Pyogenic ventriculitis with ruptured brain abscess.
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Aged↗
Biomedical subjects
Hiromichi Kawai
Publications and source records attributed to Hiromichi Kawai.
Cytomegalovirus-induced small-bowel hemorrhage in a patient with nonsystemic vasculitic neuropathy.
A 73-year-old man who was being treated with corticosteroids for nonsystemic vasculitic neuropathy developed small-bowel hemorrhage after ileostomy for ileus. Immunohistochemical staining for cytomegalovirus (CMV) antigen in the ulcer in the resected ileum was positive; thus, cytomegalovirus infection of the small intestine caused his gastrointestinal manifestations. Cytomegalovirus infection should be considered in the differential diagnosis of gastrointestinal diseases in patients with collagen vascular diseases receiving immunosuppressive agents.
Adrenal Cortex Hormones↗
Antiganglion neuron antibodies correlate with neuropathy in Sjögren's syndrome.
To investigate the possible implication of antibodies against dorsal root ganglion neuron in the pathogenesis of sensory neuropathy with Sjögren's syndrome, we examined the pathogenic role of antiganglion neuron antibodies by immunoblotting, immunohistochemistry and immunoreactive assay. Sjögren's syndrome patients without neuropathy, patients with vasculitic neuropathy and normal volunteers were evaluated as controls. Antiganglion neuron antibodies recognizing certain proteins of several different molecular weights were detected only in patients of sensory neuropathy with Sjögren's syndrome. Those antibodies labeled specific-sized neurons in the fixed ganglion and isolated ganglion neurons under the culture condition, each of which corresponded well to clinical manifestations. These results suggest that antiganglion neuron antibodies may contribute to the pathogenesis of sensory neuropathy with Sjögren's syndrome.
Aged↗
Binding of soluble myelin-associated glycoprotein to specific gangliosides induces the association of p75NTR to lipid rafts and signal transduction.
Myelin-associated glycoprotein (MAG) is a potent inhibitor of neurite outgrowth from a variety of neurons. Here we show that gangliosides, GT1b and GD1a, as well as the Nogo receptor, are functional binding partners for soluble MAG-Fc. Postnatal cerebellar neurons from mice deficient in the GalNAcT gene are insensitive to MAG with regard to neurite outgrowth and lack in the activation of RhoA. MAG-Fc or the antibody to GT1b and GD1a elicits recruitment of p75(NTR.) to lipid rafts, specialized microdomain for signal transduction. Disruption of lipid rafts results in abolishment of inhibitory effects of MAG-Fc and the Nogo peptide. These findings establish gangliosides as functional binding partners for soluble MAG. Gangliosides may play a role in translocation of p75(NTR.) to lipid rafts for initiation of the signal transduction.
Animals↗
[A case of stroke-like episode of MELAS of which progressive spread would be prevented by edaravone].
A thirty-two-year-old woman who had been diagnosed MELAS with 3243A > G mutation presented headache, nausea, decreased bilateral visual acuity, and topographical disturbance on January 1 in 2002. Although brain CT showed no fresh lesion, recurrence of stroke-like episode was considered. Immediately, she was treated with ubiquinone (210 mg/day, p.o.) and tocopherol nicotinate (300 mg/day, p.o.). She became confused on the fifth day. Diffusion weighted- and T2 weighted-MRI revealed appearance of hyperintense lesion at the right occipital lobe. We started edaravone infusion (30 mg, twice a day, div.) for two weeks with informed consent from her family. On 13th day her consciousness was improved. Edema and signal intensity of the lesion were decreased on MRI with minimal spread to the parietal lobe. She discharged on the 30th day with marked visual field loss, hemispatial neglect, and topographical amnesia. MRI after four months showed remarkable atrophy of the right occipital region. In our department, five stroke-like episodes including this case were treated with ubuiquinone and tocopherol nicotinate. This regimen was effective in prevention of progressive spread of lesions only in two episodes. Edaravone is radical scavenger used in acute cerebral infarction. Progressive spread into the neighboring regions is one of characteristics of MELAS, although its precise mechanisms are not well known. Oxidative stress induced by released free radicals through mitochondrial dysfunction might be one of factors and edaravone would make an effect through blockage of the free radicals. Edaravone could not rescue neurons in the initial lesion. Although more numbers of cases are needed to establish the effect of edaravone on MELAS, it could minimize the neurological deficits after stroke-like episode of MELAS.
Adult↗
Mice deficient in sphingosine kinase 1 are rendered lymphopenic by FTY720.
Sphingosine-1-phosphate (S1P), a lipid signaling molecule that regulates many cellular functions, is synthesized from sphingosine and ATP by the action of sphingosine kinase. Two such kinases have been identified, SPHK1 and SPHK2. To begin to investigate the physiological functions of sphingosine kinase and S1P signaling, we generated mice deficient in SPHK1. Sphk1 null mice were viable, fertile, and without any obvious abnormalities. Total SPHK activity in most Sphk1-/-tissues was substantially, but not completely, reduced indicating the presence of multiple sphingosine kinases. S1P levels in most tissues from the Sphk1-/- mice were not markedly decreased. In serum, however, there was a significant decrease in the S1P level. Although S1P signaling regulates lymphocyte trafficking, lymphocyte distribution was unaffected in lymphoid organs of Sphk1-/- mice. The immunosuppressant FTY720 was phosphorylated and elicited lymphopenia in the Sphk1 null mice showing that SPHK1 is not required for the functional activation of this sphingosine analogue prodrug. The results with these Sphk1 null mice reveal that some key physiologic processes that require S1P receptor signaling, such as vascular development and proper lymphocyte distribution, can occur in the absence of SPHK1.
Animals↗
SUMO-1 co-localized with mutant atrophin-1 with expanded polyglutamines accelerates intranuclear aggregation and cell death.
To investigate the implication of small ubiquitin-related modifier-1 (SUMO-1) in the formation of neuronal intranuclear inclusions in polyglutamine diseases, we examined the localization of SUMO-1 in dentatorubral-pallidoluysian atrophy (DRPLA) brain tissues and PC12 cells expressing truncated atrophin-1 with expanded poly-glutamine stretches. SUMO-1 was co-localized with neuronal intranuclear inclusions in DRPLA brain and the DRPLA model cells, which showed that the aggregates formed by expanded polyglutamine stretches were highly SUMOlylated. In addition, to examine the role of SUMO-1 in nuclear aggregate formation and cell death, either SUMO-1 or DeltaSUMO-1, which is a SUMOlylation defective mutant lacking the C-terminal motif, was co-transfected with atrophin-1 with expanded polyglutamine stretches. Co-transfection of DeltaSUMO-1 decreased number of the cells with nuclear aggregates and consequent apoptosis of PC12 cells, both of which were markedly enhanced by co-transfection of SUMO-1 with atrophin-1 with expanded polyglutamine stretches. These results suggest that SUMO-1 is implicated in the pathogenesis of DRPLA and accelerates aggregate formation and cell death.
Animals↗