Platelets are small, anucleated cells generated by cytoplasmic fragmentation and shedding from mature megakaryocytes. Upon vascular stimulation or injury, platelets become activated and adhere to exposed vascular endothelial cells, ultimately forming thrombi to promote blood coagulation and wound healing. In recent years, increasing evidence from in-depth studies on platelet function has revealed that autophagy plays a crucial role in platelet production and functional performance. Autophagy is an intracellular process of material recycling and reuse, involving autophagosome formation, cargo degradation, and nutrient recycling, which facilitates the maintenance of homeostasis and defense against pathogen infection. Numerous studies have demonstrated that autophagy participates in the regulation of platelet production, activation, and aggregation, and is closely implicated in the pathogenesis of platelet dysfunction-related diseases such as immune thrombocytopenia. Additionally, platelet-rich plasma therapy, by modulating the autophagic process, has shown great potential in treating osteoarthritis and promoting diabetic foot wound healing. This review thoroughly explores the potential roles of autophagy in regulating platelet production and function, as well as in platelet-related diseases. Future research should focus on the molecular mechanisms of platelet autophagy, investigate its dynamic changes under different disease conditions, and explore how autophagy modulation can improve platelet function and treat related diseases. This will provide a theoretical foundation for developing novel therapeutic strategies and is expected to bring breakthroughs in the treatment of platelet-related diseases.

Hypertension ranks among the most prevalent chronic non-communicable diseases worldwide, with its prevalence rising steadily and exerting substantial impacts on the demographic composition of voluntary blood donors and the safety of blood supply. The eligibility of hypertensive individuals for safe blood donation and the relevant screening and management strategies have long remained controversial in transfusion medicine. This article systematically reviews the epidemiological characteristics of hypertension, donation-related physiological alterations and underlying risk mechanisms. By synthesizing evidence from international multicenter studies and regulatory practices across major nations, it conducts a comprehensive analysis of blood donation safety and donor admission criteria for hypertensive patients. Available evidence demonstrates that for hypertensives with well-stabilized blood pressure and no severe cardiac, cerebral or renal complications or target organ damage, the overall incidence of adverse reactions following blood donation is comparable to that in healthy donors, and no definitive correlation has been identified between blood pressure levels and vasovagal responses. Current mainstream international management frameworks are gradually shifting from screening reliant on a single blood pressure cutoff value toward an integrated strategy combining stratified risk classification and individualized dynamic assessment, with core focus on long-term blood pressure control, consistency of medication regimens and complication status. Meanwhile, emerging technologies including artificial intelligence, ambulatory blood pressure monitoring and wearable devices have opened innovative avenues for blood donation risk evaluation and full-cycle donor management. In light of existing clinical evidence, future efforts should further refine the multi-dimensional risk stratification system, facilitate the implementation of intelligent screening and continuous monitoring technologies, and scale up health education and follow-up management for hypertensive populations. Such measures aim to appropriately expand the pool of eligible blood donors while safeguarding donation safety, ultimately achieving coordinated improvement in blood safety and blood supply capacity.

Alzheimer's disease （AD） is a chronic neurodegenerative disorder with an unclear pathogenesis and currently no cure. It is characterized by a long disease course， diverse symptoms， and a persistent， difficult-to-treat nature， which greatly affects the quality of life of elderly patients. Traditional Chinese medicine （TCM） offers significant advantages in the treatment of AD， featuring multi-component， multi-target， and multi-pathway characteristics， with few adverse reactions and good safety. Angelica sinensis is a commonly used medicinal herb. As a frequently used clinical medicine for nourishing and activating blood， it shows significant efficacy in treating blood deficiency syndrome. In recent years， studies have revealed that A. sinensis exhibits significant activity in the prevention and treatment of AD. It contains various active components such as organic acids， volatile oils， and polysaccharides， and possesses pharmacological effects including anti-inflammatory， antioxidant， hepatoprotective， and neuroprotective properties. This article summarizes and outlines the mechanisms of A. sinensis and its compound formulas in the prevention and treatment of AD， providing a reference for its clinical application and the treatment of AD.

The recombinant human thyroid-stimulating hormone (rhTSH) can be used for differentiated thyroid cancer (DTC) preparation before ¹³¹I therapy, and follow-up. Since its approval by the American Food and Drug Administration (FDA) in 1998, rhTSH has been clinically used in European countries, the United States, and other countries for nearly 30 years. In April 2024, China’s first independently developed rhTSH agent was approved. Based on clinical experience and evidence from domestic and international studies, an expert consensus on the application of rhTSH has been developed following thorough consultations among experts. The consensus offers evidence-based recommendations to guide the appropriate use of rhTSH in clinical practice.

