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K Shiratori

Publications and source records attributed to K Shiratori.

At least 19 recordsLinked to original sources
PubMed1999

Purification, molecular cloning, and genomic organization of human brain long-chain acyl-CoA hydrolase.

An acyl-CoA hydrolase, referred to as hBACH, was purified from human brain cytosol. The enzyme had a molecular mass of 100 kDa and 43-kDa subunits, and was highly active with long-chain acyl-CoAs, e.g. a maximal velocity of 295 micromol/min/mg and K(m) of 6.4 microM for palmitoyl-CoA. Acyl-CoAs with carbon chain lengths of C(8-18) were also good substrates. In human brain cytosol, 85% of palmitoyl-CoA hydrolase activity was titrated by an anti-BACH antibody, which accounted for over 75% of the enzyme activity found in the brain tissue. The cDNA isolated for hBACH, when expressed in Escherichia coli, directed the expression of palmitoyl-CoA hydrolase activity and a 44-kDa protein immunoreactive to the anti-BACH antibody, which in turn neutralized the hydrolase activity. The hBACH cDNA encoded a 338-amino acid sequence which was 95% identical to that of a rat homolog. The hBACH gene spanned about 130 kb and comprised 9 exons, and was mapped to 1p36.2 on the cytogenetic ideogram. These findings indicate that the long-chain acyl-CoA hydrolase present in the brain is well conserved between man and the rat, suggesting a conserved role for this enzyme in the mammalian brain, and enabling genetic studies on the functional analysis of acyl-CoA hydrolase.

Adult↗
PubMed1999

Expression of cholecystokinin in the pancreas during development.

We have reported that cholecystokinin-like immunoreactivity (CCK-LI) and its transcripts are expressed in rat pancreatic islets (Endocrinology 1998;139:389-96). The purpose of this study was to elucidate the ontogeny of CCK during pancreatic development in the rat. Fetal rats from day 13 (E13) to 20 (E20) and postnatal (P) rats from day 1 to adulthood were used in this study. Immunohistochemical studies of rat pancreas were carried out with rabbit antisera against CCK-8 and gastrin-17. The absorption studies were performed by using CCK-8 antiserum incubated with excess CCK-8 or gastrin-17. In situ hybridization was performed to demonstrate the CCK and gastrin transcripts in the pancreas. CCK and gastrin were first detected at E15, and they were distributed in the periphery of the islets in the fetal and neonatal pancreas. The mirror sections for CCK revealed positive cells with characteristics identical to those that stained positive for gastrin. The CCK-LI in early development was completely abolished by preabsorption with excess gastrin but not with CCK-8. These findings indicated that the CCK-LI in the fetal and neonatal pancreas was crossreacting gastrin rather than CCK-8. From weaning (P21) through adulthood, on the other hand, CCK-LI was expressed diffusely in pancreatic islets, but there were no gastrin-positive cells after weaning. In situ hybridization showed that CCK messenger RNA (mRNA) was present in rat pancreatic islets in adults but not in early development. Although CCK-positive cells were not detected in fetal and neonatal pancreatic islets, CCK was expressed in islets during and after weaning through adulthood, indicating that CCK in pancreatic islets might be developmentally regulated.

Animals↗
PubMed1999

Assessment of coronary artery bypass surgery by exercise thallium imaging.

The purpose of this study was to assess the coronary artery bypass grafting (CABG) in exercise thallium-201 scintigraphy. The study was performed on 18 consecutive patients undergoing elective surgery. We compared the results of the scintigraphic examinations, 1 week before and 1 month postoperatively. Of the 47 bypass grafts, 20 (42. 6%) grafts contributed to the improvement of the ischemic areas and 38% of the bypass grafts did not change the scintigraphic patterns after surgery. Some bypass grafts had been performed on the stenotic arteries that dominated the areas which preoperatively showed normal exercise scintigraphic patterns yet were considered to worsen in the near future. Such grafts main contribution may be to protect and to increase the overall myocardial washout ratio for prevention of an enlargement of ischemic areas.

