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Biomedical subjects

N Takeda

Publications and source records attributed to N Takeda.

At least 199 records · Page 11Linked to original sources
PubMed1998

[Clinical features in patients with delayed endolymphatic hydrops].

We report clinical features in patients with delayed endolymphatic hydrops (DEH) with juvenile unilateral deafness. Among 23 patients with DEH, 15 cases were diagnosed as ipsilateral DEH and 8 cases as contralateral DEH. The distribution of onset age showed two peaks at ages of < 30 years and > 40 years. In 80% of the ipsilateral DEH cases, the onset of episodic vertigo was at younger ages. On the other hand, in 75% of the contralateral DEH cases, the onset of fluctuation hearing loss of the contralateral ear was at older ages. Ispilateral DEH and Meniere's disease may show different pathophysiologies. The incidence of dominant negative summating potential in the better-hearing ear was 20% in the ispilateral DEH cases and 60% in the contralateral DEH cases. It is suggested that endolymphatic hydrops is in the better-hearing ear of contralateral DEH.

Adult↗
PubMed1998

[Identification of vestibular compensation-associated molecules by means of differential display].

The differential display method was used to identify gene expression which is altered in the cerebellar flocculus after unilateral labyrinthectomy (UL). Total RNA from flocculi of sham-operated and labyrinthectomized rats was isolated, amplified by PCR using arbitrary primer sets and separated by electrophoresis on a polyacrylamide gel. PCR products, whose amounts were significantly different in samples from labyrinthectomized animals and those from controls, were cut out of the gel and sequenced. One of the up-regulated products was the rat protein phosphatase 2A beta catalytic subunit mRNA and one of the down-regulated products was the rat glutamate receptor delta-2 subunit mRNA. Histochemical examination of in situ hybridization showed that those molecules were intensively localized in the Purkinje cell layer. In labyrinthectomized rats, UL-induced nystagmus gradually disappeared within 3 days after UL. These findings suggest that changes in expression of those molecules in the floccular Purkinje cells after UL is involved in vestibular compensation. So far various kinds of neural plasticity-associated molecules have been investigated, mainly by slice-in vitro studies. This study indicates that differential display is a feasible molecular biological in vivo method for investigation of the mechanism of neural plasticity.

Animals↗
PubMed1998

Molecular mechanisms of vestibular compensation in the central vestibular system--review.

Vestibular compensation consists of two stages: the inhibition of the contralesional medial vestibular nucleus (contra-MVe) activities at the acute stage after unilateral labyrinthectomy (UL) and the recovery and maintenance of the ipsilesional MVe (ipsi-MVe) spontaneous activities at the chronic stage after UL. In this paper, we reviewed molecular mechanisms of vestibular compensation in the central vestibular system using several morphological and pharmacological approaches in rats. Based on our examinations, we propose the following hypotheses: i) at the acute stage after UL, the activated neurons in the ipsi-MVe project their axons into the flocculus to inhibit the contra-MVe neurons via the NMDA receptor, nitric oxide (NO) and/or GABA-mediated signalling, resulting in the restoration of balance between intervestibular nuclear activities. ii) At the chronic stage after UL, the flocculus depresses the inhibitory effects on the ipsi-MVe neurons via protein phosphatase 2A (PP2A) beta, protein kinase C (PKC) and glutamate receptor (GluR) delta-2, to help the recovery and maintenance of ipsi-MVe activities.

Animals↗
PubMed1998

[Factors associated with participation in chest X-ray screening by young and middle aged residents].

