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Biomedical subjects

H Tsukagoshi

Publications and source records attributed to H Tsukagoshi.

At least 73 records · Page 4Linked to original sources
PubMed1993

Sympathetic skin response in patients with cerebellar degeneration.

Sudomotor function was studied based on sympathetic skin responses (SSRs) in 87 patients with various types of cerebellar degeneration. Evaluations of orthostatic hypotension and the R-R interval variation were also performed in these patients. The respective incidences of SSR abnormality and orthostatic hypotension were 44 (50.6%) of 87 and 39 (44.8%) of 87. Fourteen percent of the patients with abnormal SSRs did not have orthostatic hypotension, but 8% of the patients with normal SSRs did have orthostatic hypotension. Sympathetic skin responses were abnormal in most patients with Shy-Drager syndrome, sporadic olivopontocerebellar atrophy (OPCA), and striatonigral degeneration, whereas SSRs were normal in patients with familial OPCA, sporadic cerebellar atrophy, and familial cerebellar atrophy. We demonstrated that SSR can be used to evaluate sudomotor function in degenerative disorders of the central nervous system as well as in peripheral neuropathies. The vasomotor and sudomotor functions usually are both disturbed in patients with cerebellar degeneration, and the SSR can detect autonomic dysfunction as sensitively as does the head-up tilt test. We also concluded that sporadic OPCA differs from familial OPCA in that it has a much higher incidence of autonomic dysfunction and that degeneration of the cerebellar cortex did not affect the autonomic regulation.

Adolescent↗
PubMed1993

Inhibitory effect of a thromboxane A2 synthetase inhibitor OKY-046 on bronchial hyperresponsiveness to histamine, but not on airway wall thickening, induced by intravenous administration of leukotriene C4 in guinea-pigs.

We studied the effect of i.v.administration of leukotriene (LT) C4 on bronchial responsiveness to histamine and airway wall thickening in guinea-pigs. The infusion of 3 micrograms/kg LTC4 for 1 h induced an increase of the relative thickness of the airway wall in peripheral bronchi, found by histological examination. In analysis of airway function, the infusion of 3 micrograms/kg LTC4 for 1 h induced airway wall thickening and airway hyperresponsiveness to histamine administered i.v.at doses of 1.8 and 3.6 micrograms/kg. Thromboxane A2 synthetase inhibitor OKY-046, which was administered perorally, inhibited the LTC4-induced airway hyperresponsiveness to histamine in a dose-dependent manner at doses from 30-100 mg/kg, but not the airway wall thickening induced by LTC4.

Airway Resistance↗
PubMed1993

Action myoclonus induced by visually guided movement.

In order to determine what kind of voluntary movement induces action myoclonus, we gave two siblings with sialidosis two kinds of tasks. When the patients were asked to move their index fingers following a smoothly moving target, action myoclonus became prominent. In contrast, when they were asked to perform the same movements with their eyes closed, they could move their index fingers very smoothly. This shows that action myoclonus was induced by visually guided movement, but not by self-paced movement. Our observations might reflect a disorder of the cerebellum, which controls visually guided movement.

Adult↗
PubMed1993

Role played by NK2 receptor and cyclooxygenase activation in bradykinin B2 receptor mediated-airway effects in guinea pigs.

We have investigated the effects of SR-48968, an NK2 receptor antagonist, and indomethacin, a cyclooxygenase inhibitor, against bronchoconstriction and airway microvascular leakage induced by bradykinin (BK) in anesthetized guinea pigs. In addition, we have determined whether these effects were mediated via bradykinin B2 receptor activation, using a B2 receptor antagonist HOE 140. Lung resistance (RL) and extravasation of Evans blue dye into airway tissues were used as indexes of airway caliber and microvascular leakage, respectively. BK (15 nmol/kg i.v.) induced a significant increase in RL and leakage of dye at all airway levels, responses which were completely abolished by HOE 140 (0.13 mg/kg i.v.). SR-48968 (1.5 mg/kg i.v.) had no effect against BK-induced airway effects. Indomethacin (5 mg/kg i.v.) completely blocked the increase in RL and significantly inhibited the leakage of dye in peripheral intrapulmonary airway. In conclusion, bronchoconstriction induced by i.v. BK is mediated by release of cyclooxygenase products but not by stimulation of NK2 receptors, while the airway microvascular leakage only partly involves cyclooxygenase activation. Cyclooxygenase activation may occur following bradykinin B2 receptor stimulation.

