Association of IL-1α gene polymorphism with susceptibility to type 1 diabetes in Chinese children.

The interleukin-1α (IL-1α) gene appears to play a role in the pathogenesis of type 1 diabetes (T1D). Therefore, the aim of this study was to investigate the contribution of the IL-1 rs1800587 gene polymorphism to susceptibility to T1D in Chinese children. This case-control study included 332 Chinese children with T1D and 332 healthy controls. Identification of genetic variants of rs1800587 in the IL-1α gene was performed by polymerase chain reaction amplification. The IL-1α rs1800587 polymorphism demonstrated a significant association with T1D risk. The allelic frequency significantly differed between the T1D and control groups [odds ratio (OR) = 0.7; 95% confidence interval (CI) = 0.52-0.86; P = 0.002]. Furthermore, significant differences were observed in the dominant model (CC/CT + TT; OR = 0.6; 95%CI = 0.46-0.85; P = 0.003). In T1D patients, the prevalence of hypertension in T allele carriers was 4.2-fold higher than that in C allele carriers, (95%CI = 2.67-6.58; P < 0.001). In conclusion, the present study found evidence of a significant association between the rs1800587 polymorphism in the IL-1α gene and T1D.

MiR-577 inhibits pancreatic ß-cell function and survival by targeting fibroblast growth factor 21 (FGF-21) in pediatric diabetes.

Pancreatic ß-cell dysfunction is a central component of the pathogenesis of pediatric diabetes. MicroRNA (miRNA) have become one of the most encouraging and fruitful fields in biological research, and have been implicated as new players in the pathogenesis of diabetes and diabetes-associated complications. The role of miRNA in diabetes begins with the development of pancreatic islets. Fibroblast growth factor (FGF)-21 enhances glucose uptake in adipocytes, protecting transgenic animals from diet-induced obesity when overexpressed, and lowers blood glucose and triglyceride levels in diabetic animals (when administered); therefore, it is a good way to treat diabetes. However, the mechanism of miRNA in regulation of FGF21 is not known. In this study, FGF-21 was predicted to be the target of miR-577. Therefore, we investigated the effects of miR-577 on ß-cell function and survival by targeting FGF-21. We demonstrated that, although FGF-21 does not acutely stimulate insulin secretion in isolated islets from normal rats, it increases insulin secretion and insulin content in diabetic islets and protects ß-cells from apoptosis via the activation of extracellular signal-regulated kinase 1/2 and Akt signaling pathways.

Effect of transcription factor ZBTB20 on mouse pituitary development.

Pituitary, a critical component in the neuroendocrine system, plays an indispensable role in the regulation of body growth. The transcriptional factor ZBTB20 is widely expressed in brain tissues and participates in hippocampal development; however, the detailed molecular mechanism remains unknown. Therefore, the aim of this study was to investigate the effect of ZBTB20 on mouse pituitary development and related mechanisms in ZBTB20 gene knockout mice. The expressional profiles of ZBTB20 in various neuroendocrinal cells during the different developmental stages (from E10 to P0) were described by immunofluorescence staining. A ZBTB20 gene knockout mouse model was then generated. Real-time polymerase chain reaction and western blotting assays were used to detect the levels of five hormones: growth hormone (GH), prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and thyroid-stimulating hormone (TSH). ZBTB20 protein expression was identified from E14 until birth. A majority of the pituitary endocrinal cells were ZBTB20-positive. In ZBTB20 knockout mice, the level of GH decreased by half and PRL expression was eliminated. No significant change was observed in the other three hormones (LH, FSH, and TSH). ZBTB20, an important transcriptional factor in pituitary development, is mainly responsible for the terminal differentiation of prolactin-secreting cells, thereby regulating the secretion of the pituitary hormones.

Diagnosis of lymph node micrometastasis at the pN0 stage of lung adenocarcinoma using a combination of markers.

This study aimed to detect micrometastatic tumor cells in the lymph nodes of patients with pN0 lung adenocarcinoma using a combination of thyroid transcription factor-1 (TTF-1) expression and cytokeratin 7 (CK7) expression and to investigate the association of lymph node micrometastasis with the clinicopathological characteristics of patients with lung adenocarcinoma. A total of 54 patients with pN0 lung adenocarcinoma and whose primary tumors were positive for both TTF-1 and CK7 expression were included in this study. In total, 893 lymph nodes were obtained from these 54 patients and were analyzed for micrometastasis by immunohistochemical staining with anti-CK7 and anti-TTF-1 antibodies. CK7- and TTF-1-positive cells were found in the lymph nodes of 9 (16.7%) of 54 patients, and 21 (2.4%) of 893 lymph nodes exhibited positivity for these factors. No cells positive for both CK7 and TTF-1 were detected in the 5 lymph nodes obtained from patients with benign lung tumors. Lymph node micrometastasis was found to be associated with the differentiation grade and primary tumor position (P < 0.05). The detection of lymph node micrometastasis by a combination of CK7 and TTF-1 immunohistochemical staining provides a more accurate assessment of tumor staging for pN0 lung adenocarcinoma.