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1.  Enhancement of sensitivity of human lung adenocarcinoma cells to growth-inhibitory activity of interferon alpha by differentiation-inducing agents. 
British Journal of Cancer  1996;74(4):546-554.
A low concentration of differentiation inducers such as dimethylsulphoxide (DMSO), sodium butyrate, hexamethylene bisacetamide and sodium phenylacetate greatly enhanced the antiproliferative effect in vitro and in vivo of interferon alpha (IFN-alpha) to several human lung adenocarcinoma cells. The agents induced morphological changes in the adenocarcinoma cells and the agents together with IFN-alpha-induced alkaline phosphatase activity, which is a typical marker of type II pneumocyte maturation. To understand the mechanism of the DMSO-enhanced interferon sensitivity, we examined the effect of DMSO on high-affinity IFN-alpha receptor and interferon-stimulated promoter-binding factors. The lung adenocarcinoma cells were not impaired in IFN-alpha receptor and interferon-stimulated gene transactivation factor 3 (ISGF-3). Our data suggest that the enhancement of interferon sensitivity in the lung adenocarcinoma cells acts downstream of the activation of ISGF-3.
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PMCID: PMC2074667  PMID: 8761368
2.  Recurrent opticomyelitis associated with anti-DNA antibody. 
Two patients had frequent attacks of acute myelitis and optic neuritis. One patient lacked any other organ involvement whereas the other developed systemic manifestations of systemic lupus erythematosus 14 years after the onset. Both patients developed antinuclear and antidouble strand DNA antibodies after the onset of neurological involvement. These patients, whose neurological manifestations were indistinguishable from multiple sclerosis, were thus considered to have systemic lupus erythematosus related collagen disease.
PMCID: PMC1073142  PMID: 8089684
3.  Striatal blood flow, glucose metabolism and 18F-dopa uptake: difference in Parkinson's disease and atypical parkinsonism. 
Striatal blood flow, glucose metabolism and 18F-Dopa uptake were studied with positron emission tomography (PET) in eight non-demented patients with idiopathic Parkinson's disease and eight with atypical Parkinsonism. Patients with atypical Parkinsonism had no specific cause for the Parkinsonian symptoms and were clinically different from Parkinson's disease with lack of resting tremor and a poor response to dopaminergic drugs. Decreased 18F-Dopa uptake in the putamen was observed in patients with Parkinson's disease and atypical Parkinsonism compared with normal controls. 18F-Dopa uptake in the head of the caudate was also significantly reduced in both conditions but relatively less in Parkinson's disease. Decreased blood flow and glucose metabolism in the striatum associated with a global cerebral decrease were also observed in patients with atypical Parkinsonism compared with controls, while they were preserved in patients with Parkinson's disease, indicating affected neurons not only in the striatum but also in the cerebrum in patients with atypical Parkinsonism compared with patients with Parkinson's disease. The differences in the caudate 18F-Dopa uptake, and blood flow and glucose metabolism in the cerebrum including the striatum between Parkinson's disease and atypical Parkinsonism assessed by PET may be due to the differences in the pathophysiological mechanism between Parkinson's disease and atypical Parkinsonism.
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PMCID: PMC1014575  PMID: 1744644
4.  Abnormality in the cavernous sinus in three patients with Tolosa-Hunt syndrome: MRI and CT findings. 
Three patients with Tolosa-Hunt syndrome (THS) were examined using computed tomography (CT), orbital venography and magnetic resonance imaging (MRI). CT of the brain showed no definite abnormality in two patients, right optic nerve enlargement and an abnormal area around the orbital apex in one patient. Orbital venography showed an occlusion of the superior ophthalmic vein in one of three patients. MRI showed an abnormal soft tissue area in the cavernous sinus, with intermediate to high signal intensity on T1- or intermediate weighted images. There was clinical improvement following corticosteroid therapy and the abnormal soft tissue on MRI decreased in volume and in signal intensity, although this was equivocal in one patient. Thus MRI proved to be useful in demonstrating lesions in the cavernous sinus in patients with THS.
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PMCID: PMC1014134  PMID: 2324755
5.  Biochemical studies in mitochondrial encephalomyopathy. 
The alpha-keto acid dehydrogenase complex and its component enzymes, lactate dehydrogenase, pyruvate carboxylase, cytochrome c oxidase, succinate-cytochrome c reductase, NADH-cytochrome c reductase, and the concentration of cytochromes and enzymes of beta-oxidation in muscle from a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes were studied and no specific defect was found. These results raise the possibility that the mitochondrial changes in the patient may be secondary.
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PMCID: PMC1032463  PMID: 3681314
6.  Positron emission tomography in cases of chorea with different underlying diseases. 
Local cerebral metabolic rate for glucose (LCMRglc) was measured with positron emission tomography using the 18F-fluorodeoxy-glucose method in five patients with chorea due to different underlying diseases. Hypometabolism was observed in the striatum bilaterally in patients with Huntington's disease, choreoacanthocytosis, sporadic progressive chorea and dementia, and pseudo-Huntington form of dentato-rubro-pallido-luysian atrophy (DRPLA). The patient with hemichorea showed hypometabolism in the striatum on the contralateral side to the chorea. The patient with pseudo-Huntington form of DRPLA showed a diffusely decreased LCMRglc in other structures including the cerebral cortex, thalamus and cerebellum. These findings indicated that dysfunction of the striatum is relevant to the genesis of chorea in all these patients, even though the extent of dysfunction in other structures is different in each case.
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PMCID: PMC1032451  PMID: 2960785
7.  Familial spinocerebellar degeneration as an expression of adrenoleukodystrophy. 
A family with adrenoleukodystrophy and clinical manifestations of spinocerebellar degeneration was studied. Two adult male first cousins showed progressive limb and truncal ataxia, slurred speech and spasticity of the extremities. Brain CT scans demonstrated atrophy of the pons and cerebellum, in both cases. Very long chain fatty acids in plasma and erythrocyte membranes were elevated in the affected patients and intermediately increased in an aunt and the mother of one patient, thereby indicating homozygotes and carriers of adrenoleukodystrophy, respectively. This unusual type of adrenoleukodystrophy seems to be transmitted as an X-linked recessive trait.
PMCID: PMC1029132  PMID: 3468205
8.  Oculopharyngeal myopathy with distal and cardiomyopathy. 
Two patients are described with distinctive clinical features including an insidious onset, slow progression, bilateral ptosis, weakness of facial muscles, dysphagia, muscle atrophy, and weakness with a distal distribution in the extremities, and cardiomopathy with conduction system disorders. Electromyographic studies and muscle biopsy showed features highly suggestive of a myopathic disorder. One case is considered to be sporadic. The other seems to be a familial disorder, because of the presence of a mild atrioventricular block and right incomplete bundle branch block in the patient's son and the presence of eyelid ptosis in his sister. This may be a variant of oculopharyngeal myopathy with distal and cardiomyopathy. It will be necessary to perform long-term follow-up studies in these families.
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PMCID: PMC492768  PMID: 903774
9.  Acrylamide encephaloneuropathy due to well water pollution. 
All five members of a family developed subacutely mental confusion and/or truncal ataxia. Symptoms and signs of polyneuropathy were seen later. The well water in the patients' home contained 400 ppm acrylamide. The present cases are unique in that they are cases of acrylamide poisoning induced by oral intake and percutaneous penetration, and that central nervous system symptoms were prominent.
PMCID: PMC492032  PMID: 168322

Results 1-9 (9)