Methods: A cross-sectional survey of 251 T2DM patients was conducted using convenience sampling at two tertiary hospitals. Data on IAH, IP, FOH, and MCI were collected using standardized questionnaires. Data were analyzed and compared using SPSS 27.0 and AMOS 27.0.

Results: There were significant correlations among IAH, IP, FOH, and MCI. Higher IAH was associated with increased FOH and more negative IP, which were both linked to worse cognitive function. Mediation analysis showed that IAH indirectly affects MCI through three pathways: independently via FOH, independently via IP, and via a chained effect of FOH and IP.

Discussion: The findings underscored that the link between IAH and cognitive decline is not solely physiological, but is substantially mediated by psychological responses. Negative illness perceptions and heightened fear, triggered by the unpredictability of IAH, drive maladaptive behaviors and emotional distress that contribute to worse cognitive outcomes.

Conclusion: The findings highlighted the role of psychological factors in cognitive decline among T2DM patients with IAH. We recommend that future interventions consider the associations between these variables. Diverse interventions aimed at improving IP and FOH levels could help slow cognitive decline in patients with IAH.

Methods: Using Genome-Wide Association Study (GWAS) summary data, we conducted both univariate and multivariable Mendelian Randomization (MVMR) analyses. The primary causal inference was based on Inverse Variance Weighted (IVW), MR-Egger, weighted median, and sensitivity analyses (Cochran’s Q, MR-PRESSO). Mediation analysis was employed to quantify the proportion of effects operating through metabolite-regulated pathways.

Results: BMR was inversely associated with hyperemesis gravidarum (OR=0.73, 95% CI: 0.59-0.90, P=0.008), Intrahepatic Cholestasis of Pregnancy (ICP) (OR=0.67, 95% CI: 0.56-0.80, P<0.001), poor fetal growth (OR=0.80, 95% CI:0.71-0.90, P=0.001), and preterm delivery (OR=0.78, 95% CI:0.70-0.87, P<0.001). MVMR identified elevated BMR and mannose levels as protective against ICP, with BMR showing a positive correlation with mannose. Mediation analysis revealed that BMR reduced ICP risk partly through increased mannose (OR = 1.38, 95% CI: 1.19-1.59, P = 2.03 × 10⁻⁵), accounting for 29.93% of the effect.

Discussion: Elevated BMR significantly reduced risks of intrahepatic cholestasis (HR=0.67), fetal distress (HR=0.80), and preterm birth (HR=0.78), mediated partly by mannose levels. Mendelian randomization established causality, linking metabolic adaptation to improved pregnancy outcomes. However, these findings, based on European genetic data, limit generalizability, and unmeasured confounders may persist despite MR methods.

Conclusion: Higher BMR may lower risks of hyperemesis gravidarum, ICP, poor fetal growth, and preterm delivery. Mannose mediates the protective effect of BMR on ICP, highlighting potential metabolic pathways for intervention.

Methods: Summary statistics for 179 lipid species across 13 classes were retrieved from the GWAS Catalog, encompassing 7,174 Finnish individuals from the GeneRISK study. For AF, data were synthesized from six major studies comprising over one million subjects. Our Two-Sample MR (TSMR) approach was implemented using Inverse Variance Weighting (IVW), MR-Egger, and MR-PRESSO for sensitivity analysis. Additionally, we uniquely integrated the Mendelian Randomization-Bayesian Model Averaging (MR_BMA) method to robustly prioritize the most likely causal lipid determinants of AF, and performed bidirectional MR analysis to assess potential reverse causality.

Results: The TSMR analysis, reinforced by MR_BMA, revealed significant causal associations between specific lipid species and AF risk. In particular, Phosphatidylcholine (17:0_18:2) was associated with a decreased risk of AF (OR = 0.96, 95% CI 0.93–0.99, P<0.05), whereas Phosphatidylcholine (16:0_20:5) and Phosphatidylcholine (17:0_20:4) were linked to increased risks (OR = 1.04, 95% CI 1.01–1.07, P<0.01; and OR = 1.02, 95% CI 1.00–1.05, P<0.05, respectively). Furthermore, elevated levels of Phosphatidylethanolamine (18:0_20:4) (OR = 1.03, 95% CI 1.01–1.06, P<0.01) and Triacylglycerol (50:4) (OR = 1.04, 95% CI 1.00–1.07, P<0.05) were also associated with increased AF risk. In addition, Sphingomyelin (d34:2), Sterol ester (27:1/18:0), and Sterol ester (27:1/18:3) emerged as further risk factors, thereby expanding the spectrum of lipidomic determinants implicated in AF. The bidirectional MR analysis provided no evidence of reverse causation, reinforcing the directionality of the lipid-driven association. Sensitivity analyses demonstrated robust findings with no indication of pleiotropy or heterogeneity.

Conclusion: This study provides strong evidence for the causal role of specific lipid species in the development of AF. Our comprehensive MR analysis not only deepens our understanding of AF pathophysiology but also highlights the therapeutic potential of targeting these lipid alterations. Notably, the absence of reverse causation supports a unidirectional relationship wherein altered lipid species drive AF risk.

Case Presentation: A 48-year-old woman with poorly controlled type 2 diabetes developed necrotizing fasciitis of the right perineum secondary to an ischial tuberosity pressure ulcer. She had a prior spinal cord injury resulting in sensory dysfunction in the lower limbs, which masked significant pain. Management included surgical debridement, open wound care, antimicrobial therapy, and a free skin graft for wound closure.

Conclusion: Effective treatment of necrotizing fasciitis relies on aggressive debridement and appropriate antimicrobial therapy. This case highlights the importance of early recognition and intervention to improve clinical diagnostic and management strategies.

Materials and Methods: The key active components of YPSXZJDD were screened using UHPLC- Q Exactive Orbitrap-MS, and a Protein-Protein Interaction (PPI) network diagram was constructed to explore potential mechanisms of action. The identified components were then utilized to intervene in both cellular and animal models of hyperuricemic nephropathy, evaluating their therapeutic effects and underlying mechanisms.

Results: Catalpol and Tanshinone IIA were identified as the key active components of YPSXZJDD. These compounds significantly mitigated renal epithelial cell apoptosis and inflammation by upregulating miR-223, which in turn inhibited the NLRP3/Caspase-1 pathway. The upregulation of miR-223 led to a marked reduction in NLRP3 activity and inflammatory responses, thereby alleviating HN-induced kidney damage.

Discussion: The findings of this study underscore the critical role of miR-223 in regulating the NLRP3 inflammasome and highlight its potential as a therapeutic target for HN. The inhibition of the NLRP3/Caspase-1 pathway by miR-223 significantly reduces inflammation and renal injury, demonstrating the therapeutic efficacy of YPSXZJDD. These results offer a novel perspective on the application of traditional Chinese medicine in treating HN, highlighting the importance of miR-223 in regulating inflammation.

Conclusion: This study demonstrates that YPSXZJDD alleviates HN-induced kidney injury by upregulating miR-223 and inhibiting the NLRP3/Caspase-1 pathway. The therapeutic potential of YPSXZJDD is supported by its ability to mitigate inflammation and renal damage, offering a promising approach for HN treatment. Further research into the broader role of miR-223 in kidney disease and related conditions is warranted to expand the understanding of its therapeutic applications.

Aims: The aim of this study was to discover common diagnostic genes for LUAD and MI and analyze their molecular functions and potential drug values by applying bioinformatics analysis.

Objective: The objective was to provide a theoretical basis for further research on the pathological mechanisms of LUAD and MI, contributing to the development of novel diagnostic and therapeutic strategies for the two diseases.

Methods: In this study, the datasets of LUAD and MI were obtained from TCGA and GEO databases, and differential expression analysis was performed to screen significantly differentially expressed genes (DEGs). Subsequently, disease-related genes were identified using WGCNA analysis, and the biological functions of these genes were explored by functional enrichment analysis. After screening key genes using the protein-protein interaction (PPI) network and the cytoHubba algorithm, biomarkers were determined by LASSO and SVM-RFE machine-learning methods. Finally, immune infiltration analysis and drug prediction were performed, and biomarker expression was verified by single-cell sequencing analysis.

Results: A total of 158 differentially upregulated genes were identified between LUAD and MI. WGCNA analysis screened 86 genes that were significantly associated with both diseases and were enriched in an inflammatory response and immune regulation-related pathways, such as the IL-17 signaling pathway. Ten significant genes were identified by the PPI network and cytoHubba and then reduced to 4 using LASSO and SVM-RFE. Noticeably, MMP9 was significantly overexpressed in both diseases. Immune infiltration analysis showed that MMP9 was significantly related to multiple immune cell infiltration. Drug prediction and molecular docking analysis predicted Ilomastat and Osthole as the potential target drugs. Single-cell sequencing analysis revealed that MMP9 was high-expressed in the macrophages in LUAD tissues.

Conclusion: This study identified MMP9 as a common diagnostic gene and potential therapeutic target for both LUAD and MI and revealed its role in inflammation and immune regulation through comprehensive bioinformatics analysis. These findings provided a theoretical basis for further research on the pathological mechanisms of LUAD and MI, contributing to the development of novel diagnostic and therapeutic strategies.

Methods: The study included 157 patients diagnosed with subclinical hypothyroidism, categorised into anti-TPO-positive and anti-TPO-negative groups. A retrospective comprehensive evaluation comprising demographic data, thyroid medication status, ultrasonographic characteristics, and laboratory parameters was conducted and statistically analysed between the groups.

Results: Of 157 patients, 48.4% were anti-TPO positive. This group was significantly associated with increased levothyroxine (LT4) use and sonographic parenchymal heterogeneity. However, there were no significant differences in nodule presence, number, size, or structure. A positive correlation was found between anti-TPO and ferritin levels. In addition, a positive correlation was observed between the thyroid-stimulating hormone (TSH)/free T4 ratio and the solidity of nodules, as well as between TSH and the neutrophil-to-lymphocyte ratio (NLR). Surprisingly, a negative correlation was found between anti-TPO levels and the number of nodules, as well as the cystic characterisation of the nodules.

Discussion: In our study, higher levels of anti-TPO and TSH were associated with inflammatory markers such as ferritin and NLR, suggesting a possible link with systemic inflammation. Furthermore, anti-TPO and the TSH/T4 ratio also showed associations with specific sonographic features of the thyroid gland.

Conclusion: TSH and anti-TPO levels might be associated with systemic inflammation and thyroid sonographic findings in patients with subclinical hypothyroidism. More studies on larger patient populations should confirm the same results to suggest their clinical significance.

Objective: This study sought to explore the role and mechanism of esketamine in the LIR-ALI rat model.

Methods: The effects of esketamine on the LIR-ALI rats model were evaluated through histopathological examination, assessment of pulmonary edema, measurement of MDA and SOD levels, and analysis of inflammatory cytokine levels (IL-1β, etc.) in the bronchoalveolar fluid (BALF) and serum. Western blot analysis was used to assess the expressions of TLR4, NF-κB, and NLRP3. TLR4 agonist, LPS, was used to validate the role of NF-κB/NLRP3 pathway in LIRALI.

Results: Esketamine significantly alleviated LIR-induced ALI by reducing pulmonary edema, inflammatory cell infiltration, and oxidative stress. Elevated MDA content and suppressed SOD activity were significantly reversed by esketamine, along with inactivity of the TLR4/NF-κB/NLRP3 pathway. Esketamine treatment reduced inflammatory response in BALF and serum. TLR4 activation by LPS reversed the ameliorative effects of esketamine on LIR-ALI.

Conclusion: Esketamine protected against LIR-induced ALI by mitigating oxidative stress and suppressing the TLR4/NF-κB/NLRP3 axis. These findings highlight the potential therapeutic value of esketamine for ALI.

Aims: This study explored the mutation status of DRGs in CESC.

Objective: After analyzing the mutation profiles of DRGs in CESC, this study established a prognostic model for CESC and also explored the differences in immune infiltration (accumulation of immune system cells in tissues or organs), related enriched pathways, and drug sensitivity between high-risk and low-risk CESC groups.

Methods: The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) were accessed to source related data. The mutation profiles of DRGs in CESC were analyzed using Mutect2 software, and disulfidptosis scores were calculated by ssGSEA. WGCNA was performed to identify modular genes, which were further filtered and used to formulate a risk model by applying the survival and glmnet packages. Low- and high-risk groups of CESC patients were classified using the survminer package. GSEA was performed to conduct pathway analysis, and immune infiltration was assessed using the MCPcounter package, ESTIMATE, and TIMER algorithms. Finally, immunotherapy response and drug sensitivity were analyzed using the TIDE method and the pRRophetic package, respectively.

