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Biomedical subjects

Y Takei

Publications and source records attributed to Y Takei.

At least 235 records · Page 13Linked to original sources

Goldfish calcitonin: purification, characterization, and hypocalcemic potency.

A novel teleost calcitonin was isolated from the goldfish, Carassius auratus, and its amino acid sequence was determined to be H-Cys-Ser-Ser-Leu-Ser-Thr-Cys-Val-Leu-Gly- Lys-Leu-Ser-Gln-Glu-Leu-His-Lys-Leu-Gln-Thr-Tyr-Pro-Arg-Thr-Asn-Val-Gly- Ala-Gly-Thr-Pro-NH2. The structure of goldfish calcitonin (gCT) was similar to that of salmon calcitonin (sCT) but differed from the latter at positions 3, 27, and 29. The hypocalcemic activity of gCT was estimated to be 3,470 IU/mg by the standardized rat bioassay method, compared with a value of 3,500 IU/mg for sCT. After administration of gCT to young goldfish, the serum Ca concentration was significantly lower in some cases than in controls. However, in other cases no such difference was recognized.

Amino Acid Sequence↗

New angiotensin I isolated from a reptile, Alligator mississippiensis.

Angiotensin I (ANG I) of the American alligator Alligator mississippiensis was isolated from incubates of homologous plasma and kidney extract, and its amino acid sequence was determined as H-Asp-Arg-Val-Tyr-Val-His-Pro-Phe-Ala-Leu-OH. The presence of strongly hydrophobic alanine at position 9 is unusual among ANGs I sequenced to date. Since alanine can be converted to serine by a one-point mutation of the triplet nucleotides, the phylogenetic proximity of the alligator to birds, whose ANG I has serine at position 9, is confirmed by the chemical evolution of the hormone structure. The alligator [Asp1,Val5,Ala9] ANG I increased arterial blood pressure of conscious alligators, but it was no more potent than avian [Asp1,Val5,Ser9] ANG I. The alligator ANG I was also equipotent to the homologous ANG I in the quail and rat. It is concluded that substitutions at position 9 have little influence on the vasopressor activity of ANG I.

Alligators and Crocodiles↗

Comparison of infrared electronic endoscopy using reflection and transmission.

Twelve subjects were examined using both the reflecting type of infrared electronic endoscopy and the transmission method to visualize submucosal gastric architecture. Under transmission infrared illumination, submucosal structures were more clearly observed than by using the reflecting type. Using the transmission method, only the anterior wall of the antrum could be fully visualized, although the anterior wall of the lower corpus was recognized in only 33% of the cases. Furthermore, the upper or middle corpus and the entire posterior wall were not properly recognized using transmission illumination. The entire gastric circumference was visualized with the reflecting type illumination. Both types of infrared illumination of the gastric wall can be used complementarily for visualizing submucosal gastric architecture.

Aged↗

Role of endogenous endothelin in pathogenesis of ethanol-induced gastric mucosal injury in rats.

The major objective of this study was to elucidate the role of endogenous endothelin (ET)-1, a potent vasoconstrictor peptide, in the pathogenesis of ethanol (EtOH)-induced gastric mucosal injury. Two series of experiments were performed in anesthetized rats. First, we examined the time course of relationships among changes in ET-1 concentrations in gastric mucosal and portal plasma, gastric mucosal hemodynamics, and mucosal damage produced by EtOH. Intragastric EtOH stimulated release of endogenous ET-1 in gastric mucosal tissue. Plasma ET-1 concentrations in the portal vein also increased after intragastric EtOH administration. ET-1 concentrations in gastric mucosal tissue and portal plasma increased significantly before gastric mucosal hemorrhagic damage occurred. Moreover, 30 min after EtOH administration there were significant correlations between gastric mucosal ET-1 concentrations and both area of gastric hemorrhagic damage as well as concentration of EtOH administered intragastrically. After intragastric EtOH administration, increase in gastric mucosal hemoglobin concentration and decrease in gastric mucosal hemoglobin oxygen saturation, estimated using reflectance spectrophotometry, occurred within 2.5 min and continued throughout the experiments. The time course of microcirculatory changes correlated closely with increases in gastric mucosal ET-1 and portal plasma ET-1 concentrations after intragastric EtOH administration. Gastric microcirculatory disturbances induced by EtOH were associated with significant decreases in gastric mucosal ATP content. Second, we examined whether pretreatment with anti-ET-1 antibody protected against EtOH-induced mucosal injury by improving mucosal microcirculation. Pretreatment with anti-ET-1 antibody microscopically and macroscopically reduced gastric mucosal hemorrhagic damage induced by EtOH and significantly reduced EtOH-induced gastric microcirculatory disturbances and decreases in gastric mucosal ATP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

High-density localization of ANP receptors in chondrocytes of eel gill cartilage.

