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Biomedical subjects

H Katoh

Publications and source records attributed to H Katoh.

At least 181 records · Page 10Linked to original sources
PubMed1998

Frequent loss of gelsolin expression in non-small cell lung cancers of heavy smokers.

Most lung and bladder cancers have been shown to be associated with smoking. We have previously demonstrated the frequent loss of gelsolin expression and its tumor suppressor activity in bladder cancer (M. Tanaka et al., Cancer Res., 55: 3228-3232, 1995). Here, we examined gelsolin expression in 12 cultured non-small cell lung cancer (NSCLC) cell lines. Furthermore, we analyzed gelsolin expression in relation to patients' smoking habits in 88 surgically resected NSCLCs to investigate whether gelsolin could be a molecular target for tobacco-induced carcinogenesis of lung cancer. All 12 NSCLC cell lines showed low-to-undetectable expression of the gelsolin gene, compared to that in normal lung tissue, by Northern blot analysis. On the other hand, Southern blot analysis of genomic DNA did not show any gross rearrangements or deletions of the gene in the NSCLC cell lines. Western blot analysis of gelsolin expression showed low-to-undetectable gelsolin expression in all 12 NSCLC cell lines, compared to normal lung tissue. Immunocytochemical analysis of gelsolin expression in NSCLC cell lines showed results that were consistent with those obtained by Western blot analysis, using normal bronchial epithelial cells as a positive control: two cell lines with lower gelsolin expression by Western blot analysis had reduced but positive cytoplasmic immunostaining of gelsolin, compared with primary normal bronchial epithelial cells, whereas no such immunostaining was observed in two cell lines with much lower or undetectable gelsolin expression by Western blot analysis. Therefore, gelsolin expression was analyzed in surgically resected NSCLCs by immunohistochemistry. Reduced or undetectable gelsolin expression was observed in 48 of 88 (55 %) resected NSCLCs. Such altered gelsolin expression significantly correlated with heavy smoking of patients (> or =20 pack-years; P = 0.008 by the chi2 test and P = 0.03 by multivariate logistic regression analysis), whereas there was no significant correlation between gelsolin expression and histological type, pathological tumor-node-metastasis (pTNM) stage, or survival. These findings suggest that the frequent loss of gelsolin expression may be involved in the development of NSCLCs as a potential molecular target of tobacco-induced carcinogenesis.

Aged↗
PubMed1998

Possible role of platelet-activating factor in the in vivo expression of tissue factor in neutrophils.

BACKGROUND: Recently, we demonstrated that neutrophils express tissue factor (TF) in a model of acute obstructive cholangitis (AOC). However, the regulation of TF expression was not clear. In this study, we clarified the role of platelet-activating factor (PAF) in TF expression in neutrophils. MATERIALS AND METHODS: In a model of AOC, intravenous PAF antagonist, (SM-12502, 200 mg/kg) was administered 5 min before sepsis was induced. Normal saline was given as a control. Coagulation parameters and TF activity were monitored for 6 h. Thereafter, the liver was harvested for histological examination. RESULTS: The percentage of neutrophils which stained positive for TF was significantly reduced by SM-12502 (74.9 +/- 19.3% vs 96.3 +/- 2.8%) (P < 0.01). The number of leukocytes infiltrating the liver was also significantly reduced. Coagulation abnormalities, TF activity, and focal necrosis of the hepatocytes were reduced by SM-12502. CONCLUSIONS: SM-12502 inhibits TF expression in neutrophils which have infiltrated the liver sinusoids, reducing the subsequent infiltration of leukocytes. These results suggest that PAF plays an important role in the expression of TF in neutrophils in vivo.

Animals↗
PubMed1998

Selective hippocampal damage to hypoxia after mild closed head injury in the rat.