Results: Except for NDUFA11, ARL6IP5, EPM2AIP1, GBE1, RBM38, ULK4, and ZBTB47 were found to be the DRGs significantly mutated in CESC. The six genes were integrated to develop a RiskScore model with a relatively high Area Under the Curve (AUC) value. Significant differences between the two risk groups were determined, indicating that the model was highly reliable. Notably, the low-risk group was enriched in energy metabolism-correlated pathways, while the high-risk group was primarily enriched in immune-correlated pathways. The high-risk group showed higher immune cell activity, higher TIDE score, and more B cells than the low-risk group. Drug sensitivity study revealed that the high-risk group was more sensitive to chemotherapy drugs.

Conclusion: This study provides novel insights into CESC prognosis, immunotherapy, and drug development, contributing to the clinical treatment for CESC.

Systemic glucocorticoids are commonly prescribed in the management of COPD exacerbations; however, prolonged or repeated steroid use may lead to adrenal suppression. Although the standard steroid regimen for COPD exacerbations is short-term, frequent ED visits may result in cumulative steroid exposure, raising concerns about adrenal insufficiency and its clinical consequences.

This study investigates the potential association between steroid-induced adrenal suppression and frequent ED visits among COPD patients. It further examines the impact of steroid administration on cortisol and Adrenocorticotropic hormone (ACTH) levels.

Methods: This prospective, cross-sectional, observational study was conducted in a university- based ED. Patients with COPD, with dyspnea and who presented to the ED between 06:00-08:00 were included. Demographics, previous presentations to the ED, medications used, hormone levels, and other laboratory results were recorded.

Results: Fifty patients (82% were male) included. Sputum symptoms along with incidences of heart failure were higher in patients who received steroids in the ED. Ronchi was higher, crackles and pretibial edema were lower in the patients who received steroids in the ED. Among the patients with low cortisol levels, the frequency of patients who received steroids in the ED was higher than those who did not.

Conclusion: Primary healthcare clinicians should monitor COPD patients for potential adrenal insufficiency. Careful regulation of steroid dosages during exacerbation treatment and minimizing polypharmacy are essential to mitigate the long-term effects of prolonged steroid use.

Methods: Appropriate single nucleotide polymorphisms (SNPs) were carefully selected from publicly available GWAS databases based on rigorous criteria to ensure the validity of the Mendelian randomization (MR) analysis. Inverse variance weighting (IVW) was employed as the primary approach for assessing effect sizes, supplemented by four sensitivity analysis techniques: weighted median, simple mode, weighted mode, and MR-Egger regression tests, all aimed at ensuring the robustness and reliability of the IVW results. Reverse MR was conducted to confirm the feasibility of the mediation analysis. Lastly, Cochran’s Q test, MR Egger intercept regression, and MR-PRESSO analysis were utilized to examine heterogeneity and horizontal pleiotropy.

Results: The expression of BDH1 is inversely associated with the risk of type 2 diabetes, with an odds ratio of 0.97 (95% CI: 0.95-0.99). IgD+ CD38+ B cell absolute count (20.7%), HLA DR on dendritic cell (18.7%), BAFF-R on CD20- CD38- B cell (9.5%), CD25 on IgD⁺ CD24⁺ B cell (4.1%), and BAFF-R on IgD+ B cell (3.4%), all exhibit certain mediating effects, whereas IgD+ CD38⁺ B cell absolute count, activated and resting CD4 regulatory T cell %, CD4⁺ T cell, transitional B cell absolute count, CD28- CD8 dim T cell absolute count, CD45 on HLA DR⁺ CD8⁺ T cell, FSC-A on HLA DR⁺ natural killer, and SSC-A on plasmacytoid dendritic cell exert masking effects.

Conclusion: The findings indicate that immunocytes could serve as a crucial mediating mechanism through which BDH1 exerts its protective effect against type 2 diabetes, offering novel insights for the prevention and therapeutic management of the disease.

Aims and Objectives: This study aimed to explore the prognostic factors associated with nitrogen metabolism in bladder cancer (BC) and to construct a prognostic model.

Methods: Differential expression gene analysis was performed to identify genes associated with nitrogen metabolism by analyzing mRNA expression data from BC patients. The prognostic relationship between these genes and BC patients was analyzed using univariate Cox regression. One hundred one combinatorial machine learning methods were applied for feature selection, and key prognostic genes were identified based on the method with the highest combined score. Immunocyte infiltration analysis was carried out to assess the tumor microenvironmental characteristics of patients in different risk groups.

Results: Twenty-five genes significantly associated with prognosis were identified from nitrogen metabolism-related genes. Twenty-three most prognostically predictive signature genes were screened under feature screening with multiple machine-learning models. Immune cell infiltration analysis showed that patients in the high-risk group had significantly different immune cell infiltration, suggesting that these genes may influence BC progression by regulating immune escape mechanisms. These results provide new biomarkers and potential therapeutic targets for precision treatment and prognostic assessment of BC.

Discussion: The findings suggest that nitrogen metabolism-related genes play a key role in the prognosis of bladder cancer and may be involved in regulating the tumor immune microenvironment. Different immune environments were demonstrated in high and low Riskscore groups, implying that these genes may contribute to immune evasion and thus promote tumor progression. These observations are consistent with emerging evidence that emphasizes the interplay between metabolism and immunity during cancer development. By combining nitrogen metabolism with immune analysis, this study provides a new perspective for stratifying BC patients and identifying therapeutic targets.

Conclusion: The expression patterns of nitrogen metabolism-related genes identified can be used as effective biomarkers for bladder cancer prognosis, providing a scientific basis for personalized treatment. Future studies can further explore the specific biological functions and mechanisms of action of these genes to promote more effective clinical applications.

Methods: Data were obtained from the European FinnGen biobank and the Gene Expression Omnibus (GEO) database. Mendelian Randomization (MR) analysis was performed with instrumental variables (IVs). The study assessed causal robustness using MR methods and sensitivity analysis, followed by differential expression analysis and weighted gene co-expression network analysis (WGCNA) to screen for the core genes. Further, machine learning algorithms, such as least absolute shrinkage and selection operator (LASSO), random forest (RF), and support vector machine (SVM) algorithms, were applied to screen for key diagnostic genes. Additionally, the CIBERSORT algorithm was used to analyze immune cell infiltration, and validation was conducted using an in vitro oxidized low-density lipoprotein (ox-LDL)-induced endothelial cell model and western blot experiments.

Results: MR analysis revealed a positive causal link among vitamin B12 deficiency anemia, hemolytic anemia, and coronary heart disease, while cardiovascular events appeared to have a negative association with hemolytic anemia. Integrated bioinformatics analysis identified six core genes involved in immune response, inflammation, and lipid metabolism. To improve the accuracy of key gene screening and avoid bias from a single method, this study combined multiple machine learning algorithms for comprehensive analysis, ultimately identifying IFIH1 and APBB2 as potentially valuable diagnostic biomarkers, and revealing affected macrophages, mast cells, and T cells infiltration. In vitro experiments confirmed altered expression of IFIH1 and APBB2 upon ox-LDL treatment, supporting their role in CHD pathogenesis.

Discussion: The findings of this study suggest that vitamin B12 deficiency anemia and hemolytic anemia are potential risk factors for CHD. The identification of IFIH1 and APBB2 as key biomarkers provides novel insights into the molecular mechanisms underlying CHD development in the context of anemia, offering potential targets for early diagnosis and personalized intervention strategies.

Conclusion: This study, through the integration of MR, transcriptomics, and machine learning methods, has for the first time revealed the causal role of vitamin B12 deficiency anemia and hemolytic anemia in the occurrence of CHD, and identified IFIH1 and APBB2 as potential biomarkers. This research study has provided a new theoretical basis and research direction for understanding the molecular link between anemia and CHD and for improving clinical early warning systems.

Methods: We established a rat model of HFpEF using Dahl salt-sensitive rats and evaluated three experimental groups: control (A), HFpEF (B), and canagliflozin-treated HFpEF (C). This study carried out comprehensive analyses of cardiac structure and function, metabolomic profiling, and detailed assessment of myocardial energy metabolism, including mitochondrial respiratory capacity and ATP synthesis. Additionally, we validated our findings using H9C2 cardiomyocytes under controlled conditions.

Results: Canagliflozin treatment significantly improved cardiac remodeling markers, including reduced myocardial volume and fibrosis area, while enhancing diastolic function (E/A ratio). Metabolomic analysis revealed normalization of hypermetabolic states, with significant reductions in key metabolites, including L-lysine, D-glucose, and uridine. The treatment restored balance in multiple metabolic pathways, particularly affecting β-alanine metabolism, pyrimidine metabolism, and the citrate cycle. Notably, canagliflozin enhanced mitochondrial respiratory function, increased ATP synthesis, and optimized fatty acid utilization, as evidenced by reduced free fatty acid content.

Conclusion: Our findings demonstrated that canagliflozin exerts cardioprotective effects through multiple metabolic pathways, suggesting its potential as a therapeutic option for HFpEF. The ability of the drug to optimize energy metabolism and improve mitochondrial function represents a novel mechanism for treating this challenging condition.

Methods: MethylTarget™ sequencing targeted AIM2 cg11003133 (chr1:159076528-159076740) in RA, Ankylosing Spondylitis (AS), Psoriatic Arthritis (PsA), gout, Systemic Lupus Erythematosus (SLE), Dermatomyositis (DM), primary Sjögren's Syndrome (SS), and Healthy Controls (HC) patients. Logistic regression, random forest, and XGBoost models were applied, with Spearman’s correlation used to assess associations.

Results: RA and RF/CCP-positive patients showed significantly higher methylation at cg11003133_79/91 compared to HC and AS (FDR < 0.05), but lower levels compared to DM. Methylation at cg11003133_139 was elevated in RA compared to AS/SS (FDR = 0.04/0.03). Anti- TNF-α non-responders had higher cg11003133_79/91 methylation levels compared to HC/AS non-responders (FDR < 0.05). RF-negative RA patients had higher cg11003133_91 methylation than AS patients who failed anti-TNF-α treatment (FDR < 0.05). Haplotype CCCC correlated positively with CRP (r = 0.14, P = 0.006); TTTT was significantly negatively correlated with erythrocyte sedimentation rate, CRP, and the presence of diabetes (r = -0.18, -0.15, and -0.14; P < 0.001, 0.003, and 0.008, respectively). XGBoost and RF models achieved AUCs of 0.9911 and 0.9975 for RA versus non-RA, and 1 for RF/CCP double-negative versus double-positive RA.

Discussion: AIM2 cg11003133 methylation is strongly linked to RA, aligning with its role in inflammasome activation. While promising for diagnostics, larger validation is needed.

Conclusions: AIM2 cg11003133 methylation may serve as a diagnostic biomarker for RA and subtypes.

Methods: AKI samples were acquired from Gene Expression Omnibus (GEO) database. AKI-related module genes were identified using the “WGCNA” package. The “Limma” package was used to filter Differentially Expressed Genes (DEGs). Protein interaction networks were constructed by intersecting key modular genes with DEGs, and six algorithms (MCC, MNC, Degree, EPC, Closeness, and Radiality) in the cytoHubba plug-in were combined to screen candidate genes. Diagnostic biomarkers were cross-screened using LASSO regression with Support Vector Machine–Recursive Feature Elimination (SVM-RFE) machine learning algorithm, and their predictive performance was verified by Receiver Operating Characteristic (ROC) analysis. Transcription Factors (TFs) regulatory network was constructed applying Cytoscape 3.8.0. Finally, the prediction and molecular docking analysis of potential target drugs were performed using the DSigDB database and AutoDockTools.

Results: A total of 498 key modular genes significantly associated with AKI were screened, and 88 AKI- related DEGs and 18 candidate genes were further identified. Importantly, four biomarkers with high diagnostic value (DDX17, FUBP1, PABPN1, and SF3B1) were screened and validated using dual machine learning algorithms, including LASSO regression and SVM-RFE. The area under the ROC curve (AUC) values for these biomarkers were greater than 0.8, indicating good predictive performance. Moreover, 19 TFs and 17 miRNA of SF3B1, 10 TFs and 58 miRNA of PABPN1, 15 TFs and 60 miRNA of FUBP1, together with 13 TFs and 109 miRNA of DDX17, were screened. Drug prediction and molecular docking analysis revealed that Demecolcine and Testosterone Enanthate stably bind to certain markers.

Discussion: Four potential biomarkers closely related to AKI were identified, which may be involved in the occurrence and progression of AKI by regulating key processes such as transcription. The predicted Demecolcine and Testosterone Enanthate may also be involved in the repair of renal injury by regulating key target genes. Although further experimental validation is still needed, these may still provide new intervention strategies for the treatment of AKI.

