Integrated microbiome and metabolomic analysis of Spodoptera litura under Metarhizium flavoviride qc1401 stress.

Metarhizium spp. have emerged as an alternative to chemical pesticides for protecting crops from insect pest. Here, we investigated midgut microbial community and metabolites of Spodoptera litura at three different timepoints after infection with Metarhizium flavoviride. The innate immune system of S. litura was activated with levels of polyphenol oxidase, carboxylesterase, multifunctional oxidase, and glutathione S-transferase activity significantly increasing. Exposure to the fungal pathogen also altered bacterial abundance and diversity in host's midgut, and these changes varied depending on the time elapsed since exposure. We identified more operational taxonomic units in the treated samples as compared to the control samples at all tested time points. A total of 372 metabolites were identified, and 88, 149, and 142 differentially accumulated metabolites (DAMs) were identified between the treatment and control groups at 3 timepoints after treatment, respectively. Based on the changes of DAMs in response to M. flavoviride infection at different timepoints and significantly enriched KEGG pathways, we speculated that "tyrosine metabolism," "galactose metabolism," "ATP-binding cassette transporters," "neuroactive ligand-receptor interaction," "purine metabolism," "arginine and proline metabolism," "beta-alanine metabolism," "lysosome," and "carbon metabolism" may participate in the metabolic-level defense response. An integrated pathway-level analysis of the 16S-rDNA and metabolomic data illustrated the connections and interdependencies between the metabolic responses of S. litura and the midgut microorganisms to M. flavoviride infection. This work emphasizes the value of integrated analyses of insect-pathogen interactions, provides a framework for future studies of critical microorganisms and metabolic determinants of these interactions, establishes a theoretical basis for the sustainable use of M. flavoviride.

Analysis of Risk Factors for Death in the Coronavirus Disease 2019 (COVID-19) Population: Data Analysis from a Large General Hospital in Anhui, China.

During the coronavirus disease 2019 (COVID-19) pandemic, clinical prevention, early diagnosis, and hematological monitoring were challenging areas. This study aims to compare risk factors and hematological and biochemical data in non-survivor group patients with COVID-19 versus survivor group patients. A total of 204 patients with COVID-19 were selected as research subjects from December 2022 to January 2023. We analyzed the age, sex, time from onset to admission, and laboratory test indicators upon admission. The differences between surviving and deceased patients and mortality-related risk factors were examined. Among the 204 patients, 168 survived, whereas 36 died during hospitalization. Significant differences were observed between the two groups with COVID-19 across various factors, including age (p < 0.0001), WBC count (p < 0.0001), RBC count (p < 0.05), neutrophils (p < 0.0001), lymphocytes (p < 0.05), mean corpuscular hemoglobin concentration (MCHC) (p < 0.0001), RBC distribution width-standard deviation (RDW-SD) (p < 0.0001), RBC distribution width coefficient of variation (RDW-CV) (p < 0.0001), aspartate aminotransferase (AST) (p < 0.05), albumin (ALB) (p < 0.0001), creatinine (CR) (p < 0.0001), uric acid (UA) (p < 0.0001), blood urea nitrogen (BUN) (p < 0.0001), plasma thrombin time (TT) (p < 0.05), prothrombin time (PT) (p < 0.0001), and D-dimer (p < 0.0001). Multivariate logistic analysis revealed that older age, CR, UA, and ALB were independent factors associated with death (p < 0.05). Elderly patients with underlying diseases, abnormal routine blood test indices, and abnormal renal function and coagulation indices are at an increased worse prognosis and should be identified early. Age, UA, CR, and ALB can be used as predictors to assess the worse prognosis in the hospital.

Correlation of dyslipidemias and gallbladder polyps-A large retrospective study among Chinese population.

