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Biomedical subjects

I Wakabayashi

Publications and source records attributed to I Wakabayashi.

At least 73 records · Page 4Linked to original sources
PubMed1998

[Analysis of air pollution and prevalence rate of allergic diseases among elementary school children in Kawaguchi and Hatogaya city].

Kawaguchi and Hatogaya City are located on the northern edge of Tokyo. We analysed between air pollution and prevalence rate of allergic diseases among elementary school children in this area. A prevalence rate of allergic diseases in 1996 May and June was as follows; bronchial asthma 13.5%, atopic dermatitis 24.5%, allergic rhinitis and/or conjunctivitis 22.8%, urticaria 12.4%, food allergy 7.8% and drug allergy 2.2%, respectively. Air pollution of this area was analysed to check the levels of nitrogen dioxide (NO2), sulfur dioxide (SO2) and suspended particulate matters (SPM). NO2 pollution was relatively high in urban area, and SPM pollution was especially high around the highways. SO2 pollution was lower than the environmental standard. No relationship was found between the prevalence rate of bronchial asthma, atopic dermatitis, allergic rhinitis and/or conjunctivitis and air pollution, but it was found that these diseases are slightly related to population density (p < 0.1, p < 0.01, p < 0.1, respectively).

Air Pollutants↗
PubMed1997

Brain beta-endorphin and other opioids are involved in restraint stress-induced stimulation of the hypothalamic-pituitary-adrenal axis, the sympathetic nervous system, and the adrenal medulla in the rat.

Opiates and opioids have complex effects on the hypothalamic-pituitary-adrenal axis, and they stimulate the sympathetic nervous system. This study was designed to clarify the role of brain beta-endorphin in the mechanism by which stress increases plasma concentrations of adrenocorticotropin (ACTH), epinephrine (E), and norepinephrine (NE). Intracerebroventricular (i.c.v.) administration of beta-endorphin to rats significantly increased plasma ACTH levels at doses of 0.09, 0.3, and 1.5 nmol, and plasma E and NE levels at doses of 0.3 and 1.5 nmol. The rise of plasma ACTH, E, and NE levels by 0.3 nmol beta-endorphin was inhibited by intravenous (i.v.) administration of 2 mg/kg b.wt. naloxone. I.v. administration of anti-rat corticotropin-releasing hormone (CRH) rabbit serum completely blocked the beta-endorphin-induced ACTH secretion without affecting the secretion of E and NE. I.c.v. administration of anti-beta-endorphin rabbit gamma-globulin attenuated a 30-min restraint stress-induced rise of plasma ACTH levels without significant influence on the rise of E and NE levels, whereas i.v. administration of naloxone attenuated the restraint stress-induced rise of plasma ACTH, E and NE levels. These results suggest that i.c.v. administration of beta-endorphin stimulates the secretion of ACTH, E, and NE through opiate receptor, and that brain CRH mediates the beta-endorphin-induced secretion of ACTH. The results also suggest that brain beta-endorphin is, at least in part, involved in the restraint stress-induced stimulation of the hypothalamic-pituitary-adrenal axis, and that some opioids other than beta-endorphin are involved in the stimulatory mechanism of the autonomic nervous system and the adrenal medulla in the rat.

Adrenal Medulla↗
PubMed1997

Divergent effects of extracellular and intracellular alkalosis on Ca2+ entry pathways in vascular endothelial cells.

Modulation by alkalosis of basal leak Ca2+ entry and store-depletion-induced Ca2+ entry was investigated in the vascular endothelial cell line ECV 304. Ca2+ entry was monitored as the increase in the intracellular free Ca2+ concentration ([Ca2+]i) induced by elevation of the extracellular Ca2+ concentration. When ECV 304 cells were challenged with 100 nM thapsigargin in nominally Ca2+-free solution, [Ca2+]i increased transiently, and the increase in [Ca2+]i during a subsequent cumulative elevation of extracellular Ca2+ (from nominally Ca2+-free up to 5 mM) was markedly enhanced compared with non-stimulated cells (i.e. basal Ca2+ leak). Prolonged elevation of the extracellular pH (pHo) from 7.4 to 7.9 did not affect resting [Ca2+]i or the thapsigargin-induced [Ca2+]i transient evoked in nominally Ca2+-free solution, but increased leak Ca2+ entry as well as store-depletion-activated Ca2+ entry significantly. Basal Ca2+ leak and store-depletion-activated Ca2+ entry were enhanced either by acute elevation of pHo from 7.4 to 7.9 or by chronic alkalosis (pHo=7.9). Stimulation of Ca2+ entry by extracellular alkalosis was observed both in normal and in high extracellular K+ (110 mM) solution, suggesting that the effects of alkalosis are independent of membrane potential. The intracellular pH (pHi) increased slightly during both acute and chronic extracellular alkalosis (from 7.22+/-0.01 to 7.37+/-0.04 and 7. 45+/-0.05 respectively). Elevation of pHi to 7.60+/-0.06 at constant pHo by administration of 20 mM NH4Cl failed to stimulate, and in fact inhibited, store-depletion-activated Ca2+ entry. Our results demonstrate that a decrease in the extracellular but not the intracellular proton concentration promotes both basal and stimulated Ca2+ entry into endothelial cells.

