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T Yuki

Publications and source records attributed to T Yuki.

At least 55 records · Page 3Linked to original sources
PubMed1993

[Testicular tumor following orchiopexy. A case report].

A case of testicular tumor occurring after orchiopexy is presented. The patient, a 21-year-old male, who had undergone bilateral orchiopexy 14 years before was admitted to our clinic on February 17 in 1992 because of left testicular tumor. Computed tomography showed left inguinal and paraaortic lymphnode metastases. Left high orchiectomy was performed. The tumor was histologically diagnosed to be mixed tumors of embryonal carcinoma, yolk sac tumor and choriocarcinoma. After two courses of chemotherapy consisting of cisplatin, etoposide and bleomycin (PEB regimen), LDH and tumor markers (HCG, HCG-beta) returned to the normal range. The size of retroperitoneal metastasis was significantly reduced and inguinal metastasis disappeared. Therefore retroperitoneal and left inguinal lymphadenectomy were performed. Pathological examination of the resected retroperitoneal and left inguinal lymphnodes revealed embryonal carcinoma and no residual tumor cells, respectively. Additionally, two courses of chemotherapy were performed after surgery. His postoperative course was uneventful and ten months of follow-up showed no evidence of recurrence.

Adult↗
PubMed1993

[The evaluation of portal venous invasion of pancreatic cancer by endoscopic ultrasonography].

Thirty-six cases of pancreatic cancer including 27 cases of so-called mucin producing cancer of the pancreas, examined with endoscopic ultrasonography (EUS) and treated with surgery, were reviewed to evaluate the usefulness of EUS in the diagnosis of portal venous (PV) invasion. The detection rate of pancreatic tumors cancer by EUS was 92% in 36 cases. The detection rate of PV invasion by EUS was compared with histological results in each case. Judgement of the correlation between the tumor and the PV wall was possible in 30 cases (83%), and the overall accuracy of EUS in the diagnosis of PV invasion was 73%. It is concluded that EUS is a very useful method for diagnosis of PV invasion in cases of pancreatic cancer.

Adenocarcinoma↗
PubMed1992

[Evaluation of diet of calcium stone patients].

To clarify the relationship between renal stone formation and the diet, the consumption of various nutrients of calcium stone formers was investigated. The study included 24 male and 12 female stone formers, between 20 and 78 years old (mean 42 years). The daily consumption of nutrients was compared to the daily nutritive requirement for the Japanese. The amounts of total and animal protein ingested by all the patients were significantly larger than the daily nutritive requirements. The animal protein ratio was also significantly higher. Concerning the total protein, animal protein and animal protein ratio, male and female patients showed similar results. Salt consumption was significantly larger for all the patients and the male patients than the daily nutritive requirement for the Japanese. Female stone formers also showed this tendency. Consumption of calcium and carbohydrate by all the patients and the male patients was significantly smaller than the daily nutritive requirement. This tendency was observed for the female patients.

Adult↗
PubMed1991

[A cytoprotective role of extracellular superoxide dismutase in experimental stress ulcer models].

In an experimental stress ulcer models, we examined a pathophysiological role of EC-SOD in an extracellular fluid in guinea pig. Heparin has a releasing potency of EC-SOD into extracellular fluid from endothelial cell. In this study, we divided animals into four groups; 1) control animals, 2) animals injected with heparin (1,000 IU/kg), 3) animals injected with heparin and DDC (1 g/kg), 4) animals injected with DDC treatment. In these four groups, we measured ulcer index (UI) and lipid peroxides (LPO) of the gastric mucosa, before and serially after stress. Water-immersion, ethanol and burn were used as experimental stress. Animals injected with heparin inhibited the increase of UI and LPO of gastric mucosa induced by stress. This cytoprotective effect was abolished by DDC treatment. These results suggest that EC-SOD may be a cytoprotective factor in an extracellular fluid.

Animals↗
PubMed1990

[Effect of a spacer device used with metered dose inhaler].

Metered dose inhaler (MDI) is widely used in treatment of bronchial asthma. But adequate efficacy is not obtained if the patients use an improper technique of inhalation. The spacer device was designed to reduce such inhalation errors. Three types of spacers (pear type, tube type, paper spacer) were studied to confirm their usefulness in bronchial asthma. Bronchodilating effect of procaterol (10 micrograms/puff X 2) in conventional MDI or MDI with a spacer was evaluated. There were no significant difference in the effect on the pulmonary function after single inhalation of MDI with or without a spacer for 60 minutes. In regular use of MDI with a spacer for two weeks, PEFR and FEV1.0 were slightly improved. These results suggest that effect of MDI with a spacer may be more effective than MDI alone in regular use.

