Objective To evaluate the short-term effects of comprehensive health management interventions for stroke high-risk population screening on the prevention and treatment of ischemic stroke, and to provide reference and basis for improving and exploring health management and prevention strategies for stroke high-risk population. Methods From 2018 to 2022, 13 community health service centers in Jiading District, Shanghai were selected in the present study. Based on information push platform, stroke risk assessment and health intervention follow-up were conducted for community residents through convenience sampling. The residents were divided into a full course intervention group (intervention group) and a routine intervention group (control group) according to different health intervention measures and forms. The incidence of ischemic stroke in the two groups of survey subjects was tracked within 36 months. Results A total of 52144 subjects were included in the study. The total number of patients in the full course intervention group was 14227, with an incidence density of 577.32/100 000 (556.49/100 000-598.12/100 000), which was lower than that of the conventional intervention group (37 917), with an incidence density of 1 485.47/100 000 (1 464.99/100 000-1 505.94/100 000) (χ²=2490.212, P<0.001). The relative risk of the full course intervention group was 0.39, and the relative risk of stroke risk factors in the full course intervention group from low to high was 0.33, 0.43, 0.45, and 0.49, respectively. The incidence density of males in the full course intervention group was 660.76 (627.46/100 000 - 694.05/100 000), with a relative risk of 0.43, and the incidence density of female patients was 509.71/100 000 (483.37/100 000 - 536.05/100 000), with a relative risk of 0.35. The overall incidence density of the population under 62 years old gourp, 62-75 years old group and over 75 years old group was 197.45/100 000 (173.09/100 000 -221.80/100 000), 608.36/100 000 (580.19/100 000-636.54/100 000), and 1 025.06/100 000 (958.51/100 000-1 091.61/100 000), with relative risks of 0.51, 0.44, and 0.38, respectively. Conclusion Comprehensive health management measures can effectively reduce the short-term risk of ischemic stroke, and should be further promoted and improved to enhance the effectiveness of stroke prevention and control.

Objective To investigate the mechanism of action of the nuclear factor erythroid 2-related factor 2(Nrf2)/solute carrier family 7 member 11(SLC7A11)/glutathione peroxidase 4(GPX4)signaling pathway in non-alcoholic fatty liver disease(NAFLD),and to explore the mechanism of Gegen QinLian Decoction for the treatment of NAFLD,using in vivo and in vitro experiments.Methods Rats were fed with high-fat chow for 24 weeks to induce NAFLD,and were then divided randomly into normal(C),model(M),high-,medium-,and low-dose Gegen QinLian Decoction(GGQLT-H,GGQLT-M,GGQLT-L),and metformin(Met)groups.From week 25 onwards,the rats were administered the corresponding drugs by gavage for 2 weeks according to the grouping,until sampling.Levels of the oxidative stress markers malondialdehyde(MDA)and glutathione(GSH)in the liver tissues were measured in each group using biochemical kits and ferrous iron(Fe2+)in rat liver tissues was detected using a Fe2+kit.Nrf2,heme oxygenase-1(HO-1),SLC7A11,glutathione synthetase(GSS),GPX4,and acyl coenzyme A synthetase 4(ACSL4)mRNA levels in rat liver tissues were measured by reverse transcription quantitative polymerase chain reaction.For cellular experiments lipid acc umulation was induced in HepG2 hepatocellular carcinoma cells using 1 mmol/L free fatty acid,to mimic the NAFLD in vitro model.Different concentrations of Gegen QinLian Decoction and metformin-containing serum were added for treatment.Lipid accumulation was detected in the cells in each group by Oil red O staining.The MDA and GSH contents of HepG2 cells in the different groups were determined using appropriate kits,and the ferrous contents were detected using a cell-specific ferrous kit.Expression levels of Nrf2,HO-1,SLC7A11,GSS,GPX4,and ACSL4 mRNA was detected in each group of cells using reverse transcription quantitative polymerase chain reaction.Results In the animal experiments,MDA and Fe2+liver levels were significantly higher in the M group than in the C group,while GSH levels were significantly lower(P＜0.01).GGQLT-H,GGQLT-M and Met groups showed significantly reduced MDA and Fe2+and elevated GSH levels compared with the M group(P＜0.01,P＜0.05).High-and medium-dose Gegen QinLian Decoction and metformin increased Nrf2,HO-1,GSS,and GPX4 mRNA and decreased ACSL4 mRNA expression levels(P＜0.01,P＜0.05).In cellular experiments,lipid droplets were significantly increased in the HepG2 cell M group compared with those in the C group,and lipid droplets were significantly reduced by Gegen QinLian Decoction and metformin.MDA and Fe2+levels were significantly increased and GSH levels were significantly decreased in the HepG2 M group compared with the levels in the C group(P＜0.01),while all doses of Gegen QinLian Decoction and metformin significantly decreased MDA and Fe2+levels(P＜0.01)and increased the GSH content(P＜0.01,P＜0.05).Nrf2,GSS,GPX4,and SLC7A11 mRNA expression levels in the GGQLT-H group,Nrf2,HO-1,and SLC7A11 in the GGQLT-L group,HO-1,SLC7A11,and GSS in the GGQLT-M group,and GSS,Nrf2,and HO-1 in the Met group were all significantly increased compared with the findings in the M group(P＜0.01,P＜0.05).ACSL4 mRNA expression levels were significantly decreased in the GGQLT-M and GGQLT-L groups and the Met group(P＜0.01,P＜0.05).Conclusions Gegen QinLian Decoction can improve NAFLD by inhibiting ferroptosis,and its mechanism may he related to regulation of the Nrf2/SLC7A 11/GPX4 signaling pathway.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract, which increases the incidence of colorectal cancer (CRC). In the pathophysiology of IBD, ubiquitination/deubiquitination plays a critical regulatory function. Josephin domain containing 2 (JOSD2), a deubiquitinating enzyme, controls cell proliferation and carcinogenesis. However, its role in IBD remains unknown. Colitis mice model developed by dextran sodium sulfate (DSS) or colon tissues from individuals with ulcerative colitis and Crohn's disease showed a significant upregulation of JOSD2 expression in the macrophages. JOSD2 deficiency exacerbated the phenotypes of DSS-induced colitis by enhancing colon inflammation. DSS-challenged mice with myeloid-specific JOSD2 deletion developed severe colitis after bone marrow transplantation. Mechanistically, JOSD2 binds to the C-terminal of inosine-5'-monophosphate dehydrogenase 2 (IMPDH2) and preferentially cleaves K63-linked polyubiquitin chains at the K134 site, suppressing IMPDH2 activity and preventing activation of nuclear factor kappa B (NF-κB) and inflammation in macrophages. It was also shown that JOSD2 knockout significantly exacerbated increased azoxymethane (AOM)/DSS-induced CRC, and AAV6-mediated JOSD2 overexpression in macrophages prevented the development of colitis in mice. These outcomes reveal a novel role for JOSD2 in colitis through deubiquitinating IMPDH2, suggesting that targeting JOSD2 is a potential strategy for treating IBD.

