ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

Objective:To evaluate the cost-effectiveness and impact on mortality of health management services for the elderly aged 65 years and older in national essential public health service project.Methods:Based on the data of county-level medical institutions in Henan Province from 2019 to 2024,the Random Forest Method was used to construct a counterfactual framework to predict the hospitalization expenses under the unmanaged scenario,and then the cost-benefit ratio(BCR)and net income were calculated.Time-dependent Cox proportional hazards model was used to evaluate the effect of health management on all-cause mortality and cardiovascular and cerebrovascular disease mortality in the elderly.Results:A total of 962 955 elderly patients were included,451 119(46.85%)were included in the management group.The average hospitalization cost of the management group was significantly lower than that of the non-management group(P<0.05).Except for 2020-2021,BCRS in 2019 and 2022-2024 were 6.34,2.05,4.45 and 6.60,respectively.The risk of all-cause death was reduced by 76.96%,and the risk of cardiovascular and cerebrovascular death was reduced by 75.57%in the elderly patients included in the management group compared with those not included in the management group.Suggestions:It is necessary to establish a health outcomes-based evaluation system and promote the transformation and upgrading of the service model from single chronic disease management to"integrated health services with multi-disease management".

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

Objective:To evaluate the surgical outcomes of recalcitrant medial epicondylitis combined with recalcitrant lateral epicondylitis or without.Methods:A retrospective study was conducted to analyze the clinical data of the 41 patients who had undergone suture repair of the flexor tendon via a small incision for recalcitrant medial epicondylitis between January 2010 and December 2023 at Department of Sports Medicine, Beijing Jishuitan Hospital, Capital Medical University. There were 13 males and 28 females, with an age of (52.4±7.6) years and duration of symptoms of 12 (6, 24) months. Of the patients, 26 suffered from simple recalcitrant medial epicondylitis (the simple group) and 15 recalcitrant medial epicondylitis combined with recalcitrant lateral epicondylitis (the combined group subjected to additional suture repair of the lateral tendon). The visual analogue scale (VAS) for pain, Mayo elbow performance score (MEPS), disabilities of the arm, shoulder, and hand (DASH) score, and grip strength level were evaluated at preoperation, postoperative 3 months, and the final follow-up to evaluate the surgical efficacy. Comparisons were made within the 2 groups.Results:The follow-up time for all patients was 12 (12, 16) months. At postoperative 3 months and the final follow-up, the VAS pain score [3.0 (1.8, 5.0) points, and 0.0 (0.0, 2.0) point], MPES [85.0 (81.3, 85.0) points, and 100.0 (85.0, 100.0) points], and DASH score [18.9 (12.7, 26.7) points, and 0.0 (0.0, 7.3) point] in the simple group were significantly improved compared with those at preoperation [5.0 (4.0, 7.0) points, 70.0 (65.0, 85.0) points, and 34.9 (23.2, 46.2) points] ( P<0.05). In the simple group, the grip strength at the final follow-up (88.4%±7.0%) was significantly improved compared with that at preoperation (50.2%±14.7%) ( P<0.05), but the difference in the grip strength was not statistically significant between that at postoperative 3 months (56.2%±12.3%) and that at preoperation ( P=0.137). In the combined group, at postoperative 3 months and the final follow-up, the VAS pain score [3.0 (3.0, 4.0) points, and 0.0 (0.0, 1.0) point], MPES [85.0 (85.0, 85.0) points, and 100.0 (85.0, 100.0) points], DASH score [16.7 (13.3, 23.3) points, and 3.3 (0.0, 7.0) points], and grip strength (58.9%±11.2%, and 86.9%±5.5%) were significantly improved compared with those at preoperation [5.0 (5.0, 7.0) points, 70.0 (60.0, 70.0) points, 45.6 (33.3, 46.6) points, and 43.7%±16.1%] ( P<0.05). Follow-ups revealed no complications requiring further treatment in all the patients. Conclusions:Early clinical follow-ups show that suture repair of the affected tendon through a small incision is an effective treatment of recalcitrant medial epicondylitis. Additional suture repair of the lateral tendon can also achieve good outcomes for those combined with recalcitrant lateral epicondylitis.

