Search PubMed⌕ Search

Biomedical subjects

T Nakata

Publications and source records attributed to T Nakata.

At least 181 records · Page 10Linked to original sources

Alcohol norms, expectancies, and reasons for drinking and alcohol use in a U.S. versus a Japanese college sample.

Two hundred eighty-two students at Arizona State University in the U.S. and 339 students at Okayama University in Japan completed a questionnaire on their alcohol use, expectancies of the effects of alcohol on their own and others' moods and behaviors, the desirability of these effects, norms of significant others for levels of alcohol use and the subject's desire to comply with these norms, and reasons for drinking and not drinking alcohol. Although frequencies of current drinkers versus abstainers did not differ between the two samples, the U.S. students began regular alcohol use at a significantly earlier age, currently drank more alcohol, had higher alcohol expectancies for emotional responses, and endorsed more celebratory reasons for drinking than their Japanese counterparts. U.S. students, however, had lower expectancies for flushing and lower perceived norms for drinking. Hierarchical multiple regressions performed using data from the current drinkers indicated that expectancies of disinhibition and especially aggressiveness after alcohol use, alcohol norms, celebratory (but not pathological) reasons for drinking, and reasons for not drinking were more predictive of reported levels of alcohol use among the U.S. students as compared with the Japanese students.

Adolescent↗

Alteration of response to neuropeptide Y in the nucleus tractus solitarius of spontaneously hypertensive rats.

In normotensive rats, microinjections of neuropeptide Y (2.5 to 25 pmol) into the unilateral nucleus tractus solitarius elicited dose-dependent vasodepressor and bradycardiac responses accompanied by an inhibition of sympathetic nerve firing. After microinjections of the alpha 2-adrenergic receptor antagonist yohimbine (100 ng) into the nucleus tractus solitarius, the depressor and bradycardic responses to the injection of neuropeptide Y (25 pmol) into the nucleus tractus solitarius were significantly attenuated. In contrast, pretreatment with the alpha 1-adrenergic receptor antagonist doxazosin (200 ng) injected into the nucleus tractus solitarius did not alter these responses. In spontaneously hypertensive rats, microinjections of neuropeptide Y (25 pmol) into the nucleus tractus solitarius also elicited depressor and bradycardic responses that were significantly less than those of normotensive Wistar-Kyoto rats. However, pretreatment with yohimbine (100 ng) in the nucleus tractus solitarius did not diminish these depressor responses in spontaneously hypertensive rats. Depressor responses to neuropeptide Y, which was administered after yohimbine pretreatment, were also less in Wistar-Kyoto rats than in spontaneously hypertensive rats. The results suggest that the depressor and bradycardic responses elicited by neuropeptide Y were accompanied by the inhibition of sympathetic nerve activity. These responses may be mediated in part by alpha 2-adrenergic receptor in the nucleus tractus solitarius. The impairment of alpha 2-adrenergic receptor-mediated responses to neuropeptide Y in spontaneously hypertensive rats may contribute to the development of hypertension.

Adrenergic alpha-1 Receptor Antagonists↗

Redistribution of synapsin I and synaptophysin in response to electrical stimulation in the rat neurohypophysial nerve endings.

To understand the dynamics of synaptic vesicles and synapsin I, we have studied the localization of synapsin I and synaptophysin in resting and stimulated nerve endings by ultracryomicrotomy and colloidal gold-immunocytochemistry. First, we characterized microvesicles in resting nerve endings of the rat neurohypophysis, which was chosen as the model of nerve ending in this study. Synaptophysin was localized in microvesicles that were clustered beneath the plasma membrane. Quick-freeze deep-etching electron microscopy showed that short strands cross-linked microvesicles to each other, which highly resemble the structures observed in our studies of the presynaptic nerve terminals of central and peripheral nervous system and in vitro reconstitution of synapsin I and synaptic vesicles. Immunocytochemistry showed that synapsin I was localized to the region of cluster of microvesicles. Second, using this system, we examined localization of synapsin I and synaptophysin in nerve endings after electrical stimulation. Besides release of neurosecretory granules, clusters of microvesicles dissappeared and both microvesicles and synaptophysin were scattered over nerve endings. These changes were also confirmed by quick-freeze, freeze-substitution. Immunocytochemistry of the stimulated sample revealed that synapsin I was also scattered. The results show that microvesicles in neurohypophysis have similar characteristics of typical synaptic vesicles and synapsin I has a role as a scaffold to cross-link microvesicles to be clustered in resting nerve endings. This scaffold of synapsin I was disengaged after stimulation to redistribute microvesicles and synapsin I itself, which may be the mechanism of synapsin I to regulate the availability of synaptic vesicles for release.

