Objective: To analyze changes in tuberculosis infection among junior high school students before and after tuberculosis exposure, so as to provide a reference for improving school tuberculosis prevention and control measures and policy formulation. Methods: Retrospectively collect data on a tuberculosis outbreak that occurred in a grade of a junior high school in Chongqing in 2025, including tuberculosis screening records of students in this grade upon their enrollment in 2022 (1 156 students) and after two tuberculosis outbreaks in 2023 (206 students) and 2025 (171 students). The Wilcoxon signed rank test for paired design was used to compare the induration diameters of the subjects, and the Chi square test was adopted to analyze the rate of tuberculosis infection among students. Results: In the tuberculosis outbreak in 2023, the rate of tuberculosis infection among close contacts ( 11.84 %) and the rate of tuberculosis infection among freshrman at school enrollment (12.89%) showed no statistically significant difference ( χ 2=0.25, P >0.05). The rate of tuberculosis infection of close contacts in the 2025 tuberculosis outbreak (55.56%) was higher than that in the 2023 outbreak (11.84%) ( χ 2=30.42, P <0.01). Among the 106 students included in the cohort analysis, the median induration diameter was 3.50 (1.50, 7.50) mm in 2023 and 8.75 (4.25, 11.50) mm in 2025, with a statistically significant difference ( Z=-5.76, P <0.01). There was no statistically significant difference between the infection rate in 2022 (16.98%) and that in 2023 (10.38%) ( χ 2=1.96, P =0.16). The infection rate in 2025 (43.40%) was higher than those in 2022 and 2023 ( χ 2=17.55, 29.39, both P <0.017). The seroconversion rate of students in the same class in 2025 ( 58.00 %) was higher than that of students in different classes (16.07%), with a statistically significant difference ( χ 2=20.19, P <0.01). All 72 individuals with latent tuberculosis infections identified during the pandemic in 2023 and 2025 refused to undergo prophylactic treatment. Conclusions The lack of preventive treatment may be the underlying cause of the successive outbreaks during the epidemic. Early detection of infection sources and standardized outbreak management are crucial to controlling the spread of the epidemic.

Objective: To identify early clinical predictors associated with dysphagia and delayed swallowing recovery in patients with traumatic brain injury (TBI). Methods: In this retrospective study, we enrolled adult TBI patients admitted to the rehabilitation unit of a tertiary medical center between June 2019 and June 2023. Data on baseline characteristics, neurological status, imaging findings, and rehabilitation-related variables were collected. Swallowing function was assessed using two indicators: (1) nasogastric (NG) tube retention and (2) the Functional Oral Intake Scale (FOIS) scores at 1, 4, and 12 weeks post-injury. Regression analyses were conducted to identify predictors associated with dysphagia and swallowing recovery. Results: A total of 160 patients were included. At 1 week post-injury, longer intensive care unit (ICU) stay, poor initial sitting balance and use of sedative medication in ICU were associated with NG tube retention. At 4 weeks, lower initial Rancho Los Amigos Scale (RLAS) scores, immobility-related complications, longer hospitalization, and temporal lobe hematomas were associated with persistent NG tube dependence. By 12 weeks, older age, delayed ability to follow commands, and poor initial sitting balance remained associated with NG tube retention. FOIS outcomes were also associated with older age, delayed time to follow commands, impaired initial sitting balance, prolonged ICU stay, temporal lobe hematomas, lower initial RLAS scores, immobility-related complications, prolonged endotracheal tube placement and extended hospital stays. Conclusion Impaired cognitive status, poor physical function, immobility-related complications, and temporal lobe hematomas were key factors associated with dysphagia and delayed oral intake in individuals with TBI.

A portable molecularly imprinted(MIP)surface-enhanced Raman scattering(SERS)chip was fabricated via a green electrochemical approach for highly selective detection of bisphenol A(BPA).This MIP-AuNP/UIO-66/SPE sensor was fabricated through a single-step co-deposition process.The process involved electropolymerization onto a UIO-66 modified screen-printed electrode(SPE),by usingo-phenylenediamine(OPD)as functional monomer and BPA as template,and simultaneously electro-reduction generated gold nanoparticles(AuNPs),which served as the SERS-active substrate.Ultimately,this one-step method formed a three-dimensional porous architecture on the electrode surface.Under 785 nm laser excitation,the sensing chip exhibited a highly sensitive SERS response towards BPA.The intensity of its characteristic peak at 850 cm-1 showed a good linear relationship with logarithm of BPA concentration in the range of 1.0×10-10 to 1.0×10-6 mol/L,with a detection limit of 1.0×10-12 mol/L.More importantly,the fabricated chips maintained highly selective binding affinity for BPA in water samples even in the presence of structural analogs bisphenol F(BPF)and bisphenol S(BPS).When the chip was applied to detection of BPA in water samples from plastic bottle and paper cup,the recovery rates ranged from 94.0%to 103.0%with relative standard deviations(RSD)less than 4.7%.The developed chip offered a highly sensitive and selective solution for detection of trace BPA in complex water samples.