Airway Resistance↗
PubMed1993

Developmental studies of the expression of myosin heavy chain isoforms in cultured human muscle aneurally and innervated with fetal rat spinal cord.

To study the influence of innervation of human muscle fiber type differentiation, we performed immunohistochemical studies using three monoclonal antibodies (McAbs) to myosin heavy chain (MHC) on cultured human muscles at different developmental stages. McAbs QM 355 (McAb-1), E 35-3 (McAb-2) and SM 1-11-2 (McAb-3) bound to fiber types I, IIA, IIB and IIC, types IIA, IIB and IIC, and type I, respectively. At the mononucleated cell stage the majority was immunonegative to the three McAbs; however, a few myoblasts were immunopositive to the McAb-1. They were also weakly stained with McAb-2 but not with McAb-3. In aneurally cultured myotubes (AMs), all myotubes were stained with the McAb-1 and 92.1% of AMs were positive to the McAb-2, whereas only a few (0.9%) AMs were immunopositive to the McAb-3. In contracting muscle fibers in an innervated area (CMis), which were co-cultured with fetal rat spinal cord explants, the percentage of the McAb-3-positive CMis was significantly increased (8.3%; P < 0.01) compared with that of AMs (0.9%). The double staining with the McAbs-2 and -3 clearly showed that slow MHC-positive muscle fibers without fast MHC only appeared in CMis. This is the first report of the neuronal influence on the expression of human adult slow MHC isoform derived from adult human satellite cells in vitro.

Adenosine Triphosphatases↗
PubMed1993

Inhibition of bronchial hyperresponsiveness to histamine induced by intravenous administration of leukotriene C4 by novel thromboxane A2 receptor antagonists ONO-NT-126 and ONO-8809 in guinea-pigs.

We studied the effect of intravenous administration of leukotriene (LT) C4 on bronchial responsiveness to histamine and airway wall thickening in guinea-pigs. Guinea-pigs were killed and the lungs were fixed in formalin. Slides from paraffin-embedded sections of the lungs were stained and the airways that were cut in transverse sections were measured by tracing enlarged images using a digitizer. Moreover, airway resistance (Raw) was determined by a pulmonary mechanics analyser and we calculated two indices, an index of airway wall thickening and the one of airway hyperresponsiveness to histamine, from changes of baseline-Raw and peak-Raw following intravenous administration of histamine before and after the intravenous administration of LTC4. Intravenous administration of 3 microg/kg LTC4 for 1 hr induced an increase of the relative thickness of the airway wall in peripheral bronchi by the histological examination. In analysis of airway function, intravenous administration of 3 microg/kg LTC4 for 1 hr induced airway hyperresponsiveness to histamine with airway wall thickening. Thromboxane A2 receptor antagonists ONO-NT-126 and ONO-8809 inhibited the LTC4-induced airway hyperresponsiveness to histamine in a dose-dependent manner, but not the airway wall thickening induced by LTC4, suggesting that the effect of LTC4 on bronchial hyperresponsiveness is likely to be mediated through TXA2.

Airway Resistance↗
PubMed1993

Utilization behavior and concomitant motor neglect by bilateral frontal lobe damage.

We reported on a patient who had bilateral mesial frontal lesions, presumably of a primary cerebral malignant lymphoma. The patient presented with a combination of unusual behavioral disorders of the upper extremities, which has not yet been documented in the literature: bilateral utilization and imitation behaviors and motor neglect of the left arm. Utilization behavior was closely associated with bilateral manual grasping behavior and was caused by the bifrontal lesions. Damage to the right supplementary motor area resulted most likely in concomitant motor neglect of the left hand. Discussion includes differentiation from other related behavioral disorders.

