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H Yoshimatsu

Publications and source records attributed to H Yoshimatsu.

At least 55 records · Page 3Linked to original sources
PubMed1999

[An autopsy case of lung cancer accompanied by pneumoperitoneum].

We report a case of pneumoperitoneum at the end stage of lung cancer. The patient was an 81-year-old man who experienced only mild abdominal pain and fullness. The pneumoperitoneum spontaneously disappeared. Ruptured viscera and peritonitis were not observed at autopsy. We speculated that air had moved from the lung cancer lesion to the mediastinum, and then through the retroperitoneal space into the peritoneal space. When pneumoperitoneum is observed, lung cancer and other intrathoracic diseases should be suspected as causes. Also, it may be necessary to carefully examine the patient for fever, general appearance, abdominal findings, and laboratory findings, including white blood cell count and C-reactive protein level, and on that basis differentiate from ruptured viscus, which requires an emergency laparotomy.

Aged↗
PubMed1998

Molecular cloning of rat uncoupling protein 2 cDNA and its expression in genetically obese Zucker fatty (fa/fa) rats.

We isolated rat UCP2 cDNA, which has been proposed to play an important role in mammalian thermogenesis and body weight regulation. The nucleotide sequence of the cDNA revealed that the rat UCP2 protein is composed of 309 amino acid residues, and is 99% and 95% identical to the mouse and human proteins, respectively. The molecular weight of rat UCP2, calculated from the predicted amino acid sequence, was 33,369, and the UCP2 protein of this size was detected when the cDNA was expressed in vitro. Northern blot analysis revealed that the corresponding mRNA is approximately 1.7 kb in size, and is expressed in a variety of rat organs, with predominant expression in the heart, lung and spleen. UCP2 mRNA levels in the heart, liver, muscle and epididymal adipose tissue of Zucker fatty (fa/fa) rats were comparable to those in the lean littermates, while ob mRNA level markedly increased in the epididymal adipose tissue of Zucker (fa/fa) rats.

Amino Acid Sequence↗
PubMed1998

Satiation and masticatory function modulated by brain histamine in rats.

Both the ventromedial hypothalamus (VMH) and the mesencephalic trigeminal sensory nucleus (Me5) are densely innervated by histaminergic neurons. The depletion of neuronal histamine (HA) from the Me5 by the bilateral microinfusion of 448 nmol/rat alpha-fluoromethylhistidine (FMH), a specific suicide inhibitor of histidine decarboxylase, reduced the eating speed and prolonged meal duration, while leaving the meal size unaffected. HA depletion from the VMH increased the size of the meal and prolonged its duration, but not the eating speed. When the HA turnover rate was measured at 15 min after the scheduled feeding following fasting for less than 24 hr, the rate increased in the region including the Me5, but not in the hypothalamus. The turnover rate reached higher levels at 60 min in both regions. Gastric intubation of an isocaloric liquid diet or an equivolume of water with the liquid diet abolished the increase in HA turnover both in the Me5 region and the hypothalamus. The present findings indicate that brain HA thus modulates satiation through both the VMH and masticatory function as well as due to the action of the Me5. The HA function activated by mastication began earlier in the Me5 and later in the hypothalamus due to a signal originating from the oral proprioceptors and initiated by chewing.

Animals↗
PubMed1998

[Clinical evaluation on causes of death in patients with pulmonary tuberculosis during the past 3 years (1994 to 1996)].

We evaluated the cause of death in patients with pulmonary tuberculosis during the past 3 years (1994 to 1996). Of 502 tuberculous patients, 58 (11.6%) patients died. Most of them were aged or under poor nutritional conditions. Of 378 active tuberculous patients, 39 (10.3%) patients died (group A). Of 124 old tuberculous patients or cases with extensive sequelae of tuberculosis, 19 (23.4%) patients died (group B). In the group A, 15 patients died in spite of improvements in tuberculosis lesions. All the intubated patients with active tuberculosis died. In the group B, most of patients died of respiratory failure or pneumonia.

Adult↗
PubMed1997

Enhanced expression of uncoupling protein 2 gene in rat white adipose tissue and skeletal muscle following chronic treatment with thyroid hormone.

