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Biomedical subjects

K Tagawa

Publications and source records attributed to K Tagawa.

At least 109 records · Page 6Linked to original sources
PubMed1990

Percutaneous ethanol injection therapy for neoplasms located on the surface of the liver.

There has been a reluctance to perform percutaneous ethanol injection therapy on lesions located on the surface of the liver because of the possibility of complications. We treated 16 lesions located on the surface of the liver in 14 patients by percutaneous ethanol injection and evaluated the complications and efficacy. Bleeding and seeding of malignant cells did not occur in any case. However, transient pain after injection of ethanol was more intense in these patients than in those whose lesions were not on the surface of the liver. Histopathologic examinations, imaging findings, and decrease in the serum alpha-fetoprotein levels showed that percutaneous ethanol injection was effective for tumors located on the surface of the liver. Our experience suggests that percutaneous ethanol injection can be performed safely even when lesions are located on the surface of the liver.

Adult↗
PubMed1990

Percutaneous ethanol injection therapy of hepatocellular carcinoma: analysis of 77 patients.

Although sonographically guided percutaneous ethanol injection therapy has been attracting a great deal of attention in the treatment of liver neoplasms, few reports regarding long-term results of this therapy have been published. We report here our 4-year experience, in which ethanol injection was performed 419 times on 108 lesions in 77 patients with hepatocellular carcinoma. Histopathologic examination performed in 14 cases after the therapy revealed that the lesion was completely necrotic in 10 cases, 90% necrotic in three cases, and 70% necrotic in the remaining case. Angiography performed after the therapy showed complete disappearance of tumor stain in 37 of 42 cases treated with ethanol injection. CT after the therapy showed no enhancement of the treated lesion in 55 of 56 cases. Elevated serum levels of alpha-fetoprotein decreased in 21 of 24 cases. Ethanol injection improved the long-term prognosis of the patients. Among the 50 patients in whom there were three or fewer lesions and all lesions were treated by ethanol injection, the 1-, 2-, 3-, and 4-year survival rates were 89%, 74%, 68%, and 60%, respectively. Factors that significantly affected the prognosis were the goal of the treatment, liver function, and size of the largest lesion. Serious complications rarely occurred even in patients with severe liver dysfunction. Percutaneous ethanol injection therapy appears to be valuable for treatment of hepatocellular carcinoma.

Adult↗
PubMed1990

[Hepatic arterial infusion of etoposide in the treatment of primary liver neoplasms].

A phase 1 study of etoposide for hepatocellular carcinoma and cholangiocarcinoma was undertaken by single arterial infusion (9 cases; range of doses levels; step 1: 50 mg/m2, step 2: 75 mg/m2, step 3: 120 mg/m2). Mild leukopenia (2500/mm3 in step 2 and 2400/mm3 in step 3) was observed in 2 cases. Thrombocytopenia or anemia was not observed in these doses. Hypotension was experienced 2 hrs. after infusion in one case of step 2. The post-infusion plasma decay of etoposide was biphasic with t1/2 alpha ranging from 0.59 approximately 0.63 h and t1/2 beta ranging from 5.40 approximately 6.57 h. AUC0-24 increased in association with the increase of the doses. Hepatic artery infusion of etoposide was performed without serious complication and the dose limiting toxicity was leukopenia.

Adenoma, Bile Duct↗
PubMed1989

Different patterns of leakage of cytosolic and mitochondrial enzymes.

The mechanisms of leakage of intracellular enzymes, and especially the cytosolic and mitochondrial isozymes of aspartate aminotransferase (AST), in ischemic rat liver were studied. On recirculation of ischemic liver, cytosolic AST (cAST) promptly appeared in the blood. Release of cytosolic enzymes, including cAST and lactic dehydrogenase, resulted from disruption of blebs that protruded from parenchymal cells into the sinusoidal space. When these blebs were formed in ischemic liver, mitochondria still remained in core regions of the injured cells and were not found in the blebs. Consistent with this fact, mitochondrial AST (mAST) did not leak into the circulation from ischemic liver until most of the cAST had leaked out. This delayed leakage of mitochondrial enzymes was also consistent with the fact that the mitochondrial membranes maintained a diffusion barrier against matrix enzymes even after anoxia for 2 h, when their oxidative phosphorylation capacity had been lost. These results indicate that mitochondrial enzymes are liberated into the blood only after appreciable disintegration of the cells, probably necrosis, and that the cumulative activity of mAST in the blood should reflect the extent of necrosis in ischemic organs better than that of cAST.

