International Journal of General Medicine最新文献

Background: Acyl-CoA synthetase long-chain family member 4 (ACSL4) is an index of ferroptosis. Here, serum ACSL4 levels were examined to determine their prognostic significance and mediating roles in patients with acute intracerebral hemorrhage (ICH).

Methods: In this observational analytical study, serum ACSL4 levels were measured at admission in 317 patients with supratentorial intraparenchymal hemorrhage and at study entry in 100 controls. The National Institutes of Health Stroke Scale (NIHSS) score and hematoma volume were used as the severity metrics. Poor prognosis was designated as modified Rankin Scale (mRS) 3-6 at six months following ICH. Stroke-associated pneumonia (SAP) was defined as an acute lower airway infection within a week post-ICH. The outcome variables of interest were SAP and poor prognosis. Multifactorial means were implemented for severity and outcome analyses.

Results: Patients had significantly higher serum ACSL4 levels than controls. Serum ACSL4 levels remained linearly connected with NIHSS scores, hematoma volume, SAP, mRS scores, and poor prognosis under restricted cubic spline and kept substantially associated with them even after adjusting for other confounding factors. The independent associations with poor prognosis and SAP were robust via sensitivity analysis, and exhibited no interactions with age, sex, tobacco smoking, and others through subgroup analysis. Regarding the predictive ability for poor prognosis and SAP under the receiver operating characteristic curve, serum ACSL4 levels were statistically comparable to the NIHSS scores and hematoma volume. Using mediation analysis, serum ACSL4 levels partially mediated the associations of NIHSS scores and hematoma volume with poor prognosis and SAP, and SAP in part mediated the relationship between serum ACSL4 levels and mRS scores plus poor prognosis.

Conclusion: Enhanced serum ACSL4 levels post-ICH are significantly linked to ICH severity and clinical outcomes, and serum ACSL4 may partially interpret outcome associations, therefore extrapolating serum ACSL4 as a prognostic adjunct of ICH.

Objective: This study aimed to investigate the distribution of pathogens, the usage of antimicrobial agents, and the sensitivity analysis of antimicrobial agents in patients with urinary tract infections (UTIs) in a certain hospital from 2021 to 2023, so as to provide clinical evidence for the selection of antimicrobial agents in clinical patients with UTIs.

Methods: A retrospective review was conducted on medical records of patients diagnosed with UTI during 2021-2023. Demographic characteristics (gender, age), urine sample data, pathogen distribution, and antimicrobial prescription patterns were collected. Midstream urine specimens submitted to the microbiology laboratory were processed for bacterial culture, identification, and antibiotic susceptibility testing. Differences in resistance rates to various antimicrobials were compared among pathogens from different clinical categories.

Results: From 2021 to 2023, 623 cases of positive urine culture samples were detected. Gram-negative organisms predominated (489 isolates), particularly Escherichia coli (E. coli, 61.80%, 385 isolates). Gram-positive isolates were mainly Enterococcus faecalis (6.10%, 38 isolates) and Enterococcus faecium (E. faecalis, 4.01%, 25 isolates). Gender distribution revealed that E. coli was more frequent in females (69.87%), while other principal pathogens were more common in males. Age analysis showed higher prevalence in females at young and middle age, whereas elderly males predominated (68.60%). Susceptibility testing indicated marked interspecies differences: E. coli showed 81.56% resistance to ampicillin; Proteus mirabilis exhibited 72.73% resistance to levofloxacin; E. faecalis demonstrated 94.74% resistance to tetracycline. Conversely, cefotaxime/clavulanic acid and vancomycin retained good activity against most isolates.

Conclusion: From 2021 to 2023, E. coli was the leading UTI pathogen. There were significant differences in the susceptibility of various pathogens to antimicrobial agents. It is necessary to regularly monitor the distribution of pathogens causing UTIs and their sensitivity to antimicrobial agents to provide a scientific reference for the rational use of antimicrobial agents during treatment.

Background: Neuronal PAS domain protein 1 (NPAS1) is a protein-coding gene expressed mainly in the central nervous system and plays a key role in nervous system development. The expression and prognostic value of NPAS1 in colorectal adenocarcinoma (COAD) are unknown.

