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Background Streptococcus iniae is an important fish pathogen that cause significant economic losses to the global aquaculture industry every year. Although there have some reports on the genotype of S.iniae and its relationship with virulence, no genome-scale comparative analysis has been performed so far. In our previous work, we characterized 17 isolates of S.iniae from Trachinotus ovatus and divided them into two genotypes using RAPD and rep-PCR methods. Among them, BH15-2 was classified as designated genotype A (in RAPD) and genotype 1 (in rep-PCR), while BH16-24 was classified as genotype B and genotype 2. Herein, we compared the differences in growth, drug resistance, virulence, and genome between BH15-2 and BH16-24. Results The results showed that the growth ability of BH16-24 was significantly faster than that of BH15-2 at the exponential stage. Antimicrobial tests revealed that BH15-2 was susceptible to most of the tested antibiotics except neomycin and gentamycin. In contrast, BH16-24 was resistant to 7 antibiotics including penicillin, sulfasomizole, compound sulfamethoxazole tablets, polymyxin B, spectinomycin, rifampin and ceftazidime. Intraperitoneal challenge of T.ovatus , showed that the LD 50 value of BH15-2 was 4.0 × 10 2 CFU/g, while that of BH16-24 was 1.2 × 10 5 CFU/g. The genome of S.iniae BH15-2 was 2,175,659 bp with a GC content of 36.80%. Meanwhile, the genome of BH16-24 was 2,153,918 bp with a GC content of 36.83%. Comparative genome analysis indicated that compared with BH15-2, BH16-24 genome had a large-scale genomic inversion fragment, at the location from 502,513 bp to 1,788,813 bp, resulting in many of virulence and resistance genes differentially expression. In addition, there was a 46 kb length, intact phage sequence in BH15-2 genome, which was absent in BH16-24. Conclusion Comparative genomic studies of BH15-2 and BH16-24 showed that the main difference is a 1.28 Mbp inversion fragment. The inversion fragment may lead to abnormal expression of drug resistant and virulence genes, which is believed to be the main reason for the multiple resistance and weakened virulence of BH16-24. Our study revealed the potential mechanisms in underlying the differences of multidrug resistance and virulence among different genotypes of S.iniae .

Objective To evaluate the impact of Human Immunodeficiency Virus (HIV) infection on serum amyloid A (SAA) levels in acute pulmonary infections and assess correlations between SAA and other inflammatory markers in HIV-associated pneumonia. Methods In this retrospective case-control study, 48 HIV-positive patients with pulmonary infections (HIV group) and 55 age-matched HIV-negative controls (control group) were enrolled from Shanghai Public Health Clinical Center (2021.5–2025.5). Demographic, hospitalization duration and laboratory parameters - including SAA, white blood cell count (WBC), C-reactive protein (CRP), procalcitonin (PCT), lactate dehydrogenase (LDH), platelet count (PLT), CD4 + T cell count, and absolute lymphocyte count(ALC) - were systematically collected from both patient cohorts. For intergroup comparisons, the Mann-Whitney U test was employed, while Spearman’s rank correlation analysis was conducted to assess biomarker associations within the HIV-positive subgroup. Results Among 103 patients, the HIV group had higher male predominance (83.3% vs. 54.5%, P  = 0.02) and lower CD4 + T cell count (215.17 vs. 443.41 cells/µL, P  < 0.05). SAA (178.39 vs. 122.93 mg/L, P  = 0.032), CRP (64.27 vs. 37.07 mg/L, P  = 0.031), LDH (310.65 vs. 235.96 U/L, P  = 0.024), and hospitalization duration (16.83 vs. 13.05 days, P  = 0.013) were significantly elevated in HIV patients. SAA correlated positively with CRP ( r  = 0.4807), PCT ( r  = 0.3554), LDH ( r  = 0.3564), and PLT ( r  = 0.3094) ( P  < 0.05 for all). Conclusions Patients with HIV-associated pulmonary infections exhibited significantly elevated levels of SAA, CRP, and LDH, along with prolonged hospital stays, compared to non-HIV-infected individuals. These findings suggest that HIV infection amplifies systemic inflammatory responses, potentially contributing to extended hospitalization. The robust correlations between SAA and other biomarkers (including CRP, PCT, LDH, PLT) highlight its potential as a key component in early diagnostic panels for HIV-associated pulmonary infections.

