Human papillomavirus (HPV) DNA testing is an important method in cervical cancer screening. However, the studies on prevalence and genotype distribution of HPV among women in northeastern Guangdong Province of China are very limited. A total of 28,730 women attending the Department of Gynecology of Meizhou People’s Hospital (Huangtang Hospital), Meizhou Hospital Affiliated to Sun Yat-sen University between January 1st, 2013 and June 1st, 2015 were enrolled in this study. HPV type-specific distribution was tested using flow-through hybridization and gene chip. The overall prevalence of HPV infection was 19.81%, among which 79.09% were infected with high-risk HPV subtypes in the subjects. The 5 most predominant genotypes were HPV16, 52, 58, 18 and 81. Most HPV infections were observed in women aged 41–50 and women aged 30–59 accounted for a proportion of over 80%. Our findings suggested a high burden of HPV infection among women in northeastern Guangdong Province of China. We identified the top 5 HPV genotypes as well as the age-specific distribution of HPV infections in this area.

Despite significant advances in the management of acute coronary syndromes (ACS), there are still plenty of patients undergoing percutaneous coronary intervention (PCI) and stent implantation suffered poor prognosis and high treatment expenditure. Evidence increasingly suggests that the ratio of low-density lipoprotein cholesterol/high-density lipoprotein cholesterol (LDL-C/HDL-C) ratio might be a novel marker for the risk of atherosclerotic cardiovascular disease, but the impact of LDL-C/HDL-C ratio on 1-year prognosis of drug-eluting stent (DES) implantation patients after PCI is still not reported. Our aim of the study was to investigate the impact of LDL-C/HDL-C ratio on 1-year prognosis of DES implantation patients after PCI. Between May 2014 and July 2016, 1937 patients who were underwent primary PCI and DES implantation and achieving LDL-C with statins were enrolled and divided into two groups based on the ratio of LDL-C/HDL-C. The entire occurrence of adverse cardiovascular events according to the ratio of LDL-C/HDL-C showed that there were no significant differences in 1-year cardiovascular death (hazard ratio [HR]: 1.97, 95% confidence interval [CI]: 0.49 to 7.84, P = 0.329), myocardial infarction (MI) (HR: 1.66, 95% CI: 0.84 to 3.28, P = 0.172) and bleeding events (HR: 1.08, 95% CI: 0.83 to 1.41, P = 0.598) The cumulative incidence of target lesion revascularization (TLR) (HR: 1.43, 95% CI: 1.10 to 1.86, P = 0.007), stent thrombosis (ST) (HR: 2.04, 95% CI: 1.06 to 3.93, P = 0.037) and major adverse cardiac events (MACE) (HR: 1.54, 95% CI: 1.24 to 1.91, P < 0.001) were significantly higher in high group than in low group. Multivariate Cox regression analysis revealed that age (HR: 1.556, 95%, CI: 1.198 to 2.021, P < 0.001), together with diabetes mellitus (HR: 1.490, 95% CI: 1.142 to 1.945, P = 0.003), and ratio of LDL-C/HDL-C (HR: 1.638, 95% CI: 1.260 to 2.218, P < 0.001) were independent predictors of 1-year MACE. The Kaplan-Meier cumulative MACE-free survival curves with a log-rank test showed that the presence of high ratio of LDL-C/HDL-C was associated with higher incidences of MACE after PCI with DES implantation. The high LDL-C/HDL-C ratio was associated with cardiovascular events in patients with ACS after PCI and DES implantation.

