA) reductase inhibitors (Statins) are used to treat dyslipidemia. Generally, the statins are the substrates of CYP enzymes, P-glycoprotein (P-gp), and organic anion transporting polypeptides transporters (OATP1B1). </P><P> Objective: This review article focuses on the clinical significance of statins, and their interactions in real practice. </P><P> Methods: The databases like Medline/PubMed Central/PubMed, Google Scholar, Science Direct, Cochrane Library, Directory of open access journals (DOAJ), and reference lists were searched to identify relevant articles. </P><P> Results: Most of the drug interactions of statins result in elevated plasma concentrations and toxicity of statins due to the inhibition of CYP3A4, P-gp and/or OATP1B1 transporters. The toxicity of statins includes myopathy, rhabdomyolysis, elevated liver enzymes, acute kidney injury, and diabetes. The statins like simvastatin, lovastatin, and atorvastatin are substrates of CYP3A4 enzyme and P-glycoprotein and their concomitant use with the drugs inhibiting or inducing them would result in changes in plasma concentrations and toxicity/efficacy. However, the statins like pravastatin, rosuvastatin and pitavastatin are not substrates of CYP enzymes and hence the concomitant use of CYP inhibitors or inducers does not affect them. Almost all the statins are the substrates of OATP1B1 transporter, and the co-prescription of inhibitors of OATP1B1 elevates the plasma concentrations and muscle toxicity of statins. </P><P> Conclusion: Understanding the interacting potential of each statin will enable the prescribers, pharmacists, and other health care professionals to use statins effectively without compromising patient safety.</P>]]></description> </item><item><title><![CDATA[Enterovirus D-68 Molecular Virology, Epidemiology, and Treatment: an Update and Way Forward]]></title><link>https://www.benthamscience.comarticle/108179</link><description><![CDATA[Enterovirus D68 (EV-D68) is a single-stranded positive-sense RNA virus, and it is one of the family members of Picornaviridae. Except for EV-D68, the entire family Picornaviridae has been illustrated in literature. EV-D68 was first discovered and isolated in California, USA, in 1962. EV-D68 has resulted in respiratory disorders’ outbreaks among children worldwide, and it has been detected in cases of various neurological diseases such as acute flaccid myelitis (AFM). A recent study documented a higher number of EV-D68 cases associated with AFM in Europe in 2016 compared to the 2014 outbreak. EV-D68 is mainly diagnosed by quantitative PCR, and there is an affirmative strategy for EV-D68 detection by using pan-EV PCR on the untranslated region and/or the VP1 or VP2, followed by sequencing of the PCR products. Serological tests are limited due to cross-reactivity of the antigens between the different serotypes. Many antiviral drugs for EV-D68 have been evaluated and showed promising results. In our review, we discuss the current knowledge about EV-D68 and its role in the development of AFM.]]></description> </item><item><title><![CDATA[Understanding The Role of Inflammasome in Angina Pectoris]]></title><link>https://www.benthamscience.comarticle/112184</link><description><![CDATA[Angina pectoris, associated with coronary artery disease, a cardiovascular disease where the pain is caused by adverse oxygen supply in the myocardium, results in contractility and discomfort in the chest. Inflammasomes, triggered by stimuli due to infection and cellular stress, have been identified to play a vital role in the progression of cardiovascular disorders and, thus, causing various symptoms like angina pectoris. Nlrp3 inflammasome, a key contributor in the pathogenesis of angina pectoris, requires activation and primary signaling for the commencement of inflammation. Nlrp3 inflammasome elicits out an inflammatory response by the emission of pro-inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K<sup>+</sup> efflux and Ca<sup>2+</sup> and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process. Thus, inflammasome is considered to be one of the factors involved in the progression of coronary artery diseases and has an intricate role in the development of angina pectoris.]]></description> </item><item><title><![CDATA[Antineutrophil Cytoplasmic Antibody in Lupus Nephritis: Correlation with Clinicopathological Characteristics and Disease Activity]]></title><link>https://www.benthamscience.comarticle/112203</link><description><![CDATA[Background: Lupus nephritis (LN) represents 40%-50% of all systemic lupus erythematosus (SLE) patients, and rapidly progressive glomerulonephritis is associated with significant morbidity and mortality. Antineutrophil cytoplasmic antibody (ANCA) might be involved in the pathogenesis of LN. </p> Objective: We evaluated the role of myeloperoxidase (MPO)-ANCA, proteinase 3 (PR3)-ANCA, and anti-glomerular basement membrane autoantibodies (anti-GBM autoAb) for the diagnosis of LN. </p> Methods: In this cross-sectional study, 95 SLE patients were divided into 2 subgroups: LN group (n = 60) and non-LN group (n = 35). For further analysis, we subclassified the LN group into ANCA- positive (n = 16) and ANCA-negative (n = 44) LN patients. The entire Non-LN group was ANCA- negative. The SLE disease activity index (SLEDAI) was reported for each patient. Determination of MPO-ANCA, PR3-ANCA, and anti-GBM autoAb was performed using a novel multiplex bead-based technology in all patients. Data analyses were done using SPSS, version 20. Approval was obtained from the institutional review board of Zagazig University (ZU-IRB#6000). </p> Results: Of 95 patients with SLE, 16 patients (16.84%) had ANCA-positive LN, all of which were MPO-ANCA. There was a positive correlation between MPO-ANCA and SLEDAI, as well as with class IV LN. Receiver operating characteristic analyses revealed that the sensitivity and specificity of MPO-ANCA were 81.3% and 99.8%, respectively, in discriminating LN from systemic lupus without nephritis. </p> Conclusion: MPO-ANCA level was significantly correlated with SLEDAI, inflammatory markers, kidney function tests, and LN class IV.]]></description> </item><item><title><![CDATA[Clinical Features and Disease Damage Risk Factors in an Egyptian SLE Cohort: A Multicenter Study]]></title><link>https://www.benthamscience.comarticle/111879</link><description><![CDATA[Background: Systemic lupus erythematosus (SLE) has a variable natural history and clinical characteristics. Objectives: This study aims to evaluate the clinical and immunological characteristics, and assess the disease accrual of an Egyptian SLE cohort. </p> Methods: The study included 569 SLE patients who were collected from three different centers; demographic, laboratory data, cumulative manifestations, and comorbidities were assessed (characteristics at the time of diagnosis were recorded retrospectively, while current clinical data were recorded cross-sectionally). Evaluation of disease activity was done using Systemic Lupus Erythematosus Disease Activity Index score (SLEDAI) and damage by Systemic Lupus International Collaborative Clinics/American College of Rheumatology Damage Index (SDI). </p> Results: The median age of patients at disease onset was 25.0±10.5 years, the median disease duration was 4.0 (6.5) years, the female to male ratio was (12.5:1), and the median SLEDAI was 12.0±14.0. Family history of SLE was noticed in 4%. Antinuclear antibody was positive in all patients and 86% had positive anti-double-stranded DNA. Arthritis/arthralgia was the most frequent presenting symptom (44%) followed by fever (39%). Along the disease course; alopecia was the most common clinical manifestation (76.1%), followed by constitutional symptoms (75.9%), and nephritis (65.7%). Three hundred and five patients encountered organ damage (SDI >1); kidney damage was the most frequent (32%), followed by cardiovascular damage (24.3%). Neutropenia, hypocomplementemia, arthritis, hypertension, longer disease duration, and higher disease activity were found to be independent risk factors for disease damage. </p> Conclusions: There are some diversities and similarities in our findings compared to the previously reported data. Arthritis is the most common presenting symptom, while alopecia is the most frequent clinical finding, and a higher prevalence of nephritis was reported. Renal damage is the most frequent outcome.]]