ABSTRACT
<p><b>OBJECTIVE</b>To evaluate the efficacy and safety of nateglinide, a new antidiabetic agent, in the treatment of type 2 diabetes.</p><p><b>METHODS</b>A total of 219 treatment-naïve patients with type 2 diabetes from 6 centers were enrolled in this study and blindly divided into nateglinide group (n = 105) and repaglinide group (n = 114). In all patients, the disease was confirmed for at least three months. The whole observation lasted for 12 weeks. The efficacy indicators measured include glycohemoglobin A1c (HbA1c), fasting blood glucose, and 2 hours postprandial blood glucose, and the safety parameters measured included renal and hepatic function, serum lipids, and blood and urea profiles.</p><p><b>RESULTS</b>Similar decreases in fasting blood glucose, 2 hours postprandial blood glucose, and HbA1 c were found in both nateglinide group and repaglinide group without significant differences. No severe adverse events were noted. The hypoglycemia event reports were not significantly different between these two groups.</p><p><b>CONCLUSION</b>Nateglinide is an effective and safe drug in treating type 2 diabetes.</p>
Subject(s)
Female , Humans , Male , Middle Aged , Blood Glucose , Cyclohexanes , Therapeutic Uses , Diabetes Mellitus, Type 2 , Drug Therapy , Drug Administration Schedule , Hypoglycemic Agents , Therapeutic Uses , Phenylalanine , Therapeutic Uses , Treatment OutcomeABSTRACT
<p><b>BACKGROUND</b>Increased reactive oxygen species (ROS) formation, which in turn promotes cardiomyocytes apoptosis, is associated with the pathogenesis and progression of various cardiac diseases such as ischemia and heart failure. Recent studies have shown that over expression of heat shock protein 27 (Hsp27) confers resistance to cardiac ischemia/reperfusion injury. However, not much is known about the regulation of myocyte survival by Hsp27.</p><p><b>METHODS</b>The rat cardiac cell line H9c2, with a stable overexpression of Hsp27, was established, with empty vector transfected H9c2 cells as controls. Following the cells challenged by Hydrogen Peroxide (H2O2), lactate dehydrogenase (LDH) release, apoptosis, intracellular ROS, cell morphology, mitochondrial transmembrane potential and the activation of serine/threonine kinase Akt were determined.</p><p><b>RESULTS</b>Along with marked suppression of H2O2-induced injury by Hsp27 overexpression in H9c2 cells, ROS generation and the loss of mitochondrial membrane potential were also significantly depressed. Furthermore, augmented Akt activation was observed in Hsp27 overexpressed H9c2 cells following H2O2 exposure.</p><p><b>CONCLUSIONS</b>Hsp27 inhibits oxidative stress-induced H9c2 damage and inhibition of ROS generation and the augmentation of Akt activation may be involved in the protective signaling.</p>
Subject(s)
Animals , Humans , Rats , Apoptosis , Cell Line , HSP27 Heat-Shock Proteins , Heat-Shock Proteins , Physiology , Hydrogen Peroxide , Toxicity , Myocytes, Cardiac , Pathology , Neoplasm Proteins , Physiology , Oxidative Stress , Proto-Oncogene Proteins c-akt , Metabolism , Reactive Oxygen Species , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the sleep status of college and high schools students.</p><p><b>METHODS</b>Pittsburgh sleep quality index (PSQI) and self-manufactured questionnaires about siesta habits were used as tools. Three groups of students from medical college (MC), senior high school (SS) and junior high school (JS) were surveyed.