Hepatitis B virus （HBV） infection is the primary cause of viral hepatitis and represents a substantial disease burden in China. However， effective and safe agents capable of completely eliminating HBV DNA are still lacking. In modern medicine， anti-HBV strategies mainly target covalently closed circular DNA （cccDNA）， among other mechanisms， and multiple novel drugs are currently under clinical investigation. Traditional medicine has been shown to exert anti-HBV effects through direct pathways， such as blocking viral entry， as well as indirect pathways， including the regulation of programmed cell death. Studies have confirmed that the integration of traditional Chinese medicine （TCM） and Western medicine in treating HBV infection and its related complications offers complementary advantages， particularly in enhancing HBV clearance rates， improving liver function， preventing various complications， and delaying the progression from hepatic fibrosis to hepatocellular carcinoma. This review focuses on advances in anti-HBV research involving TCM， Western medicine， and their integrated application， aiming to provide a basis for integrated HBV therapy and new drug development.

ObjectiveTo explore the effects of Yimei Baijiang formula （YMBJF） on colitis-associated colorectal cancer （CAC） and the nuclear factor kappaB （NF-κB） signaling pathway in mice. MethodsSixty male Balb/c mice of 4-6 weeks old were randomized into 6 groups： Normal， model， capecitabine （0.83 g·kg^-1）， and low-， medium-， and high-dose （4.63， 9.25， 18.50 g·kg^-1， respectively） YMBJF. The mouse model of CAC was established by combining azoxymethane （AOM， 10 mg·kg^-1） and dextran sulfate sodium （DSS， 2%）. At the 5^th week after the start of modeling， the capecitabine group and the YMBJF groups were respectively administrated with the corresponding doses of drugs by gavage once a day for a total of 6 weeks. The body weights and general conditions of mice were measured and observed， and the disease activity index （DAI） was scored. The tumors in the colorectal tissue were counted， and the colorectal length was measured. The histological features of the colorectal tissue in each group of mice were observed by hematoxylin-eosin （HE） staining. The levels of inflammatory cytokines including interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the serum were determined by enzyme-linked immunosorbent assay （ELISA）. The expression and localization of proliferating cell nuclear antigen-67 （Ki67）， proliferating cell nuclear antigen （PCNA）， and phosphorylated nuclear transcription factor-κB p65 （p-NF-κB p65） proteins were observed by immunohistochemistry （IHC）. The apoptosis of tumor cells was observed by the TUNEL assay. The mRNA levels of IL-6，IL-1β， TNF-α， nuclear transcription factor-κB p65 （NF-κB p65）， NF-κB inhibitor alpha （IκBα）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in the colorectal tissue were quantified by Real-time polymerase chain reaction（Real-time PCR）. The protein levels of NF-κB p65， phosphorylated （p）-NF-κB p65， IκBα， p-IκBα， Bcl-2， and Bax in the colorectal tissue were determined by Western blot. ResultsCompared with the model group， each YMBJF group showed decreases in DAI and tumor number （P0.01）， and the medium-dose and high-dose YMBJF groups showed increases in colorectal length （P0.05）. In addition， each YMBJF group showed alleviated colorectal mucosal pathological injury， declined levels of IL-6， IL-1β， and TNF-α in the serum （P0.05）， reduced expression of Ki67 and PCNA （P0.01）， and down-regulated expression of p-NF-κB p65 （P0.05）. The apoptosis in the medium-dose and high-dose YMBJF groups increased （P0.01）. Each YMBJF group and the capecitabine group showed down-regulated mRNA levels of IL-1β， TNF-α， IL-6， NF-κB p65， and Bcl-2 （P0.05） and up-regulated mRNA levels of IκBα and Bax （P0.05）. The mRNA level of IκBα was up-regulated， and that of Bcl-2 was down-regulated （P0.05） in the high-dose YMBJF group. The protein levels of p-IκBα and Bcl-2 were down-regulated （P0.05） in each YMBJF group. The protein levels of IκBα and Bax were up-regulated in the medium-dose and high-dose YMBJF groups （P0.01）， while those of NF-κB p65 and p-NF-κB p65 were down-regulated （P0.05）. ConclusionYMBJF can reduce the number of tumors， reduce the levels of inflammatory factors， promote tumor cell apoptosis， and inhibit tumor cell proliferation by regulating the direct effector molecules of the NF-κB signaling pathway in the mouse model of CRC.

