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Objective Published evidence indicated that the leptin receptor (LEPR) gene polymorphisms are associated with polycystic ovary syndrome (PCOS) risk. However, studies on the association between the polymorphisms of LEPR gene are inconsistent or even controversial.Material and Methods We conducted this meta-analysis to explore the more precise relationship between LEPR polymorphisms and PCOS risk. Relevant articles were searched with five online databases up to March 1 2023. Odds ratios (OR) with 95% confidence intervals (CI) were selected to examine the statistical strength of each genetic model. Moreover, RNA secondary structure and variant effects of these loci were examined with in silico analysis.Results Overall, 11 publications were analyzed, and the pooled results did not present any significant association between rs1137101 A/G polymorphism and PCOS risk in general population and some subgroup analysis. But the significant association were observed in Asian population (AG vs. AA: OR = 0.51, 95%CI = 0.32–0.81, p = .01, I2=0%; AG + GG vs. AA: OR = 0.41, 95%CI = 0.26–0.65, p

Abstract Background Published researches have suggested some associations between PPAR‐γ and ischemic stroke (IS) development. This meta‐analysis was conducted to evaluate the association between PPAR‐γ gene polymorphisms and IS risk. Materials and methods A systematic search was conducted in PubMed, Embase, Web of Science, China National Knowledge Infrastructure, and WanFang databases. The pooled association of odd ratios (ORs) and its 95% confidence interval (CI) was calculated to assess the IS risk of PPAR‐γ rs1801282 C/G and rs3856806 C/T polymorphisms. Furthermore, the heterogeneity test, cumulative analyses, sensitivity analyses, and publication bias were conducted. Result Sixteen publications with 3786 cases and 5343 controls were identified. Overall findings indicated that rs1801282 C/G polymorphism may be associated with an increased risk for IS (GG vs. CC: OR = 2.17 95%CI = 1.09–4.35, p = .03, I2 = 0%; GG vs. CC+CG: OR = 2.15, 95%CI = 1.07–4.32, p = .03, I2 = 0%). The similar results were also found in the subgroup analysis. In addition, no significant association was observed between rs3856806 C/T polymorphism and IS risk. Conclusion In conclusion, our study showed that PPAR‐γ rs1801282 C/G polymorphism probably plays an important role in IS occurrence. The result should be verified with more studies in the future.

Evidence suggests that there is a close association between myeloperoxidase (MPO) gene rs2333227 G>A polymorphism with Alzheimer’s disease (AD) susceptibility. We conducted a meta-analysis to explore the precise association between MPO rs2333227 G>A polymorphism and AD susceptibility. Online databases were searched and the relevant information was collected. Crudeodds ratios with 95% confidence intervals were calculated. Trial sequential analysis (TSA), heterogeneity analyses, accumulative analyses, sensitivity analyses, and publication biasestests were performed. Overall, nine publications (ten independent case-controls) were included in this meta-analysis, involving 3260 participants. Pooled results revealed no significant association between MPO rs2333227 G>A polymorphism and AD susceptibility was observed. TSA showed that the present meta-analysis remained inconclusive due to insufficient evidence. In summary, the current meta-analysis indicated that the MPO rs2333227 G>A polymorphism may not be acausalfactor in the development of AD.

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. [ABSTRACT FROM AUTHOR]

There are limitations to the use of single biomarker levels, for example phosphate and tensin homology (PTEN) or vascular endothelial growth factor (VEGF), in the diagnosis of esophageal squamous cell carcinoma (ESCC). The present study therefore aimed to evaluate the clinical implications of combined detection of multiple biomarkers. The associations between PTEN and VEGF expression status, microvessel density (MVD), and the pathological characteristics of 50 patients with ESCC were determined using Χ², analysis of variance, and t-tests. The results indicated that the PTEN-positive rate was negatively correlated with ESCC histological grade (P<0.01), depth of ESCC invasion (P<0.01) and lymph node metastasis status. Furthermore, the VEGF-positive rate was correlated with lymph node metastasis status, while MVD was correlated with the depth of ESCC invasion (P<0.01) and lymph node metastasis status (P<0.05). The PTEN-positive rate was negatively correlated with the VEGF-positive rate. A higher MVD was identified in ESCC samples than that of the normal esophageal mucosa, particularly in VEGF-positive ESCC specimens compared with those of VEGF-negative specimens, and PTEN-negative ESCC specimens compared with that of the PTEN-positive ESCC specimens. These results suggested that combined detection of PTEN and VEGF levels, as well as evaluation of MVD in patients with ESCC may provide essential information for improvements in the diagnosis and prognosis of ESCC. [ABSTRACT FROM AUTHOR]

