Increased Risk of Ischemic Stroke during Sleep in Apneic Patients.

BACKGROUND AND PURPOSE:The literature indicates that obstructive sleep apnea (OSA) increases the risk of ischemic stroke. However, the causal relationship between OSA and ischemic stroke is not well established. This study examined whether preexisting OSA symptoms affect the onset of acute ischemic stroke. METHODS:We investigated consecutive patients who were admitted with acute ischemic stroke, using a standardized protocol including the Berlin Questionnaire on symptoms of OSA prior to stroke. The collected stroke data included the time of the stroke onset, risk factors, and etiologic subtypes. The association between preceding OSA symptoms and wake-up stroke (WUS) was assessed using multivariate logistic regression analysis. RESULTS:We identified 260 subjects with acute ischemic strokes with a definite onset time, of which 25.8% were WUS. The presence of preexisting witnessed or self-recognized sleep apnea was the only risk factor for WUS (adjusted odds ratio=2.055, 95% confidence interval=1.035-4.083, p=0.040). CONCLUSIONS:Preexisting symptoms suggestive of OSA were associated with the occurrence of WUS. This suggests that OSA contributes to ischemic stroke not only as a predisposing risk factor but also as a triggering factor. Treating OSA might therefore be beneficial in preventing stroke, particularly that occurring during sleep

Power Law in Firms Bankruptcy

We consider the scaling behaviors for fluctuations of the number of Korean firms bankrupted in the period from August 1 2002 to October 28 2003. We observe a power law for the distribution of the number of the bankrupted firms. The Pareto exponent is close to unity. We also consider the daily increments of the number of firms bankrupted. The probability distribution of the daily increments for the firms bankrupted follows the Gaussian distribution in central part and has a fat tail. The tail parts of the probability distribution of the daily increments for the firms bankrupted follow a power law.Comment: 3 pages, 4figure

Modelling wave-induced current at haeundae beach on orthogonal curvilinear grid by using CST3D

Haeundae Beach is sandy beach at Busan, Korea. Haeundae Beach is about 1.5 km- long enclosed by two headlands. The normal direction of the beach is between south and south-east. Tidal current at the site is not negligible, and waves are relatively high during monsoon and winter seasons. Currents were measured at nine points along Haeundae Beach on 4 June 2008 by using GPS-equipped drogues. Bathymetry around Haeundae Beach was surveyed on 7 August 2007 and 12 November 2007 by using an echo-sounder; wave, tide, and tidal current were measured between the two survey days, so that bathymetric change at the beach was obtained from the two surveys. The measured current vectors may include wave- induced current element, tidal current element, and wind-induced current. Seasonal sediment transport pattern at Haeundae Beach, Busan, Korea is known to be simple, according to previous observation. Typically sediment moves eastward, while sediment moves westward in winter. Tidal current contributes to long-term bathymetric change at the beach by transporting small-sized sediment

Role of Neuronal NADPH Oxidase 1 in the Peri-Infarct Regions after Stroke

The molecular mechanism underlying the selective vulnerability of neurons to oxidative damage caused by ischemia-reperfusion (I/R) injury remains unknown. We sought to determine the role of NADPH oxidase 1 (Nox1) in cerebral I/R-induced brain injury and survival of newborn cells in the ischemic injured region. Male Wistar rats were subjected to 90 min middle cerebral artery occlusion (MCAO) followed by reperfusion. After reperfusion, infarction size, level of superoxide and 8-hydroxy-20-deoxyguanosine (8-oxo-2dG), and Nox1 immunoreactivity were determined. RNAi-mediated knockdown of Nox1 was used to investigate the role of Nox1 in I/R-induced oxidative damage, neuronal death, motor function recovery, and ischemic neurogenesis. After I/R, Nox1 expression and 8-oxo-2dG immunoreactivity was increased in cortical neurons of the peri-infarct regions. Both infarction size and neuronal death in I/R injury were significantly reduced by adeno-associated virus (AAV)-mediated transduction of Nox1 short hairpin RNA (shRNA). AAV-mediated Nox1 knockdown enhanced functional recovery after MCAO. The level of survival and differentiation of newborn cells in the peri-infarct regions were increased by Nox1 inhibition. Our data suggest that Nox-1 may be responsible for oxidative damage to DNA, subsequent cortical neuronal degeneration, functional recovery, and regulation of ischemic neurogenesis in the peri-infarct regions after stroke