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Biomedical subjects

H Abe

Publications and source records attributed to H Abe.

At least 541 records · Page 30Linked to original sources
PubMed1996

Bone changes and mineral metabolism disorders in rats with experimental liver cirrhosis.

To investigate the pathogenesis of hepatic osteodystrophy (HOD) in parenchymal liver disease, we developed a laboratory model in animals using carbon tetrachloride (CCl4) and thioacetamide. Biochemical and histological parameters in the model were measured. In rats with both chronic non-cirrhotic liver injury and CCl4-induced cirrhosis, tibial bone volume was significantly lower than in controls. In CCl4-treated cirrhotic rats, the osteoid volume decreased while the urinary calcium/creatinine ratio increased. In all CCl4-treated rats, bone volume was significantly correlated with both the serum albumin concentration and the number of goblet cells reflecting intestinal villous atrophy. The serum concentration of vitamin D metabolites was not correlated with bone volume. Whole body retention of 47Ca was significantly lower in CCl4-treated cirrhotic rats than in controls. Furthermore, the bone volume in thioacetamide-treated cirrhotic rats was significantly lower than in controls. These data demonstrate that chronic parenchymal liver injury itself causes osteoporosis (i.e. HOD) due to a combination of low bone formation rates and high resorption rates, that HOD begins at the stage of chronic non-cirrhotic liver injury, that bone volume in HOD parallels liver damage and that the principal pathogenesis of HOD seems to be intestinal Ca malabsorption due to lower serum albumin and villous atrophy, while serum levels of vitamin D metabolites have little influence on the pathogenesis of HOD.

Animals↗
PubMed1996

Effect of dual chamber atrioventricular sequential pacing on coronary flow velocity in a patient with hypertrophic obstructive cardiomyopathy.

Effects of dual chamber AV sequential pacing on coronary flow velocity, especially systolic reversal flow, were tested in a patient with hypertrophic obstructive cardiomyopathy. AV sequential pacing with shorter AV delays reduced the systolic reversal flow in the coronary artery, and improved the pressure gradient of the left ventricular outflow tract.

Cardiac Pacing, Artificial↗
PubMed1996

Demonstration of syncope in patients after pacemaker implantation: role of head-up tilt test to distinguish neurocardiogenic vasodepressor syncope from pacemaker syndrome.

It is important to distinguish clinically neurocardiogenic syncope from pacemaker syndrome in patients after pacemaker implantation. We report two syncopal patients with AV sequential physiological pacemakers who displayed neurocardiogenic vasodepressor syncope (VDS) during head-up tilt (HUT) testing. Neurocardiogenic VDS, as a cause of syncope in patients following pacemaker implantation, might be involved in these patients as well as pacemaker syndrome. HUT is a useful diagnostic test in distinguishing neurocardiogenic VDS from pacemaker syndrome in patients with syncope following pacemaker implantation. Careful evaluations for diagnosis of pacemaker syndrome are needed in these patients.

Aged↗
PubMed1996

Irreversible sinus node dysfunction induced by resumption of lithium therapy.

We present the case of a 56-year-old woman with syncope and sinus node dysfunction after long-term lithium therapy. Following lithium discontinuation, sinus node function recovered completely. After resuming low doses of lithium, however, severe sinus node dysfunction recurred. Thereafter, sinus node function did not recover after lithium was discontinued, and a permanent pacemaker was implanted. These findings suggest that irreversible sinus node dysfunction should be recognized as a potentially fatal, albeit rare, risk of lithium therapy, and that previous recovery from sinus node dysfunction after long-term lithium treatment cannot always guarantee the reversible nature of this abnormality after resumption of lithium therapy.

Adult↗
PubMed1996

Evaluation of the somatosensory evoked blink response in patients with neurological disorders.

BACKGROUND: The somatosensory evoked blink response (SBR) is a characteristic reflex blink elicited by electrical stimulation of peripheral nerves or other anatomical sites. METHODS: 139 patients with neurological disorders were examined for presence of the SBR. Although the SBR was not usually elicitable, it was present in a subset of patients with Parkinson's disease and with hemifacial spasm. It was also present in a patient with Guillain-Barré syndrome before the recovery phase. The latency of the EMG activities responsible for the SBR was significantly shorter than that of the startle blink. CONCLUSIONS: The SBR is not a variant of the startle blink, but is a release phenomenon transmitted via the brainstem reticular formation. This response may be clinically relevant in disorders associated with brainstem lesions and abnormal blinking.

