• ISSN 1674-8301
  • CN 32-1810/R

2011 Vol. 25, No. 4

Post-translational protein modification, including phosphorylation, is generally quick and reversible, facilitat-ing rapid biologic adjustments to altered cellular physiologic demands. In addition to protein phosphorylation, other post-translational modifications have been identified. Intracellular protein O-glycosylation, the addition of the simple sugar O-linked N-acetylglucosamine (O-GlcNAc) to serine/threonine residues, is a relatively recently identified post-translational modification that has added to the complexity by which protein function is regulated. Two intracellular enzymes, O-GlcNAc transferase and O-GlcNAcase, catalyze the addition and removal, respec-tively, of O-GlcNAc to serine and threonine side-chain hydroxyl groups. Numerous proteins, including enzymes, transcription factors, receptors and structural proteins have been shown to be modified by intracellular O-glyco-sylation. In this review, the mechanism and relevance of O-GlcNAc protein modification are discussed in the con-text of cell adhesion and several representative diseases.
This present study was aimed to investigate the localizable diagnostic value of magnetoencephalography (MEG) combined with synthetic aperture magnetometry (SAM) in childhood absence epilepsy (CAE). Thirteen CAE pa-tients underwent MEG detection at resting state and after hyperventilation, and then the epileptic foci were located by SAM. In the thirteen CAE patients, epileptic foci were found in five cases (38.5%) , and they were all located in the bilateral frontal lobe, suggesting that the frontal lobe in some CAE patients may serve as the epileptic foci. Our findings indicate that MEG combined with SAM could be of diagnostic value in localizing the epileptic foci in certain CAE patients.
Epidermal growth factor (EGF) may increase cell motility, an event implicated in cancer cell invasion and me-tastasis. However, the underlying mechanisms for EGF-induced cell motility remain elusive. In this study, we found that EGF treatment could activate Ras-related C3 botulinum toxin substrate 1 (Rac1), PI3K/Akt and p21-actived kinase (PAK1) along with cell migration. Ectopic expression of PAK1 K299R, a dominant negative PAK1 mutant, could largely abolish EGF-induced cell migration. Blocking PI3K/Akt signalling with LY294002 or Akt siRNA remarkably inhibited both EGF-induced PAK1 activation and cell migration. Furthermore, expression of dominant-negative Rac1 (T17N) could largely block EGF-induced PI3K/Akt-PAK1 activation and cell migration. Interestingly, EGF could induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF-induced ROS generation, cell migration, as well as activation of PI3K/Akt and PAK, but not Rac1. Our study demonstrated that EGF-induced cell migration involves a cascade of signalling events, in-cluding activation of Rac1, generation of ROS and subsequent activation of PI3K/Akt and PAK1.
Regular use of aspirin (ASA) could reduce the risk of gastric cancer although the precise mechanism remains unclear. Down-regulation of survivin may be one of the cyclooxygenase-independent mechanisms whereby ASA induces apoptosis of gastric cancer cell. In this study, we investigated the effect of ASA on the growth, apoptosis and survivin expression of gastric cancer cell line SGC7901. The survival of cells treated with 3.0 and 10.0 mmol/L ASA for 24 h was decreased by 44.6% and 88.5%, respectively. ASA at 3.0 mmol/L inhibited the viability of SGC7901 cells in a time-dependent manner. Apoptosis analysis showed similar results with MTT assay. ASA at 3.0 and 10.0 mmol/L decreased the mRNA transcript levels of survivin and reduced survivin protein levels in SGC7901 cells also in a time-dependent manner. Our findings indicated that ASA inhibited the proliferation of SGC7901 by sup-pressing survivin at both the transcriptional and translational level.
We evaluated the effect of water storage on fluoride release and mechanical properties of compomer restorative material. Fluoride release was recorded using a specific fluoride electrode. Flexural properties and fracture tough-ness were measured using a universal testing machine. Vickers hardness was measured using a micro-hardness tester. There was initial burst of fluoride release up to 1 w, which was diminished to a low level in 1 mon and remained relatively constant over 6 mon. Flexural strength and hardness were increased up to 1 mon followed by a gradual decrease up to 6 mon. Flexural modulus was decreased gradually up to 6 mon. Fracture toughness was increased during the first week and gradually decreased over the storage period. We concluded that flexural prop-erties, fracture toughness, Vickers hardness and fluoride release of compomer were sensitive to water as well as storage time. There was a significant effect of fluoride release on the studied mechanical properties.