Administration, Inhalation↗
PubMed1989

Biochemical examination on the increased superoxide dismutase-like plasma substance observed in a state of acute gastric mucosal lesions.

When experimental acute gastric mucosal lesions were produced in guinea pig by water-immersion and restraint stress, superoxide dismutase (SOD)-like substance in the plasma increased. On analysis by gel filtration, it was shown that the molecular weight of the increased SOD-like plasma substance was about 130,000, and even after treatment with trypsin, 84% of this substance remained. Since the molecular weight of intracellular SOD is about 40,000, it seems that this substance is similar to extracellular SOD, located on the endothelial cell-surface, as previously reported by Marklund et al. Our results suggest that in the presence of acute gastric mucosal lesions, SOD-like plasma substance is not identical to intracellular SOD, which derived from cell destruction by stress or free radical-induced microvascular damage or by hemolysis. Furthermore, this substance may itself work as a scavenger of free radicals generated under conditions, such as these described in the present experiment.

Animals↗
PubMed1985

Oxygen consumption and carbon dioxide production following open heart surgery.

The VO2, VCO2 and RQ were measured in 24 patients after open heart surgery using a CO2 analyzer and O2 Consumption Calculator (Siemen Elma, Sweden). With prolonged ventilatory care, shivering was noticed in only one patient and VO2, VCO2 and RQ were rather stable and constant in patients in the Intensive Care Unit (ICU). With dopamine infusion the 3-5 kg body wt/min cardiovascular status was stable and the oxygen extraction ratio was a mean of 0.264. From those data we suggest that ventilatory support would be desirable for about 2 days for those patients in the post-operative period.

Adult↗
PubMed1985

Relationship of Mallory bodies to intermediate filaments in hepatocytes. A scanning electron microscopy study.

Livers from 12 mice fed griseofulvin for 4 to 6 months were perfused in situ with a detergent solution to extract lipid membranes leaving the cytoskeleton intact. Seven control mice were similarly studied. After 30 to 120 minutes perfusion, liver samples were examined by scanning electron microscopy and transmission electron microscopy. By light microscopy, Mallory bodies (MBs) were observed in pericentral hepatocytes. These were confirmed by transmission electron microscopy. Intermediate filaments (IFs) were observed in close apposition to MBs. Numerous IFs were seen throughout the cytoplasm. The 3-dimensional organization of the cytoskeleton and MBs were clearly visualized by scanning electron microscopy. The IFs were disorganized in the hepatocytes and formed small MBs in griseofulvin-treated mice. In the case of hepatocytes containing large MBs, there was an apparent decrease in the concentration of IFs. Transition forms of dense networks of IFs between the normal cytoskeleton and the MBs were noted in the cytoplasm between small MBs and the nucleus and also at the cell border. The IFs connected to the nucleus and invaded the MBs. The MBs appeared to form as a result of condensation or collapse of the IFs.

Animals↗
PubMed1984

Alteration of acetaldehyde metabolism in carbon tetrachloride-intoxicated rat liver: analysis using liver perfusion system.

The heptic metabolism of acetaldehyde in carbon tetrachloride (CCl4)-intoxicated rats was studied using a non-recirculating haemoglobin-free liver-perfusion system. Acetaldehyde uptake by the liver from acutely CCl4-treated animals (4.16 mmol/kg,i.p.) at 24 hr after the treatment was not significantly altered, whereas that by the liver from chronically CCl4-treated animals (2.08 mmol/kg,i.p., twice a week, for 8-12 weeks) was decreased by approximately 50% when it was determined in the presence of 0.01-5 mM acetaldehyde. In liver from rats chronically intoxicated with CCl4, the following important biochemical changes were observed: (1) The activity of low Km aldehyde dehydrogenase (ALDH) in hepatic mitochondria was decreased by approximately 75%. (2) The basal levels of the lactate/pyruvate (cytosolic [NADH]/[NAD+]) ratio as well as the beta-hydroxybutyrate/acetoacetate (mitochondrial [NADH]/[NAD+]) ratio were elevated by more than 2-fold. (3) Mitochondrial NADH oxidation was also reduced by approximately 35% of the control level. (4) The basal level of hepatic oxygen uptake was attenuated by approximately 50%, and the infusion of acetaldehyde (0.01-5.0 mM) caused a further decrease in the uptake. (5) The rate of ethanol production from acetaldehyde by the catalytic action of alcohol dehydrogenase was found to be unaltered when low concentrations of acetaldehyde (0.01-0.2 mM) were used, whereas a significant suppression of the rate of ethanol production was detected in the presence of high concentrations of acetaldehyde (0.6-5 mM).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1982

The swift increase in alcohol metabolism. Inhibition by propylthiouracil.

