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M Kawanishi

Publications and source records attributed to M Kawanishi.

At least 19 recordsLinked to original sources

Differences between Lactococcus garvieae isolated from the genus Seriola in Japan and those isolated from other animals (trout, terrestrial animals from Europe) with regard to pathogenicity, phage susceptibility and genetic characterization.

AIMS: To clarify the epidemiological relationship between Lactococcus garvieae isolates from the Seriola in Japan and isolates from other animals. METHODS AND RESULTS: A total of 32 isolates obtained from aquatic (the genus Seriola and trout) and terrestrial animals (cow, pig, cat, dog and horse) was used to evaluate its pathogenicity to yellowtail and mouse, phenotype (KG+ and KG-), its susceptibility to three bacteriophages and the pattern of pulsed field gel electrophoresis (PFGE). Lactococcus garvieae isolated from Seriola showed strong pathogenicity to yellowtail, while isolates from trout showed weak pathogenicity and those obtained from terrestrial animals showed no distinct pathogenicity. Only, the isolates from the genus Seriola in Japan showed susceptibility to the bacteriophages. The results of PFGE pattern indicate that the isolates obtained from the Seriola predict homogeneity, while there is no similarity among the isolates obtained from different animals. CONCLUSION: This experiment indicates that L. garvieae isolated from Seriola in Japan appears to be very different from the isolates obtained from other animals, and the isolates prevalent among the genus Seriola in Japan might be homogeneous. SIGNIFICANCE AND IMPACT OF THE STUDY: This study suggests that a particular genetic group that has specially adapted and acquired virulence toward yellowtail were prevalent among the genus Seriola in Japan.

Animals↗

Drug resistance and random amplified polymorphic DNA analysis of Photobacterium damselae ssp. piscicida isolates from cultured Seriola (yellowtail, amberjack and kingfish) in Japan.

AIMS: To investigate the antimicrobial susceptibility and genetic characteristics of Photobacterium damselae ssp. piscicida isolates obtained from cultured Seriola in Japan. METHODS AND RESULTS: Minimal inhibitory concentrations of 14 antimicrobials for 74 isolates from Seriola in Japan in 2002 were determined. Isolates showed high frequencies of resistance to sulfamonomethoxine (SMMX) (97.3%), oxytetracycline (OTC) (77.0%), flumequine (FMQ) (77.0%), chloramphenicol (CP) (75.7%), kanamycin (KM) (63.5%) and oxolinic acid (OA) (62.0%), but low to ampicillin (ABPC) (2.8%). All isolates were susceptible to bicozamycin (BCM), fosfomycin (FOM) and florfenicol (FF). Of these isolates, 45 (60.8%) showed same resistance pattern (SMMX-OTC-FMQ-OA-CP-KM). In random amplified polymorphic DNA (RAPD) analysis, no difference was observed among our 74 field isolates and ATCC51736 isolated from Seriola in 1974 in Japan, but different from ATCC 17911 isolated from white perch in USA. CONCLUSIONS: FF, BCM, FOM and ABPC were useful antimicrobials for treating pseudotuberculosis. However, the frequency of multidrug resistance was high. RAPD analysis showed homogeneity of isolates from Seriola in Japan. SIGNIFICANCE AND IMPACT OF THE STUDY: This study demonstrates that some antimicrobials were still useful for treating pseudotuberculosis and that P. damselae ssp. piscicida strains of same origin might have spread among Seriola in Japan since 1974.

Animals↗

A national surveillance of Shiga toxin-producing Escherichia coli in food-producing animals in Japan.

To assess the public health risk, the prevalence and anti-microbial resistance of Shiga toxin-producing Escherichia coli (STEC) among food-producing animals were studied throughout Japan. Faecal samples were collected from healthy animals of 272 cattle, 179 pigs, and 158 broilers on 596 farms in all 47 Japanese prefectures. STEC were isolated from 62 (23%) cattle and 32 (14%) pig samples but from no chicken samples. Of the bovine isolates, 19 belonged to serotypes frequently implicated in human disease (O157:H7/non-motile (NM)/H not typeable, O26:NM/H11/H21/H not typeable, O113:H21, and O145:NM). The eae genes were observed in 37% of bovine isolates; among them one O145:NM and all four O157 isolates possessed eae-gamma1, and one O145:NM, one O103:H11, and all five O26 isolates possessed eae-beta1 gene. Among the swine isolates, stx2e were dominant, and serotypes frequently implicated in human diseases or eae-positive isolates were not observed. Bovine isolates showed less anti-microbial resistance, but six isolates of 26:NM/H11 and O145:NM were multi-resistant and may need careful monitoring. Swine isolates showed various resistance patterns; chloramphenicol resistance patterns were more common than in bovine isolates. This first national study of STEC in the Japanese veterinary field should aid our understanding of Japan's STEC status.

