Objective To investigate the prevalence and related factors of sarcopenia among non–bedridden older adults in the community of Baoshan District using the China mini sarcopenia risk assessment 7 (C-MSRA-7) combined with Ishii scoring system. Methods The older individuals consulting at 20 community health stations in Baoshan District between April 2025 and June 2025 were enrolled. Data were collected using a general information questionnaire, a dietary and lifestyle habits survey, the C-MSRA-7, and the mini nutritional assessment-short form (MNA-SF). Handgrip strength and anthropometric measurements were also obtained. Individuals with both Ishii score and C-MSRA-7 results positive were classified into the sarcopenia risk group, while the remaining participants were assigned to the non–sarcopenia risk group. Differences in lifestyle habits, dietary patterns, and nutritional status between the two groups were compared. Results A total of 2 611 valid questionnaires were retrieved. Univariate analysis showed statistically significant differences in alcohol consumption, physical activity frequency, body mass index (BMI), nutritional status, activities of daily living, and regularity of three meals in sarcopenia risk group (n＝486) and non–sarcopenia risk group (n＝2 125, P<0.05). Logistic regression analysis showed that advanced age (75–84 years: OR＝2.55, 95%CI 2.03–3.21; ≥85 years: OR＝3.98, 95%CI 2.24–7.07), underweight status (OR＝2.19, 95%CI 1.50–3.19), weight loss＞2 kg (OR＝4.52, 95%CI 2.68–7.64) past 3 months, lack of regular physical activity (OR＝1.77, 95%CI 1.24–2.52) , and alcohol consumption (OR＝1.48, 95%CI 1.07–2.05) were independent risk factors for sarcopenia (P<0.05). Behaviors related to healthy diet, including daily milk consumption (OR＝0.40, 95%CI 0.30–0.52), regular three meals (OR＝0.56, 95%CI 0.41–0.78), and high-quality protein intake (OR＝0.70, 95%CI 0.52–0.94), were protective factors (P<0.05). Conclusions Sarcopenia among community–dwelling, non–bedridden older adults is closely associated with physical activity levels, dietary habits, and nutritional status. Early identification of individuals at risk, enhanced nutritional education, and timely implementation of nutritional interventions and exercise programs are recommended for this population.

Objective To explore the effect and mechanism of Gegen Qinlian decoction (GQD) on myocardial injury induced by high-fat diet combined with streptozotocin in type 2 diabetic mice through network pharmacology and animal experiments. MethodsNetwork pharmacology was applied to screen the potential signaling pathways of GQD in the intervention of diabetic heart disease (DHD). A total of 36 specific pathogen-free (SPF) male C57BL/6J mice aged 8 weeks were acclimatized for 1 week and randomly divided into a normal control group (n=6) and a model group (n=30). Mice in the model group were fed a 60% high-fat diet and 5% glucose water for 4 weeks, and were intraperitoneally injected with 100 mg/kg streptozotocin after 12 h of fasting to establish the type 2 diabetes model. Mice in the normal control group were given a conventional diet and drinking water, and were intraperitoneally injected with an equal volume of citrate buffer after 12 h of fasting at the same time point. After successful establishment of the diabetic mouse model, the model mice were randomly divided into five groups according to body weight: model control group, GQD low-dose group, GQD medium-dose group, GQD high-dose group, and metformin positive control group, with 6 mice in each group. After 6 weeks of intragastric administration of corresponding doses of GQD, metformin, and ddH₂O respectively, all mice in the six groups (one normal control group and five model groups) were anesthetized with inhaled 2% isoflurane, blood samples were collected via eyeball enucleation, and heart tissues were harvested after euthanasia by cardiac exsanguination. Hematoxylin-eosin (HE) staining and wheat germ agglutinin (WGA) staining were performed to observe the pathological damage of myocardial tissues and measure the cross-sectional area of cardiomyocytes. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of pro-inflammatory cytokines in serum. Immunohistochemical staining was adopted to determine the protein expression levels of receptor for advanced glycation end products (RAGE), nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3), and phosphorylated nuclear factor-κB p65 (p-p65) in myocardial tissues. ResultsNetwork pharmacology analysis revealed that the targets of GQD against DHD were significantly enriched in inflammatory pathways, including the advanced glycation end products (AGEs)-RAGE axis, tumor necrosis factor (TNF) and interleukin-17 (IL-17) signaling pathways. HE and WGA staining results showed that, compared with the normal control group, the model control group exhibited myocardial fiber rupture, cardiomyocyte swelling, and significantly increased cardiomyocyte cross-sectional area (P<0.05). Compared with the model control group, GQD intervention significantly ameliorated the pathological changes, including myocardial fiber rupture, cell swelling, and cardiomyocyte hypertrophy. The results of immunohistochemical staining and ELISA indicated that compared with the model control group, GQD intervention markedly downregulated the protein expression of RAGE, NLRP3, and p-p65 in myocardial tissues, as well as the levels of serum pro-inflammatory cytokines (P<0.05). ConclusionGQD can effectively alleviate myocardial pathological injury in diet-induced type 2 diabetic mice, and its mechanism may be related to inhibiting the activation of the RAGE/p-p65/NLRP3 signaling pathway and reducing myocardial inflammatory response.

