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Biomedical subjects

K Yagi

Publications and source records attributed to K Yagi.

At least 235 records · Page 13Linked to original sources
PubMed1996

Norepinephrine depletion impairs neuroendocrine responses to fear but not novel environmental stimuli in the rat.

Emotional stimuli suppress vasopressin secretion and potentiate oxytocin and prolactin secretion by the pituitary in the rat. We studied effects of central norepinephrine depletion on these hormonal responses to novel environmental or fear stimuli. Male Wistar rats were injected intracerebroventricularly with 5-amino-2,4-dihydroxy-alpha- methylphenylethylamine, a selective neurotoxin to noradrenergic fibers. The neurotoxin treatment reduced the hypothalamic content of norepinephrine by 71% but did not significantly affect the dopamine content. Novel environmental stimuli suppressed vasopressin secretion and augmented secretion of oxytocin and prolactin in the vehicle-injected rats. The neurotoxin did not block the neuroendocrine responses. Intermittently applied electric footshocks also induced the similar neuroendocrine responses in the vehicle-injected rats. The neurotoxin significantly reduced the neuroendocrine responses. The drug, however, did not significantly alter vasopressin release after continuously applied footshocks. Environmental stimuli previously paired with footshocks (conditioned fear stimuli) suppressed vasopressin secretion and augmented secretion of oxytocin and prolactin in the vehicle-injected animals. Motor activity was suppressed during the conditioned fear stimuli. The neurotoxin impaired the neuroendocrine and behavioral responses whether the drug was injected before or after the conditioning. These data demonstrate the distinction between the neural mechanisms underlying the neuroendocrine responses to fear and to novel stimuli, suggesting that noradrenergic neurons are selectively involved in the hypothalamo-hypophysial responses to fear stimuli.

Animals↗
PubMed1996

Expression of human phospholipid hydroperoxide glutathione peroxidase gene for protection of host cells from lipid hydroperoxide-mediated injury.

A cDNA encoding human phospholipid hydroperoxide glutathione peroxidase (PHGPx) was obtained by PCR amplification from human testis cDNA and was inserted into the plasmid pRc/CMV to construct an expression vector for human PHGPx. Guinea pig cell line 104C1 cells were transfected with the expression vector. One of the transfectants, designated 104Cl/O4C, expressed high glutathione peroxidase activity toward dilinoleoyl phosphatidylcholine hydroperoxide and linoleic acid hydroperoxide. Western blot analysis revealed a large amount of protein immunoreactive against anti-PHGPx antibody in the transfectant. When the cells were incubated with these hydroperoxides, the parental cells suffered from serious cell injury, whereas the transfectant was extremely resistant against lipid hydroperoxide-mediated injury.

Animals↗
PubMed1996

A benzodiazepine, chlordiazepoxide, blocks vasopressin and oxytocin release after footshocks but not osmotic stimulus in the rat.

Noxious as well as hypertonic stimuli potentiate vasopressin and oxytocin secretion in rats. Neurohypophysial vasopressin- and oxytocin-secreting neurons receive inhibitory synaptic inputs mediated by gamma-aminobutyric acid (GABA). Benzodiazepines modulate GABA-A receptor activity in a facilitatory fashion. It is thus possible that benzodiazepines suppress vasopressin and oxytocin release after noxious stimuli. To test this hypothesis, we investigated whether chlordiazepoxide impairs the enhanced release of vasopressin and oxytocin after noxious or hypertonic stimuli in male rats. Chlordiazepoxide (5-20 mg/kg, i.p.) blocked dose-dependently the vasopressin and oxytocin responses to footshocks. Chlordiazepoxide, however, did not impair the hormonal responses to hypertonic stimulus. The results demonstrate that chlordiazepoxide selectively prevents vasopressin and oxytocin release after noxious stimuli and therefore suggest that the sites of chlordiazepoxide actions are not on the vasopressin or oxytocin neurons in rats.

Animals↗
PubMed1996

Proto-oncogene expression in human glomerular diseases.

