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Biomedical subjects

K Mine

Publications and source records attributed to K Mine.

At least 19 recordsLinked to original sources
PubMed1995

Esophagoaortic fistula caused by esophageal tuberculosis: report of a case.

We report herein the case of a 73-year-old woman who was urgently admitted to hospital with severe hematemesis. An emergency endoscopy revealed a protruding lesion 36 cm from the incisors; however, respiratory insufficiency precluded surgery and despite aggressive medical treatment, the patient's respiratory status continued to deteriorate, leading to death on the 36th hospital day. An autopsy revealed the source of the hemorrhage to be a fistula connecting the esophagus and the descending aorta. Histopathologic studies showed that this fistula was caused by esophageal tuberculosis.

Aged↗
PubMed1995

Long-term spatial cognitive impairment after middle cerebral artery occlusion in rats: no involvement of the hippocampus.

The behavioral and neurochemical changes in the chronic phase of permanent occlusion of the right middle cerebral artery (MCA) in rats were investigated. One month after MCA occlusion, 23 rats were unable to solve a radial eight-arm maze task during an entire 1-month period, whereas seven rats were able to solve this task. Three months after occlusion, 19 MCA-occluded rats failed to solve the task successfully again for at least 1 month (the cognitively impaired rats), whereas 11 MCA-occluded rats were able to solve it (the cognitively unimpaired rats). The rats that underwent behavioral testing were examined for any changes in the acetylcholine (ACh) levels in the hippocampus using HPLC with electrochemical detection or the formation of long-term potentiation (LTP) in the population spike of the hippocampal CA1 field. The immunohistochemical distribution of either the microtubule-associated protein 2 (MAP2) or glial fibrillary acidic protein (GFAP) in the hippocampus of the cognitively impaired rats was also studied. In the cognitively impaired rats, neither the suppression of the induction of LTP, nor the degradation of MAP2, nor the increase in the GFAP immunoreactivity was observed in the hippocampus. The levels of ACh in the hippocampus did not change significantly among the cognitively impaired, unimpaired, and the sham-operated rats. These results suggest that MCA occlusion is capable of producing long-term spatial cognitive disturbance in rats without any evidence of neurobiological damage in the hippocampus.

Acetylcholine↗
PubMed1995

Long-term spatial cognitive impairment following middle cerebral artery occlusion in rats. A behavioral study.

Behavioral changes in the chronic phase of permanent occlusion of the right middle cerebral artery (MCA) in rats were investigated. One month after MCA occlusion, 23 rats were unable and 7 rats were able to solve a radial 8-arm maze task during a 1-month period. Three months after occlusion, 19 MCA-occluded rats failed to solve the task successfully again during at least a 1-month period (the cognitively impaired rats), and 11 MCA-occluded rats were able to solve it (the cognitively unimpaired rats). When a delay of 60 min was imposed for this task, five cognitively unimpaired rats failed to solve it. The locomotor activity of the cognitively impaired rats increased significantly 2 months after occlusion, and this increase showed good correlation with spatial cognitive deficit. However, the mean time a rat spent at each arm remained unchanged among the cognitively impaired, unimpaired, and sham-operated rats. There was no significant difference in the ratio between the cognitively impaired and unimpaired rats for disturbed motor coordination. These results suggest that MCA occlusion is capable of producing long-term spatial cognitive disturbance in rats. In addition, this spatial cognitive deficit does not seem to be primarily due to hypermotility or a disturbance in motor coordination.

Animals↗
PubMed1994

[A depressive disorder in patients with irritable bowel syndrome and non-ulcer dyspepsia].