Administration of a single large dose of ethanol (5 g/kg) to rats elevates the rates of ethanol metabolism and of oxygen consumption in perfused livers in 2-3 hr. Pretreatment with the antithyroid drug propylthiouracil (PTU) for 10 days abolished both of these effects. Under all treatment conditions studied (controls; PTU-pretreatment; acute ethanol treatment; PTU-pretreated + acute ethanol treatment),, a significant correlation between ethanol metabolism and oxygen consumption was observed (r = 0.86). It is concluded that a normal thyroidal state is required to evoKe the swift increase in alcohol metabolism (SIAM) and an elevation of oxygen consumption.

Animals↗
PubMed1982

Alteration of hepatic ethanol metabolism in CCL4-intoxicated rats: analysis using isolated liver perfusion system.

Hepatic ethanol metabolism in the liver from carbon tetrachloride (CCl4)- treated animals was studied using non-recirculating hemoglobin-free liver perfusion system. CCl4-administration decreased ethanol uptake by the liver to 56% and 30% of the control values following the acute (24 hrs. after treatment) and chronic (8-12 weeks) treatments, respectively. In addition, 4 mM fructose, a well-known agent to increase ethanol metabolism in the liver, did not increase the hepatic uptake of ethanol in CCl4-treated livers. Hepatic alcohol dehydrogenase activity was not changed following acute and chronic CCl4 treatments. The lactate/pyruvate (cytosolic NADH/NAD) ratio as well as beta-hydroxybutyrate/acetoacetate (mitochondrial NADH/NAD) ratio significantly increased, whereas both hepatic oxygen uptake and oxidation of NADH in mitochondria remarkably decreased in parallel with the magnitude of liver injury induced by CCl4. Histological studies revealed that the liver had centrilobular coagulative necrosis with fatty droplet formations at acute phase, while bridging fibrosis between central and portal areas and the pattern of cirrhosis with conspicuous changes in the mitochondria were seen at chronic phase. These data indicate that CCl4-treatment significantly reduces hepatic ethanol metabolism via the inhibition of reoxidation of NADH, a rate limiting step of ethanol metabolism in the liver.

Alcohol Dehydrogenase↗
PubMed1981

Hepatic lipogenesis and mobilization of peripheral fats in the formation of alcoholic fatty liver.

Biochemical mechanisms underlying the development of alcoholic fatty liver was investigated. Acute ethanol (EtOH) administration for 3 days by an inhalation method, and continuous EtOH treatments by feeding with liquid diet or drinking water containing EtOH induced a significant increase of hepatic triglycerides (TG). A small but significant increase of TG was also observed in the blood serum. Although hepatic acetyl CoA carboxylase activity, measured in the presence and absence of citrate, was not altered by either acute or chronic EtOH administrations, fatty acid synthetase and malic enzyme activities in the liver were increased by continuous EtOH administration, but not in the acutely EtOH-treated animals. The incorporations of [14C]palmitate and [14C]acetate into hepatic RG were also increased significantly in animals treated continuously with EtOH. The lipoprotein lipase activity in adipose tissues was activated by both acute and continuous EtOH treatments, whereas lipase activity in adipose tissues and the epinephrine-stimulated and cyclic AMP-mediated release of free fatty acid (FFA) from this tissue were not altered by these treatments. These results indicate that acute alcoholic fatty liver is caused mostly by the increased mobilization of FFA from peripheral adipose tissues via the activation of lipoprotein lipase, whereas alcoholic fatty liver induced by continuous EtOH administration involves the increased synthesis of FFA due to the activation of fatty acid synthetase and malic enzyme in the liver in addition to the increased mobilization of peripheral FFA.

Acetyl-CoA Carboxylase↗
PubMed1981

The swift increase in alcohol metabolism.