We investigated the factors that affect participation rates in chest X-ray mass screenings among 20-59 year-old residents in A city, Kagawa prefecture. 1) Participation rates in employees and non-employees were 78.3% and 33.9% respectively. In the employees whose firms do not provide health check-ups, participation rate was 15.9%. 2) Among participants, about 90% of the employees whose firms do not provide health check-ups and about 60% of non-employees utilized mass screenings provided by the local government. 3) Among non-participants, 53.7% of the employees whose firms do not provide health check-ups and 70% of the others (employees whose firms provide health check-ups and non-employees) were aware of the screening system. Most of the young did not know of the system. 4) Principal reasons for nonparticipation were "inconvenient" and "unnecessary because healthy" in job holders and "unnecessary because healthy" in non-job holders. 5) Participants had better health practices than non-participants. Participation rates of chest X-ray mass screenings were high in employees and low in non-employees. Local governments are expected to supplement the existing mass screening system at work-sites by providing accessibility screening. In tuberculosis prevention, nonparticipation in mass screenings is one of the main issues. The association between participation and health practice suggests that methods for linking with primary prevention activities are necessary for stimulating interest and promoting participation in mass screenings.

Adult↗
PubMed1998

Cardiac sarcolemmal Na(+)-Ca2+ exchange and Na(+)-K+ ATPase activities and gene expression in alloxan-induced diabetes in rats.

To determine the sequence of alterations in cardiac sarcolemmal (SL) Na(+)-Ca2+ exchange, Na(+)-K+ ATPase and Ca(2+)-transport activities during the development of diabetes, rats were made diabetic by an intravenous injection of 65 mg/kg alloxan. SL membranes were prepared from control and experimental hearts 1-12 weeks after induction of diabetes. A separate group of 4 week diabetic animals were injected with insulin (3 U/day) for an additional 4 weeks. Both Na(+)-K+ ATPase and Ca(2+)-stimulated ATPase activities were depressed as early as 10 days after alloxan administration; Mg2+ ATPase activity was not depressed throughout the experimental periods. Both Na(+)-Ca2+ exchange and ATP-dependent Ca(2+)-uptake activities were depressed in diabetic hearts 2 weeks after diabetes induction. These defects in SL Na(+)-K+ ATPase and Ca-transport activities were normalized upon treatment of diabetic animals with insulin. Northern blot analysis was employed to compare the relative mRNA abundances of alpha 1-subunit of Na(+)-K+ ATPase and Na(+)-Ca2+ exchanger in diabetic ventricular tissue vs. control samples. At 6 weeks after alloxan administration, a significant depression of the Na(+)-K+ ATPase alpha 1-subunit mRNA was noted in diabetic heart. A significant increase in the Na(+)-Ca2+ exchanger mRNA abundance was observed at 3 weeks which returned to control by 5 weeks. The results from the alloxan-rat model of diabetes support the view that SL membrane abnormalities in Na(+)-K+ ATPase, Na+Ca2+ exchange and Ca(2+)-pump activities may lead to the occurrence of intracellular Ca2+ overload during the development of diabetic cardiomyopathy but these defects may not be the consequence of depressed expression of genes specific for those SL proteins.

Alloxan↗
PubMed1998

[Standard versus long-term prednisolone with sairei-to for initial therapy in childhood steroid-responsive nephrotic syndrome: a prospective controlled study].

The most appropriate initial treatment for children with steroid-responsive nephrotic syndrome is controversial. Initial treatment with 18-week prednisolone and the Chinese herbal medicine. Sairei-to, may prevent subsequent relapse. To determine whether similar results can be obtained with a combination of just initial 8-week prednisolone and Sairei-to, we compared the effects of such treatment with those of treatment with 18-week prednisolone and Sairei-to in 196 children with steroid-responsive nephrotic syndrome. The patients were randomly assigned to receive 8-week (group 1) or 18-week (group 2) prednisolone for the initial therapy. All patients received Sairei-to for 2 years in addition to prednisolone. Eighty-eight of the 98 patients in group 1 and 83 of the 98 patients in group 2 completed their trial. At entry, the two groups of patients did not differ in their clinical and laboratory findings. During the 2-year trial, 62 group 1 patients (70%) and 54 group 2 patients (65%) had relapses, and 19 group 1 patients (21%) and 20 group 2 patients (24%) had frequent relapses. The present study demonstrates that a combination of initial 8-week prednisolone and 2-year Sairei-to is effective in children with steroid-responsive nephrotic syndrome.

