Objective. We aimed to explore whether squamous cell carcinoma antigen (SCC), cytokeratin 19 fragment (Cyfra21-1), neuron-specific enolase (NSE), and carcinoembryonic antigen (CEA) are elevated in diabetic nephropathy (DN) and the association between urinary albumin-to-creatinine ratio (UACR) and tumor markers in diabetic patients.Methods. Nondialysis patients with diabetes (n=261) and 90 healthy controls were enrolled. DN was defined as an UACR ≥ 30 mg/g in the absence of a urinary tract infection or other renal abnormalities.Results. Patients with DN had significantly higher serum SCC, Cyfra21-1, and CEA levels than those with normoalbuminuria and healthy controls. The rates of positive SCC, Cyfra21-1, and CEA significantly increased with increasing urinary albumin excretion (allPfor trend < 0.001). In contrast, NSE was not affected by DN. SCC, Cyfra21-1, and CEA were significantly and positively correlated with UACR. In logistic regression, after multivariable adjustment, increased UACR was associated with increased odds ratio of elevated tumor marker levels (allPfor trend < 0.05).Conclusions. Serum levels of SCC, Cyfra21-1, and CEA are markedly increased with increasing urinary albumin excretion, which affects the specificity for diagnosis for lung cancer. Appropriate interpretation of tumor markers in diabetic patients is mandatory to avoid unnecessary and even hazardous biopsies.

Introduction: Previous case-control studies have suggested that the –1562C/T and R279Q polymorphisms of the matrix metalloproteinase 9 gene (MMP9) are associated with coronary heart disease (CHD). However, other studies do not confirm these relationships. The objective is to assess these relationships using meta-analysis. Methods: Databases, including PubMed and ScienceDirect, were searched to access the genetic association studies. Then data were extracted. Pooled odds ratio (OR) and 95% confidence interval (CI) were calculated. Moreover, subgroup and sensitive analysis were performed. Results: The meta-analysis of the –1562C/T polymorphism included 12 studies with 8,336 cases and 3,984 controls. The –1562T allele was significantly associated with CHD (OR 1.25, 95% CI 1.08–1.45, p = 0.004). There was heterogeneity among the 12 studies (I2 = 61%, p = 0.003). The overall results were consistent and were not changed substantially by the removal of any data set. The meta-analysis of the R279Q polymorphism, including 6 studies with 6,983 cases and 3,282 controls, showed that the R279Q polymorphism was not associated with CHD (p = 0.16). Conclusions: The synthesis of available evidence supports the fact that the MMP9 –1562C/T polymorphism is a risk factor for CHD.

The global epidemic of obesity challenges the scientific and medical communities to find different treatments. Schisantherin A (Sin A), a natural compound isolated from Schisandra chinensis (Turcz.), reduces the abundance of bile salt hydrolase-producing gut bacteria in obese mice, leading to accumulation of specific conjugated bile acids (CBAs). These elevated CBAs activate a signaling axis containing Takeda G protein-coupled receptor 5, phosphorylated cAMP-responsive element binding protein 1, and signal transducer and activator of transcription 6 (TGR5–p-CREB–STAT6), wherein CREB directly binds to the STAT6 promoter. Sin A-induced STAT6 activation promoted M2-like macrophages polarization to secret slit guidance ligand 3 (SLIT3), which consequently stimulated norepinephrine release in sympathetic neurons and induced thermogenesis in adipose tissue. This study thus identifies a pathway by which Sin A interacts with gut bacteria to stimulate CBA-mediated beiging of white adipose tissue, highlighting a promising natural product-based strategy for obesity treatment.