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K Tanigawa

Publications and source records attributed to K Tanigawa.

At least 37 records · Page 2Linked to original sources
PubMed2000

Characterization of bovine and human lactoferrins as glycyrrhizin-binding proteins and their phosphorylation in vitro by casein kinase II.

The binding ability of bovine and human lactoferrins (bLF and hLF; LFs) to a glycyrrhizin (GL)-affinity column and their phosphorylation by casein kinase II (CK-II) in vitro were biochemically investigated. It was found that (i) both bLF and hLF are GL-binding proteins; (ii) purified both proteins function as phosphate acceptors of CK-II; and (iii) this phosphorylation is completely inhibited by two polyphenol-containing anti-oxidant compounds (quercetin and epigallocatechin gallate) at I microm, whereas a glycyrrhetinic acid derivative (oGA) inhibits it at one tenth the concentration of GL. The DNA-binding affinity of hLF was reduced by GL in a dose dependent manner. However, no significant effect of the CK-II-mediated hLF phosphorylation on its DNA-binding affinity was detected. These results suggest that the GL-induced inhibition of the DNA-binding affinity and the CK-II-mediated phosphorylation of hLF may be closely correlated with the anti-inflammatory effect of GL in the human body.

Animals↗
PubMed2000

Effect of epinephrine on GLUT2 protein content in mouse liver.

The intraperitoneal administration of epinephrine (EP) to mice caused a significant increase in the blood glucose level and a significant decrease in the liver glycogen content 1 h after its administration at 0.6 mg/kg (blood glucose; p < 0.01, liver glycogen; p < 0.01). The liver type glucose transporter (GLUT2) mRNA expression and protein content from mouse liver significantly increased in the intraperitoneally EP-treated mice when compared to that in normal mice (mRNA; p < 0.01, protein; p < 0.01). These results suggest that the hyperglycemic effect of EP is due, at least in part, to the increase of GLUT2 protein synthesis.

Animals↗
PubMed2000

Biochemical characterization of bovine lactoferrin as a glycyrrhizin-binding protein in vitro.

Lactoferrin (LF) from bovine colostrum was biochemically characterized as a glycyrrhizin (GL)-binding protein (gbP) in vitro. It was found that (i) bovine LF (bLF) and a synthetic bovine lactoferricin (bLFcin, the N'-terminal region of bLF at the positions 17--41) had a high affinity to a GL-affinity column; (ii) approximately 1.8 moles of GL were bound to a molecule of bLF with a binding constant of approx. 1.20x10(4) M(-1) at pH 6.8; and (iii) GL, but not glycyrrhetinic acid (GA), induced a conformational change of bLF. In addition, the glucuronic acid moiety of the GL molecule was found to be responsible for binding to bLF, because (i) no binding of GA and two glucoses-GA (Glc-Glc-GA) to bLF was detected; and (ii) a synthetic fluorinated GL (GlcA-GlcF-GA) and mono-glucuronyl-GA (mono-GlcA-GA) were bound significantly to bLF. A similar binding of GL to human LF (hLF) was also observed under the same experimental conditions. Data provided here suggest that (i) bLF contains plural GL-binding sites; and (ii) the specific binding of GL to bLF may modulate the physiological activity of bLF in vivo.

Amino Acid Sequence↗
PubMed2000

Expression and characterization of human rheumatoid factor single-chain Fv.

The variable region of heavy chain [V(H)] of human rheumatoid factor (hRF) IgM was connected with the variable region of light chain [V(L)] with the peptide-linker (GGGSGGGSGGGS) by genetic engineering method and the single-chain Fv (scFv) was expressed in E. coli. On design, scFv and scFv (tag) were planned; the latter had a detection marker at the carboxyl-terminal. These scFvs were expressed as inclusion bodies in E. coli, purified in the presence of 8 M urea by gel filtration and renatured to the active form in vitro. As a control, the Fv, non-covalently associated V(H) and V(L) fragments, was also constructed. The 3 derivatives showed almost the same binding activity to rabbit-IgG to which hRF is cross-reactive. ScFv (tag) was the most stable against urea among the 3 derivatives.