We investigated the relationship of apoB/apoA1 ratio and coronary heart disease (CHD) in persons who were overweight or obese. The subjects were divided by the body mass indexes (BMI) into the normal weight group (n=397, BMI<24 kg/m2) and the overweight group (n=400, BMI>24 kg/m2). Our results showed that the over-weight group had higher blood pressure [(130.15±19.01) mmHg vs (123.66±18.70) mmHg] and higher levels of blood sugar [(7.09±2.89) mmol/L vs (6.21±2.59) mmol/L], triglyceride [(1.93±1.19) mmol/L vs (1.44±0.85) mmol/L], total cholesterol [(4.26±1.06) mmol/L vs (4.09±0.99) mmol/L], low-density lipoprotein cholesterol (LDL-C) [(2.56±0.75) mmol/L vs (2.39±0.72) mmol/L], and apoB [(0.83±0.27) mg/L vs (0.78±0.23) mg/L], and a higher apoB/apoA1 ratio (0.83±0.27 vs 0.75±0.25) and lower levels high-density lipoprotein cholesterol [(1.10±0.26) mmol/L vs (1.21±0.31) mmol/L] and apoA1 [(1.04±0.20) mg/L vs (1.08±0.22) mg/L] than those of the normal weight group (all P < 0.05). The prevalence of CHD in the over-weight group in the lowest LDL quar-tile was almost twice greater than that of the highest apoB/apoA1 quartile, compared with the subjects in the low-est apoB/apoA1 quartile. The higher apoB/apoA1 quartile was in agreement with the higher prevalence of CHD. In the overweight and obesity group, the area under ROC curve (AUC) was the highest for apoB/apoA1 (0.655). The cut-off point of apoB/apoA1 for optimal sensitivity and specificity was at 0.80, with a sensitivity of 57.19% and a specificity of 71.72%. In conclusion, apoB and apoA1 were simple clinical indicators, and the apoB/apoA1 ratio was closely related with CHD in overweight and obese patients. The apoB/apoA1 ratio may provide some useful information in the differential diagnosis.
Remodeling of ion channels is an important mechanism of arrhythmia induced by heart failure (HF). We in-vestigated the expression of potassium channel encoding genes in the ventricles of rabbit established by volume-overload operation followed with pressure-overload. The reversible effect of these changes with bisoprolol was also evaluated. The HF group exhibited left ventricular enlargement, systolic dysfunction, prolongation of cor-rected QT interval (QTc), and increased plasma brain natriuretic peptide levels in the HF rabbits. Several potas-sium channel subunit encoding genes were consistently down-regulated in the HF rabbits. After bisoprolol treat-ment, heart function was improved significantly and QTc was shortened. Additionally, the mRNA expression of potassium channel subunit genes could be partially reversed. The down-regulated expression of potassium channel subunits Kv4.3, Kv1.4, KvLQT1, minK and Kir 2.1 may contribute to the prolongation of action potential duration in the heart of rabbits induced by volume combined with pressure overload HF. Bisoprolol could partially reverse these down-regulations and improve heart function.
The present study investigated the antiarrhythmic activity of alcoholic extract of Tinospora cordifolia (T. cor-difolia) in CaCl2 induced arrhythmia. CaCl2 (25 mg/kg) was administered by intravenous infusion (iv) to produce arrhythmia in rats. The animals were then treated with T. cordifolia extract (150, 250, and 450 mg/kg) and vera-pamil (5 mg/kg,iv). Lead II electrocardiogram was monitored. Plasma calcium, sodium and potassium levels were measured. In CaCl2 induced arrhythmia, heart rate was decreased by 41.10%, T. cordifolia at 150, 300, and 450 mg/kg decreased the heart rate by 26.30%, 29.16%, and 38.29%, respectively, and verapamil reduced the heart rate by 9.70% compared to the normal group. The PQRST waves were normalized and atrial and ventricular fi-brillation was controlled in rats treated with verapamil and T. cordifolia. CaCl2 increased calcium and sodium lev-els and decreased potassium levels in blood. T. cordifolia dose-dependently decreased calcium and sodium levels and increased potassium levels. Hence, T. cordifolia can be used in antiarrhythmic clinical settings and beneficial in atrial and ventricular fibrillation and flutter and may be indicated in ventricular tachyarrhythmia.
The aim of present study was to investigate the relationship between nerve injury-induced protein 2 (NINJ2) gene polymorphism and stroke in Chinese Han population. Fifty-two patients with large-artery atherosclerosis (LAA) infarction, 85 patients with small-artery occlusion lacunar (SAO) infarction, 50 patients with intracerebral hemorrhage (ICH) and 66 controls were included. Genotypes and alleles frequencies of the two single nucleotide polymorphisms (SNPs) of NINJ2 among different groups were analyzed and compared. In regard to rs12425791, the frequencies of the AG and AA+AG genotypes of the LAA and SAO groups were significantly higher than those in the control group; the frequency of the A allele of the SAO group was significantly higher than that of the con-trol group. In regard to rs11833579, there were not any significant differences between the case and the control groups. The SNP rs12425791 is significantly associated with ischemic stroke, and the A allele increases the sus-ceptibility to stroke. The SNP rs11833579 is not significantly associated with stroke.
The present study was aimed to investigate the effects of minocycline (MC) on the expression of nerve growth factor (NGF) and heat shock protein 70 (HSP70) following intracerebral hemorrhage (ICH) in rats, and explore the neuroprotective function of MC. Seventy-eight male SD rats were randomly assigned to three groups: the ICH control group (n = 36), ICH intervention group (n = 36) and sham operation group (n = 6). The ICH control group and ICH intervention group were subdivided into 6 subgroups at 1, 2, 4, 5, 7 and 14 d after ICH with 6 rats in each subgroup. Type IV collagenase was injected into the basal nuclei to establish the ICH model. All rats showed symptoms of the nervous system after the model was established, and the sympotsm in the ICH control group were more serious than the ICH intervention group. The number of NGF-positive cells and HSP70-positive cells in the ICH intervention group was higher than that of the ICH control group. MC administration by intraperito-neal injection can increase the expression of NGF and HSP70. MC may inhibit the activation of microglia, the in-flammatory reaction and factors, matrix metalloproteinases and apoptosis, thus protecting neurons. The change of the expression of NGF and HSP70 may be involved in the pathway of neuroprotection by MC.