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Biomedical subjects

T Teramoto

Publications and source records attributed to T Teramoto.

At least 217 records · Page 12Linked to original sources
PubMed1987

Effect of dietary cholesterol on production of lipoproteins and apolipoproteins by perfused livers from Japanese monkeys (Macaca fuscata).

Isolated livers from Japanese monkeys were perfused for the purpose of characterizing low density lipoprotein (LDL) secreted directly by the liver, and for determining whether cholesterol feeding affects the hepatic production of LDL. Perfusate containing [3H]leucine was recirculated for 60 min, followed by perfusion with fresh perfusate for two additional 2-h periods. Radiolabelled lipoproteins, which are isolated by ultracentrifugation as very low density lipoprotein (VLDL), LDL, and high density lipoprotein were 0.87 +/- 0.74, 1.83 +/- 1.47, and 0.44 +/- 0.33%, respectively, of total radiolabelled protein in the medium of the last 2-h period. Subfractionation of perfusate LDL by high performance liquid chromatography, and by concanavalin A sepharose chromatography, revealed that the newly synthesized LDL were secreted as apo E-rich particles. Cholesterol feeding resulted in a four-fold increase in hepatic secretion of newly synthesized VLDL, but not of the LDL. The distribution of radioactivity among VLDL apolipoproteins was not affected by cholesterol feeding. Incorporation of radioactivity into apo B100 of LDL decreased significantly, but that into apo E did not change. These results suggested that (i) the elevation of serum LDL in cholesterol-fed monkeys is not due to enhanced hepatic production of LDL, but probably results from intravascular metabolism of VLDL, which is of hepatic origin, and (ii) cholesterol feeding affects the hepatic apo B100 synthesis and/or release but not apo E.

Animals↗
PubMed1987

Bloom's syndrome with porokeratosis of Mibelli and multiple cancers of the skin, lung and colon.

A 38-year-old Japanese male with Bloom's syndrome (BS) and porokeratosis of Mibelli (PM) developed multiple carcinomas of the skin and lung. There were multiple, spontaneous chromosomal aberrations and frequent sister chromatid exchanges (SCE). Cutaneous delayed-type hypersensitivity reactions were defective and serum IgM was decreased. The lung cancer was treated with radiation, which was effective but caused a severe pulmonary atelectasis and esophageal stricture. The patient expired one-and-a-half years later because of pneumonia. Autopsy disclosed an adenocarcinoma of the colon. The concurrent PM was considered responsible for the occurrence of multiple skin cancers.

Adenocarcinoma↗
PubMed1986

Calmodulin-independent inhibition of platelet phospholipase A2 by calmodulin antagonists.

We tested the effects of calmodulin, two types of calmodulin antagonists, and various phospholipids on the phospholipase A2 activities of intact platelets, platelet membranes, and partially purified enzyme preparations. Trifluoperazine, chlorpromazine (phenothiazines) and N-(6-amino-hexyl)-5-chloro-1-naphthalenesulfonamide (W-7), at concentrations which antagonize the effects of calmodulin, significantly inhibited thrombin- and Ca2+ ionophore-induced production of arachidonic acid metabolites by suspensions of rabbit platelets and Ca2+-induced arachidonic acid release from phospholipids of membrane fractions, but not phospholipase A2 activity in purified enzyme preparations. The addition of acidic phospholipids, but not calmodulin, stimulated phospholipase A2 activity in purified enzyme preparations while decreasing its Km for Ca2+. The dose-response and kinetics of inhibition by calmodulin antagonists of acidic phospholipid-activated phospholipase A2 activity in purified preparations were similar to those of Ca2+-induced arachidonic acid release from membrane fractions. Calmodulin antagonists were also found to inhibit Ca2+ binding to acidic phospholipids in a similar dose-dependent manner. Our results suggest that the platelet phospholipase A2 is the key enzyme involved in arachidonic acid mobilization in platelets and is regulated by acidic phospholipids in a Ca2+-dependent manner and that calmodulin antagonists inhibit phospholipase A2 activity via an action on acidic phospholipids.

Animals↗
PubMed1986

The basic apolipoprotein A-I in the patients with familial lecithin:cholesterol acyltransferase deficiency.

