Biomedical subjects
Publications and source records attributed to Satoshi Ishikawa.
Of 1,456 strains isolated from 2001 to 2003 demonstrating resistance to either oxyimino-cephalosporin, 317 strains, isolated in 57 of 132 clinical facilities, were found to harbor bla(CTX-M) genes by PCR. Fifty-seven, 161, and 99 strains harbored bla(CTX-M) genes belonging to the bla(CTX-M-1), bla(CTX-M-2), and bla(CTX-M-9) clusters, respectively.
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To study the mechanisms involved in membrane fusion, we visualized the fusion process of giant liposomes in real time by optical dark-field microscopy. To induce membrane fusion, we used (i) influenza hemagglutinin peptide (HA), a 20-aa peptide derived from the N-terminal fusion peptide region of the HA2 subunit, and (ii) two synthetic analogue peptides of HA, a negatively (E5) and positively (K5) charged analogue. We were able to visualize membrane fusion caused by E5 or by K5 alone, as well as by the mixture of these two peptides. The HA peptide however, did not induce membrane fusion, even at an acidic pH, which has been described as the optimal condition for the fusion of large unilamellar vesicles. Surprisingly, before membrane fusion, the shrinkage of liposomes was always observed. Our results suggest that a perturbation of lipid bilayers, which probably resulted from alterations in the bending folds of membranes, is a critical factor in fusion efficiency.
BACKGROUND: Periodontal ligament (PDL) cells form mineralized nodules in vitro. Ascorbic acid is known to be required in this process, although its effect on osteoblastic differentiation of PDL cells remains unclear. The purpose of this study was to determine the role of ascorbic acid on the early osteoblastic differentiation of PDL cells, with regard to alkaline phosphatase (ALP) activity, type I collagen production and integrin expression. METHODS: Cultured PDL cells were stimulated at confluence with ascorbic acid in the presence or absence of type I collagen inhibitor and blocking antibodies to integrins. After stimulation, the cells and culture supernatants were examined for ALP activity, type I collagen production, and integrin expression. The ALP activity was measured using a colorimetric assay with p-nitrophenyl phosphate and ALP staining. Enzyme-linked immunosorbent assay (ELISA) was used to determine type I collagen production, and ELISA and flow cytometric analysis were employed for assessment of integrin expression. RESULTS: Both ALP activity and type I collagen production were upregulated when PDL cells were cultured in the presence of ascorbic acid (200 microM). Inhibitor of the formation of collagen triple helices and blocking antibodies to alpha2beta1 integrin inhibited ALP activity by 50% in ascorbic acid-stimulated PDL cells. Furthermore, ascorbic acid increased the cell surface expression of alpha2beta1 integrin. CONCLUSIONS: Our findings indicated that ascorbic acid increases the ALP activity of PDL cells via type I collagen production and also enhances the expression of alpha2beta1 integrin, which is a major receptor of type I collagen. These results suggest that ascorbic acid promotes the osteoblastic differentiation of PDL cells by modulating type I collagen-alpha2beta1 integrin interaction.
A large-volume (100 microl) injection-ETAAS with W-treated PG furnace combined with a phosphate modifier was applied to the determination of unpolluted levels of Cd in tap, snow and river-water samples. The limit of detection of 1.1 ng l(-1) was observed for a 4 w/v% NH4H2PO4 modifer. Matrix interference studies were tested for major ion species well found in fresh water. The direct determination of Cd in certified river water (12 +/- 2 ng l(-1)) was carried out and the observed value was in agreement with the certified one. The good recoveries of Cd added to real environmental water samples were also observed. This method was applied to the determination of Cd in unpolluted environmental water samples.
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Shiga toxin 1 (Stx1) of enterohemorrhagic Escherichia coli O157:H7 was cloned, and four mutant Stx1s were constructed by site-directed mutagenesis with PCR. The wild-type and mutant Stx1s with amino acid replacements at positions 167 and 170 of the A subunit were purified by one-step affinity chromatography with commercially available Globotriose Fractogel, and the mutant Stxs were used for the immunization of mice. The mutant toxins were nontoxic to Vero cells in vitro and to mice in vivo and induced the immunoglobulin G antibody against the wild-type Stx1, which neutralized the cytotoxicity of Stx1. The induced antibody titers depended on the mutation at position 170 of the A subunit. The mice immunized with the mutant Stx1s were protected against a challenge of approximately 100 times the 50% lethal dose of the wild-type Stx1, suggesting that the mutant toxins are good candidates for toxoid vaccines for infection by Stx1-producing E. coli.