Background The clinical significance of hematogenous and lymphatic metastasis in ovarian cancer has been increasingly addressed, as it plays an imperative role in the formation of both intraperitoneal and distant metastases. Our objective is to identify the key molecules and biological processes potentially related to this relatively novel metastatic route in serous ovarian cancer. Methods Since lymphovascular space invasion (LVSI) is considered as the first step of hematogenous and lymphatic dissemination, we developed a gene signature mainly based on the transcriptome profiles with available information on LVSI status in the Cancer Genome Atlas (TCGA) dataset. We then explored the underlying biological rationale and prognostic value of the identified gene signature using multiple public databases. Results We observe that primary tumors with increased risk of hematogenous and lymphatic metastasis highly express a panel of genes, namely POSTN, LUM, THBS2, COL3A1, COL5A1, COL5A2, FAP1 and FBN1. The identified geneset is characterized by enhanced deposition of extracellular matrix and extensive stromal activation. Mechanistically, both the recruitment and the activation of stromal cells, especially fibroblasts, are closely associated with lymphovascular metastasis. Survival analysis further reveals that the elevated expression of the identified genes correlates to cancer progression and poor prognosis in patients with serous ovarian cancer. Conclusions Our findings indicate that tumor stroma supports the hematogenous and lymphatic spread of ovarian cancer, increasing tumor invasiveness and ultimately resulting in worse survival. Thus stroma-targeted therapies may improve the clinical outcomes in combination with cytoreductive surgery and chemotherapy.

Cardiovascular diseases (CVDs) are major global health threats. This study explores links between anti-allergic drugs and CVD risk, providing valuable insights for clinical pharmacotherapy. Mendelian randomization (MR) analyses were performed on 139 eQTLs for anti-allergic drugs in coronary artery disease (CAD), heart failure (HF), myocardial infarction (MI), and atrial fibrillation (AF) cohorts, with validation in independent cohorts. Sensitivity analyses, transcriptomics analysis, enrichment analysis, and molecular docking were performed to evaluate the robustness of causality, potential pathways and binding affinity. Furthermore, the FAERS database evaluated the cardiovascular adverse events associated with prednisone in combination with cardiovascular drugs. Among the 11 anti-allergic drug targets significantly linked to CVDs, KAT2A inversely correlated with CAD risk, BAZ2B and CYP2C8 with AF risk, and ITGB2, TG and six other eQTLs were associated with HF risk. Notably, prednisone (targeting ITGB2, TG) and loratadine (targeting TSHR) elevated CVD risk, while zafirlukast (targeting KAT2A, POLB, BAZ2B) reduced it. The progression of CVDs may be influenced by the formation of neutrophil extracellular traps and lipid accumulation, which could potentially be affected by the administration of prednisone and similar medications. Molecular docking revealed a strong binding affinity between the cardiovascular candidate drug quercetin and zafirlukast (POLB). Pharmacovigilance analysis indicated an increased risk of adverse cardiovascular outcomes with the concurrent use of prednisone and cardiovascular drugs. The comprehensive analyses indicate that certain anti-allergic drugs may heighten the risk of CVDs, suggesting caution with medications like prednisone.

Background Non-alcoholic fatty liver disease (NAFLD), recognized as the liver manifestation of metabolic syndrome, is highly prevalent in the general population. Recent studies suggest that lipid accumulation product is significantly associated with metabolic abnormalities. The aim of this study was to assess the accuracy of lipid accumulation product (LAP) as an effective screening tool for diagnosing NAFLD in the general population. Methods A total of 40,459 subjects aged ≥18 years were enrolled in this cross-sectional study. LAP was calculated as [waist circumference (cm) – 65] × triglyceride concentration (mmol//L) in men and [waist circumference (cm) – 58] × triglyceride concentration (mmol/L) in women. Multiple logistic regression and receiver operating characteristic (ROC) analyses were performed. Results According to multiple logistic regression analyses, LAP was significantly associated with a higher prevalence and severity of NAFLD in both men and women. When assessed using ROC curve analyses, LAP exhibited high diagnostic accuracy for identifying NAFLD, and the areas under the curves (AUC) in men and women were 0.843 (95% CI 0.837, 0.849) and 0.887 (95% CI 0.882, 0.892), respectively. After further analyzed in different age groups, the diagnostic accuracy of LAP was found to be significantly better in younger age groups (aged 18-34 for men; aged 18-34 and 35-44 years for women) for both sexes. Conclusions LAP is significantly associated with the presence and severity of NAFLD, and has a high diagnostic accuracy for identifying NAFLD in the general population. The diagnostic accuracy of LAP was especially high among younger age groups.

