OBJECTIVE To systematically review the status on pharmacist competency assessment tools both domestically and internationally， providing a theoretical basis for constructing scientific and applicable pharmacist competency assessment tools in China. METHODS Through literature review and comparative analysis， 15 representative domestic and international pharmacist competency assessment tools were systematically summarized， and their theoretical foundations， core dimensions， methodological characteristics and practical applications were compared and implications were given. RESULTS &CONCLUSIONS International research has established relatively mature evaluation systems. Represented by those developed from the United Kingdom， the United States， and the International Pharmaceutical Federation， these assessment tools demonstrate scientific structure， wide application， and dynamic and international applicability. While domestic research has progressed in sub-specialties such as clinical pharmacists， licensed pharmacists and pediatric pharmacists， it still faces challenges including insufficient standardization， inadequate validation， delayed updates， and limitations in practical application. The reasons for the disparities in assessment tools between China and other countries include differences in pharmaceutical care models， varying pharmacist training systems， cultural and social background factors， as well as differences in industry management and international influence. Based on this， the author suggests promoting the development and research of assessment tools for pharmacist job competency in China from four aspects： mechanism construction， system refinement， standardization development， and practical implementation.

Objective To investigate the association between physical activity levels and blood lipids among college freshmen, and to provide scientific evidence for the health management of college freshmen. Methods An electronic questionnaire survey on physical activity was conducted on freshmen of a university, and fasting blood biochemical indicators were detected. The International Physical Activity Questionnaire (IPAQ) short form was used to evaluate the physical activity levels of the participants. Dyslipidemia was defined as an abnormality in any one of the following serum lipid parameters: total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), or non-high-density lipoprotein cholesterol. Binary logistic regression and stratified analyses were employed to explore the relationship between physical activity and blood lipids. Results A total of 3 401 participants were included, with an average age of 18.45 ± 0.92 years, and 60.5% were female. The prevalence of dyslipidemia was 17.7%, with a higher rate among males (22.1%) than females (14.8%). After adjusting for confounding factors related to blood lipids, high-intensity physical activity was negatively associated with the risk of elevated LDL-C among males (OR = 0.36, 95% CI: 0.13–0.99, P = 0.049). Conclusion Among freshmen at a medical college in Hubei Province, high-intensity physical activity is negatively associated with the risk of elevated LDL-C in males, but this association needs to be further confirmed by larger prospective cohort studies.

The therapeutic effect of human umbilical cord mesenchymal stem cells (hUCMSCs) combined with intestinal probiotics on the wound healing of diabetic mice and its potential mechanism were explored. A diabetic wound mouse model was established, and 25 male C57BL/6J mice were randomly divided into five groups: blank control group, model group, hUCMSCs treatment group, probiotics treatment group, and hUCMSCs combined with probiotics treatment group. The wound healing conditions were photographed and recorded on days 0, 3, 6, 9, and 12 after modeling, and the differences in wound healing rates among the groups were analyzed. HE and Masson staining were used to observe the histopathological changes and collagen deposition. CD31 immunofluorescence was used to detect angiogenesis. Collagen I immunohistochemistry was used to evaluate the formation of type I collagen. ELISA was used to detect the expression levels of anti-inflammatory factors (Arg1) and pro-inflammatory factors (IL-6, IL-1β, TNF-α) in wounded skin tissue and serum. The results showed that on day 12 after modeling, compared with the other groups, the combined treatment group had the most significant wound contraction and the fastest healing rate. HE and Masson staining showed that the combined treatment group had the fastest epithelialization and the most collagen deposition. Immunofluorescence and immunohistochemistry showed that the combined treatment group had the highest expression levels of CD31 and Collagen I. ELISA results indicated that the combined treatment group had higher expression levels of Arg1 in wound skin tissue and serum than the other groups, while the expression levels of IL-6, IL-1β, and TNF-α were significantly lower. These results suggest that the combined treatment of hUCMSCs and intestinal probiotics can accelerate wound healing in diabetic mice through mechanisms such as promoting angiogenesis, enhancing collagen deposition, and regulating the inflammatory microenvironment. The therapeutic effect was significantly better than that of single treatment, providing a new potential strategy for the clinical treatment of diabetic foot.