Animals↗

Drug resistance and pulsed-field gel electrophoresis patterns of Lactococcus garvieae isolates from cultured Seriola (yellowtail, amberjack and kingfish) in Japan.

AIMS: To investigate the existing antimicrobial susceptibility and genetic characteristics of Lactococcus garvieae isolates from cultured Seriola in Japan. METHODS AND RESULTS: Minimum inhibitory concentrations (MICs) of 14 antimicrobial agents for 170 isolates were determined using the agar dilution method. Seventy-five isolates (44.1%) were simultaneously resistant to erythromycin (EM) (MIC>or=2 microg ml-1), lincomycin (LCM) (MIC>or=128 microg ml-1) and oxytetracycline (OTC) (MIC>or=4 microg ml-1). Resistance to EM was grouped as intermediate- and high-level resistant by MIC values. All resistant isolates possessed ermB and tet(S) genes. The number of different bands between pulsed-field gel electrophoresis patterns of 25 isolates and two ATCC strains (isolated in 1974), determined using two enzymes (ApaI and SmaI), did not exceed 3. CONCLUSIONS: The present resistance pattern observed with ermB and tet(S) is similar to that observed in previous reports. Moreover, the genetic characteristics of L. garvieae isolates from a wide area in Japan in 2002 and ATCC strains were closely related. SIGNIFICANCE AND IMPACT OF THE STUDY: This study suggests that EM-, LCM- and OTC-resistant isolates have been present for 15 years and that L. garvieae strains with same origin have spread among Seriola spp. in Japan since 1974.

Animals↗

Treatment of cold injury-induced brain edema with a nonspecific matrix metalloproteinase inhibitor MMI270 in rats.

Blood-brain barrier (BBB) disruption is a critical event leading to vasogenic brain edema and secondary brain damage after cold injury-induced brain trauma. Matrix metalloproteinases (MMPs) are implicated in BBB disruption in this model. The purpose of this study was to examine the effects of MMI270, a synthetic nonspecific MMP inhibitor, on cold injury-induced brain edema in rats. Treatment with MMI270, a bolus injection at a dose of 30 mg/kg, was started immediately after the induction of cold injury and was continued at a dose of 40 mg/kg/day using an intraperitoneal osmotic minipump. At 24 hours after the cold injury, the brain water content and the BBB permeability to Evans Blue (EB) were determined. The secondary brain lesion was assessed using hematoxylin and eosin (H-E) staining at 7 days after the cold injury. Compared with the untreated control group, treatment with MMI270 significantly reduced the brain water content in the ipsilateral core and intermediate areas and protected the BBB integrity to EB in the ipsilateral core area. The secondary lesion was significantly smaller in the MMI270-treated animals compared with the untreated animals. Our results indicate that treatment with MMI270 in rats exhibits protection in acute brain edema formation and secondary brain lesion by attenuating the BBB permeability after cold injury.

Animals↗

Effect of hypothermia on brain edema formation following intracerebral hemorrhage in rats.