Conclusion: To conclude, four AKI biomarkers with high diagnostic value were screened by integrating multiple computational methods, revealing a new perspective on the molecular mechanism of AKI. The results provided a new theoretical basis for achieving early precision diagnosis and individualized treatment of AKI.

Methods: We thoroughly searched the Science Citation Index-Expanded (SCI-E) of the Web of Science Core Collection (WoSCC), PubMed, and the Excerpta Medica Database (Embase) to identify relevant articles on the links between NASH and DM from 2004 to 2023. The current publication trends and hotspots in this field were analyzed using the Online Analysis Platform of Literature Metrology, CiteSpace software, VOSviewer, and the R package Bibliometrix.

Results: From 2004 to 2023, 943 articles were found that focused on the links between NASH and DM with a noticeable surge in publications since 2015. The United States has taken the primary position in terms of the number of publications. It has also been the most active country in international collaborative efforts. The University of California, San Diego, and Kenneth Cusi were the most productive institution and scholar, respectively. The co-citation keywords cluster labels revealed 10 primary clusters: adiponectin, MAFLD, mortality, NASH, nonalcoholic fatty liver, SGLT2, neurodegeneration, LY2405319, autophagy, and hepatocytes. Recent studies focused on weight loss, fibrosis stage, NAFLD, mortality, and diabetes mellitus.

Discussion: Research on NASH and DM has transitioned from early mechanistic exploration to a current focus on weight management, diabetes control, and fibrosis prevention, particularly through lifestyle interventions and antidiabetic drug therapy. Future studies should integrate lifestyle adjustments with drug development, enhance international cooperation to fill regional research gaps, and achieve more effective management of NASH and DM.

Conclusion: Over the past 20 years, global publications on the relationship between NASH and DM have grown rapidly. The current research hotspots focus on weight loss, and the reduction of blood glucose and fibrosis in NASH. Maintaining a healthy diet, exercising regularly, taking appropriate medication, and being vigilant about complications are essential for delaying the progression of NASH and DM. These are also the primary future directions of research.

Registration Number: Registration number: 1020973(PROSPERO)

Case Presentation: We provide the first complete case of Graves' disease with ICPi therapy in a patient who already had Hashimoto's thyroiditis. The patient, a 52-year-old male, was diagnosed with lung adenocarcinoma and received Atezolizumab. Clinical evaluation revealed hyperthyroidism, confirmed by elevated thyroid hormones and autoantibodies (TRAb and TSAb). The patient was managed with methimazole and demonstrated a transient hyperthyroid phase followed by persistent hypothyroidism. Only 16 confirmed cases of Graves' disease induced by ICPi were reported. We conducted a review to investigate the clinical characteristics, risk factors, and prognosis trends associated with ICPi-induced Graves disease in PTAD patients. Additionally, changes in thyroid function and autoantibodies during and after ICPi treatment are examined.

Conclusion: This case underscores the importance of monitoring thyroid function and autoantibodies in patients with PATD undergoing ICPi therapy. The findings suggest distinct differences in the humoral immune response between ICPi-induced and spontaneous Graves' disease, necessitating further research into autoantibody dynamics and their relationship with cellular immunity in these patients.

Objective: This review synthesizes mechanistic insights into DAMP signaling and regulated cell death modalities in IRI, aiming to identify translational gaps and propose precision-targeted therapies.

Methods: A literature search in PubMed using keywords “IRI,” “DAMPs,” and cell death modes was conducted without date restrictions. Peer-reviewed studies on human/animal models were included, with qualitative synthesis of DAMP-cell death interactions.

Results: During ischemia, mitochondrial dysfunction releases HMGB1, ATP, and mtDNA, activating Kupffer cell TLR4/RAGE and cGAS-STING pathways, triggering NLRP3 inflammasomedriven cytokine storms. Reperfusion amplifies ROS bursts, lipid peroxidation, and iron overload, creating a self-sustaining cycle of damage. Cell death modalities exhibit spatiotemporal specificity: hepatocyte ferroptosis dominates early injury, while macrophage pyroptosis and necroptosis predominate in steatotic livers during late phases. HMGB1 lactylation and mtDNA-cGAS signaling emerge as key regulators. Machine perfusion (e.g., hypothermic oxygenated perfusion) reduces biliary complications via mitochondrial resuscitation, outperforming conventional drugbased therapies.

Conclusion: Current single-pathway targeting shows limited efficacy due to IRI’s complexity. Future strategies should integrate temporal targeting (ferroptosis inhibitors pre-reperfusion; pyroptosis blockers post-reperfusion), DAMP-neutralizing agents (anti-HMGB1 antibodies), and precision preservation combining multi-omics biomarkers with ex vivo pharmacological preconditioning. Addressing metabolic vulnerabilities in fatty livers and refining cell death-specific interventions are critical for bridging translational gaps.

Methods: Primary human orbital preadipocytes were chosen and authenticated using immunofluorescence. Cells were treated with the IGF-1R agonist ginsenoside Rg5, IGF-1R overexpression plasmid, dexamethasone (Dex), and/or DA, after which cell proliferation and differentiation were assessed by cell counting kit-8 (CCK-8), oil red O staining, real-time quantitative polymerase chain reaction, and Western blot assays.

Results: Orbital preadipocytes showed positive expression of Pref-1. Treatment with IGF-1R agonist, as well as Dex, promoted orbital adipocyte viability and lipid accumulation, and increased the expression of adiponectin and leptin. It was observed that the overexpression of IGF-1R boosted PI3K/AKT activation and elevated PPARγ and C/EBPα expressions. Importantly, DA reversed the effects of IGF-1R on cell viability, lipid accumulation, and the PI3K/AKT signaling pathway.

Discussion: This study, for the first time, revealed the molecular mechanism by which DA regulates orbital fat metabolism through targeted inhibition of the IGF-1R/PI3K/AKT signaling axis. Notably, IGF-1R overexpression partially counteracted the inhibitory effect of DA, suggesting that this component has multi-target regulatory characteristics.

Conclusion: This study not only reveals a new mechanism by which DA treats TAO but also provides theoretical support for the treatment of adipose metabolism.

Methods: Single-cell RNA sequencing (scRNA-seq) Data from 2 pre-B high hyperdiploid (HHD) ALL patients and 3 healthy pediatric bone marrow samples (GSE132509) were utilized for cell clustering using the Seurat package. Functional enrichment, pseudo-time trajectory, and cell-cell communication analyses were performed using clusterProfiler, Monocle2, and CellChat R packages, respectively. Bulk RNA-seq data of 511 cALL samples in the TARGET-ALL-P2 cohort were used to construct a prognostic model via Cox and LASSO regression. Immune infiltration differences between different risk groups were analyzed using ESTIMATE, MCP-counter, and CIBERSORT algorithms.

Results: The scRNA-seq analysis identified five cell subpopulations, with B cells demonstrating significant enrichment in cALL samples. Notably, the C2 subset was associated with cell proliferation. Ligand-receptor analysis revealed key interactions involving B cell C2. Four marker genes (CENPF, IGLL1, ANP32E, and PSMA2) were identified to build a risk model. Low-risk patients showed better survival, while high-risk patients had higher ESTIMATE scores.

Discussion: This study examined the key role of B cells in cALL, constructed a risk model with strong prognostic predictive ability applying multi-omics analysis, and primarily explored its potential mechanism in immune regulation.

Conclusion: This study revealed the critical role of B cells in cALL, and the prognostic model showed a high prediction accuracy, providing a potential target for individualized treatment of cALL.

Objective: Chinese medicines have been used effectively in the treatment of infectious disorders; thus, this study aimed to investigate the efficiency of Chinese medicine against S. aureus.

Methods: An extract of traditional Chinese medicine was prepared using nine compounds: tongcao, talc, red peony root, fennel, guangui, lychee core, dry sunflower, dianthus, and purslane, to evaluate its antibacterial activity against Staphylococcus aureus RN450RF.

Results: The minimum inhibitory concentration (MIC) of the Chinese medicine measured by the consecutive double dilution technique was 200g/L. The drug-resistant plasmid was transferred equally well under controlled laboratory conditions with a median conjugation frequency of 1.1x10⁶. The maximum activity of conjugated transfer of resistant drug plasmid of E. coli CP9 (R45) was observed at 2/1 MIC (100 g/L drug concentration), 32h time interval, with a bacterial concentration 10⁸ CFU/ml.

Conclusion: These results suggest that the secondary inhibitory concentration (1/2 MIC) of the Chinese medicine solution can promote the combination and transfer of the resistance plasmid of Chinese medicine (R45) between different strains. The drug concentration, binding time, and initial bacterial concentration have different degrees of positive promotion effects on the conjugation and transfer of drug-resistant plasmids. Traditional Chinese medicine might be a potentially huge disease management and infection control resource.

Background: Testicular cancer is a frequently diagnosed male tumor. Emerging evidence suggests that Copines family genes are implicated in a variety of cancer phenotypes and cancer progression. Analyzing the expression pattern of Copines family genes in testicular cancer may help improve the treatment efficacy of the cancer.

Objective: This study sought to characterize the expression profiles of Copines family genes in the cellular subpopulations of testicular cancer and to identify key signaling pathways through which they regulate cancer progression.

Methods: Based on single-cell transcriptomic data of testicular cancer, we classified testicular cancer cell subpopulations and analyzed the expressions of Copines family genes in each subpopulation. Cell subpopulations were grouped according to the expression levels of Copines family genes, and differentially expressed Copines family genes between the groups were screened by differential expression analysis. Functional enrichment analysis on the differentially expressed genes (DEGs) was performed with a clusterprofiler package. Functional pathways enriched by the Copines family genes were calculated by AUCell enrichment score. Copy number variation (CNV) analysis was performed using inferCNV to analyze gene mutation patterns across cellular subpopulations, and pseudotime analysis was conducted using Monocle to infer cellular differentiation pathways of cellular subpopulations.

Results: Single-cell clustering identified four major cell subpopulations, namely, NK/T cells, tumor cells, B cells, and macrophages. Notably, the control samples had a relatively small proportion of tumor cells. Further clustering of the tumor cells identified six cell subpopulations, among which multiple Copines genes, especially CPNE1 and CPNE3, showed a high expression. The testicular cancer samples were grouped by the expression patterns of Copines genes, and the DEGs between groups included GNLY, MGP1, CFD2, CCL21, SPARCL13 as well as some other genes involved in the malignant progression of cancer. Pseudotime analysis showed that the upregulated genes were enriched in cell migration and PI3K-Akt pathway, while the downregulated genes were related to immunity. This indicated that the Copines genes regulated the cellular heterogeneity and malignant transformation in testicular cancer.

Conclusion: This study revealed the potential molecular mechanism through which Copines family genes drove the progression of testicular cancer through regulating PI3K-Akt signaling pathway and cell cycle, providing a new target for the development of precision treatment targeting Copines family genes and prognostic assessment of the cancer.

Methods: Articles concerning children with MAFLD published from 2014-2023 were identified from the Science Citation Index-Expanded of the Web of Science Core Collection. CiteSpace software, VOSviewer, and the Online Analysis Platform of Literature Metrology were used to analyze the current publication trends and hotspots.

Results: The analysis identified 1,609 English-language articles on pediatric MAFLD published from 2014 to 2023. The United States emerged as the most active participant in international collaborations. The University of California San Diego (UCSD) demonstrated the highest research output among the analyzed institutions. Additionally, UCSD exhibited the most extensive collaborative network, engaging in frequent and substantive research partnerships with a diverse range of academic and scientific organizations. Valerio Nobili was found to be the most prolific author, with 67 articles. Keyword burst analysis revealed that cardiovascular risk factors were the most intense research hotspot.

Conclusion: Current research on pediatric MAFLD warrants greater attention, particularly regarding cardiovascular risk factors. This study provides valuable references for researchers, offering insights to guide future research directions and potential collaborations.

Background: FM is a chronic disease featuring widespread pain, and the immune system may be involved in the FM progression.

Objective: The objectives of this study are as follows: 1) To identify the molecular subtypes of FM based on IRGs. 2) To screen and validate the hub genes in FM. 3) To predict the transcription factor (TF) targeting hub genes and 4) To evaluate the correlation between immune cell infiltration, hallmark pathways, and hub genes.