></description> </item><item><title><![CDATA[Cytotoxic T Lymphocyte Antigen 4 Gene +49 A/G (rs231775) Polymorphism and Susceptibility to Systemic Lupus Erythematosus]]></title><link>https://www.benthamscience.comarticle/111665</link><description><![CDATA[Aim: To assess the probable role of +49AG polymorphism in susceptibility to SLE in an Egyptian population. </p> Background: Systemic lupus erythematosus (SLE) is a compound inflammatory chronic disease distinguished through the release of autoantibodies. Cytotoxic T lymphocyte associated antigen-4 is a main down controller of T-cell response; its dysregulation could affect SLE pathogenesis by altered T cells activation to self-antigens. </p> Objectives: To evaluate the CTLA-4 +49AG allelic and genotype frequency in a sample of the Egyptian population and correlate them with disease susceptibility and clinical severity. </p> Materials and methods: Including 100 patients with SLE and 100 healthy controls (age and gender matched), CTLA-4 exon 1 49 A>G Genotyping was done using Real-Time PCR. </p> Results: No difference was noticed in genotype or allele distributions of the studied polymorphism between both groups. Similar genotypes and allele frequencies were established for the 2 groups after their stratification by the age of disease onset, clinical course, or severity. </p> Conclusion: CTLA-4 +49AG gene polymorphism is not linked with the liability to develop SLE in the studied Egyptian population. Yet it is significantly related to disease severity.]]></description> </item><item><title><![CDATA[Development of New Therapeutics to Meet the Current Challenge of Drug Resistant Tuberculosis]]></title><link>https://www.benthamscience.comarticle/107710</link><description><![CDATA[Tuberculosis (TB) is a prominent infective disease and a major reason of mortality/ morbidity globally. Mycobacterium tuberculosis causes a long-lasting latent infection in a significant proportion of human population. The increasing burden of tuberculosis is mainly caused due to multi drug-resistance. The failure of conventional treatment has been observed in large number of cases. Drugs that are used to treat extensively drug-resistant tuberculosis are expensive, have limited efficacy, and have more side effects for a longer duration of time and are often associated with poor prognosis. To regulate the emergence of multidrug resistant tuberculosis, extensively drug-resistant tuberculosis and totally drug resistant tuberculosis, efforts are being made to understand the genetic/molecular basis of target drug delivery and mechanisms of drug resistance. Understanding the molecular approaches and pathology of Mycobacterium tuberculosis through whole genome sequencing may further help in the improvement of new therapeutics to meet the current challenge of global health. Understanding cellular mechanisms that trigger resistance to Mycobacterium tuberculosis infection may expose immune associates of protection, which could be an important way for vaccine development, diagnostics, and novel host-directed therapeutic strategies. The recent development of new drugs and combinational therapies for drug-resistant tuberculosis through major collaboration between industry, donors, and academia gives an improved hope to overcome the challenges in tuberculosis treatment. In this review article, an attempt was made to highlight the new developments of drug resistance to the conventional drugs and the recent progress in the development of new therapeutics for the treatment of drugresistant and non-resistant cases.]]></description> </item><item><title><![CDATA[Effect of Dietary Education on Cardiovascular Risk Factors in Rheumatoid Arthritis Patients]]></title><link>https://www.benthamscience.comarticle/109750</link><description><![CDATA[<P>Aim: The aim of this study was to investigate the effect of dietary education on cardiovascular risk factors in patients with rheumatoid arthritis. </P><P> Methods: In this randomized clinical trial, 112 patients with rheumatoid arthritis were randomly assigned into two groups, intervention and control. Dietary education was provided for the intervention group in 4 sessions; anthropometric measurements, serum levels of RF, triglycerides, cholesterol, HDL, LDL, and fasting blood sugar were measured before and three months after the intervention. Data were analyzed using SPSS software and appropriate statistical tests. </P><P> Results: The mean of total cholesterol (p <0.001), triglycerides (p = 0.004), LDL (p <0.001), systolic blood pressure (p = 0.001), diastolic blood pressure (p = 0.003), FBS and BMI (p <0.001) were decreased significantly in the intervention group after education compared the control group. </P><P> Conclusion: Traditional care for rheumatoid arthritis patients is not enough. Patients need more education in order to improve their situation.</P>]]></description> </item><item><title><![CDATA[Isolation of <i>Morganella Morganii</i> and <i>Providencia</i> Species from Clinical Samples in a Tertiary Care Hospital in North India]]></title><link>https://www.benthamscience.comarticle/104008</link><description><![CDATA[<P>Introduction: The members of the tribe Proteeae, Morganella and Providencia are being increasingly recognized as important pathogens. The spectrum of disease caused by them is wide and in reported cases, the mortality is high. Previously both of these pathogens were considered to be rare pathogens as the potential to cause nosocomial transmission and infection was not much studied. But their phenomenal evolution and increase in multidrug-resistance (MDR) strains of these pathogens are posing a major threat toward public health throughout the world. </P><P> Methods: This present study was carried out from July 2018 to December 2018 on all the pus and body fluid samples that were received in the Department of Microbiology. Samples were processed as per the standard Microbiological guidelines and also were analyzed for their antimicrobial susceptibility profile as per Clinical Laboratory Standards Institute. </P><P> Results: Out of 8425 samples received, 2140 were culture positive, amongst which 19 samples (0.89%) were positive for Providencia species (9) and Morganella morganii(10). The male : female ratio of these 19 patients was 2.8 : 1 and maximum patients (13) belonged to 20-60 years. As far as risk factors are concerned, maximum patients were diabetics (7) followed by abnormal liver function tests (6), concomitant UTI (6), history of invasive procedure (5), prior exposure to antibiotics (5) and urinary catheterization (4). About 6 were polymicrobial infections. Antibiotic susceptibility patterns revealed that Providencia strains were sensitive to ampicillin- sulbactum (77.7%) and amikacin (77.7%), while all Morganella strains were 100% sensitive to tobramycin and piperacillintazobactam. </P><P> Conclusion: This study heralds in need for more research in this area as infections caused by these two pathogens are on the rise. Moreover, resistance to antimicrobials is also an increasingly common problem thus delaying the treatment and prognosis of the disease.