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Biomedical subjects

T Kawamoto

Publications and source records attributed to T Kawamoto.

At least 271 records · Page 15Linked to original sources
PubMed1989

Metabolic improvements associated with a reduction of abdominal visceral fat caused by a new alpha-glucosidase inhibitor, AO-128, in Zucker fatty rats.

The relationship between mesenteric fat accumulation and metabolic disorder was studied in genetically obese Zucker fatty rats. These animals had high levels of plasma glucose, triglyceride and total cholesterol as well as increased liver triglyceride in comparison with lean rats. In addition, portal free fatty acid (FFA) levels were also higher in fatty rats than in lean rats. Direct measurement of fat weight revealed a substantial increase of mesenteric as well as subcutaneous fat. The volume of mesenteric fat cells was greater than that of subcutaneous fat cells in Zucker fatty rats (1.67 +/- 0.49 nl versus 1.00 +/- 0.31 nl), although the mesenteric fat cell volume was less than half of the subcutaneous fat cell volume (0.05 +/- 0.02 nl versus 0.14 +/- 0.07 nl) in lean rats. An increase in mesenteric fat cell volume was thus more predominant than that of subcutaneous fat cells in the fatty rats. Administration of AO-128 (50 p.p.m./day), a new alpha-glucosidase inhibitor, caused a substantial reduction of mesenteric fat weight accompanied by a marked decrease in fat cell volume in Zucker fatty rats. The drug also caused a significant reduction of FFA levels in the portal vein in parallel with a marked reduction of triglyceride content in the liver. These observations indicate that the fat accumulation in the markedly enlarged mesenteric fat cells is related to the elevated levels of FFA in the portal vein, which in turn may cause metabolic disorders in the liver. A new alpha-glucosidase inhibitor improves these disorders, at least in part, by preventing an enlargement of mesenteric fat cells.

Adipose Tissue↗
PubMed1989

Depressed myocardial contractility and normal ejection performance after aortic valve replacement in patients with aortic regurgitation.

Left ventricular cineangiography and pressure measurement were performed in 33 patients with chronic aortic regurgitation before and after aortic valve replacement and in 25 normal control subjects. Stress and volume were analyzed. The 33 patients were divided into three groups based on preoperative end-systolic volume index: 15 with an index of less than 100 ml/m2 (group I), 12 with an index of 100 to 200 ml/m2 (group II), and six with an index of more than 200 ml/m2 (group III). Afterload estimated as end-systolic stress, which was significantly elevated in all groups before operation, returned to normal postoperatively. Systolic pump function improved postoperatively in all groups; group I and group II showing the most improvement with group III still having an abnormal ejection fraction. The ratio of end-systolic stress to end-systolic volume index, which is an index of contractile state that is relatively independent of preload and afterload, was abnormal in each group preoperatively. Postoperatively, the ratio improved in each group (from 2.8 +/- 0.5 to 4.8 +/- 0.9 for group I, from 1.4 +/- 0.3 to 3.2 +/- 0.6 for group II, and from 0.8 +/- 0.2 to 2.6 +/- 0.8 for group III, compared with 5.9 +/- 1.0 for control subjects). Group I had normal values whereas group II and group III had subnormal ratios, suggesting a depressed contractility. All 15 patients in group I had values that fell within the 95% confidence limits of the linear inverse relationship between ejection fraction and end-systolic stress for control subjects. Nine of the 12 patients in group II and all six in group III had values that fell below the 95% confidence limits of the normal ejection fraction-end-systolic stress relationship. Aortic valve replacement may reduce afterload and improve systolic pump function in many patients with aortic regurgitation. However, there is a subgroup of patients who, despite normal or near-normal pump performance as assessed by ejection fraction, have depressed myocardial contractility characterized by an abnormal relationship between end-systolic stress and either ejection fraction or end-systolic volume.

Adolescent↗
PubMed1989

[A long-term evaluation of a Björk-Shiley valve prosthesis--eighteen year follow-up].