Methods: Two FM datasets were acquired from the Gene Expression Omnibus (GEO) database. IRGs were collected from the ImmPort database. Molecular subtypes of FM were identified using the “ConsensusClusterPlus” package. IRGs score and differentially expressed genes (DEGs) between different FM subtypes and control samples were obtained using “GSVA” and “limma” packages. Key module genes related to FM subtypes were identified using the “WGCNA” package. Hub genes were screened and verified using “glmnet” and “pROC” packages. TF-hub gene regulatory network was constructed by Cytoscape software. The correlation between immune cells, hallmark pathways, and hub genes was analyzed by the Spearman method. Finally, the DSigDB database was used to obtain associations between characterized genes and drugs, and the expression of key genes was verified using qRT-PCR.

Results: FM samples were classified into two subtypes, and the IRGs score of the C2 subtype was lower than that of the C1 subtype. Then, 184 module genes were obtained and mainly enriched in immune-related pathways. Next, 11 hub genes (TSPAN16, RILPL2, RASSF5, PGAP2, PADI2, NACC1, LRRC25, ITGAD, HIPK1, ATP6V0D1, AP1M2) were screened with good diagnostic performance. Besides, 45 TFs targeting hub genes were predicted. Most hub genes were negatively associated with CD4/CD8 T cells while positively correlated with macrophages, mast cell, monocyte, and neutrophil, as well as inflammatory response, angiogenesis pathways, etc. Molecular docking suggests that chloroquine and L-citrulline may be potent agents binding to NACC1 and PADI2. RILPL2 and ITGAD were significantly differentially expressed in FM-modeled mice.

Conclusion: This study identified two subtypes and 11 hub genes of FM based on IRGs, providing a reference for the clinical diagnosis of FM.

Materials and Methods: JTD's targets were cross-matched with genes associated with T2DM or NAFLD. SMR and co-localization analyses, utilizing eQTL and pQTL data, identified causal signals for each disease and their shared counterparts. GO/KEGG enrichment analyses were performed on these shared signals. Molecular docking assessed binding interactions. In vitro experiments, including ELISA (Enzyme-linked immunosorbent assay) and lipid staining, evaluated JTD's hypoglycemic/hypolipidemic effects, while PCR/immunofluorescence validated key molecular predictions in High-Glucose and High-Lipid (HGHL)-induced HepG2 cells.

Results: Initial network pharmacology identified 1107 JTD targets for T2DM and 1126 for NAFLD. SMR analyses revealed 78 eQTLs and 67 pQTLs for T2DM, and 40 eQTLs and 38 pQTLs for NAFLD. Eight shared causal genetic signals were identified: ADAMTS4, ALDH2, GLO1, CDH1, PDHB, PRKAB1, TCF4, and EP300. In vitro, JTD significantly attenuated hepatic gluconeogenesis and lipid deposition, downregulated IL-1β, and notably restored PRKAB1 expression in HepG2 cells treated with HGHL.

Discussion: Enrichment analysis revealed shared processes, including membrane microdomains, oxidoreductase activity, and responses to nutrient and oxygen levels. PRKAB1 exhibited a strong binding affinity with the JTD component Salsalate.

Conclusion: This study identified eight genes that are genetically predicted to be causal for the therapeutic effects of JTD on both T2DM and NAFLD, thereby establishing a genetic link between the conditions. These targets and associated pathways illuminate common underlying mechanisms, supporting JTD's potential for integrated treatment strategies and providing a basis for further investigation.

Methods: A retrospective cross-sectional analysis was conducted using data from 502 patients. Glycemic control was assessed based on HbA1c levels, and serum magnesium concentrations were evaluated concerning clinical and demographic variables. Statistical analyses included ttests, Mann-Whitney U tests, logistic regression, and ROC curve analysis.

Results: Patients with poor glycemic control had significantly lower serum magnesium levels. Magnesium levels were lower in females, particularly postmenopausal women. Magnesium levels were significantly associated with hypertension, gender, and the use of specific medications such as metformin and indapamide. Logistic regression revealed a significant inverse association between serum Magnesium levels and congestive heart failure (OR = 0.055), but not with other comorbidities. ROC analysis revealed limited predictive value of magnesium for glycemic control (AUC = 0.41).

Discussion: Although group-level differences in magnesium were evident, magnesium levels alone were not reliable predictors of glycemic control. However, the associations with CHF, HT, gender, and specific medications suggest that magnesium plays a multifaceted role in type 2 diabetes mellitus management.

Conclusion: Regular monitoring of serum magnesium may aid in identifying at-risk patients, especially those with hypertension, CHF, or on magnesium-depleting medications. Further prospective studies are needed to clarify the clinical utility of magnesium in diabetes care.

Methods: This cross-sectional study included adult participants from the 2007-2018 National Health and Nutrition Examination Survey (NHANES). The RFM was calculated as: RFM =64 - (20 × height/waist circumference) + (12 × sex), where sex is defined as 0 for men and 1 for women. Hyperuricemia was confirmed by using serum uric acid (SUA) levels ≥ 7 mg/dL in men and ≥ 6 mg/dL in women. The relationship between RFM and the risk of hyperuricemia was thoroughly investigated.

Results: A total of 29369 participants were enrolled in this study. The RFM levels in the hyperuricemia group were higher than those in the non-hyperuricemia group (P < 0.01). Logistic and linear regression indicated that RFM levels were positively associated with the risk of hyperuricemia (OR=1.08, 95% CI: 1.05-1.11, P < 0.001) and SUA levels (β=0.04, 95% CI: 0.03-0.05, P < 0.001). The relationship remained consistent across subgroups. Smooth curve fitting showed a nonlinear relationship, with an inflection point at 34.22. Above this threshold, the link between RFM levels and hyperuricemia was found to be more remarkable.

Conclusion: Higher RFM is associated with an increased risk of hyperuricemia. RFM could act as a cost-efficient and straightforward measure for hyperuricemia risk assessment.

Objectives: The aims of this study were to formulate bitter melon (BM) enriched biscuits and test their acceptability and effect on blood glucose levels (BGL).

Methods: The study consisted of 3 stages, including BM biscuits formulation and production, an acceptability test via 30 trained panelists, followed by an experimental stage using pre- and posttest- controlled randomized group design on healthy Wistar rats (Rattus norvegicus) to test the effect of BM biscuits on BGL.

Results: The biscuits were made using 0.5% bitter melon flour and 99.5% wheat flour. The BM biscuits were graded as acceptable by 93.3% of the panelists, most of whom rated them with “rather like” for their color and taste. A significant decrease in the BGL was found in after 30 days of the BM biscuits intervention (mean±SD = -9.71±1.15 mg/dL, p=0.01) in healthy Wistar rats; conversely, a significant increase in the BGL was found in the control group.

Conclusion: Biscuits enriched with bitter melon flour could be used as an alternative to low glycemic snacks without increasing blood glucose level of healthy Wistar rats.

Methods: From January 2005 to December 2019, a total of 33,990 patients were identified with ACS in the Chang Gung Research Database based on their medical history. After excluding patients without DM and baseline or subsequent HbA1C data, a cohort of 11,870 DM patients was divided into two groups: one consisting of 6,089 patients with newly diagnosed DM and the other comprising 5,781 patients with pre-existing DM.

Results: During the three-year follow-up, the pre-existing DM group experienced worse clinical outcomes, such as increased rates of re-ACS, major bleeding, cardiovascular (CV) events, and all-cause mortality. Optimal HbA1c levels for mitigating re-ACS and/or CV mortality and all-cause mortality appeared to differ between the two DM cohorts. Re-ACS and CV mortality reached their highest at an HbA1c of 6.8% for all DM patients, 6.6% for newly diagnosed, and 6.7% for pre-existing cases. The greatest all-cause mortality risk was at an HbA1c of 7.4% for all DM patients, 7.0% in newly diagnosed, and 8.2% in pre-existing patients.

Conclusion: Upon comparing newly diagnosed DM patients with those with pre-existing DM, a poorer prognosis was observed in the latter group, attributed to older age and a higher burden of comorbidities. Throughout the follow-up period, maintaining consistently low HbA1c levels did not reduce the incidence of re-ACS nor enhance survival rates.

Objective: To investigate the wound healing efficacy of the phytoconstituent fisetin, administered orally, in managing DFU in diabetic neuropathic Wistar rats.

Method: This study investigates the therapeutic potential of a phytoconstituent fisetin, in the management of wound healing in STZ-NAD induced diabetic animal model with surgically induced wounds after indication of neuropathy. Fisetin was administered orally at doses of 5, 10, and 15 mg/kg for 30 days following the induction of foot ulcers, Various parameters were measured, including blood glucose levels, HbA1c, lipid profile, pro-inflammatory cytokines, antioxidant activity, MDA, and histopathological analysis of wound healing.

Results and Discussion: Fisetin, particularly at 15 mg/kg, significantly modulates blood glucose level, HbA1c, lipid profile, and pro-inflammatory cytokines, further enhancing antioxidant activity, while reducing MDA, indicating a reduction in oxidative stress. Histopathological analysis demonstrated enhanced wound healing by increased fibroblast proliferation and collagen formation, as well as restoration of the epithelial layer. Fisetin also exhibited potential in enhancing re-epithelization, enhancing pro-angiogenic markers, diminishing inflammation, and reducing wound size.

Conclusion: Fisetin demonstrates promising potential in managing DFU by modulating metabolic conditions, reducing blood glucose, oxidative stress, and inflammation, and promoting wound healing. Future studies should focus on unraveling the detailed molecular pathways involved in fisetin's action, along with clinical trials to validate its efficacy in DFU patients.

Aims: This study aimed to assess the correlation between serum bilirubin levels and the prevalence of DR in patients diagnosed with type 2 diabetes mellitus (T2DM). Additionally, we sought to establish whether the polymorphisms of Nuclear Factor E2-Related Factor 2 (Nrf2) might modify this relationship.

Methods: A cross-sectional study was undertaken in Jiangxi, China, from May, 2012 to December, 2014. Serum bilirubin levels were assessed in 558 subjects, and the correlation between bilirubin and DR was analyzed using generalized linear models with a logit link. The study utilized odds ratios (OR) and 95% confidence intervals (CI) to evaluate the relationship, both with and without the consideration of clinical risk factors.

Results and Discussion: There was a significant inverse association between serum total bilirubin (TBiL) and the risk of DR (per 1-μmol/L increment; OR, 0.89; 95% CI: 0.84-0.94). Accordingly, when TBiL was categorized into tertiles, individuals in tertiles 2 and 3 exhibited significantly lower risks of DR compared to those in tertile 1. The OR for these tertiles was 0.54 (95% CI: 0.34-0.87) and 0.31 (95% CI: 0.19-0.52), respectively. Moreover, a stronger inverse relationship between TBiL and DR was observed in individuals carrying the CC and AC genotypes compared to those with the AA genotype. The OR for individuals with the CC/AC genotype was 0.87 (95% CI: 0.82, 0.92), while that for the AA genotype was 1.17 (95% CI: 0.95, 1.45). This difference was statistically significant (p for interaction = 0.001).

Conclusion: There was a significant inverse association between bilirubin and DR in participants with CC or AC genotype. However, this inverse association was not seen in AA genotype participants.]]> https://www.benthamscience.comarticle/148532Introduction: Hypoglycemia is a complication that can disrupt the continuity of therapy for Type 2 Diabetes Mellitus (T2DM) patients. Therefore, ambulatory T2DM patients need supportive treatment to ensure the safety of their medication. Currently, health workers lack a standardized reference for assessing the risk of hypoglycemia in these patients. Therefore, this study aimed to determine, validate, and develop a prediction score of risk factors influencing hypoglycemia in T2DM patients.

Methods: The psychometric properties method was used in this study design, including item development, content validity, criterion validity, and construct validity. During the process of item development, Focus Group Discussions (FGDs) with experts were used. Known predictors were then validated through panelists' content assessment. Risk factors for hypoglycemia from item development and content validation were tested for criterion and construct validation using a case-- control method.

Results and Discussion: Eight significant predictors caused hypoglycemia, including insulin use, SU use, insulin-SU combination use, CKD, diabetic neuropathy, uncontrolled blood glucose, >5- year DM duration, and history of severe hypoglycemia, and the total score of risk factors was 24. The categories were defined as follows: scores of 0-8 as low-risk, 9-16 as moderate-risk, and 17-24 as high-risk. There was a positive linear relationship between the total score and risk category (p<0.05; r2: 0.959).

Conclusion: This risk factor and score prediction model can be used by health workers in clinical practice to predict the risk of ambulatory hypoglycemia in T2DM patients because it meets content, criterion, and construct validity.

Methods: A literature review was conducted using the ScienceDirect, Scopus, PubMed, and Web of Science databases up to December 2024. Key search terms included “diabetes,” “sarcopenia,” “HbA1c”, “glucose,” “insulin,” and specific biomarkers such as inflammatory markers, adipokines, and myokines.