Methods: The expression and clinicopathological data of COAD from Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were analyzed. NPAS1 gene expression in colon cancer tissues was validated by Western blotting and immunohistochemical staining. Function and immune infiltration were established using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA), and single sample Gene Set Enrichment Analysis (ssGSEA). Methylation levels were analyzed utilizing the UALCAN database. NPAS1-related mutations were analyzed using cBioPortal. Single-cell and tissue-specific expression of NPAS1 was examined using the Human Protein Atlas. Protein-protein interactions and transcription factor networks of NPAS1-associated genes were analyzed with STRING and Network Analyst.

Results: Our study found that the expression level of NPAS1 was higher in normal tissues compared to COAD tissues, higher NPAS1 expression was associated with better survival outcomes. The bioinformatics analysis confirmed that NPAS1 co-expressed genes were linked to diverse signalling pathways and cellular functions. NPAS1 is correlated with CD56bright, cytotoxic and NK cells, and negatively correlated with helper T cells and Tcm cells. The DNA methylation level of NPAS1 in tumor tissues was elevated compared to normal tissues. We analyzed the mutation characteristics of NPAS1, single-cell expression profiling of NPAS1, and protein-protein interactions involving genes associated with NPAS1. These discoveries offered perspectives on the etiology, identification, and management of COAD.

Conclusion: This study revealed a significant decrease of NPAS1 expression in COAD tissues, exhibiting associations with the clinical stage, prognosis, immune infiltration, and DNA methylation of COAD.

Background: Post-stroke upper extremity motor impairment poses a significant challenge to rehabilitation. While repetitive transcranial magnetic stimulation (rTMS) and scalp acupuncture are effective individually, the precise mechanisms and synergistic efficacy of their combination remain to be fully elucidated.

Purpose: This study aims to evaluate the therapeutic efficacy of MEP-guided scalp acupuncture combined with rTMS versus rTMS alone. Additionally, it intends to investigate the underlying neuromodulation mechanisms using functional near-infrared spectroscopy (fNIRS).

Methods: This prospective, single-blind, randomized controlled trial includes patients with stroke-induced upper limb motor deficits. Participants are randomly assigned to either an experimental group (combined therapy) or a control group (rTMS alone) for a 4-week intervention. Both groups receive concurrent conventional rehabilitation. Follow-up assessments will be conducted 4 weeks after the completion of the treatment to evaluate the sustained effects.

Results: Primary clinical outcome measures include the Fugl-Meyer Assessment-Upper Extremities (FMA-UE) and maximum amplitude of Motor Evoked Potentials (MEP). Secondary clinical outcome measures include Action Research Arm Test (ARAT), Modified Barthel Index (MBI) and fNIRS data acquisition.

Conclusion: This study is expected to provide evidence for an optimized, multi-target rehabilitation regimen. By integrating clinical scales with fNIRS neuroimaging, it seeks to reveal the neural mechanisms of brain network reorganization driven by this combined therapy.

Clinical trial registration: ClinicalTrials.gov, identifier NCT07210944.

Objective: Patients on maintenance hemodialysis face a disproportionately high burden of cardiovascular disease, with major adverse cardiovascular events being the leading cause of death. However, the relative importance and specific roles of traditional versus non-traditional risk factors in this unique population require further elucidation in clinical practice. This study aimed to investigate the risk factors for major adverse cardiovascular events in patients undergoing maintenance hemodialysis, thereby providing evidence for clinical risk stratification and early intervention.

Methods: A single-center retrospective study was carried out, enrolling 196 patients with end-stage renal disease who received regular MHD (duration ≥ 6 months) between January 2021 and August 2022. According to MACE occurrence during follow-up, patients were categorized into MACE (n = 66) and non-MACE (n = 130) groups. Baseline characteristics, comorbidities, and laboratory parameters were collected. Logistic regression analysis was utilized to assess independent risk factors for MACEs, and their predictive value was evaluated using receiver operating characteristic (ROC) curve analysis.

Results: Over a 21-month follow-up, the cumulative MACE incidence was 33.67%. Multivariate analysis revealed that serum albumin was an independent protective factor for MACEs (OR = 0.679, 95% CI: 0.558-0.827, P < 0.01), whereas C-reactive protein (CRP) was an independent risk factor (OR = 1.151, 95% CI: 0.994-1.334, P = 0.046). ROC curve analysis demonstrated that the combination of serum albumin and CRP provided the best predictive performance, with an area under the curve (AUC) of 0.7224 (sensitivity 81.77%, specificity 51.52%).

Conclusion: Low serum albumin and elevated CRP are independent risk factors for MACEs in MHD patients. The combined assessment of these two biomarkers offers good predictive value for MACEs and may serve as an effective tool for clinical screening of high-risk patients.