We evaluated the long-term (18 years) results in 356 patients undergoing valve replacement with Björk-Shiley valve prosthesis (aortic, 212; mitral 120; double valve, 24) between 1970 and 1988. Actuarial survival rates of AVR and MVR were 90% (18 years) and 98% (8 years) respectively. Actuarial event free rates (including valve failure, thromboembolism, reoperation and prosthetic valve endocarditis) were 82% (18 years) for AVR and 95% (8 years) for MVR. There were no significant differences among spherical disc, convexo-concave disc and monostrut valve in actuarial survival rates and actuarial event free rates. In conclusion, this study demonstrated that Björk-Shiley valve showed a low incidence of postoperative events. These results endorse our choice of the Björk-Shiley valve prosthesis.

Follow-Up Studies↗
PubMed1988

Induction of cytochrome P-450, cytochrome b-5, NADPH-cytochrome c reductase and change of cytochrome P-450 isozymes with long-term trichloroethylene treatment.

Several reports have described the effects of trichloroethylene (TCE) on the microsomal mixed function oxidase system (MFOS). These studies suggest that repeated TCE administration induces MFOS, especially cytochrome P-450 and NADPH-cytochrome c reductase. However, it is uncertain what isozymes are induced by TCE treatment, and it is not clear how microsomal enzymes or cytochrome P-450 isozymes are altered when TCE is administered for a duration longer than 28 days. We investigated the changes of MFOS by long-term TCE treatment. Male Wistar rats were injected with TCE, 1.0 g/kg body weight once a day for 5 continuous days or 2.0 g/kg body weight twice a week for 15 days. The mean body weight of the rats treated with TCE for 15 weeks was slightly, but not significantly, less than that of the control rats. Relative liver weights (liver wt/body wt) of the TCE-treated group were however significantly larger (21%) than those of the control group. The weights of the other organs were not changed by long-term TCE treatment. Trichloroethylene treatments for 5 days and 15 weeks caused significant increases in microsomal protein, cytochrome P-450, cytochrome b-5 and NADPH-cytochrome c reductase. TCE treatments produced an increase in a polypeptide band at 52,000 molecular weight range observed with sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). This increase in similar to, but less pronounced than that induced by phenobarbital (PB) treatment. There were no remarkable changes at 56,000 molecular weight range where a band appeared after the treatment with 3-methylcholanthrene (MC). It is likely that the induction of cytochrome P-450 by TCE is relatively similar to that by PB.

Animals↗
PubMed1988

2,3,7,8-Tetrachlorodibenzo-p-dioxin causes an increase in protein kinases associated with epidermal growth factor receptor in the hepatic plasma membrane.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), administered to male rats at a single intraperitoneal (IP) injection dose of 25 micrograms/kg causes down-regulation of epidermal growth factor (EGF) receptor in the plasma membrane of rat liver which starts after two days and continues throughout the experimental period (20 days). Using monoclonal antibody to EGF receptor, it was determined that TCDD-caused EFG receptor down-regulation in the rat liver was accompanied by increased protein kinase activity. Such an increase in the protein kinase activity involves, at least in part, an activation of protein tyrosine kinase. Examination of serum samples from control and treated rats revealed no detectable difference in the level of EGF itself or EGF receptor-reacting substances (eg, hormones and other growth factors). In vivo TCDD caused early eye opening and tooth eruption and poor body weight gain and hair growth in mouse neonates similar to those observed with exogenously administered EGF. The results indicate that such EGF receptor-mediated effect of TCDD has some toxocilogical significance in vivo. Although TCDD causes significant reduction in [125I]-EGF binding in the hepatic plasma membrane in susceptible strains of mice, it has only modest effects in tolerant strains. The results are consistent with the idea that the action of TCDD on the EGF receptor is mediated through the cytosolic/nuclear TCDD receptor, which is known to be regulated by the Ah locus.

Animals↗
PubMed1988

The absorption of trichloroethylene and its metabolites from the urinary bladder of anesthetized dogs.

