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Biomedical subjects

H Tanabe

Publications and source records attributed to H Tanabe.

At least 307 records · Page 17Linked to original sources
PubMed1990

[Thrombosis of the superior cerebral vein with hemorrhagic cerebral infarction--serial MRI and pathological study of a case].

We reported an autopsy case of thrombotic occlusion of the superior cerebral vein with hemorrhagic laminar necrosis of the right parietal cortex. A 68-year-old woman was admitted to our hospital because of a severe headache and left hemiplegia of acute onset. There was a past history of hypertension, fever of unknown origin, leukocytopenia and nasal dermatitis. Magnetic resonance images (MRI) disclosed thrombosis of the superior sagittal sinus and of the right parietal cortical vein as well as right parieto-occipital cerebral infarction. Although she improved with mild sequelae, the subsequent MRI showed a recurrent thrombosis of the superior sagittal sinus. Ten months after the onset she died suddenly, presumably due to acute myocardial infarction. Pathologically, thrombotic occlusion of the right parietal cortical vein, recurrent thrombosis of the superior sagittal sinus and old hemorrhagic cortical laminar necrosis of the right parietal region were revealed. Moreover, intracranial arteritis and phlebitis were observed, as well as arteriolitis in the peripheral nerves. In our case, MRI was useful for the diagnosis and following the course of cerebral venous thrombosis. Cerebral noninfective vasculitis may well have caused the venous thrombosis.

Aged↗
PubMed1990

[Two siblings of distal hereditary motor neuropathy with choroideremia].

Two brothers, 31 and 25 years of age, with distal hereditary motor neuropathy (distal HMN) and choroideremia are reported. Their parents were second cousins. During the first decade, their visual acuity gradually diminished with night blindness, accompanied by weakness of the legs. From the third decade, they noticed weakness of the hands. The neurological signs of both cases could be summarized as follows: bilateral pes cavus, Charcot-Marie-Tooth type distal atrophy and weakness of the four limbs, no sensory deficit, hyperreflexia in the upper limbs and knees, absent ankle jerks and plantar reflexes, and severe visual impairment due to choroideremia. In addition to these signs, the younger patient showed nystagmus and limb kinetic ataxia suggesting cerebellar involvement. Muscle biopsies and EMG studies revealed chronic neurogenic changes. MCV's in the median nerves were normal, but the extensor digitorum brevis muscles were totally denervated. SCV's, the amplitude of sensory action potentials and sural nerve biopsies were normal. In both patients, elevated CSF protein without pleocytosis and high level of serum IgA & E were demonstrated. Associations of choroideremia and abnormal laboratory findings as noted in our cases have not been so far reported in distal HMN, but we suppose these disorders may be genetically related.

Adult↗
PubMed1990

[Chronic inflammatory demyelinating polyradiculoneuropathy associated with central nervous system involvement--as compared to multiple sclerosis].

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with central nervous system (CNS) demyelinating lesions has recently been reported to mimic multiple sclerosis (MS). In this paper, a series of patients with CIDP were examined to see if they had CNS involvement. CIDP patients with CNS lesions were then compared to patients with MS with peripheral nervous system (PNS) involvement for similarities. CNS and PNS involvement were detected by clinical symptoms, neurological findings, neuro-otological and neuro-ophthalmological tests, electrophysiological examinations such as electroencephalography, evoked potentials, blink reflex, conventional peripheral nerve conduction studies and electromyography, as well as computed tomography and magnetic resonance imaging (MRI). There were 7 of 17 CIDP patients with CNS involvement, but only 2 of 59 MS patients with PNS lesions were found. The rate of CIDP with CNS involvement (41.2%) was higher than that of MS with PNS lesions (3.4%). The CNS signs and symptoms of 7 CIDP patients were not so constant as their PNS symptoms, and consisted of 1 case with optic neuritis, 4 cases with cerebellar atxia and/or nystagmus, and 3 cases with spinal symptoms. These signs and symptoms are all well known in MS. Prolonged latencies on evoked potentials and high signal white matter lesions on T2 weighted MRI, indicating demyelinating CNS lesions were also similar to those found in MS. The CNS involvement in those patients with CIDP was therefore similar in character to those found in MS, but was far less severe than the PNS finding.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

[Central neurogenic hyperventilation in an awake patient with a primary cerebral lymphoma].

