Bacillus alcalophilus AV1934, isolated from human feces, was described in 1934 before microbiome studies and recent indications of novel potassium ion coupling to motility in this extremophile. Here, we report draft sequences that will facilitate an examination of whether that coupling is part of a larger cycle of potassium ion-coupled transporters.
The potassium-dependent alkaliphilic Bacillus sp. strain TS-2 was isolated from the mashed extract of a jumping spider, and its draft genome sequence was obtained. Comparative genomic analysis with a previously sequenced sodium-dependent alkaliphilic Bacillus species may reveal potassium-dependent alkaline adaptation mechanisms.
Alkaliphilic Microbacterium sp. strain TS-1, newly isolated from the jumping spider, showed Na(+)-independent growth and motility. Here, we report the draft genome sequence of this bacterium, which may provide beneficial information for Na(+)-independent alkaline adaptation mechanisms.
Title: Acetylcholine-related bowel dysmotility in homozygous mutant NCX/HOX11L.1-deficient (NCX-/-) mice-evidence that acetylcholine is implicated in causing intestinal neuronal dysplasia Yanai T, Kobayashi H, Yamataka A, Lane GJ, Miyano T, Hayakawa T, Satoh K, Kase Y, Hatano M Ref: J Pediatr Surg, 39:927, 2004 : PubMed
BACKGROUND/PURPOSE: Homozygous mutant Ncx/Hox11L.1-deficient (Ncx-/-) mice develop mega-ileo-ceco-colon (mega-ICC) with a caliber change in the proximal colon. The authors investigated the mechanism of intestinal dysmotility in these mice. METHODS: Five-week-old Ncx-/- mice with mega ICC were compared with age-matched BDF1 control mice. Jejunum, ileum, and colon were excised from all mice and 1.0-cm-long strips of each organ, each with a resting tension of 0.5g, were suspended in an organ bath filled with Tyrode's solution at 37 degrees C and bubbled with a mixture of 95% oxygen and 5% carbon dioxide. Contractile responses to acetylcholine chloride (ACh), histamine, serotonin, and barium chloride (BaCl2) were recorded isometrically. RESULTS: For ACh, Ncx-/- mice had decreased distal colon circular muscle contraction only at lower doses and decreased distal colon longitudinal muscle contraction for all doses compared with controls (P <.05 or P <.01). In the proximal colon, Ncx-/- mice had increased circular muscle contraction only at higher doses and decreased longitudinal muscle contraction only at lower doses compared with controls (P <.01 or P <.05). ACh did not affect jejunum, and there were no significant effects on ileum. There was no response to histamine and serotonin by any part of the bowel, and the response to BaCl2 was the same for both Ncx-/- mice and controls. CONCLUSIONS: Only ACh differentially affected muscle contraction in Ncx-/- mice in the proximal and distal colon. Thus, ACh is implicated in causing the bowel dysmotility seen in Ncx-/- mice and human IND.
We collected and completely sequenced 28,469 full-length complementary DNA clones from Oryza sativa L. ssp. japonica cv. Nipponbare. Through homology searches of publicly available sequence data, we assigned tentative protein functions to 21,596 clones (75.86%). Mapping of the cDNA clones to genomic DNA revealed that there are 19,000 to 20,500 transcription units in the rice genome. Protein informatics analysis against the InterPro database revealed the existence of proteins presented in rice but not in Arabidopsis. Sixty-four percent of our cDNAs are homologous to Arabidopsis proteins.
