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Biomedical subjects

T Terada

Publications and source records attributed to T Terada.

At least 307 records · Page 17Linked to original sources

Cerebral blood flow in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes.

BACKGROUND AND PURPOSE: The precise mechanism of neurological symptoms with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) is still controversial. We investigated the correlation between strokelike episodes and cerebral blood flow in two patients with MELAS and discuss the pathogenesis of strokelike episodes with MELAS. SUMMARY OF REPORT: Cerebral dynamic computed tomography and cerebral angiography were used to measure cerebral circulation in the first case, that of a 20-year-old woman with MELAS. The second subject was a 13-year-old female who was studied with xenon-enhanced computed tomography. The cerebral blood flow studies were performed 3-72 hours after the onset of strokelike episodes. Serial cerebral angiography, dynamic computed tomography, and xenon-enhanced computed tomography showed vasodilation localized in the affected cerebral cortexes during strokelike episodes, without any reduction in regional cerebral blood flow. CONCLUSIONS: Our study suggests that the strokelike episodes associated with MELAS are different in origin from ischemic stroke.

Adolescent↗

Inhibition of bovine leukocyte thioltransferase by anti-inflammatory drugs and anti-histaminic drugs.

Thioltransferase was partially purified from bovine leukocyte using sonication, heat treatment at pH 5.1, Sephadex G-50 gel filtration and isoelectric focusing techniques. Isoelectric point (pI) of 8.3 for leukocyte thioltransferase was quite different from pI of 6.5 for erythrocyte enzyme. Bovine leukocyte thioltransferase was employed in a study on the influence of 12 anti-inflammatory drugs and 7 anti-histaminic drugs. Piroxicam which is a well-known anti-inflammatory drug demonstrated the most powerful inhibitory effect on enzyme activity. Inhibition of piroxicam was noncompetitive, and the Ki value measured 55.0 microM in the experiment involving bovine leukocyte enzyme. Tranilast which is a typical anti-histaminic drug most strongly inhibited the enzyme activity and the Ki value of the medicine was 20.3 microM (noncompetitive). Bovine liver and erythrocyte thioltransferases also were effectively inhibited by both medicines similar to leukocyte enzyme.

Animals↗

Antitumor agents. II: Regio- and stereospecific syntheses of 1-beta-alkyl-1-desoxypodophyllotoxin derivatives and biological activity.

1-beta-Alkyl derivatives of 1-desoxypodophyllotoxin were synthesized, and their cytotoxicity and inhibitory effects on DNA topoisomerase II (Topo-II) and tubulin polymerization were examined. The reaction of epipodophyllotoxin derivatives (1a-c) with trimethylallylsilane in the presence of boron trifluoride etherate gave 1-beta-allylated compounds (2a-c). The regiochemistry and the beta-stereochemistry of the 1-allyl group were confirmed by comparison of the 13C-NMR spectra and NOE's (%) of 2c, podophyllotoxin (POD) and epipodophyllotoxin (1b). 1-beta-Alkyl-1-desoxypodophyllotoxin derivatives (3-8) were prepared from 2b. None of the tested compounds (3-8) showed any inhibitory effect on Topo-II. 1-beta-Propyl compound (3) and its 4'-demethyl compound (4) inhibited tubulin polymerization and the cytotoxicities of these compounds were equal to that of VP-16. 1-beta-(2,3-Dihydroxypropyl) compounds (5 and 8) and 1-beta-(2,3-diacetoxypropyl) compounds (6 and 7) showed no inhibitory effect on tubulin polymerization. Although 5 did not inhibit either Topo-II activity or tubulin polymerization, it showed a high cytotoxicity against sarcoma 180.

Animals↗

Influence of regional cerebral blood flow on event-related potential (P300).

The relationships between event-related potential (P300), higher brain functions, and regional cerebral blood flow (rCBF) were examined in 31 neurosurgical patients. The P300 latency, evaluated by an acoustic "odd-ball" paradigm, was normal in 14 and prolonged in 17 patients. Fourteen of 17 prolonged P300 patients had reduced rCBF in the right cerebral hemisphere, especially the frontal lobe and/or thalamus. There was a significant inverse relationship between P300 latency and laterality index (rt rCBF/lt rCBF) in the frontal lobe. Prolonged P300 patients revealed significant abnormalities in psychological tests compared to normal P300 patients. There were significant inverse relationships between the P300 latency and "orientation" and "memory" test scores. Decreased rCBF in the right cerebral hemisphere, especially the frontal lobe and/or thalamus, is associated with prolonged P300 latency, suggesting that the right cerebral hemisphere is important in human cognitive processes.