The relationships between psychiatric disorders and the symptoms of both irritable bowel syndrome (IBS) and non-ulcer dyspepsia (NUD) are herein investigated and discussed. Functional disorders of the small and large intestine induce irritable bowel syndrome. NUD is a syndrome that displays symptoms that might originate in the upper digestive system despite the absence of any organic disorder. In addition, it has also been suggested that the occurrence of NUD is based on a functional disorder of the upper digestive systems. Based on our studies of serious cases with both NUD and IBS, in approximately 50% of the NUD patients as well as about 50% of the IBS cases, a depressive disorder was found to be most closely related to the onset and continuance of the symptoms of either NUD or IBS. According to the evaluations of NUD and IBS as functional disorders and psychiatric disorders, the patients underwent treatment and all demonstrated a good response to the various treatment regimens. It is thus considered that NUD and IBS should be evaluated as both functional digestive disorders and psychiatric disorders.

Colonic Diseases, Functional↗
PubMed1993

Plasma-free and sulfoconjugated MHPG in major depressive disorders: differences between responders to treatment and nonresponders.

The plasma levels of free and sulfoconjugated forms of 3-methoxy-4-hydroxyphenylglycol (MHPG) were examined before and after treatment in 16 patients with unipolar major depressive disorders without melancholia. The patients were treated with intravenous administration of clomipramine for 4 weeks. Seven depressive disorder patients who showed marked improvement (the improvement group) revealed significant reduction in their plasma sulfoconjugated MHPG levels. In 6 depressive disorder patients who showed no improvement (the no-improvement group), the plasma sulfoconjugated MHPG levels showed no significant change after treatment. The remaining 3 patients, who showed ambiguous change after treatment, were excluded from the analysis. Levels of plasma-free MHPG showed significant change after treatment in neither the improvement group nor in the no-improvement group. It is suggested that levels of plasma sulfoconjugated MHPG may serve as an indicator of brain noradrenergic activity.

Adolescent↗
PubMed1992

Effects of the N-methyl-D-aspartate antagonists on the rise in [Ca2+]i following depolarization in aged rat brain synaptosomes.

The effects of non-competitive NMDA antagonists, MK-801 and dextrorphan in relation to the rise in intracellular Ca2+ concentrations ([Ca2+]i) after stimulation with 15 mM K+ in whole brain synaptosomes from young (3 months old) and aged (24 months old) Fisher344 rats were examined. A fluorescent chelating agent, Rhod-2, was employed to monitor any alterations of K(+)-evoked [Ca2+]i. In young rats, the rise in [Ca2+]i following depolarization was affected by neither dextrorphan (1, 10, 100 microM) nor MK-801 (0.1, 1, 10 microM), while in aged rats, 1 microM dextrorphan and 0.1 microM MK-801 brought about a significant increase in [Ca2+]i following depolarization. In low Mg2+ medium, 10 microM MK-801 and 100 microM dextrorphan significantly inhibited the rise in [Ca2+]i after stimulation with 15 mM K+ in young rats, while neither dextrorphan nor MK-801 could affect the rise in [Ca2+]i significantly in aged rats. When 100 microM NMDA was applied in a medium containing 1.2 mM Mg2+, the rise in [Ca2+]i following depolarization was slightly inhibited by 1 microM MK-801 in young rats, but it was not inhibited significantly by dextrorphan. In aged rats, both 100 microM dextrorphan and 10 microM MK-801 strongly inhibited the rise in [Ca2+]i following depolarization in the presence of 100 microM NMDA. Instead of NMDA, when 100 microM alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), a non-NMDA receptor agonist, was applied, dextrorphan did not inhibit the rise in [Ca2+]i. In low Mg2+ medium, 100 microM NMDA potentiated the inhibitory effect of 10 microM dextrorphan in young rats, while 100 microM dextrorphan or MK-801 did not show any further inhibition by adding 100 microM NMDA. The addition of 100 microM AMPA did not affect the effect of dextrorphan in a low Mg2+ medium in young rats. These results suggest that NMDA antagonist-mediated [Ca2+]i homeostatic system may alter through aging. In addition, the findings that NMDA potentiated the inhibitory effect of NMDA antagonist, which being further potentiated by aging or lowered extrasynaptosomal Mg2+, indicate the possibility that the Mg2+ block to NMDA receptors might be attenuated through aging.

