Risk Factors for Urinary Tract Infection in Elderly Patients with Type 2 Diabetes: A Retrospective Cohort Study.

OBJECTIVE: The risk factors of urinary tract infection in elderly patients with type 2 diabetes were investigated. METHODS: A total of 72 elderly patients admitted to our hospital from December 2019 to September 2023 because of with type 2 diabetes were retrospectively included. They were divided into the observation group (n = 35) and control group (n = 37) according to whether they had urinary tract infection. The general clinical data, clinical characteristics and the distribution of pathogenic bacteria in the observation group were collected and analysed. Then, t-tests, chi-square tests, regression analysis and receiver operating characteristic curve analysis were conducted. RESULTS: Escherichia coli (E. coli) accounted for 51.43% of the pathogenic bacteria in the observation group, whereas Klebsiella pneumoniae (K. pneumoniae) accounted for 22.86%. The remaining pathogens accounted for 2.86% each. Differences in gender, course of disease, glycosylated haemoglobin and comorbid urinary calculi were found between the groups (p < 0.05); These factors were all risk factors for concurrent urinary infection, and the odds ratios were all >1. The obtained values for gender, disease course, glycosylated haemoglobin and comorbid urinary calculi were respectively 0.594, 0.654, 0.738 and 0.696 (area under the curve); 0.971, 0.714, 0.800 and 0.743 (sensitivity); 0.216, 0.595, 0.676 and 0.649 (specificity); And 0.188, 0.309, 0.476 and 0.392 (Youden index). CONCLUSIONS: Common pathogens in elderly people with type 2 diabetes and comorbid urinary tract infection are E. coli and K. pneumoniae. Risk factors include gender, disease duration, glycosylated haemoglobin and urinary stones. The prompt identification of pathogens and risk factors facilitates clinical treatment, reducing infection incidence.

Improved repair of rabbit calvarial defects with hydroxyapatite/chitosan/polycaprolactone composite scaffold-engrafted EPCs and BMSCs.

Endothelial progenitor cells (EPCs) expressing vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) and bone marrow mesenchymal stem cells (BMSCs) expressing endogenous bone morphogenetic protein-2 (BMP-2) play the important role in new bone formation. This study investigated the effects of a porous hydroxyapatite (HA)/chitosan (CS)/polycaprolactone (PCL) composite scaffold-engrafted EPCs and BMSCs on the expression of BMP-2, VEGF, and PDGF in the calvarial defect rabbit model in vivo. It showed that a three-dimensional composite scaffold was successfully constructed by physical interaction with a pore size of 250 µm. The HA/CS/PCL scaffold degraded slowly within 10 weeks and showed non-cytotoxicity. By X-ray, micro-CT examination, and H&E staining, compared with the HA/CS/PCL group, HA/CS/PCL + EPCs, HA/CS/PCL + BMSCs, and HA/CS/PCL + EPCs + BMSCs groups performed a more obvious repair effect, and the dual factor group presented particularly significant improvement on the percentages of bone volume at week 4 and week 8, with evident bone growth. Osteogenesis marker (BMP-2) and vascularization marker (VEGF and PDGF) expression in the dual factor group were much better than those of the HA/CS/PCL control group and single factor groups. Collectively, the HA/CS/PCL composite scaffold-engrafting EPCs and BMSCs is effective to repair calvarial defects by regulating endogenous expression of BMP-2, VEGF, and PDGF. Thus, this study provides important implications for the potential clinical application of biomaterial composite scaffold-engrafted engineering cells.

Comprehensive analysis of interleukin-8 gene polymorphisms and periodontitis susceptibility.

BACKGROUND: Associations between interleukin-8 (IL-8) gene polymorphisms and periodontitis susceptibility have been investigated in many published studies, but the conclusions are still inconsistent. Therefore, we performed this systematic review and meta-analysis to review which polymorphisms have been researched and to obtain a precise result of the same polymorphism from different studies. RESULTS: Finally 10 publications involving 1938 patients and 1569 controls were yielded, including 12 polymorphisms. Six studies investigated rs4073 polymorphism; two focused on rs2227306 and rs2227307; two referred to rs2227532 and T-738A; one detected rs2230054, rs1126579 and rs1126580; one inspected A2767T, T11722T2 and C1633T, and one for rs2234671 polymorphism. Of them, IL-8 C1633T and rs1126580 polymorphisms showed positive association while the other ten polymorphisms revealed negative results. MATERIALS AND METHODS: A comprehensive literature search from PubMed, Web of Science, and Chinese National Knowledge Infrastructure was conducted for all potentially relevant studies published before January 2, 2017. Two authors selected the studies and extracted data. The pooled analysis was conducted using the RevMan 5.1 software if a polymorphism was reported by two or more studies. CONCLUSIONS: Based on current evidence, the IL-8 rs4073, A2767T, T11722T2, rs2234671, rs2230054, rs1126579, rs2227306, rs2227307, rs2227532, and T-738A polymorphisms were not associated with periodontitis susceptibility; the IL-8 C1633T and rs1126580 polymorphisms were associated with increased risk of periodontitis.

CCND1 G870A polymorphism and colorectal cancer risk: An updated meta-analysis.

