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Biomedical subjects

H Takase

Publications and source records attributed to H Takase.

At least 37 records · Page 2Linked to original sources

[Postoperative interstitial pneumonia: 2 cases after lobectomy].

Two patients with postoperative interstitial pneumonia are reported. Preoperative diagnosis was primary lung cancer without idiopathic interstitial pneumonia (IIP). Within one week after operation acute interstitial pneumonia (AIP) occurred on the nonoperated side and developed. Steroid therapy was performed but one was dead. AIP is a fatal complication after pulmonary resection and steroid therapy may be useful in some cases of postoperative AIP.

Adenocarcinoma↗

Isolation of a LIM15/DMC1 homolog from the basidiomycete Coprinus cinereus and its expression in relation to meiotic chromosome pairing.

The Escherichia coli gene recA is essential for homologous recombination and DNA repair, and homologs have been identified in eukaryotes. A basidiomycete, Coprinus cinereus, which has many advantages for the study of meiosis, was recently reported to have a homolog of one of these, RAD51. In the yeast Saccharomyces, mutations in the RAD51 gene cause defects in both somatic and meiotic cells. Based on this finding, we screened for a meiosis-specific homolog of recA, equivalent to Lilium LIM15 or Saccharomyces DMC1, in C. cinereus, and isolated a clone containing a 1.2-kb DNA fragment from a cDNA library constructed with Coprinus poly(A)+ RNA isolated from cells undergoing meiosis. The predicted amino acid sequence was 52% identical to the putative gene product of the lily cDNA clone LIM15 and 61% identical to Saccharomyces DMC1, and showed limited sequence similarity to the products of RAD52, 55, and 57. The synchrony of meiosis in Coprinus provides an ideal system for the investigation of differential gene expression in relation to meiosis and fruiting body development. Northern analysis indicated that Coprinus LIM15/DMC1 was expressed at meiotic prophase within 8 h after the onset of karyogamy, suggesting that the gene functions mostly at the stage at which the homologous chromosomes pair, but may not be essential at the point at which they recombine. The gene is not expressed in somatic cells.

Amino Acid Sequence↗

Transformation of bile acids and sterols by clostridia (fusiform bacteria) in Wistar rats.

The effects on bile acid and sterol transformation of clostridia (fusiform bacteria), the dominant intestinal bacteria in rodents (ca. 10(10) counts per g wet feces) were examined in Wistar rats. After inoculation of clostridia into germ-free rats and into rats previously inoculated solely with Escherichia coli, most of the endogenous bile acids were deconjugated, and cholic acid and chenodeoxycholic acid were 7alpha-dehydroxylated to deoxycholic acid and lithocholic acid, respectively. Tauro-beta-muricholic acid, another major bile acid in rats, was deconjugated, but only part of it (ca. 30%) was transformed into hyodeoxycholic acid. Cholesterol and sitosterol were also reduced to coprostanol and sitostanol, respectively. Escherichia coli transformed neither bile acids nor sterols. These data suggest that clostridia play an important role in the formation of secondary bile acids and coprostanol in rats.

Animals↗

A novel glycine-rich protein is associated with starch grain accumulation during anther development.

LIM14, originally identified as a lily gene associated with microsporogenesis, encodes a protein which has two distinct domains, one with glycine-serine repeats and the other with a hydrophobic signal peptide at the N-terminus. The putative LIM14 protein, however, is distinct from the glycine-rich cell wall proteins which have been described before. RNA analyses indicated that the LIM14 transcript is specifically detected in the anther from zygotene to young pollen stage. By using antibodies raised against recombinant LIM14 protein, we detected anther-specific 15 kDa protein. Immunofluorescence microscopy demonstrated that the LIM14 protein is associated with starch grains in the anther wall cells just prior to microspore mitosis and then accumulates at a higher level with the starch grains of immature pollen. We tagged LIM14 with the GUS and GFP reporter genes and introduced them into tobacco BY-2 cells. Analysis of the transformed cells revealed that the chimeric proteins are functional and specifically targeted to plastids. These results indicate that LIM14 is an anther-specific protein that may play a role in starch accumulation and amyloplast differentiation during anther development and pollen formation.

Amino Acid Sequence↗

Platelet-derived growth factor-induced vasodilatation in mesenteric resistance arteries by nitric oxide: blunted response in spontaneous hypertension.

Platelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth-muscle cells, but its effects on vasomotion remain controversial. Both vasoconstriction and vasodilatation of isolated rat aortic rings have been reported. The effects of PDGF on responses of perfused mesenteric resistance arteries from normotensive Wistar-Kyoto and spontaneously hypertensive rats were studied by using a video dimension analyzer. PDGF receptor messenger RNA (mRNA) expression in endothelial cells isolated from mesenteric arteries of both normotensive and hypertensive rats was studied by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. In both normotensive and hypertensive rats, PDGF-BB concentration-dependently induced vasodilatation (maximal response, 25 +/- 4% and 13 +/- 4% at 10(-8) M, respectively; p < 0.05, normotensive vs. hypertensive rats). Endothelium removal or preincubation with N(omega)-nitro-L-arginine methyl ester, but not indomethacin, inhibited these relaxations, indicating that these vasodilatations are endothelium dependent and mediated by nitric oxide. RT-PCR analysis showed that both PDGF-alpha and -beta receptor mRNAs were present in endothelial cells of the mesenteric arteries of normotensive as well as hypertensive rats. In addition, relaxations induced by both PDGF-AA and -AB were significantly less than those induced by PDGF-BB in both strains, suggesting that vasodilatation is mediated mainly by the PDGF-beta receptor subtype. No vasoconstriction was observed after application of PDGF-BB to both normotensive and hypertensive mesenteric arteries with or without endothelium. In rat mesenteric resistance arteries, PDGF induces endothelium-dependent vasodilatation mediated by nitric oxide. At sites where PDGF is released or locally produced, therefore, the growth factor may participate in regulating vascular tone, and this endothelium-dependent regulation is attenuated in spontaneous hypertension.

Animals↗

Facilitated expansion of pneumococcal colonization from the nose to the lower respiratory tract in mice preinfected with influenza virus.

A strain of Streptococcus pneumoniae, when inoculated intranasally in 2 microl of suspension into BALB/c mice preinfected with influenza virus, colonized first in the nose, and several days thereafter also colonized significantly in the trachea and lungs with purulent inflammation. Pneumoccocal colonization was also observed in the noses of normal mice after the same bacterial inoculation, but not apparently in the lower respiratory tract. These results suggest that pneumococcal infection may develop from the upper to the lower respiratory tract as a possible sequence preferentially in influenza virus-infected subjects.

Animals↗

[Surgical management of pulmonary disease due to nontuberculous mycobacteria].

Between 1983 and 1998, 9 patients with nontuberculous mycobacteriosis (NTM) underwent pulmonary resection. 8 patients were men and 1 was woman. Mean length of preoperative period was 20.3 months (range 6 months to 51 months). Most operative indication was localized NTM resistant to multidrug therapy. Lobectomy was performed in 7 patients, segmentectomy in one, partial resection in one. We have no operative mortality but air leaks occurred in one and he needed thoracoplasty. Mean postoperative follow up period was 67.7 months. Only one patients relapsed 34 months after the first operation. For localized NTM, early surgical management results good outcome.

Adult↗

Effects of a novel non-steroidal anti-inflammatory drug (M-5011) on bone metabolism in rats with collagen-induced arthritis.

The effects of a novel non-steroidal anti-inflammatory drug (NSAID), d-2-[4-(3-methyl-2-thienyl)phenyl]propionic acid: M-5011, and other NSAIDs (indomethacin, zaltoprofen and tiaprofenic acid) on bone metabolism in Dark Agouti (DA) strain rats with collagen-induced arthritis were evaluated. M-5011 (1.5 and 4.5 mg/kg) and other NSAIDs (1.5 mg/kg) were administered orally once a day from day 14 to day 35 after collagen immunization. In arthritic rats, paw volume and serum levels of anti-type II collagen antibody were increased on day 21 compared to those in non-immunized rats. M-5011 (4.5 mg/kg), indomethacin and zaltoprofen tended to prevent this increase in paw volume. Elevated urinary pyridinoline and deoxypyridinoline levels were found on days 28 and 35 in arthritic rats. M-5011 (4.5 mg/kg) also tended to prevent the increase in urinary pyridinoline level on day 28, but none of the other NSAIDs affected urinary deoxypyridinoline levels. Bone mineral densities in the hindpaw and vertebrae were also decreased in arthritic rats. M-5011 and tiaprofenic acid prevented this decrease in vertebral bone mineral density. These findings indicate that M-5011 partially inhibits the generalized bone loss accompanying the development of collagen-induced arthritis in rats.

Absorptiometry, Photon↗

Bile acid metabolism in analbuminemic rats.

