Stroke is the leading cause of death and disability among adults in China， and its common complications include digestive system abnormalities， cognitive impairment， depression， stroke-associated pneumonia， and hemiplegia. The combination of traditional Chinese and Western medicine has great potential in treating post-stroke complications. Xinglou Chengqitang （XLCQT） is a representative prescription of alleviating the disease in the upper part by treating the lower part. It has definite therapeutic effect and high safety. Clinically， XLCQT is often used to treat stroke and its complications. However， the quantity and quality of clinical trials of XLCQT in treating post-stroke complications need to be improved. Additionally， since the basic research is weak， the material basis and multi-target mechanism for the efficacy of this prescription are unknown. This article reviews XLCQT in terms of the pharmacodynamic basis， medicinal properties， safety evaluation， and progress in clinical research and mechanisms in treating post-stroke complications. This article summarizes 22 key active ingredients of XLCQT in treating acute stroke complicated with syndrome of phlegm heat and fu-organ excess. Among these key active ingredients， resveratrol， kaempferol， luteolin， chrysoeriol， apigenin， （+）-catechin， and adenosine have good pharmacokinetic properties and high bioavailability. The mechanisms of XLCQT in treating post-stroke complications are complex， including inflammatory response， brain-gut axis， hypothalamic-pituitary-adrenal （HPA） axis， intestinal flora， neurotrophic factors， autophagy， oxidative stress， and free radical damage. This review helps to deeply understand the pharmacodynamic basis and mechanisms of XLCQT in treating post-stroke complications and provides a theoretical basis for the clinical application of XLCQT against post-stroke complications and the development of drugs.

Obesity and its related metabolic diseases have become a major global public health threat, and its rising incidence significantly increases the risk of cardiovascular and cerebrovascular diseases, diabetes and other complications. Pancreatic lipase is a key enzyme that converts food-borne lipids into triglycerides and fatty acids, and the effective inhibition of its activity has become an important strategy for the treatment of obesity. This paper discusses the screening methods of pancreatic lipase inhibitors, and summarizes and reviews the basic principles, advantages and disadvantages and application status of traditional screening methods, modern new screening methods and virtual screening methods. In view of the problems faced by the screening methods of pancreatic lipase inhibitors, future research urgently needs to move towards a collaborative innovation path of multi-technology integration, intelligent screening and complex systematization of traditional Chinese medicine, so as to open up new research paradigms.

ObjectiveTo investigate the protective effect and underlying mechanisms of Yishen Huayu prescription （YSHYP） on transdifferentiation of mouse renal tubular epithelial cells （TCMK-1） induced by transforming growth factor-β₁ （TGF-β₁）. MethodsA transdifferentiation model was established by treating TCMK-1 cells with 10 μg·L^-1 TGF-β₁. Experimental groups were established using 2 μmol·L^-1 silent information regulator 1 （SIRT1） inhibitor EX527. These included the blank group， model group， YSHYP group （treated with 10% YSHYP-medicated serum）， valsartan group （treated with 10% valsartan-medicated serum）， EX527+TGF-β₁ group， EX527+YSHYP group， and EX527 group. Immunofluorescence was used to detect the protein localization of α-smooth muscle actin （α-SMA）， E-cadherin， and microtubule-associated protein light chain 3 （LC3）. Western blot and Real-time polymerase chain reaction （Real-time PCR） were used to assess the expression of proteins and mRNA related to transdifferentiation， autophagy， and associated signaling pathways. ResultsThe results from Real-time PCR and Western blot indicate that compared with those in the blank group， expression levels of α-SMA， ubiquitin-binding protein p62 （p62）， and acetylated forkhead box protein O1（Ac-FoxO1） were significantly increased in the model group， EX527+TGF-β₁ group， and EX527 group （P<0.01）. Compared with that in the model group， the expression of α-SMA and p62 were significantly downregulated in the YSHYP and valsartan groups （P<0.05， P<0.01）. Ac-FoxO1 protein levels were significantly reduced in the YSHYP group （P<0.05）， while the valsartan group showed no significant changes in Ac-FoxO1 levels. Compared with the YSHYP group， the valsartan group showed significant differences in p62 mRNA， α-SMA， and p62 protein expression （P<0.05）. Compared with those in the blank group， LC3， Beclin1， SIRT1， and forkhead box protein O1 （FoxO1） expression levels were significantly decreased in the model group， EX527+TGF-β₁ group， and EX527 group （P<0.01）. In the model and EX527+TGF-β₁ groups， E-cadherin expression levels were significantly reduced （P<0.01）， while the EX527 group showed no statistically significant change. Compared with the model group， E-cadherin， LC3， Beclin1， SIRT1， and FoxO1 expression levels were significantly increased in both the YSHYP and valsartan groups （P<0.01， P<0.05）. Compared with the YSHYP group， the valsartan group exhibited significant differences in LC3， SIRT1， and FoxO1 mRNA expression （P<0.05， P<0.01）. Immunofluorescence results were consistent with those of Western blot and Real-time PCR. ConclusionYSHYP may protect TCMK-1 cells by activating the SIRT1/FoxO1 pathway， thereby promoting autophagy and restoring the autophagy flux to reduce the extent of transdifferentiation of TCMK-1 cells.

