the Taiwan Stroke Registry InvestigatorsBackground-Stroke is a leading cause of death around the world. Improving the quality of stroke care is a global priority, despite the diverse healthcare economies across nations. The American Heart Association/American Stroke Association Get With the Guidelines-Stroke program (GWTG-Stroke) has improved the quality of stroke care in 790 US academic and community hospitals, with broad implications for the rest of the country. The generalizability of GWTG-Stroke across national and economic boundaries remains to be tested. 2,3 This was followed by the implementation of the American Heart Association/American Stroke Association Get With the Guidelines-Stroke program (GWTG-Stroke). 4 GWTG-Stroke was the first large-scale nationwide assessment of the quality of stroke care based on a set of predefined performance measures. The 790 participating hospitals showed substantial and sustained improve- Clinical Perspective on p 1123Stroke is the second leading cause of death globally, 5 with nations with diverse health care systems facing a similar medical and economic burden. 6 Whether the successful GWTG-Stroke is applicable beyond the United States remains to be tested. A key determinant that may hamper broad application of GWTG-Stroke around the world is the diversity of healthcare economies. It could be difficult for nations spending substantially less in healthcare dollars to apply GWTG-Stroke standards. To examine whether GWTGStroke is workable across nations with substantial disparities in health expenditures, we applied GWTG-Stroke to assess the quality of stroke care in Taiwan. Like the United States, stroke is the third leading cause of death in Taiwan. In 2008, the total cost of stroke in the United States, with 780 000 new or recurrent stroke cases, was estimated to be $65.5 billion, with direct (medical) costs constituting two thirds or $43.6 billion. 5 Taiwan, with a population of 23 million (1/13 of that of the United States), with Ϸ80 000 new or recurrent strokes a year, spent a total of US $375 million in medical costs for stroke in 2007. 7 The total medical costs per new or recurrent stroke patient were Ϸ1/10 of those spent in the United States. 5 The Taiwan Stroke Registry (TSR) is an appropriate program to assess the generalizability of GWTG-Stroke across national as well as economic boundaries. TSR, sponsored by the Department of Health (DOH), was launched in 2006. With the exception of anticoagulation for deep vein thrombosis (DVT) and measures for smoking cessation, all the parameters adapted by GWTG-Stroke for assessing quality of stroke care have been included in TSR. Methods TSR Design and the Criteria for Hospital SelectionTSR is the first nationwide effort in Taiwan to establish a reliable national stroke database for assessing the quality of stroke care and identifying areas that require improvement. TSR was designed and a TSR operation manual developed after a series of consensus conferences attended by an expert panel (16 stroke neurologists and 2 epi...

Paeoniflorin, a component in Paeonia lactiflora Pall, inhibits nuclear factor-kappaB expression in chronic hypoperfusion rat and has anti-inflammatory properties. Therefore, the aim of the present study was to investigate the effect of paeoniflorin on cerebral infarct, and the involvement of anti-inflammation. We established an animal model of cerebral infarct by occluding both the common carotid arteries and the right middle cerebral artery for 90 min, followed by reperfusion of 24 hours. The ratios of cerebral infarction area to total brain area, and neuro-deficit score were used as an index to observe the effects of paeoniflorin on cerebral infarct. ED1 (mouse anti rat CD68), interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), intercellular adhesion molecular-1 (ICAM-1), myeloperoxidase (MPO) immunostaining and apoptotic cells in the cerebral infarction region also were studied. The results indicated that both pre-treatment and post-treatment with paeoniflorin reduced the ratio of cerebral infarction area; pre-treatment with paeoniflorin also reduced the neurological deficit score. The counts of ED1, IL-1beta, TNF-alpha, ICAM-1 of microvessels and MPO immunoreactive cells and apoptotic cells were increased in the cerebral infarction region; however, these increases were reduced by Paeoniflorin pre-treatment. In conclusion, Paeoniflorin reduced cerebral infarct and neurological deficit in ischemia-reperfusion injured rats, suggesting that paeoniflorin may have a similar effect in humans and might be a suitable treatment for stroke. Paeoniflorin reduced cerebral infarct, at least in part, involves the anti-inflammatory properties.

Key Points• L5 is elevated in ischemic stroke patients, and its receptor, LOX-1, plays a critical role in increasing stroke size.• L5 induces platelet secretion of Ab to potentiate platelet activation and aggregation via LOX-1 and IKK2.L5, the most electronegative and atherogenic subfraction of low-density lipoprotein (LDL), induces platelet activation. We hypothesized that plasma L5 levels are increased in acute ischemic stroke patients and examined whether lectin-like oxidized LDL receptor-1 (LOX-1), the receptor for L5 on endothelial cells and platelets, plays a critical role in stroke. Because amyloid b (Ab) stimulates platelet aggregation, we studied whether L5 and Ab function synergistically to induce prothrombotic pathways leading to stroke. Levels of plasma L5, serum Ab, and platelet LOX-1 expression were significantly higher in acute ischemic stroke patients than in controls without metabolic syndrome (P < .01). In mice subjected to focal cerebral ischemia, L5 treatment resulted in larger infarction volumes than did phosphatebuffered saline treatment. Deficiency or neutralizing of LOX-1 reduced infarct volume up to threefold after focal cerebral ischemia in mice, illustrating the importance of LOX-1 in stroke injury. In human platelets, L5 but not L1 (the least electronegative LDL subfraction) induced Ab release via IkB kinase 2 (IKK2). Furthermore, L51Ab synergistically induced glycoprotein IIb/IIIa receptor activation; phosphorylation of IKK2, IkBa, p65, and c-Jun N-terminal kinase 1; and platelet aggregation. These effects were blocked by inhibiting IKK2, LOX-1, or nuclear factor-kB (NF-kB). Injecting L51Ab shortened tail-bleeding time by 50% (n 5 12; P < .05 vs L1-injected mice), which was prevented by the IKK2 inhibitor. Our findings suggest that, through LOX-1, atherogenic L5 potentiates Abmediated platelet activation, platelet aggregation, and hemostasis via IKK2/NF-kB signaling. L5 elevation may be a risk factor for cerebral atherothrombosis, and downregulating LOX-1 and inhibiting IKK2 may be novel antithrombotic strategies. (Blood. 2016;127(10):1336-1345