Aged↗
PubMed1993

Polyarteritis nodosa (PN) complicated with unilateral exophthalmos.

A 58-year-old woman suddenly developed right exophthalmos. A CT scan of her orbit revealed an increase in volume and density of extraocular muscles and intraorbital soft tissues that resembled exophthalmos in Graves' disease. The exophthalmos gradually improved without treatment. Two months later she developed mononeuritis multiplex in her limbs, and then showed a sudden onset of swelling of her right calf. Sural nerve biopsy was performed and the diagnosis of polyarteritis nodosa (PN) was established from the histological findings. A rare case of PN with exophthalmos is herein reported with a review of the literature.

Exophthalmos↗
PubMed1993

Hemiballism-hemichorea induced by subcortical ischemia.

Four patients presented with hemiballism-hemichorea as a clinical manifestation of white matter ischemia. These patients illustrate "positive" motor phenomena rather than limb weakness as a consequence of cerebral ischemia. In each patient, the involuntary movements disappeared following worsening of paresis. Subcortical white matter infarction in three patients and hemodynamic hypo-perfusion in the cerebral hemisphere contralateral to dyskinetic movements were possible causes. Neuroradiologically, none had pathological changes in the vicinity of the subthalamic nucleus. We presume from these observations that ischemia of the subcortical white matter, without involvement of the basal ganglia or the subthalamic nucleus, may cause hemiballism-hemichorea.

Aged↗
PubMed1993

[Corticobasal degeneration: clinico-pathological studies on two cases].

We reported two patients with clinical features of corticobasal degeneration (CBD), one with autopsy observations. Their illness began in their sixties, ran progressive course and ended in death in about five years. The initial symptom was difficulty in manipulating with the left hands. Gradually the left lower limbs and the right limbs were also involved and the left became useless. They developed Parkinsonism, myoclonus, dystonia, hyperreflexia and vertical gaze palsy. They also showed the dysfunction of the fronto-parietal cortices, including grasping reflex, motor neglect, hemispatial neglect, constructional disturbance and cortical sensory loss. Dementia did not manifest until the terminal stage. Neuro-radiological studies demonstrated mild dilatation of the right central sulcus and marked reduction in cerebral blood flow in the fronto-parietal cortices, predominant in the right. Pathological examination in one of the case confirmed the the clinical diagnosis of CBD. There was a neuronal loss affecting second and third layers of the fronto-parietal cortices, especially the right parasylvian region, associated with spongiosis in these laminae and marked gliosis in deeper layers. Swollen, poorly staining (achromatic) neurons were observed in fifth layer. The hippocampus was unaffected. In the substantia nigra, there was extensive loss of pigmented cells. No Pick bodies, senile plaques, neurofibrillary tangles were observed in any region of the brain. The initial manifestations of their illness, the motor disturbances in the left upper extremities, were distinctive features in our patients. We could find no detailed description of these symptoms in the literature. We analysed these manifestations and described the results.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[Effect of thromboxane A2 synthetase inhibitor (OKY-046) on leukotriene C4-induced airway hyperresponsiveness in guinea pigs].

In this study, we investigated the effects of peroral (p.o.) administration of a thromboxane A2 (TXA2) synthetase inhibitor, OKY-046, on the airway hyperresponsiveness (AHR) in guinea pigs induced by intravenous administration of leukotriene C4 (LTC4). A 3 micrograms/kg/hr LTC4 infusion induced airway wall thickening (AWT) and AHR to 1.8 and 3.6 micrograms/kg histamine bolus shot. OKY-046 100 mg/kg p.o. partially inhibited the AHR induced by LTC4 without inhibition of AWT. Previously, we have reported that LTC4-induced AHR was partially inhibited, to the same exert as by OKY-046, by TXA2 receptor antagonists, ONO-NT-126 and ONO-8809. These data suggest that intravenous administration of LTC4 generates TXA2, and TXA2 augments LTC4-induced AHR partially in guinea pigs.