Evidence is rapidly emerging which suggests that uncoupling protein 2 (UCP2), by virtue of its ubiquitous expression, may be important for determining basal metabolic rate. To assess the functional modulation of UCP2 gene expression in relation to body weight control, we examined the effects of hyperthyroid state induced by chronic treatment with triiodothyronine (T3) on UCP2 mRNA expression in male rats. Daily subcutaneous injection of T3 (37 pmol/100 g body weight) for 7 days increased UCP2 mRNA expression in brown adipose tissue (BAT), white adipose tissue (WAT) and the soleus muscle 1.6-, 1.6- and 1.7-fold compared to the controls, respectively, and increased UCP1 mRNA expression in BAT 1.2-fold. In contrast, the same treatment with T3 decreased both ob mRNA expression in WAT and plasma leptin level 0.5-fold for each. The present results suggest that T3 may directly increase UCP2 expression independently of leptin action.

Adipose Tissue↗
PubMed1997

Hypothalamic neuronal histamine: implications of its homeostatic control of energy metabolism.

In a series of studies on histaminergic functions in the hypothalamus, probes to manipulate activities of histaminergic neuron systems were applied to assess its physiologic and pathophysiologic implications using non-obese normal and Zucker obese rats, an animal model of genetic obesity. Food intake is suppressed by either activation of H1-receptor or inhibition of the H3-receptor in the ventromedial hypothalamus (VMH) or the paraventricular nucleus, each of which is involved in satiety regulation. Histamine neurons in the mesencephalic trigeminal sensory nucleus modulate masticatory functions, particularly eating speed through the mesencephalic trigeminal motor nucleus, and activation of the histamine neurons in the VMH suppress intake volume of feeding at meals. Energy deficiency in the brain, i.e., intraneuronal glucoprivation, activates neuronal histamine in the hypothalamus. Such low energy intake in turn accelerates glycogenolysis in the astrocytes to prevent the brain from energy deficit. Thus, both mastication and low energy intake act as afferent signals for activation of histaminergic nerve systems in the hypothalamus and result in enhancement of satiation. There is a rationale for efficacy of a very-low-calorie conventional Japanese diet as a therapeutic tool for weight reduction. Feeding circadian rhythm is modulated by manipulation of hypothalamic histamine neurons. Hypothalamic histamine neurons are activated by an increase in ambient temperature. Hypothalamic neuronal histamine controls adaptive behavior including a decrease in food intake and ambulation, and an increase in water intake to maintain body temperature to be normally constant. In addition, interleukin-1 beta, an endogenous pyrogen, enhanced turnover of neuronal histamine through prostaglandin E2 in the brain. Taken together, the histamine neuron system in the hypothalamus is essential for maintenance of thermoregulation through the direct and indirect control of adaptive behavior. Behavioral and metabolic abnormalities of obese Zucker rats including hyperphagia, disruption of feeding circadian rhythm, hyperlipidemia, hyperinsulinemia, and disturbance of thermoregulation are essentially derived from a defect in hypothalamic neuronal histamine. Abnormalities produced by depletion of neuronal histamine from the hypothalamus in normal rats mimic those of obese Zuckers. Grafting the lean Zucker fetal hypothalamus into the obese Zucker pups attenuates those abnormalities. These findings indicate that histamine nerve systems in the brain play a crucial role in maintaining homeostatic energy balance.

Adaptation, Physiological↗
PubMed1997

[The usefulness of radiotherapy in the management of intracranial meningioma: a review of 29 patients].

Twenty-nine patients with intracranial meningiomas were treated with a high-energy linear accelerator (4-10 MV. X rays and electron beams) between 1980 and 1992 at the Hiroshima Prefectural Hiroshima Hospital. We investigated the relationships between tumor size and tumor response, histological type and tumor response, and grade of operation using Simpson's classification and recurrence rate. Meningiomas were greatly reduced between 1 month and 46 months after radiotherapy, the average being 14 months. In the group with a tumor size of less than 5 cm2, 3 patients obtained CR, 5 patients NC and 1 patient PD. Tumor response was 89% in the group with a combination of CR with NC. In the group with a tumor size of 5 to 20 cm2, 2 patients obtained PR, 1 patient NC and 1 patient PD. Tumor response was 75% in the group with a combination of PR with NC. In the group with a tumor size of more than 20 cm2, 3 patients showed NC, 3 patients PD. Tumor response was 50% in the group with NC. In the group with a tumor size of less than 20 cm2, tumor response was 85%. In the group with a tumor size of more than 20 cm2, it was 50%. Though there were no statistically significant differences between the two groups, a tumor size of less than 20 cm2 had a tendency to be more responsive than one of more than 20 cm2. The response of meningioma of the transitional type was worse than that of the meningothelial type and fibroblastic type. Fourteen patients after Simpson grade II or III operation were free of recurrence. The results of this study support the role of radiotherapy for meningioma which is less than 20 cm2, and also for treatment after Simpson grade II or III operation.

