The Apparatus to Measure the Multi-point Critical Flicker Fusion Frequency (MCFF)

In this paper, we mentioned the apparatus developed to measure CFFs at the various point of the retina. Eleven CFFs measured at the central retina of both eyes (used usually} simultaneously, at the central retina of each eye separately, and at four points of the peripheral retina of each eye were analyzed together and referred to as the multi-point critical flicker fusion frequency (MCFF) . MCFF can be used to estimate the level of cortex activity, since the temporal and nasal parts of each eye are connected to different visual cortexes through the optic nerve. As the apparatus used to measure the MCFF was controlled by a micro-computer, the order of measurements and the calculation were done automatically

Association of the Trp64Arg Mutation of the β3-Adrenergic Receptor with Diabetes Mellitus, Impaired Glucose Tolerance and Lifestyle in Japanese Workers

In order to investigate whether the Trp64Arg (a missense mutation of tryptophan for arginine at position 64 codon) polymorphism of the β3-adrenergic receptor (β3-AR) gene is related to the incidence of non-insulin-dependent diabetes mellitus (NIDDM) and impaired glucose tolerance (IGT), a retrospective cohort study among Japanese workers was conducted. The subjects were Japanese workers at an occupational site in Shimane Prefecture. Informed consent was obtained from 492 workers. The baseline data were obtained at the regular health examination in 1992 and a retrospective cohort study was performed for analyzing the incidence of NIDDM and IGT in 1998. The Trp64Arg polymorphism β3-AR gene for each worker was detected by the single strand conformation polymerase analysis. Relative risks were calculated by the logistic regression analysis. The rates of Trp64Trp (TT), Trp64Arg (TA) and Arg64Arg (AA) genotypes were 66.3%, 31.1% and 2.6%, respectively. The relative risk of (TA + AA) against TT for the incidence of NIDDM and IGT by univariate analysis was 1.37 (95% incidence of NIDDM and IGT adjusted for confounders in a multiple logistic regression model including age, gender, family history, body mass index, alcohol consumption, eating habits and exercise was 1.31 (95% confidence interval, 0.65-2.67). The present findings suggested that a weak association between Trp64Arg polymorphism of the β3-AR gene and the incidence of NIDDM and IGT

Heterogeneity of immune complex-derived anti-DNA antibodies associated with lupus nephritis

Heterogeneity of immune complex-derived anti-DNA antibodies associated with lupus nephritis. The mechanisms responsible for the tissue injuries associated with lupus nephritis have not yet been well explained. We have investigated the characteristics of anti-DNA antibodies in circulating immune complexes (CIC) and in the deposits of renal glomeruli in patients with active lupus nephritis. The CIC-derived antibodies expressed anti-DNA idiotypes (Id) designated as 0-81 Id and NE-1 Id, and bound mainly to single-stranded DNA but never to glomerular basement membrane (GBM) antigens. On the other hand, the immunoglobulins (Ig) eluted from renal glomeruli of lupus patients reacted not only with DNA but also with GBM, proteoglycan, and heparan sulfate. The binding of glomeruli-deposited Ig was markedly low when GBM antigens were used after treatment with heparitinase, suggesting that some anti-DNA antibodies may bind directly to GBM antigens associated with heparan sulfate, and form in situ IC in renal glomeruli. It was also revealed that the renal eluates obtained after passing through GBM antigen-coupled Sepharose lost the binding ability with GBM but still retained DNA-binding and 0-81 Id activity, showing the participation of circulating IC-derived anti-DNA antibodies in the glomerular deposits. Theoretically there may be two mechanisms in the pathogenesis of lupus nephritis through the deposition of circulating IC and through in situ formation of anti-DNA IC in renal glomeruli. The diversity ofhistological features in lupus kidneys may be attributed to the heterogeneity of the mechanisms

Strains and mapping results.

<p>a Strains with same sequence type within a family are underlined.</p><p>b Number of variations compared with F30 genome.</p><p>Strains and mapping results.</p

Phylogenetic trees of <i>H</i>. <i>pylori</i> genomes in the families.

<p>The number of nucleotide substitutions was used as the distance matrix. The relation and age of the host is added next to the strain name. (A) Family K-1. (B)(i) Family K-2. (ii) Strains with the same MLST sequence type in Family K-2. (C) Family K-3. (D) Family K-4. (E)(i) Family K-5. (ii) Strains with the same MLST sequence type in Family K-5. The bar indicates the number of nucleotide substitutions.</p

Strains and mapping results.

<p>a Strains with same sequence type within a family are underlined.</p><p>b Number of variations compared with F30 genome.</p><p>Strains and mapping results.</p

Microevolution of Virulence-Related Genes in <i>Helicobacter pylori</i> Familial Infection

<div><p><i>Helicobacter pylori</i>, a bacterial pathogen that can infect human stomach causing gastritis, ulcers and cancer, is known to have a high degree of genome/epigenome diversity as the result of mutation and recombination. The bacteria often infect in childhood and persist for the life of the host. One of the reasons of the rapid evolution of <i>H</i>. <i>pylori</i> is that it changes its genome drastically for adaptation to a new host. To investigate microevolution and adaptation of the <i>H</i>. <i>pylori</i> genome, we undertook whole genome sequencing of the same or very similar sequence type in multi-locus sequence typing (MLST) with seven genes in members of the same family consisting of parents and children in Japan. Detection of nucleotide substitutions revealed likely transmission pathways involving children. Nonsynonymous (amino acid changing) mutations were found in virulence-related genes (<i>cag</i> genes, <i>vacA</i>, <i>hcpDX</i>, <i>tnfα</i>, <i>ggt</i>, <i>htrA</i> and the collagenase gene), outer membrane protein (OMP) genes and other cell surface-related protein genes, signal transduction genes and restriction-modification genes. We reconstructed various pathways by which <i>H</i>. <i>pylori</i> can adapt to a new human host, and our results raised the possibility that the mutational changes in virulence-related genes have a role in adaptation to a child host. Changes in restriction-modification genes might remodel the methylome and transcriptome to help adaptation. This study has provided insights into <i>H</i>. <i>pylori</i> transmission and virulence and has implications for basic research as well as clinical practice.</p></div

COG enrichment of genes with strain specific non-synonymous substitutions.

<p>a Strain used as reference strain for mapping.</p><p>b K15 and K17 were counted together because we cannot assign strain specific substitutions by comparison of two strains.</p><p>* Counts were tested by Fischer's exact test, P < 0.01</p><p>COG enrichment of genes with strain specific non-synonymous substitutions.</p