ObjectiveTo investigate the protective effect and underlying mechanisms of Yishen Huayu prescription （YSHYP） on transdifferentiation of mouse renal tubular epithelial cells （TCMK-1） induced by transforming growth factor-β₁ （TGF-β₁）. MethodsA transdifferentiation model was established by treating TCMK-1 cells with 10 μg·L^-1 TGF-β₁. Experimental groups were established using 2 μmol·L^-1 silent information regulator 1 （SIRT1） inhibitor EX527. These included the blank group， model group， YSHYP group （treated with 10% YSHYP-medicated serum）， valsartan group （treated with 10% valsartan-medicated serum）， EX527+TGF-β₁ group， EX527+YSHYP group， and EX527 group. Immunofluorescence was used to detect the protein localization of α-smooth muscle actin （α-SMA）， E-cadherin， and microtubule-associated protein light chain 3 （LC3）. Western blot and Real-time polymerase chain reaction （Real-time PCR） were used to assess the expression of proteins and mRNA related to transdifferentiation， autophagy， and associated signaling pathways. ResultsThe results from Real-time PCR and Western blot indicate that compared with those in the blank group， expression levels of α-SMA， ubiquitin-binding protein p62 （p62）， and acetylated forkhead box protein O1（Ac-FoxO1） were significantly increased in the model group， EX527+TGF-β₁ group， and EX527 group （P<0.01）. Compared with that in the model group， the expression of α-SMA and p62 were significantly downregulated in the YSHYP and valsartan groups （P<0.05， P<0.01）. Ac-FoxO1 protein levels were significantly reduced in the YSHYP group （P<0.05）， while the valsartan group showed no significant changes in Ac-FoxO1 levels. Compared with the YSHYP group， the valsartan group showed significant differences in p62 mRNA， α-SMA， and p62 protein expression （P<0.05）. Compared with those in the blank group， LC3， Beclin1， SIRT1， and forkhead box protein O1 （FoxO1） expression levels were significantly decreased in the model group， EX527+TGF-β₁ group， and EX527 group （P<0.01）. In the model and EX527+TGF-β₁ groups， E-cadherin expression levels were significantly reduced （P<0.01）， while the EX527 group showed no statistically significant change. Compared with the model group， E-cadherin， LC3， Beclin1， SIRT1， and FoxO1 expression levels were significantly increased in both the YSHYP and valsartan groups （P<0.01， P<0.05）. Compared with the YSHYP group， the valsartan group exhibited significant differences in LC3， SIRT1， and FoxO1 mRNA expression （P<0.05， P<0.01）. Immunofluorescence results were consistent with those of Western blot and Real-time PCR. ConclusionYSHYP may protect TCMK-1 cells by activating the SIRT1/FoxO1 pathway， thereby promoting autophagy and restoring the autophagy flux to reduce the extent of transdifferentiation of TCMK-1 cells.

