Monoclonal gammopathy, or paraproteinemia, involves monoclonal immunoglobulins in the blood and ranges from benign monoclonal gammopathy of undetermined significance (MGUS) to malignant multiple myeloma. Hemostatic abnormalities affect 15-30% of cases but are often under-recognized. This study presents three cases of Immunoglobulin A (IgA) monoclonal gammopathy with hemostatic dysfunction to enhance understanding of its pathophysiology and clinical impact.

Lipid metabolism and endoplasmic reticulum stress (ERS) are crucial in coronary artery disease (CAD) pathogenesis, but the exact mechanisms remain unclear. This study aims to systematically investigate the molecular interplay between lipid metabolism and ERS in CAD.

Anti-LGI1 antibody-associated encephalitis is a rare autoimmune neurological disorder, and primary Sjögren's syndrome is a systemic autoimmune disease with multisystem involvement. The coexistence of these conditions with acute cerebral infarction is extremely rare and highlights complex interactions between autoimmune and vascular mechanisms.

Irritable Bowel Syndrome (IBS) and hypothyroidism are both common conditions that significantly affect patient health. This study examines the link between IBS and hypothyroidism, focusing on how IBS impacts hypothyroidism.

This study investigated the hepatoprotective effects and mechanisms of 17β-estradiol (E2) in a mouse model of type 2 diabetes mellitus (T2DM) with non-alcoholic fatty liver disease (NAFLD).

Pancreatic cancer (PC) presents unique challenges to traditional immunotherapy due to its immunosuppressive microenvironment and low mutation burden. Research into antibody-mediated immune responses, which has been extensively applied in various cancer types, is also applicable to the study of pancreatic cancer.

Observational research has indicated a link between regulatory T-cells (Tregs) and the risk of acute respiratory distress syndrome (ARDS). However, establishing a definitive causal relationship has been challenging. This study aimed to clarify this connection using a two-sample Mendelian randomization (MR) approach.

Sarcopenia is a degenerative musculoskeletal disease affecting the elderly, significantly impairing patients' quality of life and challenging modern medicine. This study innovatively combines Traditional Chinese Medicine (TCM) theories with modern medical research to explore the mechanisms by which Gushukang granules address sarcopenia.

The interplay between LncRNA MALAT1 and hsa-miR-1 plays a crucial role in Myocardial Ischemia-Reperfusion Injury (MIRI), offering insights into the molecular mechanisms underlying cardiovascular pathologies. This study sought to elucidate their regulatory relationship and functional impact on MIRI progression.

Hirschsprung disease (HD) is a congenital disorder associated with specific missense mutations in the RET proto-oncogene. This study aimed to demonstrate the incidence of Hirschsprung disease and its clinical and pathological aspects in an Iraqi pediatric cohort from a major referral hospital in Baghdad.

Cancer-associated fibroblasts (CAFs) can promote gastric cancer (GC) progression through regulating the tumor microenvironment (TME). This study explored cell-to-fibroblast communication based on the single-cell data of GC, identified CAF-related genes linked to GC using high-dimensional weighted gene co-expression network analysis (hdWGCNA), and conducted functional mining, drug prediction, and molecular docking for these genes.

Diabetes mellitus is a global health issue, affecting over 6.2% of the population. Effective management of type II diabetes mellitus (DM II) depends largely on patients' knowledge, attitudes, and practices (KAP). This study has examined how demographic and clinical factors influence KAP among DM II patients in Punjab, India, aiming to identify knowledge gaps and behavioral trends.

Congenital hyperinsulinemia (CHI) is a clinically heterogeneous disorder that is the leading cause of persistent and recurrent hypoglycemia in infancy and childhood. There are 39 pathogenic genes associated with CHI. The forkhead box A2 (FOXA2) gene variants that induce forkhead box A2 hyperinsulinemia (FOXA2-HI) are extremely rare. This review describes the genetic pathogenesis and treatment progress of FOXA2-HI to improve clinicians' understanding of the disease.

DNA methylation, being a predictor of gene-environment interaction, a dynamic and reversible process, and a target of drugs, may help clinicians to step towards precision medicine. Epigenome-wide association studies have linked methylation changes with type 2 diabetes and glycemic control; among such frequently documented differentially methylated loci include TXNIP (Thioredoxin interacting protein) and ABCG1 (ATP-binding cassette Subfamily G Member 1). However, research evaluating the effects of antidiabetic treatment on DNA methylation is quite meager.

The high global prevalence of diabetes and treatment noncompliance is a great clinical challenge. Thus, the need for anti-diabetic medications is critical. In this regard, in vivo antidiabetic potential of the synthesized dichloroindolinone (C1 and C2) was investigated.

Introduction: Pancreatic adenocarcinoma (PAAD) is characterized by aggressive progression, driven by an immunosuppressive tumor microenvironment (TME) and mitochondrial dysfunction. Alterations in mitochondrial bioenergetics and metabolic reprogramming are crucial to tumor survival, invasion, and immune evasion. The "immune dictionary" approach provides a systematic classification of immune-related genes, offering insights into immune dysfunction and its interaction with mitochondrial pathways in the context of PAAD outcomes.

Methods: To identify differentially expressed genes (DEGs) associated with immune dysfunction and mitochondrial pathways in PAAD, data from TCGA, GTEx, and three GEO datasets were integrated. Differential gene expression was analyzed using DESeq2, applying criteria of p-value < 0.05 and |log2 fold change| > 1. Using the "immune dictionary" framework, a prognostic model was developed through LASSO-Cox regression, followed by survival analysis for validation. The expression of key genes identified in the bioinformatics analysis was validated by quantitative real- time PCR (qPCR) on paired PAAD tissue and adjacent normal samples, focusing on NOG, TNFSF9, and TNFSF10.