The apolipoprotein A-I (apo A-I) from the patients with familial lecithin: cholesterol acyltransferase (LCAT) deficiency has been characterized. More than 10% of total serum apo A-I was recovered in the bottom fraction (d greater than 1.21 g/ml) of the patients' sera, while in normal sera, only 4.3 +/- 2.7% (Mean +/- SD) of apo A-I was found in the bottom fraction. The lipoproteins of the sera from the patients were analysed by density gradient ultracentrifugation and by high performance liquid chromatography (HPLC). Our HPLC analysis has revealed that the association of apo A-I with a lipid-poor HDL, observed in the patients, is not due to ultracentrifugal artifacts. The serum apo A-I isoproteins and their relative concentrations in the three patients were analysed by two dimensional electrophoresis. The isoprotein distribution for each of the three patients was as follows: isoproteins 2 and 3; 12.3, 21.2 and 25.7%, suggesting that the basic isoforms (isoproteins 2 and 3) were increased compared to normal controls (3.5 + 2.3%). The profile of apo A-I isoproteins of the bottom fraction was almost the same as that of the patient's HDL, indicating the equivalent affinity of each isoprotein with lipid and/or protein of HDL. These observations are compatible with the suggestion that the reduction of HDL-cholesterol in familial LCAT deficiency may be due to rapid catabolism of HDL, resulting in the increase in the ratio of apo A-I isoprotein 2 and 3 (immature form of isoprotein A-I) to isoprotein 4 and 5 (mature form of apo A-I).

Adult↗
PubMed1986

[Extended radical operation of cancer of the rectum].

Extended radical operation for rectal cancer included the high ligation of inferior mesenteric artery and the dissection of lateral lymph nodes. There was no significant difference between overall survival of extended operation and conventional operation, although in Dukes B cases, 5-year survival rate was significantly higher in extended operation than in conventional. Extended operation caused high incidence of postoperative urinary and sexual dysfunction compared with conventional operation. We conclude that extended radical operation must be performed only in those patients, when tumors locate in the lower part of the rectum and invade beyond the proper muscle layer.

Humans↗
PubMed1985

Effects of arachidonic acid on the metabolism of eicosapentaenoic acid in washed human platelets.

We examined effects of arachidonic acid (AA) on eicosapentaenoic acid (EPA) metabolism in washed human platelets. Although human platelets had been considered to metabolize scarcely EPA, a simultaneous addition of EPA and AA to washed platelet suspensions stimulated markedly EPA metabolism. In addition, the stimulatory effect was more potent over the formation of thromboxane (TX) B3 than that of 12-hydroxy-5,8,10,14,17-eicosapentaenoic acid (HEPE). The stimulation by AA can be due to AA itself and/or AA metabolites. Indomethacin decreased the stimulatory effect of AA on the HEPE formation, suggesting that cyclooxygenase product(s) of AA stimulated the HEPE formation. Among the metabolites of AA investigated, prostaglandin (PG)G2 and 12-hydroperoxy-5,8,10,14-eicosatetraenoic acid had the stimulatory effect on both TXB2 and HEPE formations, whereas PGH2, PGD2, TXB2 and 12-hydroxy-5, 8,10,14-eicosatetraenoic acid were ineffective.

Arachidonic Acid↗
PubMed1985

High concentrations of arachidonic acid induce platelet aggregation and serotonin release independent of prostaglandin endoperoxides and thromboxane A2.

We examined platelet aggregation and serotonin release, induced by less than 60 micro M arachidonic acid, using washed platelet suspensions in the absence of albumin. The concentration of arachidonic acid used did not cause platelet lysis. Platelet responses induced by less than 20 micro M arachidonic acid were inhibited by aspirin, whereas those induced by above 30 micro M arachidonic acid were not inhibited, even by both aspirin and 5,8,11,14-eicosatetraynoic acid. Although phosphatidic acid and 1,2-diacylglycerol increased after the addition of arachidonic acid in aspirin-treated platelets, the amounts were not parallel to platelet aggregation. Oleic, linoleic and linolenic acids also induced platelet responses, while palmitic, stearic and arachidic acids did not. EDTA, dibutyryl cyclic AMP, apyrase and creatine phosphate/creatine phosphokinase brought about almost the same effects in platelet responses induced by the unsaturated fatty acids, other than arachidonic acid, as those induced by 40 micro M arachidonic acid. These results suggest that the mechanism of the actions of more than 30 micro M arachidonic acid on platelets is the same as that of the other unsaturated fatty acids and is independent of prostaglandin endoperoxides, thromboxane A2 and, perhaps, phosphatidic acid and 1,2-diacylglycerol.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1985

Time-dependent inhibition of the cyclooxygenase pathway by 12-hydroperoxy-5,8,10,14-eicosatetraenoic acid.