Adult↗

Comparison of purified lens glutathione S-transferase isozymes from rabbit with other species.

Two glutathione S-transferase (GST) isozymes, GST-rl1 and GST-rl2, were purified from rabbit lenses and their properties were compared with those of other animals. GST-rl1 and GST-rl2 are dimeric enzymes whose subunit sizes are 24,000 and 21,500, respectively. The substrate specificities and inhibitor sensitivities of GST-rl1 and GST-rl2 are different from each other and from those of the isozymes from other animals. GST-rl1 immunologically crossreacted with the antibody against class mu GST (rat GST Yb1-Yb1), and GST-rl2 crossreacted with the antibody against class pi GST (rat GST Yp-Yp). N-Terminal amino acid sequences of GST-rl1 and GST-rl2 have great homology with other class mu and class pi enzymes, and thus indicate that they belong to class mu and class pi, respectively. Class pi GST-rl2 is inactivated by 1,2-naphthoquinone, an oxidized metabolite of naphthalene, but class mu GST-rl1 is insensitive to it. These results are similar to those of class pi pig lens GST and class mu bovine lens GST. Thus, the expression pattern of GST isozymes in lens varies with animal species, and may relate to their variation in sensitivity to oxidative stress.

Amino Acid Sequence↗

Modulation of 3 alpha-hydroxysteroid dehydrogenase activity by the redox state of glutathione.

3 alpha-Hydroxysteroid dehydrogenase (EC 1.1.1.50), purified to homogeneity from rat liver, was strongly inactivated by incubation with a disulfide such as GSSG, L-cystine or L-cystamine, as well as an SH-reagent such as DTNB (5,5'-dithiobis(2-nitrobenzoic acid)), NEM (N-ethylmaleimide) or iodoacetic acid. The inactivation advanced with incubation time. Coenzyme (NADP+) completely protected the enzyme from this inactivation by disulfides, but neither of the substrates (androsterone and benzenedihydrodiol) did. The activity of inactivated enzyme was restored by treatment with thiols such as DTT (dithiothreitol) or GSH. In the GSH/GSSG redox buffer, the enzyme existed in an equilibrium between active (reduced) and inactive (oxidized) forms.

3-Hydroxysteroid Dehydrogenases↗

Development of human intrahepatic peribiliary glands. Histological, keratin immunohistochemical, and mucus histochemical analyses.

BACKGROUND: Intrahepatic peribiliary glands are important components of the intrahepatic biliary tree. Although the development of extrahepatic and intrahepatic bile ducts has been studied extensively, that of intrahepatic peribiliary glands is still unclear. EXPERIMENTAL DESIGN: The development of human intrahepatic peribiliary glands was examined using histology, keratin immunohistochemistry, and mucus histochemistry. RESULTS: At 7 weeks gestation, the ductal plate was present in the periportal immature hepatocytes around the portal veins at the hepatic hilum. At 10 weeks gestation, biliary cells began to bud from the ductal plate into the mesenchyme and formed double-layered cords and tubules. The double-layered cords had transformed completely into tubules by 30 weeks gestation. The tubules then gradually increased in number and aggregated to form immature peribiliary glands at approximately 40 weeks gestation. After birth, the acini of the immature peribiliary glands continued to increase in number and reached an adult state by approximately 15 years. Cytokeratin immunohistochemistry revealed that the ductal plate, precursor cords and tubules in the mesenchyme, and developing and developed peribiliary glands were positive for monoclonal anticytokeratin antibodies CAM5.2, AE1, KL1, and the polyclonal anticytokeratin antibody. Mucus acini containing neutral mucin, sialomucin, and sulfomucin were absent in fetal and neonatal peribiliary glands, appeared at 3 months after birth, and increased gradually after that time. In some cases, ectopic exocrine pancreatic tissue differentiated from the peribiliary glands. This was first observed 3 months after birth and persisted to adult life. CONCLUSIONS: These data indicate that 1) intrahepatic peribiliary glands arise from the periportal immature hepatocytes at the hepatic hilum, 2) the cytokeratin profile does not change during development of peribiliary glands, and 3) differentiation of peribiliary glands into mucus acini and ectopic exocrine pancreatic tissue occurs 3 months after birth.