</P>]]></description> </item><item><title><![CDATA[Tuberculosis: An Update on Pathophysiology, Molecular Mechanisms of Drug Resistance, Newer Anti-TB Drugs, Treatment Regimens and Host- Directed Therapies]]></title><link>https://www.benthamscience.comarticle/112378</link><description><![CDATA[Human tuberculosis (TB) is primarily caused by Mycobacterium tuberculosis (Mtb) that inhabits inside and amidst immune cells of the host with adapted physiology to regulate interdependent cellular functions with intact pathogenic potential. The complexity of this disease is attributed to various factors such as the reactivation of latent TB form after prolonged persistence, disease progression specifically in immunocompromised patients, advent of multi- and extensivelydrug resistant (MDR and XDR) Mtb strains, adverse effects of tailor-made regimens, and drug-drug interactions among anti-TB drugs and anti-HIV therapies. Thus, there is a compelling demand for newer anti-TB drugs or regimens to overcome these obstacles. Considerable multifaceted transformations in the current TB methodologies and molecular interventions underpinning hostpathogen interactions and drug resistance mechanisms may assist to overcome the emerging drug resistance. Evidently, recent scientific and clinical advances have revolutionised the diagnosis, prevention, and treatment of all forms of the disease. This review sheds light on the current understanding of the pathogenesis of TB disease, molecular mechanisms of drug-resistance, progress on the development of novel or repurposed anti-TB drugs and regimens, host-directed therapies, with particular emphasis on underlying knowledge gaps and prospective for futuristic TB control programs.]]></description> </item><item><title><![CDATA[Biochemical Markers in the Prediction of Contrast-induced Acute Kidney Injury]]></title><link>https://www.benthamscience.comarticle/106286</link><description><![CDATA[For many years clinicians have been searching for “kidney troponin”- a simple diagnostic tool to assess the risk of acute kidney injury (AKI). Recently, the rise in the variety of contrast-related procedures (contrast computed tomography (CT), percutaneous coronary intervention (PCI) and angiography) has resulted in the increased number of contrast-induced acute kidney injuries (CI-AKI). CIAKI remains an important cause of overall mortality, prolonged hospitalisation and it increases the total costs of therapy. The consequences of kidney dysfunction affect the quality of life and they may lead to disability as well. Despite extensive worldwide research, there are no sensitive and reliable methods of CI-AKI prediction. Kidney Injury Molecule 1 (KIM-1) and Neutrophil Gelatinase Lipocalin (NGAL) have been considered as kidney-specific molecules. High concentrations of these substances before the implementation of contrast-related procedures have been suggested to enable the estimation of kidney vulnerability to CI-AKI and they seem to have the predictive potential for cardiovascular events and overall mortality. According to other authors, routine determination of known inflammation factors (e.g., CRP, WBC, and neutrophil count) may be helpful in the prediction of CIAKI. However, the results of clinical trials provide contrasting results. The pathomechanism of contrast- induced nephropathy remains unclear. Due to its prevalence, the evaluation of the risk of acute kidney injury remains a serious problem to be solved. This paper reviews pathophysiology and suggested optimal markers facilitating the prediction of contrast-induced acute kidney injury.]]></description> </item><item><title><![CDATA[Drug Induced Cutaneous Manifestations due to Treatment of Gastrointestinal Disorders]]></title><link>https://www.benthamscience.comarticle/111532</link><description><![CDATA[Cutaneous manifestations due to drugs used in the treatment of gastrointestinal disorders are multiple and common. Adequate diagnosis is of great importance, bearing in mind that the therapeutic regimen depends on its diagnosis. In this review, we provided an overview of the most common drug-induced skin lesions with a detailed explanation of the disease course, presentation and treatment, having in mind that in recent years, novel therapeutic modalities have been introduced in the treatment of various gastrointestinal disorders, and that incidence of cutaneous adverse reactions has been on the rise.]]></description> </item><item><title><![CDATA[A Comprehensive Systemic Literature Review of Pericardial Decompression Syndrome: Often Unrecognized and Potentially Fatal Syndrome]]></title><link>https://www.benthamscience.comarticle/107170</link><description><![CDATA[<P>Background: Pericardial Decompression Syndrome (PDS) is defined as paradoxical hemodynamic deterioration and/or pulmonary edema, commonly associated with ventricular dysfunction. This phenomenon was first described by Vandyke in 1983. PDS is a rare but formidable complication of pericardiocentesis, which, if not managed appropriately, is fatal. PDS, as an entity, has discrete literature; this review is to understand its epidemiology, presentation, and management. </P><P> Methodology: Medline, Science Direct and Google Scholar databases were utilized to do a systemic literature search. PRISMA protocol was employed. Abstracts, case reports, case series and clinical studies were identified from 1983 to 2019. A total of 6508 articles were reviewed, out of which, 210 were short-listed, and after removal of duplicates, 49 manuscripts were included in this review. For statistical analysis, patient data was tabulated in SPSS version 20. Cases were divided into two categories surgical and percutaneous groups. t-test was conducted for continuous variable and chi-square test was conducted for categorical data used for analysis. </P><P> Results: A total of 42 full-length case reports, 2 poster abstracts, 3 case series of 2 patients, 1 case series of 4 patients and 1 case series of 5 patients were included in the study. A total of 59 cases were included in this manuscript. Our data had 45.8% (n=27) males and 54.2% (n=32) females. The mean age of patients was 48.04 ± 17 years. Pericardiocentesis was performed in 52.5% (n=31) cases, and pericardiostomy was performed in 45.8% (n=27). The most common identifiable cause of pericardial effusion was found to be malignancy in 35.6% (n=21). Twenty-three 23 cases reported pre-procedural ejection fraction, which ranged from 20%-75% with a mean of 55.8 ± 14.6%, while 26 cases reported post-procedural ejection fraction which ranged from 10%-65% with a mean of 30% ± 15.1%. Data was further divided into two categories, namely, pericardiocentesis and pericardiostomy. The outcome as death was significant in the pericardiostomy arm with a p-value of < 0.00. The use of inotropic agents for the treatment of PDS was more common in needle pericardiocentesis with a p-value of 0.04. Lastly, the computed recovery time did not yield any significance with a p-value of 0.275. </P><P> Conclusion: Pericardial decompression syndrome is a rare condition with high mortality. Operators performing pericardial drainage should be aware of this complication following drainage of cardiac tamponade, since early recognition and expeditious supportive care are the only therapeutic modalities available for adequate management of this complication.