Amino Acid Sequence↗
PubMed2000

Impairment of glucokinase translocation in cultured hepatocytes from OLETF and GK rats, animal models of type 2 diabetes.

We examined sugar-induced translocation of glucokinase in cultured hepatocytes from Otsuka Long-Evans Tokushima Fatty and Goto-Kakizaki rats, animal models of type 2 diabetes, and compared this with that in Long-Evans Tokushima Otsuka and Wistar rats, respectively, as control strains. When hepatocytes from the four strains were incubated with 5 mM glucose, glucokinase was present predominantly in the nuclei. Higher concentrations of glucose, 5 mM glucose plus 1 mM fructose, and 5 mM glucose plus 1 mM sorbitol all induced the translocation of glucokinase from the nucleus to the cytoplasm in hepatocytes from these rats. The extent of glucokinase translocation under these conditions, however, was less marked in both diabetic rat types than in the control rats. The extent of the phosphorylation of glucose as estimated by the release of 3H2O from [2- 3H] glucose is significantly lower in Goto-Kakizaki rats than in Wistar rats. The results indicate that the translocation of glucokinase is impaired in the hepatocytes of diabetic rats. They also suggest that the impaired translocation of glucokinase is associated with abnormal hepatic glucose metabolism in type 2 diabetes.

Animals↗
PubMed2000

[Modified Jekler and Lhotka operation in minimized laparotomy for achalasia].

The rationale for surgery in achalasia is to reduce lower esophageal sphincter (LES) pressure and recontruct an antireflux mechanism. Fundopexy as an antireflux procedure after LES myotomy (modified Heller myotomy), called the Jekler and Lhotka method or the Heller and Dor operation, is commonly performed as standard surgery. In our institution, this method has been used since 1982. We have performed the modified Jekler and Lhotha method including long myotomy to confirm complete reduction of LES pressure as measured by intraoperative manometry and fundopexy plus posterior wall fixation to contract the long abdominal esophagus since 1986. Satisfactory results with this procedure have been obtained and reported. Furthermore, we have recently performed this procedure with minilaparotomy. In this review, we describe the modified Jekler and Lhotha method in minimized laparotomy and evaluate this procedure using intraoperative manometry.

Esophageal Achalasia↗
PubMed1999

Effect of extract prepared from the roots of Paeonia lactiflora on endothelium-dependent relaxation and antioxidant enzyme activity in rats administered high-fat diet.

This study examined the effect of Paeoniae Radix (PR) on endothelial function and the activity of superoxide dismutase (SOD) of erythrocytes in rats administered a high-fat diet. Administration of the extract of PR increased the endothelium-dependent relaxation and the activities of SOD compared with high the cholesterol diet group significantly. Hypercholesterolaemia induced an increase of endothelial superoxide anion and endothelial dysfunction. Paeoniae Radix is suggested to have a protective effect on endothelial cells and their function.

Animals↗
PubMed1999

The role of the spleen, especially regarding changes in both thromboxane A2 and the remnant liver dysfunction after extensive hepatectomy.

The plasma levels of thromboxane B2 (TxB2) and 6-keto-prostaglandin F1alpha (6-KF) in the peripheral and portal blood increase after an extensive hepatectomy, and even more so in cases with complications. In this cell biological study, we estimated the prostanoids in the portal system to clarify which organ produces them, while also evaluating the effect of a splenectomy in conjunction with an extensive hepatectomy. Our results showed that the level of TxB2 in the splenic vein was significantly higher than that in the mesenteric vein. Furthermore, the TxA2 produced by splenic macrophages after an extensive hepatectomy was significantly more than after a sham operation. We also observed the hepatocyte damage to be less in the group that underwent an 84% hepatectomy and splenectomy than in the group that underwent the same hepatectomy without a splenectomy. It therefore appears important both to suppress the splenic macrophages from producing TxA2 and to prevent remnant hepatic dysfunction after an extensive hepatectomy.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Insulin secretion and biosynthesis by the perfused pancreas of spontaneously hypertensive rats.