OBJECTIVE: Aim to explore the association of dyslipidemias with GBP prevalence, number and size in a large Chinese population in Beijing. Dyslipidemias include hypercholesterolemia, hypertriglyceridemia, increased low density lipoprotein (LDL) and decreased high density lipoproteins (HDL). METHODS: Prevalence of GBP and its association with dyslipidemias were retrospectively investigated among subjects who underwent check-up at Health Screening Center of Xuanwu Hospital between January 2014 and December 2017. RESULTS: This study enrolled 97117 participants. Prevalence of GBP was 7.3%. There were significant differences in increased LDL (595/7107 vs 6004/90010, P = 0.000) and increased cholesterol (TC) (403/7107 vs 4846/90010,P = 0.000) between GBP group and control group, but not in decreased HDL and increased triglyceride (TG). Logistic regression analysis showed that gender, age, BMI, SBP, DBP and LDL were independently associated with GBP. People with increases LDL had 1.488 times higher risk for GBP formation. Trend of dyslipidemias prevalence change according to age was similar with that of GBP. Increased LDL group had higher GBP prevalence rate (9.0% vs 7.2%, p = 0.000), multiple GBP proportion (2.9% vs 2.2%, p = 0.000) and large polyps with diameter ≥ 5 mm proportion (3.7% vs 2.6%,p = 0.000). Comparing with control group, there was higher proportion of large polyps in Increased TC group (3.2% vs 2.7%, p = 0.019) and decreased HDL group (3.0% vs 2.6%,p = 0.028). Increased TG group had not difference with its control group in GBP prevalence, number or size. CONCLUSION: Dyslipidemias is associated with GBP formation. Dyslipidemias change according to age is consistent with GBP prevalence. Increased LDL was a more related risk factor rather than decreased HDL, increased TC or TG.

Risk factors of gallbladder polyps formation in East Asian population: A meta-analysis and systematic review.

To perform Meta-analysis to identify risk factors associated with gallbladder polyps (GBP) formation in east Asian population. Three English electronic bibliographic databases includes PubMed, Embase and Medline, with reviewed researches from 1986 to 2017. All possible risk factors of GBP formation were recorded. Meta-analyses were performed by Review Manager Software. Pooled odds ratios (OR) or the mean difference (MD) were used to determine risk factors. Sixteen studies and 227021 people were recruited, including 17261 people with GBP and 209760 without GBP. For categorical variables evaluated by OR test., risk factors of GBP formation were male gender (OR, 1.63; 95%CI, 1.42-1.87) and positive HBsAg. GBP formation were not correlated with age <50 years old, hypertension, DM, BMI ≥ 25kg/m2, smoking, drinking, HDL decrease, TC increase, TG increase, fatty liver and GBS. For continuous variables evaluated by MD test, risk factors of GBP formation were DBP (MD, 1.08; 95%CI, 0.15-2.02), mean BMI (MD,0.19; 95%CI,0.02-0.35), waist circumference (MD,1.780; 95%CI, 0.17,3.40), mean LDL (MD,0.89; 95%CI,0.03-1.75), mean HDL (MD,-1.87; 95%CI,-3.21 to -0.52). GBP formation were not correlated with mean age, SBP, mean TC, mean TG, ASL and ALT. In conclusion, risk factors of gallbladder polyp formation included male gender, higher BMI, higher waist circumference, higher DBP, higher LDL, lower HDL and positive HBsAg in east Asian population. GBP formation was not correlated with age, hypertension, DM, smoking, drinking, fatty liver, GBS, TC, TG, SBP, ASL and ALT. The mechanism of Dyslipidemias causing GBP needs deeper study in future.

Association between genetic variants in glutathione peroxidase 1 gene and risk of prostate cancer: a meta-analysis.

To examine the association between glutathione peroxidase 1 (GPx1) gene Pro198Leu polymorphism with the development and progression of prostate cancer. A comprehensive search was conducted to identify all case-control studies of GPx1 polymorphisms and prostate cancer. Statistical analysis was performed with the software program Stata, version 11.0, and Review Manage, version 4.2. A total of 7 eligible studies relating the GPx1 polymorphism to the risk of prostate cancer were identified. The results indicated no significant association between GPx1 polymorphisms and prostate cancer susceptibility in the dominant model (random effects OR 0.75, 95 % CI 0.48-1.18), recessive model (random effects OR 0.47, 95 % CI 0.22-1.01) and co-dominant genetic model (random effects OR 0.72, 95 % CI 0.43-1.21). For the analysis of GPx1 polymorphism and progression of prostate cancer, no significant association were found in the dominant model (fixed effects OR 1.20, 95 % CI 0.95-1.52), recessive model (fixed effects OR 0.69, 95 % CI 0.48-1.00) and co-dominant genetic model (fixed effects OR 0.95, 95 % CI 0.79-1.15). Egger's test showed that publication bias was not present in all the comparisons.

Association between fibroblast growth factor receptor-4 gene polymorphism and risk of prostate cancer: a meta-analysis.