</P>]]></description> </item><item><title><![CDATA[Acute Myocarditis in Children: An Overview of Treatment and Recent Patents]]></title><link>https://www.benthamscience.comarticle/104196</link><description><![CDATA[<P>Background: Pediatric myocarditis is rare but challenging. This overview summarized the current knowledge and recent patents on childhood myocarditis. </P><P> Methods: Clinical queries and keywords of “myocarditis” and “childhood” were used as search engine. </P><P> Results: Viral infections are the most common causes of acute myocarditis. Affected children often have a prodrome of fever, malaise, and myalgia. Clinical manifestations of acute myocarditis in children can be nonspecific. Some children may present with easy fatigability, poor appetite, vomiting, abdominal pain, exercise intolerance, respiratory distress/tachypnea, dyspnea at rest, orthopnea, chronic cough with wheezing, chest pain, unexplained tachycardia, hypotension, syncope, and hepatomegaly. Supraventricular arrhythmias, ventricular arrhythmias, and heart block may be present. A subset of patients have fulminant myocarditis and present with cardiovascular collapse, which may progress to severe cardiogenic shock, and even death. A high index of suspicion is crucial to its diagnosis and timely management. Cardiac magnetic resonance imaging is important in aiding clinical diagnosis while, endomyocardial biopsy remains the gold standard. The treatment consists of supportive therapy, ranging from supplemental oxygen and fluid restriction to mechanical circulatory support. Angiotensinconverting enzyme inhibitors, angio-tensin II receptor blockers, &#946;-blockers, and aldosterone antagonists might be used for the treatment of heart failure while, immunosuppression treatments remain controversial. There are a few recent patents targeting prevention or treatment of viral myocarditis, including an immunogenic composition comprising a PCV-2 antigen, glutathione-S-transferase P1, neuregulins, NF-[kappa] B inhibitor, a pharmaceutical composition which contains 2-amino-2- (2- (4-octyl phenyl) - ethyl) propane 1,3-diol, a composition containing pycnojenol, Chinese herbal concoctions, and a Korean oral rapamycin. Evidence of their efficacy is still lacking. </P><P> Conclusion: This article reviews the current literature regarding etiology, clinical manifestations, diagnosis, and management of acute myocarditis in children.</P>]]></description> </item><item><title><![CDATA[The Protective of Baicalin on Myocardial Ischemia-Reperfusion Injury]]></title><link>https://www.benthamscience.comarticle/107118</link><description><![CDATA[<P>Background: The aim of this study was to explore the inhibitory effect of baicalin on myocardial apoptosis induced by Ischemia-Reperfusion (I/R). </P><P> Methods: Sprague Dawley rats&#039; heart and myocardial cells I/R model were established in vivo and vitro, then 100 mg/kg and 10 μmol/l baicalin were administrated, respectively. The experiment was randomly divided into 4 groups (n=10): Control; I/R; IR+DMEM; and I/R+baicalin groups. Postoperation, the Left Ventricular (LV) End-Diastolic Pressure (LVEDP), the maximum velocity of LV contraction (dP/dtmax) and the maximum velocity of LV diastole (dP/dtmin) were recorded by the transthoracic echocardiography; the myocardial apoptosis percentage was analyzed by Annexin VFITC/ PI and TUNEL staining, and the apoptosis gene and protein were detected by RT-PCR and western blot. Furthermore, the protein expression of the calcium-sensing receptor (CaSR) and ERK1/2 phosphorylation were observed by western blot and Fura-2-acetoxymethyl ester. Moreover, primary rats’ cardiomyocytes were cultured and ERK1/2 specific inhibitor PD98059 was added to the culture medium. The cell survival rate, vitality and apoptosis were detected by MTT, lactate dehydrogenase (LDH) and TUNEL staining assay Kit, respectively. </P><P> Results: Our present study showed that baicalin significantly improved LV hemodynamic parameters and myocardial apoptosis in myocardial I/R injury rats. Furthermore, we found that baicalin could down-regulate the protein expression of CaSR, but up-regulate the protein expression of ERK1/2. Furthermore, when the cells were pretreated with ERK1/2 inhibitor PD98059, the cells survival rate significantly decreased, but LDH activity and apoptosis significantly increased. The results indicated that the effect of baicalin on myocardial I/R injury could be inhibited by ERK1/2 inhibitor. </P><P> Conclusion: In conclusion, our data suggests that baicalin attenuates I/R-induced myocardial injury maybe through the suppression of the CaSR/ERK1/2 signaling pathway.</P>]]></description> </item><item><title><![CDATA[The Advances on the Protective Effects of Ginsenosides on Myocardial Ischemia and Ischemia-Reperfusion Injury]]></title><link>https://www.benthamscience.comarticle/107461</link><description><![CDATA[Ginseng is a traditional medicine with a complex chemical composition, wide bioactivity and unique pharmacological action. Many studies have confirmed that ginsenosides are the active ingredients of ginseng, and ginsenosides have always been the focus of different researchers. With the development of modern separation and analysis technology, more than 150 kinds of ginsenosides have been isolated. The ginsenosides Rb1, Rb2, Rc, Rg1 and Re account for more than 80% of total ginsenosides, and other saponins, such as Rd, Rg3 and Rh2, which are minor constituents, accounting for only a small portion of the total amount. In recent years, ginsenosides have been found to possess strong pharmacological activities, such as antioxidation, clearing of oxygen free radicals, reducing calcium overload and anti-apoptosis. Ginsenosides play a protective role in ischemia-reperfusion injury. This paper reviews the protective effects of ginsenosides on myocardial ischemia and ischemiareperfusion injury.]]></description> </item><item><title><![CDATA[Cardio-Rheumatology: Two Collaborating Disciplines to Deal with the Enhanced Cardiovascular Risk in Autoimmune Rheumatic Diseases]]></title><link>https://www.benthamscience.comarticle/108386</link><description><![CDATA[In Part 1 of this Thematic Issue entitled “Systemic Autoimmune Rheumatic Diseases and Cardiology”, a panel of specialists and experts in cardiology, rheumatology, immunology and related fields discussed the cardiovascular complications of spondyloarthritides, rheumatoid arthritis, Sjogren’s syndrome and vasculitides, as well as relevant cardiovascular issues related to non-biologic and biologic disease-modifying anti-rheumatic drugs (DMARDs), and provided their recommendations for prevention and management of these complications. In part 2 of this Thematic Issue, experts discuss the enhanced cardiovascular risk conferred by additional autoimmune rheumatic diseases (ARDs), including systemic lupus erythematosus, the antiphospholipid syndrome, psoriasis and psoriatic arthritis and juvenile idiopathic arthritis. These, and the previous articles, place inflammation as the key common link to explain the enhanced risk of cardiovascular complications in patients with ARDs. It follows that treatment should probably target inflammation. From all these contemporary reviews, the conclusion that is derived further supports the notion of the emerging field of Cardio- Rheumatology where physicians and experts from these two disciplines collaborate in risk stratification and optimization of preventive strategies and drug therapies in patients with ARDs.]]></description> </item><item><title><![CDATA[Cardiovascular Disease in Juvenile Idiopathic Arthritis]]></title><link>https://www.benthamscience.comarticle/105725</link><description><![CDATA[Juvenile idiopathic arthritis (JIA), is a term used to describe a group of inflammatory disorders beginning before the age of 16 years. Although for the majority of children remission is achieved early, those with systemic or polyarticular form of the disease may present persistent symptoms in adulthood. Considering that there is overlap in the pathogenesis of JIA with adult rheumatic diseases, concerns have been raised as to whether JIA patients could be at increased cardiovascular (CV) risk in the long-term. In this review, we summarize evidence for CV involvement in JIA and present data on CV risk factors and surrogate markers of arterial disease. We also provide information on beneficial and harmful CV effects of anti-inflammatory medications in the context of JIA and suggest strategies for CV screening. Overall, patients with systemic forms of JIA demonstrate an adverse lipid profile and early arterial changes relevant to accelerated arterial disease progression. Although there is paucity of data on CV outcomes, we recommend a holistic approach in the management of JIA patients, which includes CV risk factor monitoring and lifestyle modification as well as use, when necessary, of antiinflammatory therapies with documented CV safety.]]