Search PubMed⌕ Search

Biomedical subjects

H Fukui

Publications and source records attributed to H Fukui.

At least 253 records · Page 14Linked to original sources
PubMed1994

Cysteinyl leukotrienes in the urine of patients with liver diseases.

The significance of cysteinyl leukotrienes was investigated in patients with liver diseases by measurements of leukotriene E4 and N-acetyl-leukotriene E4 in urine. A marked increase of renal cysteinyl leukotriene excretion was observed in patients with cirrhosis without and with ascites, intrahepatic cholestasis, and obstructive jaundice as compared with healthy subjects (leukotriene E4: means 82, 264, 221 and 142 versus 40 nmol/mol creatinine, respectively; N-acetyl-leukotriene E4: means 25, 64, 61 and 47 versus 13 nmol/mol creatinine, respectively). The urinary concentration of leukotriene E4 was positively correlated with the one of N-acetyl-leukotriene E4 (r = 0.81, p < 0.001). In patients with cirrhosis, the excretion of cysteinyl leukotrienes was strongly increased in patients in Child-Turcotte stage C as compared with those in Child-Turcotte stages A and B. In patients with intrahepatic cholestasis and in those with obstructive jaundice, the excretion of leukotriene E4 plus N-acetyl-leukotriene E4 was positively correlated with total serum bilirubin. In patients with cirrhosis and in those with obstructive jaundice, the cysteinyl leukotrienes in urine were negatively correlated with creatinine clearance. The elevated renal excretion of cysteinyl leukotrienes decreased after biliary drainage in patients with obstructive jaundice. These data support the concept that increased urinary excretion of cysteinyl leukotrienes in patients with cirrhosis is due to a reduced functional liver mass and that in patients with cholestasis it is mainly due to an impaired elimination into the biliary tract that results in a diversion to renal excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Primary central nervous system lymphoma in Japan--a retrospective, co-operative study by CNS-Lymphoma Study Group in Japan.

This manuscript reports the results of the first cooperative study on primary central nervous system lymphoma (PCNSL) in Japan. Of 196 patients registered, 170 were judged as having PCNSL. No patients were immunocompromised. Of the 170 patients with PCNSL, 93 were males and 77 were females. The mean was 56.7 years. One hundred and nineteen tumors were confirmed histopathologically, and 51 were diagnosed by neuroimaging alone. All the tumors were non-Hodgkin's lymphoma. According to the Working Formulation for Clinical Usage (WF), 96 out of 119 tumors were classifiable: 53 were diffuse large cell type (55.2%), 17 immunoblastic type (17.7%), 9 diffuse small cleaved type (9.4%), 6 diffuse mixed type (6.3%), 5 polymorphous type (5.2%), 5 small lymphocytic type (5.2%) and 1 small non-cleaved type (1.0%). Of 21 tumors studied immunohistochemically, 18 were B-cell type and 3 were T-cell type. Irradiated patients (144) survived significantly longer than non-irradiated patients, (median survival time, MST: 19.2 and 2.7 months, respectively; p < 0.001). There was a remarkable difference in survival among patients of the intermediate lymphomas; MST (18 months) of patients with large cell lymphoma was significantly shorter than MST (over 96 months) of patients with other intermediate grade lymphomas (small cleaved and mixed) (p < 0.001) and had no significant difference from MST (9 months) of patients with high grade lymphomas. If patients were irradiated with more than 40 Gy, higher doses and different modes of irradiation brought no further survival advantage. Chemotherapy was performed in 87 of 144 irradiated patients (60.4%). No regimens were effective in prolonging survival. Of 144 irradiated patients, a complete or partial response to initial treatment was demonstrated in 91 (63.2%) and 43 patients (29.9%), respectively. Improvement in performance status was confirmed in 82 patients (57.0%). Despite a good response to initial treatments, 88 out of 144 evaluatble patients have died of PCNSL (MST: 19 months). Multivariate analysis based on the Cox hazard model revealed that histology of tumor, age at onset, performance status, and radiotherapy were prognostic factors. Neither chemotherapy nor mode of surgery was a beneficial factor.

Adolescent↗
PubMed1994

Spontaneous passage of a colon cast in the absence of abdominal aneurysm.

