Tianyu Liang

Probiotic/synbiotic, have been proposed as a supplement to improve bone health markers. However, findings evidence remains inconsistent. This meta-analysis

Objective This study aimed to explore the association between circulating HMGB1 mRNA expression and clinical pathological characteristics and prognosis in bladder urothelial carcinoma (BUC) patients. Methods Circulating HMGB1 mRNA expression levels were assessed using real-time fluorescence quantitative PCR, and patients were categorized into low-expression and high-expression groups based on the median value. Follow-up was conducted for 3 years post-surgery, and patients were classified into non-recurrence and recurrence groups. Baseline circulating HMGB1 mRNA expression levels were compared across different clinical pathological characteristics and prognosis groups to evaluate prognostic disparities based on HMGB1 mRNA expression levels. The Western Blot (WB) experiment assesses the expression levels of HMGB1 across various tissue sections and evaluates the inhibitory effects of chemotherapeutic agents on HMGB1. Additionally, after knocking out HMGB1 in vitro cell lines, the cell proliferation is detected. Results There were no significant differences in HMGB1 mRNA expression levels among patients with varying differentiation grades, lymph node metastasis stage (N stage), primary tumor stage (T stage), or tumor diameter. However, baseline circulating HMGB1 mRNA expression levels were notably lower in surviving patients than in deceased patients. Kaplan–Meier survival analysis revealed a median survival time of 356 weeks in the low-expression group and 259 weeks in the high-expression group. Notably, the low-expression group exhibited significantly prolonged survival compared to the high-expression group (HR = 1.714, 95%CI 1.226, 2.397). WB test showed that the expression level of HMGB1 in tumor tissues of BUC patients was increased, and inhibition of HMGB1 expression could also inhibit the proliferation of tumor cells. Some common chemotherapy drugs can also significantly inhibit the proliferation of BUC cells. Conclusion HMGB1 is highly expressed in urinary bladder epithelial carcinoma, and chemotherapy drugs can effectively inhibit the expression of HMGB1. Inhibition of HMGB1 expression is helpful to inhibit the proliferation of tumor cells. Circulating HMGB1 mRNA expression levels are closely associated with tumor prognosis, with low-expression patients having a longer survival period.

Intracerebral hemorrhage (ICH) is an acute neurological disorder characterized by high mortality and disability rates. Previous studies have shown that 75% of patients who survive ICH experience varying degrees of neurological deficits. Sphk1 has been implicated in a multitude of phylogenetic processes, including innate immunity and cell proliferation. An in vivo rat model of ICH and an in vitro model of neuronal oxyhemoglobin (OxyHb) were constructed. The expression level of Sphk1 was assessed using western blotting and immunofluorescence, whereas cell death following ICH was evaluated using fluoro-Jade B and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Immunofluorescence facilitated the examination of microglial phenotypic alterations, while enzyme-linked immunosorbent assays were used to determine the concentrations of inflammatory markers. Behavioral assays were employed to assess the overall behavioral modifications of animals. Neuronal Sphk1/Sirt1 protein levels gradually increased following the induction of ICH. Elevated Sphk1 expression resulted in increased levels of anti-inflammatory microglia and reduced levels of pro-inflammatory factors. In contrast, suppression of Sphk1 expression resulted in an increased number of dead cells, thereby exacerbating neurological deficits. In vitro findings indicated that the levels of phosphorylated PI3K and AKT proteins increased in conjunction with Sphk1 expression. This study established that after ICH, Sphk1 interacts with Sirt1 to mitigate neuroinflammation, cell death, oxidative stress, and brain edema via the PI3K/AKT signaling pathway. Augmenting expression of Sphk1 significantly can ameliorate neurological impairments induced by ICH, offering novel targets and perspectives for therapeutic interventions in ICH treatment.