Results and Discussion: Aging is associated with a decline in organ and bodily system functionality, with sarcopenia being particularly prominent due to its progressive loss of muscle mass and function. This condition increases health risks and mortality in the elderly. Muscles, as the primary consumers of glucose, play a crucial role in glucose uptake; reduced mass can exacerbate insulin resistance. Sarcopenia and diabetes share common pathophysiological mechanisms, including insulin resistance, inflammation, and vascular complications. Circulating biomarkers, crucial for diabetes management, may offer insights into the early stages of sarcopenia.

Conclusion: The complex relationship between sarcopenia and diabetes, influenced by shared pathophysiological pathways, presents challenges in geriatric healthcare. Circulating biomarkers hold promise for early detection and monitoring of sarcopenia, potentially enhancing patient outcomes and quality of life. Further research is necessary to validate these connections and develop targeted treatments for individuals affected by these conditions.

Methods: A cross-sectional study was conducted with DM patients who attended two diabetes clinical centers in Jordan in the period from October 2022 to April 2023 in which data were collected through a self-administered questionnaire developed to assess patients’ understanding of DFUs, foot care outcomes expectations (FCOE), and self-efficacy about FSC.

Results and Discussion: The final sample included data from 107 patients. Patient awareness of DFUs and FCOE was good, and the level of self-efficacy for FSC was moderate to high. Multiple linear regression revealed that age was negatively associated with lower self-efficacy for FSC (β = -0.22, p = 0.03) and both confidence (self-efficacy) in FSC and living arrangements (i.e., living with family) were positively associated with higher FCOE (β = 0.19, p = 0.04 and β = 0.39, p <0.001, respectively). Diagnosis of renal failure, diagnosis of retinopathy, elevated levels of glycated hemoglobin, and the settings in which the patient is receiving care for DM were positively associated with an understanding of DFUs. Both age and history of heart attacks and coronary artery disease were negatively associated with realizing DFUs (β = -0.26, p = 0.007, and β = -0.18, p = 0.045, respectively).

Conclusion: Patients with diabetes mellitus in Jordan have good FCOE, good awareness of DFUs, and a moderate degree of self-efficacy to execute FSC. Health education and self-efficacy programs should focus on older adults with a history of heart attacks to boost their understanding of DFUs and raise their sense of self-efficacy around FSC.

Aim: The objective of this study was to identify the risk factors associated with T1D in the southern region of Iran during the year 2022.

Methods: This research employed a case-control design involving two groups (79 individuals in each group) of healthy children and adolescents diagnosed with T1D. The study assessed and compared the groups regarding various potential risk factors that may influence the development of T1D. Data analysis was performed using SPSS-22 software.

Results and Discussion: Significant differences were observed between the two groups concerning several factors, including the age at which children began kindergarten, their weight at one year and 18 months, maternal weight gain during pregnancy, delivery method, age of introduction to complementary feeding, duration of breastfeeding, use of cow's milk and vitamin D supplements before one year of age, as well as family history of T1D and other autoimmune diseases among fathers and siblings.

Conclusion: The findings indicate that, in addition to genetic predispositions, numerous environmental factors contribute to the risk of developing T1D. Consequently, it is recommended that health managers and policymakers investigate these risk factors more broadly across various regions to implement effective strategies aimed at reducing the incidence of T1D nationwide.

Methods: The anti-obesity, anti-diabetic, and antihyperlipidemic effects of E. japonica leaf extract were screened in high-fat diet-fed rats. After treatment with different E. japonica leaf extract concentrations, body weight, blood glucose levels, HbA1c, and lipid profile were determined.

Results and Discussion: The high-fat diet group treated with Loquat leaf extract >= 200 mg/ml/ kg showed significant weight loss and a beneficial lipid marker profile. However, the glycemic markers were not significantly different.

Conclusion: The findings demonstrate that E. japonica leaf extract at doses of ≥200 mg/kg significantly reduces body weight and improves lipid markers in HFD-fed rats. However, glycemic markers such as blood glucose and HbA1c were not significantly affected. These results highlight the potential of E. japonica as a natural weight loss and lipid control aid, warranting further investigation into its mechanisms and clinical applicability.

Objectives: To conduct the first comprehensive bibliometric evaluation of epigenetic studies in diabetes mellitus and its complications (2014-2024), identifying key research domains, international collaboration patterns, and innovative investigative directions to inform strategic research planning and highlight opportunities for innovative therapeutic approaches.

Methods: We interrogated the Web of Science Core Collection using stringent inclusion criteria, analyzing 1,451 publications through advanced multi-dimensional metrics in CiteSpace (6.2.R4), VOSviewer (1.6.20), and Bibliometrix (4.1.3).

Results and Discussion: A total of 1,451 original and review articles were retrieved, involving 83 countries/regions, 576 journals, and 7,645 authors. The United States produced the highest number of publications (n = 464), followed by China (n = 283) and Italy (n = 121). The International Journal of Molecular Sciences was the leading journal (66 publications), dominated by review articles (n = 53). Author collaboration networks were extensive, with Charlotte Ling emerging as the most prolific and influential author in publications, citations, and H-index. Keyword co-occurrence analyses emphasized type 2 DM, gestational DM, and diabetic nephropathy as primary research focuses, while new frontiers highlighted potential links to Alzheimer’s disease and fibroblast biology.

Conclusion: This multi-dimensional analysis provides quantitative visualization of research evolution, delineates current investigative priorities, and highlights underexplored therapeutic targets. Our findings establish a strategic framework for transdisciplinary collaboration in precision diabetology.

Methods: Adhering to the PRISMA guidelines and the principles of the Joanna Briggs Institute, a comprehensive search was conducted across multiple databases, including CINAHL, Cochrane, Embase, LILACS, PubMed, Scopus, Web of Science, Google Scholar, OPENGREY, and NDLTD. The review included studies published in any language that examined the relationship between HL, numeracy, and SMBG.

Results and Discussion: A total of 12 studies met the inclusion criteria. These studies utilized various assessment tools, such as the Brief Test of Functional Health Literacy in Adults (B-TOFHLA) and the Diabetes Numeracy Test (DNT-15), to evaluate health literacy and numeracy levels. The findings revealed a significant association between adequate HL and numeracy and improved SMBG practices. Specifically, individuals with sufficient health literacy were more likely to monitor their blood glucose levels regularly and make appropriate treatment adjustments based on their readings.

Conclusion: The results indicated that numeracy skills and health literacy are critical determinants of effective SMBG, influencing the frequency and accuracy of self-care practices in diabetes management. These findings highlight the urgent need for educational interventions tailored to enhance these skills, which could lead to improved health outcomes for individuals with diabetes.

Methods: Since diabulimia is not formally defined, a systematic review of the limited literature was conducted on November 8th, 2024, using PubMed, Scopus, and Web of Science databases. The search terms included “diabulimia”, “insulin omission”, “insulin restriction”, “eating disorders”, “disordered eating”, and “type 1 diabetes”. Out of 288 manuscripts, 19 were selected after excluding non-English articles and screening the titles and abstracts.

Results and Discussion: Eating disorders and disordered eating are common in patients with type 1 diabetes, often driven by concerns regarding body image and weight. These behaviors can complicate diabetes management, worsen glucose control, and increase the risk of complications. Diabulimia may develop as a coping mechanism, especially in adolescents with higher body mass index and a history of eating disorders. Diagnosis is challenging due to the lack of established guidelines, but poor glucose control can raise suspicion and prompt further psychological evaluation. A multidisciplinary approach, combining medical care, nutrition, mental health support, and therapy, is recommended, despite limited evidence.

Conclusion: While diabulimia is not formally recognized, understanding its impact can help healthcare professionals diagnose and manage it more effectively, improving patients’ health and well-being.

Methods: We conducted a systematic search in PubMed, CAM-QUEST®, and the Cochrane Central Register following PRISMA guidelines. We included randomized controlled trials (RCTs) assessing yoga interventions (asanas, pranayama, kriyas, and meditation) alongside standard care. Primary outcomes were fasting blood glucose (FBS), postprandial blood glucose (PPBS), HbA1c, serum insulin, and HOMA-IR. Secondary outcomes included oxidative stress markers (glutathione, malondialdehyde [MDA], superoxide dismutase [SOD]) and psychological outcomes. Meta-analyses were conducted using random-effects models in RevMan 5.4.1.

Results: Fourteen RCTs (n = 1,629 participants) were included. Yoga combined with standard care significantly improved FBS (SMD = -1.60; 95% CI: -2.27 to -0.92), PPBS (SMD = -2.16; p = 0.03), HbA1c (SMD = -0.92; 95% CI: -1.59 to -0.26), and HOMA-IR (SMD = -1.28; p = 0.002). MDA levels were significantly reduced, though glutathione and SOD showed no significant changes. Psychological well-being improved in several trials.

Discussion: Yoga appears effective in improving glycemic outcomes and insulin resistance in patients with or at risk of T2DM. It may also reduce oxidative stress and enhance psychological well- being, highlighting its potential as a holistic intervention.

Conclusion: Yoga, when integrated with standard care, offers clinically relevant benefits in managing T2DM and related metabolic risks. Further high-quality, multi-centered trials using standardized protocols are needed to validate and generalize these findings.

Methods: To identify relevant randomized controlled trials, we searched PubMed, Embase, Cochrane Library, Web of Science, and ClinicalTrials.gov. Risk Ratios (RR) and 95% Confidence Intervals (CI) were calculated using the Mantel-Haenszel approach for dichotomous outcomes. Mean Difference (MD) and 95% CI calculated by the inverse variance approach were applied to continuous outcomes.

Results: Twelve randomized controlled trials involving 7628 participants were included in this study. Compared with control groups, IDegLira has a significant hypoglycemic effect in reducing hemoglobin A1c (MD = −0.66; 95% CI [−0.85, −0.47]; p < 0.00001), fasting plasma glucose (MD = −0.90; 95% CI [−1.40, −0.41]; p = 0.0003), self-measured plasma glucose (MD = −0.82; 95% CI [−1.22, −0.42]; p < 0.0001) and achieving the hemoglobin A1c level of < 7.0% (RR = 1.66; 95% CI [1.44, 1.92]; p < 0.00001) or < 6.5% (RR = 2.13; 95% CI [1.76, 2.57]; p < 0.00001). IDegLira outperforms insulin in achieving the target of HbA1c < 7.0 or < 6.5% without hypoglycemia and weight gain. Besides, IDegLira did not increase the incidence of adverse events and serious adverse events.

Discussion: In this section, IDegLira’s benefits on simultaneously achieving glycemic control, weight loss, and reduced hypoglycemia risk were summarized. The statistical results were carefully interpreted in conjunction with clinical concerns regarding T2DM complications, adverse effects, and cost-effectiveness differences. An expanded discussion was conducted on integrating individualized HbA1c goals as a dual endpoint, without increasing body weight or the risk of hypoglycemia. Finally, the limitations of the present study were indicated.

Conclusion: IDegLira exhibits a favorable glycemic control effect and acceptable adverse effects in T2DM. Superior performance in the target glycemic control, particularly suitable for T2DM patients who do not reach the target hemoglobin A1c and have comorbid CVD or obesity.

Objective: This study aims to evaluate the potential of rosarin, a key compound derived from the root of Rhodiola rosea, in treating diabetes mellitus using a zebrafish model and in exhibiting anthelmintic (worm-expelling) activity using the Indian earthworm (Pheretima posthuma).

Methods: The study design utilizes an experimental approach, incorporating both zebrafish (Danio rerio) and earthworms (Pheretima posthuma) as subjects for testing. The zebrafish were randomly assigned to different experimental groups, including control and treatment groups (e.g., hyperglycemia induction and comparison with Metformin). The zebrafish were studied for a duration of 4 days, during which the glucose concentration was gradually increased. Zebrafish were housed in controlled aquatic environments with daily water changes and hyperglycemia in zebrafish was induced by gradually increasing the glucose concentration, starting with 50 mM for four days while closely monitoring their health and survival. The body weights, blood glucose levels and histopathological studies were noted and compared with the standard drug Metformin. Liver enzymes such as alkaline phosphatase (ALP), Aspartate aminotransferase (AST), and Alanine aminotransferase (ALT) derived from homogenate supernatants of fish viscera were determined using an autoanalyzer. Earthworms were collected from moist soil and randomly assigned to receive varying doses of test Rosarin or the standard drug albendazole in Petri dishes. Observations included changes in color, thickness, diameter, paralysis, and time to death. Dunnett’s test was used to evaluate the statistical significance, followed by one-way ANOVA.