Animals↗

Intrapulmonary lymph nodes.

We report two cases of intrapulmonary lymph nodes detected by a chest roentgenogram or CT scan. The first patient was a 61-year-old fisherman referred complaining of cough and hemosputum. Chest roentgenogram showed a subpleural small nodular shadow at the superior segment of the right lower lobe. Thoracotomy showed a small anthracotic lymph node. The other case was a 68-year-old female patient admitted for further examination of a subpleural small nodular shadow at the latero-basal segment of the left lower lobe detected on a chest CT scan. Thoracoscopic surgery revealed that the black nodule was an anthracotic lymph node. The appearance of an intrapulmonary lymph node on radiological examination is rare, however, it should be considered in the differential diagnosis of a solitary or multiple peripheral pulmonary nodules in adults. A small nodular shadow should be resected if malignancy is suspected though not proven. Subpleural intrapulmonary lymph node warrants thoracoscopic surgery.

Aged↗

Effect of an angiotensin II receptor antagonist, TCV-116, on cardiac hypertrophy and coronary circulation in spontaneously hypertensive rats.

To determine whether an angiotensin II receptor antagonist (AT antagonist) could improve the impaired coronary circulation as well as induce regression of cardiac hypertrophy in the hypertensive heart, and to elucidate whether the nitric oxide system in the coronary artery was involved in this mechanism, the AT1 antagonist, TCV-116 (10 mg/kg), was administered orally to spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY), and coronary flow was measured in the isolated hearts. High systolic blood pressure in SHR was significantly reduced by a 2-week treatment with TCV. Left ventricular (LV) hypertrophy in SHR regressed after TCV treatment, while LV weight in WKY was not reduced. Total minimum coronary vascular resistance (MCVR) obtained with adenosine (10(-5) M) infusions in a Langendorff apparatus was significantly greater in SHR than in WKY. Increased MCVR in SHR was reduced after TCV treatment. Coronary perfusion with NG-monomethyl-L-arginine monoacetate (L-NMMA) increased coronary vascular resistance (CVR) in WKY, while it failed to increase CVR in SHR. TCV treatment restored the responses to L-NMMA in SHR. These findings suggest that the AT1 antagonist, TCV-116, lowered the high blood pressure in SHR, concomitantly improving the impaired coronary circulation, and that it induced regression of the cardiac hypertrophy. The suppressed nitric oxide (NO) system in the coronary vessels in SHR appeared to be activated by TCV treatment.

Angiotensin Receptor Antagonists↗

[Quantification of reversible perfusion abnormality using exercise-stress thallium SPECT before and after coronary revascularization].

Reversible myocardial perfusion abnormality was quantified by bull's eye and unfolded surface mapping methods in exercise thallium SPECT before and after coronary revascularization in 47 patients with angina pectoris, including 34 patients with previous myocardial infarction (PMI) and 13 with effort angina (AP). There was no difference in the incidence or extent of myocardial ischemia between the 2 groups before revascularization. However, the ischemic scores were significantly smaller in PMI group preoperatively than the reductions of the ischemic scores after revascularization. The ischemic scores, preoperatively estimated reversible perfusion abnormality was 32%, 69% and 48% of the improvement of the ischemic score (extent score, severity score, and ischemic area, respectively). Using the 3 ischemic scores, the improvement of perfusion abnormality was well predicted in 70-89% of AP patients but 35-57% of PMI patients. Thus, quantitative analysis in stress thallium SPECT is useful for detecting myocardial ischemia and evaluating the effect of coronary revascularization. However, about a half of myocardial viability was underestimated in one third of PMI patients by the conventional exercise-stress thallium SPECT study.