</p><p><b>RESULTS</b>In the group MC, SS and JS, the occurrence rates of sleep disorders were 27%, 62% and 54%, respectively, and in which the appearance rates of insomnia were 17%, 19% and 19%, longing for sleep were 10%, 43% and 35% respectively. And there were no significant difference between schoolboy and schoolgirl. The occurrence rates of slack breathing were different (5/155, 1/154) significantly between group SS and JS. The distinct differences also were found in group JS and MC, in which students felt hot (10/155, 1/122) and in all the three groups, in which students felt sleepy (55/155, 62/154, 13/122) whereas the difference of sleepy between group SS and JS was comparatively distinct (55/155, 62/154). Significant differences were also found between group JS and SS, MC in average sleep time of (7.65 +/- 0.87) hours, (7.16 +/- 0.83) hours, and (7.10 +/- 0.57) hours. The time of falling asleep (median 15 min, 10 min, 20 min) and siesta habit (8/155, 19/154, 75/122) among group MC and SS, JS were different respectively and markedly, whereas siesta habit differences between group SS and JS were comparatively distinct (8/155, 19/154).</p><p><b>CONCLUSION</b>Students in high school showed higher rate of longing for sleep, and this implicated they fall short of sleep time greatly and siesta could improve their sleepy signs.</p>
Subject(s)
Adolescent , Adult , Female , Humans , Male , China , Epidemiology , Prevalence , Sleep , Physiology , Sleep Initiation and Maintenance Disorders , Epidemiology , Sleep Wake Disorders , Epidemiology , Students , Surveys and QuestionnairesABSTRACT
<p><b>AIM</b>Try to clarify the effects of HSF1 gene on the constitutively expressed alphaBC.</p><p><b>METHODS</b>To investigate the levels of constitutively expressed alphaB-Crystallin (alphaBC) in hsf1 knockout (hsf1 -/-) and hsf1 wild type (hsf1 +/+) mice myocardium by Western blot and immunohistochemistry.</p><p><b>RESULTS</b>The alphaBC levels in hsf1 -/- and hsf1 +/+ were 68.42% +/- 4.16%, 100% +/- 7.58%, respectively (P < 0.05, cytosolic fraction), and 20.53% +/- 1.01%, 37.55% +/- 1.91%, respectively (P < 0.05, pellet fraction). The alphaBC signals decreased significantly in hsf1 -/- myocardium compared with hsf1 +/+ myocardium stained with fluorescence immunohistochemistry.</p><p><b>CONCLUSION</b>hsf1 is the important, but not the only factor, which mediates the constitutively expressed alphaBC.</p>
Subject(s)
Animals , Female , Male , Mice , DNA-Binding Proteins , Genetics , Genotype , Heat Shock Transcription Factors , Mice, Knockout , Myocardium , Metabolism , Transcription Factors , Genetics , alpha-Crystallin B Chain , Genetics , MetabolismABSTRACT
Objective To determine the effect of mitochondria on the protection of heat-shock proteins B1(HSPB1) from oxidative damage in rat cardiac cell.Methods HSPB1 gene-transfected rat cardiomyocytes cell line H9c2 (HSPB1 H9c2) and empty vector transfected H9c2 (control) were established,and treated by 0-1000?mol/L H_2O_2 for 2h.And then the cell morphology, mitochondrial membrane potential and endogenous reactive oxygen species (ROS) were detected. Results (1)HSPB1 inhibited the morphological changes induced by H_2O_2 markedly.(2)HSPB1 inhibited the loss of mitochondrial membrane potential induced by H_2O_2.Following the stimulation of 0,75,150,300,500,1000?mol/L H_2O_2,mitochondrial membrane potential in HSPB1 and control H9c2 cells were (10.0?0.11)vs (7.01?0.26),(9.11?0.17)vs (6.05?0.19),(7.69?0.28)vs (5.14?0.28),(6.95?0.13)vs (4.66?0.11),(6.61?0.20)vs (1.85?0.35),(6.60?0.05)vs (1.19?0.01),respectively (all P0.05).Conclusions HSPB1 protects rat cardiomyocytes cell line(H9c2) from oxidative damage,which suggests that stabilization of mitochondrial membrane potential and the decreased endogenous reactive oxygen species after oxidative stress may be involved in the protection of HSPB1 against oxidative stress in H9c2.