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Biomedical subjects

N Hatanaka

Publications and source records attributed to N Hatanaka.

At least 37 records · Page 2Linked to original sources
PubMed1998

[A case of cerebral venous angioma detected by slow velocity-encoding phase contrast MRA: appropriate determination of velocity encode].

We report a 86-year-old woman who has been diagnosed as cerebral venous angioma by slow velocity-encoding phase contrast magnetic resonance angiography (MRA). She had developed headache for one month. T1- and T2-weighted images showed a flow void sign in the right cerebellum with gadolinium enhancement. MRA using time-of-flight sequence revealed no abnormal vascular structures. Conventional phase contrast MRA (velocity encode, 40 or 60 cm/sec) did not disclose obvious vascular abnormalities. However, slow velocity-encoding (20 cm/sec) phase contrast MRA demonstrated a well-demarcated venous angioma in the right transverse sinus. Our results of MRAs suggest that velocity encode is a crucial factor for detection of venous angioma on phase contrast MRA. Slow velocity-encoding phase contrast MRA is a beneficial tool for evaluation of venous malformations, such as venous angioma.

Aged↗
PubMed1997

Mediastinoscopic extirpation of mediastinal ectopic parathyroid gland.

We report a case of a 50-year-old man with hyperparathyroidism secondary to chronic renal failure who underwent extirpation of a mediastinal ectopic parathyroid gland by a transcervical approach under mediastinoscopy. This procedure provides an excellent approach to the mediastinal ectopic parathyroid gland, and is less invasive than median sternotomy or thoracotomy.

Choristoma↗
PubMed1996

Improvement of rat liver graft function by insulin administration to donor.

BACKGROUND & AIMS: The nutritional status of a donor is considered to be an important factor affecting organ viability. The purpose of the present study was to examine hepatic energy status in connection with posttransplantation liver function. METHODS: The following five groups of donor rat livers were prepared and stored in University of Wisconsin solution at 4 degrees C: fasted group, rats fasted for 24 hours; fed group, rats provided standard laboratory chow; fed plus insulin group, fed rats treated with insulin before harvest; fasted plus insulin group, fasted rats treated with insulin before harvest; and fed plus glucagon group, fed rats pretreated with glucagon. RESULTS: Hepatic levels of adenosine triphosphate and total adenine nucleotides were maintained in the decreasing order of the fed plus insulin, fed, fasted plus insulin, fasted, and fed plus glucagon groups during preservation. Lactate production rate and fructose 2,6-bisphosphate level increased in the order of the fed plus insulin, fed, fed plus glucagon, fasted, and fasted plus insulin groups. Liver function after transplantation evaluated by the bile flow rate and enzyme leakage was well restored in the fed plus insulin group. CONCLUSIONS: Insulin administration to nutritionally well-supported livers before harvest improved energy metabolism during preservation and liver function after transplantation.

Adenosine Triphosphate↗
PubMed1996

[Mediastinal thoracic duct cyst--a case report].

The patient, a 55-year-old asymptomatic man, was referred to our hospital in October 1995 for further investigation of a chest ++roentogenographic abnormality found during a "physical check-up". His chest X-ray showed a round shadow over the hilus of the left lung. Computed tomography revealed a homogeneous, low density mass bordering the esophagus, vertebral column, left lower pulmonary vein and descending aorta. Roentogenography after swallowing barium sulfate showed that the esophagus was compressed and displaced to the right in the anterior direction. Endoscopic ultrasound scan demonstrated a cystic mass. The preoperative findings were suggestive of an esophageal cyst or a thoracic duct cyst. On December 12, 1995, the patient was operated on. The mass was 2 x 3 x 6 cm in size, and was easily separated from the left pulmonary vein, esophagus and vertebral column by blunt and sharp dissection, but it was strongly adhered to the aorta. The wall of the cyst was incised and a chylous fluid was found inside. The mass was diagnosed as a thoracic duct cyst and was removed after clipping and cutting the thoracic duct above and below the cyst. Histopathological features of the wall of the cyst was that the luminal surface was lined by a monolayer of flat endothelium and composed of loose fibrous tissue with scattered bundles of smooth muscle. It differed from that of veins. The postoperative course was uneventful and he was discharged on the 12th postoperative day. Mediastinal thoracic duct cysts are rare and only 25 operated cases have been reported in the literature. We review and discuss these cases.

Humans↗
PubMed1995

Ca2+ release from mitochondria induces cytosolic enzyme leakage in anoxic liver.