Background: Prior research exploring the correlation between the XRCC3 Thr241Met polymorphism and the susceptibility to pancreatic cancer has yielded conflicting outcomes. To date, there has been a notable absence of studies examining this polymorphism. The primary aim of the current investigation is to elucidate the potential role of the XRCC3 Thr241Met polymorphism as a risk factor in the development of pancreatic cancer. Methods: The comprehensive literature search was meticulously conducted across primary databases, including PubMed, Embase, and CNKI (China National Knowledge Infrastructure), spanning from the inception of each database through January 2024. To synthesize the data, a meta-analysis was performed using either a fixed or random-effects model, as appropriate, to calculate the odds ratios (ORs) and their corresponding 95% confidence intervals (CIs). Results: The analysis revealed significant associations between the XRCC3 Thr241Met polymorphism and an increased risk of pancreatic cancer. This was evidenced through various genetic model comparisons: allele contrast (T vs. C: OR = 0.77, 95% CI = 0.70–0.86, P < 0.001), homozygote comparison (TT vs. CC: OR = 0.71, 95% CI = 0.58–0.88, P = 0.001), heterozygote comparison (TC vs. CC: OR = 0.67, 95% CI = 0.52–0.87, P = 0.003), and a dominant genetic model (TT/TC vs. CC: OR = 0.68, 95% CI = 0.57–0.81, P < 0.001). Additionally, subgroup analyses based on ethnicity disclosed that these associations were particularly pronounced in the Caucasian population, with all genetic models showing significance (P < 0.05). Conclusions: The XRCC3 Thr241Met polymorphism has been identified as contributing to a reduced risk of pancreatic cancer in the Caucasian population. This finding underscores the need for further research to validate and expand upon our conclusions, emphasizing the urgency for continued investigations in this domain.

The aim is to investigate the relationship between serum coagulation parameters (PT, APTT, D-D and FDP) before hospitalization and recurrence of chronic subdural hematoma (CSDH). 236 patients with CSDH who were diagnosed for the first time and had complete medical records were followed up for at least 90 days. Fifty patients (21.2%) had relapsed. Univariate analysis was conducted including general data, imaging data and test results. Serum coagulation parameters (PT, APTT, D–D and FDP) were detected for all CSDH patients. The study identified several factors that exhibited a significant correlation with chronic subdural hematoma (CSDH) recurrence. These factors included advanced age (p = 0.01), hypertension (p = 0.04), liver disease (p = 0.01), anticoagulant drug use (p = 0.01), antiplatelet drug use (p = 0.02), bilateral hematoma (p = 0.02), and single-layer hematoma (p = 0.01). In addition, the presence of fibrin/fibrinogen degradation products (FDP) exceeding 5 mg/L demonstrated a significant relationship with CSDH recurrence (P < 0.05). Notably, the combined assessment of D-dimer (D–D) and FDP exhibited a significant difference, particularly regarding recurrence within 30 days after surgery (P < 0.05). The simultaneous elevation of serum FDP and D–D levels upon admission represents a potentially novel predictor for CSDH recurrence. This finding is particularly relevant for patients who experience recurrence within 30 days following surgical intervention. Older individuals with CSDH who undergo trepanation and drainage should be closely monitored due to their relatively higher recurrence rate.

Gastric cancer is a kind of tumor with strong heterogeneity. Long noncoding RNAs (lncRNAs) acting as competing endogenous RNAs (ceRNAs) play significant roles in the development of tumors. In this study, we divided all TCGA gastric cancer patients into the whole, intestinal and diffuse cohorts for further analysis, and constructed competitive endogenous RNA network and evaluated immune cells using CIBERSORTx. The support vector machines recursive feature elimination (SVM-RFE) was used for screening significant signatures and the support vector machines (SVM) for establishing model predicting the lymph node metastasis. The performance of SVM model was good in the intestinal and diffuse cohort, while the model in the whole cohort was relatively poor. Some important co-expression patterns between immune cells and ceRNAs network indicated significant correlation CD70 with dendritic cells and so on. Our research inferred competing endogenous RNA network of lymph node metastasis and built an excellent predicting model.