></description> </item><item><title><![CDATA[Combined Brain/Heart Magnetic Resonance Imaging in Systemic Lupus Erythematosus]]></title><link>https://www.benthamscience.comarticle/100095</link><description><![CDATA[<P>Cardiovascular Disease (CVD) in Systemic Lupus Erythematosus (SLE) and Neuropsychiatric SLE (NPSLE) has an estimated prevalence of 50% and 40%, respectively and both constitute major causes of death among SLE patients. In this review, a combined brain/heart Magnetic Resonance Imaging (MRI) for SLE risk stratification has been proposed. <P> The pathophysiologic background of NPSLE includes microangiopathy, macroscopic infarcts and accelerated atherosclerosis. Classic brain MRI findings demonstrate lesions suggestive of NPSLE in 50% of the NPSLE cases, while advanced MRI indices can detect pre-clinical lesions in the majority of them, but their clinical impact still remains unknown. Cardiac involvement in SLE includes myo-pericarditis, valvular disease/endocarditis, Heart Failure (HF), coronary macro-microvascular disease, vasculitis and pulmonary hypertension. Classic and advanced Cardiovascular Magnetic Resonance (CMR) indices allow function and tissue characterization for early diagnosis and treatment follow-up of CVD in SLE. <P> Although currently, there are no clinical data supporting the combined use of brain/heart MRI in asymptomatic SLE, it may have a place in cases with clinical suspicion of brain/heart involvement, especially in patients at high risk for CVD/stroke such as SLE with antiphospholipid syndrome (SLE/APS), in whom concurrent cardiac and brain lesions have been identified. Furthermore, it may be of value in SLE with multi-organ involvement, NPSLE with concurrent cardiac involvement, and recent onset of arrhythmia and/or heart failure.</P>]]></description> </item><item><title><![CDATA[Cardiovascular Risk of Synthetic, Non-Biologic Disease-Modifying Anti- Rheumatic Drugs (DMARDs)]]></title><link>https://www.benthamscience.comarticle/101084</link><description><![CDATA[Patients with rheumatoid diseases have an increased risk of cardiovascular disease (CVD) and CVD-related death compared with the general population. Both the traditional cardiovascular risk factors and systemic inflammation are contributors to this phenomenon. This review examines the available evidence about the effects of synthetic, non-biologic disease-modifying antirheumatic drugs (DMARDs) on CVD risk. This is an important issue for clinicians when deciding on individual treatment plans in patients with rheumatic diseases. Evidence suggests that synthetic, non-biologic DMARDs such as methotrexate, sulfasalazine, hydroxychloroquine, leflunomide and tofacitinib show decreased CVD morbidity and mortality. However, the strongest data in favour of a reduction in CVD events in rheumatoid patients are shown with methotrexate, which has been the focus of most studies. Adequate proof for a favourable effect also exists for hydroxychloroquine. Larger, prospective studies and randomized clinical trials are needed to better characterize the effect of synthetic, non-biologic DMARDs on CVD outcomes in these patients. Design of future studies should include areas with lack of evidence, such as the risk for heart failure, arrhythmias and valvular heart disease. The clinically relevant question whether synthetic, non-biologic DMARDs are inferior to biologic DMARDs in terms of CVD outcomes remains not adequately addressed.]]></description> </item><item><title><![CDATA[Primary Sjögren’s Syndrome and Cardiovascular Disease]]></title><link>https://www.benthamscience.comarticle/104047</link><description><![CDATA[Sjögren’s syndrome is a rheumatic autoimmune disease that primarily affects middle-aged women and runs a slowly progressing course with sicca symptoms being the prevalent manifestation. Premature atherosclerosis and increased cardiovascular (CV) morbidity and mortality are frequently encountered in rheumatic diseases characterized by significant systemic inflammation, such as the inflammatory arthritides, systemic vasculitides and systemic lupus erythematosus. In the same context, chronic inflammation and immune aberrations underlying Sjögren’s syndrome are also reported to be associated with augmented risk of atherosclerosis. Increased CV disease (CVD) frequency has been found in recent meta-analyses. The involvement of the CV system is not a common feature of Sjögren’s syndrome; however, specific manifestations, such as autoantibody-mediated heart block, pericarditis, pulmonary arterial hypertension and dysautonomia, have been described. This review focuses on studies addressing CV morbidity in Sjögren’s syndrome and presents current data regarding distinct CV features of the disease.]]></description> </item><item><title><![CDATA[Cardiovascular Effects of Biologic Disease-Modifying Anti-Rheumatic Drugs (DMARDs)]]></title><link>https://www.benthamscience.comarticle/104517</link><description><![CDATA[The risk of cardiovascular (CV) disease is increased among patients with systemic autoimmune rheumatic diseases and remains an underserved area of medical need. Although traditional risk factors for CV disease, such as hypertension, smoking, dyslipidemia and obesity contribute to endothelial dysfunction in rheumatoid arthritis (RA), they are not enough on their own to explain the observed excess CV risk. Rather, systemic inflammation seems to play a pivotal role in both disease states. Considering the inflammatory process in autoimmune diseases, scientific interest has focused on recently introduced biologic disease-modifying agents (bDMARDS) such as inhibitors of Tumor Necrosis Factor- &#945; (ΤΝF-&#945;), Interleukins -1 (IL-1) and -6 (IL-6). Despite the widespread use of bDMARDS in RA and other chronic autoimmune inflammatory diseases, their precise impact on CV disease and outcome remains to be elucidated, while prospective randomized control trials assessing their impact on hard CV endpoints are scarce. In this review, we summarize current knowledge concerning the effect of bDMARDs on CV outcome and on the risk of developing CV disease in patients with systemic autoimmune rheumatic diseases.]]></description> </item><item><title><![CDATA[Cardiovascular Disease in the Systemic Vasculitides]]></title><link>https://www.benthamscience.comarticle/104081</link><description><![CDATA[The vasculitides are a heterogeneous group of disorders, characterized by inflammatory cell infiltration and necrosis of blood vessels that cause vascular obstruction or aneurysm formation, affecting various organs such as lungs, kidneys, skin and joints. Cardiac involvement is commonly encountered in primary systemic vasculitis and it is associated with increased morbidity and mortality. Depending on the dominant pathophysiological mechanism, heart complications may manifest in different ways, including myocardial ischemia due to impaired micro- or macrovascular circulation, progressive heart failure following valvular heart disease and myocardial dysfunction, (sub) clinical myocarditis, pericarditis, pulmonary hypertension as well as arteritis of coronary vessels. Beyond cardioprotective regimens, aggressive immunosuppression reduces the inflammatory burden and modulates the progression of cardiovascular complications. Perioperative management of inflammation, when surgical treatment is indicated, improves surgical success rates and postoperative long-term prognosis. We aim to provide an overview of the pathogenetic, diagnostic and therapeutic principles of cardiovascular involvement disease in the various forms of systemic vasculitis.]]></description> </item><item><title><![CDATA[Cardio-Rheumatology: Cardiovascular Complications in Systemic Autoimmune Rheumatic Diseases / Is Inflammation the Common Link and Target?]]