Objective To investigate the relationships of the expression of Calponin 1 and tumor ubiquitin-specific protease 1(OTUB1)with clinicopathological features in gastric cancer tissues as well as their prognostic values.Methods A total of 98 patients with gastric cancer were enrolled in this study.The qPCR was used to detect the expression levels of Calponin 1 mRNA and OTUB1 mRNA in gastric cancer tissues;the immunohistochemical staining was performed to detect the protein expres-sion levels of Calponin 1 and OTUB1;the Kaplan-Meier curve was plotted to compare the survival differences among gastric cancer patients with different expression levels of Calponin 1 and OTUB1;the Cox regression model was used to screen the influencing factors of prognosis in gastric cancer.Results Compared with adjacent tissues,the expression levels of Calponin 1 mRNA and OTUB1 mRNA in gastric cancer tissues were significantly higher(P＜0.05).The positive expression rates of Calponin 1 and OTUB1 protein in gastric cancer tissues were 63.27％and 65.31％respectively,which were significantly higher than 6.12％and 8.16％in adjacent tissues(P＜0.001).The expression levels of Calponin 1 and OTUB1 proteins were increased significantly in gastric cancer tissues of cases with stage Ⅲ ofTNM staging and lymph node metastasis(P＜0.05).The 3-year overall survival rate was 45.16％(28/62)in the Calponin 1-positive group,which was significantly lower than 83.33％(30/36)in the Calponin 1-negative group(Log-rank x2=12.990,P＜0.001).The 3-year overall survival rate was 45.31％(29/64)in the OTUB1-positive group,which was significantly lower than 85.29％(29/34)in the OTUB1-negative group(Log-rank x2=14.880,P＜0.001).The results of multivariate Cox regression showed that Calponin 1 positivity,OTUB1 positivity,stage Ⅲ ofTNM staging,and lymph node metastasis were risk factors for death in gastric cancer patients(P＜0.001).Conclusion The expressions of Calponin 1 and OTUB1 are upregulated in gastric cancer tissues and are related to TNM staging and lymph node metastasis.

Chaihu Guizhi Ganjiangtang （CGG）is a classic prescription in the Treatise on Cold Damage，which has the effects of clearing and relieving stagnation heat in Shaoyang，warming and dissolving water drink，and relieving the pivot mechanism. It is a classic prescription for treating spleen deficiency and liver depression and stopping internal stagnation caused by water drink. The formula is exquisite and well-matched and is often modified and used by ancient and modern medical practitioners to treat various miscellaneous diseases of internal and external medicine，with significant therapeutic effects. In recent years，with the rapid development of modern pharmacology，research on the micro mechanism of CGG has been continuously developed and deepened，providing new ideas for the treatment of diseases with CGG. Therefore，the authors systematically searched databases such as China National Knowledge Infrastructure，Wanfang Data Knowledge Service Platform，VIP Database， and PubMed for literature on the clinical application and pharmacological mechanism of CGG published by Chinese and foreign scholars in recent years. This article summarized the literature from two aspects：the modern clinical application and mechanism of action of CGG and elaborated on the diseases treated by CGG in modern literature，involving digestive system，respiratory system，nervous system，endocrine system，circulatory system，urinary system，gynecology，as well as its application in reducing the side effects of radiotherapy and chemotherapy， gynecology， dermatology， ophthalmology， and orthopedics. At the same time，the mechanism of CGG in treating diseases may be related to anti-inflammatory，anti-oxidative stress， regulation of immunity， anti-fibrosis， anti-tumor， improvement of gastrointestinal flora and motility， protection of liver tissue， reduction of blood lipids and blood sugar， and regulation of hormone levels.