ObjectiveTo explore the effects of Yimei Baijiang formula （YMBJF） on colitis-associated colorectal cancer （CAC） and the nuclear factor kappaB （NF-κB） signaling pathway in mice. MethodsSixty male Balb/c mice of 4-6 weeks old were randomized into 6 groups： Normal， model， capecitabine （0.83 g·kg^-1）， and low-， medium-， and high-dose （4.63， 9.25， 18.50 g·kg^-1， respectively） YMBJF. The mouse model of CAC was established by combining azoxymethane （AOM， 10 mg·kg^-1） and dextran sulfate sodium （DSS， 2%）. At the 5^th week after the start of modeling， the capecitabine group and the YMBJF groups were respectively administrated with the corresponding doses of drugs by gavage once a day for a total of 6 weeks. The body weights and general conditions of mice were measured and observed， and the disease activity index （DAI） was scored. The tumors in the colorectal tissue were counted， and the colorectal length was measured. The histological features of the colorectal tissue in each group of mice were observed by hematoxylin-eosin （HE） staining. The levels of inflammatory cytokines including interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the serum were determined by enzyme-linked immunosorbent assay （ELISA）. The expression and localization of proliferating cell nuclear antigen-67 （Ki67）， proliferating cell nuclear antigen （PCNA）， and phosphorylated nuclear transcription factor-κB p65 （p-NF-κB p65） proteins were observed by immunohistochemistry （IHC）. The apoptosis of tumor cells was observed by the TUNEL assay. The mRNA levels of IL-6，IL-1β， TNF-α， nuclear transcription factor-κB p65 （NF-κB p65）， NF-κB inhibitor alpha （IκBα）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in the colorectal tissue were quantified by Real-time polymerase chain reaction（Real-time PCR）. The protein levels of NF-κB p65， phosphorylated （p）-NF-κB p65， IκBα， p-IκBα， Bcl-2， and Bax in the colorectal tissue were determined by Western blot. ResultsCompared with the model group， each YMBJF group showed decreases in DAI and tumor number （P0.01）， and the medium-dose and high-dose YMBJF groups showed increases in colorectal length （P0.05）. In addition， each YMBJF group showed alleviated colorectal mucosal pathological injury， declined levels of IL-6， IL-1β， and TNF-α in the serum （P0.05）， reduced expression of Ki67 and PCNA （P0.01）， and down-regulated expression of p-NF-κB p65 （P0.05）. The apoptosis in the medium-dose and high-dose YMBJF groups increased （P0.01）. Each YMBJF group and the capecitabine group showed down-regulated mRNA levels of IL-1β， TNF-α， IL-6， NF-κB p65， and Bcl-2 （P0.05） and up-regulated mRNA levels of IκBα and Bax （P0.05）. The mRNA level of IκBα was up-regulated， and that of Bcl-2 was down-regulated （P0.05） in the high-dose YMBJF group. The protein levels of p-IκBα and Bcl-2 were down-regulated （P0.05） in each YMBJF group. The protein levels of IκBα and Bax were up-regulated in the medium-dose and high-dose YMBJF groups （P0.01）， while those of NF-κB p65 and p-NF-κB p65 were down-regulated （P0.05）. ConclusionYMBJF can reduce the number of tumors， reduce the levels of inflammatory factors， promote tumor cell apoptosis， and inhibit tumor cell proliferation by regulating the direct effector molecules of the NF-κB signaling pathway in the mouse model of CRC.

Work-related musculoskeletal disorders (WMSDs) represent a significant occupational health challenge among healthcare professionals globally, posing substantial threats to physical and mental well-being as well as work sustainability. Adopting preventive behaviors—including ergonomic postural adjustments, optimized work-rest scheduling, proper use of protective and assistive equipment, and regular physical activity—is essential for mitigating the risk of WMSDs. Guided by the social ecological model, the review synthesized current evidence on the determinants of WMSDs preventive behaviors across four levels: intrapersonal characteristics, work environment conditions, interpersonal support, and policy/institutional factors. The findings suggest that higher educational attainment, favorable health-related behavioral patterns, optimized ergonomic work environments, adoption of supportive collaborative systems, strong organizational support, as well as policy safeguards facilitate preventive behavior adoption. Conversely, limited prevention-related knowledge, low risk perception, insufficient physical activity, excessive workload, lack of appropriate protective equipment, inadequate ergonomic training, a prevailing culture of presenteeism, and inadequate policy implementation constitute significant barriers. Multi-dimensional intervention strategies targeting these determinants are warranted to enhance preventive behaviors, reduce the risk of WMSDs, and strengthen occupational health protection for healthcare professionals.