Anti-Inflammatory Agents↗
PubMed1997

Changes in nitric oxide synthase-like immunoreactivities in unipolar brush cells in the rat cerebellar flocculus after unilateral labyrinthectomy.

To elucidate the role of nitric oxide (NO)-mediated signaling in vestibular compensation, we examined effects of unilateral labyrinthectomy (UL) on the neuronal isoform of NO synthase (NOS) expression in the rat central vestibular system using immunohistochemical techniques. After UL, a substantial number of NOS-like immunoreactive (-LIR) neurons were observed in the granule cell layer in bilateral flocculi, and these neurons were determined to be unipolar brush cells (UB cells) by their unique morphology and location. NOS-LIR UB cells appeared by 12 h with a maximum increase in number 24 h after UL, and then gradually disappeared in accordance with the development of vestibular compensation. Continuous floccular infusion of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, or 2-phenyl-4,4,5,5-tetramethyl-1-oxyl-3-oxide (PTIO), an inhibitor of NO, caused more severe vestibulo-ocular deficits at the initial stage after UL and slightly delayed the recovery from these symptoms. All these findings suggest that up-regulation of NO production in floccular UB cells facilitates vestibular compensation, especially at the initial stage after UL.

Animals↗
PubMed1997

Risk factors and probability of vertebral body collapse in metastases of the thoracic and lumbar spine.

STUDY DESIGN: The associations between vertebral body collapse and the size or location of the metastatic lesions were analyzed statistically to estimate the critical point of collapse. OBJECTIVES: To determine risk factors for collapse, to estimate the predicted probability of collapse under various states of metastatic vertebral involvement, and to establish the criteria of impending collapse. SUMMARY OF BACKGROUND DATA: Pathologic vertebral collapse brings about severe pain and paralysis in patients with cancer. Prevention of collapse plays a significant role in maintaining or improving their quality of life. Because no previous study has clarified the critical point of vertebral collapse, however, the optimum timing for prophylactic treatment has been unclear. METHODS: The size and location of metastatic tumor from Th1 to L5 were evaluated radiologically for 100 thoracic and lumbar vertebrae with osteolytic lesions. The correlations between collapse and the following risk factors (x1-x4) were determined by means of a multivariate logistic regression model: x1, tumor size (the percentage of tumor occupancy in the vertebral body [% TO]); x2, pedicle destruction, x3, posterior element destruction; and x4, costovertebral joint destruction. RESULTS: Significant risk factors were costovertebral joint destruction (odds ratio, 10.17; P = 0.021) and tumor size (odds ratio of every 10% increment in %TO, 2.44; P = 0.032) in the thoracic region (Th1-Th10), whereas, tumor size (odds ratio of every 10% increment in %TO, 4.35; P = 0.002) and pedicle destruction (odds ratio, 297.08; P = 0.009) were main factors in the thoracolumbar and lumbar spine (Th10-L5). The criteria of impending collapse were: 50-60% involvement of the vertebral body with no destruction of other structures, or 25-30% involvement with costovertebral joint destruction in the thoracic spine; and 35-40% involvement of vertebral body, or 20-25% involvement with posterior elements destruction in thoracolumbar and lumbar spine. CONCLUSIONS: With respect to the timing and occurrence of vertebral collapse, there is a distinct discrepancy between the thoracic and thoracolumbar or lumbar spine. When a prophylactic treatment is required, the optimum timing and method of treatment should be selected according to the level and extent of the metastatic vertebral involvement.

Adult↗
PubMed1997

The metabolism of biogenic monoamines during embryogenesis and metamorphosis in two anuran species.