Brain edema is an important clinical complication of intracerebral hematoma (ICH). Hypothermia has been employed as an effective neuroprotective treatment on cerebral ischemia and contusional brain injuries. In this study, we attempted to evaluate the effects of mild hypothermia (35 degrees C) on brain edema formation at 48 hours after ICH in the rat. Brain hypothermia started at 6, 12 and 24 hours after the induction of hematoma (HT6; n = 6, HT12; n = 11, HT24; n = 6). Brain water contents in the basal ganglia was significantly reduced in the rats treated with mild hypothermia compared with the normothermic rats (NT; 82.0 +/- 0.04% vs. HT6; 78.6 +/- 0.09%: p < 0.01, HT12; 79.7 +/- 0.05%.: p < 0.01, HT24; 79.7 +/- 0.05%: p < 0.01). Differences in the brain water content were not significant among the hypothermic subgroups. The BBB disruption to Evan's blue was significantly reduced with hypothermia compared with the normothermic rats in the ipsilateral basal ganglia (42.3 +/- 4.0 vs. 23.0 +/- 5.2 ng/g wet tissue; p < 0.05). Hypothermic treatment tended to inhibit the accumulation of polymorphonuclear (PMN) leukocytes in the lesion compared with the normothermic treatment (0.78 +/- 0.13 vs. 0.51 +/- 0.16 deltaAbs/mg tissue). This study indicates that hypothermic treatment significantly reduces the brain edema formation after ICH in rats.

Animals↗

Balloon-assisted guglielmi detachable coil placement in wide-necked internal carotid-ophthalmic aneurysms: a report of four cases.

We present an endovascular technique for treating wide-necked ophthalmic aneurysms using Guglielmi detachable coils with simultaneous temporary balloon protection. Four illustrative cases of wide-necked ophthalmic aneurysms treated with Guglielmi detachable coils and a temporary balloon are presented. By blocking the parent artery with a non-detachable balloon, the coils could be safely placed in these aneurysms without herniation when the balloon was deflated. All patients exhibited embolic manifestations after the procedure, and the use of simultaneous temporary balloon protection allowed more dense intra-aneurysmal coil packing. Although this technique requires manipulation of a second microcatheter and balloon, which increases its technical difficulties and is a higher-risk procedure than the standard coil placement, it can be used for patients who are not candidates for surgery. Long-term follow-up is needed to determine the final outcome of aneurysms treated by this technique.

Aged↗

Oxidative DNA damage in cultured cells and rat lungs by carcinogenic nickel compounds.

DNA damage in cultured cells and in lungs of rats induced by nickel compounds was investigated to clarify the mechanism of nickel carcinogenesis. DNA strand breaks in cultured cells exposed to nickel compounds were measured by using a pulsed field gel electrophoresis technique. Among nickel compounds (Ni(3)S(2), NiO (black), NiO (green), and NiSO(4)), only Ni(3)S(2), which is highly carcinogenic, induced lesions of both double- and single-stranded DNA in cultured human cells (Raji and HeLa cells). Treatment of cultured HeLa cells with Ni(3)S(2) (10 microg/ml) induced a 1.5-fold increase in 8-hydroxy-2'-deoxyguanosine (8-OH-dG) compared with control, whereas NiO (black), NiO (green), and NiSO(4) did not enhance the generation of 8-OH-dG. Intratracheal instillation of Ni(3)S(2), NiO(black), and NiO(green) to Wistar rats increased 8-OH-dG in the lungs significantly. NiSO(4) induced a smaller but significant increase in 8-OH-dG. Histological studies showed that all the nickel compounds used induced inflammation in lungs of the rats. Nitric oxide (NO) generation in phagocytic cells induced by Ni(3)S(2), NiO(black), and NiO(green) was examined using macrophage cell line RAW 264.7 cells. NO generation in RAW 264.7 cells stimulated with lipopolysaccharide was enhanced by all nickel particles. Two mechanisms for nickel-induced oxidative DNA damage have been proposed as follows: all the nickel compounds used induced indirect damage through inflammation, and Ni(3)S(2) also showed direct oxidative DNA damage through H(2)O(2) formation. This double action may explain relatively high carcinogenic risk of Ni(3)S(2).

8-Hydroxy-2'-Deoxyguanosine↗

Effects of hypothermia on thrombin-induced brain edema formation.