Background Deregulation of integrins signaling had been documented to participate in multiple fundamental biological processes, and the aberrant expression of integrin family members were linked to the prognosis of various cancers. However, the role of integrins in predicting progression and prognosis of ovarian cancer patients are still largely elusive. This study is aimed to explore the prognostic values of ITGA and ITGB superfamily members in high grade serous ovarian cancers (HGSOC). Methods GSE26712 dataset was used to determine the differential expression of ITGA and ITGB superfamily member between HGSOC and normal counterparts. The Cancer Genome Altas (TGGA) and GSE9891 datasets were used to determine the prognostic values of ITGA and ITGB superfamily members in HGSOC, followed by the development of nomograms predictive of recurrence free survival (RFS) and overall survival (OS). Results ITGA6 and ITGB5 expression were significantly downregulated in HGSOC compared with that in normal counterparts. In contrast, ITGA2, ITGA5, ITGA7, ITGA8, ITGA9, ITGA10, ITGB3, ITGB4, ITGB6, and ITGB8 were all significantly upregulated in HGSOC compared with that in normal counterparts. Both univariable and multivariable analysis indicated that ITGB1 was associated with extended RFS. The ITGB1-related nomogram indicated that ITGB1 had the largest contribution to RFS, followed by FIGO stage and debulking status. The C-index for predicting RFS was 0.55 (95% CI 0.50–0.59) in TCGA dataset (training dataset) and 0.65 (95% CI 0.59–0.72) in GSE9891 dataset (validation dataset), respectively. Regarding OS, ITGB8 was associated with reduced survival suggested by both univariable and multivariable analysis. ITGA7 appeared to be associated with improved survival though without reaching statistical significance. The ITGA7/ITGB8-based nomogram showed that age at initial diagnosis had the largest contribution to OS, followed by ITGB8 and ITGA7 expression. The C-index for predicting OS was 0.65 (95% CI 0.60–0.69) in TCGA dataset (training dataset) and 0.59 (95% CI 0.51–0.66) in GSE9891 dataset (validation dataset), respectively. Conclusion In conclusion, ITGB1, ITGA7 and ITGB8 added prognostic value to the traditional clinical risk factors used to assess the clinical outcomes of HGSOC.

Background To compare the prognosis of lymphatic metastasis in type I and type II epithelial ovarian cancer (OC) and to identify the risk factors for pelvic lymph node metastases (PLNs) and para-aortic lymph node metastases (PALNs). Methods Patients diagnosed with epithelial OC were collected from the Surveillance, Epidemiology, and End Results (SEER) database. Overall survival (OS) and cancer-specific survival (CSS) were estimated. The Cox proportional hazards regression model was used to identify independent predictors of survival. Results A total of 11,275 patients with OC were enrolled, including 31.2% with type I and 68.8% with type II. Type II and high tumour stage were risk factors for lymph node involvement ( p  < 0.05). The overall rate of lymph node metastasis in type I was 11.8%, and that in type II was 36.7%. In the type I group, the lymph node metastasis rates in stages T1, T2, T3 and T X M 1 were 3.2%, 14.5%, 40.4% and 50.0%, respectively. In the type II group, these rates were 6.4%, 20.4%, 54.1% and 61.1%, respectively. Age and tumour size had little effect on lymph node metastasis, and grade 3 was not always a risk factor. For the type I group, the 10-year CSS rates of LN(-), PLN( +), PALN( +), and PLN + PALN( +) were 80.6%, 46.6%, 36.3%, and 32.3%, respectively. The prognosis of PLN ( +) was better than that of PALN ( +) in the type I group ( p  > 0.05). For the type II group, the 10-year CSS rates of LN(-), PLN( +), PALN( +), and PLN + PALN( +) were 55.6%, 18.5%, 25.7%, and 18.2%, respectively. PALN ( +) had a significantly better prognosis than PLN ( +) in the type II group ( p  < 0.05). Conclusions The clinical characteristics and prognoses of patients with type I and type II OC differed greatly. Patients with type II and higher tumour stages had poorer prognoses. Type I with PALN metastasis and type II with PLN metastasis indicated a worse prognosis. Patients with stage TI did not require lymph node dissection, especially in the type I group.