The spontaneous passage of colon cast from a 76-year-old Japanese female patient is reported. Macroscopically, the colon case was shaped like the airbladder of a fish. Histopathologically, the cast consisted of degenerated colonal mucosa, including glands. No inflammatory reaction was apparent. The patient lacked any evidence of abdominal aneurysm. Since there have been only five reported cases of colon cast in the literature, and since in all of those association with abdominal aneurysms was always described, the present study represents the first report demonstrating the formation of a colon cast in the absence of associated abdominal aneurysm. However, the patient was found to exhibit several risk factors for ischemic colitis, such as arteriosclerosis on the wall of the abdominal aorta, chronic constipation, and colonic stenosis. Her colonal mucosal surface, indeed, suggested ischemic colitis. This case report, therefore, indicates that ischemic colitis, due to various causes, may be responsible for the formation of colon casts, and that the presence of an abdominal aneurysm is not necessarily a prerequisite for colon cast formation. This report may contribute to a better understanding of the pathogenesis of colon casts.

Aged↗
PubMed1994

Tissue distribution of histamine N-methyltransferase-like immunoreactivity in rodents.

The rat kidney histamine N-methyltransferase was purified to homogeneity from Escherichia coli transfected with its recombinant cDNA. An antiserum to the enzyme was raised in rabbit by immunization with the purified protein. Western blot analysis of rat tissues with the antiserum revealed a band with identical mobility to that of purified enzyme in the extracts of kidney, jejunum, and brain, where the enzyme activity was detected. The antiserum cross-reacted with a 32K protein in mouse liver, brain, stomach, kidney and lung, and a 33K protein in guinea pig brain, stomach jejunum, spleen, lung, and kidney. The intensity of the staining in western blotting correlated well with the enzyme activity in all the tissues in these three species, suggesting that our antiserum is useful for quantifying histamine N-methyltransferase protein in rodent tissues.

Animals↗
PubMed1994

Effect of prostaglandin E1 on experimental acute hepatic failure in rabbits: prostaglandin E1 prevents the development of multiple-organ failure.

Acute hepatic failure was induced in 50 male rabbits by D-galactosamine HCl (1 g per kg bw), and the effects of prostaglandin E1 on this model were investigated. Twelve hours after the administration of D-galactosamine HCl, a continuous infusion of prostaglandin E1 (2 micrograms.kg-1.h-1 or 20 micrograms.kg-1.h-1) was started. Ten animals in each group were observed until the time of death and mean survival times were compared between the groups. Five animals in each group were used for the determination of regional blood flows and brain water content. After the injections of D-galactosamine HCl, serum aspartate transaminase and alanine transaminase activity rose markedly and prothrombin time was prolonged. The administration of prostaglandin E1 did not affect these levels. However, the survival time in the prostaglandin E1 20 micrograms.kg-1.h-1 group (48.2 +/- 10.4 h) was significantly longer (p < 0.005, p < 0.01) than those in the untreated group (24.9 +/- 5.0 h) and the prostaglandin E1 2 micrograms.kg-1.h-1 group (28.1 +/- 5.8 h). Prostaglandin E1 20 micrograms.kg-1.h-1 inhibited elevations of blood urea nitrogen and creatinine and significantly inhibited the decrease of urine volume and urinary sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗
PubMed1994

Expression and characterization of the bovine histamine H1 receptor in cDNA-transfected C6 astroglioma cells.

Rat C6 astroglioma cells (C6-bH1R cells) expressing cloned bovine histamine H1 receptors were established by transfection with a vector (pEF-BOS-bH1R) which carried a 2.7-kbp EcoRI fragment of the bovine H1 receptor cDNA [Yamashita, M. et al. (1991) Proc. Natl. Acad. Sci. USA 88, 11515-11519]. The cloned bovine H1 receptor in C6-bH1R cells was characterized by three established criteria: the [3H]mepyramine binding assay, the accumulation of inositol phosphates induced by histamine, and histamine-induced elevation of intracellular Ca2+ concentration ([Ca2+]i). The accumulation of inositol phosphates induced by histamine was time- and dose-dependent. The accumulation of inositol trisphosphate was biphasic with a prompt increase to the maximal level, followed by a sustained submaximal level. The histamine-induced accumulation of inositol phosphates was suppressed by phorbol ester, but not by pertussis toxin. Results from the [3H]-mepyramine binding assay and histamine-induced elevation of [Ca2+]i were characteristic of H1 receptors. Several compounds among tricyclic antidepressants, neuroleptics, and serotonin antagonists showed affinities to the cloned bovine H1 receptor with Ki values similar to reported values. Histamine neither induced cAMP accumulation nor attenuated forskolin-induced cAMP accumulation in C6-bH1R cells. C6-bH1R cells are particularly useful for studying the H1 receptor-mediated astroglial cell functions.