BACKGROUND: The transcription factor POU2F1 regulates the expression levels of microRNAs in neoplasia. However, the miR-29b1/a cluster modulated by POU2F1 in gastric cancer (GC) remains unknown. METHODS: Gene expression in GC cells was evaluated using reverse-transcription polymerase chain reaction (PCR), western blotting, immunohistochemistry, and RNA in situ hybridization. Co-immunoprecipitation was performed to evaluate protein interactions. Transwell migration and invasion assays were performed to investigate the biological behavior of GC cells. MiR-29b1/a cluster promoter analysis and luciferase activity assay for the 3'-UTR study were performed in GC cells. In vivo tumor metastasis was evaluated in nude mice. RESULTS: POU2F1 is overexpressed in GC cell lines and binds to the miR-29b1/a cluster promoter. POU2F1 is upregulated, whereas mature miR-29b-3p and miR-29a-3p are downregulated in GC tissues. POU2F1 promotes GC metastasis by inhibiting miR-29b-3p or miR-29a-3p expression in vitro and in vivo . Furthermore, PIK3R1 and/or PIK3R3 are direct targets of miR-29b-3p and/or miR-29a-3p , and the ectopic expression of PIK3R1 or PIK3R3 reverses the suppressive effect of mature miR-29b-3p and/or miR-29a-3p on GC cell metastasis and invasion. Additionally, the interaction of PIK3R1 with PIK3R3 promotes migration and invasion, and miR-29b-3p , miR-29a-3p , PIK3R1 , and PIK3R3 regulate migration and invasion via the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway in GC cells. In addition, POU2F1 , PIK3R1 , and PIK3R3 expression levels negatively correlated with miR-29b-3p and miR-29a-3p expression levels in GC tissue samples. CONCLUSIONS The POU2F1 - miR-29b-3p / miR-29a-3p-PIK3R1 / PIK3R1 signaling axis regulates tumor progression and may be a promising therapeutic target for GC.
MicroRNAs/metabolism* ; Humans ; Stomach Neoplasms/pathology* ; Cell Line, Tumor ; Cell Movement/physiology* ; Phosphatidylinositol 3-Kinases/metabolism* ; Animals ; Mice ; Octamer Transcription Factor-1/metabolism* ; Mice, Nude ; Class Ia Phosphatidylinositol 3-Kinase/metabolism* ; Neoplasm Invasiveness ; Gene Expression Regulation, Neoplastic/genetics* ; Male ; Immunohistochemistry ; Female

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OBJECTIVE To explore the clinical characteristics of bronchial asthma with secondary pulmonary infec-tions in children and compare the expressions of transcriptomes in peripheral blood between the bronchial asthma with secondary pulmonary infections and the bronchial asthma without the secondary pulmonary infections.METHODS The clinical data were collected from 425 children with bronchial asthma who were treated in respirato-ry medicine department of Children's Hospital of Anhui Province from Apr.2022 to Feb.2025 and were retrospec-tively analyzed.The enrolled children were divided into the infection group with 60 cases and the non-infection group with 365 cases according to the status of complication with pulmonary infections.The clinical characteristics were compared between the infection group and the non-infection group.The gene expression profile sequencing was carried out for peripheral blood mononuclear cells by transcriptome high throughput technology,and the bio-logical information was analyzed.RESULTS There were significant differences in course of asthma,frequencies times of acute attack,complication with nasosinusitis or allergic rhinitis,standardized use of antibiotics and intra-venous use of glucocorticoids between the two groups of children(P＜0.05).Totally 60 children had secondary pulmonary infections,with the infection rate 14.12％.Totally 73 strains of pathogens were isolated,43.84％of which were gram-positive bacteria,and 56.16％were gram-negative bacteria.As compared with the non-infection group,there were 1578 genes with the changed expression in the infection group,and the expressions of the genes such as nuclear factor κB were upregulated.The differentially expressed genes were primarily enriched in immuno-regulation-related pathways,including proinflammatory factor signal transduction,interacted networks of cyto-kines and its receptors,T lymphocyte activation signal transduction and other biological processes.CONCLUSION The specific clinical characteristics and abnormal immune pathways may jointly result in the pulmonary infec-tions in children with the asthma and provide theoretical bases for early identification of the children at high risk of pneumonia and targeted intervention.