Animals↗
PubMed1989

Ca2+-induced accumulation of pyrophosphate in mitochondria during acetate metabolism.

The mechanism of pyrophosphate (PPi) accumulation in rat liver during acetate metabolism was investigated. Perfusion of the liver with acetate in the presence of noradrenaline and glucagon induced marked accumulation of PPi (2 mumol/g of liver, 200 times that of control). In contrast, perfusion with glutamine, which generates PPi only in the cytosol, caused little accumulation of PPi, even in the presence of the two hormones. The site of PPi accumulation was shown to be the mitochondria by the finding that isolated mitochondria from the liver perfused with acetate and the hormones contained 50 nmol of PPi/mg of protein. The addition of an uncoupler to mitochondria with accumulated PPi caused gradual decrease in their PPi content, with concomitant release of a stoichiometric amount of Ca2+. Similar accumulation of PPi was observed when isolated mitochondria were incubated with acetate and Ca2+. These results show that an increase in cytosolic Ca2+ caused by the co-administration of the two hormones induced uptake of the ion into mitochondria, and that PPi accumulated in mitochondria only when it was generated in the organelles with an elevated concentration of Ca2+. High mitochondrial concentrations of Ca2+ are considered to inhibit inorganic pyrophosphatase through the formation of a stable complex, CaPPi-. Mitochondria with accumulated PPi had normal respiratory activities, and their adenine nucleotide concentrations were increased 2-fold rather than being decreased, the increases also being considered to be caused by their high concentration of Ca2+.

Acetates↗
PubMed1989

Pharmacokinetic analysis of single- or multiple-dose plasma drug concentration data with a microcomputer using multi-fraction absorption models.

A Basic program for multi-fraction absorption models was developed to link with another microcomputer program, MULTI, and was named MFA-MULTI. A main frame computer program SIMP, based on a simplex method using differential equations, was also operated using a microcomputer equipped with a FORTRAN compiler and a 8087 floating-point coprocessor. These two programs [MFA-MULTI and SIMP (M)] were applied to the analysis of plasma concentration data of several drugs with irregular absorption profiles. The results by MFA-MULTI and SIMP(M) for the single- or multiple-dose data were almost coincident with those obtained by a SIMP program. The result for nalidixic acid estimated using MFA-MULTI or PKM-MULTI was also compared. The plasma nalidixic acid concentration, with irregular absorption profiles due to characteristics of dissolution in the gastrointestinal tract, was found to be described by a two-fraction absorption model. The MFA-MULTI program was applied to the analysis of plasma cimetidine concentration data with double peaks in humans. Pharmacokinetic absorption behavior of a sustained-release preparation of theophylline after repetitive oral administration was adequately evaluated using MFA-MULTI. In addition, application of multi-fraction absorption models to population pharmacokinetics is discussed.

Administration, Oral↗
PubMed1989

The effect of fructose on the cellular content of adenine nucleotides in the perfused rat liver.

In order to evaluate the validity of using fructose in total parenteral nutrition, the mechanism of the resultant decrease in hepatic ATP content on fructose loading was examined using perfused rat livers. The ATP content of the livers perfused with fructose at a concentration of 2 mM or less, was about 2.8 mumol/g liver. Perfusion with 3 mM and 5 mM fructose decreased the ATP level to 1.65 and 1.50 mumol/g liver, respectively. Transient suppression of respiration occurred after the liver was perfused with fructose at a concentration of 3 mM or more, but not after 2 mM or less. Perfusion of the liver with fructose caused an accumulation of fructose 1-phosphate and a decrease in Pi. At higher concentrations of fructose, the accumulation of fructose 1-phosphate and the depletion of Pi were greater. The Pi depletion, caused by the accumulation of fructose 1-phosphate, suppressed O2 consumption and subsequently decreased the hepatic ATP content. A stoichiometric relationship was found between the total loss of adenine nucleotides in the liver and the amount of purine catabolites in the perfusate. After the administration of fructose at a concentration of 2 mM or less, however, the amount of remaining intracellular Pi was sufficient to maintain respiration and no decrease in the hepatic ATP content was observed.

Adenine Nucleotides↗
PubMed1989

A case of gallbladder cancer manifesting chylous ascites and chylothorax.

