Abstract On September 26, 2024, a municipal hospital in Jiaxing City reported a maternal case of Listeria monocytogenes infection. In order to clarify the source of infection, the Jiaxing Center for Disease Control and Prevention immediately conducted the epidemiological investigation, laboratory testing and related disposal work. The case presented with fever (37.9 ℃), gradually intensifying paroxysmal abdominal pain without obvious cause, and went to hospital on the day of onset. Due to fetal intrauterine distress, a male infant was delivered by cesarean section on the same day. The epidemiological investigation identified that the case usually consumed fruits, often store fruits such as watermelon and grapes in the refrigerator alongside raw meat, and the refrigerator had never been cleaned or disinfected, posing a risk of cross contamination. Laboratory tests on amniotic fluid sample from the pregnant woman, infant blood sample showed positive results for Listeria monocytogenes infection. One strain of Listeria monocytogenes was detected in a smear sample from the inner wall of the refrigerator, and all the strains were ST2 type. Consuming fruits contaminated with Listeria monocytogenes may be the main source of infection. Food safety education for pregnant women and their family members should be strengthened to reduce the risk of infection.

Immobilized enzyme-based enzyme electrode biosensors, characterized by high sensitivity and efficiency, strong specificity, and compact size, demonstrate broad application prospects in life science research, disease diagnosis and monitoring, etc. Immobilization of enzyme is a critical step in determining the performance (stability, sensitivity, and reproducibility) of the biosensors. Random immobilization (physical adsorption, covalent cross-linking, etc.) can easily bring about problems, such as decreased enzyme activity and relatively unstable immobilization. Whereas, directional immobilization utilizing amino acid residue mutation, affinity peptide fusion, or nucleotide-specific binding to restrict the orientation of the enzymes provides new possibilities to solve the problems caused by random immobilization. In this paper, the principles, advantages and disadvantages and the application progress of enzyme electrode biosensors of different directional immobilization strategies for enzyme molecular sensing elements by specific amino acids (lysine, histidine, cysteine, unnatural amino acid) with functional groups introduced based on site-specific mutation, affinity peptides (gold binding peptides, carbon binding peptides, carbohydrate binding domains) fused through genetic engineering, and specific binding between nucleotides and target enzymes (proteins) were reviewed, and the application fields, advantages and limitations of various immobilized enzyme interface characterization techniques were discussed, hoping to provide theoretical and technical guidance for the creation of high-performance enzyme sensing elements and the manufacture of enzyme electrode sensors.

Lipid turbidity disease is a metabolic disease featuring lipid metabolism disorders caused by many factors such as social environment， diet， and lifestyle， which is closely related to many diseases in modern medicine， such as hyperlipidemia， obesity， fatty liver， atherosclerosis， metabolic syndrome， and cardiovascular and cerebrovascular diseases， with a wide range of influence and far-reaching harm. According to the Huangdi Neijing， lipid turbidity disease reflects the pathological change of the body's physiologic grease. Grease is the thick part of body fluids， which has the function of nourishing， and it is the initial state and source of important substances in the human body such as brain， marrow， essence， and blood. Once the grease of the human body is abnormal， it can lead to lipid turbidity disease. The Huangdi Neijing also points out the physiological relationship between the transportation and transformation of body fluids and the rise and fall of the spleen and stomach， which can deduce the pathological relationship between the occurrence of lipid turbidity disease and the abnormal rise and fall of the spleen and stomach functions. Lipid turbidity disease is caused by overconsumption of fatty and sweet foods or insufficient spleen and stomach endowments， leading to disorders of the function of promoting clear and reducing turbidity in the spleen and stomach. This leads to the transformation of thick grease in body fluids into lipid turbidity， which accumulates in the body's meridians， blood vessels， skin pores， and organs， forming various forms of metabolic diseases. The research team believed that the pathological basis of lipid turbidity disease was the abnormal rise and fall of the spleen and stomach and the obstruction of the transfer of grease. According to the different locations where lipid turbidity stays， it was divided into four common pathogenesis types： ''inability to distinguish between the clear and turbid， turbid stagnation in the Ying blood''， ''spleen not rising clear， turbid accumulation in the vessels''， ''spleen dysfunction， lipid retention in the pores''， ''spleen failure to transportation and transformation， and grease accumulation in the liver''. According to the pathogenesis， it could be divided into four common syndromes， namely， turbid stagnation in the Ying blood， turbid accumulation in the vessels， lipid retention in the pores， and grease accumulation in the liver， and the corresponding prescriptions were given for syndrome differentiation and treatment， so as to guide clinical differentiation and treatment of the lipid turbidity disease.