Blinking↗
PubMed1996

Circadian rhythm and response to light of extracellular glutamate and aspartate in rat suprachiasmatic nucleus.

Extracellular concentrations of glutamate and aspartate were measured in the vicinity of rat suprachiasmatic nucleus (SCN) by means of in vivo microdialysis. The concentrations of both excitatory amino acids (EAAs) were higher during the dark phase than during the light under the light-dark cycle, showing pulsatile fluctuations throughout the day. When rats were released into the complete darkness, the 24-h pattern in the aspartate continued for at least one cycle, whereas that in the glutamate disappeared. The nocturnal increases in the EAA levels were not due to the increase of locomotor activity during the nighttime, because the 24-h rhythms were also detected in animals under urethan anesthesia. The patterns of extracellular EAA levels were changed when rats were released into the continuous light. Circadian rhythm was not detected in the glutamate, whereas the 24-h pattern was maintained in the aspartate with the levels increased to various extents. A 30-min light pulse given either at zeitgber time (ZT) 1 or ZT 13 elevated the EAA levels during the latter half of the light pulse, except glutamate by a pulse at ZT 1. The extracellular EAA levels in the vicinity of the rat SCN showed the circadian rhythm with a nocturnal peak and increased in response to the continuous light and a brief light pulse. The aspartate level is considered to be regulated by the endogenous circadian rhythm, but the glutamate levels seems to be modified by the light-dark cycle.

Anesthesia↗
PubMed1996

Aging affects development and persistence of feeding-associated circadian rhythm in rat plasma corticosterone.

Effects of aging on development and persistence of feeding-associated circadian rhythm were examined with respect to the prefeeding plasma corticosterone peak under restricted feeding. Old (20 mo), middle-aged (12 mo), and young (2.5 mo) male rats were subjected to a restricted feeding schedule for 21 days in which free access to food was limited to 2 h/day in the light phase. Prefeeding corticosterone peak was detected 1 wk after the start of the schedule in the young and 3 wk after in the old and middle-aged rats. After the restricted feeding, a feeding/ fasting cycle composed of 7 days of ad libitum feeding and 3 days of fasting was imposed four times. The persistence of feeding-associated rhythm was evaluated by examining the reappearance of the corticosterone peak at the previous meal time during each fasting period of the feeding/fasting cycle. The corticosterone peak was not detected in the old and middle-aged rats even at the first cycle, but it was still distinct at the third cycle in the young rats. In conclusion, aging impaired the development and persistence of feeding-associated circadian rhythm in rats.

Aging↗
PubMed1996

Paracrine stimulation of cell growth by cholecystokinin/gastrin through cholecystokinin-B receptor on GH3 cells in vitro.

Cholecystokinin (CCK) is detected in pituitary tumors but its role remains unknown. On the hypothesis that CCK may facilitate the cell growth in pituitary tumors, we have examined the effect of CCK on cell growth using a rat pituitary tumor cell line, GH3, cultured in a serum-free, chemically defined medium. Addition of sulfated CCK-(26-33) (CCK-8) in two different concentrations (0.5 approximately 1 nM) caused a significant increase in the number of GH3 cells. The antagonist (1 microM) for CCK-B receptor, but not CCK-A receptor, significantly inhibited the number of GH3 cells. Northern blot analysis revealed a significant expression of CCK-B receptor mRNA in GH3 cells, but not in normal rat pituitary glands. In addition, immunoreactive CCK/gastrin was detected by RIA in the GH3 cell extracts as well as the serum-free culture medium. In GH3 cell extracts, both CCK-8 and gastrin like peptides were identified by gel chromatography. These findings provided the first evidence for an autocrine/paracrine role of CCK and gastrin on stimulation of GH3 cell growth through the CCK-B receptor.

Animals↗
PubMed1996

Comparison of changes in cardiac structure after treatment in secondary hypertension.