The expression of the protein products and mRNA of c-fos, c-myc, p53, and c-raf was examined in normal renal tissues and biopsy specimens from 73 patients with various glomerular diseases. Immunofluorescent staining showed that there were cell nuclei stained for c-Fos, c-Myc, and p53, and cytoplasm positive for c-Raf, in the glomeruli of patients with proliferative types of glomerulonephritis, including IgA nephritis and lupus nephritis, and in patients with focal glomerular sclerosis. Glomerular expression of c-fos and c-myc mRNA was detected by in situ hybridization. The number of proto-oncogene-positive glomerular cells was significantly higher in lupus nephritis, IgA nephritis, and focal segmental sclerosis, as compared with minimal change nephrotic syndrome and normal specimens. In IgA nephritis, the population of glomerular cells positive for c-Fos and c-Myc and the grade of c-Raf immunoreactivity were significantly correlated with the proportion of proliferating cell nuclear antigen (PCNA)-positive glomerular cells, with histological grading of mesangial hypercellularity and matrix increase, and with the magnitude of proteinuria. These data indicate that proto-oncogene expression is associated with mesangial proliferation and matrix expansion in proliferative types of glomerulonephritis and in focal glomerular sclerosis.

Cell Nucleus↗
PubMed1996

Surgical treatment for invasive thymoma, especially when the superior vena cava is invaded.

BACKGROUND: We analyzed the operative outcome of extensive surgery for invasive thymoma, especially in those with thymomas invading the superior vena cava, the left innominate vein, or both. METHODS: We treated 41 patients with invasive thymoma, including 34 stage III, 5 stage IVa, and 2 stage IVb thymomas. Thirty-eight patients received radiotherapy preoperatively or postoperatively. In 12 patients with invasion of the superior vena cava or innominate vein, we performed angioplasty, reconstruction, or both. RESULTS: The overall 5-year survival rate was 77% and the 10-year survival rate was 59%. In the stage III group, there was a significant difference between those with complete and those with incomplete resection. Ten of 12 patients who had angioplasty with or without reconstruction of the superior vena cava or innominate vein survived without recurrence of the tumors. CONCLUSION: Angioplasty and vascular reconstruction are recommended because successful treatment for invasive thymomas depends on complete resection of the tumors.

Adolescent↗
PubMed1996

Chlordiazepoxide discriminates between the neural circuits mediating neuroendocrine responses to fear- and anxiety-producing stimuli in the rat.

Effects of a benzodiazepine, chlordiazepoxide (CDP), on neuroendocrine responses to emotional stimuli were studied in male rats. In the experiments with conditioned fear stimuli, rats received a pure tone paired with footshocks in the training session and were tested on the following day with the same environmental stimuli. CDP injected i.p. 30 min before training impaired the suppressive vasopressin and the augmentative oxytocin or adrenocorticotrophic hormone (ACTH) responses to the conditioned fear stimuli. However, the drug, administered 30 min after the training, did not significantly alter the hormonal responses to conditioned fear stimuli. CDP administered 30 min before testing also abolished the hormonal responses to conditioned fear stimuli. The stimuli which were identical to those used for training or unconditioned fear stimuli (intermittent footshocks) also produced the vasopressin, oxytocin and ACTH responses, and CDP prevented these hormonal responses. The drug, however, did not prevent the hormonal responses to novel environmental stimuli. Novel stimuli are known to produce a state of anxiety. Thus the present experiments demonstrate that CDP discriminates between the neural circuits mediating fear- and anxiety-producing stimuli in the rat.

Adrenocorticotropic Hormone↗
PubMed1996

A selective role of brainstem noradrenergic neurons in oxytocin release from the neurohypophysis following noxious stimuli in the rat.

Noxious stimuli facilitate oxytocin release from the neurohypophysis. Oxytocin-secreting hypothalamic magnocellular neurosecretory neurons receive excitatory synaptic inputs from noradrenergic neurons in the medulla oblongata. The medulla oblongata includes the A2 noradrenergic and the A1 noradrenergic cells. Here we investigated whether medullary noradrenergic neurons mediate oxytocin release after noxious stimuli in male rats. 5-Amino-2,4-dihydroxy-alpha-methylphenylethylamine, a neurotoxin selective for noradrenergic fibers, was injected into the lateral cerebral ventricle or the medulla. Seven days after the injection, the hypothalamic content of noradrenaline was decreased. In the rats injected with the neurotoxin, the release of oxytocin but not vasopressin after footshocks was impaired. Surgical ablation by suction of the caudal dorsomedial medulla including the A2 cell region did not significantly affect oxytocin release after footshocks, though the surgery abolished oxytocin release after i.v. injection of cholecystokinin octapeptide. In the rats whose A2 cell region had been ablated, an i.c.v. injected alpha 1 adrenoreceptor antagonist, benoxathian, blocked oxytocin release after footshocks. These results demonstrate that brainstem noradrenergic neurons mediate oxytocin release following noxious stimuli in the rat and suggest that responsible noradrenergic neurons are the A1 cells in the caudal ventrolateral medulla.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1996

Effect of mild hypothermia on ischemia-induced release of endothelin-1 in dog brain.