Adolescent↗

Development of human peribiliary capillary plexus: a lectin-histochemical and immunohistochemical study.

We investigated the development of human intrahepatic peribiliary capillary plexus by lectin-histochemistry and immunohistochemistry, using 40 fetal livers of various gestational ages, 52 postnatal livers of various ages, and 10 adult livers. In the earliest developmental stage of intrahepatic bile ducts ("the stage of ductal plate"), no vasculatures were found around the ductal plate, but progenitor vascular cells positive for von Willebrand factor, Ulex europaeus agglutinin I and succinylated wheat germ agglutinin appeared in the mesenchyme of the portal tracts. In "the stage of biliary cell migration into the mesenchyme," the progenitor vascular cells transformed into capillaries positive for von Willebrand factor, Ulex europaeus agglutinin I, and succinylated wheat germ agglutinin. In "the stage of bile duct formation," capillaries began to surround the bile ducts (immature peribiliary capillary plexus). The capillaries of the immature peribiliary capillary plexus proliferated and formed premature peribiliary capillary plexus around 40 wk of gestation in large bile ducts and around 6 wk after birth in small bile ducts. The former was composed of inner and outer layers, whereas the latter consisted of scattered capillaries without layer formation. The premature peribiliary capillary plexus continued to proliferate in the postnatal life and reached an adult and mature state around 15 yr. These data suggest that endothelial cells of capillaries of peribiliary capillary plexus derive from mesenchyme at the earliest stage of bile duct development and that the development and maturation of peribiliary capillary plexus progress parallel to those of the intrahepatic bile ducts.

Adult↗

An immunohistochemical survey of amylase isoenzymes in cholangiocarcinoma and hepatocellular carcinoma.

It is well known that neoplastic cells of several organs produce amylases. However, to our knowledge, alpha-amylase expression has not been reported in hepatic neoplasms. In the present study, we surveyed the expression of alpha-amylase isoenzymes in cholangiocarcinoma (CCC) (n = 18) and hepatocellular carcinoma (n = 20) by an immunohistochemical technique, using four polyclonal and monoclonal antibodies against salivary- and pancreatic-type amylases. In CCC, salivary- and pancreatic-type amylase immunoreactivity was found in the tumor cell cytoplasm in 11 (61%) and eight (44%) cases, respectively. There was a tendency for salivary- and pancreatic-type amylases to appear in the same CCC. The proportion of isoamylase-positive cases was high in well-differentiated CCC (75%), intermediate in moderately differentiated CCC (66%), and low in poorly differentiated CCC (25%). In contrast, hepatocellular carcinoma cells were negative for salivary- and pancreatic-type amylases. Intrahepatic large bile ducts of nontumorous areas frequently expressed both amylase isoenzymes, while nonneoplastic hepatocytes were negative for both isoamylases. These results suggest that biliary epithelial cells retain amylase isoenzymes after malignant transformation. The finding that the expression of amylase isoenzymes was correlated with the histologic differentiation in CCC supports this suggestion.

Adenoma, Bile Duct↗

Postmortem survey of bile duct necrosis and biloma in hepatocellular carcinoma after transcatheter arterial chemoembolization therapy: relevance to microvascular damages of peribiliary capillary plexus.

The present study was aimed at determining the incidence of bile duct necrosis and biloma in hepatocellular carcinoma (HCC) after transcatheter arterial embolization therapy (TAE) or hepatic arterial infusion chemotherapy (HAI), and also clarifying the relationship between these duct injuries and the peribiliary capillary plexus (PBP). These bile duct injuries were found in seven (12.5%) of the 56 consecutive autopsy livers with HCC and a history of TAE or HAI, whereas they were not in the 48 consecutive autopsy livers with HCC but without such a history (p < 0.02). There was a close relation between the areas of TAE and bile duct injuries. These complications were restricted to the intrahepatic large or septal bile ducts. The inner layer vessels of PBP were considerably reduced in the HCC cases with a history of TAE or HAI, irrespective of these bile duct injuries. We concluded that bile duct necrosis or biloma was not uncommon in cirrhotic livers with HCC after TAE or HAI, and that TAE or HAI might cause the reduction of the inner layer vessels of PBP which may be necessary but was insufficient for the induction of bile duct necrosis or biloma.

Adolescent↗

[Newly developed blocking balloon catheter for PTA of internal carotid artery].