Purpose: This study assessed the performance of the ultrasound-guided attenuation parameter (UGAP) in diagnosing and grading hepatic steatosis in patients with metabolic dysfunctionassociated steatotic liver disease (MASLD). Magnetic resonance imaging proton density fat fraction (MRI-PDFF) served as the reference standard. Methods: Patients with hepatic steatosis were enrolled in this prospective study and underwent UGAP measurements. MRI-PDFF values of ≥5%, ≥15%, and ≥25% were used as references for the diagnosis of steatosis grades ≥S1, ≥S2, and S3, respectively. Spearman correlation coefficients and area under the receiver operating characteristic curves (AUCs) were calculated. Results: Between July 2023 and June 2024, the study included 88 patients (median age, 40 years; interquartile range [IQR], 36 to 46 years), of whom 54.5% (48/88) were men and 45.5% (40/88) were women. Steatosis grades exhibited the following distribution: 22.7% (20/88) had S0, 50.0% (44/88) had S1, 21.6% (19/88) had S2, and 5.7% (5/88) had S3. The success rate for UGAP measurements was 100%. The median UGAP value was 0.74 dB/cm/MHz (IQR, 0.65 to 0.82 dB/ cm/MHz), and UGAP values were positively correlated with MRI-PDFF (r=0.77, P<0.001). The AUCs of UGAP for the diagnoses of ≥S1, ≥S2, and S3 steatosis were 0.91, 0.90, and 0.88, respectively. In the subgroup analysis, 98.4% (60/61) of patients had valid controlled attenuation parameter (CAP) values. UGAP measurements were positively correlated with CAP values (r=0.65, P<0.001). Conclusion Using MRI-PDFF as the reference standard, UGAP demonstrates good diagnostic performance in the detection and grading of hepatic steatosis in patients with MASLD.

OBJECTIVE To investigate the mechanisms of paeoniflorin （PF） in anti-hyperprolactinemia （HPRL）. METHODS Twenty-four female SD rats were divided into blank control group （intragastric administration of 5% gum arabic solution）， olanzapine group （model group， intragastric administration of 5 mg/kg olanzapine suspension）， and PF group （intragastric administration of 5 mg/kg olanzapine suspension， followed by gavaging with 50 mg/kg PF solution 2 hours later） with 8 rats in each group. Once a day， continuously model/administer until the plasma prolactin （PRL） levels in the olanzapine group were twice as high as those in the blank control group. PRL levels were measured. The changes in gut microbiota of rats were analyzed， including assessments of α-diversity （Simpson， Chao1， and Shannon indexes）， β-diversity， species composition analysis （at the phylum and genus levels）， and microbiome LEfSe analysis. Fecal untargeted metabolomics technology was employed to analyze the effects of PF on the fecal metabolomics of rats， including multivariate statistical analysis， screening of differential metabolites， and pathway enrichment analysis. Spearman correlation analysis was performed to examine the correlations between differential microbiota and differential fecal metabolites. RESULTS PF significantly reduced serum PRL levels of rats in olanzapine group （P＜0.05）. 16S rRNA sequencing revealed that PF improved the α-diversity and β-diversity of gut microbiota in HPRL rats （P＜0.05）， restoring them to levels similar to the blank control group. At the phylum level， PF significantly reduced the relative abundance of Firmicutes and Desulfobacterota， while increasing the relative abundance of Verrucomicrobiota in HPRL rats （all P＜0.05）. At the genus level， PF reversed the relative abundance of Desulfovibrio，Allobaculum， and Prevotellaceae_NK3B31_group， etc （all P＜0.05）. The results of LEfSe analysis revealed that PF significantly enriched microbial taxa such as Actinobacteriota，Staphylococcales， Corynebacteriales， etc （all P＜0.05）. Metabolomics analysis identified 51 differential metabolites， with key metabolic pathways enriched in steroid hormone biosynthesis， prostate cancer， ovarian steroidogenesis， etc. Correlation analysis showed that the relative abundance of gut microbiota such as Desulfovibrio and Aerococcus was significantly correlated with the levels of steroid hormone metabolites such as tetrahydrocortisol and adrenosterone （P＜0.05）. CONCLUSIONS PF alleviates PRL by modulating gut microbiota structure in HPRL rats （including significantly reducing the relative abundance of Desulfovibrio， Allobaculum and Aerococcus， as well as significantly increasing the relative abundance of Ruminococcaceae_UBA1819 and Muribaculum）， and regulating steroid hormone pathways， then exerting its anti-HPRL effect.