Endothelin-1 (ET-1) plays an important role in the physiologic or pathophysiologic regulation of cerebral circulation. To evaluate the effect of mild hypothermia on the cerebral concentration of ET-1 and on the cerebral metabolism of oxygen after complete global cerebral ischemia, we occluded the ascending aorta and caval veins of 9 dogs for 15 min. A fiberoptic catheter was inserted into the sagittal sinus to monitor venous oxygen saturation (S(SO)2) continuously. Blood samples were collected 30 min before and 30 min, 1 h, 2 h, 4 h and 6 h after the ischemic insult. Concentrations of ET-1 were assayed in the blood of the sagittal sinus and abdominal aorta. Before, during and after the aortic occlusion, we compared findings in a normothermic control Group 1 (pulmonary artery temperature 38.5 degrees C) (n = 4) with those in the mildly hypothermic Group 2 (pulmonary artery temperature 34.0 degrees C) (n = 5) by surface cooling induced before and maintained during and after ischemia for 6 h. Following ischemia, the plasma concentration difference of ET-1 (sagittal sinus--arterial) was significantly decreased in Group 2 (P < 0.05). Differences in S(SO)2 between the two groups were not statistically significant. Mild hypothermia reduced the ET-1 release in the cerebral circulation but did not improve cerebral oxygen metabolism after complete cerebral ischemia. Findings indicated that the decrease in ET-1 induced by mild hypothermia contributes to the improvement of the cerebral microcirculation after ischemia.

Animals↗
PubMed1996

Time course of coproantigen excretion in Echinococcus multilocularis infections in foxes and an alternative definitive host, golden hamsters.

Coproantigen excretion during experimental infections of Echinococcus multilocularis in foxes and an alternative definitive host, golden hamsters, was evaluated by a sandwich ELISA using a monoclonal antibody. A sigmoidal increase of antigen excretion from the developing parasites was observed in in vitro incubation of the parasites collected on different days during the first 21 days post-infection (DPI). In hamsters, the ELISA O.D. value of faeces became positive at 4 DPI. Thereafter, the O.D. value increased in semi-sigmoidal fashion in the first 42 DPI, probably reflecting the development of the parasites. In foxes, the O.D. value became positive at 6 DPI. However, contrary to that in hamsters, after the initial steep rise, the O.D. value suddenly decreased to 1/2 the level during 15-17 DPI, indicating that a large number of worms might have been expelled. The parasite eggs were detected by the sugar centrifugal-flotation technique (Ito, Yagi & Ishige, 1989) from 29 to 84 DPI but not thereafter to 125 DPI, although mature parasites were detected at 125 DPI. In contrast, positive O.D. values were obtained almost constantly until 125 DPI, indicating that the coproantigen detection assay was more sensitive than the egg detection assay. The detection limit of the coproantigen assay was roughly estimated to be around 100 worms. These observations, along with the fact that the assay was designed to detect a heat-resistant coproantigen in heat-sterilized fecal samples, indicate that the coproantigen detection assay is a safe and useful method, not only for diagnosis in the definitive host of E. multilocularis, but also for monitoring parasite development and change in parasite burden during an experimental infection.

Animals↗
PubMed1996

Extensive resection with selective cerebral perfusion for a lung cancer invading the aortic arch.

An extensive operation for lung cancer invading the aortic arch is reported. A 66-year-old man presented the recent onset of hoarseness. Chest computed tomography and magnetic resonance imaging demonstrated a tumor of the Botallo lymph node invading the aortic arch. Left pneumonectomy with combined resection of the aortic arch was performed with the use of brain-isolated cardiopulmonary bypass. The aortic arch was resected and replaced by an artificial graft. Pathological examination revealed a primary lesion of adenocarcinoma in the left upper lobe and contiguous lymph node involvement, pT4N2M0. He was discharged and followed as an outpatient, however he died of miswallowing 10 months later. Such an extensive operation may be of value in selected patients.

