ISSN 2959-409X (Print) ISSN 2960-1290 (Online) Editor-in-chief: Raees Ahmad （Xi'an Jiaotong University） Associate Editor: Zunaira Khalid （University of Lahore） Editorial Board Member: Muhammad Numan （The Second Affiliated Hospital of Xi’an Jiaotong University） Yu Diao （Xi'an Jiaotong University） The Journal of MedScien (a shortened form of Medical Science) is a comprehensive, peer-reviewed academic publication dedicated to the advancement of healthcare knowledge. We provide a professional forum for the exchange of scientific ideas, clinical observations, and breakthrough research that shapes the future of medicine. By integrating various branches of health sciences, the journal serves as a vital resource for medical students, nurses, doctors, and researchers worldwide. Our mission is to support the global healthcare community by publishing high-quality, evidence-based content that is accessible to both the practicing clinician and the academic researcher. We believe that by providing a platform for diverse perspectives—from student-led pilot studies to advanced clinical trials—we foster a more collaborative and innovative medical landscape. Scope of Subjects: The Journal of MedScien prides itself on its broad, multidisciplinary scope. We invite submissions across the full spectrum of health and life sciences, including: Medical Science: Fundamental research in anatomy, physiology, pathology, and biochemistry. Pharmaceuticals: Innovations in drug development, pharmacology, pharmacokinetics, and vaccine research. Clinical Application: Practical insights into surgical techniques, diagnostic tools, patient care, and nursing protocols. General Science: Interdisciplinary research that intersects with health, such as biotechnology, medical ethics, and public health policy. Why Publish with Us? Rigorous Peer Review: Every article undergoes a thorough evaluation by experts in the field to ensure scientific integrity and clinical relevance. Inclusive Readership: Our content is curated to be valuable for those in training (students) and those with years of professional experience (doctors and researchers). Global Reach: We aim to disseminate findings to a wide audience, ensuring that your research has a tangible impact on global health outcomes. The Journal of MedScien remains committed to the principle that better information leads to better care. We welcome your contributions to our upcoming issues. All articles will be submitted to: Google Scholar, Crossref, U.S. Librarian Database, ProQuest (part of Clarivate’s Web of Science), Ulrich's Periodicals Directory, SEMANTIC SCHOLAR, OpenAlex.
Tau Protein Pathology and Tau-Targeted Therapeutic Strategies in Alzheimer’s Disease: Mechanisms, Clinical Evidence and Future Perspectives
Alzheimer's disease (AD) is the most dominant form of dementia characterized by neurodegeneration which leads to progressive cognitive decline and memory loss, the common symptoms of AD. While amyloid-β peptide accumulation has traditionally been the primary focus of AD research, there is growing evidence that tau pathology also contributes significantly in disease progression. Tau is a microtubule-associated protein that normally stabilizes microtubules and supports axonal transport within neurons. However, abnormal hyperphosphorylation causes tau to detach from microtubules, misfold and aggregate into toxic filaments which ultimately lead to neurodegeneration and eventually cell death. This paper reviews the structure of tau protein, its physiological and pathological behaviours and tau's mechanism in terms of disease progression. This paper also examines clinical and preclinical evidences and discusses the efficacy and limitations of three tau-targeted therapeutic approaches: gosuranemab, a monoclonal antibody designed to prevent the spread of extracellular tau; BIIB080, an antisense oligonucleotide that reduces tau production by targeting MAPT mRNA; and leucomethylthioninium bis (LMTM), a tau aggregation inhibitor. Studies also suggest the potential of combination therapies targeting multiple pathological pathways to enhance efficacy. Though no tau-targeted therapy has yet to demonstrate definitive clinical benefit, continued research supports tau as an important therapeutic target and contributes to the development of more effective treatments for AD.
Research on Conservative Rehabilitation and Prevention Strategies for Patellar Dislocation Among College Students
In recent years, with the extensive popularization of campus sports activities, the number of reported knee injuries such as patellar dislocation has kept rising among college students. Although most such injuries can reset spontaneously, insufficient attention has resulted in a persistently high recurrence rate after the first dislocation, and female students face a notably higher onset risk than male students. A review of existing domestic and overseas literature shows that current research mainly focuses on surgical treatment and postoperative rehabilitation for professional athletes, while conservative intervention schemes designed for ordinary college students are relatively insufficient. By adopting the literature review method, this paper integrates research outcomes from anatomy, biomechanics and clinical rehabilitation fields to systematically sort out the stabilizing structures and injury mechanisms of patellar dislocation. On this basis, it compares the differences in injury features and rehabilitation demands between college students and professional athletes and further puts forward an intervention framework that fits campus scenarios and takes conservative training as the core. Available evidence proves that step-by-step phased conservative intervention can strengthen the stability of the patellofemoral joint, improve the overall function of the knee joint, and reduce the probability of repeated dislocation, which is applicable to early intervention and daily management of mild patellar dislocation and functional instability among college students.