></title><link>https://www.benthamscience.comarticle/106636</link><description><![CDATA[In the current Thematic Issue of Current Vascular Pharmacology (CVP), entitled “Systemic Autoimmune Rheumatic Diseases and Cardiology”, presented in two parts, Part 1 and Part 2, review articles are included from specialists in cardiology, rheumatology, immunology and related fields. These reviews discuss the cardiovascular complications of the main systemic Autoimmune Rheumatic Diseases (ARDs). For example, the underlying pathogenetic mechanisms, the role of cardiovascular imaging and recommendations for prevention and management. These articles place inflammation as the key process, linking cardiovascular complications with ARDs. From all these reviews, the conclusion is the need for collaboration between the disciplines of Rheumatology and Cardiology to establish the emerging field of Cardio- Rheumatology. This will aid to fine-tune risk stratification and optimize preventive strategies and pharmacological therapies for patients with ARDs.]]></description> </item><item><title><![CDATA[Uncommon Association Between Diabetic Ketoacidosis, Thyrotoxicosis, Cutaneous Abscess and Acute Pericarditis in an Immunocompetent Patient: A Single Case Report and Literature Review]]></title><link>https://www.benthamscience.comarticle/101907</link><description><![CDATA[<p>Introduction: The typical factors precipitating diabetic ketoacidosis (DKA) include infections (30%), cessation of antidiabetic medication (20%), and a new diagnosis of diabetes (25%). The etiology remains unknown in 25% of cases. Less frequent causes cited in the literature include severe thyrotoxicosis and, infrequently, pericarditis. Few publications have described the role of human T lymphotropic virus type 1 (HTLV-1) in endocrine and metabolic disorders. Based on a clinical case associated with several endocrine and metabolic disorders, we suggest a potential role for HTLV-1, an endemic virus in the Amazonian area, and review the literature concerning the role of this virus in thyroiditis, pericarditis and diabetes mellitus. </P><P> Case Report: A fifty-year-old Surinamese woman without any medical history was admitted for diabetic ketoacidosis. No specific anti-pancreatic autoimmunity was observed, and the C-peptide level was low, indicating atypical type-1 diabetes mellitus. DKA was associated with thyrotoxicosis in the context of thyroiditis and complicated by nonbacterial pericarditis and a Staphylococcus aureus subcutaneous abscess. The patient was infected with HTLV-1. </P><P> Conclusion: To our knowledge, this uncommon association is described for the first time. Few studies have analyzed the implications of HTLV-1 infection in thyroiditis and diabetes mellitus. We did not find any reports describing the association of pericarditis with HTLV-1 infection. Additional studies are necessary to understand the role of HTLV-1 in endocrine and cardiac disorders.</p>]]></description> </item><item><title><![CDATA[Heart Infection Prognosis Analysis by Two-dimensional Spot Tracking Imaging]]></title><link>https://www.benthamscience.comarticle/96234</link><description><![CDATA[Cardiovascular death is one of the leading causes worldwide; an accurate identification followed by diagnosing the cardiovascular disease increases the chance of a better recovery. Among different demonstrated strategies, imaging on cardiac infections yields a visible result and highly reliable compared to other analytical methods. Two-dimensional spot tracking imaging is the emerging new technology that has been used to study the function and structure of the heart and test the deformation and movement of the myocardium. Particularly, it helps to capture the images of each segment in different directions of myocardial strain values, such as valves of radial strain, longitudinal strain, and circumferential strain. In this overview, we discussed the imaging of infections in the heart by using the two-dimensional spot tracking.]]></description> </item><item><title><![CDATA[Bactericidal Activity of a Cationic Peptide on Neisseria meningitidis]]></title><link>https://www.benthamscience.comarticle/92441</link><description><![CDATA[Background: The increasing prevalence of antibiotic resistant bacteria has raised an urgent need for substitute remedies. Antimicrobial peptides (AMPs) are considered promising candidates to address infections by multidrug-resistant bacteria through new mechanisms of action that require a careful evaluation of their performance. </P><P> Objective: Identification of effective AMPs against Neisseria meningitidis, which represents a pathogen of great public health importance worldwide that is intrinsically resistant to some AMPs, such as polymyxin B. </P><P> Methods: A cationic 11-residue peptide (KLKLLLLLKLK), referred to as poly-Leu, was synthesized and its antimeningococcal activity was compared to cecropin A and poly-P (KLKPPPPPKLK) through a variety of assays. Flow cytometry was used to measure propidium iodide uptake by N. meningitidis serotype B as an indicator of the effectiveness of each peptide when added to cultures at different concentrations. </P><P> Results: The addition of the poly-Leu peptide led to a 90.3% uptake of the dye with an EC50 value of 7.9 &#181;g mL-1. In contrast, uptake was <10% in cells grown in the absence of peptides or with an identical concentration of cecropin and poly-Pro peptides. Electron micrographs indicated that the integrity of the cellular wall and internal membrane was impacted in relation to peptide concentrations, which was confirmed by the detection of released alkaline phosphatase from the periplasmic space due to disruption of the external membrane. </P><P> Conclusion: Poly-Leu peptide demonstrated definitive antimicrobial activity against N. meningitidis.</P>]]></description> </item><item><title><![CDATA[Evaluation of Serum Calprotectin Level and Disease Activity in Patients with Rheumatoid Arthritis]]></title><link>https://www.benthamscience.comarticle/95993</link><description><![CDATA[<P>Background: Rheumatoid Arthritis (RA) is the most common type of chronic inflammatory arthritis with unknown etiology marked by a symmetric, peripheral polyarthritis. Calprotectin also can be used as a biomarker of disease activity in inflammatory arthritis and other autoimmune diseases. </P><P> Objectives: In this study, we evaluated the association between serum calprotectin level and severity of RA activity. </P><P> Methods: A cross-sectional study was conducted on 44 RA patients with disease flare-up. Serum samples were obtained from all patients to measure calprotectin, ESR, CRP prior to starting the treatment and after treatment period in the remission phase. Based on Disease Activity Score 28 (DAS28), disease activity was calculated. </P><P> Results: Of 44 RA patients, 9(20.5%) were male and 35(79.5%) were female. The mean age of our cases was 53&#177;1.6 years. Seventeen (38.6%) patients had moderate DAS28 and 27(61.4%) had high DAS28. The average level of calprotectin in the flare-up phase was 347.12&#177;203.60 ng/ml and 188.04&#177;23.58 ng/ml in the remission phase. We did not find any significant association between calprotectin and tender joint count (TJC; P=0.22), swollen joint count (SJC; P=0.87), and general health (GH; P=0.59), whereas significant associations were found between the calprotectin level and ESR (p=0.001) and DAS28 (p=0.02). The average calprotectin level in moderate DAS28 (275.21&#177;217.96 ng/ml) was significantly lower than that in high DAS28 (392.4&#177;183.88 ng/ml) (p=0.05). </P><P> Conclusion: We showed that the serum level of calprotectin can be a useful and reliable biomarker in RA activity and its severity. It also can predict treatment response.