Aging↗
PubMed1992

The facilitating and suppressing effects of delta 9-tetrahydrocannabinol on the rise in intrasynaptosomal Ca2+ concentration in rats.

The effects of delta 9-tetrahydrocannabinol (delta 9-THC) on the rise in intracellular Ca2+ concentrations ([Ca2+]i) after stimulation with 15 mM or 29 mM K+ in rat whole brain synaptosomes were examined. A fluorescent chelating agent, Rhod-2, was employed to monitor any alterations of K(+)-evoked [Ca2+]i. Pretreatment with 10(-10) M delta 9-THC for 3 min enhanced K(+)-evoked [Ca2+]i significantly, while 10(-9), 10(-8) or 5 x 10(-8) M delta 9-THC significantly inhibited the K(+)-evoked [Ca2+]i. These results suggest that delta 9-THC had a biphasic effect on the K(+)-evoked Ca2+ response in rat brain synaptosomes.

Animals↗
PubMed1992

[The relation between irritable bowel syndrome and a major depression].

It has been demonstrated that physical or psychological stress induces dysfunction of bowel movement and intestinal transit in rodents and human. There have been several reports concerning the psychiatric factors involved in the onset and clinical course of irritable bowel syndrome (IBS). We investigated patients with IBS who had been markedly disturbed in their daily life, and it was concluded that the most important psychiatric factor related to the onset and the clinical course of severely impaired IBS is a major depression, fulfilling the criteria of the DSM-III-R. Especially, in diarrhea predominant type of IBS, a major depression was considered to be strongly involved in the onset and the clinical course of IBS. Most of IBS patients with a major depression can be effectively treated with antidepressants and brief psychotherapy. Concerning treatment, the psychological background should be carefully considered.

Antidepressive Agents↗
PubMed1992

[A study of the dynamics of gallbladder contraction in irritable bowel syndrome].

We examined gallbladder motility function after intramuscular injection of caerulein (0.2 micrograms/kg) to the cases of irritable bowel syndrome (IBS) by using ultrasonography. We measured gallbladder area pre and after caerulein injection (0' 5' 10' 15' 20' 25' 30' 40' 50' 60') and calculated contraction rate of gallbladder in each time. We applied one way analysis of variance among the four groups [diarrhea group (N = 9), alternative group (N = 8), constipation group (N = 8), control group (N = 15)]. Gallbladder contraction rate was low in diarrhea group and high in constipation group (p less than 0.05). And then we classified gallbladder contraction pattern to three groups (hyperkinetic, intermediate, hypokinetic). These three groups correlated bowel habits and biliary knocked pain. Therefore, constipation group showed hyperkinetic tendency and diarrhea group showed hypokinetic tendency (chi 2 analysis: p = 0.004 CMH analysis: p = 0.001). And biliary knocked pain significantly appeared in constipation group and hyperkinetic type of gallbladder (chi 2 analysis: p = 0.026, CMH analysis: p = 0.019). Consequently, it was suggested that bowel habits concerned with abnormality of gallbladder motility function in IBS.

Adolescent↗
PubMed1991

Serum pepsinogen I concentrations in peptic ulcer patients in relation to ulcer location and stage.

To investigate the relation of the serum group I pepsinogen (PG I) concentration to the location of gastric ulcers and chronicity of peptic ulcers, ulcer patients (n = 322) were compared with endoscopically normal subjects (n = 174). The mean PG I concentration was significantly higher in male control subjects (n = 90) than in female control subjects (n = 84). In male patients with ulcers in the duodenum (n = 69), antrum (n = 34), or angulus portion (the lower third of the body; n = 83), the mean serum PG I concentration was significantly higher than in the control subjects but in patients with an ulcer in the upper body (n = 49) it was similar to control values. Men with active or healing ulcers (n = 149) showed a significantly higher serum PG I concentration than those with scarred lesions (n = 86) when the abnormality was located in either the upper body or in the angulus portion. For female patients (n = 87), the results were similar. These results suggest that serum PG I concentrations reflect the stages of activity of peptic ulcer.