Very high levels of atrial natriuretic peptide (ANP) receptor were found in a quite unexpected tissue, i.e., the chondrocyte of the eel gill cartilage. 125I-labeled ANP binding assay indicated that the eel gill contains large amounts of the receptor and its levels are much higher (> 10-fold) than those in the other tissues examined, including the brain, kidney, head kidney including steroidogenic interrenal cells, and gut. Autoradiography using gill sections revealed dense localization of ANP receptors in the chondrocytes of the cartilage as well as moderate localization in the parenchymal cells. Biochemical and pharmacological characterization of the chondrocyte receptor indicated that most of the receptors are type C receptors, having a broad ligand specificity and a reduced M(r) of 68,000. Because a hyaline cartilage in which chondrocytes reside lacks blood vessels, and all metabolic exchange is by slow diffusion through the matrix, the chondrocyte localization of the type C ANP receptor is notable and may stimulate not only chondrocyte research but also studies on physiological significance of the type C receptor, which is generally considered to be merely a clearance (silent) receptor.

Animals↗

Roles of endothelin-1 and nitric oxide in the mechanism for ethanol-induced vasoconstriction in rat liver.

This study was designed to investigate the mechanism for ethanol-induced hepatic vasoconstriction in isolated perfused rat liver. Upon initiation of ethanol infusion into the portal vein at concentrations ranging from 25 to 100 mM, portal pressure began to increase in a concentration-dependent manner and reached maximal levels in 2-5 min (initial phase), followed by a gradual decrease over the period of ethanol infusion (escape phenomenon). Endothelin-1 antiserum significantly inhibited this ethanol-induced hepatic vasoconstriction by 45-80%. Cessation of infusion of endothelin-1 antiserum was followed by a subsequent increase in portal pressure. On the other hand, when a nitric oxide synthesis inhibitor, NG-monomethyl-L-arginine (L-NMMA), was infused into the portal vein simultaneously with ethanol, the initial phase of the response of portal pressure to ethanol was not altered and the peak values of portal pressure remained unchanged. However, after the peak increase in portal pressure, the rate of decrease was less than in the absence of L-NMMA. Thus, L-NMMA diminished the escape phenomenon and sustained the vasoconstriction. This study supports the hypothesis that two endothelium-derived vasoactive factors, endothelin-1 and nitric oxide, regulate hepatic vascular tone in the presence of ethanol.

Animals↗

Effects of N-omega-nitro-L-arginine methyl ester on the cerebral circulation of newborn piglets quantified in vivo by near-infrared spectroscopy.

The effects of N-omega-nitro-L-arginine methyl ester (L-NAME) on basal cerebral vascular tone, the vasodilatory effects of acetylcholine (ACh), and the cerebrovascular response to alterations in arterial carbon dioxide tension (CBVR) were investigated using near-infrared spectroscopy. Seven newborn piglets were anesthetized and mechanically ventilated; mean arterial blood pressure (MAP) was monitored and near-infrared spectroscopy used to measure changes in total cerebral Hb concentration. At the beginning of the experiment, CBVR was measured and then 10, 20, 30, and 100 mg.kg-1 L-NAME were administered sequentially; ACh (1, 2, 3, and 5 micrograms) was given before and after each injection of L-NAME. At the end of this sequence, CBVR was measured again and finally sodium nitroprusside (1.5 mg.kg-1) was administered. Ten and 20 mg.kg-1 L-NAME caused a significant decrease in total cerebral Hb concentration of -0.59 (-3.21 to -0.02) and -1.46 (-6.50 to -0.15) mumol.L-1 (median and range), respectively (Wilcoxon p < 0.05), but subsequent injections did not. Ten, 20, and 100 mg.kg-1 L-NAME caused an increase in MAP (Wilcoxon p < 0.05). ACh caused an increase in total cerebral Hb concentration and a decrease in MAP that was impaired but not abolished by L-NAME (ANOVA p < 0.05). CBVR was not affected by L-NAME. Sodium nitroprusside caused a reduction in mean (SD) MAP of 4.7 (1.6) kPa, and a slower rise in [tHb] of 13.44 (2.03) mumol.L-1. Postmortem examination of three animals revealed NADPH-diaphorase staining in neurons, cerebral blood vessels, carotid artery, and jugular vein.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

A novel angiotensin I isolated from an elasmobranch fish.