The mechanisms of elevation of cytosolic Ca2+ concentration during anoxia causing cytosolic enzyme leakage were studied in perfused rat liver. Before anoxia the Ca2+ contents in mitochondria of perfused rat liver were varied by addition of noradrenaline and glucagon, lowering Ca2+ concentration in the perfusion medium, and addition of Ca2+ channel blocker, either singly or in combination. The amount of cytosolic enzyme leakage during anoxic perfusion positively correlated with the mitochondrial Ca2+ content just before anoxia and also with Ca2+ release from mitochondria during anoxia. However, the amount of cytosolic enzyme leakage during anoxic perfusion did not correlate with the Ca2+ concentration in the perfusion medium and microsomal Ca2+ content. These data support the hypothesis that in anoxic liver, the cytosolic Ca2+ concentration is elevated to a pathological level mainly by Ca2+ release from mitochondria, causing the cytosolic enzyme leakage.

Animals↗
PubMed1994

Beneficial effects of cyclosporine on reoxygenation injury in hypoxic rat liver.

The effect of CsA on hypoxia-reoxygenation injury was studied in perfused rat livers. CsA did not attenuate hypoxic injury, as assessed by the release of lactate dehydrogenase and mitochondrial aspartate aminotransferase. During reoxygenation, the release of lactate dehydrogenase was also not affected by CsA. However, the release of mitochondrial aspartate aminotransferase into the cytosol, which indicates mitochondrial injury, was significantly reduced by CsA. The effect of CsA on mitochondrial function during hypoxia-reoxygenation was also investigated. CsA administration increased both the respiratory control ratio and the adenine nucleotide content after reoxygenation in both isolated mitochondria and perfused livers. In addition, glucose production by perfused livers after reoxygenation was increased by CsA. We conclude that the beneficial effect of CsA on hypoxia-reoxygenation injury may be partly due to protection of the mitochondria against reoxygenation injury.

Animals↗
PubMed1994

Oxygen radical-induced inhibition of alkaline phosphatase activity in reconstituted membranes.

The effects of lipid peroxidation on membrane-bound enzyme activity were examined using reconstituted membranes consisting of intestinal alkaline phosphatase (ALP) and phosphatidylcholine (PC) or dipalmitoylphosphatidylcholine (DPPC). When the PC-reconstituted membranes were incubated with ascorbic acid/Fe2+, the ALP activity decreased with increases in the thiobarbituric acid-reactive substances and conjugated diene values in a time-dependent manner. The kinetic studies on the ALP activity with varying the p-nitrophenyl phosphate or beta-glycerophosphate concentrations showed that the inhibition of the enzyme activity by treatment with these oxidizing agents is mainly due to a decrease in the Vmax value rather than a change in the Km value. The results with several antioxidants suggested that ascorbic acid/Fe(2+)-induced inhibition of the ALP activity is related to generation of .OH radicals. Modification of the reconstituted membranes with malondialdehyde, trans-2-nonenal, or n-heptaldehyde did not affect the ALP activity, suggesting that the secondary degraded products of lipid hydroperoxides had no influence on the enzyme activity. Increasing bityrosine production in the membrane constituents was observed by ascorbic acid/Fe2+ treatment, depending on the incubation time. This finding suggests the possibility that amino acid modifications in the protein molecule are induced by the treatment. Furthermore, the contribution of the lipid organization in ascorbic acid/Fe(2+)-induced inhibition of the ALP activity in the reconstituted membranes was examined by measurements of the fluorescence anisotropy of diphenylhexatriene-labeled membranes. In addition, it was found that the ALP activity in DPPC-reconstituted membranes was also inhibited by treatment with ascorbic acid/Fe2+, similar to the case in PC-reconstituted ones. On the basis of these results, a possible mechanism of ascorbic acid/Fe(2+)-induced inhibition of membrane-bound ALP activity is discussed.

Alkaline Phosphatase↗
PubMed1994

Changes in biliary glutathione level during ischemia-reperfusion of rat liver.