This study investigated the pathways to many monoamines and their metabolites in the central nervous system of the frog Rana nigromaculata and the toad Bufo bufo japonicus during embryonic development and metamorphosis. Metabolites were analyzed by three-dimensional HPLC. The two species provided evidence of similar pathways, with slightly different timetables for the development of their monoamine systems. During embryonic development, the main metabolic pathways in entire embryos were tyrosine (TYR)-->[3,4-dihydroxyphenylalanine in Bufo]-->3-hydroxytyramine-->norepinephrine or epinine (EPIN)-->epinephrine, TYR-->tyramine--> (octopamine in Rana) and TYR-->3-O-methyldopa for catecholamines, and tryptophan-->kynurenine and 5-hydroxytryptamine (5-HT)-->[5-hydroxyindoleacetic acid and N-methyl-5-hydroxytryptamine (N-MET) in Bufo]. The monoamine system in the brain was similar during metamorphosis to that during embryogenesis with a few exceptions. The most striking change was the development of the bufotenine (5-hydroxy-N, N-dimethyltryptamine) pathway from 5-HT via N-MET. EPIN and norepinephrine in Rana and octopamine in both species disappeared during metamorphosis. These results are discussed in relation to the roles of the various pathways in development.

Animals↗
PubMed1997

Different pathophysiology of cardiac hypertrophy in hypertension and hypertrophic cardiomyopathy.

In order to investigate differences in the pathophysiology of cardiac hypertrophy between patients with arterial hypertension and hypertrophic cardiomyopathy, DNA synthesis by cardiac myocytes and the effects of an angiotensin-converting enzyme inhibitor were examined in these two groups of patients. DNA synthesis and the cell cycle were investigated by flow cytometry using autopsy materials from patients with hypertension and hypertrophic cardiomyopathy. The hypertension group (n=10) included four men and six women aged 61+/-10 years (heart weight: 470+/-79 g, mean+/-s.d.); the cardiomyopathic group (n=10) included eight men and two women aged 61+/-23 years (heart weight: 615+/-211 g). The percentage of cells in G2M phase of the cell cycle was significantly decreased in the myocardium from patients with hypertrophic cardiomyopathy compared with that from hypertensive patients (cardiomyopathy v hypertension: 1.1+/-0.6 v 7.7+/-2.6%, mean+/-s.d.). Captopril, an angiotensin-converting enzyme inhibitor, was administered for 12 months to patients with hypertension (n=20) and hypertrophic cardiomyopathy (n=15). Regression of cardiac hypertrophy was assessed by echocardiography. Long-term administration of captopril achieved regression of cardiac hypertrophy in the hypertensive patients, but not in the patients with hypertrophic cardiomyopathy. In the hypertensive patients, the left ventricular mass was 234+/-9 g before treatment and 198+/-26 g after treatment (mean+/-s.d., P<0. 01). In cardiomyopathic patients, on the other hand, there was no significant difference of left ventricular mass after treatment (before v after, 305+/-85 v 285+/-90 g, mean+/-s.d.). These results suggest that the mechanism of cardiac hypertrophy differs between patients with hypertension and hypertrophic cardiomyopathy.

Aged↗
PubMed1997

Age-related changes in vertebral height ratios and vertebral fracture.

Because no gold standard for the definition of vertebral fracture exists, there has been controversy about whether mild vertebral deformities are truly fractures or simply normal variation in vertebral size and shape. The aim of this study was to assess the associations of mild variations of vertebral height ratios to definite vertebral fractures. In 479 Japanese women (aged 53.9 +/- 9.1 years) who visited our institute for a medical checkup, we performed lateral lumbar radiographs and morphometric parameters were derived by measuring the anterior (Ha), middle (Hm) and posterior (Hp) height of each vertebral body from T12 to L4. Vertebral height ratios, Ha/Hp, Hm/Hp or Hp/Hp' of adjacent vertebrae that were more than 3 SD different from vertebra-specific means of normative data were considered to indicate fractures. Forty-five women were diagnosed with at least one fracture. After excluding the subjects with vertebral fracture, we examined the associations of the variations in vertebral height ratios with age, anthropometric parameters and lumbar bone mineral density (BMD) measured by dual-energy X-ray absorptiometry. Vertebral height ratios, especially Hm/Hp in postmenopausal women, tended to decrease with age and were positively associated with BMD. No significant correlation was observed between anthropometric parameters and vertebral height ratios. Aged-related decrease in vertebral height ratios (Ha/Hp and Hm/Hp, each averaged from T12 to L4) was significant even after the correction for BMD. Mean values of height ratios of non-fractured vertebrae adjusted for age and BMD were significantly lower in postmenopausal women with vertebral fracture than in those without vertebral fracture. Logistic regression analysis showed that BMD and height ratios of non-fractured vertebrae were independent predictors of vertebral fracture risk. The results suggest that older women, and women with at least one obvious (3 SD) fracture, tend to have mild deformities which do not qualify using the 3 SD definition. These mild deformities may represent real consequences of osteoporosis, because they are more pronounced among women with obvious fracture.

