Bow hunter's syndrome (BHS), also known as rotational vertebral artery (VA) occlusion syndrome, is a rare yet treatable type of symptomatic vertebrobasilar insufficiency resulting from mechanical occlusion or stenosis of the VA during head and neck rotation or extension. The symptoms of BHS range from transient vertigo to posterior circulation stroke. The underlying pathology is dynamic stenosis or compression of the VA by abnormal bony structures with neck rotation or extension in many cases, such as osteophyte, disc herniation, cervical spondylosis, tendinous bands or tumors. Imaging approaches, such as Doppler sonography, computed tomography and angiography, as well as magnetic resonance imaging and angiography, are widely used in the diagnosis and evaluation of this syndrome. Digital subtraction angiography with head rotation remains the gold standard diagnostic method. Conservative management, surgery and endovascular procedures are the three major treatment methods for BHS, whereas some symptomatic patients may need operative treatment including surgery and endovascular procedures when conservative management is not adequate.

A dynamic increase in neutrophils after stroke significantly predicts 3-month death or major disability in acute ischaemic stroke patients receiving r-tPA treatment.

No abstract

No abstract

Increasing evidence suggests that the ubiquitin-binding histone deacetylase-6 (HDAC6) plays an important role in the clearance of misfolded proteins by autophagy. In this study, we treated PC-12 cells over-expressing human mutant (A53T) a-synuclein (a-syn) and SH-SY5Y cells with MPP + . It was found that HDAC6 expression significantly increased and mainly colocalized with a-syn in the perinuclear region to form aggresome-like bodies. HDAC6 deficiency blocked the formation of aggresome-like bodies and interfered with the autophagy in response to MPP + -induced stress. Moreover, misfolded a-syn accumulated into the nuclei, resulting in its reduced clearance, and finally, the number of apoptotic cells significantly increased. Taken together, HDAC6 participated in the degradation of MPP + -induced misfolded a-syn aggregates by regulating the aggresome-autophagy pathway. Understanding the mechanism may disclose potential therapeutic targets for synucleinopathies such as Parkinson's disease.