Our previous studies have shown selective neuronal damage in the CA3 region after mild closed head injury (CHI) combined with hypoxia. In the present studies, we examined (1) extracellular concentrations of neuroactive amino acids using in vivo microdialysis technique and (2) neuroactive amino acid binding to their receptors using quantitative autoradiography. Male SD rats were divided into five groups; sham control, mild CHI (sacrificed at 1 h or 24 h after CHI), mild CHI followed by hypoxia (1 h or 24 h). [3H]-Glutamate binding to NMDA receptors, [3H]-muscimol binding to GABAA receptors and [3H]-kainate binding to KA receptors were measured in hippocampus and cortex by quantitative autoradiography. With CHI alone, GLU and TAU levels were transiently increased by 15 min posttrauma. In the CHI with hypoxia, increases in GLU and TAU levels were sustained until 60 min following CHI. GABA level was also increased until 75 min posttrauma Pretreatment of MK-801 significantly diminished the prolonged elevation in GLU and TAU levels. (2) CHI alone did not produce prominent change in the measured receptor binding. When hypoxia was combined with CHI, significant increase in [3H] GLU binding to NMDA receptors and significant decrease in [3H]-muscimol binding to GABAA receptors were observed in CA1 and CA3 at 1 h and 24 h post-insult. These results demonstrate that selective hippocampal damage to hypoxia after mild CHI may be mediated through an increase in NMDA receptor activation and the further release of GLU and that NMDA antagonist may be beneficial in preventing secondary neuronal damage by hypoxia.

Animals↗
PubMed1998

A new inbred strain JF1 established from Japanese fancy mouse carrying the classic piebald allele.

A new inbred strain JF1 (Japanese Fancy Mouse 1) was established from a strain of fancy mouse. Morphological and genetical analysis indicated that the mouse originated from the Japanese wild mouse, Mus musculus molossinus. JF1 has characteristic coat color, black spots on the white coat, with black eyes. The mutation appeared to be linked to an old mutation piebald (s). Characterization of the causative gene for piebald, endothelin receptor type B (ednrb), demonstrated that the allele in JF1 is same as that of classic piebald allele, suggesting an identical origin of these two mutants. Possibly, classic piebald mutation was introduced from the Japanese tame mouse, which was already reported at the end of the 1700s. We showed that JF1 is a useful strain for mapping of mutant genes on laboratory strains owing to a high level of polymorphisms in microsatellite markers between JF1 and laboratory strains. The clarified genotypes of JF1 for coat color are "aa BB CC DD ss".

Alleles↗
PubMed1998

Portal vein reconstruction with conventional polytetrafluoroethylene grafts: an experimental study in dogs.

The purpose of this study was to examine the short- and long-term performance of conventional polytetrafluoroethylene (PTFE) grafts for portal vein reconstruction. The grafts were placed as a portal vein replacement in 11 mongrel dogs. At 1 month and 6 months, the grafts were then retrieved and examined for patency, while also undergoing a pathological analysis. During the observation period (at 55 days), one dog died of an unknown cause with a patent graft. The patency rates of the other 10 grafts were 83% (5/6) at 1 month and 100% (4/4) at 6 months. However, the neointima formation was incomplete even 6 months after implantation. In conclusion, although conventional PTFE grafts may be used as a synthetic alternative to autogenous vein grafts, every effort should be made to use autogenous vein grafts before considering conventional PTFE grafts.

Animals↗
PubMed1998

Gianturco stents for the venous system: a detailed pathological study.

This study was designed to examine the short-term performance of Gianturco stents placed in the venous system, in comparison with that of stents placed in the arterial system. Single-bodied modified Gianturco stents were surgically placed in six dogs (group 1), while in another six dogs, only exposure of the vessels was performed (group 2). Segments with an outer diameter 0.9 times smaller than those of the stents were targeted in the infrarenal inferior vena cava (IVC), the portal vein (PV), and the infrarenal abdominal aorta (AA). The animals were killed 4 weeks postoperatively for pathological analysis. All the segments were patent in both groups. Although the stents placed in the infrarenal IVC and PV were completely covered with neointima, those placed in the infrarenal AA were only partially covered. Furthermore, the venous stents were deeply embedded in the media, while the aortic stents remained in the intima. Medial hyperplasia occurred in the venous stents, while intimal hyperplasia occurred in the aortic stents. In conclusion, Gianturco stents placed in the IVC and PV performed better in the short term than the stents placed in the AA.

Animals↗
PubMed1998

Infected abdominal aortic aneurysm caused by Campylobacter fetus subspecies fetus: report of a case.

A 45-year old man with fever, abdominal pain, and a pulsating mass underwent an aneurysmectomy, with in situ reconstruction using a bifurcated knitted Dacron graft, for a saccular abdominal aortic aneurysm (AAA). A culture taken postoperatively grew Campylobacter fetus subspecies fetus. The administration of antibiotics sensitive to this organism was continued for 3 months, and no infection has been encountered in the 1 year since his operation. This is only the 13th documented case of AAA infected by C. fetus subspecies fetus.

Aneurysm, Infected↗
PubMed1998

Experimental study of tracheal patch reconstruction with a covered expandable metallic stent.

