Acid-activation of rat prorenin following non-proteolytic alteration.
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Amino Acid Sequence↗
Biomedical subjects
K Takeuchi
Publications and source records attributed to K Takeuchi.
CSF shunt physics: factors influencing inshunt CSF flow.
Cerebrospinal fluid (CSF) in a shunt does not have a constant flow rate. The flow fluctuates from 0.01 ml/min to 1.93 ml/min according to each patient's own daily supine rhythmic pattern. We determined and evaluated the factors influencing CSF flow in a shunt in 19 cases of hydrocephalus. Postural changes, such as head elevation, led to increases by over 0.04 ml/min in inshunt CSF flow, while inshunt CSF flow in the supine position was less than 0.04 ml/min. Respiratory changes, such as coughing and apnea-hyperventilation, also influenced inshunt CSF flow. Changes in intracranial pressure (ICP) corresponded to changes in inshunt CSF flow. Inshunt CSF flows were higher than average during the night, the flows being stimulated by increases in ICP especially during REM sleep.
Adolescent↗
Nucleotide sequence of the gene encoding novel delta-endotoxin from Bacillus thuringiensis serovar japonensis strain Buibui specific to scarabaeid beetles.
A new isolate of Bacillus thuringiensis serovar japonensis strain Buibui, which was specific to scarab beetles (M. Ohba et al., Lett. Appl. Microbiol. 14:54, 1992), was shown to have a 130-kDa insecticidal crystal protein (ICP) (H. Hori et al., J. Appl. Bacteriol. 76:307, 1994). ClaI restriction enzyme fragments of total cell DNA of the isolate were cloned into E. coli (Sato et al., Curr. Microbiol. 28:15, 1994). Whole 3480-bp nucleotide sequence of the gene encoding 130-kDa ICP was determined, and the molecular weight of the ICP was estimated to be 130,424. The strongly conserved five blocks that occur in almost all ICP genes of B. thuringiensis were detected in the ORF with the same order and almost the same intervals as elsewhere. The amino acid sequence homologies of the whole ICP or N-terminus half portion to that of the CryIIIA, B, C, D, and CryV were about 35%.
Amino Acid Sequence↗
Cine magnetic resonance imaging of aqueductal stenosis.
Cerebral aqueductal stenosis is one of the most common causes of congenital and acquired hydrocephalus, but the etiology, pathophysiology and cerebrospinal fluid (CSF) dynamics of aqueductal stenosis have yet to be clarified. Utilizing cardiac gated cine magnetic resonance (MR) imaging, we evaluated aqueductal configuration and pulsatile motion of brain and CSF flow stimulated by cardiac pulsation in five patients with non-tumoral aqueductal stenosis. Cine MR of four cases revealed obliteration of the aqueduct by thickening mesencephalic tectum, turbulent CSF flow in the III ventricle, and absence of flow-related signal void, which in all normal cases indicates CSF movement within the aqueduct. In the remaining fifth case, with proximal dilation of the aqueduct resulting from thinning of the tectum, distortion of caudal (distal) tectum related to pulsatile motion of the brain caused funnel-like narrowing of the aqueduct, leading to incomplete obstruction and the absence of upward CSF flow during diastole.
Adult↗
Comparison of the entire nucleotide and deduced amino acid sequences of the attenuated hog cholera vaccine strain GPE- and the wild-type parental strain ALD.
We have determined the complete nucleotide sequences of a live attenuated hog cholera virus (HCV) and its progenitor strain. The viral RNA of each strain consisted of 12,298 nucleotides including untranslated regions of 373 and 228 bases at the 5' and 3' end, respectively. There was a single large open reading frame spanning 11,697 nucleotides which could encode a large protein of 3,899 amino acids with a calculated molecular weight of 438-kDa. We have found 225 nucleotide difference between the two strains, of which six were located in the untranslated region. Four-sixths of these differences resulted in amino acid substitutions.
Amino Acid Sequence↗
Effects of nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester on duodenal alkaline secretory and ulcerogenic responses induced by mepirizole in rats.