Title: Correlations between plasma platelet-activating factor acetylhydrolase (PAF-AH) activity and PAF-AH genotype, age, and atherosclerosis in a Japanese population Yamada Y, Yoshida H, Ichihara S, Imaizumi T, Satoh K, Yokota M Ref: Atherosclerosis, 150:209, 2000 : PubMed
Platelet-activating factor acetylhydrolase (PAF-AH), a plasma enzyme that hydrolyzes PAF and oxidized phospholipids, is thought to be involved in protecting cells against oxidative stress. A G(994) (M allele)-->T (m allele) mutation in the plasma PAF-AH gene, which results in a Val(279)-->Phe substitution in the mature protein, leads to a loss of catalytic activity. To elucidate the relationships among PAF-AH enzyme activity, genotype, age, and atherosclerosis, we assayed these parameters in a large Japanese population (n=3932) that consisted of three groups; a control group (healthy individuals; n=1684), a risk-factor group (individuals having at least one conventional risk factor for atherosclerosis; n=1398), and a diseased group (patients who had suffered a myocardial infarction or stroke; n=850). We observed a significantly increased frequency of the m allele in the diseased group as compared with the control or risk-factor groups. Plasma PAF-AH activity increased significantly with age in women in the control group with the MM and Mm genotypes, and in men in the control group with the MM genotype, but not in men with the Mm genotype. In both the risk-factor and diseased groups, however, no correlation was observed between plasma PAF-AH activity and age in subjects with either genotype. These results suggest that in individuals with the MM genotype, plasma PAF-AH activity may be increased in response to stresses induced by PAF and/or oxidized phospholipids that might accumulate with age, but that this response is not evident or reduced in healthy individuals with the m allele, or in subjects with atherosclerotic disease, or having risk factors. Together with our previous findings, the G(994)-->T mutation in the PAF-AH gene may be one of the genetic determinants for atherosclerotic disease in the Japanese population.
Title: [Genetic risk factors for chronic obstructive pulmonary disease (COPD)] Miki M, Satoh K Ref: Nihon Rinsho, 57:1954, 1999 : PubMed
Cigarette smoking has been shown to be a major environmental risk factor predisposing to the development of chronic obstructive pulmonary disease (COPD). However, only 10-20% of cigarette smokers develop COPD, implying undue susceptibility compared with the remainder of the population at large. Studies of families and twins suggest that genetic factors also contribute to development of COPD. We review the genes which have been investigated as potential risk factors for COPD. The fully established genetic risk factor is only alpha 1-antitrypsin deficiency. Polymorphisms for the genes including alpha 1-antichymotrypsin, vitamin D-binding protein, microsomal epoxide hydrolase, cytochrome P450 1A1, Glutathione S-transferase and immunoglobulin A, have also been associated with the development of COPD. Other genetic factors are likely involved but have not yet been identified. Elucidation of additional genetic risk factors may provide useful insights into the pathogenesis of COPD. Potential interactions between the various environmental and genetic risk factors may be important determinants in development of COPD.
PURPOSE:
To evaluate pharmacologically stimulated portal flow measured by magnetic resonance (MR) imaging for assessment of liver function.
MATERIALS AND METHODS:
Pharmacologically stimulated portal flow was measured by phase contrast MR imaging in 27 patients when they were undergoing abdominal angiography for liver tumors or gall bladder cancer. The patients included 11 cases of liver cirrhosis and eight of chronic hepatitis. Pharmacological stimulation was done by infusion of 10 microg/Kg of nicardipine hydrochloride into the superior mesenteric artery through an angiographic catheter. We examined the correlation between stimulated or non-stimulated portal flow and biochemical liver function tests.
RESULTS:
Correlation coefficients and their corresponding p values between non-stimulated portal flow and the indocyanine green residual rate at 15 min after injection (ICG R15), serum albumin (ALB), total bilirubin (TB), cholinesterase (CHE), and hepaplastin test (HP) were--0.414 (0.056), 0.296 (0.134), -0.570 (0.002), 0.289 (0.153), and 0.321 (0.126), respectively, whereas those between stimulated portal flow and ICG R15, ALB, TB, CHE, and HP were--0.561 (0.007), 0.411 (0.033), -0.509 (0.007), 0.445 (0.023), and 0.494 (0.014), respectively.
CONCLUSION:
Stimulated portal flow showed better correlations with biochemical liver function tests than non-stimulated portal flow. It is suggested that stimulated portal flow measurement is more useful for the evaluation of liver function than non-stimulated portal flow measurement.