We examined effects of small dose (1 microM or less) of exogenous 12-hydroperoxy-5,8,10,14-eicosatetraenoic acid (12-HPETE) on the formation of cyclooxygenase products from exogenous arachidonic acid (AA) in washed human platelets. With a simultaneous addition of AA, 12-HPETE did not affect the formation of thromboxane (TX)B2 and 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT). However, by being preincubated with platelets before an addition of AA, 0.1 microM or greater of 12-HPETE inhibited the formation of TXB2 and HHT dose-dependently. In addition, the inhibitory effect of 12-HPETE increased as the preincubation time was prolonged. These results suggest that 12-HPETE is a strong inhibitor for the cyclooxygenase pathway.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1985

Abnormal high density lipoprotein of primary biliary cirrhosis analyzed by high performance liquid chromatography.

The lipoprotein profile of patients with primary biliary cirrhosis (PBC) has been assessed by high performance liquid chromatography (HPLC). Without exception, all subjects with PBC had an abnormal high density lipoprotein (HDL), which was larger than normal HDL. The elution time from an HPLC column of the abnormal HDL separated it clearly from normal HDL. The HDL of subjects with asymptomatic and symptomatic PBC could also be distinguished. The HDL of asymptomatic subjects was eluted between that of normal and symptomatic subjects. The lipid and protein composition of abnormal HDL was characterized by an increase in phospholipid and a decrease in protein, resulting in an increase in the ratio of phospholipid/protein. This ratio was higher in symptomatic than in asymptomatic PBC. Incubation of dimyristoyl phosphatidylcholine liposomes with normal serum resulted in the formation of an altered high density lipoprotein. These findings suggest that an overload of phospholipid may play a role in the formation of the abnormal HDL in primary biliary cirrhosis.

Adult↗
PubMed1985

Partial purification of the apolipoprotein E receptor of rat liver membrane.

The liver has two distinct lipoprotein receptors; one is the apolipoprotein (apo) B, E receptor and the other the apo-E receptor. In this study, the protein to which apo-E HDLc (cholesterol-induced high density lipoprotein containing apo-E as the predominant protein species) bound specifically was partially purified from the rat liver membrane by ion exchange chromatography and preparative gel electrophoresis. The molecular weight of the protein was estimated to be about 36K daltons and the protein bound to 125I-apo-E HDLc in a specific and saturable manner, suggesting that the protein is the apo-E receptor.

Animals↗
PubMed1985

Microangiographic findings of massive intestinal bleeding in a patient with Crohn's disease: a case report.

A 16 year old man with complaints of abdominal pain, diarrhea, high fever and loss of body weight was made a diagnosis of Crohn's disease. During the administration, he had intestinal obstruction and several episodes of massive intestinal bleeding. Selective angiography of the superior mesenteric artery demonstrated the bleeding site in the ileum. Microangiography of the surgical specimens revealed abrupt interruptions of arteriae rectae in the submucosa indicating the bleeding site from the diseased intestine.

Adolescent↗
PubMed1984

Purification of intracellular phospholipase A2 from rat spleen supernatant by reverse-phase high-performance liquid chromatography.

Intracellular phospholipase A2 was purified to homogeneity from rat spleen supernatant by reverse-phase high-performance liquid chromatography with a trifluoroacetic acid-acetonitrile solvent system. The method simplified the purification procedure, which includes three consecutive chromatographic steps. The recovery of the enzyme activity was greater than 70% with an about 23,000-fold purification. The solvent system did not affect the catalytic properties of the enzyme. Phospholipases A2 from rat spleen, human pancreatic juice, and porcine pancreas were eluted in that order from a column of octadecasilyl silica gel in a similar concentration range of acetonitrile. This result suggests that the phospholipases A2 examined have similar hydrophobicities. This method may be applicable to the purification of phospholipases A2 from other sources.