BACKGROUND: We evaluated the efficacy of tracheal patch reconstruction with a covered expandable metallic stent (EMS) with omentoplasty. METHODS: After resecting the right half of the circumferential wall of two tracheal rings in adult beagle dogs, we inserted a covered EMS to reconstruct the defect interiorly. Then, through laparotomy, we made an omental pedicle flap and wrapped it around the EMS-interposed area. For comparison with the group without omentoplasty, we periodically examined the healing process macroscopically and histologically. RESULTS: Bronchofiberscopic observations revealed that incorporation of the covered EMS progressed with the passage of time and tracheal luminal patency was maintained well in both groups. However, polyplike granulation developed gradually at both ends of the EMS. Histologically, epithelium was regenerated in the patched area 4 weeks postoperatively and the area was covered with pseudostratified ciliated epithelium at 12 weeks postoperatively. Quantitative analysis of the macroscopic and histologic findings showed that the inflammatory polyps were reduced and epithelialization was promoted in the group with omentoplasty. CONCLUSIONS: Tracheal patch reconstruction with a covered EMS, when combined with omentoplasty, promoted early epithelial regeneration and suppressed the development of inflammatory polyps.

Animals↗
PubMed1998

Heterogeneity and underlying mechanism for inotropic action of endothelin-1 in rat ventricular myocytes.

1. To clarify the mechanisms underlying the positive inotropic action of endothelin-1 (ET-1), we investigated the effect of ET-1 on twitch cell shortening and the Ca2+ transient in rat isolated ventricular myocytes loaded with a fluorescent Ca2+ indicator indo-1. 2. There was a cell-to-cell heterogeneity in response to ET-1. ET-1 (100 nM) increased twitch cell shortening in only 6 of 14 cells (44%) and the increase in twitch cell shortening was always accompanied by an increase in the amplitude of the Ca2+ transient. 3. The ET(A)- and ET(B)-receptors antagonist TAK-044 (100 nM) almost reversed both the ET-1-induced increases in twitch cell shortening and in the Ca2+ transient. In the ET-1 non-responding cells, the amplitude of the Ca2+ transient never increased. 4. Intracellular pH slightly increased (approximately 0.08 unit) after 30 min perfusion of ET-1 in rat ventricular myocytes. However, ET-1 did not change the myofilament responsiveness to Ca2+, which was assessed by (1) the relationship between the Ca2+ transient amplitude and twitch cell shortening, and by (2) the Ca2+ transient-cell shortening phase plane diagram during negative staircase. 5. We concluded that there was a cell-to-cell heterogeneity in the positive inotropic effect of ET-1, and that the ET-receptor-mediated positive inotropic effect was mainly due to an increase in the Ca2+ transient amplitude rather than to an increase in myofilament responsiveness to Ca2+.

Animals↗
PubMed1998

Inhibition of dopamine release by prostaglandin EP3 receptor via pertussis toxin-sensitive and -insensitive pathways in PC12 cells.

Prostaglandin EP3 receptor is involved in the inhibition of neurotransmitter release from presynaptic nerve terminals in various tissues. We have examined the regulation of neurotransmitter release by the EP3 receptor using a PC12 cell line that stably expresses the EP3B receptor isolated from bovine adrenal medulla. In the cells, M&B28767, an EP3 agonist, inhibited the 50 mM KCl- or 10 nM bradykinin-induced [3H]dopamine release in a concentration-dependent manner (10 pM to 0.1 microM). This inhibition was partially reversed by pretreatment with pertussis toxin, whereas under the same condition, the agonist-induced inhibition of forskolin-stimulated cyclic AMP accumulation was suppressed completely. In contrast, M&B28767 did not affect the high K(+)- or bradykinin-induced increase in intracellular Ca2+ concentration. Moreover, M&B28767 also inhibited the [3H]dopamine release induced by the Ca2+ ionophore ionomycin, and this inhibition was also partially reversed by pretreatment with pertussis toxin. These results indicate that the EP3 receptor is coupled to dual pathways, pertussis toxin-sensitive and -insensitive G-protein pathways, to regulate neurotransmitter release without changing Ca2+ influx in neuronal cells.

Adenylyl Cyclase Inhibitors↗
PubMed1998

Protection of hippocampal neurons from ischemia-induced delayed neuronal death by hepatocyte growth factor: a novel neurotrophic factor.

