Biomedical and environmental sciences : BES最新文献

Neurosyphilis (NS) is an infectious disease caused by Treponema pallidum invading the central nervous system. It can manifest at any stage of syphilis, and is often misdiagnosed due to its atypical and progressive symptoms. The increasing incidence of NS underscores the necessity for early and accurate diagnosis. Here, we present a case where routine cerebrospinal fluid metagenomic next-generation sequencing (mNGS) was used to diagnose a patient with neurosyphilis. The patient exhibited cognitive impairment and was initially diagnosed with cerebral infarction due to syphilitic cerebral arteritis. Thus, the patient was treated with dual antiplatelet therapy (aspirin and clopidogrel) and statins to stabilize the plaques. Neurosyphilis was treated with penicillin sodium injections, resulting in significant improvement in the patient's mental state. This case is a rare instance of neurosyphilis associated with cerebral infarction. These findings suggest that mNGS is a valuable tool in diagnosing neurosyphilis, potentially improving diagnostic accuracy and patient outcomes.

Objective: To analyze the relationship between Chemokine IP10 and its receptor CXCR3 during prion infection.

Methods: We investigated the increases in IP10 signals, primarily localized in neurons within the brains of scrapie-infected mice, using western blotting, ELISA, co-immunoprecipitation, immunohistochemistry, immunofluorescence assays, and RT-PCR.

Results: Both CXCR3 levels and activation were significantly higher in the brains of scrapie-infected mice and prion-infected SMB-S15 cells. Enhanced CXCR3 expression was predominantly observed in neurons and activated microglia. Morphological colocalization of PrP ^C/PrP ^Sc with IP10/CXCR3 was observed in scrapie-infected mouse brains using immunohistochemistry and immunofluorescence. immunohistochemistry (IHC) analysis of whole brain sections further revealed increased accumulation of IP10/CXCR3 specifically in brain regions with higher levels of PrP ^Sc deposits. Co-immunoprecipitation and biomolecular interaction assays revealed the molecular interactions between PrP and IP10/CXCR3. Notably, a significantly larger amount of IP10 accumulated within prion-infected SMB-S15 cells than in the normal partner cell line, SMB-PS. Importantly, resveratrol treatment effectively suppressed prion replication in SMB-S15 cells, thereby restoring the accumulation and secretion pattern of cellular IP10 similar to that observed in SMB-PS cells.

Conclusion: Our data demonstrate that the activation of IP10/CXCR3 signaling in prion-infected brain tissues coincides with PrP ^Sc deposition. Modulation of IP10/CXCR3 signaling in the brain represents a potential therapeutic target for mitigating the progression of prion diseases.

Objective: To comprehensively examine the molecular epidemiological characteristics of human rhinovirus (HRV) in Beijing.

Methods: A total of 7,151 children and adults with acute respiratory tract infections (ARTIs) were recruited from 35 sentinel hospitals in Beijing between 2018 and 2022. Their respiratory samples were obtained, and epidemiological and clinical data were collected. Nucleic acid testing for 11 respiratory pathogens, including HRV, was performed on the specimens. We sequenced VP4/VP2 or 5'UTR of HRV isolates to identify their genotypes using phylogenetic analyses.

Results: HRV was detected in 462 (6.5%) cases. A total of 105 HRV genotypes were successfully identified in 359 (77.7%) specimens, comprising 247 (68.8%) with HRV-A, 42 (11.7%) with HRV-B, and 70 (19.5%) with HRV-C. No predominant genotype was observed. HRV was prevalent year-round with two weak peaks in spring and autumn. HRV detection declined gradually between 2018 and 2022, with seven genotypes disappearing and five genotypes emerging. HRV detection rate decreased by age without resurge among old people. HRV-C was more common among children aged less than 5 years with severe community-acquired pneumonia compared to HRV-A and HRV-B. Adults infected with HRV-B had higher rates of hospitalization, intensive care unit admission, and complications than those infected with HRV-A and HRV-C.

Conclusion: HRV epidemics in Beijing were highly dispersed in genotypes, which probably resulted in a high prevalence of HRV infection, attenuated its seasonality, and made it more difficult to establish effective population immunity.