Objective:To investigate the association of monocyte-to-high-density lipoprotein cholesterol ratio (MHR) with the severity of white matter hyperintensities (WMHs) and its spatial distribution.Methods:Patients admitted to the Department of Neurology, Jiangning Hospital Affiliated to Nanjing Medical University due to various chronic diseases or physical examinations between January 2023 and December 2024 were included retrospectively. Past medical history, clinical and imaging data were collected. The Fazekas scale was used to assess the severity of WMHs. According to the scoring results of periventricular WMHs (PVWMHs) and deep WMHs (DWMHs), WMHs were divided into no/mild group (0-1 points) and moderate/severe group (2-3 points). Multivariate logistic regression analysis was used to determine independent correlation factors for the severity of WMHs, PVWMHs, and DWMHs. Results:A total of 357 patients were included, aged 65.42±9.95 years, with 198 males (55.5%). There were 193 patients (54.1%) in the no/mild group and 164 (45.9%) in the moderate/severe group. Univariate analysis showed that the proportion of patients with hypertension, diabetes, history of cerebral infarction and cerebral hemorrhage, carotid plaque, and age, serum creatinine, monocyte count and MHR in the moderate/severe group were significantly higher than those in the no/mild group (all P<0.05). Multivariate logistic regression analysis showed a significant positive correlation between MHR and the severity of WMHs (odds ratio 3.138, 95% confidence interval 1.042-9.451; P=0.042). Further analysis showed a significant positive correlation between MHR and PVWMHs (odds ratio 3.384, 95% confidence interval 1.111-10.305; P=0.032), but no independent correlation with DWMHs. In addition, age and hypertension, diabetes, history of cerebral infarction and cerebral hemorrhage were significantly positively correlated with the severity of WMHs, PVWMHs and DWMHs. Conclusion:MHR is correlated with the severity of WMHs, and higher MHR is significantly associated with PVWMHs, but not with DWMHs.

Objective:To investigate the correlation between body mass index (BMI)/high-density lipoprotein cholesterol (HDL-C) ratio and cerebral small vessel disease (CSVD) in middle-aged and elderly people.Methods:Consecutive middle-aged and elderly patients (aged ≥40 years) who were hospitalized for chronic disease examinations in the Department of Neurology, Jiangning Hospital Affiliated to Nanjing Medical University between February 2022 and May 2024 were included prospectively. According to the overall burden score of CSVD, they were divided into CSVD group (≥1) and non-CSVD group (0). According to age, they divided into middle-aged group (40-59 years old) and elderly group (≥60 years old). The demographic characteristics and clinical data were collected. Binary multivariate logistic regression analysis was used to determine the independent correlation between BMI/HDL-C ratio and CSVD. Forest plot was used to analyze the correlation between BMI/HDL-C ratio and CSVD in different age groups. Results:A total of 710 patients were included, with an age of 66.0±10.0 years and 361 were males (50.8%). There were 261 patients (36.8%) in the CSVD group and 449 (63.2%) in the non-CSVD group. The BMI/HDL-C ratio in the CSVD group was significantly higher than that in the non-CSVD group (23.60±7.00 vs. 20.78±6.40; P<0.001). Multivariate logistic regression analysis showed that BMI/HDL-C ratio was an independent risk factor for CSVD in middle-aged and elderly populations (odds ratio 1.046, 95% confidence interval 1.027-1.064; P<0.001). There were 475 patients in the elderly group, of which 198 (41.7%) had CSVD; there were 235 patients in the middle-aged group, of which 63 (26.8%) had CSVD. Forest plot analysis showed that the association between BMI/HDL-C ratio and CSVD still had statistical significance in different age groups, but the effect intensity was higher in the elderly group than in the middle-aged group. Conclusion:The BMI/HDL-C ratio is independently correlated with CSVD in middle-aged and elderly population, particularly significant in the elderly population.

After the onset of ischemic stroke, microglia undergo lipid metabolic reprogramming, especially lipid droplet accumulation, which significantly affects their polarization state and inflammatory response. Lipid droplets can exacerbate neuroinflammation by synthesizing inflammatory lipid mediators, and may also have a protective effect under certain conditions. Its metabolic reprogramming involves multiple pathway regulation such as fatty acid oxidation and cholesterol efflux. This article reviews the mechanism of changes in lipid droplet metabolism of microglia and its role in the pathological process after stroke, aiming to provide new ideas for metabolic intervention strategies.

