Mechanical thrombectomy (MT) has been demonstrated as an effective treatment for acute ischemic stroke (AIS), thanks to large vessel occlusion (LVO), especially in case of anterior cerebral artery with many randomized clinical trials (RCTs) every year. On the other hand, there is a limited number of basilar artery occlusion (BAO)-related studies which have been conducted. The fact prompts our range of case studies, which furnish BAO understanding with our experience, results and some prognosis factors of MT. This retrospective and single-center study was conducted on 22 patients who were diagnosed with BAO and underwent the treatment of MT from October 2012 to January 2018. Clinical feature such as radiological imaging, procedure complications, and intracranial hemorrhage were all documented and evaluated. All the studies' results based on performance using modified Rankin scale score (mRS) and mortality at 90 days. The results from these BAO patients study indicated that the posterior circulation Acute Stroke Prognosis Early CT Score (pcASPECTS) recorded before the intervention was 7.7 ± 1.6, while the admission National Institutes of Health Stroke Scale (NIHSS) was 17.5 ± 5.4. 15/22 cases achieved successful recanalization (TICI, Thrombolysis in Cerebral Infarction scale, of 2b-3), accounting for 68.2%. The results highlighted 50% of the favorable outcome (mRS 0-2) occupying 11 out of 22 patients in total and the overall mortality was 36.4%. The intracranial hemorrhagic complication was detected in three cases (13.6%). Placing in juxtaposition the poor-outcome group and the favorable-outcome group, we could witness statistically significant difference (P
Sphingolipid dysregulation is often associated with insulin resistance, while the enzymes controlling sphingolipid metabolism are emerging as therapeutic targets for improving insulin sensitivity. We report herein that sphingosine kinase 2 (SphK2), a key enzyme in sphingolipid catabolism, plays a critical role in the regulation of hepatic insulin signaling and glucose homeostasis both in vitro and in vivo. Hepatocyte-specific Sphk2 knockout mice exhibit pronounced insulin resistance and glucose intolerance. Likewise, SphK2-deficient hepatocytes are resistant to insulin-induced activation of the phosphoinositide 3-kinase (PI3K)-Akt-FoxO1 pathway and elevated hepatic glucose production. Mechanistically, SphK2 deficiency leads to the accumulation of sphingosine that, in turn, suppresses hepatic insulin signaling by inhibiting PI3K activation in hepatocytes. Either reexpressing functional SphK2 or pharmacologically inhibiting sphingosine production restores insulin sensitivity in SphK2-deficient hepatocytes. In conclusion, the current study provides both experimental findings and mechanistic data showing that SphK2 and sphingosine in the liver are critical regulators of insulin sensitivity and glucose homeostasis.