Changes in hepatic and biliary glutathione levels were studied in rat liver treated with tert-butyl hydroperoxide (t-BuOOH) and subjected to ischemia-reperfusion. Immediately after t-BuOOH administration, the oxidized glutathione (GSSG) values and reduced glutathione (GSSG/GSH) ratio in the bile increased dose-dependently and then returned to control level within 10 min, whereas the hepatic ATP level and bile flow rate were not affected by t-BuOOH at doses of up to 1.0 mmol/kg. These data suggested that the liver remains viable on treatment with up to 1.0 mmole/kg t-BuOOH, and that hepatocytes can rapidly dismute t-BuOOH at up to this dose. The hepatic GSH and GSSG levels did not vary appreciably during ischemia for 10 or 30 min or during subsequent reperfusion, but the GSSG/GSH ratio increased after ischemia for 30 min. The rate of bile flow and the biliary level of GSH decreased after ischemia for 30 min in proportion to the decrease in the hepatic ATP level. However, the biliary GSSG concentration did not vary on reperfusion, although GSSG secretion into the bile is also related to the hepatic ATP level. As a result, the GSSG/GSH ratio in the bile increased during reperfusion after ischemia for 30 min. This increased ratio is thought to reflect oxidation of hepatic GSH by hydroperoxide produced during reperfusion. The GSSG/GSH ratio in the bile after 30 min ischemia corresponded to that observed after a small dose (0.07 mmole/kg body wt) of t-BuOOH, which hepatocytes could dismute rapidly without loss of their viability.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1994

Enzyme release from mitochondria during reoxygenation of rat liver.

Reoxygenation-induced release of mitochondrial aspartate aminotransferase (mAST) into the cytosol was studied using perfused rat liver. As the absolute activity of mAST in the perfusate did not indicate the degree of mitochondrial enzyme release, the following 3 methods were applied: measurement of the mAST to total AST ratio in the efferent perfusate, the digitonin infusion method, and measurement of mAST activity in the cytosolic compartment isolated from perfused livers. The results by all 3 methods were consistent and showed that mitochondrial injury occurs on reoxygenation. The mitochondrial Ca2+ content was proportional to the extent of mAST release during reoxygenation, indicating involvement of Ca2+ in the enzyme release. CsA, a potent inhibitor of Ca(2+)-induced increase in permeability of the mitochondrial membrane, completely prevented mAST release on reoxygenation. We conclude that during reoxygenation of hypoxic liver, mAST leaks into the cytosol in a Ca(2+)-dependent, CsA-sensitive manner.

Animals↗
PubMed1993

Radical resection of primary malignant melanoma of the gallbladder with multiple metastases: report of a case.

We present herein an usual case of primary malignant melanoma of the gallbladder in a 51-year-old man in whom an exploratory laparotomy for melena revealed six malignant melanoma lesions located in the gallbladder, main pancreatic duct, stomach, duodenum, jejunum, and a mesenteric lymph node. Total pancreatectomy was performed and histologically, junctional activity was seen only in the gallbladder, suggesting that this was the primary site. No melanotic lesions were found on the skin or eyes. The metastases to the main pancreatic duct and gastrointestinal tract appeared likely to have occurred as a consequence of the mucosal dissemination of the tumor cells shed into the bile. The post-operative course was uneventful and combined chemotherapy was administered for 16 months. No new metastatic lesions were found until 21 months postoperatively, when metastases were detected in the brain and thoracic spinal cord. These metastatic tumors were removed surgically, but the patient died from cerebral disturbance 26 months after the initial operation. Thus, we consider that aggressive surgical therapy was effective for extending the survival time and improving the quality of life of this patient.

Adult↗
PubMed1993

Attenuation of warm ischemic injury of rat lung by inflation with room air--assessment of cellular components and the surfactant in the bronchoalveolar lavage fluid in relation to changes in cellular adenosine triphosphate.

Studies were made on the effects in rat lungs of aerobic and anaerobic conditions on the intracellular levels of adenosine triphosphate and its related metabolites, the releases of intracellular enzymes, and the secretion of pulmonary surfactant. After warm ischemia for 120 min, the ATP content of lungs inflated with air was significantly higher (8.0 +/- 1.2 mumol/g dry weight) than those of deflated lungs and lungs inflated with nitrogen (0.8 +/- 0.7 mumol/g dry weight and 2.0 +/- 0.7 mumol/g dry weight, respectively; P < 0.001). The amounts of intracellular enzymes, such as lactate dehydrogenase, cytosolic and mitochondrial aspartate aminotransferase, and protein in the bronchoalveolar lavage fluid (BALF) of air-inflated lungs were significantly less than those in BALFs of deflated and nitrogen-inflated lungs (P < 0.001). The BALF-contents of dipalmitoyl phosphatidylcholine (DPPC), the main component of alveolar surfactant of aerobic and anaerobic ischemic lung were, however, similar. During 120-min warm ischemia after lavage, air-inflated lungs secreted significantly more DPPC into the alveolar space than nitrogen-inflated lungs did (P < 0.001). We conclude that cell membranes in the lungs are damaged under anaerobic conditions, but that inflation of ischemic lungs with air is effective for protecting them from cell injury and for maintaining the intracellular level of ATP and the ability of the cells to secrete pulmonary surfactant.

1,2-Dipalmitoylphosphatidylcholine↗