Objective To evaluate the safety and efficacy of simultaneous resection for initially resectable rectal cancer with synchronous liver metastases. Methods A retrospective analysis was conducted on 305 patients with initially resectable rectal cancer with synchronous liver metastases. These patients were diagnosed at Zhongshan Hospital, Fudan University from January 2016 to June 2020. Among them, 191 underwent simultaneous rectum and liver resection and 114 underwent staged resection. Propensity score matching (PSM) was performed at a 1∶1 ratio. Clinical data were compared and Kaplan-Meier survival curves were plotted. Results After PSM, 85 patients were included in each group. General data showed no significant differences. Except for liver metastasis resection method, no statistical differences were found in primary tumor surgery approach, intraoperative blood loss, intraoperative complications, time to first flatus and defecation, 30-day mortality, and postoperative hospital stay between the simultaneous resection group and the staged resection group. The overall complication rate was higher in the simultaneous resection group (48.2% vs 29.4%, P＝0.04). Specifically, the grade Ⅱ complications were significantly higher (29.4% vs 14.1%, P＝0.016), but there’s no differences in severe complications (grade Ⅲ-Ⅴ). No statistically differences were observed in median progression-free survival (HR＝0.70, 95%CI 0.50-0.97, P＝0.103) and 5-year overall survival (HR＝0.95, 95%CI 0.63-1.44, P＝0.259). Conclusions Simultaneous resection demonstrates comparable safety and efficacy to staged resection for initially resectable rectal cancer with synchronous liver metastases.

Alzheimer’s disease (AD) is a chronic, progressive, and irreversible neurodegenerative disorder that typically begins with a subtle onset and progresses slowly. Pathologically, it is characterized by two hallmark features: the extracellular accumulation of amyloid β-protein (Aβ), forming senile plaques, and the intracellular hyperphosphorylation of tau protein, resulting in neurofibrillary tangles (NFTs). These pathological changes are accompanied by substantial neuronal and synaptic loss, particularly in critical brain regions such as the cerebral cortex and hippocampus. Clinically, AD presents as a gradual decline in memory, language abilities, and spatial orientation, significantly impairing the quality of life of affected individuals. With the aging population steadily increasing in China, the incidence of AD is rising, making it a major public health concern that requires urgent attention. The growing societal and economic burden of AD underscores the pressing need to identify effective diagnostic biomarkers and develop novel therapeutic strategies. Among the various molecular signaling pathways involved in neurological disorders, the Notch signaling pathway is especially noteworthy due to its evolutionary conservation and regulatory roles in cell proliferation, differentiation, development, and apoptosis. In the central nervous system, Notch signaling is essential for neurodevelopment and synaptic plasticity and has been implicated in several neurodegenerative processes. Although some studies suggest that Notch signaling may influence AD-related pathology, its precise role in AD remains poorly understood. In particular, the interaction between Notch signaling and non-coding RNAs (ncRNAs)—key regulators of gene expression—has received limited attention. NcRNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are known to exert extensive regulatory functions at both transcriptional and post-transcriptional levels. Dysregulation of these molecules has been widely associated with various diseases, including cancers, cardiovascular conditions, and neurodegenerative disorders. Notably, interactions between ncRNAs and major signaling pathways such as Notch can produce widespread biological effects. While such interactions have been increasingly reported in several disease models, comprehensive studies investigating the regulatory relationship between Notch signaling and ncRNAs in the context of AD remain scarce. Given the capacity of ncRNAs to modulate signaling cascades and form complex regulatory networks, a deeper understanding of their crosstalk with the Notch pathway could provide novel insights into AD pathogenesis and reveal potential targets for diagnosis and treatment. In this study, we investigated the regulatory landscape involving the Notch signaling pathway and associated ncRNAs in AD using bioinformatics approaches. By integrating data from multiple public databases, we systematically identified significantly dysregulated Notch pathway-related genes and their interacting ncRNAs in AD. Based on this analysis, we constructed a lncRNA-miRNA-mRNA regulatory network to elucidate the potential mechanisms linking Notch signaling to ncRNA-mediated gene regulation in AD pathogenesis. Furthermore, we explored the internal relationships and molecular mechanisms within this network and assessed the feasibility and clinical relevance of these molecules as early diagnostic biomarkers and potential therapeutic targets for AD. This study aims to deepen our understanding of the molecular basis of AD and offer novel strategies for its diagnosis and treatment.