We described clinical and neuropathological findings of a case of primary cerebral lymphoma with central neurogenic hyperventilation (CNH). A 54-year-old awake woman with a primary cerebral lymphoma presented hyperventilation for two weeks. Arterial blood gas showed severe respiratory alkalosis; PH 7.603, PaCO2, 10.5 mmHg, PaO2 129.8 mmHg, HCO2 10.4 mmol/L, BE -8.0, O2SAT 98.9%. Rebreathing from a paper bag, and intravenous administration of diazepam and sodium bicarbonate failed to alter the respiratory pattern. Consecutive CAT scans indicated that CNH didn't occur when the tumor extensively invaded the cerebral cortex, cerebellum, thalamus and basal ganglia but was initiated when the lymphoma invaded the brain stem. Pathological study showed lymphoma cells invaded the cerebral cortex, cerebellum, thalamus and basal ganglia severely, and the brain stem moderately and recently. Contrary to the cases reported by Plum, Lange and Bateman, the lower medulla was also involved. Possible mechanisms for CNH are discussed in relation to the pathological findings and consecutive CAT scan findings.

Brain Neoplasms↗
PubMed1990

[In vitro immunoglobulin synthesis by peripheral blood mononuclear cells from patients with myasthenia gravis].

In vitro immunoglobulin (Ig) synthesis was studied using peripheral blood mononuclear cells (PBM) from 12 patients with myasthenia gravis (MG). In cultured PBM, levels of secreted IgG, IgM and IgA measured by ELISA, as well as the number of IgG-, IgM-, and IgA-secreting cells determined by reversed plaque assay, were higher in MG than in controls; this was not dependent upon the stimulation of PBM with pokeweed mitogen (PWM). PBM from 9 of 12 MG patients synthesized anti-acetylcholine receptor (AChR) antibodies in vitro in the presence of PWM, while PBM from 7 controls did not. Patients whose PBM secreted lower levels of each Ig class also secreted fewer or no anti-AChR antibodies. Levels of anti-AChR antibodies secreted in vitro showed a high degree of correlation with titers of sera from patients (r = 0.86). The results suggest that the process of anti-AChR antibody synthesis by PBM in vitro is related to that of Ig synthesis, and that PBM plays, at least in part, an important role in the production of anti-AChR antibodies in MG.

Adult↗
PubMed1990

[Pindolol-induced rhabdomyolysis in sarcoid myopathy].

A 72-year-old man suddenly developed severe muscle weakness following the treatment with pindolol (Calvisken) for three days. Neurological examination on admission disclosed marked proximal muscle weakness with absent deep tendon reflexes. Laboratory data showed significant increase of serum CK, aldolase and myoglobin. Electromyography revealed both neurogenic and myogenic changes in all muscle tested. Skeletal muscle CT showed patchy low density areas in muscles of thigh and leg, especially in the hamstrings. Femoral muscle biopsy demonstrated a granulomatous nodule with multinucleated giant cells in the degenerated muscle fibers showing small-grouped atrophy. By Mb-PAP staining, Mb-negative fibers were randomly distributed among normally stained ones. Leu 1, 3a, 4, HLA-DR positive cells were found adjacent to the granuloma by immunoperoxidase staining. After immediate withdrawal of pindolol and treatment with steroid, he recovered muscle strength and enzyme activities were normalized in a week. Beta blockers have been known to induce muscle cramps or pain and moderate elevation of serum muscle enzymes. However, severe muscle weakness with highly elevated enzyme activities leading to rhabdomyolysis as noticed in the present case was rarely reported in the literature. Underlying sarcoid myopathy might be suspected to exaggerate this unusual case of pindolol-induced rhabdomyolysis. A careful use of pindolol is emphasized.

Aged↗
PubMed1990

[Encephalomyelitis with elevated serum antibody against Borrelia burgdorferi].

A 60-year-old female was admitted because of intermittent fever, arthralgia, itching of whole body, pretibial edema, urinary incontinence, pain of both legs and gait disturbance, after an insect bite. On admission, she had fever of 38 degrees C, and nuchal pain and stiffness. Neurological examination revealed spasticity of lower legs and increased deep tendon reflexes of all extremities. Hyperesthesia and hyperalgesia were noted on C2-4 and L5-S5 areas. Leukocyte count was 10,100/mm3 and CRP was 2+. CSF showed no pleocytosis (3/mm3, lymphocyte), but total protein (50 mg/dl) and IgG (10.5 mg/dl) were increased. On T2-weighted images of brain MRI, multiple small high signal areas were shown. The symptom improved markedly by prednisolone, but 3 months later left lateral gaze palsy appeared abruptly. A demyelinating lesion of the pons to the medulla oblongata including the left paramedian pontine reticular formation was suspected, and a corticosteroid pulse therapy was very effective. Serum titer of anti-Borrelia burgdorferi-IgG antibody by indirect immunoperoxidase method was 400 x at first and 1600 x after 3 months. Neuroborreliosis was diagnosed, but high doses of intravenous penicillin were not effective, and an immune-mediated demyelinating mechanism was probably thought to play a role in the pathogenesis of neuroborreliosis.