Recent studies have shown that thrombin plays an important role in brain edema formation after intracerebral hemorrhage (ICH). The possible mechanisms of thrombin-induced brain edema formation include blood-brain barrier (BBB) disruption and inflammatory response involving polymorphonuclear (PMN) leukocyte. Animal experiments have revealed that moderate therapeutic hypothermia improves pathological and functional outcome in various models of brain injury. In this study, we examined the effect of hypothermia on thrombin-induced brain edema formation. Effects of hypothermia on BBB permeability and the accumulation of PMN leukocytes were also determined to clarify the protective mechanism of hypothermia in this model. Anesthetized adult rats received an injection of 10 Units of thrombin into the basal ganglia. Animals were separated into the normothermic and hypothermic groups, which were housed in a room maintained at 25 degrees C and in a cold room maintained at 5 degrees C, respectively, for 24 h after the thrombin injection. The brain temperature in rats housed in a cold room reduced temporarily to approximately 30 degrees C and then gradually recovered to 35 degrees C by the end of the observation. Brain water content in the basal ganglia was significantly reduced in rats treated with hypothermia compared to the normothermic rats (84.3+/-0.2 vs. 82.4+/-0.1%; P<0.01). The decrease of brain water content was accompanied with a significant reduction in BBB permeability to Evan's blue dye and in accumulation of PMN leukocytes. This study indicates that hypothermic treatment significantly reduces thrombin-induced brain edema formation in the rat. Inhibition of thrombin-induced BBB breakdown and inflammatory response by hypothermia appear to contribute to brain protection in this model. Hypothermic treatment may provide an approach to potentially reduce ongoing edema after ICH.

Animals↗

The efficacy and safety of transvenous embolisation in the treatment of intracranial dural arteriovenous fistulas.

To evaluate the role of transvenous embolisation including its efficacy and safety in the treatment of intracranial dural arteriovenous fistulas (DAVFs), we retrospectively analysed seven cases of intracranial DAVFs treated with transvenous embolisation in combination with arterial embolisation. Four DAVFs were in the cavernous sinus, two in the transverse-sigmoid sinus, and one in the inferior petrosal sinus. The transarterial and transvenous embolic agents included fibred platinum coils (FPC) and interlocking detachable coils (IDC). In all patients, the transarterial embolisation alone had failed to cure the DAVFs. After the combined transvenous embolisation, the anatomical cure was proven in five patients, and all patients were clinically cured. There were no complications in any patient. In conclusion, the transvenous embolisation is a useful and safe approach in the management of intracranial DAVFs.

Aged↗

[Chemotherapy for gliomas based on the expression levels of drug resistant genes].

Drug resistance, which often occurs during chemotherapy, is still a great obstacle to the success of human malignancy treatment. Among many possible mechanisms of drug resistance (biological, biochemical, kinetic or pharmacological), both typical and atypical multidrug-resistance (MDR) have been extensively studied. We picked up MDR-1, MXR, MRP1, MRP2, TopoII alpha, MGMT, and GST-pi as drug-resistant gene, based on experimental data and previous reports. Expression of these genes were measured in 14 malignant glioma specimens by reverse transcription polymerase chain reaction assay. We chose anticancer drugs for each patient, based on results of drug resistant gene expression to acquire good response to drugs. Though our follow-up periods are not long enough to analyze the results of our chemotherapy, 78% (7/9) of our glioma patients who were treated with our chemotherapy are free from tumor progression. The assays, which measure the expression of drug resistant genes, are necessary to allow rapid detection of the drug-sensitivity to chemotherapy in malignant glioma patients.

Adult↗

[Multiple cerebral tuberculomas presenting with paradoxical expansion: a case report].

A 24-year-old male presented with headache. He had been treated with antituberculous drugs for 19 months. MRI revealed 4 intracranial Gd-DTPA enhanced lesions surrounded by massive edema in the right frontal, both occipital and left basal ganglionic regions. Digital subtraction angiography showed no tumor stain. Two procedures for tumor resection were performed for the right frontal and left occipital regions, the latter of which definitively diagnosed by the polymerase chain reaction method. The tumors were well demarcated, showed a rough surface, and were elastically hard. The two residual lesions responded differently to chemotherapy. The lesion in the right occipital region decreased in size, while the other in the left basal ganglionic region continued to grow gradually 26 months after the antituberculous chemotherapy was started. According to previous reports, treatment should be continued for as long as 12-30 months in cases showing paradoxical expansion. In this case, the left basal ganglionic lesion began to decrease in size after 28 months of administration of anti-tuberculous drugs. We report successful treatment of a case of multiple tuberculomas presenting with paradoxical expansion managed by a combination of surgery and continuous chemotherapy.