To investigate the role of aldosterone and the renin-angiotensin system in cardiac structure, we performed echocardiography in patients with secondary hypertension. The relation between blood pressure or hormonal influences and left ventricular hypertrophy has not been well established in secondary hypertension. Sixteen patients with primary aldosteronism and 11 with unilateral renovascular hypertension who had completely normalized blood pressure after operation or percutaneous transluminal angioplasty were evaluated by echocardiography before and after surgery or other interventional treatment. Blood pressure was not statistically different between the groups before treatment and was normalized after treatment in both groups. Left ventricular hypertrophy was mild in both groups before treatment, and its degree was not statistically different between the groups. At the end of the follow-up period, all parameters of primary aldosteronism and left ventricular mass index in patients with unilateral renovascular hypertension were significantly reduced. In patients with primary aldosteronism, changes in end-diastolic left ventricular internal dimension correlated positively with changes in left ventricular mass index (r=.58,P<.01). In patients with unilateral renovascular hypertension, changes in mean blood pressure and left ventricular mass index were significantly correlated (r=.77,P<.01). The expanded plasma volume induced by an excess of aldosterone and high blood pressure may play an important role in the increase of left ventricular mass in primary aldosteronism. In unilateral renovascular hypertension, high blood pressure mainly contributes significantly to increased left ventricular mass. Therefore, different factors may modulate the development of left ventricular hypertrophy in patients with secondary hypertension.

Adult↗
PubMed1996

Angiogenic factors in moyamoya disease.

BACKGROUND AND PURPOSE: We previously reported that the level of basic fibroblast growth factor (bFGF) is high in cerebrospinal fluid (CSF) taken from patients with moyamoya disease. The present study investigated the levels of other angiogenic growth factors in the CSF of moyamoya patients and the clinical significance of bFGF in moyamoya disease. METHODS: The levels of bFGF, interleukin-8, platelet-derived growth factor, transforming growth factor-beta, endothelial growth factor, and vascular endothelial cell growth factor in CSF, taken from 38 patients with moyamoya disease and 16 patients with atherosclerotic occlusive disease (control group), were measured by an enzyme-linked immunosorbent assay. We analyzed the correlation between the level of bFGF and the clinical factors of age, onset pattern, development of neovascularization, and cerebral circulation. RESULTS: The CSF of moyamoya patients contained a high concentration of bFGF to a significant (P < .05) extent. The bFGF level was apparently elevated in the patients in whom neovascularization from indirect revascularization, such as encephaloduroarteriosynangiosis, was well developed (P < .01). A linear correlation between the values of bFGF and cerebral vascular response to acetazolamide (r = .7; P < .05) was revealed. The other angiogenic factors were not significantly high compared with the control group. CONCLUSIONS: The elevation of bFGF in moyamoya disease seems to be specific and is not related simply to cerebral ischemia. Clinically, the bFGF level is a useful indicator to predict the efficacy of indirect revascularization after surgery.

Adult↗
PubMed1996

Surgical therapy for adult moyamoya disease. Can surgical revascularization prevent the recurrence of intracerebral hemorrhage?

BACKGROUND AND PURPOSE: It is well recognized that revascularization surgery using direct and/or indirect bypass provides effective surgical management for pediatric moyamoya disease. However, surgical treatment of the adult hemorrhagic type remains controversial. In this study, the effect of surgery for adult moyamoya disease was investigated. METHODS: We analyzed 35 patients with adult moyamoya disease (patient age, over 20 years), 24 patients with initial onset of intracerebral hemorrhage, and 11 patients with initial onset of cerebral ischemia who underwent both direct bypass surgery of the superficial temporal artery to the middle cerebral artery anastomosis and indirect revascularization of encephalo-duro-arteriomyo-synangiosis. RESULTS: Of 24 patients with hemorrhagic-type disease, 3 showed rebleeding: of 11 patients with the ischemic type, 2 showed intracerebral hemorrhage after surgery. Overall, 5 of 35 patients (14.3%) had hemorrhage after revascularization surgery (mean follow-up period, 6.4 years). Postoperative angiography revealed that direct anastomosis is effective whereas indirect revascularization is not always effective for adult moyamoya disease. Moyamoya vessels, which are supposed to be responsible for hemorrhage, decreased in 25% of patients. CONCLUSIONS: Revascularization surgery cannot always prevent rebleeding. However, a decrease in moyamoya vessels was induced by surgery, which may reduce the risk of hemorrhage more effectively than conservative treatment. In cases of adult moyamoya disease, direct bypass is particularly important, since the indirect revascularization is not as useful in adult cases as in pediatric cases.

