Intracranial aneurysm is a prevalent cerebrovascular disease,and its rupture can lead to subarachnoid hemorrhage,which is associated with high mortality and morbidity rates.Current treatment modalities for ruptured intracranial aneurysms primarily consist of surgical clipping and endovascular coiling.In recent years,the development and widespread clinical adoption of flow diverter have made these devices a prominent therapeutic option in the treatment of ruptured intracranial aneurysms.This article provides a comprehensive review of the mechanism of flow diverter,the current status of flow diverter implantation in the treatment of ruptured aneurysms,strategies for antiplatelet medication,and innovations in flow diverter materials,aiming to offer a refence for clinical decision-making in the management of ruptured aneurysms.

Intracranial aneurysm is a prevalent cerebrovascular disease,and its rupture can lead to subarachnoid hemorrhage,which is associated with high mortality and morbidity rates.Current treatment modalities for ruptured intracranial aneurysms primarily consist of surgical clipping and endovascular coiling.In recent years,the development and widespread clinical adoption of flow diverter have made these devices a prominent therapeutic option in the treatment of ruptured intracranial aneurysms.This article provides a comprehensive review of the mechanism of flow diverter,the current status of flow diverter implantation in the treatment of ruptured aneurysms,strategies for antiplatelet medication,and innovations in flow diverter materials,aiming to offer a refence for clinical decision-making in the management of ruptured aneurysms.

Humans ; Neoplasms, Second Primary/epidemiology* ; Neoplasms/epidemiology* ; Risk Factors ; Prognosis

A fundamental challenge that arises in biomedicine is the need to characterize compounds in a relevant cellular context in order to reveal potential on-target or off-target effects. Recently, the fast accumulation of gene transcriptional profiling data provides us an unprecedented opportunity to explore the protein targets of chemical compounds from the perspective of cell transcriptomics and RNA biology. Here, we propose a novel Siamese spectral-based graph convolutional network (SSGCN) model for inferring the protein targets of chemical compounds from gene transcriptional profiles. Although the gene signature of a compound perturbation only provides indirect clues of the interacting targets, and the biological networks under different experiment conditions further complicate the situation, the SSGCN model was successfully trained to learn from known compound-target pairs by uncovering the hidden correlations between compound perturbation profiles and gene knockdown profiles. On a benchmark set and a large time-split validation dataset, the model achieved higher target inference accuracy as compared to previous methods such as Connectivity Map. Further experimental validations of prediction results highlight the practical usefulness of SSGCN in either inferring the interacting targets of compound, or reversely, in finding novel inhibitors of a given target of interest.
Drug Delivery Systems ; Proteins ; Transcriptome

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Objective:To investigate the effects of different lipid-lowering regimens on blood lipids, endothelial function and safety in patients with unstable angina.Methods:Patients who admitted to Henan Provincial People's Hospital for unstable angina from September 2018 to May 2019 were randomly (random number) divided into the conventional treatment group, intensive statin group and intensive lipid-lowering group. Follow-up was performed at 1, 3, and 6 months after treatment according to the predetermined lipid-lowering regimen. Assessments included lipid profile, liver function, muscle enzymes, hypersensitive C-reactive protein (hs-CRP), endothelial function (reactive hyperemia index, RHI), ischemic events, myalgia, and discontinuation. The differences of the follow-up indicators among the three groups were analyzed.Results:A total of 375 patients were enrolled and randomly divided into three groups, 125 patients in each group. There were no significant differences in demographic data and medication among the three groups. At the 1st month, the low density lipoprotein cholesterin (LDL-C) compliance rate of the intensive statin group was significantly higher than those in the conventional treatment group ( χ2=3.939, P=0.047) and the intensive lipid-lowering group ( χ2=4.63, P=0.031). At the 3rd month, the reductions of LDL-C in the intensive statin group and the intensive lipid-lowering group were significantly better than that in the conventional treatment group( P<0.01). At the 6th month, the reduction rate of LDL-C in the intensive lipid-lowering group was higher than that in the intensive statin group ( q=4.332, P<0.01). At the 1st month, the improvement of hs-CRP and RHI in the intensive statin group was significantly better than that in the conventional treatment group( q=4.133, P<0.05). From the 3rd month of treatment, the incidence of cardiovascular events in the intensive statin group and the intensive lipid-lowering group showed a tendency to decrease compared with the conventional treatment group, but no statistically significant difference was found. At the 6th months of treatment, the withdrawal rates were significantly higher in the intensive statin group and the intensive lipid-lowering group than that in the conventional treatment group (χ 2=4.488, P=0.03 and χ2=5.039, P=0.02). There were no significant differences in the ratio of liver enzyme and muscle enzyme elevation and the incidence of myalgia among the three groups (all P>0.05). Conclusions:Intensive statin therapy can make LDL-C reach the standard in patients with unstable angina pectoris as soon as possible, significantly improve inflammation indicators and endothelial function, and has good safety.

In this study, the virtual simulation tutoring system was applied to the teaching of dental residents in the standardized training stage for the first time, including the curriculum preparation, curriculum design and teaching practice. Through the practice of the preparation of class Ⅱ holes and the tooth preparation of PFM (porcelain fused to metal) by the dental residents in the virtual simulation teaching system, the teaching arrangement of three courses as one term was explored. Each course adopted the matching interactive teaching mode. Finally, the transcripts would be given by the virtual simulation teaching system to comment and summarize. This study has laid a foundation for future promotion of virtual simulation teaching system in the standardized training stage of stomatology residents and found a new direction for improving the proficiency and accuracy of residents' clinical operation skills.