Adult↗

Postlabelling analysis of DNA adducts formed in human hepatoma cells treated with 3-nitrobenzanthrone.

3-Nitrobenzanthrone (NBA) is one of the most mutagenic nitroaromatic compounds that has been found recently in diesel exhaust and airborne particles. A [32P]-postlabelling analysis was carried out to examine the adducts in DNA from human hepatoma HepG2 cells treated with NBA. Two major and two minor adduct spots were obtained in the analysis. The structure of the compound obtained from one of the minor adduct spots was identified to be N-acetyl-3-amino-2-(2'-deoxyguanosin-3', 5'-bisphosphate-8-yl)-benzanthrone, based on identical mobility of the compound with that of synthetic standards in thin-layer chromatography and high performance liquid chromatography. This substance is the identical adduct found in our previous in vitro study. The yet-unidentified major adduct spots may be guanosin- and adenosin-benzanthrone adducts without the N-acetyl group.

Benz(a)Anthracenes↗

Amplification of pepleomycin-mediated DNA cleavage and apoptosis by unfused aromatic cations.

An important approach to improve chemotherapy of members of the bleomycin (BLM) family of antibiotics is to find compounds (amplifiers) that enhance the activity of BLM-mediated DNA cleavage and apoptosis. Using a DNA-sequencing technique and pulsed field gel electrophoresis, we have investigated whether BLM-mediated cleavage of isolated and cellular DNA is amplifed by three compounds (RW-12, LS-20, 1S-5Me) which have a conformationally flexible, unfused polyaromatic system and cationic side chain in the molecules. RW-12 enhanced most effectively both pepleomycin (PEM)-induced cytotoxicity and apoptosis. The order of the maximum enhancing effect of amplifiers on PEM-mediated DNA damage is RW-12 > LS-20 > 1S-5Me. RW-12 amplified PEM-mediated DNA cleavage most effectively not only in vitro but also in cultured cells. We have reported that the order of the DNA binding constants of these compounds is RW-12 > LS-20 > 1S-5Me. In this study, we found a good correlation between PEM-mediated cleavage of isolated DNA and cellular DNA. These results suggest that BLM amplifiers bind to DNA and by doing so enhance drug-mediated DNA degradation, ultimately leading to apoptosis. The present study on amplifiers of anticancer agents shows a novel approach to the potentially effective anticancer therapy.

Apoptosis↗

The Epstein-Barr virus latent membrane protein 1 (LMP1) enhances TNF alpha-induced apoptosis of intestine 407 epithelial cells: the role of LMP1 C-terminal activation regions 1 and 2.

Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) can protect some kinds of lymphocytes from apoptotic cell death. In contrast, the present study showed that the expression of LMP1 induced high susceptibility to tumor necrosis factor alpha (TNFalpha)-induced apoptosis in intestine 407 epithelial cells, without affecting expression of TNF receptors I and II. LMP1-deletion mutants lacking either C-terminal activation region (CTAR)-1 or CTAR-2 had ability to enhance TNFalpha-induced apoptosis, whereas the deletion of both activation regions completely abolished the induction of high susceptibility to TNFalpha. Phosphorylation of the NFkB-inhibitory molecule IkB-alpha, another biological activity of TNFalpha, was not enhanced by LMP1-expression. LMP1 upregulated antiapoptotic gene A20 expression, suggesting that A20 can not block TNFalpha-induced apoptosis in this cell system. Apoptosis triggered by TNFalpha in LMP1-expressing intestine 407 cells was blocked by inhibitors of caspases-8 and -3. It is therefore concluded that in intestine 407 epithelial cells, LMP1 enhances primarily signal cascade responsible for TNFalpha-induced apoptosis, which occurs at a level upstream of acting site of caspases-8 and -3 and that CTAR-1 and CTAR-2 are involved in enhancement of TNFalpha-induced apoptosis.

Apoptosis↗

Role of SNAP23 in insulin-induced translocation of GLUT4 in 3T3-L1 adipocytes. Mediation of complex formation between syntaxin4 and VAMP2.