Administration, Oral↗
PubMed1993

[Effect of Asthremedin on bronchial hyperresponsiveness (BHR) to histamine induced by intravenous administration of platelet activating factor (PAF) in guinea pigs].

Platelet activating factor (PAF) has been suggested to play an important role in the pathogenesis of bronchial asthma. In the present study, the effect of i.c. administration of asthremedin on bronchial hyperresponsiveness (BHR) induced by i.v. administration of PAF was investigated in guinea pigs. Changes of airway wall thickness and ratio of bronchial smooth muscle constriction by histamine were calculated from dynamic respiratory resistance. Administration of PAF induced airway wall thickening. The ratio of bronchial smooth muscle constriction by histamine was enhanced by administration of PAF. Asthremedin did not inhibit airway wall thickening by PAF, but inhibited BHR to histamine induced by PAF.

Adrenocorticotropic Hormone↗
PubMed1993

[Deep peroneal nerve palsy associated with hypothyroidism].

Carpal tunnel syndrome is well known to be associated with hypothyroidism, but other mononeuropathies have been rarely reported. We report a 65-year-old male who showed right deep peroneal nerve palsy caused by hypothyroidism. The patient was admitted to our hospital because of general fatigue and right drop foot. On admission, bilateral pretibial pitting edema was observed, predominant on the right side. There was no muscle contraction in the right anterior tibial muscle and extensor hallucis longus in addition to slight weakness of the proximal muscles; whereas, muscle atrophy of the anterior tibial muscle was not noted. There was no sensory disturbance. On an electrophysiological examination, there was no muscle action potentials by the stimulation of the right deep peroneal nerve. Other nerves showed normal results both in the conduction velocity and in the compound action potential. Two months after the administration of levothyroxine sodium (0.025 mg/day), the right deep peroneal nerve palsy was completely recovered, associated with disappearance of pretibial edema. It is not yet determined which of axonopathy or demyelination is dominantly responsible for neuropathy associated with hypothyroidism. These results suggested a conduction block in deep peroneal nerve associated with focal edema. It is necessary to consider hypothyroidism as well as trauma, diabetes mellitus, and vasculitis when investigating mononeuropathy of deep peroneal nerve.

Action Potentials↗
PubMed1993

[Bronchial hyperresponsiveness to histamine induced by intravenous administration of 9 alpha,11 beta-prostaglandin F2 (9 alpha,11 beta-PGF2) in guinea pigs].

The effects of intravenous administration of 9 alpha,11 beta-PGF2, a stable metabolite of prostaglandin D2 (PGD2), on bronchial smooth muscle in guinea pigs were investigated by measurement of dynamic compliance and dynamic respiratory resistance using a formula to exclude the effects of differences in airway wall thickness. With this formula, the ratio of bronchial smooth muscle constriction by histamine can be estimated as an index of bronchial hyperresponsiveness to histamine. Administration of 9 alpha,11 beta-PGF2 induced airway wall edema. The ratio of bronchial smooth muscle constriction by histamine was significantly enhanced by the administration of 9 alpha,11 beta-PGF2a. TXA2 antagonists, ONO-NT-128 and ONO-8809, inhibited the effect of 9 alpha,11 beta-PGF2 administration. These results suggest that 9 alpha,11 beta-PGF2 act as important mediators affecting bronchial hyperresponsiveness, and TXA2 may play a role in 9 alpha,11 beta-PGF2-induced airway wall edema and bronchial hyperresponsiveness to histamine.

Animals↗
PubMed1993

[Alcoholic cerebellar degeneration with pyramidal sign--in relation to alcoholic myelopathy].