Alkalosis↗
PubMed1997

Extracellular Ca2+-dependent contractile action of phorbol 12,13-dibutyrate on gall bladder from guinea pig.

The effects of phorbol 12,13 dibutyrate (PDBu) on the isometric tone of gall bladder strips isolated from guinea pig were investigated. PDBu caused the development of a contractile force at concentrations of 5 nM to 1 microM, which was abolished by staurosporine (30 nM). The contraction was completely inhibited in Ca2+-free solution and by pretreatment with verapamil (1 microM) or nifedipine (1 microM). A lower concentration of PDBu (1 nM) potentiated the contractile response to KCl: it increased the sensitivity, but not the reactivity of KCl-induced contraction. Ca2+-induced contraction in the solution with 15 mM KCl was significantly augmented by the pretreatment with 1 nM PDBu. However, PDBu (1 nM) affected neither Ca2+-induced contraction in the presence of Ca2+ ionophore A23187 (0.7 microM) and verapamil (1 microM) nor Ba2+-induced contraction in the Ca2+-free solution. These results suggest that activation of protein kinase C induces completely extracellular Ca2+-dependent contraction by activating the voltage-dependent Ca2+ channels in gall bladder of guinea pig.

Animals↗
PubMed1997

Daunorubicin-induced smooth muscle contraction: involvement of Ca2+ entry mechanism.

The mechanisms of the smooth muscle contractile action of daunorubicin were investigated using guinea-pig aortae, and the involvement of the Ca2+ entry mechanism was compared among different smooth-muscle preparations. In the aorta, daunorubicin showed a concentration-dependent contractile action at concentrations of 10-200 microM. The contractile response to daunorubicin was completely dependent on extracellular Ca2+, but only slightly sensitive to verapamil or nifedipine. Trifluoperazine abolished the contraction by daunorubicin, but no significant effect was noted with amiloride, phentolamine, indomethacin or staurosporine. The order of potency (sensitivity) for daunorubicin-induced smooth muscle contraction was oesophagus = gall bladder = iliac artery > bronchus = aorta, while that of maximum reactivity was iliac artery = aorta > bronchus = oesophagus = gall bladder. In the portal vein, daunorubicin showed no contractile action. Although the smooth muscle contraction induced by daunorubicin was strongly dependent on extracellular Ca2+ in the aorta, iliac artery, bronchus, oesophagus and gall bladder, its sensitivity to verapamil varied among the different smooth muscle preparations, with the sensitivity being iliac artery = gall bladder > bronchus = oesophagus > aorta. These results suggest that daunorubicin has contractile action on various kinds of smooth muscle, mainly via the transplasmalemmal Ca2+ entry mechanism, but the degree of involvement of the voltage-dependent Ca2+ channel differs among the different smooth muscle preparations.

Animals↗
PubMed1997

A comparative analysis of the transplant potential of umbilical cord blood versus mobilized peripheral blood stem cells.

Human umbilical cord blood (UCB) is currently considered as a third source of hematopoietic stem cells for transplantation, following the bone marrow and growth-factor-mobilized peripheral blood (MPB). To evaluate the potential benefits of UCB, we performed a comparative study of the properties of the stem cells in UCB and MPB samples. CD 34+ cell determination and CFU-GM colony assay showed a lower frequency of committed progenitors in UCB than in MPB. In contrast, a higher of the CD 34+ CD 38- subset in UCB suggested that more primitive, multipotent progenitors are enriched in UCB than in MPB. Phenotypic analysis of UCB lymphocytes revealed a reduced level of T cell subsets, especially cytotoxic CD 8+ lymphocytes, which might minimize graft versus host disease in clinical practice. In conclusion, UCB is an attractive alternative source for stem cell transplantation, but ex vivo expansion of stem/progenitor cells could be effective for attaining rapid and safer hemopoietic reconstruction.

Blood Cell Count↗
PubMed1997

Microinjection of rat GH but not human IGF-I into a defined area of the hypothalamus inhibits endogenous GH secretion in rats.