Adult↗
PubMed1996

Stimulus-dependent disorganization of actin filaments induced by overexpression of cofilin in C2 myoblasts.

Actin depolymerizing factor (ADF)/cofilin is a widely distributed family of actin-binding proteins which regulate actin polymerization in a pH-dependent manner. In cultured cells, cofilin, as well as ADF, translocates from the cytoplasm into the nucleus together with actin and forms rod-like structures in response to heat shock or dimethylsulfoxide (DMSO) treatment. In order to study in vivo interaction of cofilin with actin, we examined the effects of cofilin overexpression on actin cytoskeleton in C2 myoblasts. Interestingly, no remarkable effect was observed on phalloidin-stained patterns in cells overexpressing cofilin as compared with normal cells. However, upon treatment with DMSO, cytoplasmic actin filaments were disrupted and intranuclear rod structures containing cofilin and actin were apparently larger and thicker in cells overexpressing cofilin than in normal cells. Heat shock also stimulated disruption of microfilaments and formation of both intranuclear and prominent cytoplasmic cofilin-actin rods in cofilin-transfected cells, suggesting that DMSO-treatment or heat shock triggers cofilin-actin interaction. We further found that a myosin ATPase inhibitor (BDM) induced a reduction in cytoplasmic staining with phalloidin in cofilin-transfected cells. The results suggest that myosin activity might be involved in the regulation of cofilin-actin interactions in vivo.

Actin Cytoskeleton↗
PubMed1996

Differences in mechanisms for cell-free NADPH oxidase activation between arachidonate and sodium dodecyl sulfate.

Mechanisms for the cell-free activation of NADPH oxidase by sodium dodecyl sulfate (SDS) and arachidonate were compared in relation to their responsiveness to short chain diacylglycerols. The plasma membrane and cytosol prepared from guinea pig neutrophils were used for the cell-free system. The activation of NADPH oxidase by SDS was enhanced about 5- to 10-fold by 1,2-dioctanoylglycerol (diC8), but not by either 1,2-dihexanoylglycerol (diC6) or 1,2-didecanoylglycerol (diC10). However, none of these diacylglycerols potentiated the NADPH oxidase activation by arachidonate. The maximal extent of activation by the combination of SDS and diC8 was similar to that by arachidonate alone. In the presence of sufficient amounts of diC8 and SDS, GTP gamma S potentiated the activation of NADPH oxidase. The potentiating activity of diC8 was preserved in the membrane fraction, not in the cytosol fraction. These results suggest that arachidonate may possess the functions of both SDS and diC8 in the activation. In addition, diC8 and GTP gamma S seem to independently enhance the NADPH oxidase activation.

Animals↗
PubMed1996

Intracellular fate of 2-NBDG, a fluorescent probe for glucose uptake activity, in Escherichia coli cells.

A fluorescent derivative of D-glucose, 2-NBDG, which was previously developed for the evaluation of glucose uptake activity by living cells, was used on Escherichia coli cells and its fate after incorporation in the cells was investigated. 2-NBDG was converted to another fluorescent derivative (2-NBDG metabolite) immediately after it was taken by E. coli cells. This 2-NBDG metabolite was then decomposed to non-fluorescent forms. 2-NBDG metabolite was decomposed into the original 2-NBDG by G6Pase with concurrent liberation of inorganic phosphate. Furthermore, FAB/MS analysis showed that its molecular weight was 420, the same value as that of 2-NBDG 6-phosphate. These indicate 2-NBDG metabolite should be 2-NBDG 6-phosphate. Based on these results, the feasibility of 2-NBDG as a fluorescent non-toxic probe for glucose uptake activity and its application to viability assessment of various living systems are discussed.

4-Chloro-7-nitrobenzofurazan↗
PubMed1996

Different effects of alcohol and salt on 24-hour blood pressure and heart rate in hypertensive patients.