Aim To explore the mechanism of the effect of siRNA-mediated MAGE-3 silencing on intesti-nal flora,gastric mucosal PTEN expression and liver metastasis in rats with gastric cancer based on MAPK/ERK signaling pathway.Methods Thirty rats were randomly divided into the normal(CO)group,model(MO)group,and MAGE-3 silenced(SM)group,with 10 rats in each group.The model of MO group and SM group was established by MNNG gavage meth-od.After successful modeling,the SM group was intri-toneally injected with 20 μg·kg-1 shRNA MAGE-3 lentiviral vector.The number of intestinal flora in rats was detected by selective medium of intestinal flora,the expression of PTEN in gastric mucosa was detected by immunohistochemistry,liver metastasis was detected by HE staining,and the protein expression of MAPK/ERK signaling pathway was detected by Western blot.The regulatory effect of siRNA-mediated MAGE-3 si-lencing on MAPK/ERK signaling pathway was verified in vitro.Results Compared with CO group,the con-tents of Enterococcus and Escherichia coli,the protein expressions of P-MEK1,P-ERK1 and P-ELK1 in MO group increased(P＜0.05),while the contents of Lactobacillus and Bifidobacterium and the expression of PTEN decreased(P＜0.05).In SM group,the con-tents ofEnterococcus,Escherichiacoli,P-MEK1,P-ERK1 and P-ELK1 protein expressions decreased(P＜0.05),while the contents of Lactobacillus,Bifidobac-terium and PTEN expression increased(P＜0.05).Compared with group CO,the protein expressions of P-MEK1,p-ERK1 and P-ELK1 in group MO were not significantly different(P＞0.05),while the protein expressions of P-MEK1,p-ERK1 and P-ELK1 in group SM were reduced compared with group MO(P＜0.05).Conclusions siRNA-mediated MAGE-3 si-lencing can significantly improve intestinal flora,pro-mote the expression of PTEN in gastric mucosa,and inhibit liver metastasis in rats with gastric cancer.The mechanism may be related to the inhibition of MAPK/ERK signaling pathway.

Bovine rotavirus(BRV)is an important pathogen causing diarrhea in calves.To understand the genomic charac-teristics and genetic variations in bovine rotavirus,and to further enrich data on the biological characteristics of rotavirus,we aimed to amplify 11 gene segments of the isolated and cultured G6P[1]bovine rotavirus BLL strain,perform whole genome se-quencing,and analyze the molecular characteristics.MEGA7.0 and DNAMAN software were used for homology and typing a-nalysis,and the whole genome phylogenetic tree was constructed to analyze genetic evolution relationships.The complete geno-type of the BLL strain was G6-P[1]-I2-R2-C2-M2-A3-N2-T6-E2-H3.Phylogenetic analysis of the VP7 and VP4 genes of the BLL strain showed that the VP7 gene had the highest homology with RVA/Cow-wt/HB01/China/2021,and the VP4 gene of the BLL strain was in the same branch as RVA/Human-tc/ISR/Ro8059/1995.From the sequence alignment of VP8*amino acids,the sialic acid domain of the BLL strain was found to be similar to that in other P[1]strains,but different from those in other types of strains,except for residue 189,which was the same as that in Ro8059 but different from that in other strains.The results suggested that the BLL strain might potentially infect humans.Therefore,continued monitoring and study of the biological characteristics of this strain are necessary to provide more information and evidence supporting further research on the cross-species transmission of group A rotavirus in China.

Objective To explore an experimental protocol for differentiating human-induced pluripotent stem cells(iPSCs)into highly pure midbrain dopaminergic(DA)neurons.Methods By optimizing a blend of small molecules and recombinant human growth factors,iPSCs were induced to differentiate into ventral midbrain floor plate DA progenitor cells and subsequently into mature substantia nigra pars compacta DA neurons.Throughout the differentiation process,Real-time PCR and immunofluorescent staining were utilized as a method for quality assessment.Results iPSCs firstly differentiate into dopaminergic precursor cells,and then gradually differentiate into DA neurons expressing tyrosine hydroxylase(TH).Conclusion The protocol successfully yields approximately high purity tyrosine hydroxylase-positive(TH+)DA neurons.This differentiation technique offers an effective cellular model for studying the physiological mechanisms and pathogenesis of Parkinson's disease,providing valuable insights for future research and potential therapeutic strategies.

Recent studies have indicated that the expression of ubiquitin-specific protease 51 (USP51), a novel deubiquitinating enzyme (DUB) that mediates protein degradation as part of the ubiquitin‒proteasome system (UPS), is associated with tumor progression and therapeutic resistance in multiple malignancies. However, the underlying mechanisms and signaling networks involved in USP51-mediated regulation of malignant phenotypes remain largely unknown. The present study provides evidence of USP51's functions as the prominent DUB in chemoresistant triple-negative breast cancer (TNBC) cells. At the molecular level, ectopic expression of USP51 stabilized the 78 kDa Glucose-Regulated Protein (GRP78) protein through deubiquitination, thereby increasing its expression and localization on the cell surface. Furthermore, the upregulation of cell surface GRP78 increased the activity of ATP binding cassette subfamily B member 1 (ABCB1), the main efflux pump of doxorubicin (DOX), ultimately decreasing its accumulation in TNBC cells and promoting the development of drug resistance both in vitro and in vivo. Clinically, we found significant correlations among USP51, GRP78, and ABCB1 expression in TNBC patients with chemoresistance. Elevated USP51, GRP78, and ABCB1 levels were also strongly associated with a poor patient prognosis. Importantly, we revealed an alternative intervention for specific pharmacological targeting of USP51 for TNBC cell chemosensitization. In conclusion, these findings collectively indicate that the USP51/GRP78/ABCB1 network is a key contributor to the malignant progression and chemotherapeutic resistance of TNBC cells, underscoring the pivotal role of USP51 as a novel therapeutic target for cancer management.