Antibodies, Bacterial↗
PubMed1990

[Postpolio late progressive muscular atrophy--clinical and epidemiologic analyses in 4 Japanese cases].

Four Japanese cases of postpolio progressive muscular atrophy (PPMA) of late onset were clinically studied to characterize their clinical features and discussed upon the epidemiologic viewpoint. Four male patients were included with mean age of 43.5 (30-59) years on examination, diagnosed as PPMA after the criteria by Alter (1982) and Dalakas (1986). All suffered from polio at age 10 month to 8 years (mean: 3y) between 1931 and 1957 with residual motor paresis in one limb or two. Twenty-eight to 55 (mean: 40.3) years later, subsequent muscle weakness and atrophy appeared in the limb seemingly unaffected by the initial polio attack. Marked fasciculations and occasional myalgias were noticed without sensory disturbance and bulbar as well as upper motor neuron signs. Laboratory examinations revealed moderate elevations of serum CK and protein content in SCF. No significant elevation of polio virus antibody titers was found in both serum and CSF. Electromyography showed neurogenic changes of various degrees by muscle tested. Muscle CT disclosed patchy distribution of atrophied muscles with fatty replacement in all extremities. Spinal cord MRI images were unremarkable. Scatters of small grouped atrophy and fiber type grouping were noticed on muscle biopsy specimens. These findings summarized in our cases are generally compatible with those of hereby reported PPMA cases. On reviewing the western literature and the great epidemic of polio around 1960 in Japan, an increasing number of patients with PPMA can be anticipated in near future; possibly in 10 years.

Adult↗
PubMed1989

Detection of dystrophin on two-dimensional gel electrophoresis.

A protein with MW approximately 350 k daltons and pI approximately 5.5, which was deleted in the dystrophic mouse (C57BL/10ScSn-mdx), was detected on two-dimensional gel electrophoresis with silver staining. Deletion of this protein was uniformly observed in the dystrophic mouse extensor digitus longus, soleus and cardiac muscle. This protein specifically reacted with the monoclonal antibody against the chemically synthesized N-terminal fragment of human dystrophin. The protein reacting with this monoclonal antibody was also detected in rabbit back-muscle, rat extensor digitus longus and human skeletal muscle at the same position as the mouse muscle protein, on the two-dimensional gel electrophoresis. Our results show that dystrophin is solubilized in 8M guanidine HCl and that the modified two-dimensional gel electrophoresis can be applied to separate dystrophin.

Animals↗
PubMed1989

Cause of early skeletal relapse after mandibular setback.

The present study was undertaken to examine the factors that might be responsible for the skeletal relapse occurring during the period of intermaxillary fixation after mandibular setback osteotomy. Fifteen patients, treated for absolute mandibular prognathism by modified sagittal split ramus osteotomy and fixation by skeletal suspension wiring, were evaluated cephalometrically by reference to the degree of postsurgical superior shift of the gonial region of the distal segment as a parameter of relapse since such a shift was evident despite the use of wiring. It was found that the degree of inadvertent anteroposterior rotation of the proximal segment at surgery, rather than the extent and pattern of surgical repositioning of the distal segment, was significantly correlated with the degree of shift. This result emphasizes the justification of preserving the proximal segment in its exact original anatomic site, in addition to the use of skeletal fixation, to ensure predictable stability after mandibular setback osteotomy.

Adolescent↗
PubMed1989

Identification of a gene that shortens clonal life span of Paramecium tetraurelia.

We have isolated a Paramecium tetraurelia mutant that divides slowly in daily reisolation cultures and repeats short clonal life spans after successive autogamies. Here we show, using breeding analysis, that a recessive mutation is responsible for the low fission rate and that this low rate is closely related to the short clonal life span. We conclude that a single pleiotropic gene controls these traits and have named it jumyo. In an attempt to further characterize the jumyo mutant, we have revealed that it has a culture life span similar to that of the wild-type cells and that, when mass cultured, it can divide as rapidly as wild-type cells. There was strong evidence that the mutant cells excreted into culture medium some substance that promotes their cell division. These findings may not only present supporting evidence for the hypothesis that the cellular life span is genetically programmed but also give a material basis for the study of the controlling mechanism of cell division in relation to the clonal life span.

Animals↗