Introduction: Sepsis is associated with high mortality. Early intervention is crucial to reducing sepsis-related mortality. This study aims to assess the clinical potential of S100A8/A9 and resistin as novel biomarkers for predicting mortality risk in sepsis patients.Method: Serum samples were collected and analyzed from 141 adult sepsis patients (discovery cohort), 43 non-sepsis intensive care units (ICU) patients, 15 healthy volunteers, and 55 sepsis patients along with 17 non-sepsis ICU patients (validation cohort). The 28-day mortality and sequential organ failure assessment (SOFA) scores of the participants were compared. Additionally, the predictive ability of S100A8/A9 and resistin for sepsis mortality was evaluated using the area under the receiver operating characteristic curve at ICU admission.Results: The concentrations of S100A8/A9 and resistin in sepsis patients were noticeably increased relative to non-sepsis patients and healthy controls. Serum S100A8/A9 concentrations in surviving sepsis patients were significantly higher than in non-surviving patients. On the day of admission, serum resistin concentrations in Gram-negative (G-) sepsis patients were considerably elevated relative to Gram-positive (G+) infected sepsis patients. Among sepsis patients admitted to the ICU, the AUC for S100A8/A9 in predicting 28-day mortality was 0.617 (P = 0.032; 95% confidence bounds 0.513–0.721), and for SOFA was 0.750 (P < 0.0001; 95% confidence bounds 0.660–0.840). Sepsis patients with high serum S100A8/A9 concentrations (≥ 377.53 ng/mL) had a higher survival rate relative to those with low concentrations (<377.53 ng/mL). In the validation cohort, the AUC for S100A8/A9 and 28-day mortality was 0.708 (P = 0.032; 95% confidence bounds 0.563–0.854), and for SOFA was 0.698 (P = 0.025; 95% confidence bounds 0.550–0.845). Additionally, sepsis patients with high serum S100A8/A9 concentrations (≥ 377.53 ng/mL) also had a higher survival rate relative to those with lower concentrations (< 377.53 ng/mL). Furthermore, serum resistin levels in patients with a normal phenotype and mixed phenotype with hyperinflammation were predictive of mortality, with an AUC of 0.810 (P = 0.034; 95% confidence bounds 0.605–1.00) and 0.708 (P = 0.015; 95% confidence bounds 0.571–0.846). In patients with a normal sepsis phenotype, those with high serum resistin levels (≥ 63.695 ng/mL) had a lower survival rate compared to those with low resistin levels (< 63.695 ng/mL). In contrast, in patients with a mixed phenotype with hyperinflammation, those with high serum resistin levels (≥ 107.64 ng/mL) had a higher survival rate compared to those with lower resistin levels (< 107.64 ng/mL).Discussion: Sepsis, the leading cause of death in intensive care unit patients. Identifying reliable biomarkers is essential for improving both the diagnosis and treatment of sepsis. We found that serum S100A8/A9 concentration at ICU admission is a significant predictor of 28-day mortality risk in sepsis patients. Additionally, resistin levels at ICU admission play an important role in predicting 28-day mortality risk in patients with both normal and mixed phenotypes with hyperinflammation. These findings suggest that S100A8/A9 and resistin could serve as effective biomarkers. Moreover, these findings could guide early clinical decisions in the treatment of sepsis patients.

BACKGROUND:Cytochrome P450 (CYP) 2C19 is an enzyme involved in the bioactivation of various important therapeutic drugs, from pro-drugs to an active inhibitor of platelet action. Variants in the CYP2C19 gene influence the pharmacokinetics and clinica...

Background: Understanding the mechanism behind sepsis-associated encephalopathy (SAE) remains a formidable task. This study endeavors to shed light on the complex cellular and molecular alterations that occur in the brains of a mouse model with SAE, ultimately unraveling the underlying mechanisms of this condition. Methods: We established a murine model using intraperitoneal injection of lipopolysaccharide (LPS) in wild type and Anxa1^−/− mice and collected brain tissues for analysis at 0-hour, 12-hour, 24-hour, and 72-hour post-injection. Utilizing advanced techniques such as single-nucleus RNA sequencing (snRNA-seq) and Stereo-seq, we conducted a comprehensive characterization of the cellular responses and molecular patterns within the brain. Results: Our study uncovered notable temporal differences in the response to LPS challenge between Anxa1^−/− (annexin A1 knockout) and wild type mice, specifically at the 12-hour and 24-hour time points following injection. We observed a significant increase in the proportion of Astro-2 and Micro-2 cells in these mice. These cells exhibited a colocalization pattern with the vascular subtype Vas-1, forming a distinct region known as V1A2M2, where Astro-2 and Micro-2 cells surrounded Vas-1. Moreover, through further analysis, we discovered significant upregulation of ligands and receptors such as Timp1-Cd63, Timp1-Itgb1, Timp1-Lrp1, as well as Ccl2-Ackr1 and Cxcl2-Ackr1 within this region. In addition, we observed a notable increase in the expression of Cd14-Itgb1, Cd14-Tlr2, and Cd14-C3ar1 in regions enriched with Micro-2 cells. Additionally, Cxcl10-Sdc4 showed broad upregulation in brain regions containing both Micro-2 and Astro-2 cells. Notably, upon LPS challenge, there was an observed increase in Anxa1 expression in the mouse brain. Furthermore, our study revealed a noteworthy increase in mortality rates following Anxa1 knockdown. However, we did not observe substantial differences in the types, numbers, or distribution of other brain cells between Anxa1^−/− and wildtype mice over time. Nevertheless, when comparing the 24-hour post LPS injection time point, we observed a significant decrease in the proportion and distribution of Micro-2 and Astro-2 cells in the vicinity of blood vessels in Anxa1^−/− mice. Additionally, we noted reduced expression levels of several ligand-receptor pairs including Cd14-Tlr2, Cd14-C3ar1, Cd14-Itgb1, Cxcl10-Sdc4, Ccl2-Ackr1, and Cxcl2-Ackr1. Conclusions: By combining snRNA-seq and Stereo-seq techniques, our study successfully identified a distinctive cellular colocalization, referred to as a special pathological niche, comprising Astro-2, Micro-2, and Vas-1 cells. Furthermore, we observed an upregulation of ligand-receptor pairs within this niche. These findings suggest a potential association between this cellular arrangement and the underlying mechanisms contributing to SAE or the increased mortality observed in Anxa1 knockdown mice.