Adult↗
PubMed1996

Ornithine decarboxylase activity in rat intestinal mucosa and liver is stimulated by central administration of 2-deoxy-D-glucose but not of 2,5-anhydro-D-mannitol.

It has been shown that 2-deoxy-D-glucose (2-DG) inhibits glucose utilization and elicits feeding through the lateral hypothalamus. In contrast, 2,5-anhydro-D-mannitol (2,5-AM), blocking glycogenolysis and/or gluconeogenesis, elicits feeding through the ventromedial hypothalamus. The aim of the present study was to determine whether ornithine decarboxylase (ODC) activity in the rat small intestine is stimulated by infusion into the third ventricle of 2-DG or of 2,5-AM. Under anesthesia, a cannula was implanted into the third ventricle one week before the experiment. Each rat was infused with 6, 12, and 24 mumol 2-DG or 2,5-AM into the third ventricle without disturbing the behavior. Ingestive behavior was observed for one h after the infusion. ODC activity in the intestinal mucosa and the liver was measured 2 h after the infusion. Additionally, ODC activity was measured in vagotomized rats. Both test solutions elicit feeding at 24 mumol/rat. Infusion of 2-DG into the cerebroventricle significantly increased ODC activity in the duodenal and jejunal mucosa and the liver. In contrast to 2-DG, infusion of 2,5-AM did not increase ODC activity in the intestinal mucosa or liver. Truncal vagotomy attenuated the increase of ODC activity in the intestinal mucosa and liver induced by 2-DG. The present study showed that 2-DG, but not 2,5-AM, increased ODC activity in the peripheral organs, indicating that glucose-metabolism at specific sites of the central nervous system, including the lateral hypothalamus, is important for stimulatory signals to ODC activity. It is also indicated that the stimulatory signals from the central nervous system are mediated, at least in part, via the efferent vagal nerve.

Animals↗
PubMed1996

[A patient with Goodpasture's syndrome revealed a poor prognosis regardless of receiving intensive therapy from an early stage after onset].

Goodpasture's syndrome has been reported as a disease that has a favorable prognosis when the patient receives intensive immunosuppressive drug-therapy from an early stage after onset. The present report describes a 50-year-old woman, who exhibited progressive renal failure accompanied by pulmonary hemorrhage, and an increase in serum level of antiglomerular basement membrane (GBM) antibody. Initial histological examination of a renal specimen indicated a severe fibrocellular crescentic glomerulonephritis with a linear deposition of Ig-G and C3 along the glomerular capillary wall. The patient was thus diagnosed as having Goodpasture's syndrome. Therapy with pulse treatment of steroid (corticosteroid hormone), immunosuppressive agents, or plasma-exchange for the removal of anti-GBM antibody was adopted a week after the clinical onset. However, histological amelioration of the glomeruli did not occur with this treatment in the second biopsy, while glomerular damage advanced progressively. In contrast to other patients with Goodpasture's syndrome, our case revealed an unfavorable outcome regardless of receiving intensive therapy from an early period after onset, which suggests that more intensive therapy of another approach to this patient may have been necessary.

Anti-Glomerular Basement Membrane Disease↗
PubMed1995

alpha-amylase inhibitor increases plasma 3-hydroxybutyric acid in food-restricted rats.