Adult↗

Induction and release of manganese superoxide dismutase from mitochondria of human umbilical vein endothelial cells by tumor necrosis factor-alpha and interleukin-1 alpha.

The effects of tumor necrosis factor-alpha (TNF alpha) on cultured human umbilical vein endothelial cells (EC) and 2 cancer cell lines, A549 and ME180, were compared. The effects of interleukin-1 alpha (IL-1 alpha) on EC were also examined. While A549 cells were fairly resistant to the cytolytic effects of TNF alpha and IL-1 alpha, ME180 cells were sensitive. EC were also less sensitive to TNF alpha than ME180 cells, as judged by viability of individual cells and by the release of lactate dehydrogenase (LDH) into the medium. Both manganese superoxide dismutase (Mn-SOD) and its mRNA were markedly induced by these cytokines in EC and in A549 cells but not in ME180 cells. The levels of Mn-SOD in the conditioned medium of EC were markedly increased after stimulation with cytokines, whereas those in ME180 and A549 cells were relatively low. The amount of Mn-SOD released appears to be comparable to that from cells lysed due to the cytocidal effect of cytokines, as assessed by measuring intra- and extra-cellular LDH activity. These data suggest that, in vivo, the TNF alpha and IL-1 alpha produced by cancer cells and other cells may induce Mn-SOD in vascular endothelial cells as well as other host tissues, resulting in release of a relatively large amount of this protein into the serum.

Blotting, Northern↗

The primary structure of rat brain (cytoplasmic) dynein heavy chain, a cytoplasmic motor enzyme.

Overlapping cDNA clones encoding the heavy chain of rat brain cytoplasmic dynein have been isolated. The isolated cDNA clones contain an open reading frame of 13,932 bp encoding 4644 aa (M(r), 532,213). The deduced protein sequence of the heavy chain of rat brain dynein shows significant similarity to sea urchin flagellar beta-dynein (27.0% identical) and to Dictyostelium cytoplasmic dynein (53.5% identical) throughout the entire sequence. The heavy chain of rat brain (cytoplasmic) dynein contains four putative nucleotide-binding consensus sequences [GX4GK(T/S)] in the central one-third region that are highly similar to those of sea urchin and Dictyostelium dyneins. The N-terminal one-third of the heavy chain of rat brain (cytoplasmic) dynein shows high similarity (43.8% identical) to that of Dictyostelium cytoplasmic dynein but poor similarity (19.4% identical) to that of sea urchin flagellar dynein. These results suggested that the C-terminal two-thirds of the dynein molecule is conserved and plays an essential role in microtubule-dependent motility activity, whereas the N-terminal regions are different between cytoplasmic and flagellar dyneins.

Amino Acid Sequence↗

Expression of superoxide dismutase (SOD) in adenomyosis.

OBJECTIVE: To assess the expression of Cu,Zn-SOD and Mn-SOD in peritoneal fluid and ectopic endometrium from women with adenomyosis. STUDY DESIGN: The levels of Cu,Zn-SOD and Mn-SOD were measured in peritoneal fluid from infertile women who did not have endometriosis (n = 27), women with adenomyosis (n = 22), and women with endometriosis (n = 15). The expression of Cu,Zn-SOD and Mn-SOD messenger ribonucleic acids in ectopic endometrium was investigated by Northern blot analysis. Mn-SOD in ectopic endometrium was investigated by immunohistochemical staining. RESULTS: The levels of Cu,Zn-SOD and Mn-SOD were significantly higher in the peritoneal fluid from women with adenomyosis than in those with endometriosis or infertile women. Mn-SOD was highly expressed in ectopic endometrium, but Cu,Zn-SOD was not. Mn-SOD was detected in ectopic endometrium of women with adenomyosis. CONCLUSIONS: These data show that reactive oxygen produced in adenomyosis may induce Mn-SOD in ectopic endometrium, which results in the release of relatively large amounts of this protein into the peritoneal fluid. These results suggest that free radicals may play a role in the pathogenesis of adenomyosis, the same as they do in other inflammatory processes.

Ascitic Fluid↗

Localization of dynamin: widespread distribution in mature neurons and association with membranous organelles.

