RESUMO
Mutations in mitochondrial DNA have been found to be associated with hypertension. Of these, mitochondrial transfer RNA (mt-tRNA) is a hot spot for these pathogenic mutations. It is generally believed that these mutations may result in the failure of mt-tRNA metabolism, thereby worsening mitochondrial dysfunction and resulting in hypertension. mt-tRNA is known for its high frequency of polymorphisms and mutations, and the number of reports regarding mt-tRNA mutations and hypertension is increasing significantly. To better understand the molecular basis of maternally inherited hypertension, we reassessed the link between four mt-tRNA mutations (G15927A in tRNA(Thr), C7492T in tRNA(Ser(UCN)), A4386G in tRNA(Gln), and C14686T in tRNA(Glu)) and hypertension. We first used the phylogenetic approach to investigate the deleterious roles of these mutations, then we used RNA Fold Web Server to predict the minimum free energy of these mt-tRNAs with and without mutations. Using the pathogenicity scoring system, we found that the G15927A and C7492T mutations are classified as pathogenic while all other studied mutations are neutral polymorphisms. Our study provides valuable information for the detection of pathogenic mt-tRNA mutations in hypertension.
Assuntos
DNA Mitocondrial/genética , Hipertensão/genética , Filogenia , RNA de Transferência/genética , Humanos , Hipertensão/patologia , Mitocôndrias/genética , Mutação , Polimorfismo GenéticoRESUMO
Hyperglycemia is common in critical patients and high blood glucose levels have a negative effect on their prognosis. The aim of this study was to investigate the effect of hyperglycemia and glycosylated hemoglobin (GHb) in critical patients. A total of 648 critical patients were enrolled in the study and received a random blood glucose test when they entered the emergency department. If blood glucose was more than 11.1 mM, a GHb test was followed within 24 h. All patients were followed up for 28 days. According to diabetes mellitus (DM) history, GHb value, and outcome of follow-up, patients were divided into different groups, and mortality rates were calculated, respectively. Hyperglycemia was found in 67.44% (437/648) of patients, and 51.49% (225/437) and 48.51% (212/437) had normal and elevated GHb levels, respectively. At the end of the follow-up period, 14 of the normal GHb patients and 32 of the elevated GHb patients died (6.22 and 15.09%, respectively). In the normal GHb group, 53 had a DM history, 23 were newly diagnosed with DM, and 149 had hospital-related hyperglycemia (HRH); the mortality rates were 11.32% (6/53), 8.70% (2/23), and 4.03% (6/149), respectively. In the elevated GHb group, 114 had a DM history, 83 were newly diagnosed with DM, and 15 had HRH; the mortality rates were 13.16% (15/114), 19.27% (16/83), and 6.67% (1/15), respectively. Hyperglycemia and GHb might play important roles in the prognosis and assessment for critical patients, and the prognosis would vary according to the different causes of hyperglycemia.