The bile acid concentrations in the serum, liver, bile, intestines, and feces of 3- and 19-mon-old male and female Nagase analbuminemic (NA) rats were compared with those in Sprague-Dawley (SD) rats. There was no significant difference in the bile acid levels between NA and SD rats. However, increased biosynthesis and pool size of cholic acid (CD) derivatives and decreased levels of chenodeoxycholic acid (CDCA) derivatives (increased CA/CDCA ratio) were detected in male NA rats as compared to SD rats. The CA/CDCA ratio in female NA rats was not different from that in their SD counterparts. There were no significant differences between NA and SD rats in the biliary bile flow, bile acid levels in the small and large intestines, fecal bile acid excretion, bile acid concentration in the portal and systemic circulation, and in the pool size of bile acids. The blood lipid concentrations were significantly higher in the NA rats than in the SD rats. The hepatic levels of lipids were not significantly different between the two rat strains. In conclusion, this study showed that metabolism of bile acids in NA rats is not significantly affected, and that the hypercholesterolemia observed in these strains is not related to abnormalities of bile acid metabolism.

Animals↗

Effect of chronic nitric oxide deficiency on angiotensin II-induced hypertrophy of rat basilar artery.

BACKGROUND AND PURPOSE: Although in vitro studies suggest that nitric oxide has an inhibitory effect on cellular proliferation and migration, in vivo experiments failed to support this conclusion. The present study was designed to determine the effect of endogenous nitric oxide on angiotensin II-induced hypertrophy of small arteries in vivo. METHODS: Angiotensin II (200 ng/kg per minute), alone or in combination with N(omega)-nitro-L-arginine methyl ester (L-NAME) (60 mg/kg per day), was administered for 2 weeks in normotensive rats. Basilar arteries were harvested, and their geometry was determined in perfused and pressurized conditions. RESULTS: Angiotensin II increased media thickness, media-lumen ratio, and cross-sectional area of the arteries, confirming the presence of hypertrophic remodeling. The concomitant administration of L-NAME, an inhibitor of nitric oxide synthesis, prevented vascular hypertrophy. The remodeling of the basilar artery geometry in the combined treatment was of eutrophic nature, similar to that observed with the administration of L-NAME alone. CONCLUSIONS: Our results suggest that endogenous nitric oxide does not inhibit angiotensin II-induced vascular hypertrophy in vivo. Nitric oxide may even be a necessary factor for hypertrophy to develop.

Analysis of Variance↗

Angiotensin II increases tissue endothelin and induces vascular hypertrophy: reversal by ET(A)-receptor antagonist.

BACKGROUND: In vitro studies on vascular smooth muscle cells suggest that endothelin has a stimulating effect on cellular proliferation. This study was designed to determine the endogenous effect of endothelin on angiotensin II-induced hypertrophy of small arteries in vivo. METHODS AND RESULTS: Two weeks of angiotensin II administration (200 ng x kg[-1] x min[-1]) increased media thickness, media/lumen ratio, and cross-sectional area of basilar and small mesenteric arteries, confirming the proliferative properties of angiotensin II. The tissue levels of endothelin-1 were elevated in mesenteric arteries after angiotensin II administration. The administration of the selective and specific ET(A)-receptor antagonist LU135252 (50 mg x kg[-1] x d[-1]) in combination with angiotensin II prevented the changes of vascular geometry and partially reduced the increase in blood pressure induced by angiotensin II. Indeed, part of the effect on the vascular structure of the endothelin-receptor antagonist seemed pressure-independent. CONCLUSIONS: Our results therefore demonstrate that angiotensin II increases the production of endothelin in the blood vessel wall that, via ET(A) receptors, mediates changes in vascular structure of the cerebral and mesenteric circulation. Endothelin antagonists may therefore be of value to reduce blood pressure and to prevent vascular structural changes in conditions of increased activity of the renin-angiotensin system.

Angiotensin II↗

Bile acid metabolism in young-old parabiotic rats.

Serum cholesterol, triglyceride and phospholipid levels, liver cholesterol concentration, bile flow, biliary cholesterol, phospholipid and bile acid secretion rates, fecal sterol and bile acid levels and their bile acid compositions were examined in young-old parabiotic rats and compared with those in young and old control rats and young-young parabiotic rats. Bile acid composition was expressed in terms of the cholic acid group/chenodeoxycholic acid group (CA/CDCA) ratio. Body weight (BW) gain decreased after parabiosis especially in old rats, but the liver weight (g/100 g BW), diet-intake, feces dry weight, liver cholesterol concentration and fecal sterol level were almost the same in all the groups. The biliary bile acid secretion rate was higher and the fecal bile acid level was lower in old rats than those in young rats but both the levels became comparable with those in young rats after parabiosis of old rats with young rats. Young rats, however, showed no changes in these levels after parabiosis. The serum cholesterol level and the biliary and fecal CA/CDCA ratios in old rats were higher than those in young rats but decreased after parabiosis with young rats, although they were still higher than those in young rats. The serum cholesterol level in young rats increased after parabiosis with old rats, but not after parabiosis with young rats, and the fecal bile acid level and the CA/CDCA ratio were not changed in either case. It is concluded from these findings that the serum cholesterol level and the CA/CDCA ratio increased with age and that these increases were prevented after parabiosis with young rats while young rats, although their serum cholesterol level was increased, showed no increase in the CA/CDCA ratio after parabiosis with old rats.