Objective To investigate the mechanism by which Biejiajian Pill(BJJP)regulates ferroptosis in hepatocellular carcinoma(HCC)cells through the p62/Keap1/NRF2 pathway and to provide an experimental basis for its application in the prevention and treatment of HCC.Methods Huh7 HCC cells were divided into a normal control group,a BJJP drug serum group,an erastin(a ferroptosis inducer)group,a BJJP drug serum+erastin group,and BJJP drug serum+ferrostatin-1(Fer-1)(a ferroptosis inhibitor)group.BJJP drug serum was prepared with animals treated with BJJP and CCK-8 assay was performed to determine the optimal concentration and duration of BJJP intervention.The levels of intracellular iron(Fe),reduced glutathione(GSH),lipid peroxides(MDA),and reactive oxygen species(ROS)were measured.Western blot was performed to determine the expression levels of FTH1,GPX4,xCT,SLC40A1,Keapl,p62,and NRF2.JC-1 staining was performed to measure mitochondrial membrane potential,and cell immunofluorescence was performed to determine the expression of p62 and Keap1.Results According to the CCK-8 assay results,the cell inhibition rate was highest when BJJP was administered at a high dose of 2.2 g/kg(P＜0.001).Furthermore,the inhibition rate of Huh7 cells was highest when Huh7 cells were treated with high-dose BJJP drug serum for 48 h.Therefore,the serum concentration of high-dose BJJP and 48 h were selected as the treatment dose and duration for the subsequent experiment.Compared with the control group,the BJJP drug serum group,the erastin group,and the BJJP drug serum+erastin group showed increased iron content,decreased GSH content,increased MDA levels,increased ROS aggregation,decreased FTH1,GPX4,xCT,SLC40A1,p62,and NRF2 contents,increased Keap1 content,and decreased mitochondrial membrane potential(P＜0.05).Conclusion BJJP regulates ferroptosis in Huh7 HCC cells by inhibiting the p62/Keap1/NRF2 pathway,demonstrating potentials as a therapeutic agent for HCC.

Objective To prepare a dissolvable microneedle(MN)patch loaded with sodium houttuyfonate(SH)combined with erythromycin(ERY)(SH+ERY-MN patch),to characterize its properties,and to investigate its synergistic anti-acne effects and the mechanisms involved.Methods The SH+ERY-MN patch was prepared by two-step centrifugation.The morphology and skin puncture performance of the microneedles were evaluated using scanning electron microscopy,puncture tests,and other methods.The combined antibacterial effect was assessed using the checkerboard assay.The in vitro anti-inflammatory effect of the SH+ERY-MN patch was evaluated by quantitative PCR(qPCR)and enzyme-linked immunosorbent assay(ELISA).The therapeutic effect of the SH+ERY-MN patch on acnes in mice was investigated using an animal model.Results The microneedle patch prepared in the study had well-aligned microneedles,excellent needle shape,and good mechanical properties,which could effectively penetrate the skin to reach the superficial dermis.The minimum inhibitory concentration(MIC)of ERY against acne was 1.28 mg/mL.When ERY was combined with SH,the results showed that the fractional inhibitory concentration(FIC)was 0.375,indicating that the medication combination had a synergistic antibacterial effect.In particular,the MIC value of ERY in combination was 1/4 of that of ERY used alone.The results of in vitro qPCR showed that SH+ERY-MN could downregulate the production of interleukin(IL)-1β,IL-18,tumor necrosis factor α(TNF-α),inhibitor of κB(I-κB),Toll-like receptor 4(TLR4),NLR family pyrin domain containing 3(NLRP3),and cysteine-aspartic proteases(Caspase-1)induced by Propionibacterium acnes(PA)in cell culture supernatant(P＜0.05).According to the in vivo findings,SH+ERY-MN had a significant anti-acne effect and effectively alleviated cytokine-mediated inflammatory responses.The results of qPCR and ELISA showed that SH+ERY-MN could effectively reduce the levels of IL-1β,IL-18,NLRP3,and Caspase-1 in the serum of the mouse acne inflammation model(P＜0.01),and had good antibacterial and anti-inflammatory effects.Conclusion SH+ERY-MN patch was successfully prepared and demonstrated obvious anti-acne effects.The SH+ERY-MN patch enhances the transdermal delivery of SH combined with ERY.It provides an innovative method for acne treatment and creates new possibilities for achieving effective drug delivery and improving therapeutic efficacy.

Objective To establish a homozygous zebrafish map3k15 knockout line using CRISPR/Cas9 gene editing technology so to provide an animal model for investigation of potential role of map3k15 in renal diseases.Methods 1)Analyzing the expression pattern of map3k15 in zebrafish;2)Establishing a homozygous map3k15 knockout zebrafish line using CRISPR/Cas9;3)Observing the phenotypic effects of map3k15 deficiency in ze-brafish.Results 1)map3k15 was expressed in the zebrafish pronephros,and map3k15/map3k15 protein was found highly conserved across species;2)map3k15-/-mutant zebrafish model was constructed with+2 bp mutation and+1 bp mutation;3)map3k15 mutant zebrafish exhibited edema in yolk sac,pericardium and head during embryonic development.Conclusions A homozygous zebrafish map3k15 knockout line is successfully developed which may provide an important model for future research on the role of map3k15 in renal development and disease.