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Articles by Y Nagahama
Total Records ( 2 ) for Y Nagahama
  Y Nagahama , T Okina , N Suzuki and M. Matsuda
 

The aim of this study was to investigate the association between psychotic symptoms in dementia with Lewy bodies and brain perfusion on single photon emission tomography. Based on factor analysis in 145 patients, psychotic symptoms were classified into five symptom domains (factor 1 to 4-related symptoms and delusions). The relationship between each symptom domain and brain perfusion was assessed in 100 patients with dementia with Lewy bodies, while accounting for the effects of age, sex, dementia severity, parkinsonism and dysphoria. Factor 1 symptoms (Capgras syndrome, phantom boarder, reduplication of person and place and misidentification of person) represented misidentifications, and were significantly related to hypoperfusion in the left hippocampus, insula, ventral striatum and bilateral inferior frontal gyri. Factor 3 symptoms (visual hallucination of person and feeling of presence) represented hallucinations of person and were related to hypoperfusion in the left ventral occipital gyrus and bilateral parietal areas. Delusions of theft and persecution were associated with relative hyperperfusion in the right rostral medial frontal cortex, left medial superior frontal gyrus and bilateral dorsolateral frontal cortices. This study revealed that different psychotic symptoms in dementia with Lewy bodies were associated with distinguishable cerebral networks. Visual hallucinations were related to dysfunction of the parietal and occipital association cortices, misidentifications were related to dysfunction of the limbic-paralimbic structures and delusions were related to dysfunction of the frontal cortices. Our findings provide important insights into the pathophysiological mechanisms underlying psychotic symptoms in dementia with Lewy bodies.

  J Hirahashi , K Hishikawa , S Kaname , N Tsuboi , Y Wang , D. I Simon , G Stavrakis , T Shimosawa , L Xiao , Y Nagahama , K Suzuki , T Fujita and T. N. Mayadas
 

Background— Inflammation and thrombosis coexist in several disorders. Although it is recognized that leukocytes may induce a procoagulant state at sites of inflammation, the critical molecular determinants of this process remain largely unknown.

Methods and Results— To examine mechanisms of inflammation-induced thrombosis, we developed a murine model of thrombotic glomerulonephritis (TGN), a known cause of acute renal failure in patients. This model, induced by lipopolysaccharide and antibody to the glomerular basement membrane, led to rapid glomerular neutrophil recruitment, thrombotic glomerular lesions with endothelial cell injury, and renal dysfunction. In mice immunodepleted of neutrophils or lacking the leukocyte-specific integrin Mac-1, neutrophil recruitment, endothelial injury, glomerular thrombosis, and acute renal failure were markedly attenuated despite the robust generation of renal cytokines. Neutrophil elastase is a likely effector of Mac-1 because its activity was reduced in Mac-1–deficient mice and the phenotype in mice deficient in Mac-1 or neutrophil elastase was similar. Platelets accumulated in glomerular capillaries within 4 hours of TGN before evidence of thrombosis. Platelet immunodepletion before TGN markedly exacerbated hematuria (hemorrhage), inflammation, and injury, whereas thrombocytopenic Mac-1–deficient mice remained resistant to disease, indicating that initial glomerular platelet deposition protects the vessel wall from neutrophil-mediated sequelae. The subsequent thrombosis relied on the interaction of Mac-1 on recruited neutrophils with glycoprotein Ib on platelets as antibody-mediated disruption of this interaction attenuated TGN without affecting renal neutrophil accumulation.

Conclusions— These observations establish Mac-1 on neutrophils as a critical molecular link between inflammation and thrombosis and suggest it as an attractive target for antithrombotic therapy.

 
 
 
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