Advances in Hydrogel Applications in Wound Healing and Tissue Regeneration
Hydrogel has received wide attention in the field of biomedicine in recent years due to its high-water content, good biocompatibility and structural characteristics similar to human tissues. This article reviews the classification, basic properties and application of Hydrogel in wound repair and tissue regeneration. According to the material source and functional characteristics, hydrogel can be divided into natural hydrogel, synthetic hydrogel and smart hydrogel. Studies show that hydrogel can accelerate wound healing by maintaining a humid environment, exerting antibacterial and anti-inflammatory effects, and promoting cell proliferation and angiogenesis. At the same time, hydrogel has also shown good application prospects in the fields of skin regeneration, bone regeneration and cartilage repair. Although hydrogel still has problems such as insufficient mechanical strength, difficult to accurately control the degradation rate and limited clinical application data, with the continuous development of material design and preparation technology, the new smart hydrogel and the research of multifunctional hydrogel is constantly advancing. In general, as a biomaterial with development potential, hydrogel has a broad application prospect in the fields of regenerative medicine and tissue engineering in the future.
The role of TNF - α signaling pathway in rheumatoid arthritis and the therapeutic progress of TNF-α monoclonal antibodies
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic synovitis and progressive joint destruction. Tumor necrosis factor - α (TNF - α) plays a central regulatory role in its inflammatory network. At present, biological agents such as TNF - α monoclonal antibodies (mAbs) have been widely used in clinical practice, significantly improving the prognosis of RA patients. But some patients have problems with poor treatment efficacy or infection. The differences and safety issues between different drugs still need further research. This article analyzes the immune imbalance mechanism of RA and the activation process of TNF - α signaling pathway, explores the mechanism of action and safety characteristics of TNF - α inhibitor drugs (adalimumab, infliximab, etanercept), and reviews the research progress of new inhibitors such as biosimilars. TNF - α inhibitors can effectively block downstream inflammatory signals and alleviate joint damage. However, there are significant differences in patients' response to treatment, and issues related to infection risk and immunogenicity limit the long-term use of drugs. This study provides a theoretical reference for investigating the mechanism of TNF - α targeted therapy for rheumatoid arthritis. At the same time, future research should focus on exploring biomarkers for predicting treatment response, optimizing individualized combination therapy, and developing new drugs for nontumor necrosis factor pathways to cover a wider range of patients.
Mechanism of Action and Clinical Analysis of Semaglutide in Weight Loss
Semaglutide is a long-acting Glucagon-Like Peptide-1 Receptor Agonist (GLP-1RA). It was initially applied in the treatment of type 2 diabetes mellitus, and later widely used in obesity management due to its prominent weightloss effect. As a novel long-acting GLP-1RA weight-loss drug, compared with traditional GLP-1RAs, it undergoes molecular structural modification to achieve reversible albumin binding, which reduces renal clearance and degradation by dipeptidyl peptidase Ⅳ. Meanwhile, it maintains high affinity to GLP-1 receptors, extending its half-life to 156 hours. The long half-life supports onceweekly injection, greatly improving patients' treatment compliance. Its structure is highly similar to natural human GLP-1, with an amino acid sequence homology of 94%. For the above reasons, it has attracted increasing attention. Accordingly, there is a growing demand for comparing the efficacy of semaglutide with that of other weightloss drugs. This article systematically summarizes the core weight-loss mechanism of semaglutide, efficacy data from large-scale clinical trials, characteristics of adverse reactions and clinical safety, and compares semaglutide with several other weight-loss drugs to clarify their differences and efficacy gaps. It aims to provide objective scientific evidence for the rational clinical application of relevant drugs and scientific weight loss for the public.
Immune Regulatory Mechanism of Alpha1-Antitrypsin in Type 1 Diabetes and Its Clinical Application Progress
Type 1 Diabetes (T1D) is an autoimmune disease-causing selective destruction of pancreatic β-cells, requiring lifelong insulin. Current treatments cannot prevent β-cells loss or restore immune tolerance, highlighting the need for diseasemodifying therapies. Alpha-1 antitrypsin (AAT) has attracted attention due to its multiple mechanisms of action in T1D. It can regulate NKDC interactions, boost Treg function, and inhibit Th1 and CD8+ T cells. It also suppresses the NFκB/IL-1β pathway and upregulates IL1Ra. These actions reduce β-cell apoptosis and increase β-cell mass. Clinical studies show safety of AAT in new-onset T1D and islet autotransplantation, but efficacy outcomes have not been consistently met, partly due to insufficient dosing (90 mg/kg/week) and compensatory endogenous AAT elevation. Different reactions related to gender have been observed in female patients. Future larger-dose, placebo-controlled trials with gender are needed. Engineered mesenchymal stem cells overexpressing AAT and gene delivery strategies provide an effective way to achieve sustained and localized AAT expression, and are expected to overcome the current challenges in clinical translation.