Objective:To investigate the clinical manifestations and genetic characteristics of a child with glycogen storage disease type Ⅲ (GSD-Ⅲ) complicated with Guillain-Barré syndrome (GBS) caused by AGL gene variants, and to analyze the pathogenesis, potential correlation, treatment and prognosis of the two diseases. Methods:A child with GSD-Ⅲ who visited the General Hospital of Ningxia Medical University due to " limb weakness for more than ten days" in July 2024 was selected as the study subject. Clinical data of the child were collected. Peripheral blood samples of the child and his parents were collected for whole exome sequencing and Sanger sequencing. Candidate variants were verified, and pathogenicity analysis was conducted for the variant sites. This study was approved by the Medical Ethics Committee of General Hospital of Ningxia Medical University (Ethics No.: KYLL-2025-1984).Results:The child has presented with inability to stand or walk independently, difficulty in grasping, accompanied by numbness and pain at the distal end, choking when drinking water, occasional non-projectile vomiting, and enlargement of liver and spleen. Laboratory tests showed abnormal liver function and a significant increase in creatine kinase. Color Doppler ultrasound of the heart showed an enlarged left atrium and mild regurgitation of mitral and tricuspid valves. Genetic testing confirmed that he has harbored compound heterozygous variants of the AGL gene, namely c. 1611G>A (p.E537E) and c. 579del (p.W194Gfs*7), which were inherited from his father and mother, respectively. According to the guidelines from the American Collage for Medical Genetics and Genomics (ACMG), the two variants were respectively predicted as variant of unknown significance (PM2_Supporting+ PM3+ PP3_Supporting) and likely pathogenic (PVS1+ PM2_Supporting). Electrophysiological examination confirmed that the child had severe damage to the motor and sensory nerves accompanied by axonal injury, which was consistent with the axonal variant type of GBS -acute motor and sensory axonal neuropathy. After a clear diagnosis, the child was treated with intravenous human immunoglobulin. His condition deteriorated progressively, presenting with breathing difficulties, liver failure, and gastrointestinal bleeding, and eventually deceased due to multiple organ failures. Conclusion:The etiology of GSD-Ⅲ and GBS involves multiple aspects such as genetics, metabolism and immunity. In clinical practice, it should be noted that similar clinical manifestations may occur in both conditions. Close attention should be paid to the patients′ blood glucose, blood gas, coagulation function and liver function, etc. Clinical intervention should be carried out as early as possible to improve the prognosis.