A case of gallbladder cancer manifesting both chylous ascites and chylothorax was reported. A 66-year-old man was hospitalized with milky ascites. The patient was diagnosed as having gallbladder cancer based on findings of endoscopic retrograde cholangiopancreatography (ERCP) and celiac angiography. The diagnosis of chylous ascites was confirmed by the presence of microscopically visible free fat and the biochemical analysis of the fluid. The patient also gradually developed chylous thoracic effusion. Autopsy revealed lymphogenous metastasis in multiple retroperitoneal and mediastinal nodes. Chylothorax and chyloperitoneum are relatively rare. Only five cases have been reported in Japan that manifested both conditions.

Adenocarcinoma↗
PubMed1989

Electroencephalographic correlates of blood flow and oxygen metabolism provided by positron emission tomography in patients with cerebral infarction.

Quantitative EEG data were analyzed statistically with respect to cortical cerebral blood flow (CBF) and oxygen metabolism (CMRO2) measured by positron emission tomography in 47 patients with unilateral cerebral infarction. Relative value of the square root of average power was used as a percentage power fraction (PPF) for each frequency category. Power ratio index (PRI) was calculated by dividing the combined delta-PPF and theta-PPF by the combined alpha-PPF and beta-PPF. Delta-PPF, theta-PPF and PRI correlated negatively with regional CBF (rCBF) and CMRO2 (rCMRO2) whereas alpha-PPF and beta-PPF correlated positively. In the acute stage, delta-PPF, alpha-PPF and PRI correlated with rCBF at all but the frontopolar region whereas the correlation with rCMRO2 was poor. Alpha-PPF and PRI correlated also with rCMRO2 in the frontal, central, parietal and occipital regions while delta-PPF correlated with rCBF only in the parietal and occipital regions in the subacute stage. In the chronic stage, all EEG quotients correlated significantly with both rCBF and CMRO2 in the central and parietal regions. In the frontopolar region, only the theta-PPF correlated with rCBF throughout. In the comparison of hemispheric mean values, the correlations were always closer for the affected hemisphere than for the contralateral hemisphere. Although hemispheric mean CBF and CMRO2 were significantly lower in patients with cortical infarcts on CT than in those with small subcortical infarcts, there was no significant difference in the EEG data between the 2 groups.

Brain↗
PubMed1989

Involvement of Ca2+ release and activation of phospholipase A2 in mitochondrial dysfunction during anoxia.

During anoxic incubation, depletion of mitochondrial ATP was followed by release of Ca2+ with concomitant increase in the rate of state 4 respiration due to disruption of the diffusion barrier against protons. The external addition of ATP and its non-metabolizable analog, beta,gamma-methylene adenosine 5'-triphosphate, prevented both the release of Ca2+ and increase in the rate of state 4 respiration. Addition of EGTA, which did not prevent release of the ion, resulted in little increase in the respiration rate. Addition of an inhibitor of mitochondrial phospholipase A2, such as quinacrine, dibucaine, or chlorpromazine, also prevented increase in the respiration rate without affecting Ca2+ release from mitochondria during anoxic incubation. Non-esterified polyunsaturated fatty acids were also found to be liberated from anoxic mitochondria. External addition of the ATP-analog, EGTA, and inhibitors of phospholipase A2 suppressed the liberation of non-esterified polyunsaturated fatty acids. Melittin and Ca2+, which activate phospholipase A2, increased the rate of state 4 respiration and the liberation of fatty acids. These findings support the hypothesis proposed previously that the following sequence changes occurs in mitochondria during anoxia; depletion of ATP, liberation of free calcium from mitochondria, and disruption of the diffusion barrier against H+ of the inner membrane. The results also indicate another event; activation of phospholipase A2 by release Ca2+ which results in H+ leakiness of the inner membrane.

Animals↗
PubMed1989

[Non-verbal facial and topographic visual object agnosia--a problem of familiarity in prosopagnosia and topographic disorientation].