Aducanumab and Lecanemab: Target Specificity, Mechanisms and Clinical Outcomes in Alzheimer’s Disease
Alzheimer's disease (AD) is one of the major unmet medical needs as a neurodegenerative disease associated with cognitive impairment and amyloid-beta (Aβ) accumulation. Unfortunately, current drug development for AD is based on treatment with only symptomatic therapies; there is no available drug able to influence the disease process. Anti-Aβ monoclonal antibodies have been shown as the promising strategy for AD therapy. However, little is known about the dissimilarities of these drugs in terms of target, mechanisms, and clinical effects. This review discusses the differences between two anti-Aβ antibodies – aducanumab and lecanemab, including target selectivity, mechanisms of action, structure, and clinical effectiveness. In particular, this review demonstrates that aducanumab interacts with the insoluble form of the protein, causing serious side effects, whereas lecanemab selectively binds the dangerous soluble protofibrillar form of Aβ. The importance of the state of Aβ aggregation for AD treatment has been revealed through the analysis of the drugs.
Advances in Clinical Research on CRISPR-Cas9 for the Treatment of Common Monogenic Diseases
CRISPR-Cas9 gene editing technology has achieved milestone breakthroughs in the treatment of monogenic hereditary diseases. We systematically review the latest clinical research progress of this technology in treating common monogenic disorders, summarizing key efficacy data, safety outcomes, and current major obstacles. On this basis, we analyze the shift in application logic when extending from monogenic diseases to specific cancers and long COVID syndrome, that is, moving from defect repair to engineering modification and immunomodulation. For cancer, we discuss the prospects of CRISPR in CAR-T enhancement and oncogene disruption, as well as challenges such as tumor heterogeneity and delivery bottlenecks. For long COVID, we explore its value as a research tool and the prospects for direct therapy. Finally, we propose strategies to address common challenges including delivery optimization, off-target detection standardization, and ethical regulation. The success of CRISPR-Cas9 in monogenic diseases represents the prelude to precision medicine, whereas conquering complex diseases will require systematic leaps in target discovery, delivery technology, and safety profiles.
The Treatment Strategies for Kawasaki Disease without Response to Intravenous Immunoglobulin (IVIG)
Background: Kawasaki Disease (KD) is an acute vasculitis that occurs predominantly in children. The standard treatment is initial therapy with intravenous immunoglobulin (IVIG), but some patients develop resistance to IVIG, which increases their risk of developing coronary artery lesions. This review aims to analyze and summarize the causes and pathological mechanisms of IVIG resistance, as well as other treatment strategies. Results: Studies have found that IVIG resistance is mediated by multiple factors including genetic susceptibility, immune dysregulation, and changes in vascular endothelial cell characteristics, with persistently elevated pro-inflammatory cytokines as the core manifestation. Second-dose IVIG, glucocorticoids, and infliximab as second-line treatments each have their advantages and disadvantages. A second IVIG dose is currently the preferred treatment for IVIG non-responders in KD, while infliximab is more effective in controlling fever and coronary inflammation. Combination therapy may be a better option. However, existing predictive models remain limited, with obvious heterogeneity in clinical data. Conclusion: The pathogenesis of Kawasaki disease remains unclear. Current treatment options still carry risks and controversies. Further experimental research is needed to elucidate resistance mechanisms, construct predictive models, conduct heterogeneous experiments, and promote international collaboration to achieve breakthroughs in the treatment of this disease.
CD4+ T-Cell Program Dynamics Under PD-1/PD-L1 Blockade in NSCLC
Immune checkpoint blockade (ICB) targeting PD-1/PDL1 has transformed non-small cell lung cancer (NSCLC) therapy, yet durable benefit remains limited to a subset of patients. While most mechanistic and biomarker frameworks emphasize CD8+ T cells, accumulating single-cell, TCR, and spatial evidence indicates that CD4+ T cells can act as system-level organizers of antitumor immunity and resistance. This paper synthesizes NSCLC studies from 2018-2025 and weighs conclusions using an evidence-tier framework that prioritizes intrapatient longitudinal sampling (paired tumor biopsies and/or serial blood) and spatially resolved profiling. Findings are integrated across five recurring CD4 programs: TLSassociated CXCL13+ Tfh-like states, Th1-oriented helper/effector states, Th17-linked inflammatory states, FOXP3+ regulatory T cells (Tregs), and proliferative/activation-toexhaustion trajectories. Across the strongest longitudinal tumor evidence, response most consistently aligns with coordinated on-therapy remodeling that strengthens TLS/Tfh organization and Th1-oriented output, whereas non-response is repeatedly linked to persistence or accumulation of activated intratumoral Treg states. Th17-associated signals show more variable directionality and remain lower-confidence under PD-1/PD-L1 blockade in NSCLC. Clonal tracking further connects benefit to productive proliferative bursts and blood-tumor clonal exchange within tumor-relevant T-cell pools. Together, these data support biomarker and treatment strategies that move beyond single markers toward composite, timeaware readouts capturing baseline immune infrastructure, suppressive balance, and on-therapy state transitions, and motivate rational combinations that relieve suppressive constraints while preserving productive CD4 help.