Aged↗
PubMed1998

Evidence for the existence of CCK-producing cells in rat pancreatic islets.

BACKGROUND: Although the existence of cholecystokinin-like immunoreactivity (CCK-LI) in rat pancreas had been reported previously, it was never clearly demonstrated whether CCK is produced in rat pancreatic islets. AIMS: The purpose of this study was to elucidate the source of the CCK-LI, the molecular properties of CCK, and the expression of the CCK gene in islet cells. METHODS: Immunohistochemical studies of rat pancreas were carried out with different rabbit antisera against CCK-8 and CCK-related peptide including N-terminal CCK-33 (1-22) and gastrin-17, and colocalization with known islet hormones including insulin, glucagon, somatostatin, and pancreatic polypeptide was investigated. The major molecular form of CCK in the islets was determined by HPLC. RT-PCR and in situ hybridization were performed to demonstrate the presence of the CCK transcript in the pancreas. RESULTS: CCK-LI was found in the center of the islets, colocalized with insulin in B cells. The major molecular form of CCK in the islets was CCK-8. A 350-nucleotide fragment of PCR-amplified CCK cDNA was detected in the islet as well as the duodenum by RT-PCR. In situ hybridization showed that CCK messenger RNA was located in a large portion of the islets, and this was consistent with the immunohistochemical findings. CONCLUSION: CCK messenger RNA and immunoreactivity are expressed in adult rat pancreatic islets, indicating that CCK-producing cells are present in adult rat islets.

Animals↗
PubMed1998

Lectin-binding patterns in the olfactory epithelium and vomeronasal organ of the common marmoset.

The patterns of expression of sugar residues in the olfactory epithelium and vomeronasal organ of the common marmoset were studied lectin-histochemically. Eight lectins including DBA, BSL-I, RCA-I, s-WGA, PNA, ECL, UEA-I and Con A bound to the free border of the olfactory epithelium, and 6 lectins including DBA, RCA-I, s-WGA, PNA, ECL and UEA-I bound to that of the vomeronasal organ. UEA-I bound to all dendrites of the olfactory receptor cells, and 6 lectins including BSL-I, RCA-I, s-WGA, PNA, ECL and Con A bound to only a part of dendrites of the olfactory receptor cells. ECL and UEA-I bound to all dendrites of the vomeronasal receptor cells, and s-WGA, PNA and Con A bound to only a part of dendrites of the vomeronasal receptor cells. Seven lectins including RCA-I, s-WGA, BSL-II, PNA, ECL, UEA-I and Con A bound to all the olfactory receptor cell bodies, and BSL-I bound to only a part of them. Six lectins including RCA-I, s-WGA, PNA, ECL, UEA-I and Con A bound to all the vomeronasal receptor cell bodies, and BSL-II bound to only a part of them. These results showed that a smaller number of lectins bound to the free border, dendrites and cell bodies of the receptor cells in the vomeronasal organ than those in the olfactory epithelium, suggesting that the vomeronasal organ is less active in some physiological functions with which sugar residues are associated than the olfactory epithelium in the common marmoset.

Animals↗
PubMed1997

Evidence for a significant role of gastrin in cysteamine-induced hypersecretion of gastric acid.

Cysteamine has been known to stimulate gastric acid secretion and to induce duodenal ulcers in rats. We investigated the role of gastrin in cysteamine-induced acid hypersecretion in the perfused rat stomach. Intravenous infusion of cysteamine (75 mg/kg/h) resulted in a significant increase in acid secretion, which was accompanied by a marked increase in the plasma gastrin concentration. The cysteamine-induced increase in gastric acid secretion was completely blocked by i.v. injection of anti-gastrin rabbit serum (500 microliters). In addition, i.v. infusion of a CCK-B/gastrin receptor antagonist (L-365,260) (1 mg/kg/h) also suppressed the cysteamine-induced increase in acid secretion. Atropine significantly, but only partially, inhibited the increase. The elevated plasma gastrin levels induced by cysteamine were unaffected by atropine and L-365,260. In conclusion, cysteamine-induced acid hypersecretion is mediated mainly by cysteamine-induced gastrin release and partially by cholinergic factors. Furthermore, gastrin release caused by cysteamine appears to be independent of cholinergic tone.