The inhibition of nitric oxide (NO) production by NO synthase inhibitors stimulates HCO3- secretion in the rat duodenal mucosa. Therefore, we examined the effects of NG-nitro-L-arginine methyl ester (L-NAME, the NO synthase inhibitor) and nitroprusside (the exogenous NO donor) on the duodenal HCO3- and ulcerogenic responses in anesthetized rats. Animals were administered mepirizole (200 mg/kg, subcutaneously) for induction of duodenal ulcers, and gastric acid and duodenal HCO3- secretions were measured with or without pretreatment with L-NAME (5 mg/kg, intravenously) or nitroprusside (4 mg/kg, intravenously). Mepirizole increased acid secretion, decreased the acid-induced duodenal HCO3- secretion, and induced hemorrhagic lesions in the proximal duodenum. The inhibition of NO production by L-NAME potentiated the acid secretory response, increased the duodenal HCO3- secretion, and prevented the duodenal lesions, and these changes were all antagonized by simultaneous administration of L-arginine (200 mg/kg, intravenously) but not D-arginine. On the other hand, nitroprusside slightly reduced the acid response but further decreased the HCO3- output, resulting in aggravation of duodenal lesions induced by mepirizole. These data suggest that the inhibition of endogenous NO production by the NO synthase inhibitor L-NAME increases duodenal HCO3- secretion and protects the duodenal mucosa against acid injury.
Animals↗
Mechanism of gastric alkaline response in the stomach after damage. Roles of nitric oxide and prostaglandins.
The gastric mucosa responds to hypertonic NaCl by significantly decreasing acid secretion. We examined the role of nitric oxide (NO) in this phenomenon in comparison with endogenous prostaglandins (PGs). A rat stomach was mounted in an ex vivo chamber, perfused with saline, and the potential difference (PD), pH, and acid/alkaline responses were measured before and after the application of hypertonic NaCl (1 mol/liter) with or without pretreatment with NG-nitro-L-arginine methyl ester (L-NAME; an inhibitor of NO biosynthesis) or indomethacin (a cyclooxygenase inhibitor). NaCl at 1 M caused a PD reduction, a decrease in acid secretion, and an increase in luminal HCO3-. Prior administration of L-NAME (5 mg/kg, intravenously) as well as indomethacin (5 mg/kg, subcutaneously) did not affect PD and HCO3- responses, but significantly attenuated the inhibitory effect of 1 M NaCl on acid secretion, although the effect of L-NAME was more potent when compared to indomethacin. This effect of L-NAME was antagonized by the simultaneous administration of L-arginine but not by D-arginine (200 mg/kg, intravenously), whereas the effect of indomethacin was completely reversed by PGE2 (100 micrograms/kg, intravenously). The histamine-stimulated acid secretion in the normal stomach was significantly decreased by nitroprusside (the exogenous NO donor; 4 mg/kg, intravenously) and PGE2, but not by either L-NAME or indomethacin. These results suggest that in addition to PGs, NO is involved in the mechanism of the gastric alkaline response after damage with 1 M NaCl. Irritation of the gastric mucosa by hypertonic NaCl may release endogenous NO and PGs, both of which in turn inhibit acid secretion and unmask luminal alkalinization due to HCO3- flux in the damaged portion.
Animals↗
Irritant and protective action of urea-urease ammonia in rat gastric mucosa. Different effects of ammonia and ammonium ion.