The liver regenerative capacity is crucial for patients with end-stage liver disease following partial hepatectomy (PHx). The specific bacteria and mechanisms regulating liver regeneration post-PHx remain unclear. This study demonstrated dynamic changes in the abundance of Parabacteroides distasonis (P. distasonis) post-PHx, correlating with hepatocyte proliferation. Treatment with live P. distasonis significantly promoted hepatocyte proliferation and liver regeneration after PHx. Targeted metabolomics revealed a significant positive correlation between P. distasonis and β-hydroxybutyric acid (BHB), as well as hyodeoxycholic acid and 3-hydroxyphenylacetic acid in the gut after PHx. Notably, treatment with BHB, but not hyodeoxycholic acid or 3-hydroxyphenylacetic acid, significantly promoted hepatocyte proliferation and liver regeneration in mice after PHx. Moreover, STAT3 inhibitor Stattic attenuated the promotive effects of BHB on cell proliferation and liver regeneration both in vitro and in vivo. Mechanistically, P. distasonis upregulated the expression of fatty acid oxidation-related proteins, and increased BHB levels in the liver, and then BHB activated the STAT3 signaling pathway to promote liver regeneration. This study, for the first time, identifies the involvement of P. distasonis and its associated metabolite BHB in promoting liver regeneration after PHx, providing new insights for considering P. distasonis and BHB as potential strategies for promoting hepatic regeneration.

The 97th Annual Meeting of the Japanese Gastric Cancer Association was held from March 12 to March 14,2025,in Nagoya,Japan.The conference was chaired by Professor Kazuhiro Uyama from Fujita Medical University and attracted nearly 2 000 scholars from around the world,including Japan,China,the republic of Korea,the United States,and Europe.With the theme of"Digital Innovation in Gastric Tumors,"the conference focused on the application of artificial intelligence,robotic surgery,and other innovations in the treatment of gastric cancer.It explored how high-precision and highly reproducible robotic surgical techniques are transforming traditional approaches to gastric cancer surgery,along with topics such as digital innovation,future medical policies,and strategies that herald a new era in healthcare.The meeting featured one main venue and 60 sub-venues with different themes,ultimately accepting 1 003 submissions.A total of 158 oral presentations covering 80 topics and 203 poster presentations were delivered.Among them,approximately 145 lectures were related to robotic surgery for gastric cancer,and when including poster presentations,nearly 255 topics were associated with gastric cancer robotic surgery.Additionally,the 7th edition of the Japanese Gastric Cancer Treatment Guidelines was released during the meeting.Our team had the honor of participating in this prestigious event.Drawing from our experience at both this conference and the 17th Annual Meeting of the Japanese Society for Robotic Surgery held in Utsunomiya,Japan,from March 7 to March 8,2025,we provide a detailed report on the latest advancements in robotic surgery for gastric cancer,hoping to offer valuable insights and references for fellow surgeons both in China and abroad.