Molecular epidemiological studies have revealed a closer association between cyclin D1 (CCND1) polymorphism and the risk of colorectal cancer; however, the results were inconsistent. The aim of the present meta-analysis was to investigate the association between CCND1 G870A polymorphism and colorectal cancer risk. Online electronic databases (PubMed and Embase) were searched. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess the association between CCND1 G870A polymorphism and the risk of colorectal cancer. In addition, heterogeneity, publication bias and sensitivity analysis were performed to guarantee the statistical power. In total, 23 published case-control studies with 6,320 patients and 8,252 controls were selected. Significantly increased risks were observed in four genetic models (A vs. G: OR=1.09, 95% CI=1.00-1.18, I2=54.3%; GA vs. GG: OR=1.13, 95% CI=1.04-1.24, I2=18.2%; AA vs. GG, OR=1.17: 95% CI=1.00-1.38, I2=52.5%; GA+AA vs. GG: OR=1.14, 95% CI=1.05-1.24, I2=33.8%). Similarly, significant associations were also identified in the stratified analysis in the cancer subtype of sporadic colorectal cancer (GA vs. GG: OR=1.21, 95% CI=1.04-1.42, I2=24.1%; GA+AA vs. GG: OR=1.18, 95% CI=1.02-1.37, I2=35.0%), Caucasian population (GA vs. GG, OR=1.14, 95% CI=1.02-1.28, I2=19.8%; GA+AA vs. GG, OR=1.14, 95% CI=1.02-1.27, I2=37.5%) and other subgroups of control design and genotyping type. The present updated meta-analysis suggested that CCND1 G870A may present an increased risk for developing colorectal cancer, particularly in sporadic colorectal cancer and a Caucasian population.

Oral sex and risk of oral cancer: a meta-analysis of observational studies.

OBJECTIVE: Association between oral sex and oral cancer is a highlighted topic all the time; however, many published epidemiological studies remain failed to obtain a consistent conclusion. We performed this meta-analysis to ascertain whether oral sex is a risk factor or a risk marker for oral cancer. METHOD: The PubMed database was searched up to 30 August 2013 (latest updated on 21 December 2014) for relevant observational studies that tested the association between oral sex and oral cancer risk. After data extraction from eligible studies, the meta-analysis was conducted using the Comprehensive Meta-Analysis software. RESULTS: Finally we yielded six case-control studies and one cross-sectional study with 5553 individuals. The results based on random-effects model indicated that there was no significant association between oral sex and risk of oral cancer (OR 1.15, 95% CI 0.86 to 1.54; P = 0.33). Sensitivity analysis showed that the result was robust and subgroups analyses also revealed similar results. Publication bias was not detected. CONCLUSION: Current evidence suggests that oral sex is a risk marker rather than an independent risk factor for oral cancer. However, the practitioners should assure they are without sexually transmitted diseases and with good oral health, and at least cleaned carefully and thoroughly before oral sex.

No association between MTHFR A1298C gene polymorphism and head and neck cancer risk: a meta-analysis based on 9,952 subjects.

OBJECTIVE: Findings for associations between the methylenetetrahydrofolate reductase (MTHFR) A1298C gene polymorphism and head and neck cancer risk have been conflicting. We therefore performed a meta-analysis to derive a more precise relationship. METHODS: Ten published case-control studies were collected and odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the association between MTHFR A1298C polymorphism and head and neck cancer risk. Sensitivity analysis and publication bias assessment also were performed to guarantee the statistical power. RESULTS: Overall, no significant association between MTHFR A1298C polymorphism and head and neck cancer risk was found in this meta-analysis (C vs. A: OR=1.04, 95%CI=0.87- 1.25, P=0.668, P heterogeneity<0.001; CC vs. AA: OR=1.07, 95%CI=0.70-1.65, P=0.748, P heterogeneity<0.001; AC vs. AA: OR=1.06, 95%CI=0.88-1.27, P=0.565, P heterogeneity<0.001; CC+AC vs. AA: OR=1.06, 95%CI=0.86-1.30, P=0.571, P heterogeneity<0.001; CC vs. AA+AC: OR=1.02, 95%CI=0.69-1.52, P=0.910, P heterogeneity<0.001). Similar results were also been found in succeeding analysis of HWE and stratified analysis of ethnicity. CONCLUSIONS: In conclusion, our meta-analysis demonstrates that MTHFR A1298C polymorphism may not be a risk factor for developing head and neck cancer.

Association between XPD Asp312Asn polymorphism and esophageal cancer susceptibility: a meta-analysis.

OBJECTIVE: To investigate the association between xeroderma pigmentosum group D (XPD) Asp312Asn polymorphism and esophageal cancer (EC) susceptibility by meta-analysis. METHODS: We searched PubMed up to April 9th, 2012, to identify relevant papers, and 8 published case-control studies including 2165 EC patients and 3141 healthy controls were yielded. Odds ratios (ORs) with relevant 95% confidence intervals (CIs) were applied to assess the association between XPD Asp312Asn polymorphism and EC susceptibility with the Comprehensive Meta-Analysis software, version 2.2. RESULTS: Overall, the meta-analysis results suggested the XPD Asp312Asn polymorphism to be significantly associated with EC susceptibility [(Asn/Asn+Asp/Asn) vs. Asp/Asp: OR=1.20, 95%CI=1.05-1.36, p=0.01; and Asp/Asn vs. Asp/Asp: OR=1.15, 95%CI=1.01-1.31, p=0.04]. In the subgroup analysis by ethnicity and cancer type, significantly associations were found for Caucasian populations [(Asn/Asn+Asp/Asn) vs. Asp/Asp: OR=1.26, 95%CI=1.08-1.47, p<0.001; Asp/Asn vs. Asp/Asp: OR=1.19, 95%CI=1.02- 1.40, p=0.03] and esophageal squamous cell carcinoma [(Asn/Asn+Asp/Asn) vs. Asp/Asp: OR=1.19, 95%CI=1.01-1.41, p=0.04]. There was no heterogeneity and no publication bias existed. CONCLUSIONS: This meta-analysis shows that the XPD Asp312Asn polymorphism may be a risk factor for developing EC, especially for Caucasian populations and esophageal squamous cell carcinoma.