Adult↗
PubMed1990

Differential calcium dependence between the release of endogenous dopamine and noradrenaline from rat brain synaptosomes.

The characteristics of the release of endogenous dopamine and noradrenaline from rat brain synaptosomes were studied using HPLC with an electrochemical detector. The spontaneous release of dopamine and noradrenaline was inhibited by approximately 50-60% in a Ca2(+)-free medium or a 100 microM La3(+)-containing medium. Also, the high-K+ (30 mM)-evoked release of dopamine and noradrenaline was inhibited by approximately 50-60% in a Ca2(+)-free medium or a 100 microM La3(+)-containing medium. From these results, the ratio of the Ca2(+)-dependent component to the total release of noradrenaline seemed to be similar to that of dopamine. On the other hand, 20 microM La3+ or 1 microM diltiazem inhibited both the spontaneous and 30 mM K(+)-evoked release of dopamine by approximately 50-60% but inhibited neither the spontaneous nor the 30 mM K(+)-evoked release of noradrenaline. The K(+)-evoked rise in intrasynaptosomal Ca2+ concentration was mostly blocked in Ca2(+)-free medium or 100 microM La3(+)-containing medium but was only partially blocked by 20 microM La3+ or 1 microM diltiazem. These data indicate alternative possibilities in that the Ca2(+)-dependent release of noradrenaline might be less sensitive to a change of intracellular Ca2+ concentration than that of dopamine and that the calcium channels directly involved in the noradrenaline release may be more resistant to diltiazem and La3+ than those involved in the dopamine release.

Animals↗
PubMed1990

Psychogenic vomiting: the relation between patterns of vomiting and psychiatric diagnoses.

Fifty nine patients admitted with a diagnosis of psychogenic vomiting were classified into five patterns of vomiting: continuous, habitual postprandial, irregular vomiting, nausea, and self induced. The psychiatric disorders related to the onset of vomiting were either a major depression or a conversion disorder. Continuous vomiting was usually due to a conversion disorder, while in many cases of habitual postprandial and irregular vomiting, major depression was observed. The patients' psychiatric disorders and vomiting patterns often changed during the clinical course. Assessing the psychiatric problems and vomiting patterns is important in the diagnosis and treatment of psychogenic vomiting.

Adolescent↗
PubMed1990

Effects of anticonvulsants on the electroconvulsive threshold lowered by DA, 5-HT or GABA depletion.

A cannula was chronically implanted in the rat ventriculus, and anticonvulsants were administered through the cannula. The effects of the anticonvulsants applied, intraventricully, were investigated on the decreased electroconvulsive threshold induced by pretreatment with alpha-methyl-p-tyrosine (alpha-MT), p-chlorophenylalanine (PCPA) or allylglycine. The TRH analog, DN-1417, valproate (VPA), and phenobarbital (PB) raised the electroconvulsive threshold which had been lowered by alpha-MT. The reduced electroconvulsive threshold from PCPA was raised by DN-1417, but not by VPA or PB. The allylglycine induced lowering of the electroconvulsive threshold was raised by VPA and PB, but not by DN-1417. Phenytoin had no anticonvulsant effect on rats pretreated with these drugs. From these results, it was concluded that the anticonvulsant action of DN-1417 could be due to enhancement of dopamine and/or serotonin turnover.

Animals↗
PubMed1990

The Na(+)-dependent release of endogenous dopamine and noradrenaline from rat brain synaptosomes.