OBJECTIVES: To examine the association between fibroblast growth factor receptor-4 (FGFR-4) genetic polymorphisms (Gly-388Arg) and prostate cancer susceptibility. METHODS: A comprehensive search was conducted to identify all case-control studies of FGFR-4 polymorphisms and prostate cancer risk. Statistical analysis was performed with the software program Stata, version 8.0, and Review Manage, version 4.2. RESULTS: A total of 4 eligible studies, including 2,618 cases and 2,305 controls, relating the FGFR-4 polymorphism to the risk of prostate cancer were identified. The overall results indicated a significant association between FGFR-4 polymorphisms and prostate cancer. In the subgroup analysis by ethnicity, a significant association was found between European descent for recessive model (random effects OR 0.82, 95% CI 0.72-0.93) and co-dominant genetic model (random effects OR 0.83, 95% CI 0.68-1.00). Sensitivity analysis also found a significant association in the recessive (random effects OR 0.68, 95% CI 0.49-0.95) or the co-dominant (random effects OR 0.68, 95% CI 0.49-0.96) models. Egger's test showed that publication bias was not present in any of the comparisons. CONCLUSIONS: Gly-388Arg polymorphism of FGFR-4 most likely contributes to susceptibility to prostate cancer, especially in men of European descent.

Association between manganese superoxide dismutase gene polymorphism and risk of prostate cancer: a meta-analysis.

OBJECTIVES: To examine the association between 2 mitochondrial manganese superoxide dismutase (MnSOD) genetic polymorphisms (Ala-9Val and Ala-16Val) and prostate cancer susceptibility. METHODS: A comprehensive search was conducted to identify all case-control studies of MnSOD polymorphisms and prostate cancer risk. Statistical analysis was performed with the software program Stata, version 8.0, and Review Manage, version 4.2. RESULTS: A total of 9 eligible studies, including 3268 cases and 5907 controls, relating the MnSOD polymorphism to the risk of prostate cancer were identified. For the Ala-9Val polymorphism, 5 studies, including 889 cases and 1841 controls, found no significant associations between MnSOD polymorphism and the risk of developing prostate cancer in the recessive, dominant, and co-dominant models. In the sensitivity analysis, exclusion of the study with the controls not in Hardy-Weinberg equilibrium, no significant associations were also found in the recessive (odds ratio [OR] 1.29, 95% confidence interval [CI] 0.66-2.50), dominant (OR 1.35, 95% CI 0.84-2.17), and co-dominant (OR 1.33, 95% CI 0.87-2.01) models. For the Ala-16Val polymorphism, 4 studies, including 2379 cases and 4066 controls, found no significant association between MnSOD polymorphism and the risk of developing prostate cancer in both co-dominant (OR 1.08, 95% CI 1.00-1.16), recessive (OR 1.06, 95% CI 0.94-1.20) and dominant (OR 1.14, 95% CI 1.00-1.28) models. CONCLUSIONS: No significant association was found between the Ala-9Val and Ala-16Val polymorphisms in MnSOD and prostate cancer susceptibility.

Additional gene therapy with rAAV-wt-p53 enhanced the efficacy of cisplatin in human bladder cancer cells.

OBJECTIVE: Gene therapy is defined as the treatment of an acquired or inherited disease by transfer of genetic material. The most common strategies in gene therapy of bladder cancer are corrective, inductive and cytotoxic gene therapy. Mutations in the p53 tumor suppressor gene are the most common molecular genetic abnormalities in bladder cancer and p53 gene transfer in the human bladder cancer cell line by adenoviral or other vectors was demonstrated to be cytotoxic. However, so far there has been no report of adeno-associated virus-2 vector-mediated p53 gene deliveries in bladder cancer. In this study, wild-type p53 cDNA was transfected into the bladder cancer cells, using the adeno-associated virus-2 vector, and the capability of rAAV-wt-p53 gene therapy in bladder cancer was evaluated in vitro. METHOD: Bladder cancer cell lines 5637 were transduced with adeno-associated virus-2 vectors containing wild-type human p53 gene (rAAV-wt-p53). Gene expression and transcriptional activation of p53 was determined by Western blot analysis. The cellular growth inhibition and apoptosis of rAAV-mediated p53 transfection were assessed by flow cytometry. The combination effect of rAAV-wt-p53 and cisplatin was measured by MTT assay. RESULTS: The virus rAAV efficiently enters the cells and expresses its gene products. The gene product of rAAV-wt-p53 is cytotoxic to bladder cancer cells. The bladder cell line 5637 was found to experience a synergistic killing effect when rAAV-wt-p53 was used in combination with cisplatin. CONCLUSION: rAAV-mediated p53 gene transfer could offer a powerful novel therapeutic approach in bladder cancer.