In order to examine the absorption of trichloroethylene (TRI) and its metabolites from the urinary bladder of dogs, we injected TRI and its metabolites, i.e., chloral hydrate (CH), free trichloroethanol (F-TCE), trichloroacetic acid (TCA) and conjugated trichloroethanol (Conj-TCE), into the urinary bladder of anesthetized dogs, and measured the agents and their respective metabolites in the blood or serum, urine and bile. The percentage of water absorbed from the urinary bladder was 10-20% 2 h after the administration of all substances. The percentage of agents absorbed was 60-70% for the TRI and TCA groups, and 50-60% for the CH, F-TCE and Conj-TCE groups 2 h after administration. The combined urinary and biliary excretion rates of the absorbed materials from the urinary bladder 2 h after administration were 46% for F-TCE, 30% for CH, 6% for Conj-TCE and 0.5-1.0% for TRI and TCA. Urinary re-excretion rates of the total excreted amounts were 65-70% in TRI, CH and F-TCE groups, about 50% in TCA and 99% in Conj-TCE group. It is possible that all of the substances administered, particularly F-TCE, are metabolized to Conj-TCE in the urinary bladder.

Animals↗
PubMed1988

Metabolism of chloral hydrate in the anoxic perfused liver.

The metabolism of chloral hydrate (CH) under anoxic conditions was investigated in the non-recirculating, hemoglobin-free liver perfusion system. CH uptake in the anoxic liver decreased to about 80% of that in the oxygen-supplied liver. The reduction of CH to trichloroethanol (TCE) increased and the oxidation of CH to trichloroacetic acid (TCA) decreased. The TCE/TCA ratio increased; however, the total trichloro compounds, that is TCE and TCA, were not significantly altered by anoxia. Though approximate 14% of the CH infused into the oxygen-supplied liver was changed to substances other than TCE or TCA, the unknown part was a very small portion in the anoxic liver. The decrease in CH uptake, by the anoxic liver, is thought to be equivalent to the decrease of the unknown metabolites. The TCE/TCA ratio under anoxia was also altered by pyruvate or lactate infusion.

Animals↗
PubMed1988

Intestinal absorption of chloral hydrate, free trichloroethanol and trichloroacetic acid in dogs.

In order to examine the intestinal absorption of chloral hydrate (CH), free trichloroethanol (F-TCE) and trichloroacetic acid (TCA), an intestinal circulation system in dogs was developed using jejunal, ileal and colonic loops, and solutions of CH, F-TCE and TCA were circulated within them. The concentrations of these substances and their metabolites in the serum, urine, bile and circulates were then measured. In all groups, the fraction of water absorbed from the intestine was about 10% of the administered volume two hours after administration. The absorbed fraction of CH was about 50% in the jejunum and ileum, and about 40% in the colon. The absorbed fraction of F-TCE was about 60% in the jejunum, 50-60% in the ileum and about 40% in the colon, while the figures for TCA were about 40-50% in the jejunum and about 30-40% in the ileum and colon. The combined biliary and urinary excretion ratios of the administered substances and their respective metabolites to the total amounts absorbed from the intestine were about 25-30% for F-TCE, 10-15% for CH and 0.1-0.2% for TCA in all parts of the intestine two hours after administration.

Animals↗
PubMed1988

Identification of the human beta-actin enhancer and its binding factor.

An enhancer of the human beta-actin gene and a factor that specifically interacts with it were detected. A mobility shift assay showed that the factor bound to the 25-base-pair sequence (between +759 and +783 downstream from the cap site) with high specificity. This finding correlated with those of DNase I protection and exonuclease III digestion assays. This binding region of the beta-actin enhancer contained a hyphenated dyad symmetry and an enhancer core-like sequence. In vitro competition experiments indicated that the factor did not bind to the simian virus 40 enhancer core region.

Acetyltransferases↗
PubMed1988

Amplification of the structurally and functionally altered epidermal growth factor receptor gene (c-erbB) in human brain tumors.