Tissue distribution and intracellular localization of dynamin by immunoblotting and immunocytochemistry is investigated in this study. Dynamin was widely expressed in all the neurons we examined, and was especially abundant in the central nervous system after maturation, although its expression presented regional heterogeneity. Dynamin was present most abundantly in cerebellar Purkinje cells and hippocampal pyramidal cells, and to a lesser extent in motor neurons and peripheral nerves. However, dynamin was nearly absent in cells such as anterior pituitary cells and adrenal medullary cells which secrete mainly dense cored vesicles. Dynamin was localized not only in cell bodies, axons, and synapses but also in dendrites. Subcellular fractionation indicated that dynamin existed in the membrane fraction as well as in the soluble fraction. In ligated peripheral nerves, dynamin colocalized with tubulovesicular membranous organelles transported mainly anterogradely. By transfection of dynamin cDNA into mouse fibroblast L-cells, we showed it colocalized with some membranous organelles but not with microtubules. Our results show that dynamin is associated with membranous organelles in vivo, although a certain amount of dynamin also exists in the soluble fraction and is distributed diffusely throughout mature neurons. The data suggest that dynamin's fundamental role involves membrane trafficking in neurons in the central nervous system rather than in sliding microtubules as a motor protein.

Amino Acid Sequence↗

Thermal drift is enough to drive a single microtubule along its axis even in the absence of motor proteins.

One-dimensional diffusion of microtubules (MTs), a back-and-forth motion of MTs due to thermal diffusion, was reported in dynein motility assay. The interaction between MTs and dynein that allows such motion was implicated in its importance in the force generating cycle of dynein ATPase cycle. However, it was not known whether the phenomenon is special to motor proteins. Here we show two independent examples of one-dimensional diffusion of MTs in the absence of motor proteins. Dynamin, a MT-activated GTPase, causes a nucleotide dependent back-and-forth movement of single MT up to 1 micron along the longitudinal axes, although the MT never showed unidirectional consistent movement. Quantitative analysis of the motion and its nucleotide condition indicates that the motion is due to a thermal driven diffusion, restricted to one dimension, under the weak interaction between MT and dynamin. However, specific protein-protein interaction is not essential for the motion, because similar back-and-forth movement of MT was achieved on coverslips coated with only 0.8% methylcellulose. Both cases demonstrate that thermal diffusion could provide a considerable sliding of MTs only if MTs are restricted on the surface appropriately.

Animals↗

High copper and iron levels and expression of Mn-superoxide dismutase in mutant rats displaying hereditary hepatitis and hepatoma (LEC rats).

The LEC rat is a mutant strain displaying hereditary hepatitis and hepatoma. We established enzyme-linked immunosorbent assays of Cu,Zn- and Mn-superoxide dismutase (Cu,Zn- and Mn-SOD) and measured the levels of both SODs in various organs of LEC and Wistar rats. Mn-SOD concentrations were higher in LEC rats than in Wistar rats in most tissues. Cu,Zn-SOD levels of liver, kidney and intestine were lower in LEC rats than in Wistar rats. Atomic absorbtion techniques indicated that in addition to high Cu concentrations as previously reported, LEC rat livers contained high Fe concentrations relative to those in Wistar rat livers. These data suggest that increased concentrations of Fe and Cu and decreased levels of Cu,Zn-SOD may facilitate the Fenton reaction to produce hydroxyl radicals in the tissues of the LEC rat. To compensate for the decreased scavenging effects due to low levels of Cu,Zn-SOD, an adaptive increase of Mn-SOD may occur in the process of hepatitis and hepatocarcinogenesis in LEC rats.

Animals↗

Manganese-superoxide dismutase in endothelial cells: localization and mechanism of induction.

Mechanisms of Mn-superoxide dismutase (Mn-SOD) expression in human umbilical endothelial cells were investigated by Northern blot analysis, enzyme-linked immunosorbent assay, and immunoelectron microscopy. The Mn-SOD in human endothelial cells was markedly induced by the cytokines tumor necrosis factor (TNF), interleukin-1, and lipopolysaccharide as well as by phorbol esters [12-O-tetradecanoylphorbol 13-acetate (TPA)]. The induction was partially blocked by dexamethasone and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine, a potent inhibitor of protein kinase C (PKC). In endothelial cells in which PKC had been desensitized to TPA by pretreatment for 24 h, addition of TNF caused overexpression of Mn-SOD. These facts suggested that at least two separate signal-transducing pathways are involved in expression of the Mn-SOD gene. Immunoelectron-microscopic studies showed that Mn-SOD was localized to the mitochondrial matrix of the capillary vascular endothelial cells of cardiac tissues and cultured endothelial cells. Mn-SOD, which is normally abundant in endothelial cells relative to other cell types, may play an important protective role against stresses such as ischemia and inflammation.