Insulin secretory activity was compared in the spontaneously hypertensive rat (SHR) versus the normotensive Wistar-Kyoto (WKY) rat and Wistar rat. When the isolated pancreas was perfused with 16.7 mmol/L glucose, insulin release was significantly greater in the SHR versus the other groups. On the other hand, there was no difference in arginine (19 mmol/L)-induced insulin secretion among the three groups. To determine insulin biosynthesis during glucose stimulation, the pancreas was perfused with 16.7 mmol/L glucose for 180 minutes. Insulin secretion was greater in SHR versus WKY and Wistar rats, but the net increase in insulin content was not different between the three groups. These results strongly suggest that in vivo hyperinsulinemia in the SHR is associated with increased in vitro insulin secretion in response to glucose. The mechanisms by which enhanced glucose-induced insulin secretion is linked to hypertension in the SHR remain unclear.

Animals↗
PubMed1999

Effect of pregnancy on insulin metabolism in spontaneously hypertensive rats.

Several lines of evidence suggest that insulin resistance and/or hyperinsulinemia may play an important role in the pathogenesis of hypertension. We studied the effect of pregnancy on insulin metabolism in spontaneously hypertensive rats (SHRs) and in Wistar-Kyoto rats (WKYs) as a control. Pregnancy markedly reduced blood pressure in both strains of rats, but insulin resistance as determined by the hyperinsulinemic glucose clamp (10 mU/kg/min) increased in SHRs and was unchanged in WKYs. The plasma insulin response to an intravenous glucose challenge in SHRs was low and did not change with pregnancy. Therefore, it is suggested that the regulation of blood pressure in these animals is linked to an unknown factor rather than to insulin resistance and hyperinsulinemia. Fetuses from SHRs had a lower body weight and plasma glucose level and higher plasma insulin and pancreatic insulin levels than those from WKYs. Thus, fetal hyperinsulinemia in the SHR may be linked to the development of hypertension in adulthood.

Animals↗
PubMed1999

Nitric oxide metabolism in canine sepsis: relation to regional blood flow.

PURPOSE: To investigate the role of nitric oxide (NO) in early endotoxemia on the systemic and regional blood flow by measuring the plasma nitrite/nitrate (NOx) and blood nitrosyl-hemoglobin (NO-Hb) levels. MATERIALS AND METHODS: This was a prospective, controlled, experimental study conducted in an animal research laboratory on 15 male mongrel dogs. Escherichia coli endotoxin (1 mg/kg) was injected intravenously. RESULTS: Hepatic, renal, and iliac blood flow and cardiac output (CO) were measured before and 15, 30, 45, 90 and 180 minutes after injection of Escherichia coli endotoxin (1 mg/kg) (n = 6). NOx efflux from the organs was calculated by measuring plasma NOx levels. The arterial blood levels of NO-Hb were also measured (n = 4). As control studies, blood samples from dogs (n = 5) without exposure to endotoxin were assayed at 180 minutes for NOx and NO-Hb. Following endotoxin injection, mean arterial pressure decreased and reached its lowest value at 90 minutes (baseline vs. 90 minutes: 119.1+/-5.8 vs. 82.5+/-16.7 mm Hg, P<.0001). Hepatic artery blood flow increased significantly (baseline vs. 180 minutes: 23.6+/-12.0 vs. 170.0+/-68.4 mL/ min, P<.0001). There were no significant changes in plasma levels of NOx, uptake or release of NOx across the measured vascular beds, NO-Hb levels at any time point. In the portal system, the portal vein flow correlated with NOx release (R = 0.69, P<.0001). CONCLUSION: In the early phase of endotoxemia in the dog, the significant reduction in systemic vascular resistance and hepatic arterial resistance are not associated with any measurable NOx release in the systemic circulation or the liver.