By using Southern blot analysis, we found that in two cases of human glioblastoma multiforme, cells carried amplified c-erbB genes which bore short deletion mutations within the ligand-binding domain of the epidermal growth factor (EGF) receptor. The products of these mutated c-erbB genes were about 30 kilodalton (kDa) smaller than the normal 170-kDa EGF receptor, and the tumor cell membrane fractions containing the 140-kDa abnormal EGF receptor showed a significant elevation of tyrosine kinase activity without its ligand. In view of the similarity to the activated viral and cellular erbB genes in the avian system, these mutated and overexpressed EGF receptors might play a role in the onset or development of human glioblastoma cells.

Animals↗
PubMed1988

Morphological studies of the neuromuscular mechanism shifting from sucking to biting of mice.

In order to give a neuroanatomical evidence to the mechanism of shifting from sucking to biting, we investigated in prenatal, newborn and postnatal mice whether there is a time difference in the neurogenesis of the neurons relative to sucking and biting or in the histogenesis of their peripheral effector organs by the HRP labeling technique and electron microscopy. The results obtained are as follows. (1) At birth the facial motoneurons exceed the trigeminal motoneurons in cell area and development. (2) After birth, the trigeminal motoneurons grow rapidly and outstrip the growth of the facial motoneurons at the age of 6 days. (3) Thereafter, the cell area of both neuron types continues to increase gradually. (4) The initial sign of the alpha motor end plates is found in the orbicularis oris muscle innervated by the facial nerve in 17-day-old fetuses, while that of the trigeminal nerve is delayed in the masseter muscle of 18-day-old fetuses. (5) The initial sign of the muscle spindle appears with the sensory terminals in the masseter muscle of 17-day-old fetuses and the fundamental structure of the muscle spindle is formed in 4-day-old youngs. (6) Myelination of the facial nerve begins in 3-day-old youngs, while that of the trigeminal nerve becomes apparent in 4- or 5-day-old youngs. From these bases, it is obvious that the facial nerve elements related to sucking are firstly developed at birth and that the differentiation of the trigeminal nerve elements related to biting is rapidly accelerated after birth.

Animals↗
PubMed1988

Evaluation of long-term results of bicuspidalization annuloplasty for functional tricuspid regurgitation. A seventeen-year experience with 133 consecutive patients.

Between 1968 and 1985, 133 consecutive patients underwent bicuspidalization annuloplasty for moderate to severe functional tricuspid regurgitation associated with mitral or combined mitral and aortic valve disease. Over this period, the incidence of tricuspid valve replacement was only 2.3% (3/136 patients). There were 18 early deaths (13.5%) in the entire series--three (5.0%) of 60 patients in the last 5 years of the study--and 10 late deaths (8.7%). Actuarial survival rate for the entire series, excluding early deaths, was 91.0% +/- 3.0% at 10 and 17 years. There were seven reoperations (6.1%) on the tricuspid valve, needed because of residual or recurrent mitral valve lesions after the initial operation. Actuarial rates of freedom from reoperation on the tricuspid valve were 93.6% +/- 3.0% (10 years) and 69.7% +/- 16% (17 years) for the entire series: 78% +/- 10% (15 years) for the open mitral commissurotomy plus tricuspid annuloplasty group (44 patients); 90% +/- 9.0% (15 years) for the mitral plus tricuspid annuloplasty group (10); 75.2% +/- 22% (17 years) for the mitral replacement plus tricuspid annuloplasty group (58); and 92.6% +/- 7.0% (16 years) for the combined aortic and mitral valve surgery plus tricuspid annuloplasty group (21). Ninety-eight percent of the survivors were in New York Heart Association class I or II postoperatively. Of 21 randomly selected patients investigated by pulsed Doppler echocardiography, 14 (67%) had no regurgitation or grade 1/4 tricuspid regurgitation and the remaining seven (33%) had grade 2/4 regurgitation postoperatively. Our experiences suggest that bicuspidalization annuloplasty can be a reliable method in the vast majority of patients with functional tricuspid regurgitation.

Actuarial Analysis↗