Objective: In this study, we analyzed the transcriptome sequences of Kupffer cells exposed to simulated microgravity for 3 d and conducted biological experiments to determine how microgravity initiates apoptosis in Kupffer cells.

Methods: Rotary cell culture system was used to construct a simulated microgravity model. GO and KEGG analyses were conducted using the DAVID database. GSEA was performed using the R language. The STRING database was used to conduct PPI analysis. qPCR was used to measure the IL1B, TNFA, CASP3, CASP9, and BCL2L11 mRNA expressions . Western Blotting was performed to detect the level of proteins CASP3 and CASP 9. Flow cytometry was used to detect apoptosis and mitochondrial membrane cells. Transmission electron microscopy was used to detect changes in the ultrastructure of Kupffer cells.

Results: Transcriptome Sequencing indicated that simulated microgravity affected apoptosis and the inflammatory state of Kupffer cells. Simulated microgravity improved the CASP3, CASP9, and BCL2L11 expressions in Kupffer cells. Annexin-V/ PI and JC-1 assays showed that simulated microgravity promoted apoptosis in Kupffer cells. Simulated microgravity causes M1 polarization in Kupffer cells.

Conclusion: Our study found that simulated microgravity facilitated the apoptosis of Kupffer cells through the mitochondrial pathway and activated Kupffer cells into M1 polarization, which can secrete TNFA to promote apoptosis.

Objective: This study aimed to explore the spatial heterogeneity and risk factors for dental caries in 12-year-old children in Shanxi province, China.

Methods: The data encompassed 3,721 participants from the two most recent oral health surveys conducted across 16 districts in Shanxi Province in 2015 and 2018. Eighteen specific variables were analyzed to examine the interplay between socioeconomic factors, medical resources and environmental conditions. The Geo-detector model was employed to assess the impacts and interactions of these ecological factors.

Results: Socioeconomic factors ( Q = 0.30, P < 0.05) exhibited a more substantial impact compared to environmental ( Q = 0.19, P < 0.05) and medical resource factors ( Q = 0.25, P < 0.05). Notably, the urban population percentage (UPP) demonstrated the most significant explanatory power for the spatial heterogeneity in caries prevalence, as denoted by its highest q-value ( q = 0.51, P < 0.05). Additionally, the spatial distribution's heterogeneity of caries was significantly affected by SO ₂ concentration ( q = 0.39, P < 0.05) and water fluoride levels ( q = 0.27, P < 0.05) among environmental factors.

Conclusion: The prevalence of caries exhibited spatial heterogeneity, escalating from North to South in Shanxi Province, China, influenced by socioeconomic factors, medical resources, and environmental conditions to varying extents.

Objective: Previous studies on the association between lipid profiles and chronic kidney disease (CKD) have yielded inconsistent results and no defined thresholds for blood lipids.

Methods: A prospective cohort study including 32,351 subjects who completed baseline and follow-up surveys over 5 years was conducted. Restricted cubic splines and Cox models were used to examine the association between the lipid profiles and CKD. A regression discontinuity design was used to determine the cutoff value of lipid profiles that was significantly associated with increased the risk of CKD.

Results: Over a median follow-up time of 2.2 (0.5, 4.2) years, 648 (2.00%) subjects developed CKD. The lipid profiles that were significantly and linearly related to CKD included total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), TC/HDL-C, and TG/HDL-C, whereas low-density lipoprotein cholesterol (LDL-C) and LDL-C/HDL-C were nonlinearly correlated with CKD. TC, TG, TC/HDL-C, and TG/HDL-C showed an upward jump at the cutoff value, increasing the risk of CKD by 0.90%, 1.50%, 2.30%, and 1.60%, respectively, whereas HDL-C showed a downward jump at the cutoff value, reducing this risk by 1.0%. Female and participants with dyslipidemia had a higher risk of CKD, while the cutoff values for the different characteristics of the population were different.

Conclusion: There was a significant association between lipid profiles and CKD in a prospective cohort from Northwest China, while TG, TC/HDL-C, and TG/HDL-C showed a stronger risk association. The specific cutoff values of lipid profiles may provide a clinical reference for screening or diagnosing CKD risk.