ABSTRACT
OBJECTIVE: To explore the correlations of interleukin-6 (IL-6) and C-reactive protein (CRP) gene polymorphisms with pulmonary heart disease (PHD). PATIENTS AND METHODS: A total of 98 patients with PHD and 102 healthy persons receiving physical examinations were enrolled. Their general clinical information was collected, and the levels of IL-6 and CRP in the plasma were determined. The pulmonary functions and blood gas were detected, and the TaqMan-minor groove binder (MGB) probe was used to detect the polymorphisms of IL-6 rs1800796 and CRP rs1800796. RESULTS: Observation group had higher levels of IL-6 and CRP than control group (p<0.05). The forced expiratory volume in 1 second (FEV1) (%), FEV1/forced vital capacity (FVC) ratio (%), and arterial partial pressure of oxygen (PaO2) in observation group were lower than those in control group (p<0.05), but the arterial partial pressure of carbon dioxide (PaCO2) was higher than that in control group (p<0.05). There were differences in the distribution frequencies of the genotypes and alleles of IL-6 rs1800796 and CRP rs1800796 between the two groups (p<0.05). CONCLUSIONS: IL-6 and CRP are correlated with the onset of PHD, and there are also correlations between the polymorphisms of IL-6 rs1800796 and CRP rs2794521 and the disease.
Subject(s)
C-Reactive Protein/genetics , Interleukin-6/genetics , Pulmonary Heart Disease/genetics , Blood Gas Analysis , Carbon Dioxide/metabolism , Case-Control Studies , Female , Forced Expiratory Volume , Genetic Predisposition to Disease , Humans , Male , Middle Aged , Oxygen/metabolism , Partial Pressure , Polymorphism, Single Nucleotide , Pulmonary Heart Disease/metabolism , Pulmonary Heart Disease/physiopathology , Vital CapacityABSTRACT
BACKGROUND: Traumatic brain injury (TBI) is a serious neurodisorder commonly caused by sports related events or violence. It is the leading cause of disability in people under 40. AIM: In order to elucidate the molecular mechanism of the secondary injury after TBI. MATERIALS AND METHODS: In this study, we downloaded gene expression profile on TBI model with sham controls for gene set enrichment analysis and pathway analysis. RESULTS: At a q-value of 5%, 361 genes were up-regulated and 373 were down-regulated in samples obtained at 48 hours after TBI. Functional analyses revealed that steroid biosynthesis, cell cycle, metal ion transport, inflammation and apoptosis were significantly dysregulated during the late period after trauma. In addition, MAPK3 (mitogen-activated protein kinase 3), was identified as the hub node in the protein-protein interaction (PPI) network constructed by the differentially expressed genes (DEGs). CONCLUSIONS: Further elucidation of genes and proteins in our study may reveal their potential as novel therapeutic targets.