A standardized questionnaire has not been established for screening or diagnostic assessment of patients with multiple chemical sensitivity (MCS) in Japan. In the US, Miller and Prihoda (1999a,b) developed a questionnaire that could be used internationally, the Quick Environment Exposure Sensitivity Inventory (QEESI), to assist researchers and clinicians in evaluating patients and populations for chemical sensitivity. The Japanese version of QEESI was subsequently translated by Ishikawa and Miyata (1999). The present study was performed to investigate the reliability and validity of QEESI (Japanese version) for research purposes and for evaluation of patients with MCS in Japan. A total of 498 subjects were recruited from the general population of Miyagi prefecture, Japan. The factor structure in QEESI was analyzed with 40 items on four subscales except for the items in 'Masking' using principal components analysis with Promax rotation. The results showed that 30 items on three subscales, 'Chemical Inhalant Intolerances,' 'Symptom Severity,' and 'Life Impact' except for 'Other Intolerances' were consistent with those reported for the US population by Miller and Prihoda (1999a). Cronbach's alpha reliability coefficient ranged between 0.87 and 0.94 indicating high internal consistency in the 30 items on three subscales. Next, we compared the mean scores on three subscales of QEESI in two groups: 131 self-reported MCS group who were new outpatients at the Environmental Medical Center in Kitasato Institute Hospital, and 131 members of the general population (controls) who were matched for both gender and age with the self-reported MCS group. Mean scores on each subscale for the self-reported MCS group were significantly greater than those for controls (P <0.001). Mean scores on all of the 30 items on three subscales for the self-reported MCS group were also significantly greater than for the controls (P <0.001). These findings indicated that the 30 items on three subscales in QEESI can be used for surveys and for diagnostic assessment of patients with MCS as well as for comparative studies between patients in Japan and in other countries.
A 60-year-old man was admitted for investigation of an abnormality detected in chest radiography: a giant tumor with calcification in the right middle lung field. A computed tomography (CT) scan revealed multiple tumors with calcification on the posterior chest wall. Histological analysis of the tumor specimen obtained by surgical biopsy demonstrated an increasing number of plasma cells accompanied with the deposition of amyloid. A bone marrow biopsy contained over 50% of plasma cells. We therefore diagnosed these tumors as multiple myeloma. It has been reported that multiple myeloma is usually characterized by osteolytic lesions; osteosclerotic changes are rare. Multiple myeloma should be taken into account as one of the causes of a chest wall tumor even if it is diffusely calcified.
Since symptoms typical for multiple chemical sensitivity (MCS) are induced by exposure to low levels of chemicals, we hypothesize that MCS represents an impaired recognition of odors or an increased emotional reaction to common odors. Twenty-five subjects with MCS, 20 women and 5 men, and 50 gender-and-age matched controls participated in this study. The University of Pennsylvania Smell Identification Test (UPSIT) and the Cross-Cultural Smell Identification Test (CC-SIT) were administered. In addition to selecting the most probable odor among the four, the subjects were asked their impression of each odor. Odor identifiability evaluated by the scores of two tests, were almost equal in MCS and control groups. The mean CC-SIT odor per person with pleasant feeling was lower in MCS than in controls. The mean odor per person creating an unpleasant sensation was higher in MCS than in the controls. Gingerbread was the only odor making MCS subjects more pleasant than the controls. Nine out of 40 UPSIT odors were felt as unpleasant by MCS subjects more than by controls. This study indicates that MCS subjects are able to identify the odors equally as well as the controls but feel unpleasant to a larger number of odors than the controls. Despite unknown mechanisms of the altered odor perception in MCS, the application of these tests for diagnostic procedure of MCS is proposed.
OBJECTIVE: This study was conducted to confirm the definition of multiple chemical sensitivity (MCS) in actual life: that multiple symptoms are provoked in multiple organs by exposure to, and ameliorated by avoidance of, multiple chemicals at low levels. We used the Ecological Momentary Assessment to monitor everyday symptoms and the active sampling and passive sampling methods to measure environmental chemical exposure. METHODS: Eighteen patients with MCS, diagnosed according to the 1999 consensus criteria, and 12 healthy controls participated in this study. Fourteen patients and 12 controls underwent 1-week measurement of physical and psychologic symptoms and of the levels of exposure to various chemicals. Linear mixed models were used to test the hypotheses regarding the symptom profile of MCS patients. RESULTS: Some causative chemicals were detected in 11 of 14 MCS patients. Two other patients did not report any hypersensitivity episodes, whereas passive sampling showed far less exposure to chemicals than control subjects. Another subject reported episodic symptoms but was excluded from the following analyses because no possible chemical was detected. Eleven of the 17 physical symptoms and all four mood subscales examined were significantly aggravated in the interview based on "patient-initiated symptom prompts." On the other hand, there were no differences in physical symptoms or mood subscales between MCS patients and control subjects in the interview based on "random prompts." CONCLUSIONS: MCS patients do not have either somatic or psychologic symptoms under chemical-free conditions, and symptoms may be provoked only when exposed to chemicals.