Results: Fifty-two DEGs associated with immune and mitochondrial dysfunction were identified. Gene set enrichment analysis revealed critical pathways, including IL-4 signaling, NF-κB activation, and autophagy. The LASSO-Cox model identified 12 prognostic genes that effectively stratified patients into high- and low-risk groups with high predictive accuracy. Validation confirmed significant differential expression patterns, consistent with computational findings.

Discussion: This study, utilizing the immune dictionary framework, systematically analyzed immune- related and mitochondria-related genes in PAAD, identifying 12 DEGs for prognostic modeling. It revealed significant correlations between immune evasion and mitochondrial dysfunction, offering novel targets for personalized therapy.

Conclusion: This study presents an innovative immune dictionary approach to identify key immune- and mitochondria-related DEGs in PAAD, providing potential targets for new therapeutic strategies and personalized treatment approaches.

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Introduction: Obesity, a global health crisis, necessitates innovative therapeutic strategies. Traditional Chinese Medicine (TCM), including Erchen Decoction (ECD), offers potential benefits; however, the molecular mechanisms underlying ECD's anti-obesity effects, particularly on lipid metabolism, remain unclear. This study investigates the mechanism by which ECD improves lipid metabolism through the AMPK/SIRT1/PGC-1α signaling pathway.

Methods: AML-12 hepatocytes were cultured and divided into Control, Model (palmitic acid-induced lipid deposition), and treatment groups (ECD serum: 2%, 4%, 8%; orlistat: 10 μM). Cell viability, lipid accumulation, and triglyceride (TG) content were measured. Key lipid metabolism genes (p-AMPK/AMPK, SIRT1, PPARα, PGC-1α, Nrf2, TFAM) were evaluated using RT-qPCR, Western Blot, and immunofluorescence. Network pharmacology analysis identified ECD's targets and pathways.

Results: The Model group showed increased lipid droplets and TG content, with reduced AMPK, SIRT1, PPARα, PGC-1α, Nrf2, and TFAM expression compared to Control. ECD treatment significantly decreased lipid droplets and TG content (at all doses), with the 4% dose being the most effective. ECD up-regulated all tested genes, confirmed by immunofluorescence (p-AMPK, SIRT1, PGC-1α). Network pharmacology highlighted the overlap between ECD and obesity pathways, with a particular emphasis on lipid metabolism.

Discussion: ECD improves lipid metabolism in AML-12 hepatocytes by activating the AMPK/ SIRT1/PGC-1α pathway, consistent with prior research. The upregulation of Nrf2 and TFAM indicates enhanced mitochondrial function and resistance to oxidative stress. Limitations include the use of in vitro models; future studies should focus on clinical translation and dosage optimization. Conclusion: ECD regulates lipid metabolism via the AMPK/SIRT1/PGC-1α pathway, providing a scientific basis for its clinical use in obesity-related diseases. This study highlights ECD as a promising therapeutic strategy for improving lipid metabolism and reducing obesity-associated risks.

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Introduction: Autoimmune thyroiditis (AIT), a prevalent autoimmune disorder, can severely impair patients' quality of life when progressing to hypothyroidism. This investigation seeks to systematically evaluate the therapeutic efficacy of Buzhong Yiqi Decoction (BZYQ) against iodine-induced AIT while elucidating its underlying molecular mechanisms.

Methods: NOD.H-2 mice received daily 0.05% sodium iodide gavage for 8 weeks to induce AIT. Thyroid histopathology was evaluated by HE staining. Serum autoantibody levels and lactate concentrations were measured. Western blotting analyzed PTEN, p-PI3K/PI3K, p-AKT/AKT, GLUT1, HK2, PKM2, and LDHA protein expression in thyroid tissues. Immunofluorescence staining localized the expression of HK2 and RORγt in thyroid sections. Flow cytometry quantified the proportion of Th17 cells within splenic lymphocytes.

Results: BZYQ reduced thyroid structural damage and lymphocytic infiltration in AIT mice, accompanied by significant reductions in serum TGAb and TPOAb levels. Notably, BZYQ modulated glycolysis to decrease lactate levels and the proportion of Th17 cells. Mechanistically, BZYQ upregulated PTEN expression to suppress downstream p-PI3K, p-AKT, GLUT1, HK2, PKM2, and LDHA expression, thereby achieving regulation of immunometabolic pathways.

Discussion: This study provides experimental evidence for broadening the modern clinical applications of this classical formula. However, the related mechanisms still require further rigorous clinical studies for validation.

Conclusion: BZYQ modulates Th17 differentiation via the PTEN/AKT-immunometabolic axis in AIT.

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Anemia has been linked to an increased risk of coronary heart disease (CHD), yet the underlying causal relationship remains unclear. This study aimed to investigate the bidirectional associations between anemia and CHD using a multi-method approach.

Sepsis is a Systemic Inflammatory Response (SIR) caused by invading pathogens. We aimed to characterize infiltrating cells in sepsis and provide novel insight for the treatment of sepsis.

Polycystic ovary syndrome (PCOS) is a complex endocrine disorder characterized by hyperandrogenism, ovarian dysfunction, and metabolic abnormalities. It affects between 4% and 21% of females of fertile age. The present review provides a comprehensive analysis of PCOS, covering pathophysiology, diagnostic criteria, prevalence, biochemical markers, and demographic influences. It examines genetic, hormonal, and lifestyle variables, contributing to the conditions, highlighting ethnic disparities in prevalence.