Case report: Acute ischemic stroke caused by intracranial artery dissection in a patient with skull fractures.

The intracranial artery dissection (IAD) is an uncommon but life-threatening disease. The IAD would develop a significant cerebral infarction due to unrecognized contrecoup brain injury. We report a 53-year-old man fell to develop blunt cerebrovascular injuries (BCVIs) more than 2 months ago. During his rehabilitation, he often had a transient left headache and underwent short-term right limb weakness twice, but he did not care. He was hospitalized again because of suffering right limb weakness for more than 4 h. The brain computed tomography angiography (CTA) showed subtotal occlusion of the left middle cerebral artery M1 segment, and the vascular morphology displayed the IAD. The patient was then treated with balloon dilation and a self-expanding stent. This case highlights that IAD may show delayed onset with no initial typical symptom. By early detecting of abnormal signs and symptoms, serious traumatic brain injury may be avoided.

Annexin A5 is essential for PKCθ translocation during T-cell activation.

T-cell activation is a critical part of the adaptive immune system, enabling responses to foreign cells and external stimulus. In this process, T-cell antigen receptor (TCR) activation stimulates translocation of the downstream kinase PKCθ to the membrane, leading to NF-κB activation and thus transcription of relevant genes. However, the details of how PKCθ is recruited to the membrane remain enigmatic. It is known that annexin A5 (ANXA5), a calcium-dependent membrane-binding protein, has been reported to mediate PKCδ activation by interaction with PKCδ, a homologue of PKCθ, which implicates a potential role of ANXA5 involved in PKCθ signaling. Here we demonstrate that ANXA5 does play a critical role in the recruitment of PKCθ to the membrane during T-cell activation. ANXA5 knockout in Jurkat T cells substantially inhibited the membrane translocation of PKCθ upon TCR engagement and blocked the recruitment of CARMA1-BCL10-MALT1 signalosome, which provides a platform for the catalytic activation of IKKs and subsequent activation of canonical NF-κB signaling in activated T cells. As a result, NF-κB activation was impaired in ANXA5-KO T cells. T-cell activation was also suppressed by ANAX5 knockdown in primary T cells. These results demonstrated a novel role of ANXA5 in PKC translocation and PKC signaling during T-cell activation.