Animals↗
PubMed1997

[The mechanisms of the inhibition of gastric acid secretion induced by intraduodenal amino acids in rats].

We investigated the effect of intraduodenal amino acids (AA) on gastric acid secretion and gastrin release, and possible role of endogenous secretin on this phenomenon in vivo in rats. Intraduodenal administration of mixed AA solution (140 mg/hr, pH6.5) resulted in significant inhibition of gastric acid secretion and gastrin release stimulated by intragastric perfusion of peptone (0.5%). Intravenous infusion of secretin (0.05CU/kg/hr) also inhibited peptone-stimulated gastric acid secretion and gastrin release. Furthermore, the AA-induced suppression of gastric acid secretion was significantly blocked by intravenous injection of rabbit anti-secretin serum. In conclusion, intraduodenal AA inhibit peptone-stimulated gastric acid secretion and gastrin release, and endogenous secretin released by AA is attributed to this suppression. Thus, the result of this study indicates that intestinal AA regulate gastric secretory function mediated by AA-released endogenous secretin in the intestinal phase.

Amino Acids↗
PubMed1996

Duration of anti-cholecystokinin (CCK) action on the rat exocrine pancreas of new CCK receptor antagonist FK480 administered orally.

We assessed the duration of the anti-cholecystokinin (CCK) action of FK480, a new non-peptide CCK-A receptor antagonist developed in Japan, in an in vivo study in rats, comparing it with CR 1505. Pancreatic exocrine secretion stimulated by intravenous infusion of CCK-8 (0.06 microgram/kg per h) was measured at intervals of 0-24 h after the oral administration of FK480 (1.5 mg/kg) and CR 1505 (30 mg/kg). FK480 significantly inhibited both CCK-stimulated pancreatic juice volume flow and amylase output 0, 4, 8, and 12 h after oral administration, whereas the inhibitory effect of CR 1505 had completely disappeared by 8 h after oral administration. It was concluded that orally administered FK480 has a prolonged anti-CCK action.

Administration, Oral↗
PubMed1996

Bucillamine induced pulmonary injury occurs with immunoglobulin decrease.

We describe pulmonary involvement in 3 patients with rheumatoid arthritis treated with bucillamine. In all 3, synovitis was in remission. The common radiological characteristic was mottled dense infiltrates, in which were air bronchograms, in the bilateral central lung, sparing the periphery. Lung biopsies in 2 cases revealed organizing exudates in the alveolar ducts and alveoli, and cellular infiltration into alveoli and septa. Serum immunoglobulin (Ig) levels decreased markedly at the time of involvement. After discontinuation of bucillamine, lung injury resolved without exacerbation of synovitis and Ig levels increased. A mechanism involving decreased Ig concentration is suggested.

Aged↗
PubMed1995

Pharmacokinetics of single-dose intravenous amikacin in critically ill patients undergoing slow hemodialysis.

OBJECTIVE: The pharmacokinetics of amikacin were studied in patients undergoing slow hemodialysis (HD). DESIGN: Slow HD was performed at the dialysate flow rate of 30 ml/min. After a single intravenous dose of amikacin 5 mg/kg, pharmacokinetic variables were calculated by fitting individual concentration-time curves to a two-compartment open model. PATIENTS: 6 critically ill patients with renal failure were entered into the study. RESULTS: The volume of distribution was 0.35 +/- 0.03 l/kg. Total body clearance was 35.1 +/- 2.3 ml/min with an elimination half-life of 10.5 h. During a 10.5 h session of slow HD, the serum amikacin concentration decreased from the peak level of 21.3 +/- 1.2 mg/l to 7.2 +/- 0.9 mg/l. CONCLUSION: Slow HD eliminate amikacin more efficiently than other types of slowly performed renal replacement therapy and had profound effects on the pharmacokinetics. Amikacin elimination by this approach should be taken into consideration for designing a dosage schedule during the treatment.