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.

Objective To investigate the effect of microglia activation regulated by C-X3-C motif chemokine ligand 1(CX3CL1)-C-X3-C motif chemokine receptor 1(CX3CR1)pathway on memory function in hemorrhagic shock/resuscitation rats.Methods The experiment was divided into two parts.In the first part,the rats were randomly divided into sham group,model-0.5 hour group,model-1.5 hour group,model-3 hour group,10 rats in each group.There were differences in the time of hemorrhagic shock among each group.In the second part,rats were randomly divided into control group and CX3CL1 group,10 rats in each group.The rats in CX3CL1 group were treated with CX3CL1 protein factor(intraventricular injection),and the rats in control group were treated with saline.All rats were trained in Morris water maze experiments before model construction,and tests of Morris water maze experiments were carried out after 4 days of model construction.After completion,the whole brains were taken for HE staining and immunohistochemical staining.Cerebrospinal fluid was taken for detection of inflammatory cytokines,and hippocampus tissues were taken for Real-time PCR detection and Western blotting detection.Results Compared with the sham group,the escape latency of rats in model group increased,the number of platform crossings and the resident time in the third quadrant decreased.The neuronal state was impaired in HE staining in model group.In addition,compared with the sham group,the expression of ionized calcium binding adaptor molecule-1(Iba1)in the brain of the rats in model group increased,the contents of tumor necrosis factor-α(TNF-α)and interleukin(IL)-6 in the cerebrospinal fluid increased,and the M1-type microglia markers CD16,TNF-α,IL-1β and inducible nitric oxide synthase(iNOS)mRNA content increased.At the same time,compared with the sham group,the expressions of CX3CL1 and CX3CR1 in the brain of model group decreased,and the expressions of phosphorylated nuclear factor-κB(p-NF-κB)and nucleotide binding oligomerization domain(NOD)-like receptor protein 3(NLRP3)increased.However,compared with the control group,rats in CX3CL1 group had reduced escape latency,increased platform crossing times and quadrantⅢresident time,and recovered neuronal states.In addition,the expression of Iba1 in the brain of CX3CL1 group decreased,the contents of TNF-α and IL-6 in the cerebrospinal fluid decreased,the mRNA contents of M1-type microglia markers like CD16,TNF-α,IL-1β and iNOS decreased,and the mRNA contents of markers of M2-type microglia glial like CD206,transforming growth factor-β(TGF-β),arginase-1(Arg1),Chitinase 3-like protein 1(Ym 1)increased.Conclusion CX3CL1 can help inhibit the excessive activation of microglia,induce the polarization of microglia to M2 type,inhibit the polarization of M1 type,reduce the release of inflammatory cytokines,and alleviate the memory function damage induced by hemorrhagic shock/resuscitation.

Objective:To analyze the current situation of the development and allocation of medical and health resources in Liaoning Province,and provide references and guidance for relevant departments to optimize and balance the allocation of medical resources.Methods:Based on data from the Liaoning Provincial Bureau of Statistics,a comparative analysis was conducted on the development and allocation of medical resources in Liaoning Province from the dimensions of time and geography.Indicators such as Lorentz curve,Gini coefficient,and health resource density index were used to quantitatively evaluate the equity of medical and health resource allocation and distribution in Liaoning Province.Results:The allocation level of medical resources in central cities is relatively high,while the northwest region of the province is relatively weak.Conclusion:In recent years,the allocation of medical resources in various regions of the province has been improved,but differences still exist.These differences can be gradually reduced through policy guidance,introduction of information technology,and strengthening of human resource construction.