It is believed that the renin-angiotensin system evolved initially in primitive bony fishes and is absent from elasmobranchs. We have isolated angiotensin I from the incubates of plasma and kidney extracts of an elasmobranch fish, Triakis scyllia, using eel vasopressor activity as an assay system. Its sequence was determined to be H-Asn-Arg-Pro-Tyr-Ile-His-Pro-Phe-Gln-Leu-OH. Dogfish angiotensin I is teleost-like because of an asparagine residue at position 1 but it is mammalian-like because of an isoleucine residue at position 5. The unique and most important substitution in dogfish angiotensin I is a proline residue at position 3 which may cause significant changes in its tertiary structure. A glutamine residue at position 9 is also unique among all angiotensin Is sequenced to date. Dogfish angiotensin I is more potent than rat angiotensin I in its vasopressor activity in the dogfish but the relationship is reversed in the rat. Thus angiotensin receptors as well as the hormone molecules appear to have evolved during vertebrate phylogeny. Our findings establish the elasmobranch renin-angiotensin system and support the hypothesis that the renin-angiotensin system is a phylogenetically old hormonal system which plays important roles in cardiovascular and fluid homeostasis.

Amino Acid Sequence↗

Immunohistochemical study of hemangioblastoma with special reference to its cytogenesis.

The cytogenesis of so-called hemangioblastoma arising in the central nervous system was investigated using the immunoreactivity to various proteins in cerebellar hemangioblastomas, extracerebellar hemangioblastomas, cerebral hemangiopericytomas, and hemangioendotheliomas, as well as a variety of meningiomas. The antisera used included vimentin, glial fibrillary acidic protein, epithelial membrane antigen, factor VIII-related antigen, and cytokeratin. Lipid-laden cells often encountered in partially degenerated meningiomas revealed almost identical reactivity patterns as the lipid-laden cells, i.e., so-called stroma cells, of hemangioblastomas. The results indicate that the so-called hemangioblastoma of the central nervous system is derived from arachnoid cells in meningotheliomatous meningiomas by way of cellular degeneration.

Adult↗

Development of neoglycoproteins conjugated with natural oligosaccharides through carboxyl residues of proteins and its application to recombinant human interleukin 1.

In order to develop glycosylated cytokines, neoglycoproteins were synthesized utilizing naturally occurring oligosaccharides. High mannose type oligosaccharide-asparagine (Asn)s, containing Man8GN2-Asn, Man7GN2-Asn and Man6GN2-Asn, were obtained from quail ovalbumin and were coupled to bovine serum albumin (BSA) by carbodiimide-mediated coupling. Major reaction occurred between amino residues of oligosaccharide-Asns and carboxyl residues of BSA. Approximately one molecules of oligosaccharides-Asns were coupled to per molecule of BSA with 50% yield of glycosylation. Among the oligosaccharides, Man6GN2-Asn appeared to be conjugated predominantly. While this strategy was applied to recombinant human interleukin 1 alpha (IL-1 alpha), three molecules of oligosaccharide-Asns were introduced into per molecule of IL-1 with 10% yield of glycosylation.

Animals↗

Evaluation of effective portal venous flow in chronic liver diseases using echo-Doppler flowmetry combined with per jejunal portal scintigraphy.

Portal circulation changes due to the progression of chronic liver disease and portal venous flow are also affected by pharmacotherapy. Thus, noninvasive measurement of effective portal venous flow (EPVF) is highly desirable. We evaluated EPVF under steady-state conditions using echo-Doppler flowmetry combined with per jejunal portal scintigraphy in 32 patients with chronic liver disease. After introduodenal administration of 37 MBq (1 mCi) of 123I-iodoamphetamine, scintigraphy of the pulmonary and hepatic regions was performed and a portosystemic shunt index (SI) calculated. EPVF was calculated as follows: EPVF = PVFx (1-SI/100). EPVF in chronic hepatitis, compensated cirrhosis and decompensated cirrhosis was 12.0 +/- 1.8 ml/min/kg, 10.3 +/- 1.6 ml/min/kg and 8.0 +/- 2.5 ml/min/kg, respectively. There were significant differences in EPVF between all groups, although PVF was similar in each group. EPVF correlated with liver function tests and was a better indicator of liver function than PVF. Measurement of EPVF may provide useful information in the management of patients with chronic liver disease.