In recent years, prosopagnosia is defined as the "loss of ability to recognize the well-acquainted persons like the family members by their physiognomy." There are many reports based on this definition. However, from the viewpoint of symptomatology, there are many problems not entirely solved yet. And the mechanism of its manifestation is not clearly explained. Topographic disorientation, which often accompanies prosopagnosia, is studied even less. From the results of the postmortem examination in the literature, bilateral occipito-temporal lesions have been known to cause prosopagnosia. However, the recent radiographical examination by the computed tomography revealed that the prosopagnosia is also caused by the right occipito-temporal lesions only. We experienced a case with prosopagnosia and topographic disorientation which were considered to be caused by infarction in the territory of the right posterior cerebral artery. Detailed symptomatological, morphological and functional examinations were carried out by means of various psychological testing, X-ray computed tomography (CT), magnetic resonance imaging (MRI) and positron emission tomography (PET). The patient was a 70-year-old right-handed man who suffered from sudden visual loss on both eyes, and was admitted to our hospital after four weeks. On examination, a decrease of visual acuity and right homonymous hemianopsia were recognized. When visual acuity was recovered, he was unable to recognize the faces of his relatives and friends, with whom he has been well acquainted for many years. He also found his own house, the buildings and streets around it as entirely unfamiliar. Seven months after the onset of the disease, examination showed he had definite prosopagnosia and topographic disorientation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

NMR-invisible ATP in rat heart and its change in ischemia.

The subcellular compartmentalization of adenosine 5'-triphosphate (ATP) in isolated perfused rat heart and its relation to energy depletion in ischemia were examined by 31P nuclear magnetic resonance (31P-NMR) spectroscopy and chemical analyses. The signal intensities of the beta-phosphate of ATP and creatine phosphate in the 31P-NMR were standardized by the intracellular volume ratio measured with 23Na-NMR to determine the actual content of each. During aerobic perfusion the ATP content determined by NMR (13.7 +/- 2.2 mumol/g dry weight) was significantly lower than that found by chemical analysis (22.4 +/- 0.7 mumol/g dry weight), while the creatine phosphate contents determined by the two methods were the same. During ischemia at 33 degrees C, the signal of the beta-phosphate of ATP in the 31P-NMR spectrum decreased progressively, disappearing completely after 16 min. But at this time 5.7 +/- 1.7 mumol/g dry weight of myocardial ATP was still detected by chemical analysis. These results indicated that there were two different compartments of intracellular ATP in the heart, only one of which is detectable by 31P-NMR spectroscopy, and that during ischemia the ATP that is detectable, which seems to be the free ATP in the cytosol, decreased more rapidly than the ATP in the other compartment.

Adenosine Triphosphate↗
PubMed1988

Changes in aerobic and anaerobic ATP-synthesizing activities in hypoxic mouse brain.

The changes in cerebral metabolism in mice in severe hypoxia were investigated by analyses of changes in the levels of energy metabolites and near-infrared spectrophotometric assessment of the states of hemoglobin and cytochrome oxidase. Under 4.4% O2, the contribution of anaerobic ATP production was at most about 20% of the demand. However, the cerebral ATP level was kept at the control level until about 1 min before death. Pentobarbital anesthesia, which reduced the cerebral rate of metabolism, prolonged the survival time, although anaerobic ATP production still did not support ATP demand. Under these conditions, deoxygenation of hemoglobin and reduction of cytochrome oxidase proceeded rapidly within 1 min. Hemoglobin reached the maximum state of deoxygenation in the middle phase of hypoxia, with no further change until death. However, cytochrome oxidase was reduced slowly with one phase of partial reoxidation due to increase of cerebral blood volume, and reached the completely reduced state at death. From these results it was concluded that the aerobic ATP synthesis, which supplied more than 80% of the cerebral demand, decreased gradually because of limitation of oxygen supply, and that the failure of oxidative phosphorylation to meet demand triggered the decrease in the cellular ATP level that led to death.

Adenosine Diphosphate↗
PubMed1988

Molecular cloning and expression of a gene for a factor which stabilizes formation of inhibitor-mitochondrial ATPase complex from Saccharomyces cerevisiae.

Stabilizing factor, a 9 kDa protein, stabilizes and facilitates formation of the complex between mitochondrial ATP synthase and its intrinsic inhibitor protein. A clone containing the gene encoding the 9 kDa protein was selected from a yeast genomic library to determine the structure of its precursor protein. As deduced from the nucleotide sequence, the precursor of the yeast 9 kDa stabilizing factor contains 86 amino acid residues and has a molecular weight of 10,062. From the predicted sequence we infer that the stabilizing factor precursor contains a presequence of 23 amino acid residues at its amino terminus. We also used S1 mapping to determine the initiation site of transcription under glucose-repressed or derepressed conditions. These experiments suggest that transcription of this gene starts at three different sites and that only one of them is not affected by the presence of glucose.

Adaptor Proteins, Signal Transducing↗