Objective:To analyze the epidemic trend of influenza-like illness（ILI）cases，etiological detection results，and the evolution of the hemagglutinin（HA）gene of the predominant strains in Hanzhong City，Shaanxi Province during the 2018-2024 influenza seasons.Methods:ILI sentinel surveillance data and network laboratory test results during the 2018-2024 influenza seasons in Hanzhong City，Shaanxi Province were collected for descriptive analysis. The HA gene sequences of 25 predominant strains were obtained through whole-genome deep sequencing method，and then compared with the vaccine strains recommended by the World Health Organization in the same period to analyze the evolution of the virus.Results:A total of 37 770 cases of ILI were reported in Hanzhong City during the 2018-2024 influenza seasons，and the proportion of total ILI cases（ILI%）was 2.87%（37 770/1 316 009）. The epidemic trend of ILI showed an obvious epidemic peak in winter and spring（from December of the current year to March of the following year）. The specimens with the highest positive rate were of type A（H3N2）（39.12%，365/933），and the predominant epidemic strains in each influenza season alternated among A（H1N1）pdm09（in the 2018-2019 and 2022-2023 influenza seasons），A（H3N2）（in the 2019-2020 and 2023-2024 influenza seasons）and B（Victoria）（in the 2021-2022 influenza season）. The phylogenetic relationship gradually became more distant over time across different influenza seasons. Among them，the epidemic strains of A（H1N1）pdm09 belonged to the 6B.1 clade，and the evolution mainly occurred in the Sa and Sb regions of the HA epitope. Meanwhile，the epidemic strains of A（H3N2）belonged to the 3C clade，and the evolution mainly took place in the A，B and C regions of the HA epitope. The strains of the B（Victoria）lineage belonged to the V1a.3a.2 clade，and the evolution mainly occurred in the 120-loop，150-loop，and 190-helix regions of the HA epitope.Conclusions:The influenza epidemic in Hanzhong City has obvious seasonality，and the amino acids of the epidemic strains have shown a certain degree of variation over the years. In future prevention and control work，influenza surveillance should be continuously strengthened，and the change trend of the predominant circulating strains should be closely monitored.

OBJECTIVE: To investigate the clinical manifestations and genetic characteristics of a child with glycogen storage disease type III (GSD-III) complicated with Guillain-Barré syndrome (GBS) caused by AGL gene variants, and to analyze the pathogenesis, potential correlation, treatment and prognosis of the two diseases. METHODS: A child with GSD-III who visited the General Hospital of Ningxia Medical University due to "limb weakness for more than ten days" in July 2024 was selected as the study subject. Clinical data of the child were collected. Peripheral blood samples of the child and his parents were collected for whole exome sequencing and Sanger sequencing. Candidate variants were verified, and pathogenicity analysis was conducted for the variant sites. This study was approved by the Medical Ethics Committee of General Hospital of Ningxia Medical University (Ethics No.: KYLL-2025-1984). RESULTS: The child has presented with inability to stand or walk independently, difficulty in grasping, accompanied by numbness and pain at the distal end, choking when drinking water, occasional non-projectile vomiting, and enlargement of liver and spleen. Laboratory tests showed abnormal liver function and a significant increase in creatine kinase. Color Doppler ultrasound of the heart showed an enlarged left atrium and mild regurgitation of mitral and tricuspid valves. Genetic testing confirmed that he has harbored compound heterozygous variants of the AGL gene, namely c.1611G>A (p.E537E) and c.579del (p.W194Gfs*7), which were inherited from his father and mother, respectively. According to the guidelines from the American Collage for Medical Genetics and Genomics (ACMG), the two variants were respectively predicted as variant of unknown significance (PM2_Supporting+PM3+PP3_Supporting) and likely pathogenic (PVS1+PM2_Supporting). Electrophysiological examination confirmed that the child had severe damage to the motor and sensory nerves accompanied by axonal injury, which was consistent with the axonal variant type of GBS -acute motor and sensory axonal neuropathy. After a clear diagnosis, the child was treated with intravenous human immunoglobulin. His condition deteriorated progressively, presenting with breathing difficulties, liver failure, and gastrointestinal bleeding, and eventually deceased due to multiple organ failures. CONCLUSION The etiology of GSD-III and GBS involves multiple aspects such as genetics, metabolism and immunity. In clinical practice, it should be noted that similar clinical manifestations may occur in both conditions. Close attention should be paid to the patients' blood glucose, blood gas, coagulation function and liver function, etc. Clinical intervention should be carried out as early as possible to improve the prognosis.
Humans ; Male ; Guillain-Barre Syndrome/complications* ; Glycogen Storage Disease Type III/complications* ; Mutation ; Child