Objective To investigate MRI diagnosis of intracranial extra-encephalon cavernous angiomas.Methods In 9 intracranial extra-encephalon cavernous angiomas,5 masses located in the parasellar,2 masses in the lateral ventricle triangle,1 mass in the fourth ventricle and 1 mass in temporal subdural space.The MRI features of the masses were analyzed.Results 5 parasellar cavernous angiomas enclosed the ipsilateral internal carotid artery and extended the saddle.The masses showed homogeneous low intensity on T1WI,high intensity on T2WI,obvious enhancement on enhanced scan.Of 2 cavernous angiomas in the right lateral ventricle triangle, 1 mass showed homogeneous low intensity on T 1WI,high intensity on T2WI,obvious enhancement on enhanced scan;the other mass showed isointensity on T1WI,slight high intensity on T2WI,high intensity on DWI,low intensity on SWI and patchy enhancement on enhanced scan.1 cavernous angioma located in the fourth ventricular showed mixed intensity on T 1WI and T2WI,low signal rim around the mass on T2WI,inhomogeneous high intensity on DWI sequence and little enhancement on enhanced scan.1 mass located in temporal subdural space showed homogeneous low intensity on T 1WI,high intensity on T2WI,low intensity on DWI,isointensity on SWI and homogeneous obvious enhancement on enhanced scan.Conclusion The MRI findings of the intracranial extra-encephalon cavernous angiomas are characteristic.Most masses show homogeneous low intensity on T1WI,high intensity on T2WI and obvious enhancement on enhanced scan.The masses should mainly be distinguished from meningiomas.

Objective To explore the mechanism of thymoquinone (TQ) on NSCLC cytotoxicity.Methods SK-MES-1 was inoculated into 96-well plates and cultured at 20,40,60,80 and 100 μmol/L TQ for 24 h,and the IC50 of TQ was calculated.SK-MES-1 was cultured in close proximity to IC50 concentration TQ,and time-dependent was observed.The ERK inhibitor U0126 and the p38 inhibitor SB203580 were applied to SK-MES-1 and 95-D,respectively,then TQ-activated MAPK-mediated cytotoxicity were observed.The SK-MES-1 expression of p-p38,p38,p-ERK1/2,ERK1/2,pJNK and JNK protein were detected by U0126 pretreatment for 1 h and TQ-cultured for 30 min.Results ① TQ was used to mediate NSCLC cells in a concentration and time-dependent manner,and the viability of NSCLC cells was decreased.② The cell viability of 30 μmol/L TQ and 10 μmol/L U0126 +30 μmol/L TQ showed significant differences (P =0.000),but no significant difference was found when compared with 10 μmol/L SB203580 + 30 μmol/L TQ (P =1.00).10 μmol/L SB203580 + 30 μmol/L TQ was significantly different from 10 μmol/L U0126 + 30 μmol/L TQ (P =0.000).60μmol/LTQ,10μmol/LU0126 + 60μmol/LTQ,10μmol/LSB203580 + 60 μmol/L TQ showed no significant differences between every two groups (P ＞ 0.0 5).With the increase of TQ concentration,the protective effect of SB203580 on 95-D cells gradually decreased,and 10 μmol/L SB203580 +40 μmol/L TQ group was significantly different from 40 μmol/L TQ group (P =0.033).③ Western blot analysis showed that U0126 could significantly inhibit the phosphorylation of ERK1/2,phosphorylated p38 increased with the increasing of TQ concentration.However,ERK1/2 phosphorylation decreased,and JNK phosphorylation did not change significantly.Conclusion TQ can mediate NSCLC cytotoxicity through phosphorylation of p38 pathway,but not ERK1/2 pathway.

Objective To explore the mechanism of thymoquinone (TQ) on NSCLC cytotoxicity.Methods SK-MES-1 was inoculated into 96-well plates and cultured at 20,40,60,80 and 100 μmol/L TQ for 24 h,and the IC50 of TQ was calculated.SK-MES-1 was cultured in close proximity to IC50 concentration TQ,and time-dependent was observed.The ERK inhibitor U0126 and the p38 inhibitor SB203580 were applied to SK-MES-1 and 95-D,respectively,then TQ-activated MAPK-mediated cytotoxicity were observed.The SK-MES-1 expression of p-p38,p38,p-ERK1/2,ERK1/2,pJNK and JNK protein were detected by U0126 pretreatment for 1 h and TQ-cultured for 30 min.Results ① TQ was used to mediate NSCLC cells in a concentration and time-dependent manner,and the viability of NSCLC cells was decreased.② The cell viability of 30 μmol/L TQ and 10 μmol/L U0126 +30 μmol/L TQ showed significant differences (P =0.000),but no significant difference was found when compared with 10 μmol/L SB203580 + 30 μmol/L TQ (P =1.00).10 μmol/L SB203580 + 30 μmol/L TQ was significantly different from 10 μmol/L U0126 + 30 μmol/L TQ (P =0.000).60μmol/LTQ,10μmol/LU0126 + 60μmol/LTQ,10μmol/LSB203580 + 60 μmol/L TQ showed no significant differences between every two groups (P ＞ 0.0 5).With the increase of TQ concentration,the protective effect of SB203580 on 95-D cells gradually decreased,and 10 μmol/L SB203580 +40 μmol/L TQ group was significantly different from 40 μmol/L TQ group (P =0.033).③ Western blot analysis showed that U0126 could significantly inhibit the phosphorylation of ERK1/2,phosphorylated p38 increased with the increasing of TQ concentration.However,ERK1/2 phosphorylation decreased,and JNK phosphorylation did not change significantly.Conclusion TQ can mediate NSCLC cytotoxicity through phosphorylation of p38 pathway,but not ERK1/2 pathway.