The effect on energy metabolism of delayed absorption of starch by inhibition of alpha-amylase was examined by considering levels of plasma glucose and 3-hydroxybutyric acid (3-OHBA) in rats. Addition of alpha-amylase inhibitor (alpha AI) to a high starch diet delayed the plasma glucose response after feeding: peak plasma glucose levels in the control group occurred 15 min after feeding, whereas in the alpha AI group this peak did not occur until 30 min after. The total plasma glucose response was not different between the two groups. Plasma 3-OHBA levels 1 day after food restriction increased approximately five-fold in both groups. After 3 days of food restriction, the alpha AI group maintained the same level of plasma 3-OHBA as after 1 day of food restriction, while the control group showed significantly decreased levels of 3-OHBA. After 3 days of food restriction, plasma insulin levels were significantly decreased in the alpha AI group compared with the corresponding levels of the control group and with levels before the restriction. There was no significant difference in body weight between the two groups. These findings suggest that delayed hyperglycemia due to delayed absorption of starch following alpha AI loading may attenuate insulin secretion, leading to altered metabolism of 3-OHBA during the delayed response to energy deficit.

3-Hydroxybutyric Acid↗
PubMed1995

Effects of auricular acupuncture stimulation on nonobese, healthy volunteer subjects.

Effects of auricular acupuncture stimulation on nonobese healthy volunteers were investigated. Subjects (n = 35) averaged 34.5 years old, and BMI was 25.3 kg/m2. Small (0.15 x 2.0 mm) auricular needles were applied intracutaneously into the bilateral cavum conchae that was identified by having less than 100 k omega resistance. Body weight was measured four times a day and charted by the subjects themselves. Results showed that, in the period 11-2, in which only body weight was measured, without auricular acupuncture stimulations, 57.1% of the subjects reduced their body weight. This indicates that charting body weight themselves might be useful to maintain their weight. In the auricular acupuncture treated period, 19 (70.4%) out of 27 decreased (p < 0.01), 5 (18.5%) was increased, and 3 (11.1%) had no change in body weight. In conclusion, the results suggest that success in maintaining weight reduction can be attributed to graphic illustration of one's weight pattern. Bilateral auricular acupuncture stimulation can also reduce body weight of healthy non-obese subjects. This is consistent with the suggestion that it might be effective in the treatment of obese patients.

Acupuncture Points↗
PubMed1995

Hypothalamic neuronal histamine modulates adaptive behavior and thermogenesis in response to endogenous pyrogen.

Homeostatic involvement of hypothalamic neuronal histamine in adaptive behavior and thermogenesis was investigated when interleukin-1 beta (IL-1 beta), one of the endogenous pyrogens, was infused peripherally in rats. IL-1 beta decreased food and water intake and elevated body temperature. Depletion of neuronal histamine in the hypothalamus induced by alpha-fluoromethylhistidine, a suicide inhibitor of the histamine synthesizing enzyme histidine decarboxylase (HDC), attenuated the suppressive effect of IL-1 beta on food intake, facilitated the inhibitory effect on water intake, and enhanced its thermogenic effect. Simultaneously IL-1 beta increased activity of HDC and histamine-N-methyltransferase (HMT), a neuronal histamine catabolizing enzyme. Pretreatment with indomethacin completely blocked those increases in turnover of neuronal histamine induced by IL-1 beta. Hypothalamic prostaglandin E2 (PGE2) activated by peripheral IL-1 beta, but not peripheral PGE2, increased both activities of HDC and HMT. Ginsenoside Rg1, a major component of panax ginseng, modulated the suppressive effects of IL-1 beta on ingestive behavior, resulting in a lowering of body temperature. The findings suggest that the effects of IL-1 beta on ingestive behavior and thermogenesis may be modulated by dynamics of hypothalamic neuronal histamine through activation of hypothalamic PGE2 which is elevated by peripheral IL-1 beta.

Adaptation, Physiological↗
PubMed1995

Ginsenoside Rg1 modulates ingestive behavior and thermal response induced by interleukin-1 beta in rats.

Effects of ginsenoside Rg1 (Rg1), a major component of panax ginseng, on changes in ingestive behavior and rectal temperature induced by interleukin-1 beta (IL-1 beta) were investigated in rats. Intraperitoneal (ip) injection of IL-1 beta suppressed food and water intake and elevated rectal temperature. The suppressive effect of IL-1 beta on water intake was converted to an increase when 4.0 mM Rg1 was continuously infused into the third cerebroventricle (ICV) at a rate of 0.966 microliters/h. The elevation of rectal temperature induced by IL-1 beta was attenuated by ICV infusion of Rg1. The feeding suppression caused by IL-1 beta was unaffected by ICV infusion of Rg1. These results suggest that sustained ICV infusion of Rg1 may modulate the effects of IL-1 beta on ingestive behaviors, i.e., increase in water intake and sustained decrease in food intake, resulting in a lowering of body temperature.