Animals↗
PubMed1994

Purification and characterization of diamine oxidase (histaminase) from rat small intestine.

Diamine oxidase (DAO) was purified to homogeneity from rat small intestine, and its biochemical and immunochemical properties were studied. DAO was suggested to be a dimer of a 92 kDa subunit, and its isoelectric point was found to be 6.0. Histamine, putrescine, N tau-methylhistamine, and cadaverine were good substrates, with Km values ranging from 9.4 to 16.0 microM. Spermine and spermidine were not substrates. Both an immunoprecipitation study and Ouchterlony's double diffusion test involving antiserum against the purified DAO showed that the immunological properties of the DAOs from rat small intestine, thymus, and placenta were identical. Among small intestinal DAOs from different species, this antibody reacted to the guinea pig enzyme as strongly as to the rat enzyme, but the reaction was much weaker to the mouse enzyme than to the rat enzyme. The DAOs from rabbit and dog small intestine, pig kidney, and human placenta showed no reactivity toward this antibody.

Amine Oxidase (Copper-Containing)↗
PubMed1994

Interleukin-1 beta inhibits gastric histamine secretion and synthesis in the rat.

Interleukin-1 beta (IL-1 beta) is the most potent inhibitor of gastric acid secretion known at present. Although histamine has been shown to be an important mediator of gastric acid secretion, the effect of IL-1 beta on gastric histamine mobilization has not been studied. In the present study, the effects of IL-1 beta on gastric acid secretion and gastric histamine mobilization were investigated in conscious rats with both gastric and vesical fistulas. IL-1 beta (5 micrograms/kg iv) significantly inhibited basal acid secretion but did not affect basal urinary histamine excretion and fundic histidine decarboxylase (HDC) activity. Gastrin-17-I (1 nmol.kg-1.h-1) caused a marked increase in acid secretion, urinary histamine secretion, and fundic HDC activity. IL-1 beta (5 micrograms/kg iv) completely inhibited gastrin-induced acid secretion and partially inhibited urinary histamine excretion and fundic HDC activity. Pretreatment with indomethacin (10 mg/kg ip) partially reversed the inhibitory effects of IL-1 beta on gastrin-stimulated fundic HDC activity and acid secretion. These findings indicate that IL-1 beta inhibits gastric histamine mobilization through both prostaglandin-dependent and prostaglandin-independent pathways. Furthermore, it is suggested that the inhibitory action of IL-1 beta on gastric acid secretion is mediated by the inhibition of gastric histamine mobilization.

Animals↗
PubMed1994

Physical exercise increases bone mineral density in postmenopausal women.

To examine whether physical exercise is beneficial in preventing postmenopausal osteoporosis, we measured bone mineral density (BMD) in three distinct groups of healthy postmenopausal Japanese women aged 49-61 yrs: 11 volleyball players (V) and 5 joggers (J), and 9 controls (C) who had not been participating in regular physical activity. BMD was measured at the lumbar spine (L2-L4) and proximal femur using dual energy X-ray absorptiometry, and at the radius using single X-ray photon absorptiometry. Serum levels of estradiol (E2), parathyroid hormone (PTH) and calcitonin were also measured by radioimmunoassay. Osteocalcin was determined by enzyme immunoassay. BMD in the lumbar spine was greater in the V and J groups than in the C group (P < 0.01). The J group had a significantly lower PTH level than the C group. In contrast to weight-bearing bones, we found no significant differences in BMD at the radius among the three groups. BMD at the distal radius was negatively correlated with years after menopause in both the V group and the J group significantly. These results indicate that regular physical exercise has a positive effect on the maintenance of bone mineral in postmenopausal women and that the protective action is localized in skeletal sites used predominantly for the sport without opposing the negative regulation caused by estrogen deficiency in systemic bones.