ABSTRACT This case report documents a recurrent pulmonary infection caused by Schizophyllum commune in a 59‐year‐old woman with repeated admissions for cough and sputum production. Using mNGS on BALF, S. commune sequences were identified. The patient's clinical symptoms, lab results, and imaging features aligned with six criteria from Asano's assessment table, confirming ABPM. During treatment, bronchoscopic airway clearance, antifungal agents, and inhaled corticosteroids proved effective. The case highlights mNGS's role in diagnosing rare fungal infections and the need for individualised antifungal therapy. Azithromycin's potential anti‐inflammatory effects were noted, though its specific application in ABPM requires further study. Caution is advised in future use, with more research needed on its mechanism in such cases. Schizophyllum commune (SC), commonly known as the oyster mushroom, is a basidiomycete fungus widespread in nature. This case report documents a recurrent pulmonary infection caused by S. commune in a 59‐year‐old woman with repeated admissions for cough and sputum production.

Aims Sphingosine-1-phosphate receptor 2 (S1PR2) is a G-protein-coupled receptor that regulates sphingosine-1-phosphate-triggered cellular response. However, the role of S1PR2 in diabetes-induced glomerular endothelial cell dysfunction remains unclear. This study aims to investigate the effect of S1PR2 blockade on the morphology and function of mitochondria in human renal glomerular endothelial cells (HRGECs). Methods HRGECs were pretreated with a S1PR2 antagonist (JTE-013) or a Rho-associated coiled coil-containing protein kinase 1 (ROCK1) inhibitor (Y27632) for 30 min and then cultured with normal glucose (5.5 mM) or high glucose (30 mM) for 72 h. The protein expression levels of RhoA, ROCK1, and Dynmin-related protein-1(Drp1) were evaluated by immunoblotting; mitochondrial morphology was observed by electron microscopy; intracellular levels of ATP, ROS, and Ca 2+ were measured by ATPlite, DCF-DA, and Rhod-2 AM assays, respectively. Additionally, the permeability, apoptosis, and migration of cells were determined to evaluate the effects of S1PR2 and ROCK1 inhibition on high glucose-induced endothelial dysfunction. Results High glucose induced mitochondrial fission and dysfunction, indicated by increased mitochondrial fragmentation, ROS generation, and calcium overload but decreased ATP production. High glucose also induced endothelial cell dysfunction, indicated by increased permeability and apoptosis but decreased migration. However, inhibition of either S1PR2 or ROCK1 almost completely blocked these high glucose-mediated cellular responses. Furthermore, inhibiting S1PR2 resulted in the deceased expression of RhoA, ROCK1, and Drp1 while inhibiting ROCK1 led to the downregulated expression of Drp1. Conclusions S1PR2 antagonist modulates the morphology and function of mitochondria in HRGECs via the positive regulation of the RhoA/ROCK1/Drp1 signaling pathway, suggesting that the S1PR2/ROCK1 pathway may play a crucial role in high glucose milieu.

Background Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, and its prevalence is likely to rise even further. To help understand the pathogenesis and early prevention of progressive NAFLD, this large-scale study was designed to explore the potential association between homocysteine and the prevalence of NAFLD. Methods A total of 7203 subjects aged 18 years or older were enrolled in this cross-sectional study. The association of homocysteine with the prevalence of NAFLD, in the total sample and stratified by subgroups, was examined using multiple logistic regression analyses. Results Subjects in the higher quartiles of homocysteine had a higher prevalence of NAFLD. After multivariate adjustment, the odds ratio (OR) for NAFLD in the highest compared with the lowest quartile of homocysteine was 2.08 (95% confidence interval [CI] 1.61, 2.67). Moreover, in the subgroup analyses, we found an effect modification by gender, body mass index (BMI) and smoking status on the association between homocysteine and the prevalence of NAFLD ( P for interaction: 0.001, 0.002 and <0.001, respectively). A stronger association was observed in female, obese and non-smoking adults than in male, normal weight and smoking subjects. Conclusion Homocysteine was significantly associated with the prevalence of NAFLD, particularly in female, obese or non-smoking adults.