It has been surmised that GH exerts feedback action on the hypothalamus and thereby regulates its own secretion. Our previous studies suggested that GH acts on somatostatin neurons in the hypothalamic periventricular nucleus (PeV) and neuropeptide Y (NPY) neurons in the hypothalamic arcuate nucleus (ARC). However, there remains uncertainty whether GH acts directly or indirectly through the generation of IGFs on the hypothalamus to regulate its own secretion. To examine this, rat GH (rGH) or human IGF-I was injected directly into a defined area of the hypothalamus, and the blood GH profile was observed in conscious male rats. In the rats given 0.5 microgram rGH into the ARC or PeV bilaterally, GH secretion was inhibited, and the inhibition lasted for 12 h. During the period of inhibition, the duration and amplitude of GH pulses were significantly decreased and the episodic secretion of GH appeared irregularly compared with the vehicle-injected control rats. In control rats given the vehicle or those given rGH into the lateral hypothalamus, the blood GH profile did not change and pulsatile GH secretion was produced every 3 h. When 0.1 microgram IGF-I was injected into the ARC or PeV bilaterally, the blood GH secretory pattern was not affected. Together with the results of our previous studies showing that c-fos gene expression was induced by systemic administration of GH and that GH receptor mRNA was contained in somatostatin neurons in the PeV and NPY neurons in the ARC, the data of the present study indicate that GH, but not IGF-I, acts on the cells in the ARC and the PeV or in their vicinity to inhibit its own secretion, presumably by activating the somatostatin and NPY neurons.

Animals↗
PubMed1997

Herbal medicine-associated lead intoxication.

A female patient visited our hospital with abdominal pain and anemia. Examination for a gastrointestinal disease gave no diagnostic information. Laboratory studies of the parameters of heme biosynthesis revealed an enzymatic inhibition by lead. The diagnosis of lead poisoning was confirmed by detection of an elevated blood lead level. Excessive lead ingestion was thought to be caused by herbal medicines and/or by an earthen teapot.

Abdominal Pain↗
PubMed1997

Cushing's syndrome due to bilateral adrenocortical adenomas with different pathological features.

A 48-year-old woman with Cushing's syndrome due to bilateral adrenocortical adenomas is reported. The patient presented with a typical Cushingoid appearance. The serum cortisol level was elevated with loss of the diurnal rhythm and the plasma adrenocorticotropic hormone (ACTH) level was undetectable. Dynamic testing showed no suppression of urinary 17-OHCS by high-dose dexamethasone and no stimulation by metyrapone. An abdominal computed tomography (CT) scan showed bilateral adrenal tumors. Bilateral adrenalectomy was performed. The right adrenal gland contained a tumor that was encapsulated and consisted mainly of compact cells. The surrounding cortex was atrophic. The left adrenal gland contained an encapsulated tumor composed predominantly of clear cells. There were numerous small adrenocortical nodules in the surrounding cortex. Immunohistochemical analysis of steroidogenic enzymes (P450scc, 3beta-HSD, P450c21, P450c17 and P450c11) was performed. Immunoreactivity of all the enzymes was intense in the compact cells of the right adrenocortical adenoma, while the adjacent non-neoplastic cortex was negative for the enzymes. In the left adrenal tumor, the immunoreactivity of 3beta-HSD was intense, while that of P450c17 was weak. In the adrenocortical nodules, 3beta-HSD activity was sporadically observed. G protein genes encoding Gs alpha and Gi2 were examined for activating mutations at codons 201 and 227 (Gs alpha) and codons 179 and 205 (Gi2 alpha) in the bilateral adrenal tumors, but no mutations were found. The bilateral adenomas of this patient showed marked differences in microscopic and immunohistochemical studies, suggesting that the capacity of steroidogenesis differs between the right and left tumors.

Adrenal Cortex Neoplasms↗
PubMed1997

Acute lymphoblastic leukemia with isolated adrenocorticotropic hormone deficiency.

A 57-year-old female was admitted to our hospital because of Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL). On admission, disturbance of consciousness and hyponatremia were recognized. The patient's endocrinological data showed low levels of adrenocorticotropic hormone (ACTH) (less than 5 pg/ml) and cortisol (5.9 microg/dl). Other anterior pituitary hormones were normal. Plasma ACTH and cortisol did not respond to the corticotropin releasing factor (CRF) test. A diagnosis of isolated ACTH deficiency was made. This is a rare case of isolated ACTH deficiency complicated with hematological malignancies.

Adrenocorticotropic Hormone↗
PubMed1997

[Potentiating effect of ethanol on alpha 1 adrenergic receptor mediated contraction of thoracic aorta from guinea pig].