Aged↗
PubMed1994

[Interferon treatment for chronic hepatitis C].

To determine the factors influencing the response to interferon (IFN) therapy, we studied 156 patients with chronic hepatitis C who underwent IFN alpha treatment Either 9MU of recombinant IFN alpha 2a or 3MU of natural IFN alpha was administered daily for 2 weeks and then three times a week for 22 weeks. IFN responses were divided into three types on the basis of the results of the polymerase chain reaction (PCR) assay detecting the 5 noncoding regions of HCV in sera. A complete response (CR) was defined as sustained elimination of HCV for at least 6 months after treatment, partial response (PR) as HCV elimination for a limited period, no response (NR) as continuously HCV-RNA positive. HCV genotyping was done by PCR with genotype-specific primers, by analyzing the variations in nucleotide sequence within the core region of HCV, namely HCV-I, -II, -III and -IV. Quantitation of serum HCV-RNA was performed by competitive PCR assay using synthetic mutant RNA. CR was obtained in 43 patients, PR in 64, and NR in 49. The IFN responses, CR/PR/NR, were 7/10/3 in 20 patients with chronic persistent hepatitis histologically, 34/38/24 in 96 patients with chronic active hepatitis (CAH)2A, and 2/16/22 in 40 with CAH2B. Median values of pretreatment serum HCV-RNA amount (copies/ml) in CR, PR, and NR groups were 10(3.55), 10(4.56) and 10(5.97), respectively. On HCV genotyping of sera from 114 patients, HCV-I, -II, -III, -IV and mixed (II+of) were seen in 1, 94, 11, 6 and 2 patients, respectively. CR/PR/NR in patients infected with HCV-I, -II, -III, -IV and -II + IV were 0/0/1, 28/26/40, 3/5/3, 1/3/2 and 0/1/1, respectively. Patients who had low viremia levels were likely to show good IFN responses, and those who had progressed liver histologies were resistant to IFN therapy.

Chronic Disease↗
PubMed1994

Does the [3H]mepyramine binding site represent the histamine H1 receptor? Re-examination of the histamine H1 receptor with quinine.

Mepyramine is a potent H1 receptor antagonist, and [3H]mepyramine generally is used to label histamine H1 receptors. However, we found that [3H]mepyramine labeled not only the H1 receptor but also a [3H]mepyramine binding protein (MBP) in the liver, which protein appears to be related to the subfamily of debrisoquine 4-hydroxylase (cytochrome P450IID) isozymes. The binding of [3H]mepyramine to the cloned H1 receptor was not affected by 1 microM quinine, an inhibitor of debrisoquine 4-hydroxylase. On the other hand, the binding to MBP in the liver membranes was completely inhibited by 1 microM quinine. These data indicate that the labeling by [3H]mepyramine of H1 receptors and MBP can be completely separated with 1 microM quinine. The majority of [3H] mepyramine binding sites in the cerebral cortex, thalamus and hypothalamus, hippocampus, heart, aorta, lung and spleen were H1 receptors. On the other hand, almost all [3H]mepyramine binding sites in the liver and kidney were MBP. Both H1 receptors and MBP were expressed in the stomach, ileum, cerebellum and adrenal gland. Kd values of [3H]mepyramine for membranes from the cerebellum and stomach in the presence of quinine, which tissues contain both H1 receptors and MBP, approached that value of the cloned H1 receptor. The improved [3H]mepyramine binding assay using quinine is a precise method to characterize H1 receptors by the separate determination of H1 receptors and MBP.

Animals↗
PubMed1994

Effect of alcohol on the endotoxin binding protein produced in the liver.

The Kupffer cell-hepatocyte interaction in the process of endotoxin clearance and the effect of alcohol on it were investigated in a newly developed rat Kupffer cell-hepatocyte culture system. The hepatic production of endotoxin binding protein was increased when the Kupffer cells were preincubated in the medium containing ethanol, and the resultant culture supernatant was added to the hepatocyte culture system. The amount of endotoxin binding protein produced by the hepatocytes was increased as the ethanol concentration in the culture medium of Kupffer cells was increased. This endotoxin binding protein was proved to enhance the uptake of endotoxin and suppressed the production of tumor necrosis factor in the Kupffer cells. When Kupffer cells and hepatocytes were isolated from chronically alcohol-fed rats, further addition of ethanol to the culture medium of Kupffer cells did not affect the hepatic production of endotoxin binding protein. The increase in hepatic production of endotoxin binding protein may serve as a defence mechanism against endotoxicity. There is a possibility that an impairment of the defence mechanism has a pivotal role in the development of endotoxemia and endotoxicity in chronic alcoholics.