The common functional cyclin D1 (CCND1) G870A polymorphism may influence the risk of esophageal cancer. However, the conclusions of previous studies have been inconsistent for the association between the CCND1 G870A polymorphism and esophageal cancer risk. A meta-analysis of 11 published case-control studies was performed, including 2,111 patients with esophageal cancer and 3,232 controls, to investigate the association between the CCND1 G870A polymorphism and esophageal cancer risk. The odds ratio (OR) with a 95% confidence interval (CI) was applied to assess the association between the CCND1 G870A polymorphism and esophageal cancer risk. A significant association between the CCND1 G870A polymorphism and esophageal cancer risk was observed for the allele contrast (A vs. G: OR, 1.23; 95% CI, 1.02-1.48; P = 0.029), codominant (AA vs. GG: OR, 1.58; 95% CI; 1.06-2.35; P = 0.024) and recessive models (AA vs. GG + GA: OR, 1.33, 95% CI, 1.03-1.73; P = 0.030). However, in the stratified analysis by ethnicity, study design and pathology, there was no significant association detected in these genetic models. In conclusion, results of the meta-analysis suggested that the CCND1 G870A polymorphism is a potential risk factor in the development of esophageal cancer. [ABSTRACT FROM AUTHOR]

Aim: To investigate the effect of GW4064 on the expression of adipokines and their receptors during differentiation of 3T3-L1 preadipocytes and in HepG2 cells., Methods: The mRNA expression of farnesoid X receptor (FXR), peroxisome proliferator-activated receptor-gamma 2 (PPAR-γ2), adiponectin, leptin, resistin, adiponectin receptor 1 (AdipoR1), adiponectin receptor 2 (AdipoR2), and the long isoform of leptin receptor (OB-Rb) and protein levels of adiponectin, leptin, and resistin were determined using fluorescent real-time PCR and enzyme linked immunosorbent assay, respectively, on days 0, 2, 4, 6, and 8 during the differentiation of 3T3-L1 preadipocytes exposed to GW4064. Moreover, mRNA expression of AdipoR2 and OB-Rb was also examined using fluorescent real-time PCR at 0, 12, 24, and 48 h in HepG2 cells treated with GW4064., Results: The mRNA expression of FXR, PPAR-γ2, adiponectin, leptin, resistin, AdipoR1, AdipoR2, and OB-Rb and protein levels of adiponectin, leptin, and resistin increased along with differentiation of 3T3-L1 preadipocytes (P < 0.05 for all). The mRNA expression of FXR, PPAR-γ2, adiponectin, leptin, and AdipoR2 in 3T3-L1 preadipocytes, and AdipoR2 and OB-Rb in HepG2 cells was significantly increased after treatment with GW4064, when compared with the control group (P < 0.05 for all). A similar trend was observed for protein levels of adipokines (including adiponectin, leptin and resistin). However, the expression of resistin, AdipoR1, and OB-Rb in 3T3-L1 cells did not change after treatment with GW4064., Conclusion: The FXR agonist through regulating, at least partially, the expression of adipokines and their receptors could offer an innovative way for counteracting the progress of metabolic diseases such as nonalcoholic fatty liver disease.

The protective immune response against porcine circovirus 2 (PCV2) infection in mice was characterized using flow cytometric analysis (FCM), assays of antibody (of different IgG isotypes) and viraemia, and histopathological examination. An open reading frame 2 plasmid (pORF2) and the capsid protein (Cap) of PCV2 were used as DNA and subunit vaccines, respectively. In FCM analysis, although pORF2 and Cap alone showed comparable efficacy in eliciting lymphoproliferative responses and Cap-specific CD4(+) T cells, pORF2 was superior to the Cap protein in triggering CD8(+) T cells. A virus neutralization assay showed that pORF2 evoked stronger recall virus-neutralizing (VN) antibody responses than the Cap protein on PCV2 challenge. Correspondingly, VN antibody kinetics coincided with those of Cap-specific IgG2a, but not with the kinetics of IgG and IgG1. Following virus challenge, real-time PCR and histopathological analysis confirmed that only low viral DNA loads and mild microscopic lesions appeared in pORF2-immunized mice. These findings indicate that CD8(+) T cells and VN antibody responses correlating mainly with Cap-specific IgG2a play crucial roles in protecting against PCV2 infection, and that the protective immunity induced by the pORF2 plasmid is superior to that induced by the PCV2 Cap protein.