The effects of urea-urease-ammonia on the rat gastric mucosa were examined and compared with those of NH4OH and NH4Cl. The mucosal application of urea with urease produced a reduction in potential difference (PD) in a dose-related manner for urea, and a significant drop was observed by > 0.1% urea in the presence of 100 units urease. Such PD reduction was also observed when the mucosa was exposed to either NH4OH (> 0.03%) or NH4Cl (> 1%); delta PD (20 mV) caused by 0.3% NH4OH and 3% NH4Cl was equivalent to that induced by 0.5% urea+urease (100 units). The combined oral administration of urea (approximately 6%) and urease (100 units) did not induce any macroscopic damage in the gastric mucosa. NH4Cl given orally had no or little effect on the mucosa at any dose levels even at 10%, while NH4OH given orally caused hemorrhagic lesions in the mucosa at the dose of > 0.3%. In contrast, both urea+urease and NH4Cl given prior to HCl/ethanol protected the gastric mucosa against damage in a dose-related manner, and a significant effect was obtained by urea at > 0.5% and by NH4Cl at > 1%. NH4OH was also effective in reducing the severity of HCl/ethanol-induced gastric lesions at lower dose (0.3%). The protective effect of urea+urease was attenuated significantly by prior administration of indomethacin or coadministration of hydroxyurea, while that of NH4Cl or NH4OH was mitigated by indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)
Ammonia↗
Protein kinase C activation in the heart: effects on calcium and contractile proteins.
BACKGROUND: Cardiac contractile function is dependent on the energetic state of the heart, intracellular calcium levels, and the interaction of the contractile proteins with both adenosine triphosphate and calcium. Protein kinase C (PKC) is a ubiquitous intracellular mediator that has been found in the heart and has been shown to phosphorylate proteins that regulate calcium homeostasis (calcium channels) and the contractile proteins themselves (troponin I and troponin T). METHODS: To determine the role of PKC activation on cardiac contractile function, direct activation of PKC was achieved by the infusion of phorbol 12-myristate 13-acetate, an activating phorbol ester. The effects of PKC activation were evaluated in Langendorff-perfused rabbit hearts. Contractile function, high-energy phosphate content (phosphorous-31 nuclear magnetic resonance spectroscopy), oxygen consumption, and intracellular calcium levels (calcium fluorescent dye Rhod-2) were determined. RESULTS: Activation of PKC in the heart by phorbol 12-myristate 13-acetate resulted in a significant decrease in both systolic and diastolic function while oxygen consumption and adenosine triphosphate production remained unchanged. Both baseline and peak intracellular calcium levels decreased, which may contribute to the impaired systolic function. CONCLUSIONS: Activation of PKC in the heart leads to significant loss of contractile function without affecting energetics. The effect is most likely due to alteration in cytosolic calcium regulation and altered contractile sensitivity to calcium.
Adenosine Triphosphate↗
Body stalk anomaly: prenatal diagnosis.
Body stalk anomaly is a severe body wall defect, with maldevelopment of the hindgut and the presence of a very rudimentary umbilical cord. A case of prenatally-diagnosed body stalk anomaly is presented along with the discussion of the prenatal diagnosis and its management. Autopsy of the fetus showed abnormalities compatible with the maldevelopment of embryonic body folding. Prenatal ultrasonographic diagnosis of body stalk anomaly would permit the early termination of pregnancy or avoidance of surgical intervention.
Abdominal Muscles↗
Bilateral tubal pregnancy treated with laparoscopy.
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Adult↗
Inhibition by angiotensin II type 1 receptor antagonist of cardiac phenotypic modulation after myocardial infarction.
The purpose of this study was to examine the cardiac phenotype and remodeling after myocardial infarction and the effect of the angiotensin II type 1 (AT1) receptor antagonist (TCV-116) on the gene expression. Myocardial infarction in rats was produced by ligation of the coronary artery. TCV-116 (10 mg/kg/day) was administered orally to rats from 1 day after myocardial infarction. At 1, 2 and 3 weeks after myocardial infarction, blood pressure and heart rate were measured, and the heart was removed. The left ventricle was measured for infarct size and weight, and then the total RNA from the non-ischemic left ventricle was extracted. mRNAs in the non-ischemic left ventricle were measured by Northern blot analysis. The weight of the non-ischemic left ventricle was significantly increased 3 weeks after infarction. This was completely prevented by TCV-116 treatment. mRNA levels for beta-myosin heavy chain (beta-MHC), atrial natriuretic polypeptide (ANP), collagen types I and III and transforming growth factor-beta 1 (TGF-beta 1) in the non-ischemic left ventricle were increased by a factor of 3.0, 6.7, 7.9, 4.0 and 1.4 (P < 0.01), respectively, 1 week after infarction. There was no increase in alpha-skeletal actin mRNA at 1 and 2 weeks, but it was increased by a factor of 2.9 (P < 0.05) at 3 weeks. On the other hand, there was no change in alpha-MHC mRNA during the 3 weeks. TCV-116 significantly suppressed the increased gene expression of beta-MHC and alpha-skeletal actin in the non-ischemic myocardium at all time points, and also suppressed the expression of ANP at 2 and 3 weeks. However, TCV-116 failed to inhibit the expression of collagen I and III mRNAs at 1 and 3 weeks. These results show that myocardial infarction causes a rapid shift of myocytes to fetal phenotype and a rapid activation of collagen genes in the non-ischemic myocardium. AT1 receptor may be responsible for the phenotypic modulation of myocytes following myocardial infarction.