Animals↗
PubMed1993

Emetic effects of anticancer drugs and involvement of visceral afferent fibers and 5-HT3 receptors in dogs.

The emetic effects of five anticancer drugs, cyclophosphamide, nitrogen mustard-N-oxide, actinomycin D, 5-fluorouracil and L-asparaginase, and the effects of bilateral abdominal vagotomy and bilateral greater splanchnic nerve section or a 5-HT3 receptor antagonist on the emesis induced by these drugs were investigated in dogs. Cyclophosphamide (20 mg/kg, i.v.), nitrogen mustard-N-oxide (5 mg/kg, i.v.) and actinomycin D (50 micrograms/kg, i.v.) caused vomiting in dogs with a long latency period. 5-Fluorouracil (5 mg/kg, i.v.) and L-asparaginase (2000 K.U./kg, i.v.) failed to induce vomiting. Bilateral abdominal vagotomy and bilateral greater splanchnic nerve section completely inhibited the vomiting induced by the former three anticancer drugs. Furthermore, the vomiting was inhibited completely by intravenous administration of ICS205930 (2 x 0.1 mg/kg), a 5-HT3 receptor antagonist. These results suggest that activation of visceral afferents through 5-HT3 receptors mediates the vomiting induced by cyclophosphamide, nitrogen mustard-N-oxide and actinomycin D.

Animals↗
PubMed1993

Somatostatin inhibits gastrin-induced histamine secretion and synthesis in the rat.

Somatostatin is a potent inhibitor of gastric acid secretion. However, the effect of somatostatin on gastric histamine secretion and synthesis has not been well understood, despite the fact that histamine plays a key role in the regulation of gastric acid secretion. This study was designed to determine the effect of somatostatin on gastric histamine mobilization and acid secretion in conscious rats. In conscious rats with a gastric fistula, a 4 h intravenous infusion of gastrin-17 I (1 nmol/kg/h) evoked a marked increase in fundic histidine decarboxylase activity (the sole histamine-forming enzyme) and reduced fundic histamine content with a concomitant increase in gastric acid secretion. Somatostatin-14 (10 nmol/kg/h) significantly inhibited gastrin-induced gastric acid secretion and fundic histidine decarboxylase activity and prevented a gastrin-induced decrease in fundic histamine content. In conscious rats with a vesical fistula, somatostatin-14 (10 nmol/kg/h) significantly inhibited the urinary histamine excretion induced by a gastrin-17 I (1 nmol/kg/h) infusion. These findings suggest that the inhibitory action of somatostatin on gastrin-induced acid secretion is mediated by the inhibition of histamine mobilization.

Animals↗
PubMed1993

Involvement of 5-HT3 receptors and vagal afferents in copper sulfate- and cisplatin-induced emesis in monkeys.

The emetic effects of copper sulfate and cisplatin and the potential involvement of vagal afferent fibers and 5-HT3 receptors in the emesis were investigated in cynomolgus monkeys. Retching and vomiting induced by both oral (100 mg/kg) and intravenous (20 mg/kg) copper sulfate were inhibited markedly by abdominal vagotomy. Furthermore, the emetic response induced by oral copper sulfate was strongly inhibited by intravenous ICS 205-930 (0.1 mg/kg), a 5-HT3 receptor antagonist. Cisplatin (3 mg/kg, i.v.) caused severe retching and vomiting, and the number of emetic responses was much greater than that in other species. The emetic response induced by cisplatin was inhibited markedly by abdominal vagotomy or concurrent administration of ICS 205-930 (3 x 0.1 mg/kg, i.v.). These results suggest that the monkey is more sensitive to cisplatin than other species and that the vagal afferent terminals and 5-HT3 receptors play an important role in the emetic response induced by copper sulfate and cisplatin.

Administration, Oral↗