Reviewing Traditional and Novel Approaches to Managing Anemia of Chronic Kidney Disease
Anemia is a common complication of chronic kidney disease (CKD). If not managed appropriately, anemia can be highly debilitating and potentially life-threatening for CKD patients. Various treatments have been developed to alleviate CKD-associated anemia, with the main goals of restoring circulating iron, promoting erythropoiesis, and downregulating hepcidin. Mainstream treatment options include iron supplements, erythropoiesis-stimulating agents (ESAs), hepcidin antagonists, and blood transfusion. However, the therapeutic efficacy of current CKD anemia treatments is hindered by extensive adverse effects, most notably iron overload and ESA resistance. HIF-PH (hypoxia-induced factor prolyl hydroxylase) inhibitors are a novel class of orally bioavailable drugs for CKD anemia. HIF-PH inhibitors adopt a distinct mechanism, stimulating erythropoiesis via transcriptional regulation of the hypoxia-activated erythropoietin (EPO) gene. This review summarizes existing and emerging therapeutic strategies for CKD-associated anemia, with particular emphasis on HIF-PH inhibitors and their clinical potential and risks.
hypoxia-inducible factor prolyl hydroxylase inhibitors
Potential Mechanisms Underlying Ferroptosis-Associated NK Cell Dysfunction and Its Regulatory Networks in the Tumor Microenvironment
Ferroptosis is a regulated form of cell death characterized by iron-dependent lipid peroxidation. Its role in tumor immunity has attracted increasing attention in recent years. Natural killer (NK) cells are important antitumor immune effector cells, whereas metabolic reprogramming and oxidative stress in the tumor microenvironment (TME) may promote their functional exhaustion and ferroptotic cell death. This review summarizes the potential effects of cancer-associated fibroblasts (CAFs), the kynurenine metabolic pathway, and the tumor microenvironment itself on NK cell ferroptosis. Existing studies suggest that CAFs-induced NK cell ferroptosis can occur through dysregulated iron metabolism and ferritinophagy. In addition, the accumulation of kynurenine may further promote iron-dependent lipid peroxidation in NK cells. The amino acid transporter SLC7A5 may participate in this process by mediating kynurenine uptake, although direct evidence remains limited. Moreover, nutrient deprivation, lipid metabolic reprogramming, and redox imbalance in the TME may collectively increase the susceptibility of NK cells to ferroptosis. Ferroptosis of NK cells may be an important mechanism connecting tumor metabolic reprogramming and immune dysfunction, and is expected to become a new direction for immunotherapy intervention.
Pembrolizumab in the Precision Immunotherapy of Sinonasal Malignancies
Sinonasal carcinoma constitutes a rare subset of head and neck tumors. The majority of patients are diagnosed at a locally advanced stage, and the prognosis following recurrence or metastasis is extremely poor. Pembrolizumab is a humanized monoclonal antibody that targets programmed death-1 (PD-1) and reactivates T-cell-mediated antitumor immunity by disrupting the PD-1/PD-L1 signaling axis. This review systematically summarizes the research progress of this agent in treating these malignancies, focusing on its mechanism, key clinical data, current indications, and safety management. Published evidence indicates that combining this antibody with chemotherapy yields encouraging efficacy as frontline therapy for recurrent/metastatic sinonasal squamous cell carcinoma (SSCC). A phase II trial demonstrated that 12 of 20 patients achieved a response, resulting in an objective response rate (ORR) of 60% and a disease control rate (DCR) of 100%, with a median progression-free survival (PFS) of 12.2 months. Individuals with a PD-L1 combined positive score (CPS) ≥20 derived more pronounced benefit, and the overall toxicity was manageable. Future efforts should aim to refine biomarker-driven strategies, explore combination regimens, and accumulate evidence for rare pathological subtypes, thereby advancing precision immunotherapy for these tumors.
The Anti-Inflammatory Effects and Mechanisms of Baicalin on Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a common chronic autoimmune disease clinically, with persistent synovial inflammation as its core pathological feature. However, current treatment strategies often face limitations in efficacy and significant side effects. Baicalin, the main active flavonoid component of the traditional Chinese medicine Scutellaria baicalensis, possesses various pharmacological activities, including but not limited to anti-inflammatory, antioxidant, and immunomodulatory effects. This article focuses on exploring how the anti-inflammatory effect of baicalin plays a role in the treatment of RA, systematically discussing the molecular mechanism of baicalin from the perspectives of NF-κB and TLR signaling pathways and their synergistic regulatory effects, and showcasing the research progress of baicalin in current treatment. Studies have shown that baicalin can significantly downregulate the expression and release of pro-inflammatory cytokines such as TNF-α and IL-1β by inhibiting the activation of TLR2 and TLR4 receptors and blocking the TLR and NF-κB signaling pathways. Furthermore, baicalin can inhibit the abnormal proliferation of synovial fibroblasts, induce their apoptosis, alleviate synovial inflammation and pannus formation, and delay the pathological progression of rheumatoid arthritis. Currently, the main problem facing baicalin is its low bioavailability. In the future, priority should be given to researching its drug delivery system and conducting high-quality clinical trials to facilitate the clinical translation and application of baicalin in the treatment of RA.