AIM:To investigate the therapeutic effects and potential mechanism of pachymic acid(PA)on li-popolysaccharide(LPS)-induced acute kidney injury(AKI)in mice.METHODS:(1)Genes related to AKI were screened using the DAVID database.Core genes were identified by intersecting related genes and analyzed using Cyto-scape software.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)analyses were performed through the DAVID database for the cross-targets.Molecular docking and activity assays were conducted on the primary core targets.(2)A total of 100 C57BL/6J mice were randomly divided into five groups:normal control(NC),model(LPS),solvent control(LPS+DMSO),and treatment groups(LPS+PA-10 and LPS+PA-20),with 20 mice in each group.The LPS-AKI model was established by intraperitoneal injection of 18 mg/kg LPS.The treatment groups received 10 mg/kg and 20 mg/kg PA,respectively,and the solvent control group was administered an equivalent dose of DMSO.Mice were euthanized 24 h after injection.Serum was collected for biochemical analysis,and Western blot was used to detect neutro-phil gelatinase-associated lipocalin(NGAL),kidney injury molecule-1(KIM-1),caspase-3,cleaved caspase-3,interleu-kin-1β(IL-1β),and monocyte chemoattractant protein-1(MCP-1)protein expression.RT-qPCR was employed to detect inflammatory factor mRNA levels.Molecular docking was used to simulate the optimal binding site of PA to caspase-3.En-zyme activity assays were performed to assess caspase protein activity,and renal lesions were observed via hematoxylin and eosin(HE)staining.Apoptosis was detected by TUNEL staining.RESULTS:(1)Thirty-one potential targets of PA against AKI were identified through network pharmacology.GO and KEGG enrichment analyses indicated that these tar-gets were primarily involved in immune response,inflammatory processes,apoptosis and survival,angiogenesis and hemo-dynamics,oxidative stress,and endoplasmic reticulum stress.Key targets included CASP3(caspase-3),PTGS2,BCL2,CCL2,and CYP219.(2)PA treatment improved renal function and reduced tubular epithelial injury.It significantly de-creased NGAL,KIM-1,and cleaved caspase-3 protein levels,as well as inflammatory factors TNF-α,IL-1β,and MCP-1 mRNA and protein expression.PA also reduced apoptosis of renal tubular epithelial cells.Enzyme activity assays and mo-lecular docking revealed that PA exerted its anti-apoptotic effect by directly binding to caspase-3,thereby inhibiting its ac-tivation by caspase-8.CONCLUSION:PA demonstrated a therapeutic effect in LPS-AKI,potentially through the inhibi-tion of inflammatory factor synthesis and release,as well as the inhibition of caspase-3 activation by caspase-8,reducing apoptosis in renal tubular epithelial cells.

Objective:To observe the intervention effect of personalized nutrition program combined with rehabilitation training in stroke rehabilitation patients.Methods:86 stroke rehabilitation patients who were admitted to our hospital from January 2023 to June 2024 were prospectively selected,they were divided into control group and study group according to the random number table method,with 43 cases in each group,the control group received rehabilitation training,while the study group received personalized nutrition program combine with rehabilitation training.Simple Fugl Meyer motor function(FMA)score,immune function indicators[immunoglobulin(Ig)A,IgG,complement C3,IgM,complement C4],National Institutes of Health Stroke Scale(NIHSS),nutritional status indicators[albumin(ALB),prealbumin(PA),total protein(TP),hemoglobin(HB)],Stroke Specific Quality of Life Scale(SS-QOL),Barthel Index(BI)score were compared between the two groups.Results:NIHSS score in the study group at 8 weeks after intervention was lower than that in the control group,and SS-QOL score,BI score,FMA score,IgM,IgA,IgG,complement C3,complement C4,ALB,HB,TP and PA were higher than those in the control group(P＜0.05).Conclusion:Personalized nutrition program combined with rehabilitation training in stroke rehabilitation patients,can reduce neurological damage,improve limb motor function,enhance nutritional status,immunity,and quality of life.