Adult↗
PubMed1997

Comparison of gelatin particle agglutination and hemagglutination inhibition tests for measles seroepidemiology studies.

The prevalence of measles antibody in Japan was surveyed with a newly developed gelatin particle agglutination (PA) test, and the results compared with those of the hemagglutination inhibition (HI) test. The two age-distribution curves of the PA antibody-positive rates at > or = 1:8 and > or = 1:32 were almost the same in all the age groups, except the less-than-1-year-old group for which the rate at > or = 1:8 was higher than that at > or = 1:32 (p < 0.05, chi 2 test). In the vaccinated children, all groups older-than-1-year of age had antibody-positive levels of 96% or more. In contrast, in the unvaccinated children, there was a sharp increase in antibody-positive rates between the 1- and 4-year-old groups, indicative that about 80% of the children were infected by wild measles virus at these ages. A significant number of PA antibody-positive specimens were antibody-negative (< 1:8) by HI. The percentage of specimens in this category, PA (+) but HI (-), was greatest in infants less than one year old, and least in young children, but it increased with age to 97% of the HI (-) specimens from adults of more than 20 years of age. The PA test therefore detected some measles antibodies that HI could not. This test is simple and useful for making serosurveys in both developed and developing countries.

Adolescent↗
PubMed1997

Myosin light-chain phosphorylation in diabetic cardiomyopathy in rats.

The regulatory myosin light chain (MLC) is phosphorylated in cardiac muscle by Ca2+/calmodulin-dependent MLC kinase (MLCK) and is considered to play a modulatory role in the activation of myofibrillar adenosine triphosphatase (ATPase) and the process of force generation. Since the depression in cardiac contractile function in chronic diabetes is associated with a decrease in myofibrillar ATPase activity, we investigated changes in MLC phosphorylation in diabetic heart. Rats were made diabetic by injecting streptozotocin (65 mg/kg intravenously), and the hearts were removed 8 weeks later; some 6-week diabetic animals were injected with insulin (3 U/d) for 2 weeks. Changes in the relative MLC and MLCK protein contents were measured by electrophoresis and immunoblot assay, whereas phosphorylated and unphosphorylated MLCs were separated on 10% acrylamide/urea gel and identified by Western blot. MLC and MLCK contents were decreased markedly (40% to 45%) and MLC phosphorylation was decreased significantly (30% to 45%) in the diabetic rat heart homogenate in comparison to control values. The changes in MLC and MLCK content in diabetic heart were partially reversible, whereas changes in MLC phosphorylation were normalized upon treatment with insulin. These results suggest that decreased protein contents of MLC and MLCK and phosphorylation of MLC may contribute to the depression of cardiac myofibriliar ATPase activity and heart dysfunction in diabetic cardiomyopathy.

Adenosine Triphosphatases↗
PubMed1997

Histamine release from the hypothalamus induced by gravity change in rats and space motion sickness.