The subcortical visual pathway is generally thought to be involved in dangerous information processing, such as fear processing and defensive behavior. A recent study, published in Human Brain Mapping, shows a new function of the subcortical pathway involved in the fast processing of non-emotional object perception. Rapid object processing is a critical function of visual system. Topological perception theory proposes that the initial perception of objects begins with the extraction of topological property (TP). However, the mechanism of rapid TP processing remains unclear. The researchers investigated the subcortical mechanism of TP processing with transcranial magnetic stimulation (TMS). They find that a subcortical magnocellular pathway is responsible for the early processing of TP, and this subcortical processing of TP accelerates object recognition. Based on their findings, we propose a novel training approach called subcortical magnocellular pathway training (SMPT), aimed at improving the efficiency of the subcortical M pathway to restore visual and attentional functions in disorders associated with subcortical pathway dysfunction.

ObjectiveTo understand the infection characteristics and drug resistance of carbapenem-resistant Serratia marcescens (CRSM) in a general hospital in Shanghai, and to provide a theoretical basis for clinical anti-infective treatment and prevention of drug-resistant bacteria. MethodsClinical data on cases with CRSM infections detected in clinical specimens at a gradeⅢ level A general hospital in Shanghai from June 2022 to June 2024 were retrospectively collected, and their clinical distributions, factors of hospital-acquired infections, prognosis, and drug-resistant situation were analyzed simultaneously. ResultsA total of 38 cases with CRSM were detected from June 2022 to June 2024, and the number of CRSM strains accounted for 25.00% (38/152) of the number of SM strains. The 38 CRSM infection samples were all derived from sputum. CRSM were distributed in 9 clinical departments, and the top 3 departments having the highest percentages of CRSM among SM strains, were intensive care unit (ICU) (78.79%, 26/33), gastrointestinal surgery department (57.14%, 4/7), and thyroid hernia surgery department (50.00%, 1/2). Among the 38 patients with CRSM infections, 8 cases were identified as hospital-acquired infection, resulting in a hospital-acquired infection rate of 21.05. The mortality rate of the 38 cases of CRSM infected patients within 30 days after detection of CRSM was 23.68% (9/38). The results of multivariate logistic regression analysis showed that sequential organ failure assessment (SOFA) score ≥6.5 points (OR=15.33, P<0.001), septic shock (OR=4.85, P=0.032), and suffering from neoplastic diseases (OR=0.12, P=0.018) were the related factors for death within 30 days after the detection of CRSM in patients with CRSM infection. The results of drug sensitivity test showed that the 38 cases of CRSM exhibited 100.00% (38/38) sensitivity to trimethoprim/sulfamethoxazole, tigecycline, or ceftazidime/avibactam; demonstrated high resistance toβ-lactams except for ceftazidime (18.42%, 7/38), the latter of which was one of the third-generation of cephalosporins; showed elevated resistance to fluoroquinolones [levofloxacin (89.47%, 35/38), ciprofloxacin (94.74%, 36/38)]; maintained good tetracycline sensitivity [doxycycline (97.37%, 37/38), minocycline (76.32%, 29/38)]; and displayed high susceptibility to the aminoglycoside gentamicin (94.74%, 36/38) and elevated resistance to tobramycin (86.84%, 34/38). The detection rate of serine carbapenemase in the 38 strains of CRSM was 100.00%, while all strains tested negative for metallo-β-lactamases. ConclusionFrom June 2022 to June 2024, the detection rate of CRSM in a gradeⅢ level A general hospital in Shanghai was relatively high, especially in the ICU. CRSM has a high resistance rate to commonly used antibacterial drugs such as the first and second-generation cephalosporins, quinolones, and polypeptide antibacterial drugs. Therefore the dynamics of drug-resistant bacteria should be tracked in a timely manner to guide the rational clinical application of antibacterial drugs.

