Deficiency of the Nox2 (gp91phox) catalytic subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a genetic cause of X-linked chronic granulomatous disease, a condition in which patients are prone to infection resulting from the loss of oxidant production by neutrophils. Some studies have suggested a role for superoxide derived from Nox2 NADPH oxidase in platelet activation and thrombosis, but data are conflicting. Using a rigorous and comprehensive approach, we tested the hypothesis that genetic deficiency of Nox2 attenuates platelet activation and arterial thrombosis. Our study was designed to test the genotype differences within male and female mice. Using chloromethyl-dichlorodihydrofluorescein diacetate, a fluorescent dye, as well as high-performance liquid chromatography analysis with dihydroethidium as a probe to detect intracellular reactive oxygen species (ROS), we observed no genotype differences in ROS levels in platelets. Similarly, there were no genotype-dependent differences in levels of mitochondrial ROS. In addition, we did not observe any genotype-associated differences in platelet activation, adhesion, secretion, or aggregation in male or female mice. Platelets from chronic granulomatous disease patients exhibited similar adhesion and aggregation responses as platelets from healthy subjects. Susceptibility to carotid artery thrombosis in a photochemical injury model was similar in wild-type and Nox2-deficient male or female mice. Our findings indicate that Nox2 NADPH oxidase is not an essential source of platelet ROS or a mediator of platelet activation or arterial thrombosis in large vessels, such as the carotid artery.

BACKGROUND: Successful reperfusion is one of the strongest predictors of functional outcomes after mechanical thrombectomy (MT). Despite continuous advancements in MT technology and techniques, reperfusion failure still occurs in ≈15% to 30% of patients with large vessel occlusion strokes undergoing MT. We aim to evaluate the safety and efficacy of rescue intracranial stenting for large vessel occlusion stroke after failed MT. METHODS: The SAINT (Stenting and Angioplasty in Neurothrombectomy) Study is a retrospective analysis of prospectively collected data from 14 comprehensive stroke centers through January 2015 to December 2020. Patients were included if they had anterior circulation large vessel occlusion stroke due to intracranial internal carotid artery and middle cerebral artery-M1/M2 segments and failed MT. The cohort was divided into 2 groups: rescue intracranial stenting and failed recanalization (modified Thrombolysis in Cerebral Ischemia score 0–1). Propensity score matching was used to balance the 2 groups. The primary outcome was the shift in the degree of disability as measured by the modified Rankin Scale at 90 days. Secondary outcomes included functional independence (90-day modified Rankin Scale score 0–2). Safety measures included symptomatic intracranial hemorrhage and 90-day mortality. RESULTS: A total of 499 patients were included in the analysis. Compared with the failed reperfusion group, rescue intracranial stenting had a favorable shift in the overall modified Rankin Scale score distribution (acOR, 2.31 [95% CI, 1.61–3.32]; P <0.001), higher rates of functional independence (35.1% versus 7%; adjusted odds ratio [aOR], 6.33 [95% CI, 3.14–12.76]; P <0.001), and lower mortality (28% versus 46.5%; aOR, 0.55 [95% CI, 0.31–0.96]; P =0.04) at 90 days. Rates of symptomatic intracerebral hemorrhage were comparable across both groups (7.1% versus 10.2%; aOR, 0.99 [95% CI, 0.42–2.34]; P =0.98). The matched cohort analysis demonstrated similar results. Specifically, rescue intracranial stenting (n=107) had a favorable shift in the overall modified Rankin Scale score distribution (acOR, 3.74 [95% CI, 2.16–6.57]; P <0.001), higher rates of functional independence (34.6% versus 6.5%; aOR, 10.91 [95% CI, 4.11–28.92]; P <0.001), and lower mortality (29.9% versus 43%; aOR, 0.49 [95% CI, 0.25–0.94]; P =0.03) at 90 days with similar rates of symptomatic intracerebral hemorrhage (7.5% versus 11.2%; aOR, 0.87 [95% CI, 0.31–2.42]; P =0.79) compared with patients who failed to reperfuse (n=107). There was no heterogeneity of treatment effect across the prespecified subgroups for improvement in functional outcomes. CONCLUSIONS: Acute intracranial stenting appears to be a safe and effective rescue strategy in patients with large vessel occlusion stroke who failed MT. Randomized multicenter trials are warranted.

Background: Surgical management is considered one of the effective treatment modality for liver hydatid. However the choice of surgery is debatable. This study aims to compare the outcome of radical surgery (RS) and conservative surgery (CS) in liver hydatid disease.Methods: This is retrospective analysis of prospectively maintained institutional data of surgically treated liver hydatid from January 2012 to January 2019. The basis of diagnosis was typical imaging, confirmatory Hydatid serology and/or Intraoperative details. The clinical presentation, radiological data, operative detail, post-operative outcome, post-operative recurrence data was analysed.Results: Sixty-four patients underwent surgery during the study period and were included. RS was done in 27 (42.2%) patients and CS in 37 (57.8%) patients. The mean age was 35.6 (13-72) years. The mean size of the cyst was 10.3 ± 2.9 cm. The cyst location was peripheral in 81.5% and 56.8% in RS and CS groups respectively. Intraoperative Cyst biliary communication was detected in 48.1% of RS & 35.1% in CS group of patients. The post-operative bile leak was significantly less in RS group (7.4% vs 27.0%, p = 0.047). Postoperative endoscopic stenting for persistent biliary fistula was necessitated in five of CS and only one patient from RS group. None of RS patients had recurrence while 3 patients of CS developed recurrence. Conclusion:Radical surgery reduces post-operative bile leak and prevents recurrence and may be preferable to conservative surgery.

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