ObjectiveThis study leverages structural data from antigen-antibody complexes of the influenza A virus neuraminidase (NA) protein to investigate the spatial recognition relationship between the antigenic epitopes and antibody paratopes. MethodsStructural data on NA protein antigen-antibody complexes were comprehensively collected from the SAbDab database, and processed to obtain the amino acid sequences and spatial distribution information on antigenic epitopes and corresponding antibody paratopes. Statistical analysis was conducted on the antibody sequences, frequency of use of genes, amino acid preferences, and the lengths of complementarity determining regions (CDR). Epitope hotspots for antibody binding were analyzed, and the spatial structural similarity of antibody paratopes was calculated and subjected to clustering, which allowed for a comprehensively exploration of the spatial recognition relationship between antigenic epitopes and antibodies. The specificity of antibodies targeting different antigenic epitope clusters was further validated through bio-layer interferometry (BLI) experiments. ResultsThe collected data revealed that the antigen-antibody complex structure data of influenza A virus NA protein in SAbDab database were mainly from H3N2, H7N9 and H1N1 subtypes. The hotspot regions of antigen epitopes were primarily located around the catalytic active site. The antibodies used for structural analysis were primarily derived from human and murine sources. Among murine antibodies, the most frequently used V-J gene combination was IGHV1-12*01/IGHJ2*01, while for human antibodies, the most common combination was IGHV1-69*01/IGHJ6*01. There were significant differences in the lengths and usage preferences of heavy chain CDR amino acids between antibodies that bind within the catalytic active site and those that bind to regions outside the catalytic active site. The results revealed that structurally similar antibodies could recognize the same epitopes, indicating a specific spatial recognition between antibody and antigen epitopes. Structural overlap in the binding regions was observed for antibodies with similar paratope structures, and the competitive binding of these antibodies to the epitope was confirmed through BLI experiments. ConclusionThe antigen epitopes of NA protein mainly ditributed around the catalytic active site and its surrounding loops. Spatial complementarity and electrostatic interactions play crucial roles in the recognition and binding of antibodies to antigenic epitopes in the catalytic region. There existed a spatial recognition relationship between antigens and antibodies that was independent of the uniqueness of antibody sequences, which means that antibodies with different sequences could potentially form similar local spatial structures and recognize the same epitopes.

Early-life stress (ES) leads to cognitive dysfunction in female adolescents, but the underlying neural mechanisms remain elusive. Recent evidence suggests that the cell adhesion molecules NECTIN1 and NECTIN3 play a role in cognition and ES-related cognitive deficits in male rodents. In this study, we aimed to investigate whether and how nectins contribute to ES-induced cognitive dysfunction in female adolescents. Applying the well-established limited bedding and nesting material paradigm, we found that ES impairs recognition memory, suppresses prefrontal NECTIN1 and hippocampal NECTIN3 expression, and upregulates corticotropin-releasing hormone (Crh) and its receptor 1 (Crhr1) mRNA levels in the hippocampus of adolescent female mice. Genetic experiments revealed that the reduction of dorsal CA1 (dCA1) NECTIN3 mediates ES-induced object recognition memory deficits, as knocking down dCA1 NECTIN3 impaired animals' performance in the novel object recognition task, while overexpression of dCA1 NECTIN3 successfully reversed the ES-induced deficits. Notably, prefrontal NECTIN1 knockdown did not result in significant cognitive impairments. Furthermore, acute systemic administration of antalarmin, a CRHR1 antagonist, upregulated hippocampal NECTIN3 levels and rescued object and spatial memory deficits in stressed mice. Our findings underscore the critical role of dCA1 NECTIN3 in mediating ES-induced object recognition memory deficits in adolescent female mice, highlighting it as a potential therapeutic target for stress-related psychiatric disorders in women.
Animals ; Female ; Mice ; CA1 Region, Hippocampal/metabolism* ; Cell Adhesion Molecules/metabolism* ; CRF Receptor, Type 1/metabolism* ; Memory Disorders/etiology* ; Mice, Inbred C57BL ; Nectins/genetics* ; Receptors, Corticotropin-Releasing Hormone/antagonists & inhibitors* ; Recognition, Psychology/physiology* ; Stress, Psychological/complications*