Animals↗
PubMed1984

Analysis of apolipoproteins in high density lipoproteins by high performance liquid chromatography.

A simple and rapid method for the analysis of apolipoproteins in high density lipoprotein (HDL) by high performance liquid chromatography (HPLC) has been developed (Kinoshita et al. (1983) J. Biochem. 94, 615-617). With this method, using a sodium phosphate buffer containing 0.1% sodium dodecyl sulfate (SDS) as an eluent, apolipoproteins can be analyzed from a very small amount of HDL fraction without delipidation using organic solvents. Separation profiles of apolipoproteins by this method were examined using several techniques. The elution pattern monitored by A280 can give precise quantitative as well as qualitative information about size-distribution of apolipoproteins, except for the apo C group. Moreover, separation of apo E from apo A-I was found to be improved by column elongation.

Apolipoproteins↗
PubMed1984

Cytogenetic studies in a patient with porokeratosis of Mibelli, multiple cancers and a forme fruste of Werner's syndrome.

A 49-year-old man with extensive porokeratosis of Mibelli (PM) developed a squamous cell carcinoma and several carcinomas-in-situ within the lesional skin. The patient also had diabetes mellitus and a short stature with a prematurely aged appearance. The patient's father and two siblings also had PM. The patient died from metastatic squamous cell carcinoma, and at autopsy an adenocarcinoma of the descending colon was also found. Fibroblasts cultured from both the PM-affected and unaffected skin showed chromosomal abnormalities and a decreased lifespan. Cellular sensitivity to ultraviolet rays measured by unscheduled DNA synthesis and colony-forming ability were within normal limits. An association with a forme fruste of Werner's syndrome was suspected.

Adenocarcinoma↗
PubMed1984

Characterization of lipoprotein produced by the perfused rhesus monkey liver.

Isolated livers from rhesus monkeys (Macaca mulatta) were perfused in order to asses the nature of newly synthesized hepatic lipoprotein. Perfusate containing [3H]leucine was recirculated for 1.5 hr, followed by an additional 2.5-hr perfusion with fresh perfusate. Equilibrium density gradient ultracentrifugation clearly separated VLDL from LDL. The apoprotein composition of VLDL secreted by the liver was similar to that of serum VLDL. The perfusate LDL contained some poorly radiolabeled, apoB-rich material, which appeared to be contaminating serum LDL. There was also some material of an LDL-like density, which was rich in radiolabeled apoE. Rate zonal density gradient ultracentrifugation fractionated HDL. All perfusate HDL fractions had a decreased cholesteryl ester/unesterified cholesterol ratio, compared to serum HDL. Serum HDL distributed in one symmetric peak near the middle of the gradient, with coincident peaks of apoA-I and apoA-II. The least dense fractions of the perfusate gradient were rich in radiolabeled apoE. The middle of the perfusate gradient contained particles rich in radiolabeled apoA-I and apoA-II. The peak of apoA-I was offset from the apoA-II peak towards the denser end of the gradient. The dense end of the HDL gradient contained lipoprotein-free apoA-I, apoE, and small amounts of apoA-II, probably resulting from the relative instability of nascent lipoprotein compared to serum lipoprotein. Perfusate HDL apoA-I isoforms were more basic than serum apoA-I isoforms. Preliminary experiments, using noncentrifugal methods, suggest that some hepatic apoA-I is secreted in a lipoprotein-free form. In conclusion, the isolated rhesus monkey liver produces VLDL similar to serum VLDL, but produces LDL and HDL which differ in several important aspects from serum LDL and HDL.

Animals↗
PubMed1984

[Radical operation for rectal cancer to preserve anorectal, urinary and sexual function].

Recently, preservation of physiological functions have become to be considered in the operative treatment for rectal cancer. Dysfunction caused following radical operation for rectal cancer is divided into two parts as follows, (1) disturbance or loss of anorectal function due to sacrifice of the anus in abdomino-perineal resection and decrease function as fecal reservoir following anal sphincter preserving resection of the rectum. (2) anorectal, urinary and sexual dysfunction following surgical injury to the autonomic nerves by pelvic lymph nodes dissection. Our conceptions of the indication for sphincter preserving operation and for wide dissection of pelvic lymph nodes which cause severe dysfunction of urinary and sexual functions postoperatively were discussed.

Anal Canal↗