Freely moving rats were exposed to 2 g hypergravity in an animal centrifuge device to produce motion sickness. Histamine release from the anterior hypothalamus of the rats was measured in vivo with a microdialysis technique. After a 2-h load of 2 g hypergravity, rats ate kaolin. Because pica, eating a nonnutritive substance such as kaolin, is a behavioral index of motion sickness in rats, this finding indicates that the rats suffered from motion sickness. During 2 g hypergravity for 2-h, histamine release from the hypothalamus was transiently increased. In contrast, neither the transient increase of histamine release nor the kaolin consumption were induced by 2 g hypergravity in bilaterally labyrinthectomized rats. Pretreatment with alpha-fluoromethylhistidine, an inhibitor of histamine-synthesizing enzyme, decreased both the basal and hypergravity-induced releases of histamine from the hypothalamus and suppressed the kaolin consumption induced by hypergravity. Taken together, these findings suggest that the vestibular information of changes in gravity activate the histaminergic neuron system, resulting in the development of motion sickness. More prolonged stimulation, a 4-h load of 2 g hypergravity, induced significant increase of kaolin consumption on postdays 1-3, though rats ate kaolin on postdays 1-2 after 2 g hypergravity for 2 h. During 2 g hypergravity for 4 h, the initial transient increase of histamine release was followed by the gradual increase of histamine release after the end of centrifugation. It is suggested that rats adapted to the hypergravity environment after centrifugation for 4 h, but not 2 h, so that the change in gravity from 2 g to 1 g became a provocative stimulation. We, therefore, concluded that motion sickness in rats induced by a negative change in gravity can be used as a simulation of space motion sickness, which is induced by exposure to microgravity. Histaminergic activation in the development of motion sickness induced by negative change in gravity might be an underlying mechanism of space motion sickness.

Animals↗
PubMed1997

Role of the flocculus in the development of vestibular compensation: immunohistochemical studies with retrograde tracing and flocculectomy using Fos expression as a marker in the rat brainstem.

After unilateral labyrinthectomy in rats, Fos-like immunoreactive neurons appeared in the ipsilateral medial vestibular nucleus, contralateral prepositus hypoglossal nucleus and contralateral inferior olive beta subnucleus. and thereafter gradually disappeared in accordance with the development of vestibular compensation. This finding indicated that the activation of these nuclei is the initial event of vestibular compensation. In the present study, retrograde tracing experiments revealed that these Fos-like immunoreactive neurons project a proportion of their axons to the vestibulocerebellum (uvula-nodulus, flocculus). Before vestibular compensation was accomplished, right, left or bilateral flocculectomy was performed in right-labyrinthectomized rats. All these treatments caused reappearance of unilateral labyrinthectomy-induced behavioral deficits and Fos expression in the left medial vestibular nucleus and right prepositus hypoglossal nucleus. Since floccular efferents are GABAergic, these results indicate that the neurons in which Fos expression was detected by flocculectomy had been inhibited after unilateral labyrinthectomy by floccular Purkinje neurons and that disinhibition of these neurons induced by flocculectomy caused decompensation. Based on our present findings, we propose a hypothesis that the bilateral flocculus serves the restoration of balance between intervestibular nuclear activities to induce vestibular compensation after unilateral labyrinthectomy.

Animals↗
PubMed1997

Neurons in rostral ventrolateral medulla mediate vestibular inhibition of locus coeruleus in rats.

The effects of caloric vestibular stimulation on the central noradrenergic neurons system were examined in the rat. In urethane-anesthetized rats, caloric stimulation inhibited the spontaneous activity of noradrenergic locus coeruleus neurons and increased systemic blood pressure. Electrical and chemical lesions in the ventrolateral medulla attenuated both the locus coeruleus inhibition and the blood pressure increase in response to caloric stimulation. Neither the neuronal inhibition nor the pressor effect was attenuated by any deafferentation of the forebrain or baroreceptors, or lesioning of the nucleus tractus solitarius. These findings indicate that the caloric stimulation-induced locus coeruleus inhibition is mediated by neurons in the ventrolateral medulla, and that these neurons also mediate the vestibulo-pressor responses. The locus coeruleus inhibition via the ventrolateral medulla is, however, considered to be independent of ventrolateral medulla-mediated systemic pressor effect. Collectively these findings suggest that the ventrolateral medulla is the major origin of inhibitory vestibular input to the noradrenergic neurons of the locus coeruleus, and that the ventrolateral medulla plays an important role in the vestibulo-autonomic response.

Animals↗