Objective: Gestational diabetes mellitus (GDM) is a common pregnancy complication with adverse maternal and neonatal consequences. Probiotics have been proposed as a non-pharmacological intervention, but their effectiveness remains controversial. This study aimed to evaluate the methodological quality and reported efficacy evidence of systematic reviews and meta-analyses (SRs/MAs) on probiotic supplementation in pregnant women with GDM.

Methods: Four electronic databases were searched for English-language SRs/MAs published between 2017 and 2024 that examined probiotic supplementation in women with GDM. Methodological quality was assessed using PRISMA 2020, AMSTAR 2, and ROBIS, and reported efficacy outcomes were systematically synthesized.

Results: A total of 16 SRs/MAs were included. According to the AMSTAR-2 assessment, four studies were rated as low quality, while the remaining studies were rated very low. The PRISMA assessment showed that 8 of the 27 items had reporting completeness above 80%, whereas items 5, 8, and 22 showed completeness below 60%; at the study level, 12 SRs/MAs achieved overall PRISMA reporting completeness above 80%. The ROBIS scale assessment results showed that all SRs/MAs were rated as low risk of bias in Phase 1, Domain 1, Domain 3, and six items of Domain 4, as well as 12 items in Phase 3. However, in Domain 2, all SRs/MAs were rated as high risk. Regarding efficacy evaluation, probiotic supplementation significantly improved FPG, insulin-related indices (FSI, HOMA-IR, HOMA-B, QUICKI), and lipid profiles (TG, TC, HDL-C, VLDL-C). In addition, probiotics showed effects on markers of inflammation (CRP) and oxidative stress (NO, MDA, GSH, TAC) and indicated benefits in reducing neonatal risks. However, heterogeneity and overlap among primary studies were identified.

Conclusion: Probiotic supplementation demonstrates efficacy in improving metabolic biomarkers related to GDM and maternal and neonatal outcomes. Nevertheless, the overall certainty of evidence is limited by suboptimal methodological quality, heterogeneity, and overlap among primary studies.

Objective: Semaglutide shows potential in cardiovascular protection, yet its specific role and mechanism in H/R injury are unclear. Given the role of autophagy in cardiomyocyte protection and the unclear mechanism of semaglutide in H/R - induced injury, this study aims to assess semaglutide's protective effects on AC16 cardiomyocytes in an H/R model and probe its mechanism, focusing on autophagy.

Methods: AC16 cardiomyocytes were subjected to H/R to simulate H/R injury. Cells were divided into five groups: Control, H/R, H/R+Semaglutide, H/R+ Semaglutide+Rapamycin (autophagy activator), and H/R+Semaglutide+3-Methyladenine (3-MA, autophagy inhibitor). Cell viability, injury (LDH release), oxidative stress (MDA, SOD), and inflammation (IL-6, TGF-β) were assessed. Protein levels of cleaved caspase-3, caspase-9, Bax, Bcl-2, and the autophagy-related protein FUNDC1 were analyzed by Western blot.

Results: H/R treatment significantly decreased cell viability and increased LDH release, indicating severe cellular injury (P< 0.05). Semaglutide treatment effectively restored cell viability and reduced LDH release. Furthermore, Semaglutide significantly attenuated H/R-induced oxidative stress, as shown by decreased MDA levels and restored SOD activity (P< 0.05). The inflammatory response, characterized by elevated IL-6 and TGF-β, was also markedly suppressed by Semaglutide (P< 0.05). Flow cytometry analysis revealed that Semaglutide significantly reduced the apoptosis rate. Western blotting confirmed that Semaglutide downregulated pro-apoptotic proteins (cleaved caspase-3, caspase-9, Bax) and upregulated the anti-apoptotic protein Bcl-2. Importantly, Semaglutide increased the expression of FUNDC1. The protective effects were enhanced by Rapamycin and attenuated by 3-MA, indicating that autophagy is involved in the cardioprotection.

Conclusion: Semaglutide shows substantial protective efficacy in safeguarding AC16 from H/R-triggered injury. It operates by mitigating oxidative stress, dampening inflammatory processes, inhibiting apoptotic pathways. Importantly, this investigation revealed that the cardioprotective effect, to a considerable degree, mediated through its promotion of autophagy.

Background and objective: Osteoporosis (OP) is a metabolic disease characterized by reduced bone mass and increased fracture risk. Tryptophan metabolism may play a crucial role in its pathogenesis, although the underlying mechanisms remain unclear. This study aimed to identify key regulatory genes and elucidate molecular mechanisms through integrated transcriptomic analysis.