Results and Discussion: Zebrafish (Danio rerio), three-month-old (500-1000 mg) and Pheretima posthuma (14 cm) were used for this research. The results confirm that the rosarin glycoside at 50 mg/ml showed significant anti-diabetic activity by decreasing blood glucose levels (82.1 ± 0.5 mg/dl) with p<0.001, 95% CI (81.628- 82.572) limits and body weights (2.0 ± 0.047 g) when equated with diabetic control (Blood glucose levels= 135 ± 3.14 mg/dl and body weights =13.4 ± 0.11 g). ALT, AST and ALP levels significantly decreased in the rosarin group when equated to diabetic control. The anti-diabetic effect of rosarin is comparable with standard Metformin (50 mg/ml). In anthelmintic activity, rosarin (75 mg/ml) significantly decreased the length of the worm (9.5 ± 0.36 cm), time of paralysis (22 ± 0.76 minutes) and time of death (40 ± 0.76 minutes). Albendazole (50 mg/ml) is used as a standard drug. The study employed one-way ANOVA to compare the means of various experimental groups, followed by Dunnett's test for post-hoc analysis to evaluate the differences between the treatment groups and the control group.

Conclusion: The results of the current research indicate that rosarin has significantly reduced the blood glucose levels in zebrafish and decreased the time of paralysis and death in earthworms, suggesting its antidiabetic and anthelmintic activity and hence it is further recommended as an ideal candidate for therapy of diabetes and worm infestations.

Objectives: This study aimed to determine the effect of a health education program on knowledge, medication adherence, and HbA1c in rural patients with type 2 diabetes.

Methods: This experimental study was conducted in Ilam County, Iran. Participants were selected via multistage cluster sampling and randomly assigned to either the intervention group (n=43) or the control group (n=42). The intervention group underwent a one-month educational program based on self-regulation theory, consisting of 12 sessions, while the control group received no educational intervention. Data were collected at baseline, three months, and six months using a diabetes knowledge test (DKT), the Iranian version of the Morisky Medication Adherence Scale-8 (IVMMAS-8), and laboratory measurements of HbA1c. Statistical analysis was performed using SPSS version 16, employing chi-square tests, independent sample t-tests, repeated-measures ANOVA, and Bonferroni correction at a significance level of 0.05.

Results and Discussion: After 3 and 6 months, the intervention group showed significant improvements in diabetes knowledge and medication adherence and a significant reduction in HbA1c levels compared to the control group (p<0.001). No significant changes were observed in the control group over time (p>0.05).

Conclusion: This study demonstrated that health education based on self-regulation theory can effectively increase knowledge, improve treatment adherence, and decrease HbA1c levels in rural patients with type 2 diabetes.

Materials and Methods: We performed a cross-sectional analysis involving 140 participants with T2DM and 70 healthy control subjects. The DNA samples were analyzed for the FTO gene variant rs9939609 using ARMS-PCR. FTO gene association with diabetes-related microvascular and macrovascular complications was assessed through multivariate logistic regression, with unadjusted odds ratios (OR) and 95% confidence intervals. A p-value below 0.05 was considered statistically significant.

Results and Discussion: The genotypic distribution of the FTO gene variant adhered to Hardy- Weinberg equilibrium in the study participants (p>0.05). The AA genotype exhibited a robust association with elevated BMI, HbA1C, SBP, DBP, TGs and decreased HDL-C levels relative to the AT and TT genotypes with (p=0.002). FTO genotype frequency increased from AA to AT to TT in both macrovascular (CVD) and microvascular complications (retinopathy, nephropathy, and neuropathy). Moreover, risk allele(A) was also significantly contributed to CVD (p=0.001), retinopathy (p=0.004), nephropathy (p=0.001), and neuropathy (p=0.002). AA genotype of the FTO gene rs9939609 showed the tendency to increase the risk of CVD (OR, 1.21; 95% CI, 1.07-1.70; p=0.04) and retinopathy (OR, 1.18; 95% CI, 1.02-1.87; p=0.001) while no significant changes were recorded in diabetic nephropathy (OR,1.56; 95%CI,1.2-2.43; p=0.67) and neuropathy (OR, 2.49; 95%, 1.52-4.1; p=0.06).

Conclusion: Our data indicate that the FTO gene variant rs9939609 is linked to an elevated risk of both microvascular & macrovascular complications in individuals with T2DM.

Methods: A retrospective observational study of 246 patients with T2DM whose data were retrieved from the Proficiency Health Diagnostic Lab System in Al Ain. Data were analyzed using the Statistical Package for the Social Sciences (SPSS) program.

Results and Discussion: The prevalence of T2DM was found to be higher in gender (male), age (≥45 years), ethnicity (Middle Eastern), BMI (≥25), family history, and metabolic syndrome (hypertension and dyslipidemia). TAS was found to be significantly higher in patients with comorbidities, than in those without, particularly dyslipidemia and micro-albuminuria (p<0.05). TAS was weakly positively correlated with various T2DM biochemical parameters (p<0.05), except for Fasting blood glucose (FBG) (p=0.061). TAS was weakly negatively correlated with BMI (≥25) (p=0.042). Albumin-to-creatinine ratio (ACR) was statistically higher in hypertensives than normotensives (p=0.049). Duration of disease was only significantly correlated with ACR (r=0.325, p=0.001). Uric acid levels were statistically higher in patients with microalbuminuria than in patients without microalbuminuria (p=0.001).

Conclusion: TAS was higher in patients with dyslipidemia and microalbuminuria, suggesting the influence of other factors such as uric acid and lipid-lowering agents. TAS could be an important factor in the management of T2DM cases. This needs to be further investigated in future studies to fill the gap found in the literature.

Materials and Methods: We conducted an exploratory study involving 96 T2D Iraqi patients (Asian Arabic), examining the distribution of the ABO rs2073823 polymorphism and its correlation with MVCs. We assessed levels of inflammatory markers (TNF-α, IL-6, sE-selectin, sP-selectin), glycemic markers, renal function biomarkers, and lipid profiles. Adjustment was made for confounding factors including age, gender, body mass index, duration of diabetes, and hypertension.

Results: Among the participants, 75% had MVCs, including DR (42%) and DN (65%). The ABO rs2073823 “A/A” genotype was associated with a reduced risk of MVCs under co-dominant (OR=0.16, p=0.045) and recessive models (OR=0.14, p=0.031). This protective effect remained significant after adjusting for confounding factors (OR=0.11, p=0.022). The “A/A” genotype was also linked to lower levels of total cholesterol, LDL-cholesterol, triglycerides, and sP-selectin. Patients with MVCs exhibited significantly higher levels of TNF-α, IL-6, and sP-selectin.

Conclusion: The ABO rs2073823 polymorphism, particularly the “A/A” genotype, is associated with a decreased risk of MVCs in T2D patients and influences lipid metabolism and inflammatory markers. These findings suggest a genetic basis for the susceptibility to MVCs and highlight the role of the ABO gene in modulating inflammation and endothelial function in T2D. Further research is needed to validate these associations and explore potential therapeutic implications.

Methods: The wounds were created by excision (n=30) and incision (n=30) in rats. The Group IIV were diabetic rats treated with simple ointment BP, 10% weight-based povidone-iodine (10% PI), ointment of 5% w/w EEMS (5% w/w OEEMS), and 10% w/w EEMS (10% w/w OEEMS). Group 1 acted as a control and was treated with simple ointment BP. The wound area in the diabetic control groups was 292.33 ± 0.8 mm2 on the 18th day.

Results: Rats treated with 10% PI, 5% OEEMS, and 10% OEEMS showed a significant reduction in wound area of 68.33 ± 1.29, 248.33 ± 1.30, and 61 ± 1.91 mm², respectively, on the 18th day as compared to the control group. Rats treated with 10% PI, 5% w/w OEEMS, and 10% w/w OEEMS showed a significant increment in wound-breaking strength, respectively, as compared to diabetic rats on day 10 in the incision wound model.

Conclusion: The results demonstrated that the OEEMS has potent wound-healing properties in diabetic rats.

Objective: The objective of this study was to reveal the therapeutic effect and illuminate the possible mechanism of PN for osteoporosis.

Methods: The Traditional Chinese Medicine Database and Analysis Platform was searched to screen the potent ingredients of the PN and to analyze the potential therapeutic targets for osteoporosis. We excavated four disease databases to collect osteoporosis-related genes. After integrating the gene expression profile of osteoporosis and the chemical-protein data of PN, a protein-protein interaction network was constructed to demonstrate the interactions among the gene products. GO function, KEGG pathway, and docking analyses were executed.

Results: Network pharmacology obtained 31 active ingredients and 134 targets for the treatment of osteoporosis. The key components were beta-elemene, quercetin, methyl palmitate, oleic acid, and hexanal. The results of GO and KEGG analyses showed that Panax notoginseng was beneficial for osteoporosis by influencing the main pathways including AGE-RAGE signaling pathway in diabetic complications, TNF signaling pathway, IL-17 signaling pathway, p53 signaling pathway, NF-kappa B signaling pathway, PI3K-Akt signaling pathway, MAPK signaling pathway, FoxO signaling pathway, and Wnt signaling pathway, modulating inflammation, metabolism, cell proliferation, cell survival, growth and angiogenesis. Panax notoginseng intervened in osteoporosis through multi-components, multi-targets, and multi-pathways.

Conclusion: This study illustrates the mechanism of Panax notoginseng for osteoporosis, providing broader insights for novel research and developments of the Panax species for osteoporosis.

Background: MORC protein family genes are a highly conserved nucleoprotein superfamily whose members share a common domain but have distinct biological functions. Previous studies have analyzed the roles of MORCs as epigenetic regulators and chromatin remodulators; however, the involvement of MORCs in the development and pathogenesis of CRC was less examined.

Objective: The current work examined the role of the MORCs as the therapeutic and prognostic markers for CRC.

Methods: The expressions and prognostic significance of MORC family genes in CRC were explored. The role of these genes in tumor immunity was comprehensively analyzed in terms of their functions in immune cell infiltration, tumor microenvironment (TME), and their interaction with immune regulatory genes such as immunosuppressive genes, immune checkpoints and immunostimulatory genes. The relations between MORC family genes, tumor mutation burden (TMB), DNA, mismatch repair (MMR), RNA methylation, microsatellite instability (MSI), and drug sensitivity were investigated using the R statistical software. The expressions of MORC4 in 150 CRC tissues and 60 paracancer tissues were detected by immunohistochemical method. CRC cell proliferation, migration, and invasion were measured by cell counting kit-8 (CCK-8), scratch assay, and transwell cell invasion assay.

Results: The expressions of MORC2 and MORC4 were significantly upregulated, whereas those of MORC1 and MORC3 were noticeably downregulated in CRC in comparison to their expressions in normal colorectal mucosal tissues. Patients with high-expressed MORC2 showed a more unfavorable prognosis than those with a low MORC2 level. Functional annotation analysis identified 100 MORC family genes with the most significant negative or positive correlations to diabetic cardiomyopathy, amyotrophic lateral sclerosis, oxidative phosphorylation, Huntington’s disease, thermogenesis, Parkinson’s disease, olfactory transduction, Alzheimer’s disease, prion disease. MORC3 expression was positively correlated with Stromal score, Immune score and ESTIMATE score, while MORC2 expression was negatively related to the three scores in CRC, these correlations were not statistically significant. Additionally, the MORC family genes were significantly positively correlated with tumor-infiltrating immune cells such as T helper cells and exhibited close relations to some immunosuppressive genes such as CXCR4 and PVR, immunostimulatory genes such as TGFBR1, KDR, and CD160 as well as some immune checkpoint genes. It was found that the expressions of some members of MORC family genes were positively correlated with DNA methylation, MSI, TMB, MMRs, and drug sensitivity in CRC and that the mRNA and protein levels of MORC4 were remarkably upregulated in CRC tissues than in adjacent normal tissues (P<0.05). In the MORC4 knockdown group, DLD-1 cell proliferation was more inhibited than in the negative control (NC) and siRNA groups (P<0.05). Furthermore, the migratory capacity of DLD-1 cells and the number of cells crossing the basement membrane in the MORC4 knockdown group were reduced compared to the NC and siRNA groups (all P<0.05).

Conclusion: The expressions of MORC family genes were significantly different in CRC samples, which was related to the immune cell infiltration and prognosis of CRC. Thus, the MORC family genes were considered as markers for indicating the clinical immunotherapy and prognostic outcome of CRC.

Materials and Methods: We recruited 28 healthy individuals and 53 CD patients, 47 of whom completed the entire UST therapy. Oral samples and clinical data were collected. The clinical response and clinical remission were defined based on the CDAI score. Oral samples were analyzed by 16S rRNA gene sequencing. The analysis of sequence data was performed by QIIME and R.