Next-Generation HER2-Targeted ADCs: Comparative Mechanisms and Efficacy of T-DXd versus T-DM1 in Breast Cancer
Breast cancer is widely regarded as the most prevalent cancer across populations worldwide, among which HER2-positive breast cancer represents a key subtype. A comparative analysis of two prominent HER2-directed antibody–drug conjugates (ADCs), namely trastuzumab emtansine (T-DM1) and trastuzumab deruxtecan (T-DXd), is presented in this study. Both take trastuzumab as the targeting basis, but they differ significantly in payload type, linker design and drug release mode. T-DM1 mainly acts on tumor cells with high HER2 expression and can effectively internalize the drug. Its released products have poor membrane permeability with relatively limited bystander effects. In contrast, T-DXd has a higher drug-toantibody ratio. The free toxins released by it can diffuse across cell membranes, generate effects on surrounding tumor cells and produce a bystander effect. Therefore, it also shows certain strengths in overcoming tumor heterogeneity and partial drug resistance. Existing clinical studies have shown that in advanced HER2-positive breast cancer, T-DXd presents superior disease control, survival benefits and remission effects compared with T-DM1. In HER2-low expression breast cancer, T-DXd also exhibits broader application potential, while the efficacy of T-DM1 is relatively limited. In general, nextgeneration ADCs have significantly improved the efficacy of HER2-targeting therapy through structural optimization. Further improvements are still needed in reducing toxicity, delaying drug resistance and promoting individualized treatment in the future.
Molecular Mechanisms and Therapeutic Advances in Androgenetic Alopecia
Androgenetic alopecia (AGA), also known as seborrheic alopecia, is the most common type of hair loss in clinical practice, accounting for about 80% of all types of hair loss. In China, the prevalence among men and women is approximately 21.3% and 6%, respectively, affecting a wide population. Although it does not threaten physical health, it seriously impacts patients' mental health and quality of life and has shown a trend toward younger onset in recent years. This article provides a systematic review of the clinical features of AGA, influencing factors, molecular mechanisms, and mainstream drug treatment strategies, with a focus on the core roles of 5α-reductase and androgen receptor (AR) in disease pathogenesis. It explores the mechanisms of action, clinical efficacy, and safety of various drugs such as minoxidil and finasteride, and summarizes research advances in new drug delivery methods and combination therapy strategies. Studies have found that the pathogenesis of AGA is the result of multiple factors, including abnormal androgen metabolism, polygenic inheritance, and microinflammation, with the collaborative regulation of type II 5α-reductase and AR being a key link in disease development. Existing therapeutic drugs still have limitations, while new delivery methods and combination therapies can effectively improve efficacy. Personalized treatment and the exploration of new targets are future research directions. This article reviews recent research findings in the field of AGA, identifies current research shortcomings, and provides references for optimizing clinical diagnosis and treatment as well as for subsequent related studies.
Multi-target Mechanism of Action of Curcumin in Rheumatoid Arthritis and Clinical Application
Rheumatoid arthritis (RA) has become a common disease that poses a significant threat to human health, and its conventional therapeutic approaches exhibit certain limitations. In recent years, increasing attention has been directed toward the clinical application and underlying mechanisms of Curcumin in the treatment of RA. This article presents a literature review that systematically summarizes the pathogenesis of RA, the pharmacological properties of curcumin, its mechanisms of action in RA, as well as relevant clinical studies and their application within the framework of traditional Chinese medicine (TCM) syndrome differentiation. Existing evidence suggests that curcumin can effectively alleviate clinical symptoms in patients with RA and improve overall therapeutic outcomes. Its core mechanisms are primarily associated with the modulation of anti-inflammatory pathways. Meanwhile, the majority of studies have validated its role as a foundational therapeutic agent. In conclusion, curcumin demonstrates a certain degree of feasibility in the treatment of RA; however, further high-quality clinical trials are required to verify its safety and to strengthen the evidence base for its clinical feasibility.
The Treatment of Oral Squamous Cell Carcinoma with PD-1/PD-L1 Inhibitors
Oral squamous cell carcinoma (OSCC) often presents insidiously and has a high proportion of late-stage diagnosis, with a five-year survival rate of only 50% to 60% for traditional combined treatment, indicating a poor overall prognosis. Immunotherapy has now become a hotspot in tumor research, yet there are still many research shortcomings in the immunotherapy of OSCC. This article reviews the application of PD-1/PD-L1 inhibitors in OSCC. The results show that this target is highly expressed in cancer tissues, promoting tumor progression and indicating a poor prognosis. These drugs can rebuild the body's anti-tumor immunity and effectively improve the survival outcomes of patients with advanced disease and platinum resistance. However, the efficacy of monotherapy is limited, with an effective rate of only 20% to 30%, accompanied by the risk of resistance and various adverse reactions. This study provides a theoretical reference for the clinical practice of immunotherapy for OSCC. Currently, the mechanisms of resistance and individualized treatment options remain unclear. In the future, it is necessary to precisely screen suitable candidates, continuously optimize combination treatment modes, and promote the standardized development of immunotherapy for OSCC.
