Background Optic nerve injury is one of the most common and serious complications in traumatic brain injury (TBI). Alleviating degree of optic nerve injury is important to cure of TBI. This study explored the role of long noncoding RNA (lncRNA) GAS5 in mice retinal ganglion cells (RGCs) suffered to H2O 2 injury. Methods Primary RGC (PRGCs) were treated with H2O 2 to simulate an in vitro oxidation stress model. LncRNA GAS5 and miR‐124 expressions were knocked down by cell transfection with short‐hairpin RNA against GAS5 and miR‐124 inhibitor, and the transfection efficiency was determined by qRT‐PCR. Cell viability, apoptotic cell rate, and production of reactive oxygen species (ROS) was analyzed by CCK‐8 assay, PI/FITC‐Annexin V method, and DCFH‐DA fluorometric assay. Cell apoptosis‐associated proteins as well as activations of JAK/STAT3 signaling and JNK signaling were analyzed by Western blot. Results H2O 2 treatment‐induced cell injury was inhibited by lncRNA GAS5 silence. Specifically, knockdown of GAS5 improved viability of primary PRGCs, inhibited apoptosis, decreased ROS expression, increased antiapoptosis proteins’ expressions, and decreased proapoptosis proteins’ expressions. It was also found that miR‐124 inhibitor treatment impaired the cell protective effect of GAS5 silence, indicating low level of GAS5 protected PRGCs via upregulating miR‐124. GAS5 silence might exert cytoprotection effect via activating JAK/STAT3 signaling pathway and inhibiting activation of JNK signaling pathway. Conclusion Knocking down lncRNA GAS5 alleviated H2O 2‐induced injury in PRGCs via upregulation of miR‐124, which might dependent on activation of JAK/STAT3 signaling pathway and inhibition of JNK signaling pathway.
Background: Atherosclerotic acute carotid occlusion is a specific type of stroke, and controversy exists regarding the surgical strategy, that is, whether an internal carotid artery stent should be placed immediately after opening the occluded vessel. There is no objective evaluation system for this procedure. In a previous study, we summarized an evaluation decision system Emergent Carotid Artery Stent placement decision Evaluation System (ECASES) for emergency stent placement. Study design: This is a prospective, single-center, randomized controlled trial. Patients with acute ischemic stroke caused by atherosclerotic carotid artery occlusion confirmed by imaging (computed tomography/magnetic resonance angiography/digital subtraction angiography) will be randomly divided into the study and control groups, with 101 patients in each group. The study group will undergo surgery according to the ECASES system and the control group will undergo surgery according to the operator’s experience. The postoperative outcomes of the 2 groups will be compared. Study outcomes: Primary outcome: Neurological functional status (modified Rankin Scale and National Institutes of Health Stroke Scale scores) of patients 90 days postoperatively. Secondary outcomes: neurological function changes, hemorrhage events, cerebral edema, postoperative modified treatment in cerebral infarction grade, new cerebral infarction, and reocclusion of responsible vessels. Discussion: Currently, no prospective controlled data exist regarding the efficacy and safety of carotid stenting in the acute phase. Previously, we had developed an ECASES stent placement system for acute carotid artery occlusion. The present study will evaluate the efficacy and safety of ECASES in a randomized, double-blind prospective study and clarify its guiding significance in acute atherosclerotic carotid artery occlusion surgery.
Background: Trigeminal neuralgia (TN) is a common cranial nerve disease. Objective: To investigate the relationship between the trigeminal nerve and the responsible blood vessel in patients with unilateral vascular trigeminal neuralgia (VTN). Methods: Thirty patients with unilateral VTN were confirmed by microvascular decompression. Results: Among the 30 patients, the responsible blood vessels were present in 30 cases on the affected side and 17 cases on the uninfected side (1). The location of the intersection of the trigeminal nerve and the responsible blood vessel: the affected side is located 2/5 behind the trigeminal nerve cisternal segment; the healthy side is located 3/5 anterior to the cisternal segment (2). Symptomatic vessels were located within the cistern between the origin and 2/5ths of the cistern length, and non-symptomatic vessels were located beyond the 2/5ths location (3). Direction of intersection: on the affected side, the responsible vessel was located inside and above the trigeminal nerve in 27 cases, (27/30, 90%), and outside and below the trigeminal nerve in 3 cases (3/30, 10%). On the unaffected side, the responsible vessel was located inside and above the nerve in 16 cases (16/17, 94%) and outside and below the nerve in 1 case (1/17, 5.8%) (4). Intersection form: 3 cases (3/30, 10%) on the affected side, the responsible blood vessel contacted the trigeminal nerve, in 26 cases (26/30, 86%) the responsible blood vessel compressed the trigeminal nerve, and in 1 case (1/30, 5%) the responsible blood vessel caused the trigeminal nerve to be twisted; 8 cases (8/17, 47%) of the contralateral side contacted the trigeminal nerve with the responsible blood vessel, and in 9 cases (9/17, 53%) the responsible blood vessel compressed the trigeminal nerve. Conclusion: Patients with unilateral VTN have differences in the location and form of the intersection of the trigeminal nerve and the responsible vessel on the affected side and the contralateral side.
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