Aged↗
PubMed1995

Chronic pancreatitis caused by an autoimmune abnormality. Proposal of the concept of autoimmune pancreatitis.

Several authors have reported a case of chronic pancreatitis associated with Sjögren's syndrome in which an autoimmune mechanism may have been involved in the etiology and in which steroid therapy was effective. We recently encountered a patient with pancreatitis who had hyperglobulinemia, was autoantibody-positive, and responded to steroid therapy. This patient, however, failed to show any evidence of association with Sjögren's syndrome or other collagen diseases. Although the concept of autoimmune hepatitis and the criteria for diagnosing it have been established, autoimmune pancreatitis has not yet been defined as a clinical entity. We report a case of chronic pancreatitis in which an autoimmune mechanism is involved in the etiology and summarize the cases of pancreatitis suspected of being caused by an autoimmune mechanism in the Japanese and English literature.

Aged↗
PubMed1995

Effect of a novel cholecystokinin receptor antagonist, FK480, administered intraduodenally, on pancreatic secretion in rats.

The effect of a new cholecystokinin (CCK)-A receptor antagonist, FK480, developed in Japan, on pancreatic exocrine secretion stimulated by exogenous CCK and intraduodenal casein was investigated in vivo when administered to anesthetized rats intraduodenally, and its CCK antagonistic activity was compared with that of CR 1505. Intraduodenal administration of FK480 at graded doses of 0.0016-1.0 mg/kg-h produced dose-dependent inhibition of pancreatic juice volume and amylase output stimulated by intravenous infusion of CCK-8 at a dose of 0.06 micrograms/kg-h. The half-maximal inhibitory dose (ID50) of FK480 for CCK-8-stimulated amylase secretion was 0.025 mg/kg-h, whereas the ID50 of CR 1505 was 5.2 mg/kg-h, indicating that FK480 is 208 times more potent than CR 1505. Moreover, intraduodenal FK480 (0.2 mg/kg-h) significantly suppressed pancreatic juice volume and amylase output augmented by intraduodenal infusion of casein (400 mg/h). It is concluded that FK480 administered intraduodenally has a significant, potent inhibitory action on the exocrine pancreas stimulated by exogenous CCK and intraduodenal casein.

Amylases↗
PubMed1995

Appropriate intravenous doses of L-thyroxine and magnesium in a thyroidectomized patient with thyroid and parathyroid carcinomas receiving total parenteral nutrition during acute necrotizing pancreatitis.

A totally thyroidectomized patient with thyroid and parathyroid carcinomas, which had developed after neck irradiation in childhood, became hypercalcemic due to pulmonary metastases. The hypercalcemia was ameliorated by intermittent iv administration of bisphosphonate for 3.5 years, but this gradually became refractory to the bisphosphonate treatment. After right thoracotomy for resection of pulmonary metastases, acute necrotizing pancreatitis developed. The patient was therefore placed on total parenteral nutrition supplemented with T4 and a restricted dose of magnesium. Thyroxine(T4) (30 micrograms/day, iv) was not sufficient to maintain euthyroidism, but a higher dose (60 micrograms/day) elicited mild hyperthyroidism to the same extent as that elicited by an oral dose of 100 micrograms/day. The present case showed that the appropriate iv dose of T4 in this thyroidectomized patient with acute pancreatitis was about 60% of the oral dose. Furthermore, bisphosphonates (pamidronate and alendronate) and magnesium depletion were very effective in controlling the hypercalcemia.

Acute Disease↗