Animals↗
PubMed1999

Mild therapeutic hypothermia for postischemic vasoconstriction in the perfused rat liver.

BACKGROUND: Mild hypothermia, a promising therapy being evaluated for various clinical situations, may suppress the formation of reactive oxygen species during reperfusion and may ameliorate microcirculatory perfusion failure (the "no-reflow phenomenon"). METHODS: Isolated rat livers underwent 30 min of perfusion, 2.5 h of ischemia, and 3 h of reperfusion. The temperature was maintained at 34 degrees C (mild hypothermia, n = 5) or 38 degrees C (normothermia, n = 6) for all three periods by perfusion of a modified Krebs Henseleit solution, air surface cooling, or both. A third group of livers was normothermic before and during ischemia and mildly hypothermic during reperfusion (reperfusion hypothermia, n = 6). Control livers had 3 h of perfusion at normothermia. Chemiluminescence (a measure of the generation of reactive oxygen species) and hepatic vascular resistance were monitored simultaneously to evaluate the effect of temperature on the formation of reactive oxygen species and the development of no reflow. Also measured were thiobarbituric acid reactive species and lactate dehydrogenase, as indicators of oxidative stress and cell injury. RESULTS: Mild hypothermia decreased formation of reactive oxygen species and postischemic increases in vascular resistance. Reperfusion hypothermia also decreased postischemic increases in vascular resistance, but not as effectively as did mild hypothermia. Levels of thiobarbituric acid reactive species were lower for reperfusion hypothermia than for mild hypothermia at only 0 and 30 min of reperfusion. Lactate dehydrogenase was significant only at 0 min of reperfusion for the normothermic group. Oxygen consumption did not change. CONCLUSION: The prevention of hepatic vascular injury by suppression of oxidative stress may be an important protective mechanism of mild hypothermia.

Animals↗
PubMed1999

Fasting augments lipid peroxidation during reperfusion after ischemia in the perfused rat liver.

OBJECTIVE: To test the hypothesis that fasting would aggravate postischemic lipid peroxidation in a perfused rat liver model. DESIGN: Prospective, randomized study in a rat perfused liver model. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Livers isolated from fed and fasted male Sprague-Dawley rats (n = 16) were exposed to 2.5 hrs of normothermic (38 degrees C) ischemia followed by 2 hrs of reperfusion. MEASUREMENTS AND MAIN RESULTS: Lipid peroxidation was measured by chemiluminescence and thiobarbituric acid reactive substances (TBARS). Injury parameters, potassium, lactate dehydrogenase efflux, and oxygen extraction were measured every 30 mins. Chemiluminescence and TBARS were greater in the fasted ischemic group during reperfusion. (fasted vs. fed: chemiluminescence, 946.8+/-205.5 [SEM] vs. 98.1+/-8.2 counts per second, p = .0004; thiobarbituric acid reactive substances, 1.11+/-0.25 vs. 0.21+/-0.032 nM/g of liver wt/min, p = .0019). Potassium efflux in the fasted group was greater than in the fed group. (1.568+/-0.082 vs. 1.28+/-0.079 microEq/g liver weight/min, p = .0184). Fasted livers extracted less oxygen after ischemia (1.94+/-0.22 vs. 1.14+/-0.46 microM/g liver wt/min, p = .0048). Lactate dehydrogenase levels showed no significant differences. CONCLUSION: Fasting augmented lipid peroxidation markedly. Nutrition may be an important mechanism that protects organs from oxidative injury.

Animals↗
PubMed1999

A new Ca-antagonist, azelnidipine, reduced blood pressure during exercise without augmentation of sympathetic nervous system in essential hypertension: a randomized, double-blind, placebo-controlled trial.