Age-related sarcopenia is a progressive, systemic skeletal muscle disorder associated with aging. It is primarily characterized by a significant decline in muscle mass, strength, and physical function, rather than being an inevitable consequence of normal aging. Despite ongoing research, there is still no globally unified consensus among physicians regarding the diagnostic criteria and clinical indicators of this condition. Nonetheless, regardless of the diagnostic standards applied, the prevalence of age-related sarcopenia remains alarmingly high. With the global population aging at an accelerating rate, its incidence is expected to rise further, posing a significant public health challenge. Age-related sarcopenia not only markedly increases the risk of physical disability but also profoundly affects patients’ quality of life, independence, and overall survival. As such, the development of effective prevention and treatment strategies to mitigate its dual burden on both societal and individual health has become an urgent and critical priority. Skeletal muscle regeneration, a vital physiological process for maintaining muscle health, is significantly impaired in age-related sarcopenia and is considered one of its primary underlying causes. Skeletal muscle satellite cells (MSCs), also known as muscle stem cells, play a pivotal role in generating new muscle fibers and maintaining muscle mass and function. A decline in both the number and functionality of MSCs is closely linked to the onset and progression of sarcopenia. This dysfunction is driven by alterations in intrinsic MSC mechanisms—such as Notch, Wnt/β‑Catenin, and mTOR signaling pathways—as well as changes in transcription factors and epigenetic modifications. Additionally, the MSC microenvironment, including both the direct niche formed by skeletal muscle fibers and their secreted cytokines, and the indirect niche composed of extracellular matrix proteins and various cell types, undergoes age-related changes. Mitochondrial dysfunction and chronic inflammation further contribute to MSC impairment, ultimately leading to the development of sarcopenia. Currently, there are no approved pharmacological treatments for age-related sarcopenia. Nutritional intervention and exercise remain the cornerstone of therapeutic strategies. Adequate protein intake, coupled with sufficient energy provision, is fundamental to both the prevention and treatment of this condition. Adjuvant therapies, such as dietary supplements and caloric restriction, offer additional therapeutic potential. Exercise promotes muscle regeneration and ameliorates sarcopenia by acting on MSCs through various mechanisms, including mechanical stress, myokine secretion, distant cytokine signaling, immune modulation, and epigenetic regulation. When combined with a structured exercise regimen, adequate protein intake has been shown to be particularly effective in preventing age-related sarcopenia. However, traditional interventions may be inadequate for patients with limited mobility, poor overall health, or advanced sarcopenia. Emerging therapeutic strategies—such as miRNA mimics or inhibitors, gut microbiota transplantation, and stem cell therapy—present promising new directions for MSC-based interventions. This review comprehensively examines recent advances in MSC-mediated muscle regeneration in age-related sarcopenia and systematically discusses therapeutic strategies targeting MSC regulation to enhance muscle mass and strength. The goal is to provide a theoretical foundation and identify future research directions for the prevention and treatment of this increasingly prevalent condition.