Both syntaxin4 and VAMP2 are implicated in insulin regulation of glucose transporter-4 (GLUT4) trafficking in adipocytes as target (t) soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) and vesicle (v)-SNARE proteins, respectively, which mediate fusion of GLUT4-containing vesicles with the plasma membrane. Synaptosome-associated 23-kDa protein (SNAP23) is a widely expressed isoform of SNAP25, the principal t-SNARE of neuronal cells, and colocalizes with syntaxin4 in the plasma membrane of 3T3-L1 adipocytes. In the present study, two SNAP23 mutants, SNAP23-DeltaC8 (amino acids 1 to 202) and SNAP23-DeltaC49 (amino acids 1 to 161), were generated to determine whether SNAP23 is required for insulin-induced translocation of GLUT4 to the plasma membrane in 3T3-L1 adipocytes. Wild-type SNAP23 (SNAP23-WT) promoted the interaction between syntaxin4 and VAMP2 both in vitro and in vivo. Although SNAP23-DeltaC49 bound to neither syntaxin4 nor VAMP2, the SNAP23-DeltaC8 mutant bound to syntaxin4 but not to VAMP2. In addition, although SNAP23-DeltaC8 bound to syntaxin4, it did not mediate the interaction between syntaxin4 and VAMP2. Moreover, overexpression of SNAP23-DeltaC8 in 3T3-L1 adipocytes by adenovirus-mediated gene transfer inhibited insulin-induced translocation of GLUT4 but not that of GLUT1. In contrast, overexpression of neither SNAP23-WT nor SNAP23-DeltaC49 in 3T3-L1 adipocytes affected the translocation of GLUT4 or GLUT1. Together, these results demonstrate that SNAP23 contributes to insulin-dependent trafficking of GLUT4 to the plasma membrane in 3T3-L1 adipocytes by mediating the interaction between t-SNARE (syntaxin4) and v-SNARE (VAMP2).

3T3 Cells↗

Participation of the conjugated diene part for potent cytotoxicity of callystatin A, a spongean polyketide.

5-epi, 10-epi, 8-Deethyl, and 10-demethyl analogues of callystatin A, a potent cytotoxic spongean polyketide, were synthesized to elucidate structure-requirement for cytotoxic potency. Inversion of the asymmetric center at C-10 in callystatin A minimally affected the activity, while lack of the 10-methyl group in callystatin A decreased cytotoxicity. In addition, the C-5 epimer and the 8-deethyl analogue of callystatin A showed weaker cytotoxicity.

Animals↗

High incidence of reflux oesophagitis after eradication therapy for Helicobacter pylori: impacts of hiatal hernia and corpus gastritis.

BACKGROUND: Although several recent studies have shown that the eradication of Helicobacter pylori provokes reflux oesophagitis, the results are conflicting. AIM: To investigate the prevalence of reflux oesophagitis in patients after eradication of H. pylori and consider its association with hiatal hernia and corpus gastritis. METHODS: A total of 286 patients who underwent H. pylori eradication therapy and 286 age- and disease-matched H. pylori-positive controls who did not undergo eradication therapy were followed prospectively. All patients and controls underwent endoscopy at 1-year intervals or when upper gastrointestinal symptoms recurred. The presence of hiatal hernia and histology of the gastric corpus were evaluated at the time of initial endoscopy. RESULTS: The estimated prevalence of reflux oesophagitis within 3 years was 18% after eradication therapy and 0.3% without therapy. Patients who developed reflux oesophagitis after therapy had a greater prevalence of hiatal hernia (P=0.0008) and more severe corpus gastritis (P=0.0005) before therapy. Cumulative prevalence of reflux oesophagitis was 26% in patients with hiatal hernia, 7.7% in those without hiatal hernia, 33% in those with corpus atrophic gastritis and 13% in those without corpus atrophic gastritis. When patients had both hiatal hernia and corpus gastritis, the prevalence of reflux oesophagitis was 37%. The newly developed reflux oesophagitis was classified as mild in 35 out of 36 (97%) patients who developed reflux oesophagitis after eradication therapy. CONCLUSIONS: Eradication of H. pylori increased the prevalence of reflux oesophagitis in our patient group. The presence of hiatal hernia and corpus gastritis are closely related to the development of reflux oesophagitis after H. pylori eradication therapy.

Adolescent↗