This article combined the pathogenic characteristics of "latent wind" with the theory of collateral diseases to clarify the pathological features of tumor blood vessels， including their active proliferation， high permeabi-lity， and promotion of metastasis. The theory framework of "latent wind in collaterals" as the tumor mechanism was proposed， which suggests that at the site of tumor lesions， the collaterals inherit the nature of latent wind to grow excessively， adopt an open and discharge nature to leak essence， and tumor toxins， characterized by their rapid movement and frequent changes， spread and metastasize， driving the progression of malignant tumors. Focusing on the fundamental pathogenesis of "latent wind in collaterals"， specific clinical treatment principles and methods centered on treating wind are proposed， including regulating qi and dispelling wind， clearing heat and extinguishing wind， unblocking collaterals and expelling wind， and reinforcing healthy qi to calm wind， so as to provide references for enhancing the precision of traditional Chinese medicine in treating malignant tumors.

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

Myocardial fibrosis （MF）， characterized by decreased cardiac function and myocardial compliance， is a pathological process and a progression factor in various cardiovascular diseases. The nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 （NLRP3） inflammasome is closely related to the development of MF. Recent studies have shown that traditional Chinese medicine （TCM） can regulate the NLRP3 inflammasome to alleviate MF. Based on this， this article systematically summarizes the research progress on the mechanisms by which TCM regulates the NLRP3 inflammasome to improve MF. It is found that active ingredients of TCM， such as alkaloids （lycorine，vincristine，bufalin）， saponins （astragaloside Ⅳ， diosgenin，ginsenoside Rg3）， terpenoids （celastrol，oridonin）， and phenols （polydatin，curcumin，phloridzin） as well as TCM formulas （Zhachong shisanwei pills，Zhilong huoxue tongyu capsules， Luqi formula） can inhibit the activation of the NLRP3 inflammasome， thereby suppressing the release of inflammatory factors such as interleukin-1β and IL-18， reducing inflammatory damage to myocardial tissue， alleviating excessive deposition of the extracellular matrix， and thus exerting the effect of improving MF.

“Inflammation-cancer” transformation of chronic atrophic gastritis （CAG） refers to the process in which the gastric mucosa， in the context of CAG， progresses through stages of precancerous lesions of gastric cancer （PLGC）， such as intestinal metaplasia and dysplasia， and eventually develops into gastric cancer （GC）. In China， the incidence and mortality rates of GC rank among the highest in the world， and the proportion of GC cases caused by gastric mucosal infection and inflammation has been increasing. Modern medical treatments for CAG and PLGC mainly rely on drug therapy， endoscopic resection， and regular surveillance. Although these disease management strategies are relatively mature， they present limitations in early lesion prevention and recurrence risk control. Therefore， it is imperative to identify therapeutic approaches for CAG and PLGC that offer preventive， reversible， and recurrence-reducing benefits. With advances in research on the mechanisms underlying inflammation-cancer transformation and the integration of traditional Chinese and Western medicine， the advantages of TCM in preventing and even reversing early-stage CAG and PLGC have gradually become apparent. This review explored the mechanisms of inflammation-cancer transformation in CAG from five aspects： inflammatory microenvironment， autophagy， glycolysis， bile acids， and ferroptosis. In conjunction with TCM theory and a deeper understanding of the distinct mechanisms involved in the inflammation-cancer transformation of CAG， this review further discussed the specific mechanisms through which TCM intervened in treating CAG and PLGC， with the aim of providing theoretical support and therapeutic insights for future clinical applications.

“Inflammation-cancer” transformation of chronic atrophic gastritis （CAG） refers to the process in which the gastric mucosa， in the context of CAG， progresses through stages of precancerous lesions of gastric cancer （PLGC）， such as intestinal metaplasia and dysplasia， and eventually develops into gastric cancer （GC）. In China， the incidence and mortality rates of GC rank among the highest in the world， and the proportion of GC cases caused by gastric mucosal infection and inflammation has been increasing. Modern medical treatments for CAG and PLGC mainly rely on drug therapy， endoscopic resection， and regular surveillance. Although these disease management strategies are relatively mature， they present limitations in early lesion prevention and recurrence risk control. Therefore， it is imperative to identify therapeutic approaches for CAG and PLGC that offer preventive， reversible， and recurrence-reducing benefits. With advances in research on the mechanisms underlying inflammation-cancer transformation and the integration of traditional Chinese and Western medicine， the advantages of TCM in preventing and even reversing early-stage CAG and PLGC have gradually become apparent. This review explored the mechanisms of inflammation-cancer transformation in CAG from five aspects： inflammatory microenvironment， autophagy， glycolysis， bile acids， and ferroptosis. In conjunction with TCM theory and a deeper understanding of the distinct mechanisms involved in the inflammation-cancer transformation of CAG， this review further discussed the specific mechanisms through which TCM intervened in treating CAG and PLGC， with the aim of providing theoretical support and therapeutic insights for future clinical applications.