Gastric intubation of female Sprague-Dawley rats with 5 g of ethanol/kg body wt doubled oxygen and ethanol uptake by the isolated perfused rat liver after only 2-5 h of treatment (Swift Increase in Alcohol Metabolism). Diminished ATP generation via glycolysis accounts for a portion of the increased oxygen uptake. These data indicate that at least part of the stimulated oxygen uptake after treatment with ethanol is a result of lower rates of glycolytic ATP generation resulting from hormone action. The ADP not phosphorylated in the cytocol enters the mitochondrion where it stimulates oxygen uptake.

Adenosine Diphosphate↗
PubMed1980

Metabolic changes after prior treatment with ethanol. Evidence against in involvement of the Na+ + K+-activated ATPase in the increase in ethanol metabolism.

In perfused rat liver, the inhibition of ethanol uptake by ouabain does not follow the rapid inhibition of the Na+ K+- activated ATPase as assessed by changes in perfusate [K+] (half-time, t 1/2 = 2--3 min), but correlated rather with the slow inhibition of oxygen uptake (maximal inhibition = 40% in 20 min). The data indicate that ouabain exerts its effect on ethanol metabolism via the following sequence of events; inhibition of the sodium pump is followed gradually by a perturbation of the intracellular cation milieu; this leads to an inhibition of the mitochondrial respiratory chain, resulting in diminished rate of NADH oxidation, which in turn causes in inhibition of ethanol metabolism.

Animals↗
PubMed1980

The swift increase in alcohol metabolism. Time course for the increase in hepatic oxygen uptake and the involvement of glycolysis.

Gastric intubation of female Sprague-Dawley rats with 5 g of ethanol/kg body wt. nearly doubled oxygen uptake by the isolated perfused rat liver maximally after only 2.5 h of treatment (Swift Increase in Alcohol Metabolism). Inhibition of enhanced oxygen uptake by KCN (2mM) and 4-methylpyrazole (0.8 mM) suggested the involvement of the mitochondrial respiratory chain and alcohol dehydrogenase in this phenomenon. Glycolysis was depressed after ethanol treatment. Diminished ATP generation via glycolysis accounts for a portion (23-50%) of the increased oxygen uptake, assuming that other rates of biosynthesis remain constant. Injection of adrenaline (2 mg/kg) 1 h before perfusion mimicked partially the action of ethanol on hepatic oxygen uptake. The increases produced by ethanol and adrenaline were not additive, suggesting that adrenaline is involved in the action of ethanol. Moreover, the increase in hepatic oxygen uptake produced by 2.5 h of ethanol treatment could be blocked by either alpha-(phenoxybenzamine; 40 mg/kg) or beta-(propranolol; 40 mg/kg) adrenergic blocking agents. Blood glucose increased after ethanol treatment, supporting the involvement of glycogenolytic hormones in this effect. These data indicate that at least part of the stimulated oxygen uptake after treatment with ethanol is a result of lower rates of glycolytic ATP generation resulting from hormone (e.g. adrenaline etc.) action. The ADP not phosphorylated in the cytosol enters the mitochondria, where it stimulates oxygen uptake.

Alcohol Oxidoreductases↗
PubMed1980

Mechanism of the swift increase in alcohol metabolism ("SIAM") in the rat.

Gastric intubation of female Sprague-Dawley rats (80-150 g) with one large dose (5 g/kg) of ethanol nearly doubled oxygen uptake of the isolated, perfused rat liver in only 2.5 hours. This increased hepatic respiration can account for the Swift Increase in Alcohol Metabolism (SIAM). Inhibition of enhanced oxygen and ethanol uptake by KCN (2 mM) and 4-methylpyrazole (0.8 mM) indicated the involvement of the mitochondrial respiratory chain and alcohol dehydrogenase in this phenomenon, respectively. Epinephrine (2 mg/kg, i.p.) mimicked the increase in respiration observed with ethanol; however, the effects of epinephrine and ethanol were not additive. Pretreatment with alpha- and beta-adrenergic blocking agents, hypophysectomy and adrenalectomy prevented the increase in oxygen and ethanol uptake due to ethanol treatment. These data suggest that hormones including epinephrine are involved in the mechanism of SIAM. Hormone action in all likelihood activates a number of metabolic ATPase activities which lead to elevated oxygen uptake. One such process involved in the activation of oxygen uptake is diminished glycolysis, a ATP producing reaction sequence. The ADP not phosphorylated in the cytosol then enters the mitochondria where it stimulates oxygen uptake and NADH reoxidation. This ultimately leads to an acceleration of ADH-dependent ethanol metabolism.

Animals↗