Aging↗

Fertility investigations in the F1 hybrid and backcross progeny of cattle (Bos taurus) and yak (B. grunniens) in Mongolia.

Investigations conducted in Mongolia into the sterility of the male khainag, an F1 hybrid animal resulting from crossing cattle (Bos taurus, 2n = 60) with yaks (B. grunniens, 2n = 60), are reported. Reduced numbers of spermatogonia appear to characterise the testicular tubules of the khainag, and despite the identical cytological appearance of the two parental karyotypes, synaptic anomalies are seen at meiotic prophase in primary spermatocytes. The female khainag is fertile and can be backcrossed to cattle or yak bulls to produce a B1 backcross animal, the ortoom. Further backcrossing of ortoom females to cattle or yaks will yield a B2 backcross animal, the usanguzee. The impression is gained of better meiotic pairing in the backcross animals than in the khainag. The "Haldane Rule" is followed perfectly by the cattle x yak hybrid; namely, sterility is confined to the male.

Animal Husbandry↗

Effects of chronic ETA-receptor blockade in angiotensin II-induced hypertension.

Angiotensin II, a constrictor and mitogen of vascular smooth muscle cells, affects the release of endothelium-derived factors such as nitric oxide or endothelin-1. This study investigated the influence of endothelin-1, using the selective endothelin A receptor antagonist LU135252, on blood pressure and endothelial function in angiotensin II-induced hypertension in the rat. Two weeks of angiotensin II administration (200 ng/kg per minute) increased systolic blood pressure (+35 +/- 5 mm Hg; tail-cuff method) compared with placebo (P < .05). LU135252 alone did not affect systolic pressure but lowered the angiotensin II-induced pressure increase (P < .05). In isolated aortic rings, endothelium-dependent relaxations to acetylcholine were reduced in the angiotensin II group (P < .05 versus placebo) and improved by concomitant chronic LU135252 treatment (P < .05 versus angiotensin II). Blood pressure elevation strongly correlated with impaired endothelium-dependent relaxations to acetylcholine (r = -.967). LU135252 did not affect endothelium-independent relaxations to sodium nitroprusside, which were diminished after angiotensin II treatment (P < .05). In quiescent rings, chronic angiotensin II administration enhanced endothelium-dependent contractions to acetylcholine, which were reduced by LU135252 (P < .05). Impaired contractions to endothelin-1 and norepinephrine in the angiotensin II group were normalized after treatment with LU135252 (P < .05). Thus, chronic therapy with LU135252 partially prevents angiotensin II-induced hypertension and the alternations of the endothelial function observed in this experimental model.

Acetylcholine↗

Blood pressure and vascular effects of endothelin blockade in chronic nitric oxide-deficient hypertension.

Because nitric oxide inhibits the synthesis and vasoconstrictor effect of endothelin-1, the effect of endothelin-1 may be enhanced under conditions of chronic inhibition of nitric oxide synthesis. We studied the effect of chronic therapy with bosentan, a combined endothelin-A/endothelin-B receptor antagonist, on blood pressure and vascular function and structure of small arteries as well as on the reactivity of the aorta in N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. Six-week-old Wistar-Kyoto rats were randomly treated for 6 weeks with placebo (control), L-NAME (70 mg/kg per day), or L-NAME plus bosentan (100 mg/kg per day). The treatments were stopped 2 to 3 days before the in vitro experiments so that only the long-term effects of the drugs could be observed. L-NAME increased systolic blood pressure: bosentan did not prevent this effect although the initial blood pressure rise was delayed (P=NS versus L-NAME group). Bosentan administration did not modify the structural alteration of the resistance vessels induced by L-NAME, nor did it improve endothelium-dependent relaxation of resistance vessels or the aorta. However, bosentan therapy markedly increased endothelium-dependent contraction to acetylcholine, which was slightly enhanced by L-NAME. In contrast, bosentan inhibited aortic endothelium-dependent contractions when applied acutely in vitro. This observation, together with the increased maximal vasoconstriction to the thromboxane A2 receptor agonist U46619 after 2 weeks of bosentan administration, suggests that bosentan also interacts with the receptors mediating endothelium-dependent contractions. In conclusion, our experiments suggest a minor role of endothelin in chronic L-NAME-induced hypertension as well as in the concomitant alterations of vascular structure.

Animals↗