Hepatocyte growth factor (HGF), a natural ligand for the c-met protooncogene product, exhibits mitogenic, motogenic, and morphogenic activities for regeneration of the liver, kidney, and lung. Recently, HGF was clearly shown to enhance neurite outgrowth in vitro. To determine whether HGF has a neuroprotective action against the death of neurons in vivo, we studied the effect of HGF on delayed neuronal death in the hippocampus after 5-minute transient forebrain ischemia in Mongolian gerbils. Continuous postischemic intrastriatal administration of human recombinant HGF (10 or 30 micrograms) for 7 days potently prevented the delayed death of hippocampal neurons under both anesthetized and awake conditions. Even when HGF infusion started 6 hours after ischemia (i.e., in a delayed manner), HGF exhibited a neuroprotective action. We conclude that HGF, a novel neurotrophic factor, has a profound neuroprotective effect against postischemic delayed neuronal death in the hippocampus, which may have implications for the development of new therapeutic strategies for ischemic neuronal damage in humans.

Animals↗
PubMed1998

Changes in phenytoin concentrations in blood and cerebrospinal fluid caused by direct hemoperfusion in a patient intoxicated with phenytoin.

We performed direct hemoperfusion (DHP) 5 times on a patient with consciousness disorder and phenytoin intoxication. We then measured the phenytoin concentrations in her cerebrospinal fluid (CSF) and blood at various times. After the first DHP session, consciousness began to improve, and it normalized after the fourth DHP session when the blood concentration of phenytoin had decreased from 54.0 microg/ml to 16.5 microg/ml. The average plasma phenytoin elimination rate of DHP was 18.0% over 120-180 min. The concentration of phenytoin in the CSF decreased as that in the blood was lowered by DHP. The average reduction rate of phenytoin in the CSF after a DHP session was 23.7%, which was similar to the rate of elimination from the blood. The CSF/blood phenytoin ratio was 0.17, and no marked changes were detected before or after a DHP session.

Acute Disease↗
PubMed1998

Photosynthetic electron transport involved in PxcA-dependent proton extrusion in Synechocystis sp. Strain PCC6803: effect of pxcA inactivation on CO2, HCO3-, and NO3- uptake.

The product of pxcA (formerly known as cotA) is involved in light-induced Na+-dependent proton extrusion. In the presence of 2, 5-dimethyl-p-benzoquinone, net proton extrusion by Synechocystis sp. strain PCC6803 ceased after 1 min of illumination and a postillumination influx of protons was observed, suggesting that the PxcA-dependent, light-dependent proton extrusion equilibrates with a light-independent influx of protons. A photosystem I (PS I) deletion mutant extruded a large number of protons in the light. Thus, PS II-dependent electron transfer and proton translocation are major factors in light-driven proton extrusion, presumably mediated by ATP synthesis. Inhibition of CO2 fixation by glyceraldehyde in a cytochrome c oxidase (COX) deletion mutant strongly inhibited the proton extrusion. Leakage of PS II-generated electrons to oxygen via COX appears to be required for proton extrusion when CO2 fixation is inhibited. At pH 8.0, NO3- uptake activity was very low in the pxcA mutant at low [Na+] (approximately 100 microM). At pH 6.5, the pxcA strain did not take up CO2 or NO3- at low [Na+] and showed very low CO2 uptake activity even at 15 mM Na+. A possible role of PxcA-dependent proton exchange in charge and pH homeostasis during uptake of CO2, HCO3-, and NO3- is discussed.

Bacterial Proteins↗
PubMed1998

Cloning and mapping of the mouse Gpx2 gene encoding gastrointestinal glutathione peroxidase.

Gastrointestinal glutathione peroxidase (GSHPx-GI) is an enzyme expressed in intestinal epithelial cells and may reduce hydroperoxides generated from the ingested diet. We isolated a genomic clone containing the mouse Gpx2 gene encoding 190 amino acids of GSHPx-GI. This gene is composed of two exons and an intron. The nucleotide sequence of the coding region was 89.9% identical with that of the human GPX2 gene. A TGA opal codon predicted to encode a selenocysteine was identified at codon 40. A genomic clone containing a pseudogene for the Gpx2 gene was also isolated. The nucleotide sequence of the pseudogene was 98.3% identical with that of the mouse Gpx2 gene and showed characteristics of a processed pseudogene. Linkage analysis using backcross mouse progeny indicated the mouse Cpx2 gene and its pseudogene to be located on mouse chromosomes 12 and 7, respectively.

Amino Acid Sequence↗