Correlation Studies and Literature Review of Medullary Artery Occlusion After Intracranial Vertebral Artery Stenting.

BACKGROUND: Stenosis of the target intracranial vertebral artery is one of the major causes of posterior circulation ischemic stroke. The objective of this paper is to explore methods for reducing the occurrence of medullary artery occlusion after intracranial vertebral artery stenting. CASE DESCRIPTION: The current research presents a retrospective analysis of 48 patients who received Gateway-Wingspan stent angioplasty to treat severe stenosis of the intracranial vertebral artery, evaluates the results of stenosis remission and perfusion improvement after stent angioplasty, and explores the causes of postoperative medullary artery occlusion. A total of 49 Wingspan stents were implanted in the 48 patients, with a surgical success rate of 100%. After stent implantation, the patients' rates of intracranial vertebral artery stenosis dropped from 75.9% ± 6.3% to 28.4% ± 5.1%. Transcranial Doppler or cranial computed tomography angiography 3 months after surgery showed that none of the patients suffered from in-stent restenosis. Within 24 hours after surgery, medullary perforating artery occlusion occurred in 2 patients, probably because atherosclerotic plaque in the stenotic area became less stable and displaced under the mechanical action of postoperative saccule and stent. As a result, the medullary artery was blocked. After drug and rehabilitation therapies, the patients' symptoms were alleviated. CONCLUSIONS: Perforating artery occlusion after intracranial vertebral artery stenting can be prevented by strict assessment and preparation before surgery, correct choices of saccule and stent during operation, and other measures. However, large sample data are needed for verification.

Asiatic acid protects differentiated PC12 cells from Aß25-35-induced apoptosis and tau hyperphosphorylation via regulating PI3K/Akt/GSK-3ß signaling.

Amyloid ß (Aß) peptide can cause neurotoxicity in Alzheimer's disease (AD). The main purpose of the present study is to investigate the protective role of asiatic acid (AA) against Aß25-35-induced neurotoxicity in neuronally differentiated PC12 cells. Differentiated PC12 cells were pretreated with 5, 10 or 20 µM AA before treatment with 20 µM Aß25-35. The viability and apoptosis of differentiated PC12 cells were determined by MTT assay and Annexin V-FITC/PI double staining, respectively. The mitochondrial membrane potential (MMP) of differentiated PC12 cells was analyzed by JC-1 staining. The expression levels of proteins were detected by western blot analysis. We found that AA significantly increased the viability of differentiated PC12 cells but attenuated the mitochondria-mediated apoptosis dose-dependently when challenging with Aß25-35. Besides, the results of western blot analysis showed that AA prevented IκBα degradation and p65 nuclear translocation, and promoted the phosphorylation of Akt and GSK-3ß in Aß25-35-treated differentiated PC12 cells. Moreover, LY294002, a specific PI3K inhibitor, was found to abolish the beneficial effects of AA on Aß25-35-induced apoptosis and tau protein hyperphosphorylation. Our findings demonstrated that AA protects differentiated PC12 cells from Aß25-35-induced apoptosis and tau protein hyperphosphorylation, which might be partially mediated by the activation of the PI3K/Akt/GSK-3ß signaling pathway.

p38 mitogen-activated protein kinase gene silencing rescues rat hippocampal neurons from ketamine-induced apoptosis: An in vitro study.

Ketamine (KTM) is an anesthetic drug with several advantages, including the elevation of cardiac output and blood pressure. However, KTM may also induce the apoptosis of hippocampal neurons. Notably, p38 mitogen­activated protein kinase (p38MAPK) has previously been studied for its role in neuronal injury. Therefore, the present study evaluated the effect of lentivirus­mediated p38MAPK gene silencing on KTM­induced apoptosis of rat hippocampal neurons. Hippocampal neurons were extracted from neonatal Sprague­Dawley rats, and then treated with KTM, p38MAPK­short hairpin RNA or SB203580 (an inhibitor of p38MAPK). Next, the expression levels of p38MAPK and apoptosis­associated genes, including caspase­3, B­cell lymphoma 2 (Bcl­2) and Bcl­2­associated X protein (Bax), were detected. In addition, cell viability and apoptosis were determined using an MTT assay and flow cytometry, respectively. Finally, telomerase activity of hippocampal neurons was detected by ELISA. The results revealed that silencing of p38MAPK in KTM­treated cells decreased the expression levels of p38MAPK, caspase­3 and Bax, and the extent of p38MAPK phosphorylation, while it increased the expression of Bcl­2. Furthermore, silencing p38MAPK promoted cell viability, cell cycle progression and the telomerase activity of hippocampal neurons, and inhibited the apoptosis of hippocampal neurons. Taken together, the results suggested an inhibitory role of lentivirus­mediated p38MAPK gene silencing on KTM­induced apoptosis of rat hippocampal neurons. Thus, p38MAPK gene silencing may serve as a potential target for preventing the KTM­induced apoptosis of hippocampal neurons.

A fast response & recovery H2S gas sensor based on α-Fe2O3 nanoparticles with ppb level detection limit.

H2S gas sensor based on α-Fe2O3 nanoparticles was fabricated by post-thermal annealing of Fe3O4 precursor which was synthesized using a facile hydrothermal route. The characteristic techniques including X-ray diffraction (XRD), scanning electron microscopy (SEM), and transmission electron microscopy (TEM) were adopted to characterize the chemical composition and microstructure of the obtained samples. Gas-sensing performance of the sensor was investigated at different operation temperatures from 100°C to 400°C. Results showed that the sensor exhibited the best sensitivity, reproducibility and long-term stability for detecting H2S gas at an operating temperature of 300°C. The detection limit towards H2S gas was 0.05 ppm, and the response time and recovery time was 30s and 5s, respectively. In addition, sensing mechanism of the sensor towards H2S was discussed.