Molecular Mechanism and Clinical Optimization of Isotretinoin in the Treatment of Acne
Acne is a very common chronic inflammatory skin disease that can cause permanent scarring and psychological problems. Oral isotretinoin is the first choice for severe and persistent acne. To this day, the exact molecular mechanism of action is not well-known, and thus it has not been applied in clinical practice. With the latest research, this paper will systematically explain the current molecular mechanisms of isotretinoin in the treatment of acne and evaluate its clinical effect and improvement direction. Isotretinoin has some anti-inflammatory and normalising effects on the secretion of the outer layer, changes in cell division of keratinocytes, etc. Based on the above clinical studies, the usual dose of isotretinoin has good clearance in severe acne; a low-dose regimen can also be used to treat mild acne and rosacea. Combination of Laser and Phototherapy Treatment. Generally speaking, the amount of dry skin and mucous membranes after a single dose varies among individuals. Based on current research, it has not been found that isotretinoin causes depression or inflammatory bowel disease. In the future, through nanomedicine formulations, molecular modification and combination therapy, it is expected that isotretinoin will be more effective and safer.
Efficacy Analysis of Guizhi Fuling Wan in the Treatment of Primary Dysmenorrhea
Primary dysmenorrhea is a highly prevalent benign gynecological disorder among women of childbearing age. Its core pathogenesis lies in the excessive synthesis and release of endometrial prostaglandin F2α(PGF2α). Guizhi Fuling Wan(GZFLW), a classic prescription in traditional Chinese medicine (TCM) for promoting blood circulation and resolving blood stasis, has been widely used in the clinical treatment of this disease. This paper systematically reviews the molecular mechanisms and clinical evidence of GZFLW in the treatment of primary dysmenorrhea. It can alleviate uterine smooth muscle spasm and pain through effecting the Nuclear Factor-κB (NF-κB)/Cyclooxygenase-2 (COX-2)/PGF2α Signaling Pathway, downregulating Oxytocin Receptor (OTR) Protein Expression and regulating small molecules in uterine tissues, with synergetic therapeutic efficacy with Non-Steroidal Anti-inflammatory Drugs (NSAIDs) and a favorable safety profile. In view of the limitations of existing studies, which are mostly focused on combination medication and lack comparative studies with other TCM preparations. Monotherapy research can be explored in the future to improve the relevant evidence-based foundation.
Mechanisms and Clinical Application of Methotrexate in Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a systemic, chronic autoimmune disease that can severely damage the patient's joints and place a great burden on their work and life. Methotrexate (MTX) is currently the firstchoice drug for treating RA. It achieves the therapeutic goal of RA by inhibiting immune responses, promoting the release of adenosine from cells, and inhibiting angiogenesis. However, the efficacy and side effects of MTX vary significantly among individuals, and longterm, high-dose use of MTX can cause serious adverse reactions in some patients, forcing them to discontinue the medication. This article comprehensively analyzes the pathological mechanisms of RA and the molecular and cellular mechanisms of MTX on RA, concluding that the clinical efficacy of MTX and MTX combined with Wind-Dispelling and Dampness-Removing Pain-Relieving Decoction or cannabidiol (CBD) can effectively improve clinical outcomes. It provides a reference for future research on combination therapy with MTX, and the issue of the considerable differences in the clinical efficacy of MTX has not been resolved. Future research can focus on the individual differences in MTX.
The Neuroprotective Mechanism of Gastrodin in the Intervention of Alzheimer's Disease
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the core pathological features of β-amyloid (Aβ) deposition and excessive phosphorylation of Tau protein. Its pathological changes can induce oxidative stress, neuroinflammation and neuronal apoptosis, ultimately leading to cognitive dysfunction. Gastrodin, as the main active component of the traditional Chinese medicine Gastrodia elata, has attracted extensive attention due to its good blood-brain barrier penetration ability and multi-target neuroprotective effects. This article systematically reviews the molecular mechanisms and preclinical research evidence of gastrodin in the intervention of AD. At the molecular level, gastrodin exerts antioxidant stress, inhibits neuroinflammation, blocks neuronal apoptosis and protects the blood-brain barrier by regulating multiple signaling pathways. Animal experiments have shown that gastrodin can effectively reduce Aβ deposition and Tau protein phosphorylation, improve mitochondrial energy metabolism, and significantly enhance the learning and memory ability of AD model animals. In conclusion, gastrodin exerts neuroprotective effects through a multi-target network system of "antioxidant-anti-inflammatory-anti-apoptotic", showing great potential as an innovative drug for AD or a neuroprotective agent.