Houpo Sanwutang， included in the Catalogue of Ancient Classical Prescriptions （Second Batch）， was first recorded in the Synopsis of Golden Chamber written by ZHANG Zhongjing from the Eastern Han dynasty and was modified by successive generations of medical experts. A total of 37 pieces of effective data involving 37 ancient Chinese medical books were retrieved from different databases. Through literature mining， statistical analysis， and data processing， combined with modern articles， this study employed bibliometrics to investigate the historical origin， composition， decoction methods， clinical application， and other key information. The results showed that the medicinal origin of Houpo Sanwutang was clearly documented in classic books. Based on the conversion of the measurements from the Han Dynasty， it is recommended that 110.4 g Magnolia Officinalis Cortex， 55.2 g Rhei Radix et Rhizoma， and 72 g Aurantii Fructus Immaturus should be taken. Magnolia Officinalis Cortex and Aurantii Fructus Immaturus should be decocted with 2 400 mL water first， and 1 000 mL should be taken from the decocted liquid. Following this， Rhei Radix et Rhizoma should be added for further decoction， and then 600 mL should be taken from the decocted liquid. A single dose of administration is 200 mL， and the medication can be stopped when patients restore smooth bowel movement. Houpo Sanwutang has the effect of moving Qi， relieving stuffiness and fullness， removing food stagnation， and regulating bowels. It can be used in treating abdominal distending pain， guarding， constipation， and other diseases with the pathogenesis of stagnated heat and stagnated Qi in the stomach. The above results provide reference for the future development and research of Houpo Sanwutang.

T7 RNA polymerase (T7 RNAP) is one of the simplest known RNA polymerases. Its unique structural features make it a critical model for studying the mechanisms of RNA synthesis. This review systematically examines the static crystal structure of T7 RNAP, beginning with an in-depth examination of its characteristic “thumb”, “palm”, and “finger” domains, which form the classic “right-hand-like” architecture. By detailing these structural elements, this review establishes a foundation for understanding the overall organization of T7 RNAP. This review systematically maps the functional roles of secondary structural elements and their subdomains in transcriptional catalysis, progressively elucidating the fundamental relationships between structure and function. Further, the intrinsic flexibility of T7 RNAP and its applications in research are also discussed. Additionally, the review presents the structural diagrams of the enzyme at different stages of the transcription process, and through these diagrams, it provides a detailed description of the complete transcription process of T7 RNAP. By integrating structural dynamics and kinetics analyses, the review constructs a comprehensive framework that bridges static structure to dynamic processes. Despite its advantages, T7 RNAP has a notable limitation: it generates double-stranded RNA (dsRNA) as a byproduct. The presence of dsRNA not only compromises the purity of mRNA products but also elicits nonspecific immune responses, which pose significant challenges for biotechnological and therapeutic applications. The review provides a detailed exploration of the mechanisms underlying dsRNA formation during T7 RNAP catalysis, reviews current strategies to mitigate this issue, and highlights recent progress in the field. A key focus is the semi-rational design of T7 RNAP mutants engineered to minimize dsRNA generation and enhance catalytic performance. Beyond its role in transcription, T7 RNAP exhibits rapid development and extensive application in fields, including gene editing, biosensing, and mRNA vaccines. This review systematically examines the structure-function relationships of T7 RNAP, elucidates the mechanisms of dsRNA formation, and discusses engineering strategies to optimize its performance. It further explores the engineering optimization and functional expansion of T7 RNAP. Furthermore, this review also addresses the pressing issues that currently need resolution, discusses the major challenges in the practical application of T7 RNAP, and provides an outlook on potential future research directions. In summary, this review provides a comprehensive analysis of T7 RNAP, ranging from its structural architecture to cutting-edge applications. We systematically examine: (1) the characteristic right-hand domains (thumb, palm, fingers) that define its minimalistic structure; (2) the structure-function relationships underlying transcriptional catalysis; and (3) the dynamic transitions during the complete transcription cycle. While highlighting T7 RNAP’s versatility in gene editing, biosensing, and mRNA vaccine production, we critically address its major limitation—dsRNA byproduct formation—and evaluate engineering solutions including semi-rationally designed mutants. By synthesizing current knowledge and identifying key challenges, this work aims to provide novel insights for the development and application of T7 RNAP and to foster further thought and progress in related fields.