Objective To explore the potential mechanism of Gegen qinlian decoction(GGQLD)containing serum in ameliorating nonalcoholic fatty liver disease(NAFLD)in human hepatocellular carcinoma HepG2 cells based on transcriptomics.Methods An in vitro model of NAFLD was constructed by free fatty acid(FFA)-induced fat accumulation in HepG2 cells,and cells were treated with different proportions of GGQLD and pioglitazone-containing serum.The lipid deposition in each group was detected by oil red O staining,and the lipid content in each group was evaluated by triglyceride level.Transcriptome technology was used to detect the differentially expressed genes between the intervention groups,and GO annotation analysis,KEGG enrichment analysis and protein interaction(PPI)network analysis were performed to verify the differentially expressed genes by RT-PCR.Results Compared with normal control group,the number of red lipid droplets in the model control group increased,and the triglyceride content increased significantly(P＜0.01).Compared with model control group,the content of red lipid droplets in the GGQLD medium dose group showed a decreasing trend,and the intracellular triglyceride content decreased significantly(P＜0.05).A total of 608 differentially expressed genes were identified by transcriptome analysis,of which 163 differentially expressed genes were up-regulated and 445 differentially expressed genes were down-regulated.GO enrichment analysis showed that the differentially expressed genes were mainly involved in the regulation of MAP kinase phosphatase activity.KEGG analysis showed that the differentially expressed genes were mainly involved in MAPK signaling pathway.RT-PCR results showed that GGQLD up-regulated the expression level of MAP2K6 mRNA and down-regulated the expression levels of FOSL1,CTSL,DUSP5,DUSP1,JUN,HSPA6,IL1A,IL11 and RELB mRNA,which may be mainly involved in MAPK signaling pathway.Conclusion GGQLD has the effect of improving NAFLD,which may be related to MAPK signaling pathway.

The 97th Annual Meeting of the Japanese Gastric Cancer Association was held from March 12 to March 14,2025,in Nagoya,Japan.The conference was chaired by Professor Kazuhiro Uyama from Fujita Medical University and attracted nearly 2 000 scholars from around the world,including Japan,China,the republic of Korea,the United States,and Europe.With the theme of"Digital Innovation in Gastric Tumors,"the conference focused on the application of artificial intelligence,robotic surgery,and other innovations in the treatment of gastric cancer.It explored how high-precision and highly reproducible robotic surgical techniques are transforming traditional approaches to gastric cancer surgery,along with topics such as digital innovation,future medical policies,and strategies that herald a new era in healthcare.The meeting featured one main venue and 60 sub-venues with different themes,ultimately accepting 1 003 submissions.A total of 158 oral presentations covering 80 topics and 203 poster presentations were delivered.Among them,approximately 145 lectures were related to robotic surgery for gastric cancer,and when including poster presentations,nearly 255 topics were associated with gastric cancer robotic surgery.Additionally,the 7th edition of the Japanese Gastric Cancer Treatment Guidelines was released during the meeting.Our team had the honor of participating in this prestigious event.Drawing from our experience at both this conference and the 17th Annual Meeting of the Japanese Society for Robotic Surgery held in Utsunomiya,Japan,from March 7 to March 8,2025,we provide a detailed report on the latest advancements in robotic surgery for gastric cancer,hoping to offer valuable insights and references for fellow surgeons both in China and abroad.

Objective To establish a human luminal breast cancer stem cell(BCSC)model and investigate the inhibitory effects of astragaloside Ⅳ(AS-Ⅳ)on BCSC growth.Methods MCF-7 breast cancer cells were cultured in stem cell-specific medium to induce BCSC formation.The BCSCs were then divided into a blank control group and an AS-Ⅳ treatment group,both groups were given PBS or AS-Ⅳ treatment.Morphological changes were observed after intervention.The therapeutic efficacy of AS-Ⅳ was evaluated using 3D spheroid formation and cell viability assays.Transcriptomic profiling and gene expression analysis were performed to elucidate the underlying mechanisms.Results Compared with the MCF7 breast cancer cells,MCF7 breast cancer stem cell mammospheres exhibited accelerated growth(P＜0.01)and significantly increased expression of the stemness marker ALDH1A1(P＜0.01).Further comparison with the blank control group revealed that astragaloside Ⅳ(AS-Ⅳ)treatment significantly inhibited MCF7 breast cancer stem cell proliferation(P＜0.001)and slowed mammosphere growth(P＜0.01).Transcriptomic analysis demonstrated that differentially expressed genes(DEGs)induced by stem cell modeling and AS-Ⅳ intervention were enriched in the cellular senescence signaling pathway.AS-Ⅳ intervention substantially increased the number of SA-β-gal-positive cells(P＜0.01).RT-PCR analysis confirmed that AS-Ⅳsignificantly upregulated mRNA expression of IL-1α(P＜0.01),P21(P＜0.001),and P53(P＜0.05)in MCF7 breast cancer stem cells.Conclusion Astragaloside Ⅳ suppresses the growth of human luminal breast cancer stem cells by inducing cellular senescence.