Two cases of alcoholic cerebellar degeneration with pyramidal sign were reported. Patient 1 with alcohol dependence syndrome was a 46-year-old woman. After the alcohol abuse of about eight years, she complained of gait disturbance. The gait disturbance progressively worsened in about two months and she could not ambulate freely by herself. Neurological examination revealed nystagmus, ataxic and spastic gait, slight weakness and spasticity of the lower extremities, hyperreflexia of the extremities, bilateral Babinski's signs, and incoordination of the lower extremities. Examination of liver function and serum B12 was normal. Cranial CT scan and MRI revealed atrophy of the cerebellar vermis and dorsal part of the cerebellum. Though neurological signs slightly improved after the admission to our hospital and the abstinence from alcohol abuse, ataxic gait and hyperreflexia of the extremities have continued. Patient 2 was a 58-year-old man. He was a heavy drinker, but was not a patient with alcohol dependence syndrome. After the heavy drinking of about 40 years, he complained of gait disturbance. The gait disturbance had progressively worsened in about four months. Neurological examination revealed ataxic gait, hyperreflexia of the lower extremities, and bilateral Babinski's signs. Laboratory examination revealed slight liver dysfunction with minimal GPT and moderate gamma-GTP elevation. Examination of serum B12 was normal. Cranial CT scan and MRI revealed atrophy of the cerebellar vermis. Though bilateral Babinski's signs disappeared after the abstinence from heavy drinking, ataxic gait and hyperreflexia of the lower extremities have continued. Alcoholic myelopathy without hepatic cirrhosis was rarely reported. In the relation of alcoholic cerebellar degeneration to alcoholic myelopathy, our cases are interesting and important.

Alcoholism↗
PubMed1993

[Effect of thromboxane A2 (TXA2) antagonists on bronchial hyperresponsiveness induced by intravenous administration of leukotriene C4 (LTC4) in guinea pigs].

Effects of TXA2 antagonists on bronchial hyperresponsiveness induced by intravenous administration of LTC4 in guinea pigs were investigated by measurement of dynamic compliance and dynamic respiratory resistance, using a formula to exclude the effects of changes in airway wall thickness. With the formula, the ratio of bronchial smooth muscle constriction by histamine can be estimated as an index of bronchial hyperresponsiveness to histamine. Administration of LTC4 induced airway wall edema. The ratio of bronchial smooth muscle constriction by histamine was enhanced by the administration of LTC4. TXA2 antagonists, ONO-NT-126 and ONO-8809, inhibited the increased ratio of bronchial smooth muscle constriction of LTC4. On the other hand, the antagonists showed no significant effects on airway wall edema by LTC4. These results suggest TXA2 may play a role in LTC4-induced bronchial hyperresponsiveness to histamine.

Animals↗
PubMed1992

Selective loss of nigral neurons in Alzheimer's disease: a morphometric study.

Loss of neurons from the substantia nigra (SN), which is sometimes observed in Alzheimer's disease (AD), was quantitatively analyzed in 10 cases of presenile AD and 19 age-matched controls. On sections from the upper and lower portions of the SN, the pigmented zone (zona compacta) and the non-pigmented zone (zona reticulata) were delineated, and these zones were partitioned into quarters: medial, mid-medial, mid-lateral and lateral. This approach clarified topographical preference of neuronal depletion in the SN of AD; namely (1) pigmented neurons were more severely affected than non-pigmented neurons, (2) neuronal depletion was more marked in the lower SN (-38%, P less than 0.001), where the pigmented neurons in the medial quarter were most severely affected (-51%, P less than 0.001), (3) in the upper SN (neuronal loss: -21%, P less than 0.01), the pigmented neurons in the mid-medial quarter were most severely affected (-43%, P less than 0.01). These findings suggest that some groups of nigral neurons are primarily involved in presenile AD. Gallyas staining after bleaching of melanin pigments uncovered a large number of neurofibrillary tangles (NFTs) mainly in the pigmented zone, especially in the medial quarter. A large number of NFTs, scarse senile plaques, and substantial depletion of neurons form an unique combination of Alzheimer pathology in the SN not well recognized so far.

Aged↗