Multiple endocrine neoplasia type 1 (MEN1) is a syndrome characterized by the occurrence of two or more endocrine gland tumors. Here, we show a case of a 52-year-old man diagnosed with MEN1 through gastrinoma, parathyroid adenoma and gene detection. The MEN1 patient’s case was complicated with relapsed primary hyperparathyroidism (PHPT), and they received ultrasound-guided radiofrequency ablation (RFA). The patient had a remarkable recovery after RFA treatment for the relapsed PHPT. It might be an alternative treatment for MEN1 patients with poor conditions such as high surgical risk, unwillingness to choose parathyroid surgery or those unable to tolerate surgery. Individualized therapy significantly benefits the prognosis of MEN1 patients.
IntroductionThe incidence of osteoporosis (OP) keeps increasing due to global aging of the population. Therefore, identifying the diagnostic and prognostic biomarkers of OP is of great significance.MethodsmRNA data from OP and non-OP samples were obtained from GEO database, which were divided into training set (GSE35959) and testing sets (GSE7158, GSE62402, GSE7429 and GSE56815). Gene modules most significantly related to OP were revealed using weighted gene co-expression network analysis (WGCNA) and differentially expressed genes (DEGs) between OP and normal samples in training set were identified using limma R package. Thereafter, above two gene sets were intersected to obtain the genes potentially related to OP. Protein-protein interaction (PPI) pairs were screened by STRING database and visualized using Cytoscape, while the plug-in cytoHubba was used to screen hub genes by determining their topological parameters. Afterwards, a diagnostic model was constructed using those hub genes, whose creditability was further evaluated by testing sets.ResultsThe results of WGCNA analysis found the Black module was most significantly related to OP, which included altogether 1286 genes. Meanwhile, 2771 DEGs were discovered between OP patients and the normal controls. After taking the intersection, 479 genes were identified potentially correlated with the development of OP. Subsequently, six hub genes were discovered through PPI network construction and node topological analysis. Finally, we constructed a support vector machine model based on these six genes, which can accurately classified training and testing set samples into OP and normal groups.ConclusionOur current study constructed a six hub genes-based diagnostic model for OP. Our findings may shed some light on the research of the early diagnosis for OP and had certain practical significance.
Denitrosylase S-nitrosoglutathione reductase (GSNOR) regulates the equilibrium of total cellular S-nitrosylation levels, a key redox-based post-translational modification that is frequently dysregulated in various diseases. However, the effects and underlying mechanisms of GSNOR on brain microvascular endothelial cells (BMECs) under hypoxia conditions are unknown. In this study, a photothrombosis model was used to induced cerebral ischemia injury in the male C57BL6 mice injury. BMECs were subjected with oxygen-glucose deprivation (OGD) for 6 h to establish the ischemic cell models in vitro. Increased GSNOR levels and S-nitrosylation dysfunctions were observed in cerebral ischemic injury. GSNOR knockdown rescued OGD-induced ischemic injury in BMECs. HIF-1α S-nitrosylation was significantly increased in BMECs after GSNOR knockdown. We investigated the effects of GSNOR on mitochondrial functions and revealed the relationship between HIF-1α translocation and downstream signaling, including mitochondrial bioenergetic functions and activation of mitophagy in BMECs. GSNOR knockdown alleviated OGD-induced mitochondrial impairments. Moreover, GSNOR reduced excessive mitochondrial reactive oxygen species (ROS) production, thereby, alleviating mitochondrial oxidative stress. GSNOR knockdown also enhanced the disturbance of cellular bioenergetic functions and BNIP3L/NIX-mediated mitophagy. Expression levels of mitophagy-related proteins, such as LC3B, BNIP3L/NIX, and FUNDC1were significantly elevated in GSNOR knockdown detected by western blot. These results suggest that the knockdown of GSNOR knockdown alleviates mitochondrial toxicity by promoting HIF-1α S-nitrosylation-associated repair of mitochondrial functions and activating mitophagy in BMECs. Understanding the protective effects of GSNOR provides a novel strategy for developing potential therapies targets for ischemic injury in BMECs.
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