Endo-beta-N-acetylglucosaminidase (ENGase) is widely distributed in various organisms. The first reported ENGase activity was detected in Diplococcus pneumoniae in 1971. The protein (Endo D) was purified and its peptide sequence was determined in 1974. Three ENGases (Endo F1-F3) were discovered in Flavobacterium meningosepticum from 1982 to 1993. After that, the activity was detected from different species of bacteria, yeast, fungal, plant, mice, human, etc. Multiple ENGases were detected in some species, such as Arabidopsis thaliana and Trichoderma atroviride. The first preliminary crystallographic analysis of ENGase was conducted in 1994. But to date, only a few ENGases structures have been obtained, and the structure of human ENGase is still missing. The currently identified ENGases were distributed in the GH18 or GH85 families in Carbohydrate-Active enZyme (CAZy) database. GH18 ENGase only has hydrolytic activity, but GH85 ENGase has both hydrolytic and transglycosylation activity. Although ENGases of the two families have similar (β/α)8-TIM barrel structures, the active sites are slightly different. ENGase is an effective tool for glycan detection andglycan editing. Biochemically, ENGase can specifically hydrolyze β‑1,4 glycosidic bond between the twoN-acetylglucosamines (GlcNAc) on core pentasaccharide presented on glycopeptides and/or glycoproteins. Different ENGases may have different substrate specificity. The hydrolysis products are oligosaccharide chains and a GlcNAc or glycopeptides or glycoproteins with a GlcNAc. Conditionally, it can use the two products to produce a new glycopeptides or glycoprotein. Although ENGase is a common presentation in cell, its biological function remains unclear. Accumulated evidences demonstrated that ENGase is a none essential gene for living and a key regulator for differentiation. No ENGase gene was detected in the genomes of Saccharomyces cerevisiae and three other yeast species. Its expression was extremely low in lung. As glycoproteins are not produced by prokaryotic cells, a role for nutrition and/or microbial-host interaction was predicted for bacterium produced enzymes. In the embryonic lethality phenotype of the Ngly1-deficient mice can be partially rescued by Engase knockout, suggesting down regulation of Engase might be a solution for stress induced adaptation. Potential impacts of ENGase regulation on health and disease were presented. Rabeprazole, a drug used for stomach pain as a proton inhibitor, was identified as an inhibitor for ENGase. ENGases have been applied in vitro to produce antibodies with a designated glycan. The two step reactions were achieved by a pair of ENGase dominated for hydrolysis of substrate glycoprotein and synthesis of new glycoprotein with a free glycan of designed structure, respectively. In addition, ENGase was also been used in cell surface glycan editing. New application scenarios and new detection methods for glycobiological engineering are quickly opened up by the two functions of ENGase, especially in antibody remodeling and antibody drug conjugates. The discovery, distribution, structure property, enzymatic characteristics and recent researches in topical model organisms of ENGase were reviewed in this paper. Possible biological functions and mechanisms of ENGase, including differentiation, digestion of glycoproteins for nutrition and stress responding were hypothesised. In addition, the role of ENGase in glycan editing and synthetic biology was discussed. We hope this paper may provide insights for ENGase research and lay a solid foundation for applied and translational glycomics.