AIM:To automatically identify and quantitatively assess myopia-related fundus structural changes by combining non-mydriatic color fundus photography with an artificial intelligence(AI)-powered quantitative fundus analysis system and to further analyze the correlations between these fundus parameters and spherical equivalent(SE), axial length(AL), and age, providing the objective basis for monitoring myopia progression and supporting the formulation of personalized myopia prevention and control strategies. METHODS:A cross-sectional study was conducted enrolling myopic patients aged 18-50 y who underwent myopia screening from March 2023 to December 2023. Patients were stratified into three groups based on SE: the -3.00 D

Objective: To analyze the impact of premature death due to four major chronic diseases on life expectancy in Yangpu District, Shanghai Municipality from 2010 to 2021, so as to provide the evidence for formulating chronic disease prevention and control strategies. Methods : Mortality data of registered residents in Yangpu District from 2010 to 2021 were collected through the Death Information Registration and Management System of the Shanghai Municipal Disease Control and Prevention Information Management Platform. The premature death probability of malignant tumors, diabetes, cardiovascular and cerebrovascular diseases, and chronic respiratory diseases, and life expectancy of residents were calculated using the abridged life table method. Trends in premature death probability for four types of chronic diseases were analyzed using the average annual percent change (AAPC). The impact of premature death probability due to four chronic diseases on life expectancy was assessed by Arriaga's decomposition method. Results : The premature death probability due to four major chronic diseases in Yangpu District decreased from 9.88% in 2010 to 9.22% in 2021, showing an overall declining trend (AAPC=-0.540%, P<0.05). Among females, the premature death probability declined from 6.71% to 4.90% (AAPC=-2.715%, P<0.05), whereas no statistically significant trend was observed in males (P>0.05). Life expectancy increased from 82.52 years in 2010 to 84.50 years in 2021, with an overall upward trend (AAPC=0.244%, P<0.05). Life expectancy rose by 1.71 years for males and 2.34 years for females (AAPC=0.197% and 0.303%,both P<0.05). Declines in premature death probability from malignant tumors (AAPC=-0.967%, P< 0.05) and chronic respiratory diseases (AAPC=-3.071%, P<0.05) contributed to gains in life expectancy of 0.30 years and 0.03 years, with contribution rates of 12.18% and 1.29%, respectively. Changes in premature death probability due to diabetes as well as cardiovascular and cerebrovascular diseases were not statistically significant (both P>0.05), resulting in reductions in life expectancy of 0.05 years and 0.10 years, with contribution rates of -2.40% and -5.05%, respectively. Notably, an increase in premature death probability due to cardiovascular and cerebrovascular diseases among males (AAPC=1.673%) contributed to a decrease of 0.22 years in male life expectancy, whereas a decrease among females (AAPC=-3.824%) contributed to an increase of 0.03 years in female life expectancy, with contribution rates of -13.03% and 1.14%, respectively. Conclusions From 2010 to 2021, Yangpu District experienced an overall decline in premature death probability due to four major chronic diseases and an increase in life expectancy. Greater attention should be paid to the negative impacts of premature death probability from diabetes as well as cardiovascular and cerebrovascular diseases among males on life expectancy.

Biolinguistics is an interdisciplinary discipline dedicated to exploring the biological foundation of human language and its origin. Speech and language disorders along with the language evolution are the centers of biolinguistics. Recently, the study of the vocal behavior of animals by neuroimaging, neurophysiological technologies as well as identifying and manipulating specific neural circuits by the cellular and molecular technologies has significantly advanced the understanding of the neurobiology of human language. This paper takes three types of prevalent speech and language disorders-developmental dyslexia, post-stroke aphasia and autism spectrum disorder-as examples to review how the researchers constructed the knockout mice, middle-cerebral-artery-occlusion rats and songbird models to simulate the endophenotypes like auditory processing, neural migration, brain lateralization and ultrasonic vocalization so as to reveal the functions of the candidate genes like KIAA0319,astrotactin 2 and how neuroplasticity contributes to the restructuring of linguistic function. Regarding the language evolution, this paper focuses on how the research of primates and songbirds elucidates the coevolutionary path of human language in terms of anatomical structure, neural mechanism and cognition, as well as the multi-modal origin. These studies lead to the findings like "anatomical simplification leads to the neurocognitive complexification" and "the gesture, language ,and music are intertwined in terms of origin". At the end of the paper, the challenges regarding ethics and cross-species translation are discussed. Future research needs to adhere to "3R" principles and construct multi-species joint validation systems, and integrate the frontier technologies such as pluripotent stem cell models and brain organoids.