This study was carried out to evaluate the effect of a new long-acting calcium-channel antagonist, azelnidipine, on hemodynamic and neural responses to exercise. Ten patients (age, 36-69 years) with mild essential hypertension were enrolled in this study. A randomized, double-blind, crossover treatment of azelnidipine at a dose of 8.0 mg once daily for 4 weeks was performed. After a 4-week placebo period, the patients exercised in a submaximal test by using an ergometer with azelnidipine or placebo treatment. The changes caused by exercise in arterial blood pressure (BP), heart rate, cardiac output (CO), and systemic vascular resistance were evaluated. In addition, the plasma norepinephrine (NE), epinephrine (E), plasma renin activity, and plasma aldosterone concentration were determined at rest, at peak exercise, and at the recovery period. Both the SBP and diastolic (D) BP were decreased at rest by azelnidipine treatment (from 158 +/- 10/97 +/- 7 to 145 +/- 14/90 +/- 9 mm Hg). Azelnidipine significantly decreased both SBP and DBP during exercise (SBP, F = 6.09, p < 0.05, Fi = 0.612, NS; DBP, F = 17.78, p < 0.001, Fi = 0.298, NS). No significant changes in the resting heart rate and CO were observed, and the exercise-induced increase of these parameters was also not affected by azelnidipine. Azelnidipine produced no significant change of the resting plasma NE and E levels and an exercise-induced increase of plasma NE. In conclusion, these results indicate that azelnidipine, different from another dihydropyridine-type calcium channel antagonists, does not produce any changes in the hemodynamic and neurohumoral response to exercise, and it may be beneficial for patients with mild essential hypertension.

Adult↗
PubMed1999

Effect of Uncariae ramulus et Uncus on endothelium in spontaneously hypertensive rats.

The protective effect of the extract of Uncariae ramulus et Uncus (URE) against endothelium disorder due to hypertension was investigated. We administered low (150 mg/kg/day) and high (450 mg/kg/day) doses of URE orally to spontaneously hypertensive rats for 8 weeks. Endothelium dependent vasodilatation by acetylcholine increased significantly in the high URE group compared with the control group. Endothelium dependent vasocontraction by xanthine oxidase decreased significantly in the high URE group compared with the control group. Serum NO2-/NO3- were tended to increase in the high URE group. It is suggested that URE may have a protective effect for the endothelium against the influence of hypertension.

Acetylcholine↗
PubMed1999

Mesalazine-induced eosinophilic pneumonia.

A 35-year-old woman with a 6-month history of ulcerative colitis and treatment with oral mesalazine (5-aminosalicylic acid) developed dry cough, low-grade fever and bilaterally wandering pulmonary infiltrates. Improvement in clinical symptoms and radiological abnormalities occurred spontaneously after discontinuation of mesalazine. The transbronchial lung biopsy demonstrated the organizing stage of eosinophilic pneumonia. Drug lymphocyte stimulation test was positive for mesalazine and negative for sulfasalazine and sulfapyridine. The present case indicates that although mesalazine-induced eosinophilic pneumonia is an extremely rare entity, its possibility should be fully considered in patients developing unexplained respiratory symptoms while on mesalazine therapy.

Adult↗
PubMed1999

Construction of the single-chain Fv from 196-14 antibody toward ovarian cancer-associated antigen CA125.

The variable regions of heavy- and light-chains of mouse monoclonal antibody 196-14 toward ovarian cancer-associated antigen CA125 were linked with a peptide linker (GSTSGSGKSSEGKG) and a histidine tag was attached at the carboxyl terminal. This single-chain Fv (scFv) with a histidine tag was expressed in Escherichia coli as an inclusion body. The inclusion body was solubilized with guanidium chloride, followed by purification on nickel nitrilotriacetic acid agarose column and refolding into the active form. The scFv thus obtained bound to the Siso cells, which express CA125, and may recognize the same epitope as the parental 196-14 antibody IgG does.

Animals↗