The Molecular Mechanisms and Current Clinical Applications of Paeoniflorin in Rheumatoid Arthritis
Rheumatoid arthritis (RA) is an autoimmune disease and a debilitating condition that significantly impacts patients’ lives, placing a considerable burden on healthcare systems and society as a whole. At the same time, natural medicinal compounds are gradually emerging as a key area of research due to their notable advantage of holistic regulation. Therefore, this paper concentrate data from a wide range of literature sources. To offers a more comprehensive perspective on the role and recent developments regarding paeoniflorin in the treatment of RA. Paeoniflorin is the principal constituent of white peony root. Research find that, the paeoniflorin exerts anti-inflammatory and antioxidant effects by modulating multiple signalling pathways and regulating relevant lncRNA. Furthermore, a highly selective inhibitor from paeoniflorin, Ritlecitinib, is currently in Phase II clinal trials. The paper according to the limitations of paeoniflorin, put forward to the prospects for its use in the treatment of RA. And it is expect that this will bring about higher therapeutic effects, reducing the economic burden.
Analysis of the Mechanism of Action and Therapeutic Efficacy of Semaglutide in the Treatment of Type 2 Diabetes Mellitus
How to control Type 2 Diabetes Mellitus (T2DM) has been one of the most important current health issues which should be given priority to. Against this background, Semaglutide has created a new breakthrough point for this predicament: while protecting the cardiovascular system and liver, it controls the patient's blood glucose level through two pathways. This article focuses on analyzing the mechanism of action of semaglutide and explores its current shortcomings. As a glucagon-like peptide-1 (GLP- 1) receptor agonist, semaglutide achieves both blood sugar lowering and weight loss via a multifaceted mechanism. In the field of T2DM treatment, large-scale clinical trials have confirmed that semaglutide not only has a strong hypoglycemic effect, but also lowers risk of hypoglycemia and clearly protect the cardiovascular, and has become the first-line choice for patients with cardiovascular diseases or high-risk factors. Future research should focus on a more comprehensive evaluation of the drug's safety, while also emphasizing its clinical benefits.
Synergistic Regulation of Glucolipid Metabolism by Ginseng Polysaccharides and Ginsenosides: Divergent Microbiota Modulation and Convergent Activation of Intestinal Gluconeogenesis
Ginseng polysaccharides (GPS) and ginsenosides are two major bioactive components of Panax ginseng, both exhibiting regulatory effects on glucolipid metabolism. Traditional research has focused on individual components, but recent evidence suggests that they may exert synergistic effects mediated by the gut microbiota [1,2]. This review systematically summarizes the mechanisms by which GPS and ginsenosides cooperatively regulate glucolipid metabolism via the gut–organ axis. The gut– organ axis is defined as the bidirectional communication network linking the gut microbiota (via its metabolites, such as short‑chain fatty acids and succinate) to distal organs (liver, pancreas, and brain). The available evidence indicates that GPS act as prebiotics, modulating gut microbiota composition, promoting short‑chain fatty acids (SCFAs) production, and enhancing the biotransformation of ginsenosides [1,6]. Ginsenosides are metabolized by the gut microbiota into highly active metabolites (e.g., Compound K) and differentially enrich Proteobacteria and succinate [2,8]. GPS and ginsenosides jointly activate intestinal gluconeogenesis (IGN) through complementary pathways (SCFAs via FFAR2/FFAR3, succinate via SUCNR1), and the resulting portal vein glucose signal further influences systemic energy homeostasis via the gut‑liver and gut‑brain axes [2,8]. This "divergent microbiota modulation–convergent target engagement" synergistic pattern provides a mechanistic explanation for the multi‑component metabolic regulation of ginseng and offers a new mechanistic perspective for the health management of metabolic diseases.