National biological standards for antibiotics are critical components of the antibiotic quality control system and serve as reference materials for measuring and calibrating the biological activity of antibiotics. This article systematically reviews the classification, definition of potency units, and current research status of commercially available national antibiotic biological standards in China. At present, these standards can be categorized based on chemical structure, number of components, and development methods. The definition of potency units has evolved from an early “arbitrarily assigned unit” to “being represented by the mass of the antibiotic salt” and, more recently, to the current mainstream approach of “being represented by the mass of the active ingredient”. This evolution reflects a shift in quality control philosophy from primarily biological analysis to a system dominated by chemical analysis supplemented by biological methods. Current research focuses on optimizing potency determination methods, studying the unification of content and potency, and implementing dual quality control of both the potency and the ratio/content of active components in multi-component antibiotics. For complex multi-component antibiotics, the microbiological assay based on biological activity remains irreplaceable in quality control. Future efforts should emphasize further method optimization, ensuring batch-to-batch consistency of standards, and advancing precision quality control as key research priorities for antibiotic biological standards.

Metabolic associated fatty liver disease (MAFLD) is fundamentally driven by an imbalance in hepatic fatty-acid flux: the influx of fatty acids exceeds the liver’s capacity for disposal, resulting in excessive hepatic lipid accumulation, predominantly in the form of triglycerides (TGs). The occurrence and progression of MAFLD depend on disordered regulation across multiple metabolic steps, including fatty-acid uptake, de novo lipogenesis (DNL), fatty-acid oxidation (FAO), and very low-density lipoprotein (VLDL) export. Forkhead box protein O1 (FOXO1) is a key transcriptional regulator within the hepatic network coordinating glucose and lipid metabolism. Under metabolic stress and insulin resistance (IR), FOXO1 expression is frequently increased, whereas its inhibitory phosphorylation is reduced. These changes enhance FOXO1 nuclear localization and transcriptional activity, thereby reprogramming the expression of genes related to metabolism in the liver. Because hepatic lipid deposition is the central pathological feature of MAFLD, the functional status of FOXO1 directly influences hepatic lipid homeostasis. Growing evidence suggests that FOXO1 can exert bidirectional, environment-dependent effects on hepatic lipid accumulation; however, the molecular basis for this functional switch remains incompletely understood. This review systematically summarizes the biological functions and regulatory mechanisms of FOXO1 and its roles in hepatic lipid metabolism, with a particular focus on its crosstalk with insulin signaling. FOXO1 expression is shaped by RNA modifications and epigenetic regulation mediated by non-coding RNAs. Its transcriptional output is precisely governed by post-translational modifications—such as phosphorylation and acetylation—as well as by coordinated nucleocytoplasmic shuttling. Notably, these regulatory patterns vary markedly across nutritional states, degrees of insulin resistance, and stages of disease. In the fed state, insulin/IGF-1 signaling activates the PI3K-AKT pathway, promoting the inhibitory phosphorylation of FOXO1 and facilitating additional modifications, including acetylation, methylation, and ubiquitination. Together, these events drive FOXO1 export from the nucleus and dampen its transcriptional activity, suppressing gluconeogenesis and constraining lipogenic programs. Conversely, during fasting or when insulin signaling is weakened, FOXO1 inhibition is relieved. FOXO1 accumulates in the nucleus, binds to DNA, and regulates the transcription of downstream target genes. Mechanistically, FOXO1 can aggravate hepatic lipid accumulation by activating genes involved in TG synthesis while repressing FAO-related pathways, thereby favoring storage over oxidation. However, under specific conditions, FOXO1 may also alleviate the hepatic lipid burden by promoting TG hydrolysis and enhancing VLDL secretion, thereby reducing the net hepatic lipid load. In addition, lipotoxic signals mediated by ceramides and diacylglycerols (Cer/DAG) activate atypical protein kinase C (aPKC), further exacerbating the disruption of the AKT-FOXO1 axis. This vicious cycle ultimately produces a metabolic paradox in which increased hepatic glucose output coexists with persistent, insulin-independent lipogenesis, accelerating MAFLD progression. Importantly, FOXO1 regulation is not uniform: during early metabolic overload, insulin-mediated suppression may remain effective, whereas in advanced insulin resistance, the loss of AKT control permits sustained FOXO1 activity. Such stage-dependent dynamics may help explain why FOXO1 can either promote steatosis or, in certain contexts, support programs that facilitate lipid turnover. Accordingly, interventions should be liver-specific and tuned to the disease stage, aiming to curb maladaptive FOXO1 signaling while preserving its capacity to promote triglyceride hydrolysis and VLDL secretion when advantageous. Overall, this review offers an important perspective on MAFLD pathogenesis, emphasizing FOXO1 as a potential therapeutic target and providing a theoretical basis for developing liver-specific, disease-course-dependent precision interventions.