Numerous studies on the formation and consolidation of memory have shown that memory processes are characterized by phase-dependent and dynamic regulation. Memory retrieval, as the only representation of memory content and an active form of memory processing that induces memory reconsolidation, has attracted increasing attention in recent years. Although the molecular mechanisms specific to memory retrieval-induced reconsolidation have been gradually revealed, an understanding of the time-dependent regulatory mechanisms of this process is still lacking. In this study, we applied a transcriptome analysis of memory retrieval at different time points in the recent memory stage. Differential expression analysis and Short Time-series Expression Miner (STEM) depicting temporal gene expression patterns indicated that most differential gene expression occurred at 48 h, and the STEM cluster showing the greatest transcriptional upregulation at 48 h demonstrated the most significant difference. We then screened the differentially-expressed genes associated with that met the expression patterns of those cluster-identified genes that have been reported to be involved in learning and memory processes in addition to dipeptidyl peptidase 9 (DPP9). Further quantitative polymerase chain reaction verification and pharmacological intervention suggested that DPP9 is involved in 48-h fear memory retrieval and viral vector-mediated overexpression of DPP9 countered the 48-h retrieval-induced attenuation of fear memory. Taken together, our findings suggest that temporal gene expression patterns are induced by recent memory retrieval and provide hitherto undocumented evidence of the role of DPP9 in the retrieval-induced reconsolidation of fear memory.
Animals ; Fear/physiology* ; Male ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases/genetics* ; Memory Consolidation/physiology* ; Time Factors ; Mental Recall/drug effects* ; Mice ; Gene Expression Profiling

OBJECTIVE: To assess the independent and combined effects of air pollutants, meteorological factors, and greenspace exposure on new tuberculosis (TB) cases. METHODS: TB case data from Shanghai (2013-2018) were obtained from the Shanghai Center for Disease Control and Prevention. Environmental data on air pollutants, meteorological variables, and greenspace exposure were obtained from the National Tibetan Plateau Data Center. We employed a distributed-lag nonlinear model to assess the effects of these environmental factors on TB cases. RESULTS: Increased TB risk was linked to PM _2.5, PM ₁₀, and rainfall, whereas NO ₂, SO ₂, and air pressure were associated with a reduced risk. Specifically, the strongest cumulative effects occurred at various lags: PM _2.5 ( RR = 1.166, 95% CI: 1.026-1.325) at 0-19 weeks; PM ₁₀ ( RR = 1.167, 95% CI: 1.028-1.324) at 0-18 weeks; NO ₂ ( RR = 0.968, 95% CI: 0.938-0.999) at 0-1 weeks; SO ₂ ( RR = 0.945, 95% CI: 0.894-0.999) at 0-2 weeks; air pressure ( RR = 0.604, 95% CI: 0.447-0.816) at 0-8 weeks; and rainfall ( RR = 1.404, 95% CI: 1.076-1.833) at 0-22 weeks. Green space exposure did not significantly impact TB cases. Additionally, low temperatures amplified the effect of PM _2.5 on TB. CONCLUSION Exposure to PM _2.5, PM ₁₀, and rainfall increased the risk of TB, highlighting the need to address air pollutants for the prevention of TB in Shanghai.
China/epidemiology* ; Humans ; Air Pollutants/analysis* ; Tuberculosis/epidemiology* ; Incidence ; Meteorological Concepts ; Particulate Matter/adverse effects* ; Environmental Exposure ; Male ; Female ; Adult ; Air Pollution ; Middle Aged