Blotting, Northern↗

Cardiovascular change and hypothalamic norepinephrine release in response to environmental stress.

The major objective of this study was to compare the magnitude and duration of cardiovascular (CV) responses to acute environmental stresses with the associated patterns of noradrenergic activity in the paraventricular nucleus (PVN) and posterior nucleus (PH) of the hypothalamus. Simultaneous microdialysis samples of extracellular norepinephrine (NE) were collected at 5-min intervals from PVN and PH and the CV responses were recorded before, during, and for 15 min after acute shaker (cage oscillation) stress or inhalation of ether vapor in freely moving rats. Five minutes of shaker stress, 60 and 150 cycles/min, elicited pressor responses coupled with increases in dialysate NE from both PVN and PH in a frequency-dependent manner. Tachycardia occurred at 150 but not 60 cycles/min. Ten minutes after 60 cycles/min and 15 min after 150 cycles/min, NE efflux in PH was still increased, whereas in PVN it returned to control as had arterial pressure and heart rate. Ether vapor elicited a transient CV response but a continuing efflux of NE in PH and PVN. Urethan anesthesia raised baseline values of dialysate NE in PH and PVN but significantly attenuated cardiovascular and dialysate NE responses to shaker stress. We conclude that acute environmental stress simultaneously elicits CV responses and the efflux of NE from PVN and PH but, during or after stress, CV values may return to control levels while NE efflux remains elevated in PVN and/or PH.

Administration, Inhalation↗

A novel member of the dynamin family of GTP-binding proteins is expressed specifically in the testis.

Dynamin is a member of a new GTPase family, which includes the mouse Mx protein, the yeast VPS1 and the Drosophila shibire gene product. A high homology with the shibire product suggests a role for dynamin in the endocytotic process, but it is expressed only in mature neurons. We identified two additional dynamin-like proteins in rats, by using the polymerase chain reaction with degenerate primers corresponding to the GTP-binding areas conserved between dynamin and VPS1. The full coding sequence of one of them, dynamin-2, revealed that it has 848 amino acids and has great similarity with brain dynamin and the shibire product. Northern blot analysis and in situ hybridization revealed its expression to be specific to the seminiferous tubules in the testis. Dynamin-2 (testis type dynamin) was expressed in germ-cell-depleted testis as well, indicating its expression in Sertoli cells. Our data imply that a number of dynamin family proteins, which are products of distinct genes, may play different roles specific to each cell type in the same rat.

Amino Acid Sequence↗

Coronary stenosis and steal phenomenon in coronary-pulmonary fistula--assessment with stress thallium tomography after coronary angioplasty and fistulectomy.

We present a 46-year-old male with unstable angina and bilateral coronary-to-pulmonary artery fistulae in whom reversible myocardial ischemia was detected by exercise-stress thallium-201 single-photon emission computed tomography (SPECT). Coronary angiography revealed a 99% stenosis at the proximal site of the left descending coronary artery and bilateral coronary-to-pulmonary artery fistulae with a saccular aneurysm. Percutaneous transluminal coronary angioplasty abolished chest pain and electrocardiographic changes. However, definitely improved, but still present, stress-induced perfusion abnormalities were demonstrated by an exercise-stress thallium-201 SPECT study. Myocardial ischemia was the only serious complication related to the coronary fistulae, and after they were surgically resected, the reversible perfusion abnormality was no longer observed. These findings suggest that coronary-to-pulmonary artery fistulae potentiated the myocardial ischemia in patient with coronary stenosis leading to unstable angina and prolonged the presence of coronary perfusion abnormality on stress thallium scans probably through a coronary steal phenomenon.

Angina, Unstable↗