The Type III Secretion System (T3SS) serves as a pivotal virulence apparatus for numerous Gram-negative bacterial pathogens, enabling them to infect both animal and plant hosts. Functioning as a molecular syringe, the T3SS directly translocates bacterial effector proteins from the bacterial cytoplasm into the interior of eukaryotic host cells. These effectors are central weapons that precisely manipulate a wide spectrum of host cellular physiological processes, ranging from cytoskeletal dynamics to immune signaling, to establish a favorable niche for bacterial survival and proliferation. Among the diverse arsenal of T3SS effectors, the YopJ family constitutes a critical group of virulence factors. Members of this family are characterized by a conserved catalytic triad structure—a hallmark of the CE clan of cysteine proteases that has been evolutionarily repurposed to confer acetyltransferase activity. A defining and intriguing feature of these enzymes is their stringent dependence on a host-derived eukaryotic cofactor, inositol hexakisphosphate (IP₆), for allosteric activation. This requirement acts as a sophisticated molecular safeguard, ensuring enzymatic activity only within the appropriate host environment, thereby preventing detrimental effects on the bacterium itself. While seminal studies on individual members such as Yersinia’s YopJ and Salmonella’s AvrA have provided deep mechanistic insights, a systematic and integrative understanding of the structure-function relationships across the entire family remains fragmented. Key questions persist regarding how a conserved catalytic core has diverged to recognize distinct host substrates in different kingdoms of life. To address this gap, this article provides a systematic review of the YopJ family, focusing on three interconnected aspects: their structural features, their catalytic mechanism, and their divergent immunosuppressive strategies in animal versus plant hosts. By conducting a comparative analysis of the sequences and resolved three-dimensional structures of three representative members (e.g., HopZ1a, PopP2, AvrA), we elucidate regions of significant variation embedded within the conserved core catalytic architecture. These variable regions, often involving surface loops and substrate-binding interfaces, are crucial determinants of target specificity and functional specialization. The functional divergence of this effector family is most apparent when comparing their modes of action in different hosts. In animal hosts, YopJ-family effectors primarily sabotage innate immune signaling pathways. They achieve this by acetylating key serine and threonine residues within the activation loops of critical kinases in the MAPK and NF‑κB pathways. This post-translational modification blocks the phosphorylation and subsequent activation of these kinases, leading to potent suppression of inflammatory cytokine production. Conversely, in plant hosts, the strategy broadens to dismantle the two-tiered plant immune system. YopJ homologs target a more diverse set of substrates, including immune-associated receptor-like cytoplasmic kinases (RLCKs), microtubule networks via tubulin acetylation (which disrupts cellular trafficking and signaling), and transcription factors central to defense gene regulation. This multi-target approach effectively suppresses both Pattern-Triggered Immunity (PTI) and Effector-Triggered Immunity (ETI). In conclusion, this synthesis aims to deepen the mechanistic understanding of YopJ family-mediated pathogenesis by integrating structural biology with cellular function across host kingdoms. Elucidating the precise molecular basis for substrate selection—how conserved platforms achieve target diversity—is a major frontier. Furthermore, this knowledge provides a vital theoretical foundation for developing novel anti-virulence strategies. Targeting the conserved IP₆-binding pocket or the catalytic acetyltransferase activity itself represents a promising avenue for designing broad-spectrum inhibitors that could disarm this critical family of bacterial effectors, potentially offering new therapeutic approaches against a range of pathogenic bacteria.