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White matter is primarily composed of myelin and myelinated axons. Structural and functional completeness of myelin is critical for the reliable and efficient transmission of information. White matter injury has been associated with the development of many demyelinating diseases. Despite a variety of scientific advances aimed at promoting re-myelination, their benefit has proven at best to be marginal. Research suggests that the failure of the re-myelination process may be the result of an unfavorable microenvironment. Astrocytes, are the most ample and diverse type of glial cells in central nervous system (CNS) which display multiple functions for the cells of the oligodendrocytes lineage. As such, much attention has recently been drawn to astrocyte function in terms of white matter myelin repair. They are different in white matter from those in gray matter in specific regards to development, morphology, location, protein expression and other supportive functions. During the process of demyelination and re-myelination, the functions of astrocytes are dynamic in that they are able to change functions in accordance to different time points, triggers or reactive pathways resulting in vastly different biologic effects. They have pivotal effects on oligodendrocytes and other cell types in the oligodendrocyte lineage by serving as an energy supplier, a participant of immunological and inflammatory functions, a source of trophic factors and iron and a sustainer of homeostasis. Astrocytic impairment has been shown to be directly linked to the development of neuromyelities optica (NMO). In addition, astroctyes have also been implicated in other white matter conditions such as psychiatric disorders and neurodegenerative diseases such as Alzheimer’s disease (AD), multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS). Inhibiting specifically detrimental signaling pathways in astrocytes while preserving their beneficial functions may be a promising approach for remyelination strategies. As such, the ability to manipulate astrocyte function represents a novel therapeutic approach that can repair the damaged myelin that is known to occur in a variety of white matter-related disorders.

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It has been confirmed that apoptosis, autophagy and necrosis are the three major modes of cell death. For a long time, necrosis is regarded as a deranged or accidental cell demise. In recent years, there is evidence showing that necrotic cell death can be a well regulated and orchestrated event, which is also known as programmed cell death or "necroptosis". Necroptosis can be triggered by a variety of external stimuli and regulated by a caspase-independent pathway. It plays a key role in the pathogenesis of some diseases including neurological diseases. In the past two decades, a variety of studies have revealed that the necroptosis related pathway is activated in stroke, and plays a crucial role in the pathogenesis of stroke. Moreover, necroptosis may serve as a potential target in the therapy of stroke because genetic or pharmacological inhibition of necroptosis has been shown to be neuroprotective in stroke in vitro and in vivo. In this review, we briefly summarize recent advances in necroptosis, introduce the mechanism and strategies targeting necroptosis in stroke, and finally propose some issues in the treatment of stroke by targeting necroptosis.

This study compared three β-aminopropionitrile (BAPN) treatment rats to find the optimal BAPN model for thoracic aortic dissection and aneurysm in one study. Sixty rats were divided into five groups: control, injected control, 0.25% and 0.4% BAPN treatment (orally), and 667 mg/kg/day BAPN injection subcutaneously. Incidence of aortic dissection and aneurysm, aortic weight and diameter were measured directly. Thickness of media and area of aorta were measured by hematoxylin and eosin and Victoria blue staining. The mortality, incidence of aortic dissection and the rupture rate of dissected aneurysm in 0.25% group was much higher than in the other two BAPN treatment groups. The diameter of thoracic aorta in 0.25% and the whole aorta in 0.4% group significantly increased. Media thickness and area of thoracic aorta were increased by 91% and 54% in 0.25% group, and by 17% and 12% in the BAPN injection group. Thickness and area were increased by 49% and 35% on thoracic aorta, and 29% and 46% on abdominal aorta in 0.4% group. In conclusion, 0.25%, 0.4% and BAPN injection groups might be appropriate for aortic dissection and pharmaceutical study, thoracic-abdominal aortic aneurysm or dilation and biomechanical research, respectively.

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The sensory symptoms occur earlier than the motor symptoms in SCD patients. SCD patients may have sensory deficit level. Normal or even elevated serum levels of vitamin B12 may occur in patients with SCD.