Phosphodiesterase III inhibition promotes differentiation and survival of oligodendrocyte progenitors and enhances regeneration of ischemic white matter lesions in the adult mammalian brain.

Vascular dementia is caused by blockage of blood supply to the brain, which causes ischemia and subsequent lesions primarily in the white matter, a key characteristic of the disease. In this study, we used a chronic cerebral hypoperfusion rat model to show that the regeneration of white matter damaged by hypoperfusion is enhanced by inhibiting phosphodiesterase III. A rat model of chronic cerebral hypoperfusion was prepared by bilateral common carotid artery ligation.

Clustering of risk factors increases the incidence of echolucent carotid plaque in stroke patients.

Background: The purpose of this study was to assess the influence of clusters of risk factors on the incidence of echolucent carotid plaque in stroke patients.

Methods: A retrospective analysis of 413 stroke patients who had undergone carotid ultrasonography was performed. High-resolution B-mode ultrasonography was used to evaluate the characteristics of carotid plaque.

Cilostazol protects against brain white matter damage and cognitive impairment in a rat model of chronic cerebral hypoperfusion.

Background And Purpose: White matter lesions contribute to cognitive impairment in poststroke patients. The present study was designed to assess the neuroprotective mechanisms of cilostazol, a potent inhibitor of type III phosphodiesterase, through signaling pathways that lead to activation of transcription factor cAMP-responsive element binding protein (CREB) phosphorylation using rat chronic cerebral hypoperfusion model.

Methods: Rats underwent bilateral common carotid artery ligation.

[An 80-year-old woman with progressive stroke, who had rheumatoid arthritis and antiphospholipid syndrome].

We report an 80-year-old woman who had rheumatoid arthritis and antiphospholipid syndrome. She was treated for rheumatoid arthritis since her thirties. At 76 years of age, she was diagnosed antiphospholipid syndrome serologically.