Correlation analysis of ankle-brachial index and brachial-ankle pulse wave velocity with cardiac structures and functions in patients with essential hypertension.

OBJECTIVE: To investigate the correlation of ankle-brachial index (ABI) and brachial-ankle pulse wave velocity (baPWV) with cardiac structures and functions changes in patients with essential hypertension (EH). PATIENTS AND METHODS: A total of 202 patients with hypertension meeting the inclusion criteria were recruited in our hospital from June 2016 to August 2017. They were divided into 4 groups: the low ABI value group, the normal ABI value group, the increased baPWV value group and the normal baPWV group. Clinical data were collected, including medical histories and received physical examinations, blood pressure measurement, biochemical tests and other examinations through the automatic atherosclerosis tester (VP-l00) and echocardiography. RESULTS: Interventricular septal thickness (IVST) of the low ABI value group was significantly larger than that of the normal ABI value group (p<0.05). Compared with those of the normal ABI value group, left ventricular ejection fraction (LVEF) and the ratio of peak velocity flow in the E wave to peak velocity flow in the A wave (E/A) of the low ABI value group were significantly decreased (p<0.05). Left atrium diameter (LAD) and IVST of the increased baPWV group were significantly greater than those of the normal baPWV group (p<0.05), and left ventricular ejection fraction (LVEF) of the former was smaller than that of the latter (p<0.05). Correlation analyses showed that ABI was negatively correlated with IVST (r=-0.713, p<0.05) but positively correlated with LVEF and E/A (r=0.685 and 0.572, respectively, p<0.05); baPWV was positively related to LAD and LVST (r=0.413 and 0.527, respectively, p<0.05) but negatively related to LVEF (r=-0.546, p<0.05). CONCLUSIONS: ABI and baPWV are significantly associated with changes in cardiac structures and functions in patients with EH, which provide a basis for early intervention in clinical.

CYP1A2-163C/A (rs762551) polymorphism and bladder cancer risk: a case-control study.

To date, no study has investigated the association between CYP1A2-163C/A polymorphism and bladder cancer risk in a Chinese population. Here, we extracted genomic DNA from peripheral white blood cells, and differentiated CYP1A2 alleles by polymerase chain reaction-based restriction fragment length polymorphism methods. Differences in genotype frequencies between the cases and controls were evaluated using a chi-square test. The odds ratio (OR) and its 95% confidence interval (CI) were calculated using an unconditional logistic regression model. This revealed that the -163A allele was present at a significantly increased frequency in bladder cancer patients compared to healthy controls (44.10 vs 22.25%, P < 0.001). The prevalence of CC genotype, CA genotype, and AA genotype was 34.91, 41.98, and 23.11% in bladder cancer patients, and 64.00, 27.50, and 8.5% in the controls, respectively. Therefore, significant differences in the frequencies of -163 genotypes were found between bladder cancer patients and controls (P < 0.001). We found that the AA genotype was significantly associated with increased bladder cancer risk (OR = 3.72; 95%CI = 1.55-7.16; P = 0.02), and the -163A carriers were at increased risk of bladder cancer in a multivariate COX regression model (OR = 4.89, 95%CI = 2.78-10.87, P = 0.01). We conclude that the CYP1A2-163C/A polymorphism is associated with increased susceptibility to bladder cancer in the Chinese population.

Magnetic mediation effect of a C impurity in a Mn-doped Zn12O12 nanocluster: a case of multiple exchange interactions.

The stability and exchange interaction mechanism of a doped Zn12O12 cluster with Mn and C atoms were investigated by first-principles calculations. For the Mn-doped Zn12O12 cluster, it is identified that a superexchange interaction deriving the hybridization between the Mn 3d(2/x)-2/y and O 2p(xy) orbitals dominates the Mn(↑)-Mn(↓) antiferromagnetic coupling, although a direct exchange interaction deriving the Mn-Mn bonding is also found. In order to turn the Mn spin state in the Mn-doped Zn12O12 cluster, C doping is undertaken to change the magnetic interactions of these impurities. It is proved that the C incorporation into the Mn-doped Zn12O12 cluster destroys the short-ranged antiferromagnetic coupling, where multiple exchange interactions take over, including the direct exchange interaction and the kinetic p-d exchange interaction partially due to the geometric distortion and surface effect with dangling bonds (sp(2)-like hybrids). It is concluded that the kinetic p-d exchange interaction plays a dominant role in Mn/C-doped Zn12O12 clusters.

Retinal degeneration in the nervous mutant mouse. IV. Inner retinal changes.

We have recently noted that the inner nuclear layer (INL) and the inner plexiform layer (IPL) were significantly thinner in mice homozygous for the nervous defect (nr / nr) than in control (nr /+ or +/+) littermates. Here, we have carried out a series of anatomical studies to further understand these inner retinal changes. At postnatal day (P) 13, there was no difference in the inner retina between nervous and control mice, while a significant difference was observed at P30. Similar changes were not seen in other mouse models of photoreceptor degeneration. There was a significant reduction in the density of cells in the INL that were stained by antibodies against the inhibitory neurotransmitters GABA and glycine. These results indicate that the nervous defect causes a degeneration of one or more sub-types of amacrine cells, in addition to the loss of cerebellar Purkinje cells and retinal photoreceptors that is known to occur in these mutant animals. Finally, evidence is provided that photoreceptors die by an apoptotic pathway in nervous mice.

Retinal degeneration in the nervous mutant mouse. III. Electrophysiological studies of the visual pathway.

The nervous (nr) mutation induces a progressive and severe degeneration of cerebellar Purkinje cells and retinal photoreceptors that is virtually complete within the first few months of life. Previous studies of the retina in nervous (nr/nr) mice have focused primarily on the structural abnormalities seen at the level of the photoreceptor cell bodies and outer segments. Here, we have carried out a series of functional studies of the visual pathway in nervous mice and have quantified the status of the inner retinal cell and plexiform layers. Affected animals were obtained by mating nr/+ heterozygotes and screening the offspring for the ataxia characteristic of nervous animals; phenotypically normal littermates (i.e. nr/+ or +/+) were used as controls. As described previously, there is a substantial loss of photoreceptors cells in the nervous retina and a marked shortening of the inner and outer segments. These changes are accompanied by a more modest decline in the thickness of the inner plexiform and inner nuclear layers. These anatomic abnormalities were accompanied by reproducible changes in visual function, as measured with the electroretinogram (ERG) and visual evoked potential (VEP). The dark-adapted ERGs of nervous and control mice had similar waveforms, although the nervous responses were substantially smaller in amplitude. The reductions in the amplitude of the ERG a-wave corresponded to the loss of photoreceptor cells and shortened outer segments seen histologically. Nevertheless, the kinetics of the leading edge of the a-wave did not differ between nervous and control mice, indicating that the rod outer segments of nervous mice continue to respond to light in a normal fashion. The amplitudes of cone ERGs were also reduced in nervous mice, although the extent of this reduction in any given animal was always less than that for rod-mediated ERG components. Overall, this result is consistent with cone involvement occurring only as a secondary effect of rod photoreceptor degeneration. The peak latencies of VEPs of nervous mice were slower than those of control littermates. These functional abnormalities correspond well to the structural changes induced by the nervous mutation, which does not appear to prevent visual signals from being transmitted centrally, beyond the limitations imposed by the degenerative process.