Actins↗
High potassium-evoked release of ATP from rabbit pulmonary artery via endogenous noradrenaline.
1. High potassium 30 mM and noradrenaline at 10 microM significantly evoked the release of ATP and produced remarkable vasoconstriction in the rabbit pulmonary artery. 2. Phentolamine and prazosin at 0.1 microM inhibited ATP release but not vasoconstriction by 30 mM potassium. 3. 30 mM potassium significantly evoked the release of noradrenaline. 4. There was a significant positive correlation between the amounts of release of total purines, sum of ATP, ADP, AMP and adenosine, and noradrenaline evoked by 30 mM potassium. 5. 30 mM potassium-evoked ATP release was significantly reduced by denudation of endothelium.
Adenosine Triphosphate↗
Viremia induced by influenza virus.
A mouse model of influenza A/PR/8 virus infection was adopted to investigate the blood and various tissues of intranasally infected mice for the presence of viral RNA by using the nested polymerase chain reaction. The nucleoprotein gene was detected in the red blood cell fraction from 1 to 5 days post-inoculation, while it was found in the lung and brain up to 14 days and in the liver, spleen, kidney, heart, and skeletal muscle up to 7 days. The virus-specific messenger RNA was transiently found in these organs. When mice received the uv-inactivated virus, viremia did not occur. The prior transfer of the hyperimmune serum prevented pneumonia but not bronchitis, and viremia was totally abolished. These results suggest: (1) viremia occurs during the acute phase of infection, (2) the virus is present in various organs and there the virus gene is transiently expressed, and (3) the virus enters the blood stream possibly through capillaries of the infected alveolar wall. Viremia may influence the pathogenesis of influenza.
Animals↗
Intra-arterial administration of the angiogenesis inhibitor TNP-470 blocks liver metastasis in a rabbit model.
We evaluated the best route of administration of TNP-470, an angiogenesis inhibitor, by comparing the anti-tumour effects and toxicity following injection via the hepatic artery, the portal vein, or the jugular vein in a rabbit model of liver metastases. Following the injections of 1 x 10(6) VX2 carcinoma cells into the portal vein of rabbits, 50 mg of TNP-470 was injected continuously into the hepatic artery, portal vein, or jugular vein for 7 days. The number of tumours on the surface of the liver was counted 14 days following the start of the infusion, and the serum glutamic-oxaloacetic transamine (GOT), glutamic-pyruvic transaminase (GPT) and total bilirubin concentrations were examined. In addition, a coloured silicon rubber was injected into the vessels of the liver to visualise the capillary networks around the tumours and assess the degree of suppression of angiogenesis by TNP-470. The mean number of tumours following intra-arterial injection (17.5 +/- 2.9) was significantly less than the control (237.0 +/- 34.0) (P < 0.05). The mean numbers of the tumours following intraportal (89.1 +/- 16.0) and intravenous (140.6 +/- 31.2) injection were both less than the controls (215.3 +/- 45.5, 284.8 +/- 55.4 respectively), but the differences were not significant. We conclude that intra-arterial injection of TNP-470 is the most effective method for preventing liver metastases in this model.
Animals↗
High glucose augments angiotensin II action by inhibiting NO synthesis in in vitro microperfused rabbit afferent arterioles.