Animals↗
PubMed1995

Hypothalamic neuronal histamine modulates physiological responses induced by interleukin-1 beta.

Dynamic involvement of hypothalamic histamine in ingestive behavior and thermogenesis induced by interleukin-1 beta (IL-1 beta) was examined in rats. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta decreased food and water intake and elevated body temperature. However, depletion of neuronal histamine induced by intraperitoneal injection of 160 mumol/rat alpha-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase (HDC), attenuated the suppressive effect of IL-1 beta on food intake, facilitated the suppressive effect on drinking, and enhanced the elevating effect on rectal temperature. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta increased hypothalamic histamine turnover rate. The same dose of IL-1 beta also increased activity of HDC and histamine-N-methyltransferase (HMT). These results suggest that IL-1 beta may stimulate synthesis and release of hypothalamic histamine in presynaptic terminals by activation of HDC and facilitate degradation of extracellular histamine by activation of MHT. These changes in the dynamics of hypothalamic histamine modulate IL-1 beta-induced ingestive behavior and body temperature.

Animals↗
PubMed1995

Histamine effect on ornithine decarboxylase of rat intestine in cases of ischemia-reperfusion compared with refeeding.

Our previous study suggested that histamine might enhance the increase of ornithine decarboxylase activity in injured intestinal mucosa. To test this hypothesis, we measured histamine content in mesenteric lymph and ornithine decarboxylase activity in intestinal mucosa after ischemia-reperfusion in the rat. We examined the effect of alpha-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase, on ornithine decarboxylase activity after ischemia-reperfusion and compared this with its effect on the rat after refeeding. Ischemia-reperfusion was performed by 15-min occlusion of the superior mesenteric artery. After ischemia-reperfusion, histamine content in mesenteric lymph increased, and this increase was completely suppressed by alpha-fluoromethylhistidine pretreatment. In contrast to ischemia-reperfusion, histamine content in mesenteric lymph did not change after refeeding. Ornithine decarboxylase activity increased markedly 3 and 6 hr after ischemia-reperfusion and refeeding, whereas alpha-fluoromethylhistidine attenuated the increase in ornithine decarboxylase activity only in the ischemia-reperfusion group. These results indicate that increase in histamine synthesis in the intestinal mucosa plays an important role in the increase of ornithine decarboxylase activity after ischemia-reperfusion but that histamine is not related to the increase in ornithine decarboxylase activity after refeeding.

Animals↗
PubMed1995

Homeostatic maintenance regulated by hypothalamic neuronal histamine.

By manipulating hypothalamic neuronal histamine, its effects on brain functions related to homeostatic energy balance were assessed in non-obese normal and genetically obese Zucker rats. Feeding behavior was suppressed and drinking was accelerated by either activation of H1 receptors or inhibition of H3 receptors in the ventromedial hypothalamic nucleus (VMH) and the paraventricular nucleus, each of which is a satiety center. Energy deficiency in the brain, i.e., intraneuronal glucoprivation, produced satiation through histaminergic activation of VMH neurons. Such low energy intake in turn induced glycogenolysis in the astrocytes to protect energy deficit in the brain. Histamine neurons in the mesencephalic trigeminal nucleus (Me5) regulated masticatory functions, particularly eating speed, and those in the VMH controlled intake volume at meals. Hypothalamic histamine neurons were activated by high ambient temperature and also by interleukin-1beta, an endogenous pyrogen, through prostaglandin E2 to maintain homeostatic thermoregulation. Behavioral and metabolic abnormalities of obese Zuckers were the result of a defect in hypothalamic neuronal histamine. Abnormalities produced by depletion of neuronal histamine from the normal hypothalamus mimicked those of obese Zuckers. Grafting the lean fetal hypothalamus into the obese pups attenuated those abnormalities.

Animals↗