Platelet-activating factor (PAF) acetylhydrolase is an enzyme that inactivates PAF. Deficiency of this enzyme is caused by a missense mutation in the gene. We previously found a higher prevalence of this mutation in patients with ischemic stroke. This fact suggests that the mutation might enhance the risk for stroke through its association with hypertension. We have addressed this hypothesis by analyzing the prevalence of the mutation in hypertension. We studied 138 patients with essential hypertension, 99 patients with brain hemorrhage, and 270 healthy controls. Genomic DNA was analyzed for the mutant allele by the polymerase-chain reaction. The prevalence of the mutation was 29.3% (27.4% heterozygotes and 1.9% homozygotes) in controls and 36.2% in hypertensives and the difference was not significant. The prevalence in patients with brain hemorrhage was significantly higher than the control: 32.6% heterozygotes and 6.1% homozygotes (p <0.05). PAF acetylhydrolase deficiency may be a genetic risk factor for vascular diseases.
Title: A mutation in plasma platelet-activating factor acetylhydrolase (Val279-->Phe) is a genetic risk factor for stroke Hiramoto M, Yoshida H, Imaizumi T, Yoshimizu N, Satoh K Ref: Stroke, 28:2417, 1997 : PubMed
BACKGROUND AND PURPOSE: Platelet-activating factor (PAF) is a phospholipid with multiple actions that include thrombosis and inflammation. It is inactivated by a plasma enzyme, PAF acetylhydrolase. Deficiency of this enzyme in plasma is caused by a missense mutation in the gene (Val279-->Phe). We have studied a possible association of this mutation with the risk of stroke. SUBJECTS AND METHODS: We studied 120 consecutive patients with cerebral thrombosis. The control group consisted of 134 patients matched for age and sex with minor complaints but without stroke. Genomic DNA was analyzed for the mutant allele by a specific polymerase-chain reaction. Plasma PAF acetylhydrolase activity was determined by the method of Stafforini et al. RESULTS: The prevalence of the mutant gene was 43.4% in stroke patients (39.2% heterozygotes and 4.2% homozygotes), which was significantly higher than the 25.4% in control subjects (22.4% heterozygotes and 3.0% homozygotes) (chi 2 = 9.22, P < .01). The prevalence was slightly higher in stroke patients without hypertension than those with hypertension, but the difference was not significant. The patients with family histories of stroke had a slightly higher but not a significant prevalence of the mutant gene as compared with those without family histories of stroke. Plasma PAF acetylhydrolase activity was higher in patients than in control subjects, in normal subjects, or patients with a heterozygous genotype. CONCLUSIONS: These results suggest that plasma PAF acetylhydrolase deficiency may be a risk factor for stroke. This may explain the relatively high prevalence of stroke in Japan, as the mutation is more common among Japanese than Caucasians.
Deficiency of plasma platelet-activating factor (PAF) acetylhydrolase is an autosomal recessive syndrome that has been associated with severe asthma in Japanese children. Acquired deficiency has been described in several human diseases usually associated with severe inflammation. PAF acetylhydrolase catalyzes the degradation of PAF and related phospholipids, which have proinflammatory, allergic, and prothrombotic properties. Thus, a deficiency in the degradation of these lipids should increase the susceptibility to inflammatory and allergic disorders. Miwa et al. reported that PAF acetylhydrolase activity is absent in 4% of the Japanese population, which suggests that it could be a common factor in such disorders, but the molecular basis of the defect is unknown. We show that inherited deficiency of PAF acetylhydrolase is the result of a point mutation in exon 9 and that this mutation completely abolishes enzymatic activity. This mutation is the cause of the lack of enzymatic activity as expression in E. coli of a construct harboring the mutation results in an inactive protein. This mutation as a heterozygous trait is present in 27% in the Japanese population. This finding will allow rapid identification of subjects predisposed to severe asthma and other PAF-mediated disorders.