Methods: OP-related datasets from Gene Expression Omnibus were analyzed using differential expression analysis, weighted gene co-expression network analysis, and tryptophan metabolism gene sets. Machine learning algorithms were applied to screen key genes and construct diagnostic models. Regulatory networks including protein-protein interaction, competing endogenous RNA, and transcriptional regulation were established. Key findings were validated through independent datasets, Mendelian Randomization, single-cell analysis, and RT-qPCR.

Results: Two key genes were identified: DVL1 (significantly downregulated) and RBM39 (significantly upregulated) in OP patients. DVL1 negatively correlated with resting memory CD4+ T cells and eosinophils, while RBM39 positively correlated with memory B cells and M2 macrophages. DVL1 (AUC = 0.75) and RBM39 (AUC = 0.91) demonstrated consistent expression patterns and excellent diagnostic performance. Functional enrichment revealed significant involvement in apoptosis, autophagy, and signaling pathways. Transcription factor YY1 was identified as a key regulator in the molecular network.

Conclusion: This bioinformatic study reveals the potential role of tryptophan metabolism in OP pathogenesis and identifies DVL1 and RBM39 as candidate diagnostic biomarkers and therapeutic targets through computational analysis. These findings are inferential based on transcriptomic data mining and require further validation through experimental approaches. Future studies should include functional characterization in cellular and animal models, prospective clinical cohort validation, and mechanistic investigations to confirm the diagnostic and therapeutic value of these candidates. If validated, these findings could provide a molecular foundation for developing non-invasive diagnostic tools and precision medicine approaches in OP management, potentially improving early detection and personalized treatment strategies for patients at risk of osteoporotic fractures.

Objective: To investigate the association between cognitive impairment and multimodal magnetic resonance imaging (MRI) markers in patients with cerebral microbleeds (CMBs), and to identify imaging predictors of CMB-related cognitive dysfunction.

Methods: This retrospective case-control study included 71 patients with CMBs confirmed by MRI between August 2022 and February 2024 and 65 age-matched healthy controls. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA). All participants underwent multimodal MRI, including susceptibility-weighted imaging (SWI) for CMB detection and diffusion tensor imaging (DTI) for quantitative assessment of fractional anisotropy (FA) and apparent diffusion coefficient (ADC) in predefined brain regions. Spearman correlation analysis was performed to evaluate associations between CMB burden, DTI parameters, and cognitive scores. Multivariate linear regression analysis was used to identify independent risk factors for cognitive impairment.

Results: Compared with controls, patients with CMBs had significantly lower MoCA scores and higher CMB burden (both P < 0.05). FA values in the frontal-temporal lobe, parietal lobe, and basal ganglia were significantly reduced, while ADC values were increased (all P < 0.05). CMB number was negatively correlated with MoCA scores (r = -0.643, P < 0.001). Decreased FA and increased ADC in the frontal-temporal lobe and basal ganglia were significantly associated with cognitive decline. Regression analysis showed that CMB burden ≥10, reduced FA, elevated ADC, and basal ganglia involvement were independent risk factors for cognitive impairment.

Conclusion: Cognitive impairment in CMB patients is closely associated with lesion burden and microstructural white matter alterations detected by multimodal MRI. These imaging markers may facilitate early risk stratification and targeted monitoring, although longitudinal validation is warranted.

Pelvic inflammatory disease (PID) is an inflammatory process of the upper genital tract that is mainly caused by sexually transmitted infections (STI). It can cause tubal factor infertility, ectopic pregnancy, or chronic pelvic pain. In recent years, its incidence has increased annually owing to various factors, such as sexually transmitted diseases and intrauterine surgery. Although empirical treatment, such as antibiotics or surgery, can alleviate the symptoms of pelvic inflammatory disease, the obstetric outcome is not ideal and the recurrence rate is high, which places a heavy physical and mental burden on women. Traditional Chinese medicine (TCM) is a complementary therapy to Western medicine that has a complete theoretical and practical system and has attracted international attention because of its excellent curative effect. An increasing number of people are accepting and trying to use traditional Chinese medicine to treat gynecological diseases, including infertility, polycystic ovary syndrome, and PID; however, its efficacy and mechanism are still controversial. Therefore, this article summarizes the related research on traditional Chinese medicine and Western medicine in the treatment of PID for clinical reference.