</P>]]></description> </item><item><title><![CDATA[Natural Alkaloids Intervening the Insulin Pathway: New Hopes for Anti-Diabetic Agents?]]></title><link>https://www.benthamscience.comarticle/90095</link><description><![CDATA[Background: Accumulating experimental data supports the capacity of natural compounds to intervene in complicated molecular pathways underlying the pathogenesis of certain human morbidities. Among them, diabetes is now a world’s epidemic associated with increased risk of death; thus, the detection of novel anti-diabetic agents and/or adjuvants is of vital importance. Alkaloids represent a diverse group of natural products with a range of therapeutic properties; during the last 20 years, published research on their anti-diabetic capacity has been tremendously increased. <p></p> Purpose: To discuss current concepts on the anti-diabetic impact of certain alkaloids, with special reference to their molecular targets throughout the insulin-signaling pathway. <p></p> Methodology: Upon in-depth search in the SCOPUS and PUBMED databases, the literature on alkaloids with insulin secretion/sensitization properties was critically reviewed. <p></p> Results: In-vitro and in-vivo evidence supports the effect of berberine, trigonelline, piperine, oxymatrine, vindoneline, evodiamine and neferine on insulin-signaling and related cascades in beta-cells, myocytes, adipocytes, hepatocytes and other cells. Associated receptors, kinases, hormones and cytokines, are affected in terms of gene transcription, protein expression, activity and/or phosphorylation. Pathophysiological processes associated with insulin resistance, beta-cell failure, oxidative stress and inflammation, as well as clinical phenotype are also influenced. <p></p> Discussion: Growing evidence suggests the ability of specific alkaloids to intervene in the insulin-signal transduction pathway, reverse molecular defects resulting in insulin resistance and glucose intolerance and improve disease complications, in-vitro and in-vivo. Future indepth molecular studies are expected to elucidate their exact mechanism of action, while large clinical trials are urgently needed to assess their potential as anti-diabetic agents.]]></description> </item><item><title><![CDATA[Research Progress on Brucellosis]]></title><link>https://www.benthamscience.comarticle/90324</link><description><![CDATA[Brucellosis is a debilitating febrile illness caused by an intracellular Brucella. The disease is distributed in humans and animals widely, especially in developing countries. Ten species are included in the genus Brucella nowadays; four species of them are pathogenic to humans, which make brucellosis a zoonosis with more than 500,000 new cases reported annually. For human brucellosis, the most pathogenic species is B. melitensis followed by B. suis, while B. abortus is the mildest type of brucellosis. The infection mechanism of Brucella is complicated and mostly relies on its virulence factors. The therapy of the disease contains vaccination and antibiotic. However, there are some defects in currently available vaccines such as the lower protective level and safety. Thus, safe and efficient vaccines for brucellosis are still awaited. The dual therapy of antibacterial is effective in the treatment of brucellosis if a rapid and exact detection method is found.]]></description> </item><item><title><![CDATA[Impaired Myocardial MIF/AMPK Activation Aggravates Myocardial Ischemia Reperfusion Injury in High-Fat Diet-Induced Obesity]]></title><link>https://www.benthamscience.comarticle/97553</link><description><![CDATA[<P>Background: Obese patients are more sensitive to myocardial ischemia, which has been linked with high mortality rates. The following study investigates the effects of impaired macrophage Migration Inhibitory Factor (MIF)/AMP-Activated Protein Kinase (AMPK) activation on increased susceptibility to myocardial ischemia/reperfusion (I/R) in high-fat diet-induced obesity. </P><P> Methods: Male C57BL/6J mice were fed with a normal diet (10% kcal as fat, lean group) or a high-fat diet (60kcal as fat, obese group) for 12 consecutive weeks. To detect the MIF expression and AMPK activation in response to I/R in isolated hearts from lean and obese mice, myocardial samples were collected from left ventricular areas at different time points. To determine whether MIF supplementation is protective against I/R injury, recombined MIF (10 ng/mL) was applied before ischemia. Myocardial infarct size was estimated by triphenyltetrazolium staining. Western blot was used to detect myocardial MIF expression, AMPK activation and membrane glucose transporter 4 (Glut4) expression. </P><P> Results: The expression of MIF was remarkably higher in obese group compared to lean group. Ischemia increased myocardial MIF expression and phosphorylation of AMPK in lean mice, whereas it had no significant effect on obese mice. Furthermore, administration of recombinant MIF increased ischemic AMPK activation and membrane Glut4 expression in both lean and obese mice, while it reduced the infarct size in lean mice only. </P><P> Conclusion: An impaired MIF/AMPK activation response and consequent reduced membrane Glut4 expression may play an important role in increasing myocardial susceptibility to I/R in obesity.</P>]]></description> </item><item><title><![CDATA[Tubular and Glomerular Biomarkers of Acute Kidney Injury in Newborns]]></title><link>https://www.benthamscience.comarticle/97499</link><description><![CDATA[<P>Background: Acute Kidney Injury (AKI) is a sudden decrease in kidney function. In the early period, the highest percentage of AKI occurs among newborns hospitalized in the neonatal intensive care units, especially premature neonates. The prognosis of AKI depends on the type and severity of the cause of an injury, the accuracy and the time of diagnosis and treatment. The concentration of serum creatinine is still the main diagnostic test, although it changes in the course of AKI later than glomerular filtration rate GFR. In addition, the reliability of the determination of creatinine level is limited because it depends on many factors. New studies have presented other, more useful laboratory markers of renal function that can be measured in serum and/or in urine. </P><P> Objective: The aim of the work was to present the latest data about tubular and glomerular biomarkers of acute kidney injury in newborns. </P><P> Methods: We undertook a structured search of bibliographic databases for peer-reviewed research literature by using focused review topics. According to the conceptual framework, the main idea of research literature has been summarized and presented in this study. </P><P> Results: The concentrations of some novel biomarkers are higher in serum and/or urine of term and preterm newborns with AKI, especially in the course of perinatal asphyxia. </P><P> Conclusion: In this systematic review of the literature, we have highlighted the usefulness of biomarkers in predicting tubular and/or glomerular injury in newborns. However, novel biomarkers need to prove their clinical applicability, accuracy, and cost-effectiveness prior to their implementation in clinical practice.</P>]]></description> </item><item><title><![CDATA[Inflammatory Biomarkers in Atrial Fibrillation]]></title><link>https://www.benthamscience.comarticle/85021</link><description><![CDATA[During the last few years, a significant number of studies have attempted to clarify the underlying mechanisms that lead to the presentation of atrial fibrillation (AF). Inflammation is a key component of the pathophysiological processes that lead to the development of AF; the amplification of inflammatory pathways triggers AF, and, in tandem, AF increases the inflammatory state. Indeed, the plasma levels of several inflammatory biomarkers are elevated in patients with AF. In addition, the levels of specific inflammatory biomarkers may provide information regarding to the AF duration. Several small studies have assessed the role of anti-inflammatory treatment in atrial fibrillation but the results have been contradictory. Large-scale studies are needed to evaluate the role of inflammation in AF and whether anti-inflammatory medications should be routinely administered to patients with AF.]]