Using aortic strips isolated from guinea pigs, effects of ethanol on vascular smooth muscle tonus were studied. 50mM of ethanol significantly potentiated the contractions induced by norepinephrine and phenylephrine, but did not influence those induced by KCl and clonidine. Furthermore, ethanol significantly augmented the contraction induced by phenylephrine in the presence of verapamil, and did not have any effects on the contractions induced by A23187, Ba2+, PDBu and BAY K 8644. These results indicate that ethanol potentiates the alpha 1 adrenergic receptor-mediated contraction, depending on the extracellular calcium influx via the receptor-operated calcium channel.

Adrenergic alpha-Agonists↗
PubMed1997

Relationship between mortality rate of stomach cancer and cerebrovascular disease and concentrations of magnesium and calcium in well water in Hyogo prefecture.

The concentration of Mg, Ca and total hardness of well and tap water were examined in 98 towns and cities in Hyogo prefecture. The annual mortality rates of stomach cancer and CVD in these areas during 1975-1979 were analyzed by the concentration of Mg and Ca in well water. The mortality rate of stomach cancer was correlated significantly positively to Mg2+/Ca2+ ratio of well water, and a similar tendency was shown in tap water. A covariance analysis indicated Mg2+ to be correlated significantly to the mortality rate of stomach cancer. Thus, it is suggested that the relatively high concentration of Mg2+ compared to Ca2+ in drinking water might be one of the causes of stomach cancer in Japanese. But the concentration of Ca2+ was correlated significantly negatively to the mortality rate of CVD.

Calcium↗
PubMed1996

Increased pituitary growth hormone-releasing factor (GRF) receptor messenger ribonucleic acid expression in food-deprived rats.

In prolonged food-deprived rats, growth hormone (GH) secretion in response to exogenous GH-releasing factor (GRF) is enhanced both in vivo and in vitro. We tested the hypothesis that, in fasted rats, GRF receptors in the pituitary may be up-regulated. The expression of mRNA for the GRF receptor in the pituitary and GRF binding to the pituitary membrane were examined in adult male Wistar rats deprived of food for 72 h. The level of GRF receptor mRNA in the pituitary was significantly increased after 48 h food deprivation and was more than 3 times the level in control rats after 72 h food deprivation. GRF binding to the pituitary was significantly increased after 72 h food deprivation. The results of the present study provide evidence regarding changes in the GH axis in fasted rats, involving increased pituitary responsiveness to GRF and an increase in the pituitary membrane GRF receptor concentration.

Animals↗
PubMed1996

Inhibitory effect of neuropeptide Y on growth hormone secretion in rats is mediated by both Y1- and Y2-receptor subtypes and abolished after anterolateral deafferentation of the medial basal hypothalamus.

Neuropeptide Y (NPY) may play a physiological role in the regulation of growth hormone (GH) secretion by acting via somatostatin (SS) in the periventricular nucleus (PeV), as well as via the GH-releasing factor in the arcuate nucleus (ARC) of the medial basal hypothalamus (MBH). The objectives of the present study were to determine the neuron structures and receptor subtypes necessary for mediating the inhibitory effect of NPY on GH secretion in unanesthetized male rats. To eliminate the influence of hypophyseotropic SS, anterolateral deafferentation (ALC) of the hypothalamus was performed. Intracerebroventricular (i.c.v.) administration of 1.17 nmol of NPY decreased the blood level of GH for 3-4 h in sham-operated rats, while the procedure was without effect in ALC rats. The i.c.v. administration of 1.17 nmol of a Y1-receptor agonist ([Leu31, Pro34]-NPY) or a Y2-receptor agonist (NPY 13-36 and NPY 3-36) similarly suppressed the blood GH level. The data support the hypothesis that neuron structures anterolateral to the MBH are required for NPY-induced inhibition of GH secretion that is mediated via Y1- and Y2-receptor subtypes. Combined with data of other investigators, SS is likely the neurohumoral mediator of the effect of NPY on GH secretion.

Afferent Pathways↗
PubMed1996

Neuropeptide Y reverses corticotropin-releasing hormone- and psychological stress-caused shortening of sodium pentobarbital-induced sleep in rats.

Intracerebroventricular injection of neuropeptide Y (NPY) prolonged sodium pentobarbital (PhNa)-induced sleep in rats. The prolongation of PbNa-induced sleep by NPY was blocked by naloxone. Both corticotropin-releasing hormone and psychological stress caused shortening of PbNa-induced sleep, and the shortening was reversed by NPY. These results suggest that NPY has a sedative action and that an opioid system in the brain mediates at least in part the action of NPY.

Animals↗