To compare the influences of alcohol and salt intake on 24-h blood pressure (BP), we studied short-term effects of repeated alcohol ingestion and dietary salt intake in hypertensive patients. Thirty-two Japanese men with mild to moderate essential hypertension (54 +/- 1 years old, mean +/- SE) were examined. Sixteen patients were given alcohol (1 ml/kg) with dinner for 7 d after a 7-d control period with an isocaloric beverage. Another group consisting of 16 age- and weight-matched patients consumed a low-sodium diet (25 mmol/d) for 7 d, followed by a high-sodium diet (250 mmol/d) for 7 d. Twenty-four-hour BP was measured at the end of each period. Average 24-h BP in the alcohol period (137 +/- 4/83 +/- 2 mmHg) was similar to that in the control period (138 +/- 4/84 +/- 2 mmHg). However, BP in the alcohol period was significantly lower in the evening, but significantly higher in the morning than that in the control period. Heart rate increased for several hours after alcohol ingestion, resulting in a significant increase in 24-h heart rate (67 +/- 2 vs. 64 +/- 2 beats/min). Average 24-h BP was higher in the high salt period (144 +/- 4/89 +/- 4 mmHg) than in the low salt period (135 +/- 3/85 +/- 3 mmHg, p < 0.05). The pressor effect of high salt intake was sustained throughout the day and was associated with a decrease in 24-h heart rate (60 +/- 2 vs. 66 +/- 2 beats/min). In conclusion, short-term repeated intake of alcohol may have little effect on average 24-h BP while it causes an evening fall and a morning rise in BP, and high salt intake raises BP throughout the day. Alcohol consumption increases and salt loading decreases 24-h heart rate.

Adult↗
PubMed1996

Short stature caused by a mutant growth hormone with an antagonistic effect.

The molecular basis of biologically inactive GH remained unclear until recently. We have very recently reported a child with short stature and a mutant GH caused by a single missense mutation in the GH-1 gene, which itself cannot transduce the GH-signal to the cells but can blunt the action of wild-type GH by virtue of its greater affinity for the GH binding protein (GHBP)/GH receptor. Briefly the clinical features of the patient are: At the age of 4.9 years his height was 81.7 cm (-6.1 SD) and bone age was 2 years. The patient's serum insulin-like growth factor-1 (IGF-1) concentration was 34 ng/ml. The basal serum GH concentration ranged from 7.0 to 14.0 ng/ml and peak concentrations after insulin hypoglycemia, arginine and L-dopa were 38.0, 15.0 and 35.0 ng/ml, respectively. A heterozygous single base substitution was identified in the GH-1 gene of the proband, predicted to convert codon 77 from arginine to cysteine. Isoelectric focusing revealed the presence of an abnormal GH peak in addition to a normal GH peak. The affinity of expressed mutant GH to GHBP was approximately 6 times higher than that of wild-type GH. The mutant GH not only failed to stimulate tyrosine phosphorylation by itself, but it also inhibited the activity of wild-type GH when added simultaneously even in a one tenth dose of wild-type GH. The child whom we reported is therefore the first case of short stature caused by mutant GH with an antagonistic effect.

Age Determination by Skeleton↗
PubMed1996

No correlation of growth hormone receptor gene mutation P561T with body height.

Analysis of the growth hormone receptor (GHR) gene in GH insensitivity syndrome revealed various mutations, mainly in the gene encoding the extracellular domain of GHR. On the other hand, the mutation of the gene encoding the cytoplasmic domain of GHR was not found. We have reported, in the cytoplasmic domain of a GHR gene, mutation P561T in a patient with Noonan syndrome who showed a blunted insulin-like growth factor I (IGF-I) response to an acute injection of GH. However, her mother possessing the same mutation had no growth failure. To clarify the significance of the GHR gene mutation P561T, 96 volunteers (41 males aged 21-80 years; 55 females, aged 20-80 years, were tested for the presence of this mutation. By the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, three of the 41 males and 11 of the 55 females examined revealed heterozygous missense mutation P561T. The body height (cm) was 168 +/- 5.3 (mean +/- SD) in three males with the mutation and 164.1 +/- 5.8 in 38 males without the mutation. The difference between them was not statistically significant. The body height in 11 females with the mutation was 152.6 +/- 5.4, which did not differ significantly from 151.3 +/- 6.2 in 44 females without the mutation. These findings suggest that the heterozygous missense mutation P561T in the cytoplasmic domain of GHR does not play a significant role in determining the final body height.

Adult↗