Objective To evaluate the reliability and validity and perform cost-consequence analysis of the brief version of the Montreal cognitive assessment(MoCA)for identifying cognitive impairment in a community-based population ≥50 years of age.Methods The internal consistency and retest reliability of the brief version of the MoCA were analyzed,and the area under the curve(AUC),sensitivity,and specificity were determined to discriminate mild cognitive impairment(MCI)and dementia with the clinical dementia rating(CDR)as the diagnostic criterion.The consistency between the brief version and the full version was analyzed by the Kappa test and the Bland-Altman method,and the number of individuals entering the diagnostic assessment and the overall assessment time were estimated and compared between the two versions.Results A total of 303 individuals were included in this study,of whom 192,94,and 17 had normal cognitive function,MCI,and dementia,respectively.The Cronbach's α and re-test coefficients of the brief version of MoCA were 0.754 and 0.711(P<0.001),respectively.The brief version showed the AUC,sensitivity,and specificity of 0.889,74.5%,and 93.8% for identifying MCI,and 0.994,100%,and 93.8% for identifying dementia,respectively.When the brief version of MoCA was used to identify 94 patients with MCI in 303 individuals,107 individuals required additional diagnostic assessment,with an overall assessment time of 142.4 h,which represented decreases of 21.3% and 32.7%,respectively,compared with those of the full version.When the brief version of MoCA was used to identify 17 patients with dementia in 303 individuals,35 individuals required additional diagnostic assessment,with an overall assessment time of 70.4 h,a decrease of 29.5% in the time cost compared with the full version.Conclusions The brief version of MoCA can identify cognitively impaired individuals in a community-based middle-aged and elderly population,with diagnostic validity comparable to that of the full version but less time cost and fewer individuals needing additional diagnostic assessment to detect true-positive cases.It could be expanded for use in the community-based primary screening setting.
Humans ; Aged ; Middle Aged ; Cognitive Dysfunction/diagnosis* ; Male ; Female ; Mental Status and Dementia Tests ; Reproducibility of Results ; Dementia/diagnosis* ; Sensitivity and Specificity ; Aged, 80 and over ; Cost-Benefit Analysis

This study was aimed at identifying the pathogenic bacteria responsible for the death of a young tiger at the Fujian Meihua Mountain South China Tiger Breeding Research Institute.Tissue samples from the lungs,liver,and intestines of the deceased tiger were collected,and the bacteria were cultured inasterile environment.The bacterial strains were characterized according to their morphological and molecular biological properties,including assessment of virulence genes and antibiotic resistance genes,mouse lethality tests,and antibiotic susceptibility evaluations.A predominant bacterial strain isolated from the liver of the deceased tiger was identified as enterotoxigenic Escherichia coli(ETEC)strain Tiger22513F.Phylogenetic analysis of the 16S rRNA gene revealed that the Tiger22513F strain exhibited close genetic similarity to the reference strain ETEC(MF919609.1),with 99.9%nucleotide similarity,and resided on the same evolutionary branch.The Tiger22513F strain contained 11 antibiotic resistance genes(tetA,sul1,sul3,cmlA,floR,blaTEM,blaSHV,blaCMY-2,qnrA,qnrS,and qnrD)along with five virulence genes(VT1,fyuA,tsh,iucD,and ST).Mouse lethality tests indicated significant pathogenicity toward mice,affecting primarily the lungs,liver,and intestines.Antibiotic susceptibility testing demonstrated that this strain exhibited resistance to various classes of beta-lactam antibiotics,as well as quinolones and aminoglycosides.This investigation successfully isolated a multi-drug resistant enterotoxigenic Escherichia coli strain with pronounced pathogenicity from the liver of a deceased tiger;thus providing valuable scientific insights for clinical diagnosis,as well as prevention and control measures,against ETEC infections in South China tigers.

Objective To systematically evaluate the safety and efficacy of replacing tyrosine kinase inhibitors(TKIs)with similar drugs after they cause liver injury,based on case reports and case series studies.Methods PubMed,Embase,Cochrane,Web of Science,CNKI,Wanfang,and VIP databases were searched up to October 2023.Two reviewers independently screened the literature,extracted data,and assessed the quality of the studies.Descriptive and statistical analyses were performed.Results Twenty-six studies(22 case reports and 4 case series)were included,involving 75 patients who switched to similar drugs for TKI-induced liver injury,primarily targeting the epidermal growth factor receptor(EGFR),anaplastic lymphoma kinase(ALK),and multiple targets.The results indicate that majority of patients have favorable safety profiles after switching drugs,with normal liver function or no severe liver injury.Only one patient reported a serious liver adverse reaction,characterized by(grade 3 total bilirubin elevation).In terms of clinical efficacy,most patients responded well to the new TKIs,maintaining stable disease,or showing no progression during follow-up.Disease progression occurred in only two patients who switched from gefitinib to erlotinib after dose reduction due to non-hepatic adverse effects.Additionally,one patient who switched from erlotinib to afatinib experienced worsening tumor symptoms.Conclusion Evidence from published case reports and case series suggests that continuing treatment with similar drugs after TKI-induced liver injury,targeting EGFR,ALK,and multiple targets,demonstrates a certain degree of safety,efficacy,and clinical practicability.This can be a strategy after TKI discontinuation due to liver injury.However,there are no clear guidelines on drug selection,timing,and dosage,and further research is urgently needed.