Objective: To investigate the changes of serum high-sensitivity C-reactive protein(hs-CRP) and plasma D-dimer levels and their relationship with the volume of cerebral infarc-tion in patients with acute cerebral infarction. Methods: The levels of serum hs-CRP and plasma D-dimer in the cerebral infarction group were significantly higher than those in the control group (P ＜0.05); as compared with the patients with moderate infarction (5-10 cm3) and small infarction (≤ 5 cm3), the levels of serum hs-CRP and plasma D-dimer in patients with large cerebral infarction (≥ 10 cm3 ) increased significantly (P ＜ 0.05). Conclusions: Measuring the levels of serum hs-CRP and plasma D-dimer may contribute to the early diagnosis of cerebral infarction and the prediction of the volume of cerebral infarction.

Sirtuin is a type of deacetylase acted on histone. Sirtuin 1 (SIRT1) is the most homologous to the homologue of silent information regulator 2 (SIR2) in mammals. Its main function is to regulate the body energy metabolism, cell senescence and response to stress. SIRTI inhibits apoptosis through the interaction of several transcription factors involving in stress response. It is a neuroprotective gent.

Venous thromboembolism,including deep vein thrombosis and pulmonary embolism,is one of the common complications after stroke,and it also significantly increases the mortality in patients with stroke.Because of limb paralysis,prolonged bed rest,and specific hypercoagulable state,the patients with stroke become the high risk population of thrombosis.The preventive measures manly including physical and drug prevention.Clinical studies have confirmed that anticoagulation therapy for the prevention of venous thromboembolism is effective in patients with ischemic stroke.However,for patients with spontaneous intracerebral hemorrhage,whether anticoagulant drugs can be used and how to use them have not yet reached consensus,mainly on account of the risks of rebleeding or hematora enlargement.This article reviews the related literatures in recent years and summarizes the advances in research on the prevention and treatment of venous thrombosis in patients with intracerebral hemorrhage.

Oxidative stress is one of the important pathological mechanisms of neuron damage in ischemic stroke.Antioxidant therapy has become one of the important measures for ischemic brain injury.This article reviews the advances in research on the antioxidant therapy of ischemic stroke.

Peroxisome proliferative-activated receptor (PPAR) γ coactivator-1α (PGC-1α) is a transcriptional coactivator of PPARγ.PGC-1α can bind with many different transcription factors.It plays a number of functions in the different tissues and the process of biological reaction.Recent studies have shown that PGC-1α signaling pathway has a neuroprotective effect.This article reviews the neuroprotective effect of PGC-1α in cerebral ischernia and its possible mechanisms.

The aquaporins (AQPs) are a group of highly selective water channel protein family. The content of AQP4 in the astrocytes of the brain is the highest. It is the most vital protein in central nerve system. It participates in a series of pathologic processes of cerebrovascular disorders, brain contusion, tumor, and inflammation caused cerebral edema.However, the mechanism of AQP4 in the process of cerebral edema formation remains controversial. Selective modulation of the expression of AQP4 and intervention in part of its role may provide novel ideas and means for the treatment of edema after cerebral ischemia in clinical practice.

Neurogenic pulmonary edema (NPE) is a fatal complication after severe injury of central nervous system. Various cerebrovascular diseases are the common causes of NPE. The mortality of NPE is high. Its pathogenesis involves a variety of factors; however, its exact mechanism remains obscure. This article reviews the advances in pathogenesis and treatment of cerebrovascular diseases complicated with NPE in recent years.

Cocaine-and amphetamine-regulated transcript(CART) peptides are endogenous neurotransmitters with important roles in a number of physiological and pathological processes in vivo.Many studies suggested that CART is widely distributed in the central nervous system,and it has some central protective effects.This article reviews the recent progress in research on the protective effect of CART on cerebral ischemia and its mechanisms.

10% to 15% of patients with ischemic stroke may have hemorrhagic transformation.Its treatment is more complex,mainly includes blood pressure management,reversing coagulopathy,and treatment of complications (including increased intracranial pressure).The current research is mainly to find the therapeutic regimen of hemorrhagic transformation after anticoagulation and thrombolytic therapy in order to improve the prognosis in patients with stroke.

Objective To investigate the effects on brain tissue p38 mitogen-activated protein kinase (MAPK) and aquaporin 4 (AQP4) and neuroprotective effect of edarvone after focal cerebral ischemia and reperfusion in mice.Methods A total of 196 healthy male Kunming mice were randomly divided into four groups:a sham operation group,an ischemia-reperfusion group,a saline control group,and an edaravone group (n =49 in each group).A middle cerebral artery occlusion (MCAO) mothod was used to induce a cerebral ischemia-reperfusion model.At 2 h after ischemia,immediately after reperfusion in the edaravone group and the saline control group,edaravone (5 mg/kg) and the same volume of saline were injected intraperitoneally in mice,then repeated once every 24 h.At 2 h after MCAO,the brain water content and infarct volume at different time points after reperfusion (12 h,24 h,48 h,and 3 d) were measured respectively.At 24 h after MCAO,the expressions of AQP4 and p38 MAPK in the brain tissue of ischemic peripheral cortex were measured by Western blotting.Results The volumes of cerebral infarction (all P ＜ 0.01) and the brain water contents (all P ＜0.05) in the edaravone group were decreased than those in the ischemia-reperfusion group and saline control group at different time points,and they were most significant at 48 h.After 24-h reperfusion,the expression levels of AQP4 (0.985 ± 0.129,1.024 ± 0.117,0.713 ± 0.231) and phospho-p38 MAPK (1.123 ± 0.142,1.214 ± 0.096,0.986 ± 0.087) in the brain tissue of ischemic peripheral cortex in the ischemia-reperfusion group,the saline control group,and the edaravone group were upregulated significantly than those in the sham operation group (AQP4:0.265 ± 0.123;phospho-p38 MAPK:0.465 ±0.023;all P ＜0.01),but edaravone group were significantly lower than the ischemia-reperfusion group and the saline control group (all P ＜ 0.05).Conclusions Edaravone can downregulate the expression level of AQP4 and effectively protect cerebral ischemia reperfusion injury in mice,Its mechanism may be associated with the inhibition of p38 MAPK pathway.