We have developed a new blocking balloon system for percutaneous transluminal angioplasty (PTA) of the internal carotid artery (ICA). A latex balloon (BALT) is attached on the top of a Superselector infusion-type catheter (TORAY) which is used as a blocking balloon catheter. It can be navigated into the distal part of the ICA under torque control as well as flow control by withdrawing the core wire. Our PTA procedure is as follows, 1) insert the sheath catheter 8-9 F in size, 2) insert the PTA balloon catheter (Accent balloon, Cook) with a blocking balloon catheter through the sheath catheter, 3) navigate the blocking balloon into the distal part of the ICA, 4) introduce the PTA balloon to the stenotic portion after occlusion of the distal ICA by the blocking balloon, 5) PTA, 6) wash the lumen of the ICA with saline, 7) deflate the blocking balloon and withdraw the system. We performed PTA for 5 ICA lesions in 4 cases and got successful dilatations for all of them without complications. Our blocking balloon system is useful for performing the PTA of the ICA safely.

Aged↗

Pancreatic lipase is a useful phenotypic marker of intrahepatic large and septal bile ducts, peribiliary glands, and their malignant counterparts.

Expression of pancreatic lipase in normal, proliferating, and carcinomatous epithelia of the intrahepatic biliary tree was examined by immunohistochemistry in 82 normal livers, 35 hepatolithiatic livers, 11 cholangiocarcinomas (CCs) associated with hepatolithiasis, 34 CCs, and four combined hepatocellular-cholangiocellular carcinomas. The intrahepatic biliary tree was anatomically divided into large ducts, septal ducts, interlobular ducts, bile ductules, and peribiliary glands. In hepatolithiasis, large ducts, septal ducts, and peribiliary glands showed marked proliferation and dysplasia. In normal livers and hepatolithiasis, expression of pancreatic lipase was found in large ducts in 91% and 94%, in septal ducts in 95% and 94%, and in peribiliary glands in 93% and 94%, respectively. Interlobular ducts, bile ductules, and hepatocytes were negative for pancreatic lipase. The immunoreactivity of pancreatic lipase was coarse granular, and was regularly present in the supranuclear and to a lesser degree paranuclear cytoplasm of the epithelial cells. All cases of CCs with hepatolithiasis, which arised from large ducts, expressed pancreatic lipase. In CCs, pancreatic lipase was expressed in the perinuclear cytoplasm of cancer cells in 67% in the hilar type and in 24% in the peripheral type (P < 0.02). The combined hepatocellular-cholangiocellular carcinomas failed to express pancreatic lipase in both elements. These data suggest that large ducts, septal ducts, and peribiliary glands contain pancreatic lipase in normal and proliferative conditions, and that CCs probably arising from these ductal elements continue to express pancreatic lipase. Thus, pancreatic lipase could be a phenotypic marker of large ducts, septal ducts and peribiliary glands as well as their malignant counterparts.

Adenoma, Bile Duct↗

The role of 16,16-dimethyl prostaglandin E2 on the intrahepatic biliary branches in dogs.

We studied the effects of the oral administration of a stable prostaglandin E2 analog, 16,16-dimethyl prostaglandin E2, on the intrahepatic biliary branches in a canine model. Obstructive cholestasis with a bacterial infection was induced surgically in two liver lobes in healthy mongrel dogs, and 16,16-dimethyl prostaglandin E2 was administered orally. We examined the morphological changes in the intrahepatic biliary branches and quantitatively estimated density of mucus-producing glandular elements in the ductal wall by counting these glands per unit area. Dogs treated with 16,16-dimethyl prostaglandin E2 (group 1) demonstrated fibrous thickening of the ductal wall, moderate infiltration by inflammatory cells and severe adenomatous hyperplasia of the bile duct epithelium, including striking proliferation of the mucous glands. The mean number of these mucous glands per unit area (4 mm2) was 43.0 +/- 9.0 (mean +/- S.D.; range = 36 to 56). In contrast, in a control group whose members did not receive 16,16-dimethyl prostaglandin E2 (group 2), the mean number of mucous glands per unit area was 19.4 +/- 8.0 (range = 10 to 29), significantly lower than that in group 1, although histological examination revealed chronic inflammation in the region of the large bile duct similar to that in group 1. These findings suggest that the increase in the number of mucous glands that typically occur in the setting of bile stasis and biliary infection is enhanced by 16,16-dimethyl prostaglandin E2.

16,16-Dimethylprostaglandin E2↗