Preglomerular afferent arteriole (Af-Art) is a crucial vascular segment in the control of glomerular hemodynamics. We have recently reported that vascular reactivity of Af-Art is modulated by nitric oxide (NO). However, little is known about its reactivity under pathophysiological conditions such as diabetes, which is often accompanied by abnormal glomerular hemodynamics. In the present study, we examined the direct effects of high glucose, the hallmark of diabetes, on the vascular reactivity of Af-Art. Rabbit Af-Arts were microperfused for three hours with medium 199 containing either normal (5.5 mM; NG-Af-Arts) or high concentrations (30 mM; HG30-Af-Arts) of glucose, and then vascular reactivity was examined. Sensitivity to angiotensin II (Ang II) was significantly higher in HG30-Af-Arts than in NG-Af-Arts. Ang II began to cause significant constriction from 10(-9) M in NG-Af-Arts (18 +/- 3%, N = 6, P < 0.01) and from 10(-11) M in HG30-Af-Arts (9 +/- 2%, N = 6, P < 0.01). NO synthesis inhibition with 10(-4) M nitro-L-arginine methyl ester (L-NAME) increased the sensitivity to Ang II in NG-Af-Arts without affecting Ang II action in HG30-Af-Arts. In L-NAME-pretreated NG-Af-Arts, Ang II began to cause constriction from 10(-11) M (11 +/- 3%, N = 6, P < 0.01). Thus, pretreatment with L-NAME abolished the difference in sensitivity to Ang II between NG- and HG30-Af-Arts, suggesting impaired NO synthesis in HG30-Af-Arts.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
Association of p120, a tyrosine kinase substrate, with E-cadherin/catenin complexes.
p120 was originally identified as a substrate of pp60src and several receptor tyrosine kinases, but its function is not known. Recent studies revealed that this protein shows homology to a group of proteins, beta-catenin/Armadillo and plakoglobin (gamma-catenin), which are associated with the cell adhesion molecules cadherins. In this study, we examined whether p120 is associated with E-cadherin using the human carcinoma cell line HT29, as well as other cell lines, which express both of these proteins. When proteins that copurified with E-cadherin were analyzed, not only alpha-catenin, beta-catenin, and plakoglobin but also p120 were detected. Conversely, immunoprecipitates of p120 contained E-cadherin and all the catenins, although a large subpopulation of p120 was not associated with E-cadherin. Analysis of these immunoprecipitates suggests that 20% or less of the extractable E-cadherin is associated with p120. When p120 immunoprecipitation was performed with cell lysates depleted of E-cadherin, beta-catenin was no longer coprecipitated, and the amount of plakoglobin copurified was greatly reduced. This finding suggests that there are various forms of p120 complexes, including p120/E-cadherin/beta-catenin and p120/E-cadherin/plakoglobin complexes; this association profile contrasts with the mutually exclusive association of beta-catenin and plakoglobin with cadherins. When the COOH-terminal catenin binding site was truncated from E-cadherin, not only beta-catenin but also p120 did not coprecipitate with this mutated E-cadherin. Immunocytological studies showed that p120 colocalized with E-cadherin at cell-cell contact sites, even after non-ionic detergent extraction. Treatment of cells with hepatocyte growth factor/scatter factor altered the level of tyrosine phosphorylation of p120 as well as of beta-catenin and plakoglobin. These results suggest that p120 associates with E-cadherin at its COOH-terminal region, but the mechanism for this association differs from that for the association of beta-catenin and plakoglobin with E-cadherin, and thus, that p120, whose function could be modulated by growth factors, may play a unique role in regulation of the cadherin-catenin adhesion system.
Binding Sites↗
In vivo induction of apoptosis by influenza virus.
Intranasal exposure of mice to influenza virus led to cell death in bronchial/bronchiolar epithelial cells, alveolar cells and lymphoid cells. These cells displayed fragmentation of nuclei and chromatin condensation. Nick end-labelling of DNA in situ confirmed that such apoptotic cells had fragmented DNA. These results suggest that the influenza virus induces apoptosis in vivo.
Animals↗