Adult↗

[A case of long-term survival in a patient with small cell lung carcinoma with syndrome of inappropriate secretion of anti-diuretic hormone].

A 73-year-old man was admitted on April 1984 because of an abnormal shadow on chest X-ray. He was diagnosed as having small cell lung carcinoma (oat cell type) with inappropriate secretion of antidiuretic hormone (SIADH). Initial chemotherapy with cyclophosphamide, ACNU, vincristine, adriamycin, cis-platinum and etoposide was administered. The mass subsequently disappeared, and the serum sodium level normalized. About 2 years later, the patient developed a relapse of the primary lesion with hyponatremia. The same regimen as the initial chemotherapy was initiated and a complete response was again obtained. Similar episodes were repeated four times, and he died in April 1991. This patient survived for about seven years after the initial treatment without maintenance chemotherapy.

Aged↗

Receptor-mediated formation of multilayer aggregates of primary cultured adult rat hepatocytes on lactose-substituted polystyrene.

We used a lactose-substituted polystyrene, poly-N-p-vinylbenzyl-D-lactonamide (PVLA), as a substratum for adult rat hepatocytes in primary culture. Spherical-shaped hepatocytes attached on PVLA substratum formed stable multilayer aggregates anchored on substratum through the stimulation of epidermal growth factor (EGF). The cells required calcium ion essentially to form the aggregates. The formation of multilayer aggregates was inhibited by colchicine, but not by cytochalasin B. The inhibition was also observed by added PVLA molecules in the culture medium and by treating surfaces of PVLA-coated dishes with allo A lectin. It was suggested that adult rat hepatocytes attached on PVLA substratum required the specific interaction between asialoglycoprotein receptors on the cell surface and PVLA substratum to form anchored multilayer aggregates.

Animals↗

A GTP-binding protein in rat liver nuclei serving as the specific substrate of pertussis toxin-catalyzed ADP-ribosylation.

The ADP-ribosyl moiety of NAD was transferred to a 40-kDa protein when rat liver nuclei were incubated with pertussis toxin. The 40-kDa substrate in the nuclei displayed unique properties as follows, some of which were apparently distinct from those observed with the toxin-substrate GTP-binding protein (Gi) in the liver plasma membranes. 1) The nuclear 40-kDa protein was recognized with antibodies reacting with the alpha-subunits (alpha i-1 and alpha i-2) of Gi, but not with anti-Go-alpha-subunit antibody. 2) The nuclear protein had a higher mobility than alpha-subunit of the plasma membrane-bound Gi upon electrophoresis with a urea/sodium dodecyl sulfate-containing polyacrylamide gel. 3) The nuclear protein was not extracted from the nuclei with 1% Triton X-100, whereas Gi was easily solubilized from the plasma membranes. 4) There was a beta gamma-subunit-like activity in the nuclei, which was assayed by an ability to support pertussis toxin-catalyzed ADP-ribosylation of a purified alpha-subunit of Gi. Moreover, a 36-kDa protein in the nuclei was recognized with antibody raised against purified beta-subunits of Gi. 5) Pertussis toxin-induced ADP-ribosylation of the nuclear protein was selectively inhibited by the addition of a nonhydrolyzable GTP analogue, and its inhibitory action was competitively blocked by the simultaneous addition of GDP or its analogues, as had been observed with plasma membrane-bound Gi. It thus appeared that a novel form of alpha beta gamma-trimeric GTP-binding protein serving as the substrate of pertussis toxin was present in rat liver nuclei. In order to examine a possible role of the nuclear GTP-binding protein, rats were injected with carbon tetrachloride, a necrosis inducer of hepatocytes. There was a marked increase in the nuclear substrate activity from 3-6 days after the injection, without a significant change in the activity of Gi in the plasma membranes. The time course of the increase corresponded with a recovering stage from the hepatocyte necrosis. These results suggested that the nuclear GTP-binding protein found in the present study might be involved at some stages in the hepatocyte growth.

Adenosine Diphosphate Ribose↗