Results: We revealed the oral microbial difference between the Healthy Control (HC) group and the CD group. The enrichment of Fusobacteria, Leptotrichia, Capnocytophaga, and Campylobacter, and the diminution of Haemophilus and Rothia were observed in the CD group. Differences in oral microbiota were also identified among patients with different efficacy of UST. Compared to the response and remission groups, both the non-response and non-remission groups showed significantly higher levels of Fusobacteria and Leptotrichia. Predictive models for clinical response and clinical remission in UST were developed based on oral microbiota, with the Area Under the Curve (AUC) value of 0.944 and 0.930, respectively.

Conclusion: Oral microbiota was relevant to the UST efficacy in patients with CD based on the predictive model. These findings suggest that oral microbiota could serve as a non-invasive prognostic biomarker for UST treatment in CD patients.

Objective: The objective of the study was to determine the relationship of CBC parameters with renal parameters and liver function tests and to develop the hypothesis that curcumin may be the best and non-invasive drug for coronavirus.

Materials & Methods: The differences between the results of 91 confirmed cases of COVID-19 (symptomatic and asymptomatic) and 100 controls were assessed by an independent t-test and Mann- Witney U Wilcoxon test. Microscopy, hematological tools, and techniques were used to assess the improvements/abnormalities in blood components and parameters.

Results: This is a case control study along with the feasibility of curcumin as COVID treatment. The association between parameters was assessed by Pearson & Spearman correlation analysis. The level of significance was p < 0.05. Changes were observed in urea (p = 0.000), creatinine (p = 0.02), total bilirubin (p = 0.000), SGPT (ALT) (p = 0.000), RBC (p = 0.001), HGB (p = 0.001), MCV (p = 0.002), MCH (p = 0.03), MPV, PDW, NE%, LY%, and MO% EO% (p = 0.00), in comparison to normal controls. Differences in the correlation of electrolytes, RPM, and LFT tests along with CBC parameters in Pakistani and Chinese individuals provided a new idea for using various diagnostic and therapeutic tools in different ethnic groups. The COVID-19 infected blood components and parameters showed rapid improvement/recovery, especially the total count of platelets and WBCs (lymphocytes and basophils), HGB, HCT, MCV, and MCH.

Conclusion: Curcumin drugs can be used as an immediate remedy/treatment to cure COVID-19 patients.

Methods: A cohort of thirty mice was divided into three groups: control, T1 diabetic, and T1 diabetic groups that received vitamin D treatment. For each mouse in the three groups, measurements were taken of body weight, blood glucose levels, glycated hemoglobin (HbA1c), lipid profile, cardiac enzymes, troponin I, adropin, nitric oxide (NO), endothelin-1, and Vascular endothelial growth factor (VEGF). In addition, measurements were taken for the overall lymphocyte count, as well as the CD3⁺, CD4⁺, CD8⁺, CD4⁺, CD25⁺, and CD8⁺ CD25⁺ cell counts in all mice.

Results: The diabetic mice that received vitamin D treatment exhibited significant reductions in blood glucose levels, HbA1c levels, lipid profile, cardiac enzymes, troponin I, endothelin-1, and VEGF levels as compared to the untreated diabetic group (p < 0.01). Furthermore, there was an observed rise in adropin and NO levels in diabetic mice that received vitamin D treatment compared to the untreated diabetic group (p < 0.05). The diabetic mice treated with vitamin D exhibited a substantial decrease in total lymphocyte counts compared to the untreated diabetic and control animals (p < 0.0001). Regarding the CD3+ subset, it was shown that diabetic mice subjected to vitamin D treatment had notably elevated levels of these cells compared to both the untreated diabetic and control groups (p < 0.0001). In addition, the administration of vitamin D resulted in a substantial decrease in the numbers of CD4+ and CD8+ cells in the group of individuals with diabetes (p < 0.0001). The diabetes group that received vitamin D treatment had significantly reduced populations of CD4+ CD25+ and CD8+ CD25+ compared to the untreated diabetic group (p < 0.0001).

Conclusion: Vitamin D maintains the integrity of the cardiovascular system through the reduction of blood glucose levels and lipid profile. Moreover, its supplementation prevents atherosclerotic CVD by suppressing inflammatory reactions.

Purpose: This study aimed to investigate the impact of different levels of TSH on visual associative learning in SCH and determine if these impairments were reversed with LT-4.

Methods: A total of 134 participants were included in this cross-sectional study. Group 1: 35 healthy controls; patients with SCH (Group 2: 33 newly identified cases; Group 3: 32 patients on LT-4 with elevated TSH; Group 4: 34 euthyroid but on LT-4). A thyroid profile and a neuropsychological clinical assessment were done. The visual PAL task was performed on CANTAB.

Results: PAL was significantly impaired (p = <0.05) in all 3 patient groups as compared to Group 1. The PAL total errors (adjusted) scores were significantly higher in Groups 2 and 3, indicating that associative learning is definitely impaired in SCH, reaching levels previously seen in patients with AD.

Conclusion: Our findings encourage screening for visual associative learning or memory retrieval in patients with SCH. The study present has established a more reasonable threshold of TSH 2.5mIU/L to encourage examination of associative learning and the initiation of LT-4 in SCH. Poor PAL task performance in patients with SCH may have significant implications in clinical settings for suspecting AD

Case presentation: A 27-year-old female, not having a known chronic disease and occasionally consulting doctors due to bone pain, weakness, and fatigue, visited the emergency department with the complaint of a nosebleed four years ago. The patient was found to have hepatosplenomegaly in physical examination and was referred to the hematology clinic because of pancytopenia. According to the physical examination and laboratory results, the desired leukocyte glucocerebrosidase level was 0.4 micromol/lt/hour (normal range > 2.5). Homozygous mutations of p.L483P and L483P were observed in genetic tests. Based on these results, the patient was diagnosed with GD. Although the patient received regular weekly treatment for 4 years, no significant change was observed in the spleen size. The patient was admitted to the hospital in April 2022 with complaints of abdominal fullness and indigestion. Her quality of life was deteriorating due to massive splenomegaly. A splenectomy was performed on the patient. In our case, splenic gaucheroma, a rare complication of Gaucher’s disease, was found to be present.

Conclusion: These masses, which are a rare complication of GD, have started to be better recognized by radiologists and clinicians thanks to the case series shared, and it is clear that there is a need for standardization and further research in this field. With an increase in the number of cases and experiences in this field, there will inevitably be different and new developments in follow-up and treatment approaches.

Objective: This study aimed to investigate the protective effects of H₂ on high glucose-induced oxidative damage and apoptosis in human skin cells.

Methods: HaCaT keratinocytes and HSF fibroblasts were treated with high glucose or AGEs. Cell viability, oxidative stress markers, inflammatory cytokines, and apoptosis were analyzed. AGEs/RAGE/NF-κB signaling was evaluated via Western blot.

Results: H₂ treatment significantly reduced ROS, MDA, IL-1β, and TNF-α levels, while enhancing SOD and GSH activity. It also inhibited AGEs/RAGE/NF-κB signaling and apoptosis.

Conclusion: Hydrogen therapy protects against oxidative stress and inflammation induced by high glucose or AGEs, offering potential as an adjunctive treatment for diabetic wound healing.

Case Presentation: We report the case of a patient with a pituitary lesion who presented with hypopituitarism, diabetes insipidus, and visual field defect and was misdiagnosed as a possible cystic pituitary adenoma. Endoscopic endonasal transsphenoidal surgery (ETSS) was performed, and surprisingly, only pus was found, and complete resection of the lesion was achieved. Coagulase-negative staphylococci were detected in the culture, and appropriate antibiotic therapy was administered for six weeks. Diabetes insipidus and hypopituitarism did not improve. One year later, the abscess recurred, and a second operation with complete resection was performed.

Conclusion: Knowledge of primary pituitary abscess, a rare infectious disease, is essential for early detection and successful treatment. Most patients have a chronic and silent prediagnostic course with symptoms that are not specific to pituitary abscess alone. The primary treatment option is EETS, followed by long-term, relevant antibiotics. The disease can be resistant and recur despite appropriate treatment, especially in patients with risk factors. Therefore, long-term follow-up of patients is essential.

Objective: The present work aims to explore and compare the systemic anti-inflammatory effects of two different types of Curcumin: a traditional fat-soluble formulation (95% Curcumin) and an innovative standardized reconstituted water-soluble one (Curcuin), made in micelles in aqueous solution.

Methods: Research was conducted on 30 patients, 15 patients were treated with turmeric (Curcuma longa L., rhizome) dried extract titled 95% Curcumin (Curcumin 425mg/day) conjugated with piperine, and 15 patients were treated with Curcumin (turmeric 286 mg dried extract titled 35%; Curcuminoids 100 mg/day, standardized water-soluble) made in micelles in highly absorbed aqueous solution. We considered the quantitative variations of laboratory parameters: Erythrocyte Sedimentation Rate (ESR), C-reactive protein (CRP), Ferritin (24 to 336 ng/mL for adult males), and cholesterol LDL.

Results and Discussion: Patients treated with dried extract titled 95% Curcumin, for 90 days, show a lower value of ESR, CRP, Ferritin, and LDL cholesterol compared with the same laboratory parameters before the introduction of Curcumin into the diet. Also, patients treated with Curcuin report a lower value of ESR, CRP, Ferritin, and LDL cholesterol after the introduction of turmeric dried extract in the diet, but with a major significance compared with those obtained with 95% Curcumin conjugated with piperine.

Conclusion: As we had hypothesized, both turmeric-derived extracts have successfully reduced ESR, CRP, Ferritin, and cholesterol LDL values, exerting an anti-inflammatory action and anti-cholesterolemic action. These results suggest a possible use of Curcumin and in particular Curcuin as a coadjuvant for the treatment of inflammatory disease and to decrease cholesterol levels. However, additional investigation is needed to resolve doubts regarding Curcumin dosage form, dose, and medication frequency.

Aims: This study aimed to comprehensively clarify the correlation between ulcerative colitis (UC) and liquid-liquid phase separation (LLPS).

Objectives: In this study, bioinformatics analyses and public databases were applied to screen and validate key genes associated with LLPS in UC. Furthermore, the roles of these key genes in UC were comprehensively analyzed.

Methods: Based on the single-cell transcriptomic data of UC obtained from the Gene Expression Omnibus (GEO) database, differences between patients with UC and their controls were compared using the limma package. The single-cell data were then filtered and normalized by the ‘Seurat’ package and subjected to dimension reduction by the Uniform Manifold Approximation and Projection (UMAP) algorithm. The LLPS-related genes (LLPSRGs) were searched on the Dr- LLPS website to obtain cross-correlated genes, which were scored using the ssGSEA algorithm. Next, functional enrichment, interaction network, immune landscape, and diagnostic and drug prediction of the LLPSRGs were comprehensively explored. Finally, the results were validated using external datasets and quantitative real-time PCR (qRT-PCR).

Results: A total of eight cell types in UC were classified, namely, fibroblasts, macrophages, endothelial cells, neutrophils, NK cells, B cells, epithelial cells, and T cells. The intersection between differently expressed genes (DEGs) among the eight cell types identified 44 key genes, which were predominantly enriched in immune- and infection-related pathways. According to receiver operating characteristic (ROC) curves, PLA2G2A, GZMK, CD69, HSP90B1, and S100A11 reached an AUC value of 0.94, 0.95, 0.86, 0.89, and 0.93, respectively. Drug prediction revealed that decitabine, tetrachlorodibenzodioxin, tetradecanoylphorbol acetate, thapsigargin, and cisplatin were the potential small molecular compounds for PLA2G2A, GZMK, CD69, HSP90B1, and S100A11. Immune cell infiltration analysis demonstrated that the infiltration of CD4 memory T cell activation, macrophage M1, T macrophage M0, neutrophils, and mast cell activation was higher in the UC group than in the normal group.

Conclusion: The LLPSRGs play crucial roles in UC and can be used as prognostic and diagnostic markers for UC. The current findings contribute to the management of UC.

Objective: The present study delved into the underlying mechanisms of Jisheng Shenqi Pill (JSP) in the treatment of DKD.

Methods: The active constituents and prospective targets of JSP were identified from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), while DKD-associated disease targets were obtained from the GeneCards database. Subsequently, Gene Ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to assess the overlapping segment of drugs and disease targets. Meanwhile, a component-target-pathway network was constructed to identify pivotal components, targets, and pathways. Molecular docking and molecular dynamics simulation were also carried out to validate the binding efficacy of the pivotal components with the targets. Finally, animal experiments were conducted to corroborate the efficacy of the aforementioned targets and pathways.

