A new combination of cytochromes occurring in Pseudomonas riboflavina.
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Biomedical subjects
Publications and source records attributed to K Arima.
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Arima, Kei (University of Tokyo, Tokyo, Japan), and Tetuo Oka. Cyanide resistance in Achromobacter. I. Induced formation of cytochrome a(2) and its role in cyanide-resistant respiration. J. Bacteriol. 90:734-743. 1965.-By following the cytochrome concentrations during the growth cycle and under various conditions (aerobic, aerobic plus KCN, reduced aeration, anaerobic plus NaNO(3)) in Achromobacter strain D, a close relationship between the formation of cytochrome a(2) (and a(1)) and the difficulty of oxygen utilization was demonstrated. Cytochrome o, which was the only oxidase found in aerobic log-phase cells, was present in bacterial cells grown under various conditions; the amount present had no relation to the degree of cyanide resistance. On the other hand, cytochrome a(2) (and a(1)) was inducible, and a close relation was observed between the amount of cytochrome and resistance to cyanide. Spectrophotometric observations indicated that, among the cytochromes present in resistant cells, cytochrome a(2) could be oxidized most easily in the presence of cyanide and that cytochrome b(1) could be oxidized without the oxidation of cytochrome a(1). We concluded that cytochrome a(2) is a cyanide-resistant oxidase capable of catalyzing the oxidation of cytochromes in the presence of cyanide. Cytochrome a(2) is also resistant to azide, an inhibitor of cytochrome oxidase.
Oka, Tetuo (University of Tokyo, Tokyo, Japan), and Kei Arima. Cyanide resistance in Achromobacter. II. Mechanism of cyanide resistance. J. Bacteriol. 90:744-747. 1965.-Photochemical data showed that the only oxidase found in the cyanide-sensitive cells of Achromobacter was cytochrome o, and that cyanide-resistant cells contained at least two oxidases. The oxidase responsible for cyanide resistance was a pigment the CO compound of which had its absorption band at a wavelength longer than 580 mmu. In addition, kinetic data suggested that there were two oxidases having different affinities for cyanide. From the data presented, resistance to cyanide in Achromobacter strain D was attributed to the induced formation of cytochrome a(2), which has a very low affinity for cyanide. Several characteristics of cytochrome a(2) as a cytochrome oxidase are summarized.
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Arima, Kei (University of Tokyo, Tokyo, Japan) and Yasuo Kobayashi. Bacterial oxidation of dipicolinic acid. I. Isolation of microorganisms, their culture conditions, and end products. J. Bacteriol. 84:759-764. 1962.-In a study of the metabolic pathway(s) of dipicolinic acid (DPA) in microorganisms, 436 strains of soil microorganisms were isolated by use of an enrichment culture technique. Most of them were bacteria, and one of them, Achromobacter, which had the strongest DPA-oxidizing activity, was used for the following experiments. In DPA-free medium, the enzymes which oxidize DPA were not produced. The best culture condition for enzyme production and cell growth was: Nutrient Broth supplemented with 0.1% DPA, 30 C, and 20 hr of shake culture. End products were oxalic acid, NH(3), and CO(2). Oxalic acid was not oxidized further by this bacterium. The over-all reaction equation of DPA oxidation was determined.
We present the first reported case of hypersensitivity pneumonitis (HP) due to Aspergillus glaucus in a mushroom worker. The Aspergillus glaucus group is one of the most popular storage fungi and a possible subsidiary etiologic agent of farmer's lung, but no case of hypersensitivity pneumonitis (HP) due to A. glaucus has been reported. This first case may demonstrate the etiologic role of A. glaucus in HP and in farmer's lung.
We investigated the effect of cigarette smoking on the prevalence of summer-type hypersensitivity pneumonitis (SHP) caused by Trichosporon cutaneum. In the adult family members of SHP patients, we found that 27 of 41 (65.9%) nonsmokers were SHP patients, compared with 3 of 11 (27.3%) smokers (p less than .05). Also, the prevalence of anti-T. cutaneum antibody was significantly lower in the smokers (p less than .05). A questionnaire provided to 209 SHP patients revealed that the smoking rates of male and female SHP patients were significantly lower (p less than .01) than rates in the normal Japanese population. However, no difference was found in serum anti-T. cutaneum antibody activities or the bronchoalveolar lavage lymphocyte phenotypes for smoking and nonsmoking SHP patients. It was concluded that cigarette smoking had a suppressive effect on the outbreak of SHP, but smoking caused no further suppression after the disease was established.