Objective To observe the effect of remifentanil-based fast-track anesthesia on the quality of anesthesia recovery in children with congenital heart disease underwent transcatheter closure.Methods Children with congenital heart disease who underwent transcatheter closure were divided into treatment group and control group according to the anesthesia plan.The anesthesia plan of the control group was as follows:anesthesia induction(intramuscular injection of ketamine at 4 mg·kg-1,intravenous injection of propofol at 2.5 mg·kg-1,fentanyl at 10 μg·kg-1and cisatracurium at 0.1 mg·kg-1)and anesthesia maintenance(fentanyl at0.4μg·kg-1·min-1 and propofol at 8 μg·kg-1·min-1).The anesthesia plan of the treatment group was as follows:anesthesia induction(intramuscular injection of ketamine at 5 mg·kg-,intravenous injection of midazolam at 0.1 mg·kg-1,sufentanil at 1.0 μg·kg-1 and cisatracurium at 0.1 mg·kg-1)and anesthesia maintenance(remifentanil at 0.5 μg·kg-1·min-1 and propofol at 8 μg·kg-1·min-1).Anesthesia recovery,facial expression,leg posture,activity,crying and comfortability(FLACC)of 5 pain scores,Ramsay score,hemodynamics,myocardial injury indexes,and adverse drug reactions were compared between the two groups.Results There were 64 cases in treatment group and 56 cases in control group.The spontaneous respiration recovery time,call time and extubation time of the treatment group were(4.87±1.22),(10.16±2.58)and(12.55±3.19)min,shorter than those in control group,which were(5.49±1.35),(13.34±3.27)and(15.67±3.62)min(all P＜0.05).At 1 h and 2 h after operation,Ramsay scores of treatment group were 2.58±0.35 and 3.69±0.42,were lower than 3.02±0.47 and 4.24±0.39 in control group(all P＜0.05).At 1 h and 2 h after operation,the FLACC scores of the treatment group were 3.03±0.81 and 3.75±0.84,lower than 3.78±0.62 and 4.36±0.51 in control group(all P＜0.05).Mean arterial pressure(MAP)of treatment group at the insertion of laryngeal mask,the insertion of occluder and the end of the operation were(102.45±10.26),(94.18±8.37)and(91.46±10.15)mmHg,lower than those in control group,which were(107.84±10.11),(100.57±9.84)and(97.33±8.53)mmHg(all P＜0.05).On day 1 and day 3 after operation,serum creatine kinase isoenzyme(CK-MB)levels in the treatment group were(10.03±2.58)and(8.65±2.16)U·L-1,lower than those in control group,which were(12.44±3.07)and(10.16±2.35)U·L-1(all P＜0.05).On day 1 and day 3 after operation,serum cardiac troponin Ⅰ(cTn Ⅰ)levels in treatment group[(0.07±0.02)and(0.04±0.01)μg·L-1]were lower than those in control group[(0.09±0.03)and(0.06±0.02)μg·L-1](all P＜0.05).The incidence of adverse anesthesia reactions in treatment group was 6.25％(4 cases/64 cases),lower than 17.86％(10 cases/56 cases)in control group(P＜0.05).Conclusion Remifentanil-based fast-track anesthesia can improve the quality of anesthesia recovery in children with congenital heart disease undergoing transcatheter closure,with good sedative and analgesic effects,stable hemodynamics during operation,and low incidence of adverse drug reactions.

Objective To investigate the effects of simvastatin mediated adenylate activated protein kinase/peroxisome proliferator-activated receptor-γ-coactivator 1 α(AMPK/PGC-1α)pathway on neural function in rats with Parkinson's disease.Methods Parkinson's disease model was established in SD rats.After successful modeling,they were divided into model group,positive group(1.67 mg·kg-1 metoba),experimental-L group(10 mg·kg-1 simvastatin),experimental-H group(20 mg·kg-1 simvastatin),BML-275 group(20 mg·kg-1 simvastatin+0.25 mg·kg-1 AMPK inhibitor BML-275)and 10 normal rats were selected as control group.Enzyme-linked immunosorbent assay(ELISA)was used to detect dopamine(DA),3,4 dihydroxyphenylacetic acid(DOPAC),homovanillic acid(HVA),5-hydroxyindoleacetic acid(5-HIAA),5-hydroxytryptamine(5-HT);Western blot was used to detect the expression of tyrosine hydroxylase(TH)and AMPK/PGC-1α pathway-related proteins;TH expression was detected by immunohistochemistry,malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)were detected by kit.Results The DA of control group,model group,experimental-H group and BML-275 group were(495.63±34.30),(207.53±24.10),(429.39±44.89)and(285.55±20.79)pg·mL-1,respectively;DOPAC were(33.38±2.48),(17.70±1.31),(29.12±1.72)and(20.67±1.45)ng·mL-1,respectively;HVA were(58.75±6.25),(25.27±2.00),(46.16±2.83)and(30.58±1.91)ng·mL-1,respectively;5-HT were(5.62±0.45),(2.37±0.13),(4.42±0.26)and(3.23±0.29)ng·mL-1,respectively;5-HIAA were(11.11±1.08),(3.88±0.30),(7.99±0.63)and(6.04±0.51)ng·mL-1,respectively;p-AMPK protein expression were 0.98±0.06,0.35±0.04,0.80±0.05 and 0.21±0.02,respectively;PGC-1α protein expression were 1.12±0.11,0.40±0.04,0.90±0.08 and 0.58±0.05,respectively.There were statistically significant differences in the above indexes between control group and model group,and between model group and experimental-H group and inhibitor group(all P＜0.05).Conclusion Simvastatin can improve the neural function of Parkinson's disease rats by regulating AMPK/PGC-1α pathway.