Results: According to bioinformatics analysis, the primary targets included JUN, TNF, and BAX, while the pivotal pathways involved were AGE/RAGE and PI3K/AKT signaling cascades. In vivo experiments demonstrated that JSP effectively mitigated renal impairment in DKD by reducing renal inflammation and apoptosis. This effect was presumably achieved by modulating the AGERAGE axis and the PI3K/AKT signaling pathway.

Conclusion: Our findings imply that JSP could ameliorate renal inflammation and apoptosis in DKD mice by modulating the AGE/RAGE axis and the PI3K/AKT signaling pathway. These findings provide valuable insights into traditional Chinese medicine-based treatments for DKD.

Methods: Registered under CRD42024501460 on the PROSPERO platform, we searched eight major databases, including Web of Science, PubMed, Cochrane, Embase, China National Knowledge Infrastructure, Wanfang database, Chinese Scientific Journals Database, and Chinese Biomedicine Database, from inception to December 2023 for randomized controlled trials on Ling Gui Zhu Gan Decoction in non-alcoholic fatty liver disease treatment. We extracted data on total efficiency, TC, TG, ALT, AST, GGT, and HOMA-IR, analyzing results with RevMan 5.4 software.

Results: Twelve studies met the inclusion criteria, encompassing 970 cases. Ling Gui Zhu Gan Decoction, alone or combined with standard therapy, significantly improved non-alcoholic fatty liver disease outcomes, regardless of treatment duration. Only one study reported adverse events, including bloating, diarrhea, nausea, vomiting, and rash.

Conclusion: Ling Gui Zhu Gan Decoction appears to be an effective and safe option for non-alcoholic fatty liver disease treatment. However, due to limited studies and methodological weakness, further rigorous randomized controlled trials are necessary for conclusive results.

Case Presentation: An 18-year-old male with no previous medical history presented to the emergency department complaining of a rapidly enlarging painful neck mass in left anterior latero-cervical region progressively worsening over the last two weeks, accompanied by dysphagia and fever. Blood tests showed the presence of thyroiditis (suppressed TSH with increased free thyroxine, elevated inflammation markers and neutrophilic leucocytosis). Neck ultrasonography and CT showed a large abscess involving the left thyroid lobe and extending to the ipsilateral laterocervical region, suggesting the diagnosis of AST. Prompt antibiotic therapy was started and subsequent surgical drainage of the abscess was performed, resulting in a rapid clinical recovery and the restoration of normal thyroid function. The bacterial culture of the abscess showed exclusively the presence of Gemella morbillorum.

Conclusion: We present the first documented case of AST caused by Gemella morbillorum in an otherwise healthy young man. Although rare, AST in immunocompetent patients is possible; prompt diagnosis and treatment of this condition are fundamental to avoid severe complications.

Objective: We aimed to explore the potential targets and mechanisms of action of BZYQ in DN.

Materials and Methods: A DN rat model was induced using a high-fat and high-sugar diet combined with intraperitoneal injection of streptozotocin (STZ), followed by treatment with different doses of BZYQ. Initially, the protective effects of BZYQ on renal tissue were assessed by measuring fasting blood glucose (FBG), total cholesterol (TC), triglycerides (TG), 24-hour urinary total protein (24h-UTP), urinary albumin (ALB), and serum creatinine (SCr) after administration, along with performing hematoxylin-eosin (HE) staining. Subsequently, transcriptomics and bioinformatics approaches were employed to identify the action targets and potential mechanisms of BZYQ in DN rats. Finally, real-time PCR and Western blot analyses were conducted to validate key targets and mechanisms.

Results: We observed significant improvements in renal injury in DN rats treated with medium and high doses of BZYQ. Transcriptomic and bioinformatic analyses identified NLRP3, ASC, caspase- 1, GSDMD, IL-1β, and IL-18 as hub genes, along with differential expression of immune-related transcription factors T-bet and GATA-3 in various transcriptomes. In the validation phase, the mRNA and protein expressions of NLRP3, ASC, caspase-1, GSDMD, IL-18, IL-1β, and T-bet were significantly elevated in the DN rat model group, while GATA-3 mRNA and protein levels were significantly decreased; BZYQ was able to reverse these changes.

Conclusion: BZYQ has been found to have a protective effect on renal tissue damage in DN rats, potentially related to the inhibition of NLRP3 inflammasome pathway activation and the improvement of Th1/Th2 immune cell balance.

Case Presentation: Hypocalcemia was detected two weeks after the first denosumab administration, during routine biochemical evaluation. The patient reported only a mild nonspecific paresthesia after medical questioning, without relevant clinical symptoms. Despite the severity of the hypocalcemia, serum calcium levels began to improve after a short period of low-dose calcium and calcitriol therapy, though complete stabilization and normalization occurred after several weeks.

Conclusion: This case highlights the importance to consider severe paucisymptomatic or asymptomatic hypocalcemia as a possible side effect in bone-metastatic patients treated with denosumab. It is advisable to monitor serum calcium levels even in the absence of typical hypocalcemia-related symptoms.

Methods: We searched the Web of Science for studies related to DR RNA research before July 2024 and then used CiteSpace and VOSviewer to generate knowledge visualization maps.

Results: A total of 1,103 articles related to RNA research in DR were retrieved. China has the most articles, followed by the USA and Japan. Wayne State University, Nanjing Medical University, and Shanghai Jiao Tong University were the three most productive institutions. Investigative Ophthalmology & Visual Science was the most popular journal in this field. Kowluru, Renu A from Wayne State University published the most number of articles. Keyword analysis showed that the research hotspot in this field is the role of miRNAs in apoptosis and neovascularization in DR. Non-coding RNAs and extracellular vesicles are future research trends.

Conclusion: The results of this bibliometric study provide information on the current status and trends in the field of RNA research in DR. RNA research could lead to new diagnostic methods and therapeutic strategies for DR. Our findings can help researchers understand the current status of RNA research in DR and identify new directions for further research.

Aims: This study aimed to investigate the associations of chronic hepatitis B (CHB) and fatty liver diseases with the incidence of metabolic syndrome (MetS) in young adults, which have not been verified before.

Objective: The associations between NAFLD, NASH, and CHB and the incidence of new-onset MetS remain inconclusive in young adults.

Methods: This cohort study included 2,614 military personnel aged 18-39 years who were free of baseline MetS in 2014 and were followed for the incidence of MetS in each annual health examination until the end of 2020. CHB was defined by the presence of the hepatitis B surface antigen with an established diagnosis history. NAFLD and NASH were defined by the ultrasound finding with an elevated alanine transaminase (27-53.9 and ≥54 U/L in men and 15-29.9 and ≥30 U/L in women, respectively). MetS was defined based on the International Diabetes Federation criteria. Multivariable Cox regression analysis was used to determine the associations between hepatitis and incident MetS.

Results: During a mean follow-up of 6.0 years, 582 new-onset MetS cases occurred (22.3%). NAFLD and NASH were associated with a greater risk of new-onset MetS (hazard ratios (HRs) and 95% confidence intervals: 1.47 (1.21-1.79) and 1.66 (1.16-2.39), respectively), while no association for CHB was found (HR: 1.31 (0.88-1.96)).

Conclusion: This study found that NAFLD and NASH, while not CHB, were independent risk factors of new-onset MetS with adjustments for potential covariates, e.g., physical activity and fitness in young adults.

Case Presentation: We report the clinical history and therapeutic management of a 59-year-old man diagnosed with arginine vasopressin deficiency (AVP-D) due to an infundibulo-neurohypophysitis (INH) that occurred after the patient had inhaled spray film containing toluene. In consideration of the clinical signs and radiological imaging suggestive of INH, therapy with desmopressin and corticosteroids was instituted, with gradual improvement of polyuria and resolution of the radiological features of INH.

Conclusion: To our knowledge, we described the first case of INH, manifested with AVP-D, secondary to toluene exposure. In addition, the endocrine effects of toluene inhalation were discussed. Finally, given the scarcity of data available, an overview of all the known toxic substances inducing AVP-D was also provided.

Background/Introduction: Type 1 diabetes mellitus is the most common disorder with difficult management, affecting the quality of life. Stem cell therapy has been proven to have regenerative ability. The current study has involved using the existing stem cell therapy and modifying it.

Objective: The objective of this study was to manage hyperglycemia in a diabetic rodent model by using hypoxia-preconditioned BFP-MSCs, and to study their effect on serum and pancreatic insulin and pancreatic regeneration.

Methods: In this study, the Streptozotocin (STZ)-induced diabetes rat model was used. The diabetic rats were administered the test therapy, i.e., hypoxia-preconditioned BFP-derived MSCs in three doses by intramuscular route. Thereafter, monitoring of blood glucose levels was carried out till the end of the study. Changes in the serum insulin and pancreatic insulin were also observed. Histopathology of the pancreas was performed to assess the effect of preconditioned stem cells on pancreatic regeneration.

Results/Discussion: The effect of hypoxia-preconditioned BFP-derived MSCs on the body weight and that of food-water intake was non-significant. Their effect on blood glucose levels was found to be significant (p < 0.0001). After the administration of test therapy, the blood glucose level in the test group decreased, ultimately resulting in the management of diabetes. Histopathology of the pancreas showed regeneration of the pancreatic cells in the test group.

Conclusion: The above research findings suggest that hypoxia-preconditioned BFP-derived MSCs can be considered a promising therapy in the management of type 1 diabetes. Stem cell therapy can be the future of the management of diabetes; however, further research is needed on the current therapy.

Methods: The study employed 7-8-month-old AB strain zebrafish and induced T2DM models by continuous exposure to a 2% glucose solution for 14 days. Control, model, gardenoside low-, medium-, and high-dose groups (2.5 mg/L, 5 mg/L, 10 mg/L), and a metformin group were established. Parameters such as zebrafish body weight, fasting blood glucose levels, and behavioral analyses were monitored. Fructosamine levels were measured using ELISA, while real-time polymerase chain reaction (Real-time PCR) was employed to assess the relative expression levels of INS, IRS, NF-κB, IL-1β, and IL-6 genes. Intestinal histological examination was conducted to observe inflammation levels.

Results: Compared to the control group, the model group exhibited significantly increased blood glucose levels, weight gain, and fructosamine content. High-speed locomotion time increased, while low-speed locomotion time decreased. Relative expression levels of INS, NF-κB, IL-1β, and IL-6 genes were elevated (P < 0.0001), whereas IRS relative expression levels decreased (P < 0.001). In comparison to the model group, the gardenoside and metformin groups demonstrated reduced blood glucose levels and no significant change in body weight. The gardenoside low and medium dose groups, as well as the metformin group, showed reduced high-speed locomotion time and increased low-speed locomotion time. The relative expression levels of INS, NF- κB, IL-1β, and IL-6 genes in the gardenoside and metformin groups decreased (P < 0.01 or P < 0.0001), while IRS relative expression levels increased (P < 0.001 or P < 0.0001).

Conclusion: Gardenoside may suppress inflammatory responses, alleviate insulin resistance, and ameliorate diabetes-related inflammatory symptoms, potentially through the regulation of the INS/NF-κB signaling pathway.

Methods: In this study, the characteristics of the articles on “diabetes and osteoporosis” retrieved and downloaded from the Web of Science Core Collection (WoSCC) database from January 1, 2011 to December 1, 2022 were analyzed by bibliometrics to clarify the evolution and theme trends between the two diseases. Citespace software was used for data analysis and visualization, including countries, academic institutions, journals, authors, subject categories, keywords, references, and citations. In addition, some important subtopics identified by bibliometric characterization were further discussed and reviewed.

Results: Finally, 3372 articles were included in the analysis, including a total of 96 countries, 407 organizations, 1161 journals, and 617 keywords. Articles related to diabetes and osteoporosis were first published in 2011 and then showed an increasing trend year by year. The United States, China, Italy, England, and Japan were the top 5 countries associated with the largest number of publications. University of California-San Francisco, China Medical University, University of Toronto, Shanghai Jiao Tong University, and Mayo Clinic were the top 5 academic institutions in terms of the number of published papers. The top 5 authors with the highest number of publications were William D, Ann V, Nicola, Peter, and Toshitsugu. Osteoporosis International has published 130 articles in this field, ranking first among highly productive journals. In addition to diabetes and osteoporosis, the most frequently used keywords were bone mineral density, obesity, and fracture.

Conclusion: More and more studies have been conducted on diabetes and osteoporosis, and the current research mainly focuses on the pathogenesis of various chronic diseases. In the future, more attention may be paid to the prevention and management of these two chronic diseases and the production and application of new drugs.