Regional abnormalities of brain connectivity may be an important substrate for the expression of schizophrenia, a severe form of mental illness. Brain imaging and postmortem morphometric studies indicate hippocampal structure is abnormal in schizophrenia. To study molecular components of hippocampal connectivity the presynaptic proteins SNAP-25 and synaptophysin were assayed in postmortem samples. Immunocytochemical studies indicated reduced SNAP-25 immunoreactivity in schizophrenia compared to controls, particularly in the terminal fields of entorhinal cortex projections. Although there were no overall changes in synaptophysin immunoreactivity, in the granule cell layer of the dentate gyrus synaptophysin immunoreactivity was increased in schizophrenia. These results indicate that disconnection of a subset of hippocampal circuitry from the entorhinal cortex, as well as intrinsic changes in hippocampal connectivity, may contribute to the mechanism of illness in schizophrenia.
PURPOSE: To determine whether spleen size is related to the severity of esophageal varices or associated gastric varices and liver functions in patients with cirrhosis. METHOD: The authors retrospectively studied spleen size on CT (splenic index [SI] = length x width x height of the spleen), liver functions, and the results of esophagogastric endoscopy in 110 patients with cirrhosis. They also analyzed SI in 112 controls. RESULTS: In controls, body weight, height, and age affected the SI. The SI in patients with uncompensated cirrhosis was greater compared with the SI in those with well-compensated disease (p = 0.0363). The SI in patients with esophageal varices was greater than in patients without esophageal varices (p<0.0001), but patients with and without gastric varices had similar SI values. The SI in patients with the red color signs (red wale marking, cherry red spot, and hematocystic spot) on esophageal varices or with risky varices (enlarged tortuous varices with beady, nodular, or tumor shape associated with red color signs) was greater than in patients without these signs (p = 0.0029 and p = 0.0030, respectively). CONCLUSION: The SI is a good indicator of the severity of esophageal varices and hepatic functional reserve in patients with cirrhosis.
The Notch3 gene has been recently identified as a causative gene for cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). To investigate the genetic contribution of Notch mutations in familial cases with vascular leukoencephalopathy, we screened 13 patients from 11 unrelated families, which were selected on the basis of magnetic resonance imaging findings and positive family history. We identified three different missense mutations in 5 patients from 4 families. Two (Arg90Cys and Arg133Cys) are the same as previously reported in Caucasian patients, the other (Cys174Phe) is a novel mutation causing a loss of a cysteine in epidermal-growth-factor-like repeats of Notch3. These data indicate that the CADASIL Notch3 mutations were found in approximately 35% of familial cases with leukoencephalopathy, suggesting genetic heterogeneity of the disease.
We screened for tau gene mutations among 24 Japanese (6 familial and 18 sporadic cases) and 4 Polish patients with frontotemporal dementia (FTD) using PCR-SSCP analysis followed by DNA sequencing. We identified 2 missense mutations in exon 10: N279K and P301L in 2 Japanese patients with familial FTD. Additionally 3 DNA polymorphisms: 2 known (3' exon 3 + 9, A --> G and exon 7, codon 176, G --> A) and 1 new (exon 8, codon 185, T --> C) were identified in 1 Polish patient. Tau mutations were not found in subjects with a negative family history suggesting that tau mutations do not account for most sporadic cases of FTD. We also found no association of apolipoprotein E4 allele with FTD.
Electron microscopic studies of peripheral blood mononuclear cells (PBMC) in chronic type C hepatitis revealed several interesting structures after interferon-alpha (IFN-alpha) therapy. Fifteen of 20 patients were treated with IFN-alpha. Tubuloreticular inclusions (TRI) were observed in only one patient who did not receive therapy. In contrast, TRI were observed in 10 of 15 (66.7%) patients who underwent the therapy for 2 weeks to 6 months. Cylindric confronting cisternae (CCC) were identified in the cytoplasm of PBMC in 4 of 16 (25%) patients who underwent the therapy. CCC were found only after IFN-alpha therapy. The appearance of both TRI and CCC in the PBMC was significantly correlated to IFN-alpha therapy. Although there is little evidence about the morphogenesis of TRI and CCC, these structures may be a host response to IFN-alpha induced by hepatitis C virus infection.
A 60-year-old woman with a history of hypertension and chronic headache initially presented with irritative personality change and mild but steadily progressive dementia and oral tendency, left-sided hemiplegia, intense nuchal stiffness, and swallowing difficulty in the later stage. She died of bronchopneumonia at the age of 76. The brain showed marked loss of nerve cells with gliosis in the cerebral cortex and fibrillary gliosis in the white matter in addition to the typical pathological findings of progressive supranuclear palsy (PSP): extensive subcortical neurofibrillary tangles (NFTs) and loss of nerve cells with gliosis accentuated in the globus pallidus, Luys body and substantia nigra. In many case reports on PSP, the cerebral cortex is described as normal or within normal limits [Jellinger 1971, Steele et al. 1964], and to our knowledge, there is no reported case of severe cortical atrophy as seen in this case. The differential diagnosis of this case is also discussed.