></description> </item><item><title><![CDATA[Redox State in Atrial Fibrillation Pathogenesis and Relevant Therapeutic Approaches]]></title><link>https://www.benthamscience.comarticle/84835</link><description><![CDATA[<P>Background: Myocardial redox state is a critical determinant of atrial biology, regulating cardiomyocyte apoptosis, ion channel function, and cardiac hypertrophy/fibrosis and function. Nevertheless, it remains unclear whether the targeting of atrial redox state is a rational therapeutic strategy for atrial fibrillation prevention. </P><P> Objective: To review the role of atrial redox state and anti-oxidant therapies in atrial fibrillation. </P><P> Method: Published literature in Medline was searched for experimental and clinical evidence linking myocardial redox state with atrial fibrillation pathogenesis as well as studies looking into the role of redoxtargeting therapies in the prevention of atrial fibrillation. </P><P> Results: Data from animal models have shown that altered myocardial nitroso-redox balance and NADPH oxidases activity are causally involved in the pathogenesis of atrial fibrillation. Similarly experimental animal data supports that increased reactive oxygen / nitrogen species formation in the atrial tissue is associated with altered electrophysiological properties of atrial myocytes and electrical remodeling, favoring atrial fibrillation development. In humans, randomized clinical studies using redox-related therapeutic approaches (e.g. statins or antioxidant agents) have not documented any benefits in the prevention of atrial fibrillation development (mainly post-operative atrial fibrillation risk). </P><P> Conclusion: Despite strong experimental and translational data supporting the role of atrial redox state in atrial fibrillation pathogenesis, such mechanistic evidence has not been translated to clinical benefits in atrial fibrillation risk in randomized clinical studies using redox-related therapies.</P>]]></description> </item><item><title><![CDATA[Cancer Therapeutics-Related Cardiovascular Complications. Mechanisms, Diagnosis and Treatment]]></title><link>https://www.benthamscience.comarticle/95687</link><description><![CDATA[Background: Chemotherapy regimens have improved prognosis and mortality of patients with malignant diseases. The development of therapies, however, has widened the cardiotoxic spectrum and the cardiacrelated effects of antineoplastic drugs. </P><P> Methods: A review of the literature under the search terms anthracyclines, oncology, cardiotoxicity, cardiooncology, chemotherapy and heart failure was used for the identification of the most relevant articles. </P><P> Results: Considerable variability exists in patients’ characteristics, in mechanisms involved in cardiomyopathy progression and in its physical history, as well as in modalities used to screen myocardial competence. The anthracyclines and particularly doxorubicin are the most widely used antineoplastic drugs. Monoclonal antibodies, tyrosine kinase inhibitors and other targeted therapies have been associated with cardiovascular side-effects, such as cardiomyopathy and congestive heart failure. Moreover, some of these agents are associated with an increased risk of coronary artery disease with or without myocardial infarction. The current standard for the detection of cardiac toxicity is serial echocardiography. Biomarkers though could be proved helpful, they can be tested at closer intervals and are highly accurate and reproducible. Of note, a growing body of data has emerged suggesting that some agents could have cardioprotective properties. </P><P> Conclusion: Since the number of long-term survivors following the diagnosis and treatment of malignant disease will continue to increase, cardio-oncology will continue to evolve. Therefore, a better understanding of potential cardiovascular effects of chemotherapeutic regiments and the earlier identification and treatment of high-risk patients would be the focus of research in the future.]]></description> </item><item><title><![CDATA[The Cellular Uptake and Apoptotic Efficiency of Colchicine is Correlated with Downregulation of MMP-9 mRNA Expression in SW480 Colon Cancer Cells]]></title><link>https://www.benthamscience.comarticle/92538</link><description><![CDATA[Background: Colchicine, a tricyclic alkaloid, is commonly used in treatment due to its antiinflammatory and anti-fibrotic effects. Besides its toxicity at high doses, colchicine is reported for its potential anticancer effects at lower concentrations. The present study aimed to evaluate the anticancer effects of colchicine in SW480 cells. </P><P> Methods: The effect of colchicine on cell proliferation was determined by MTT assay. The cellular colchicine uptake was measured by HPLC analysis. The apoptotic effects was evaluated by annexin v binding assay and MMP-9 mRNA expression was determined by RT-PCR experiments. </P><P> Results: Colchicine showed significant cytotoxicity at 10 ng/ml and higher concentrations and caused a cell cycle arrest of SW480 cells at G2/M phase. The results of HPLC analysis showed that colchicine uptake was increased in correlation with treated concentrations. Colchicine concentrations have increased the amount of apoptotic cell population. The elisa and western blot measurements showed that colchicine led to nuclear translocation of NF-&#954;B proteins and increased caspase levels. The real time PCR experiments showed that colchicine has inhibitory effect on MMP-9 mRNA expression in a concentration dependent manner. </P><P> Conclusion: These results illustrated that low dose colchicine efficiently induced cell death and apoptosis of SW480 cells and the inhibition of MMP-9 mRNA levels was significantly correlated with the amount of cellular colchicine uptake, suggesting that colchicine has a potential value in the treatment of human colorectal cancer.]]></description> </item><item><title><![CDATA[Recurrent Episodes of Pericardial Effusion as Isolated Manifestation of Tuberculosis: Case Report]]></title><link>https://www.benthamscience.comarticle/84216</link><description><![CDATA[Background: Recurrent episodes of isolated pericardial effusion due to tuberculosis, leading to reduced Left Ventricle Ejection Fraction (LVEF), are uncommon. </P><P> Methods: This is a case report of a previously healthy 32-years old male with tuberculous induced pericardial effusion as isolated manifestation. The only known exposure of tuberculosis was a brother with whom the patient did not have physical contact during the last year. The pericardial effusion repeatedly appeared after being drained a total of three times. Due to recurrent episodes of pericardial effusion, severe thickening of the pericardium, pericardial adherences and increasing affection on the heart, pericardiectomy was ultimately performed. </P><P> Results: Biochemical examination, chest X-ray, computed tomography of thorax and abdomen and cytology report did not reveal any signs of malignancy, connective tissue disease or other infections including extra-pulmonary/pulmonary tuberculosis. However, the pericardial biopsy was Polymerase Chain Reaction positive (PCR) for tuberculosis DNA and showed granulomatous inflammation with necrosis. After 6 months anti-tuberculous therapy, biochemical parameters, LVEF and the clinical condition of the patient were normalized. </P><P> Conclusion: Tuberculosis can be difficult to diagnose when it only manifests as pericardial effusion especially if the time for exposure is long before the appearance of symptoms and admission.]]></description> </item></channel></rss>