Peripheral Blood Aging-Related Gene Signatures Enable Temporal Stage Discrimination in Intracerebral Hemorrhage: An Integrative Analysis with Exploratory m6A Profiling of IRS1
Intracerebral hemorrhage (ICH) is a life-threatening neurological emergency with disproportionately high mortality and disability rates, particularly among elderly individuals. Aging is the most critical non-modifiable risk factor for ICH, yet the transcriptomic changes associated with aging during ICH temporal progression remain poorly characterized. Peripheral blood transcriptomics offers a non-invasive window into the systemic molecular response following hemorrhagic brain injury; however, no study has systematically interrogated the aging-related transcriptomic landscape across different post-ICH stages at the peripheral blood level. We retrieved the peripheral blood gene expression dataset GSE125512 from the Gene Expression Omnibus (GEO) database, comprising samples from 22 ICH patients collected at 24 hours and 72 hours post-onset. Differential expression analysis was performed using DESeq2, and the resulting differentially expressed genes (DEGs) were intersected with aging-related genes (ARGs) curated from the Human Ageing Genomic Resources (HAGR) GenAge database. The aging-related DEGs were subjected to Gene Ontology (GO) and KEGG pathway enrichment analyses, protein-protein interaction (PPI) network construction, and logistic regressionbased modeling. Cross-species validation was performed using a murine ICH single-cell RNA sequencing dataset (GSE167593). A total of 218 DEGs were identified between the 24-hour and 72-hour post-ICH groups, comprising 178 upregulated and 40 downregulated genes. Intersection with 109 ARGs yielded 6 aging-related hub genes: CD24, EGF, ICAM1, IRS1, MYB, and VEGFA. Functional enrichment analysis revealed significant enrichment in pathways related to neuroinflammation, PI3K-AKT signaling, and cellular senescence. A machine learning-based temporal unprogression model incorporating the 6 hub genes achieved an area under the receiver operating characteristic curve (AUC) of 0.70, with IRS1 and ICAM1 identified as the highest-weighted stage-discriminative features. Five of the 6 hub genes (EGF, ICAM1, IRS1, MYB, and VEGFA) demonstrated conserved expression in the murine ICH single-cell dataset, with CD24 showing species-specific absence potentially attributable to ortholog nomenclature differences or low cell-type-specific expression. This study presents a systematic characterization of aging-related transcriptomic dysregulation in ICH and identifies a 6-gene peripheral blood signature associated with temporal stage discrimination. The identified hub genes—particularly CD24, ICAM1, and VEGFA—show a potential regulatory association with neuroinflammation, blood-brain barrier disruption, and vascular remodeling pathways altered during ICH progression in the context of aging. This integrative bioinformatics and machine learning framework may provide a useful reference for aging-related biomarker discovery in hemorrhagic stroke and related neurological disorders.
The Neuroscience of Mindful Tea Rituals: Effects on Attention and Learning
The paper is about the impact of mindfulness-based tea brewing rituals on attention and learning through the physiological events that take place in the brain, particularly in the prefrontal cortex. It discusses what the studies have to say about the functions, brain waves, prediction errors, and the effects of the compounds in tea on the brain. Some studies have shown that attention, in a certain way, can improve the functioning of the prefrontal cortex of the brain, quiet the noise in the brain, and increase cognitive control. Moreover, the compounds in tea, such as L-theanine, can also have an impact on the brain, making the individual calm yet alert, which is important for maintaining attention. Therefore, the physiological events that take place in the body due to tea can help maintain the brain in an optimal state for learning.
Exploring the Role of Dopamine in Curiosity-Driven Learning Using Reinforcement Learning Models
Curiosity-driven learning is a core feature of biological intelligence, manifested in the active exploration of environments by organisms even in the absence of external rewards. This study integrates neurobiological findings with reinforcement learning theory to construct a unified computational framework that reconceptualizes dopamine as an encoder of "total prediction error." In this framework, behavioral selection maximizes total value, which comprises both external rewards and intrinsic informational value. Intrinsic rewards are quantified based on novelty or prediction error, while the weight assigned to exploration is dynamically modulated by the prefrontal cortex. Dopamine neurons encode total prediction error, thereby extending the conventional role of dopamine from a reward prediction error encoder to a more general encoder of violated expectations. The hippocampus generates intrinsic reward signals, the prefrontal cortex regulates the exploration weight, the ventral tegmental area integrates these signals to compute total prediction error, and the striatum translates this error into action selection. This model bridges the explanatory gap between neuroscience and computational theory, offering a unified perspective on the intrinsic motivation underlying curiosity and exploratory behavior. In practical terms, it also provides new insights into the mechanisms of psychiatric disorders.
Mechanisms of Molecular Glue Degraders and Their Applications in Hematological Malignancies
Molecular glue degraders (MGDs) belong to a category of small-molecule compounds that bring E3 ubiquitin ligases and target proteins close to each other, thereby initiating the ubiquitination process and the subsequent breakdown of the target proteins. In the past few years, these substances have shown considerable therapeutic potential in the treatment of hematological malignancies. This review comprehensively summarizes the action mechanisms of MGDs, sorts out their preclinical and clinical advances in hematological cancers, and explores the existing challenges as well as future development directions. MGDs offer a new approach for cancer treatment, yet further research is needed to clarify their resistance mechanisms and improve the precision of target selection.
Multifactorial Pathogenesis, Diagnosis, and Therapeutic Strategies in Alzheimer’s Disease
Alzheimer's disease (AD) has traditionally been explained by the amyloid cascade hypothesis as its core mechanism. However, the limitations of single-target therapies reflect that AD cannot be simply explained by a linear pathogenic mechanism. This review examines key mechanisms including the Aβ-tau axis, neuroinflammation, genetic factors, and mitochondrial metabolic abnormalities, proposing that AD pathogenesis should instead be modeled as a multifactorial pathological network. Different pathological nodes amplify disease severity collectively, with multiple factors synergistically driving neuronal network dysfunction and cognitive decline. The review also examines trends in blood biomarkers, imaging, and digital metrics, exploring stratified diagnostics and nodetargeted therapies for multifactorial pathogenesis. This model integrates diverse mechanisms into a comprehensive disease network, providing a theoretical foundation for precision medicine.