Proteomics-based prognostic signature and nomogram construction of hypoxia microenvironment on deteriorating glioblastoma (GBM) pathogenesis.

The present study aimed to construct and evaluate a novel experiment-based hypoxia signature to help evaluations of GBM patient status. First, the 426 proteins, which were previously found to be differentially expressed between normal and hypoxia groups in glioblastoma cells with statistical significance, were converted into the corresponding genes, among which 212 genes were found annotated in TCGA. Second, after evaluated by single-variable Cox analysis, 19 different expressed genes (DEGs) with prognostic value were identified.

Exploratory meta-analysis on dose-related efficacy and complications of rhBMP-2 in anterior cervical discectomy and fusion: 1,539,021 cases from 2003 to 2017 studies.

Background/objective: Anterior cervical discectomy and fusion (ACDF), commonly using autogenous iliac bone graft may be limited by donor site availability, donor-site morbidity, lower fusion rate among specific patients and longer surgical time. Surgeons used rhBMP-2 as an alternative in order to fill these clinical needs. However, studies comparing with and without rhBMP-2 in ACDF have reported conflicting results on efficacy and complications.

Genetic Profiles Playing Opposite Roles of Pathogenesis in Schizophrenia and Glioma.

Background: Patients diagnosed with schizophrenia were found having lower risks to develop cancers, including glioma. Based on this epidemiology, we hypothesized that there were gene profiles playing opposite roles in pathogenesis of schizophrenia and glioma.

Methods: Based on GEO datasets and TCGA, key genes of schizophrenia genes on the opposite development of glioma were screened by different expressed genes (DEGs) screening, weighted gene coexpression network analysis (WGCNA), disease-specific survival (DSS), and glioma grading and verified by gene set enrichment analysis (GSEA).

The Drug Developments of Hydrogen Sulfide on Cardiovascular Disease.

The recognition of hydrogen sulfide (HS) has been evolved from a toxic gas to a physiological mediator, exhibiting properties similar to NO and CO. On the one hand, HS is produced from L-cysteine by enzymes of cystathionine -lyase (CSE) and cystathionine -synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3MST) in combination with aspartate aminotransferase (AAT) (also called as cysteine aminotransferase, CAT); on the other hand, HS is produced from D-cysteine by enzymes of D-amino acid oxidase (DAO). Besides sulfide salt, several sulfide-releasing compounds have been synthesized, including organosulfur compounds, Lawesson's reagent and analogs, and plant-derived natural products.

The Pharmacological Effects of S-Propargyl-Cysteine, a Novel Endogenous H2S-Producing Compound.

S-propargyl-cysteine (SPRC), also named as ZYZ-802, is a structural analog of S-allylcysteine (SAC), the most abundant constituent of aged garlic extract. SPRC becomes a derivative of the amino acid cysteine, which contains sulfur atom, by changing allyl group in SAC to propargyl group in SPRC. Another analog of SPRC and SAC is S-propyl cysteine (SPC), which has propyl group instead in its cysteine structure.

Hydrogen sulfide protects HUVECs against hydrogen peroxide induced mitochondrial dysfunction and oxidative stress.

Background: Hydrogen sulfide (H₂S) has been shown to have cytoprotective effects in models of hypertension, ischemia/reperfusion and Alzheimer's disease. However, little is known about its effects or mechanisms of action in atherosclerosis. Therefore, in the current study we evaluated the pharmacological effects of H₂S on antioxidant defenses and mitochondria protection against hydrogen peroxide (H₂O₂) induced endothelial cells damage.

Neuronal injury in rat model of permanent focal cerebral ischemia is associated with activation of autophagic and lysosomal pathways.

It has been reported that ischemic insult increases the formation of autophagosomes and activates autophagy. However, the role of autophagy in ischemic neuronal damage remains elusive. This study was taken to assess the role of autophagy in ischemic brain damage.

Inflammatory mechanism in ischemic neuronal injury.

Inflammation has been implicated as a secondary mechanism underlying neuronal injury induced by ischemia. A variety of experimental models, including thromboembolic stroke, focal and global ischemia, have been used to evaluate contributions of inflammation to neuronal damage. The vasculature endothelium promotes inflammation through upregulation of adhesion molecules such as intercellular adhesion molecule (ICAM), E-selectin, and P-selectin that bind to circulating leukocytes and facilitate migration of leukocytes into the central nervous system (CNS).