The involvement of intrasynaptosomal-free Ca++ concentration [( Ca++]i) in Na(+)-dependent release of endogenous dopamine and noradrenaline from rat brain synaptosomes was studied. The release of endogenous dopamine and noradrenaline from rat whole brain synaptosomes were measured using high-performance liquid chromatography with electrochemical detector. The change of [Ca++]i was measured fluorometrically using a Ca++ indicator, Quin-2. Whether extracellular Ca++ was present or not, 30 microM veratridine, a Na(+)-ionophore, increased the release of endogenous dopamine and noradrenaline. In the presence of 1.25 mM Ca++, 30 microM veratridine increased [Ca++]i. In contrast, in the absence of extracellular Ca++, veratridine did not affect [Ca++]i. Ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) increased the release of dopamine and noradrenaline in Ca-Mg-free medium. This stimulatory effect of EGTA seemed to be the result of an increase in the influx of Na+ through Ca++ channels in the absence of divalent cation. In Ca-Mg-free medium, EGTA caused a slight decrease in [Ca++]i. The EGTA-stimulated release of dopamine and noradrenaline was blocked by La which also significantly blocked the decrease in [Ca++]i observed after the addition of EGTA. These results suggest that the Na(+)-dependent release of dopamine and noradrenaline may not depend on a change in [Ca++]i. Veratridine (30 microM)-induced release of dopamine and noradrenaline were detected simultaneously. However, the time needed to induce the maximal stimulatory effect of veratridine on the release of dopamine was apparently shorter than that of noradrenaline. This delay might suggest that the Na(+)-dependent release process of dopamine is not similar to that of noradrenaline.

Amiloride↗
PubMed1989

Ascorbic acid suppresses the deconjugation of noradrenaline but not dopamine in plasma.

The characteristics of hydrolysis of sulfoconjugated noradrenaline (NA) and dopamine (DA) in plasma using sulfatase were investigated. Ascorbic acid has been used as an antioxidant during the hydrolysis of conjugated NA or DA. Hydrolysis of NA sulfates was considerably inhibited by adding ascorbic acid (0.5-10 mM), and slightly inhibited by adding dithiothreitol (1-10 mM). In contrast, the hydrolysis of DA sulfates was not affected after either ascorbic acid or DTT treatment. On the basis of these findings, the levels of NA sulfates previously reported are found to be markedly lower than the actual levels of NA sulfates in human plasma.

Ascorbic Acid↗
PubMed1989

Relationship of calcium and adenylate cyclase messenger systems in rat brain synaptosomes.

The effects of cyclic AMP on the rise in cytosolic free calcium concentration, [Ca2+]i, after stimulation with 15 mM K+ in rat brain synaptosomes were investigated. The fluorescent chelating agent Quin-2 was employed to monitor alterations of K+-evoked [Ca2+]i. Under normoxic conditions, clonidine (1, 10 microM), an alpha 2-adrenoceptor agonist, decreased the 15 mM K+-evoked [Ca2+]i. Although yohimbine (1, 10 microM), an alpha 2-adrenoceptor antagonist, had little or no effect on K+-evoked [Ca2+]i, the inhibitory effects of clonidine were blocked by yohimbine. 8-Bromo cyclic AMP, a cyclic AMP analogue, (50-500 microM), increased K+-evoked [Ca2+]i in a dose-dependent manner. The addition of cyclic AMP analogues subsequent to clonidine treatment reversed the clonidine-induced suppression of K+-evoked [Ca2+]i. On the other hand, under hypoxic conditions, K+-evoked [Ca2+]i was reduced by about 50-60%. 8-Bromo cyclic AMP and the adenylate cyclase activators, yohimbine (1-10 microM) and isoproterenol, a beta-adrenoceptor agonist, (0.1-10 microM), transiently reversed the reduction of the K+-evoked [Ca2+]i caused by hypoxia. These results indicate that the activation of alpha 2-adrenoceptor produces a rapid, sustained decrease in [Ca2+]i which may be due to a decrease in the levels of intracellular cyclic AMP. In addition, the increase in cellular levels of cyclic AMP reversed the reduction of the Ca2+ response to high K+ stimulation caused by hypoxia. If this is so, there is the possibility that increased cyclic AMP might improve the hypoxic damage.

Adenylyl Cyclases↗