In recent years,more and more attention has been given to aspirin resistance.Researchers have explored the mechanisms of this important phenomenon from several aspects,including patient compliance,laboratory tests,aspirin dose,genetics,and drug interactions.Many appropriate management methods of aspirin resistance have been proposed,such as improving patient compliance,avoiding drug interactions,adjusting dose,and adding other antiplatelet drugs with potential application value.This article reviews the advances in research on the mechanisms of aspirin resistance.

and drug development; therefore, it has received wide attention in the field of life sciences.

Ischemic stroke is one of the most important complications of malignant tumors. The etiology and pathogenesis of ischemic stroke in patients with cancer are very complicated, it includes either traditional vascular risk factors such as hypertension, diabetes and hyperlipidemia or the risk factors associated with the pathophysiological state of tumors such as hypercoagulable state, tumor emboli, and thrombotic endocarditis. In addition, various treatment methods associated with tumors, such as radiotherapy, chemotherapy and endocrine therapy, can also increase the risk of ischemic stroke. Because of the complexity of the etiology and pathogenesis, the treatment methods for ischemic stroke in patients with cancer are also different with common practice. Identification of the causes and selection of targeted therapies are crucial for the prevention ad treatment of tumor-associated ischemic stroke. With the increase of the survival rate in patients with cancer, ischemic stroke in patients with cancer is also receiving increasing attention. This article reviews advances in etiology, pathogenesis and treatment of ischemic stroke in patients with cancer.

In recent years,researchers have carried out a lot of studies about endogenous and exogenous protective mechanisms of ischemic brain injury and have found that cerebral ischemia can stimulate cell proliferation and neurogenesis.This article reviews the cerebral ischemia induced neural stem cell proliferation,the protection mechanisms of directional migration and differentiation,as well as the promoting effects of the application of exogenous factors on neurogenesis after ischemia.

Ischemic preconditioning may mobilize self-protective mechanisms to induce endogenous neuroprotection through a variety of ways.It has potential clinical application value.Anti-apoptosis is an important part in the protective mechanisms of ischemic preconditioning Caspase family is the key molecule during the apoptotic execution process.It plays an important role in the neuronal apoptosis after cerebral ischemia.This article reviews the ischemic preconditioning-induced neuroprotective mechanisms and the roles of caspase family in neuronal apoptosis after cerebral ischemia.

Cerebral ischemic postconditioning refers to conduct a series of intermittent occlusion in order to reduce ischemia-reperfusion injury during the early reperfusion after cerebral ischemia.Because of its good prospects for clinical application,it has attracted widespread attention in recent years.This article reviews the neuroprotective mechanisms of ischemic postconditioning.

A large number of animal experiments have confirmed that ischemic preconditioning can produce a powerful organ protective effect,but the progress and results of the conversion of animal experiments to clinical trials are unsatisfactory.It has great significance for studying of molecular mechanisms of ischemic preconditioning mediated neuroprotection,searching for safe and effective preconditioning induced ways which can be converted to clinical practice,improving the tolerance of nerve tissue ischemia and hypoxia in stroke and surgical patients and achieving a safe and effective neuroprotection.This article reviews the molecular mechanisms of ischemic preconditioning mediated neuroprotection from the aspects of pretreatment of activated receptor,mitochondria,transcription factor,and protein kinase.

Most patients with ischemic stroke are accompanied by osteopenia and osteoporosis, especially in the hemiplegic side, which seriously affects the prognosis of the patients.At the same time, osteoporosis is also an independent risk factor for ischemic stroke.Among the many treatment options, rehabilitation training plays an important role in the prevention and treatment of osteoporosis.In recent years, it has gradually aroused the interest of researchers.This article reviews the relationship between osteoporosis and ischemic stroke, as well as the rehabilitation treatment of osteoporosis.

Objective To investigate the effect of GM 1 on vasospasm after subarachnoid hemorrhage.Methods Twenty-five wistar rats receiving intracisternal injection of 0.15 ml autologous nonheparinized blood or 0.15 ml saline two times were divided into five groups as follows: control group, cerebral vasospasm (CVS) group, Nimodipine group, GM 1 therapy group and GM 1 prevent group. The cortical regional cerebral blood flow (rCBF) was measured by hydrogenate clearance method at 0, 0.5, 1, 3 and 6h respectively. After perfusion and fixation, capillary vessels in temporal lobe cortex were labeled with anti-factor Ⅷ and observed by microvascular graphic analysis. Results (1) Compared with control group, rCBFs in CVS group, Nimodipine group and GM 1 therapy group were apparently decreased after second intracisternal blood injection (all P

Objective To create a stable and reliable model for cerebral ischemia.Methods (1)Distal middle cerebral artery occlusion (dMCAO) model: SD rats of 270-350 g in weight were anesthetized using isoflurane.Both common carotid arteries (CCA) were exposed and occluded for 30 min.Via a bone window between the left eye and ear, the exposed left middle cerebral artery was cauterized and cut during bilateral CCA occlusion.(2) Evaluation of the model: microPET study was performed at 10 h after surgery.microMRI scan were done at 24 h.TTC staining were done at 48 h.Behavioral tests, including vibrissaeelicited forelimb placement test, were done from day 2 to 60 after surgery.Tissue damage was evaluated using cresyl-violet staining Mortality was also observed.Results Infarction areas were 54.50% ± 3.15%(95% CI:49.49-59.51 ) using microPET scanning, 45.30% ± 2.35% (95% CI:42.94-47.86) using microMRI scanning, 43.39% ± 2.33% (95% CI:40.94-45.84)using TTC staining, and 30.10% ±2.22% (95% CI:28.05-32.15) using CV staining.The behavioral test scores were lower in the ischemic group than in the sham control group.This dMCAO model was successfully performed in all rats, and the mortality rate was 0.Conclusions Our results suggest that permanent dMCAO plus bilateral CCA occlusion for 30 min can produce a stable and reliable model suitable for research on cerebral ischemia.