Neuroform atlas stent treatment for 533 intracranial aneurysms in a large Chinese cohort: complication risk factor analysis.

BACKGROUND: The newest generation of Neuroform Atlas stent™ (Stryker, Fremont, California) represents a recent advance of cerebral laser-cut microstents for the treatment of intracranial wide-necked aneurysms, and postoperative complications have been observed among Western patients. We assessed predictors of complications, morbidity, and unfavourable outcomes in a large cohort of patients with aneurysms that were treated with Neuroform Atlas stents in China. METHODS: This retrospective study included subjects who were treated with Atlas stents in China from November 2020 to January 2022. RESULTS: A total of 522 consecutive patients (mean age, 58.9 ± 9.9 years; female, 65.3% [341/522]) with 533 aneurysms were included in the study. In the early postoperative period, the neurological morbidity rate was 7.3% (38/522), the ischaemic stroke rate was 5.0% (26/522), the aneurysm rupture subarachnoid haemorrhage rate was 2.3% (12/522), and the mRS score deterioration rate was 5.4% (28/522). The mortality rate was 0.8% (4/522) in the postoperative period. The rate of neurological morbidity during the follow-up period was 1.2% (6/486). In the multifactor prediction analysis, cerebral infarction, Hunt-Hess grade (3-5), procedure duration, stent length and coil protrusion into the parent artery were found to be independent predictors of neurologic morbidity. The procedure duration, stent length and coil protrusion into the parent artery were found to be independent predictors of mRS score deterioration. CONCLUSIONS: The incidence of SCA (stent-assisted coiling)-related complications with the Atlas stent in this study population was comparable to that in Western populations. We identified the procedure duration and stent length as novel independent predictors of SCA-related ischaemic stroke, neurological morbidity, and mRS score deterioration among the Chinese population.

Dexmedetomidine alleviates blood-brain barrier disruption in rats after cerebral ischemia-reperfusion by suppressing JNK and p38 MAPK signaling.

Dexmedetomidine displays multiple mechanisms of neuroprotection in ameliorating ischemic brain injury. In this study, we explored the beneficial effects of dexmedetomidine on blood-brain barrier (BBB) integrity and neuroinflammation in cerebral ischemia/reperfusion injury. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 1.5 h and reperfusion for 24 h to establish a rat model of cerebral ischemia/reperfusion injury. Dexmedetomidine (9 􀁐g/kg) was administered to rats 30 min after MCAO through intravenous injection, and SB203580 (a p38 MAPK inhibitor, 200 􀁐g/kg) was injected intraperitoneally 30 min before MCAO. Brain damages were evaluated by 2,3,5-triphenyltetrazolium chloride staining, hematoxylin-eosin staining, Nissl staining, and brain water content assessment. BBB permeability was examined by Evans blue staining. Expression levels of claudin-5, zonula occludens-1, occludin, and matrix metalloproteinase-9 (MMP-9) as well as M1/M2 phenotypes-associated markers were assessed using immunofluorescence, RT-qPCR, Western blotting, and gelatin zymography. Enzyme-linked immunosorbent assay was used to examine inflammatory cytokine levels. We found that dexmedetomidine or SB203580 attenuated infarct volume, brain edema, BBB permeability, and neuroinflammation, and promoted M2 microglial polarization after cerebral ischemia/reperfusion injury. Increased MMP-9 activity by ischemia/reperfusion injury was inhibited by dexmedetomidine or SB203580. Dexmedetomidine inhibited the activation of the ERK, JNK, and p38 MAPK pathways. Moreover, activation of JNK or p38 MAPK reversed the protective effects of dexmedetomidine against ischemic brain injury. Overall, dexmedetomidine ameliorated brain injury by alleviating BBB permeability and promoting M2 polarization in experimental cerebral ischemia/reperfusion injury model by inhibiting the activation of JNK and p38 MAPK pathways.

Spontaneous direct carotid-cavernous fistula with acute visual loss in an elderly patient: case report and review of the literature.

Carotid-cavernous fistulas are acquired vascular lesions, representing abnormal connections caused by a direct shunt or dural branches of the internal carotid artery and/or the external carotid artery connected to the cavernous sinus. We present an interesting, rare case of a spontaneous fistula with acute vision loss in an older patient. The patient was diagnosed with a direct carotid-cavernous fistula based on the clinical and radiological findings. We concluded that early diagnosis and etiological treatment could improve the prognosis of this type of carotid-cavernous fistula.

Fabrication of current confinement aperture structure by transforming a conductive GaN:Si epitaxial layer into an insulating GaOx layer.

We report here a simple and robust process to convert embedded conductive GaN epilayers into insulating GaOx and demonstrate its efficacy in vertical current blocking and lateral current steering in a working LED device. The fabrication processes consist of laser scribing, electrochemical (EC) wet-etching, photoelectrochemical (PEC) oxidation, and thermal oxidization of a sacrificial n(+)-GaN:Si layer. The conversion of GaN is made possible through an intermediate stage of porosification where the standard n-type GaN epilayers can be laterally and selectively anodized into a nanoporous (NP) texture while keeping the rest of the layers intact. The fibrous texture of NP GaN with an average wall thickness of less than 100 nm dramatically increases the surface-to-volume ratio and facilitates a rapid oxidation process of GaN into GaOX. The GaOX aperture was formed on the n-side of the LED between the active region and the n-type GaN layer. The wavelength blueshift phenomena of electroluminescence spectra is observed in the treated aperture-emission LED structure (441.5 nm) when compared to nontreated LED structure (443.7 nm) at 0.1 mA. The observation of aperture-confined electroluminescence from an InGaN LED structure suggests that the NP GaN based oxidation will play an enabling role in the design and fabrication of III-nitride photonic devices.