Adenocarcinoma↗
PubMed1996

A simple procedure for large-scale purification of 9-cis beta-carotene from Dunaliella bardawil.

For experiments designed to obtain reliable data on the metabolic pathway and biological function of 9-cis beta-carotene, sufficient quantity of this substance in pure form is needed. For this purpose, we decided to purify 9-cis beta-carotene from the dry powder of the alga Dunaliella bardawil. By use of both silica gel and ODS open column chromatography and high-performance liquid chromatography (HPLC) on an ODS column and by treatment of the sample with ethanol, we could obtain this carotenoid as fine needle-shaped orange crystals. They were found to be highly pure as judged by analytical HPLC, absorption spectrum, and nuclear magnetic resonance analysis.

Chlorophyta↗
PubMed1996

Alpha-class isozymes of glutathione S-transferase in rat liver cytosol possess glutathione peroxidase activity toward phospholipid hydroperoxide.

Selenium-independent enzymes, found in the liver cytosol of selenium deficient rats, that are capable of reducing dilinoleoyl phosphatidylcholine hydroperoxide in the presence of reduced glutathione [Guan et al., (1995) Biochem. Mol. Biol. Int., 37, 1103-1110] were purified to homogeneity by use of successive chromatography on glutathione affinity and Mono P columns. The molecular weight of the purified protein was estimated by gel filtration to be approximately 50 kDa. Upon isoelectric focusing, the purified preparation showed two protein bands having pI values of 8.6 and 8.8. Both proteins had reactivity against both 1-chloro-2,4-dinitrobenzene and dilinoleoyl phosphatidylcholine hydroperoxide in the presence of reduced glutathione. Each of them consisted of two subunits having molecular weights of 24.3 kDa and 26 kDa, as estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The large subunit was identified as rat glutathione S-transferase (GST) 2 (Yc subunit) based on the amino-terminal amino acid sequence analysis. The small subunit was considered to be most probably rat GST 1 (Ya subunit). From these results, we conclude that the basic alpha-class isozymes of GST in rat liver cytosol possess glutathione peroxidase activity toward phospholipid hydroperoxide.

Animals↗
PubMed1996

Effects of clobazam and its active metabolite on GABA-activated currents in rat cerebral neurons in culture.

PURPOSE: The antiepileptic effects of clobazam, a 1,5-benzodiazepine, have been well documented in animal experiments and clinical trials. However, the drug's mechanisms of antiepileptic actions are still undetermined. The purpose of this study was to learn how clobazam and its active metabolite modulate gamma-aminobutyric acid (GABA)-activated currents in rat cerebral neurons in culture. METHODS: Whole-cell voltage-clamp recordings were performed on cultured cerebral neurons of the rat. Clobazam or its metabolite N-desmethylclobazam was dissolved in the extracellular solution and applied for 2 s by pressure ejection from a micropipette. To maintain GABA-activated currents, 2 mM Mg adenosine triphosphate (ATP) was added to the intracellular solution. RESULTS: GABA elicited outward currents that were mediated by GABAA receptor-coupled Cl- channels. Applying clobazam with 10 microM GABA elicited enhanced outward currents. Flumazenil, an antagonist of the benzodiazepine receptor, inhibited the enhancing effect of clobazam. The enhancement ratio increased as much as 2.28-fold in a dose-dependent manner at a concentration of 3 microM clobazam. However, it started to decrease at a concentration of 10 microM clobazam. The metabolite N-desmethylclobazam was tested in the same manner, and exhibited an identical dose-dependent enhancement of GABA-activated currents. CONCLUSIONS: The antiepileptic effects of the 1,5-benzodiazepines are attributed to the enhancement of GABAergic inhibitory neurotransmission. The antiepileptic effects of clobazam are thought to depend mainly on its active metabolite N-desmethylclobazam, which is present in high concentrations in patients who receive long-term clobazam. Clobazam's enhancement of GABA-activated currents was most marked on weaker GABA currents. We therefore infer that clobazam acts more efficiently on tissues in which the release of GABA is diminished.

Animals↗