Objective To investigate the clinical relevance and diagnostic or prognostic value of ST3β-galactoside α-2, 3-sialyltransferase 1 (ST3GAL1) in glioma and to confirm its role in promoting malignant phenotypes. Methods Using data from The Cancer Genome Atlas (TCGA) database, we analyzed the correlation between ST3GAL1 expression levels in glioma and clinical parameters to evaluate its diagnostic and prognostic value. The impact of ST3GAL1 on malignant phenotypes of glioma cells-including proliferation, cell cycle progression, apoptosis, and invasion was further validated through ST3GAL1 knockdown experiments. Results The expression level of ST3GAL1 was significantly higher in glioma tissues compared to healthy brain tissues and showed a strong correlation with clinical characteristics of glioma patients. Survival analysis and receiver operating characteristic (ROC) curve demonstrated that ST3GAL1 could serve as a potential diagnostic and prognostic biomarker for glioma. Knockdown of ST3GAL1 suppressed proliferation, invasion, and migration capabilities of glioma cell lines, and induced G1-phase cell cycle arrest. Conclusion ST3GAL1 promotes malignant phenotypes in glioma and plays a critical role in its malignant progression, suggesting its potential as a biomarker for glioma diagnosis and prognosis.
Humans ; Sialyltransferases/metabolism* ; Glioma/diagnosis* ; Cell Proliferation/genetics* ; Cell Line, Tumor ; Brain Neoplasms/enzymology* ; beta-Galactoside alpha-2,3-Sialyltransferase ; Disease Progression ; Prognosis ; Cell Movement/genetics* ; Apoptosis/genetics* ; Male ; Female ; Gene Expression Regulation, Neoplastic ; Biomarkers, Tumor/metabolism* ; Middle Aged

Zebrafish larvae are useful for identifying chemicals against lateral line (LL) hair cell (HC) damage and this type of chemical screen mainly focuses on searching for protectors against cell death. To expand the candidate pool of HC protectors, a self-built acoustic escape response (AER)-detecting system was developed to apply both low-frequency near-field sound transmission and AER image acquisition/processing modules. The device quickly confirmed the changed LL HC functions caused by most known ototoxins, protectors, and neural transmission modifiers, or knockdown of LL HC-expressing genes. With ten devices wired in tandem, five 'hit' chemicals were identified from 124 cyclin-dependent kinase inhibitors to partially restore cisplatin-damaged AER in less than a day. AS2863619, ribociclib, and SU9516 among the hits, protected the HCs in the mouse cochlea. Therefore, using free-swimming larval zebrafish, the self-made AER-detecting device can efficiently identify compounds that are protective against HC damage, including cell death and loss-of-function.
Animals ; Zebrafish ; Hair Cells, Auditory/physiology* ; Lateral Line System/cytology* ; Escape Reaction/physiology* ; Larva ; Mice ; Cisplatin/toxicity* ; Drug Evaluation, Preclinical/methods*

Microglial functions are linked to Ca²⁺ signaling, with endoplasmic reticulum (ER) calcium stores playing a crucial role. Microglial abnormality is a hallmark of Alzheimer's disease (AD), but how ER Ca²⁺ receptors regulate microglial functions under physiological and AD conditions remains unclear. We found reduced ryanodine receptor 2 (Ryr2) expression in microglia from an AD mouse model. Modulation of RyR2 using S107, a RyR-Calstabin stabilizer, blunted spontaneous Ca²⁺ transients in controls and normalized Ca²⁺ transients in AD mice. S107 enhanced ATP-induced migration and phagocytosis while reducing ramification in control microglia; however, these effects were absent in AD microglia. Our findings indicate that RyR2 stabilization promotes an activation state shift in control microglia, a mechanism impaired in AD. These results highlight the role of ER Ca²⁺ receptors in both homeostatic and AD microglia, providing insights into microglial Ca²⁺ malfunctions in AD.
Animals ; Microglia/pathology* ; Alzheimer Disease/pathology* ; Phagocytosis/drug effects* ; Ryanodine Receptor Calcium Release Channel/metabolism* ; Disease Models, Animal ; Mice ; Cell Movement/drug effects* ; Mice, Transgenic ; Calcium Signaling/physiology* ; Calcium/metabolism* ; Mice, Inbred C57BL ; Male ; Endoplasmic Reticulum/metabolism*