Objective To explore the potential mechanism of action of paeoniflorin in diabetes mellitus,the related targets and pathways were preliminarily discussed,based on the network pharmacology and molecular docking technology.Methods Analyze the potential targets of paeoniflorin using the Swiss Target Prediction database.Genecards and OMIM databases yielded the genes of diabetes-related illnesses.After taking the intersection of the two,protein-protein interaction network(PPI)was established using STRING and Cytoscape programs to search for key genes with strong correlation and complete gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis.Use AutoDockTools and Pymol programs to complete protein molecule docking validation.Results The pharmacologically-related study revealed 63 targets associated with paeoniflorin,4 758 genes related to diabetes,and 50 intersection targets.15 key genes including vascular endothelial growth factor A(VEGFA),epidermal growth factor receptor(EGFR),V-Ha-ras harvey(HRAS),V-src sarcoma(SRC)and heat shock protein hs 90-alpha(HSP90AA1)were screened.RAs-associated protein 1,Ras,calcium and other signaling pathways were obtained by KEGG pathway analysis.Molecular docking results showed that paeoniflorin had good binding ability with key genes.Conclusion Paeoniflorin can treat diabetes through multiple targets and pathways,and this mechanism can provide a basis for the application of paeoniflorin in anti diabetes and drug research and development.

Objective:To understand the major cognition, major choice motivation and the relationship between the two of medical students, and provide references and suggestions for the selection of talents in various majors of medical schools and the effective development of enrollment work.Methods:This study selected undergraduates of Batch 2019 from Peking University Health Science Center as the survey objects, conducted a questionnaire survey on their major cognition, major choice motivation and influencing factors, and used principal component analysis and Spearman rank correlation analysis.Results:The study found that the major cognition scores of 640 undergraduates of Batch 2019 from Peking University Health Science Center were clinical medicine (3.24±0.89) > stomatology (2.89±1.00) > basic medicine (2.66±1.02) > pharmacy (2.54±0.97) > preventive medicine (2.29±0.93) > nursing medicine (2.21±0.99) > medical laboratory (1.98±0.95) > medical English (1.95±0.93). Six major motivation factors for professional choice were school and professional strength, professional learning and job prospects, own factors, Peking University sentiments and the influence of others, medical factors, school policies, and the contribution rates were 34.60%, 12.97%, 7.42%, 6.00%, 5.59% and 5.37%, respectively. Major cognition scores and major choice motivation factors were positively correlated with each other to some extent.Conclusions:At present, students' major cognition level of medical majors still has a large room for improvement, and the motivational factors of major choice are more complicated, among which "the school and professional strength" and "the prospects of study and work" are important factors. Medical schools should focus on strengthening major publicity, improving students' major cognition, attracting aspiring students to apply for medical majors from many aspects, and improving the training quality of medical professionals.