Background Accumulating evidence suggests that anoikis resistance is a key process in cancer cell metastasis, making it an attractive therapeutic target. Therefore, anoikis may become a new treatment for gastric cancer. Methods We used the univariate Cox regression method to screen gastric cancer-related anoikis genes, and a prognostic risk model was established. We analyzed differences between high- and low-risk groups in terms of tumor infiltrating immune cells, gene mutation signatures, and treatment of gastric cancer. Analysis of model associated genes at single-cell resolution was performed. Results We filtered to 12 anoikis-related genes and built a prognostic risk model using seven of them, which performed well in multiple datasets. Patients with CCDC178 mutations had a worse prognosis. We also found that patients at low risk were more likely to benefit from chemotherapy and immunotherapy. ERBB2 was found to be highly expressed in epithelial cells and fibroblasts. Our analysis also indicated that gastric cancer samples with high infiltration of iCAFs had a worse prognosis. Conclusion Seven anoikis-related genes were selected to establish a risk model. The model can be used to predict the prognosis of patients and guide the drug treatment, which provides a new idea for the evaluation and treatment of gastric cancer patients.

Odontogenic brain and pulmonary abscesses are extremely rare infectious diseases. It is mainly caused by the upward or downward transmission of local infection or blood-borne spread. In recent years, with the wide application of some novel testing methods in clinical practice, the diagnosis of unexplained infections such as odontogenic abscesses in different organs has gradually become clear. We report a case of a 21-year-old male who was healthy and had not received any oral treatment before onset. He started with acute gastroenteritis-related symptoms, then developed meningitis-related symptoms seven days later with septic shock. No obvious abscess lesions were found on head computed tomography (CT) at admission, and the etiology was not clear by routine examination, which was very easy to misdiagnose as a serious infection caused by intestinal pathogens. But odontogenic pathogens were found both in his blood and cerebrospinal fluid through metagenomic next-generation sequencing (mNGS) analysis. Subsequently, rechecked imaging examination displayed multiple brain and pulmonary abscesses. Finally, it was diagnosed as an odontogenic brain and pulmonary abscess. After an extremely lengthy anti-infection course (13 weeks of intravenous antibiotics plus 2 weeks of oral antibiotics) and surgery, the patient was improved and discharged from the hospital. From this case, we could see that the development of new diagnostic technologies such as mNGS plays an important role in the early and confirmed diagnosis of diseases previously difficult to diagnose such as odontogenic polymicrobial infections and ultimately helps to improve the prognosis of these patients.

Background: Increasing evidences show a clinical significance in the interaction between hypoxia and prostate cancer. However, reliable prognostic signatures based on hypoxia have not been established yet.Methods: We screened hypoxia-related gene modules by weighted gene co-expression network analysis (WGCNA) and established a hypoxia-related prognostic risk score (HPRS) model by univariate Cox and LASSO-Cox analyses. In addition, enriched pathways, genomic mutations, and tumor-infiltrating immune cells in HPRS subgroups were analyzed and compared. HPRS was also estimated to predict immune checkpoint blockade (ICB) therapy response.Results: A hypoxia-related 22-gene prognostic model was established. Furthermore, three independent validation cohorts showed moderate performance in predicting biochemical recurrence-free (BCR-free) survival. HPRS could be a useful tool in selecting patients who can benefit from ICB therapy. The CIBERSORT results in our study demonstrated that hypoxia might act on multiple T cells, activated NK cells, and macrophages M1 in various ways, suggesting that hypoxia might exert its anti-tumor effects by suppressing T cells and NK cells.Conclusion: Hypoxia plays an important role in the progression of prostate cancer. The hypoxia-derived signatures are promising biomarkers to predict biochemical recurrence-free survival and ICB therapy responses in patients with prostate cancer.