Cerebral small vessel disease represents a group of common vascular disorders involving pathological changes in arterioles,capillaries and venules,with microvascular investigation remaining a key challenge in stroke.With high signal-to-noise ratio and high contrast enabled by enhanced field strength,7T MRI can surpass the resolution limits of 3T MRI,revealing structural and functional abnormalities in cerebral small vessels below 400 μm,as well as detecting subtle lesions in brain tissue.This paper reviews the research progress of multimodal high-resolution imaging techniques based on 7T MRI,such as time-of-flight angiography,phase contrast imaging and susceptibility imaging,in the study of cerebral small vessel disease.Utilizing these technologies,7T MRI can clearly display the structure of cerebral small vessels,such as the lenticulostriate arteries and deep medullary veins,and measure functional parameters like flow velocity and susceptibility.Additionally,it can sensitively detect cerebral microbleeds and cortical cerebral microinfarct.These imaging data provide valuable information for detecting early features of cerebral small vessel disease and assessing its progression,offering new insights into its pathogenesis.Combined with artificial intelligence-based image analysis methods,7T MRI holds great promise for early diagnosis and progression evaluation in cerebral small vessel disease.

Objective To investigate the short-term efficacy of arthroscopic total internal suture combined with platelet-rich plasma(PRP)in the treatment of lateral meniscal popliteal hiatus area injuries.Methods Forty-eight patients diagnosed with lateral meniscal popliteal hiatus area injuries in our hospital from January 2020 to December 2022 were selected and divided into Fast-Fix total internal suture group(FF group,n=23)and Fast-Fix total internal suture combined with PRP group(PRP group,n=25)according to treatment methods.The positive rate of McMurray test at 6 and 12 months after surgery,the preoperative and postoperative visual analogue scale(VAS)of pain,the International Knee Documentation Committee(IKDC)scores,the Lysholm Knee Function Scores,and the Knee Society Scores(KSS)were compared between the two groups.Results No adverse events such as vascular and nerve injury,fever and infection occurred in both groups.There was no significant difference between the two groups in the positive rates of McMurray test at 6 and 12 months(χ2=0.880,P=0.348;Fisher's exact test,P=0.479).In the PRP group,25 cases were followed up for11-14 months,with an average of(12.2±0.8)months;in the FF group,23 cases were followed up for11-14 months,with an average of(12.8±0.8)months.The VAS scores at 6 months and 12 months after surgery were significantly lower than those before surgery in both groups(all P=0.000).The VAS scores of the PRP group at 6 and 12 months after surgery were significantly lower than those of the FF group(P<0.05).Both groups showed significant improvements in IKDC,Lysholm,and KSS scores at 6 and 12 months after surgery compared to preoperative levels(all P=0.000).The IKDC,Lysholm,and KSS scores of the PRP group at 6 and 12 months after surgery were significantly higher than those of the FF group(P<0.05).Conclusion Compared to Fast-Fix total internal suture alone,PRP joint cavity adjuvant therapy based on Fast-Fix total internal suture surgery could reduce the postoperative pain of patients,and promote the functional recovery of the knee joint,which is more recommended in clinical practice.

With the advancement of the "New Medical Science" reform, the "Medicine+X" model has emerged as a key direction for the future development of medical education. Multidisciplinary integration places higher demands on both educators and students. Emerging technologies, such as intelligent tutoring systems, adaptive learning platforms, intelligent campus management systems, and ChatGPT, have made personalized learning possible. Such approaches offer notable advantages, including improving learning efficiency, enhancing motivation, eliminating the spatiotemporal constraints of clinical education, and alleviating teachers′ workloads. Nevertheless, the application of artificial intelligence in personalized medical education still faces multiple challenges, such as issues of data quality and reliability, the need for faculty development, shifts in educational paradigms, and ethical considerations. This study explored the current status of artificial intelligence in personalized medical education and offered recommendations to promote its development, including strengthening the integration of technology and education, enhancing the digital literacy of educators, establishing ethical guidelines, and fostering multi-stakeholder collaboration.