简介：Primaryhemifacialspasm(HFS)isadisorderthatcausesfrequentinvoluntarycontractionsinthemusclesononesideoftheface,duetoabloodvesselcompressingthenerveatitsrootexitzone(REZ)fromthebrainstem.Numerousprospectiveandretrospectivecaseserieshaveconfirmedtheefficacyofmicrovasculardecompression(MVD)ofthefacialnerveinpatientswithHFS.However,whileMVDiseffective,therearestillsignificantpostoperativecomplications.Inthispaper,recenttechnologicaladvancesrelatedtoMVD(suchaslateralspreadresponse,brainstemauditoryevokespotential,threedimensionaltimeofflightmagneticresonanceangiography,intraoperativeneuroendoscopy)arereviewedforthepurposesofimprovingMVDtreatmentefficacyandreducingpostoperativecomplications.

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简介：Brainmicrovascularendothelialcellsformtheinterfacebetweennervoustissueandcirculatingblood,andregulatecentralnervoussystemhomeostasis.Brainmicrovascularendothelialcellsdifferfromperipheralendothelialcellswithregardsexpressionofspecificiontransportersandreceptors,andcontainfewerfenestrationsandpinocytoticvesicles.Brainmicrovascularendothelialcellsalsosynthesizeseveralfactorsthatinfluencebloodvesselfunction.Thisreviewdescribesthemorphologicalcharacteristicsandfunctionsofbrainmicrovascularendothelialcells,andsummarizescurrentknowledgeregardingchangesinbrainmicrovascularendothelialcellsduringstrokeprogressionandtherapies.Futurestudiesshouldfocusonidentifyingmechanismsunderlyingsuchchangesanddevelopingpossibleneuroprotectivetherapeuticinterventions.

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简介：AbstractBackground:Vitamin D deficiency has been reported to be associated with diabetic microvascular complications, but previous studies have only focused on the relationship between vitamin D and specific complications. Therefore, we aimed to explore the relationship between vitamin D level and diabetic microvascular complications in general, including diabetic retinopathy (DR), diabetic nephropathy (DN), and diabetic peripheral neuropathy (DPN).Methods:This was a cross-sectional study of 815 patients with type 2 diabetes mellitus (T2DM). Clinical information and laboratory results were collected from the medical records. The relationship between vitamin D and the three diabetic microvascular complications was investigated.Results:The serum 25-hydroxyvitamin D (25 [OH] D) level of patients with DPN and/or DN was significantly lower than that of T2DM patients without any microvascular complications (P < 0.01). Univariate analysis showed that the 25 (OH) D level was related to DPN and DN, but not DR. After adjustment, the 25 (OH) D level was confirmed to be an independent protective factor for DPN (odds ratio [OR]: 0.968, P = 0.004]) and DN (OR: 0.962, P = 0.006). The prevalence of DPN and DN increased significantly as the serum 25 (OH) D levels decreased. Furthermore, patients with both DPN and DN had the lowest concentration of serum 25 (OH) D (P < 0.001), and the prevalence of macroalbuminuria increased more abruptly than that of microalbuminuria across the 25 (OH) D tertiles. Among the patients with vitamin D insufficiency, those with DPN presented more comorbid macroalbuminuria than those without DPN (15.32% vs. 4.91%; P = 0.001).Conclusions:Vitamin D deficiency is independently associated with higher risk of DPN and DN, but not DR, in T2DM patients. Further, it may be a potential predictor for both the occurrence and severity of DPN and DN.

简介：AbstractBackground:Angiopoietin-2 (Ang-2) is a type of endothelial growth factor involved in angiogenesis and vascular remodeling. Circulating Ang-2 levels are elevated in patients with obstructive coronary artery disease (CAD). This study aimed to evaluate the association between serum Ang-2 levels and coronary microvascular dysfunction in patients without obstructive CAD.Methods:A total of 125 patients with angina in the absence of obstructive CAD were included in this cross-sectional study. Coronary flow reserve (CFR) was measured in the distal left anterior descending coronary artery by trans-thoracic Doppler echocardiography. The patients were divided into the following two sub-groups according to CFR: the impaired CFR group with CFR values <2.5 and the preserved CFR group with CFR values ≥2.5. Serum Ang-2 levels were determined using enzyme-linked immunosorbent assay. Independent predictors for impaired CFR were identified by binary logistic regression analysis. The receiver-operating characteristic curve was determined to evaluate the ability of serum Ang-2 in predicting impaired CFR.Results:We found that age, percentage of female sex, N-terminal pro-B-type natriuretic peptide levels, Ang-2 levels (763.3 ± 264.9 vs. 579.7 ± 169.3 pg/mL, P < 0.001), and the left atrial volume index were significantly higher in patients with impaired CFR than in patients with preserved CFR. Serum Ang-2 levels were negatively correlated with CFR (r = -0.386, P < 0.001). Binary logistic regression analysis showed that Ang-2 (odds ratio: 1.004, 95% confidence interval [CI]: 1.001-1.006, P = 0.003) and age (odds ratio: 1.088, 95% CI: 1.023-1.156, P = 0.007) were independently associated with impaired CFR. Furthermore, Ang-2 was a significant predictor of impaired CFR on the receiver-operating characteristic curve (P < 0.001). The area under the curve was 0.712 (95% CI: 0.612-0.813).Conclusions:High serum Ang-2 levels are independently associated with impaired CFR in patients with angina in the absence of obstructive CAD.

简介：AIM:Toinvestigatewhether15-Lipoxygenase-1(15-LOX-1)playsanimportantroleintheregulationofangiogenesis,inhibitinghypoxia-inducedproliferationofretinalmicrovascularendothelialcells(RMVECs)andtheunderlyingmechanism.METHODS:PrimaryRMVECswereisolatedfromtheretinasofC57/BL6JmiceandidentifiedbyanevaluationforFITC-markedCD31.ThehypoxiamodelswereestablishedwiththeBio-bagandevaluatedwithablood-gasanalyzer.ExperimentswereperformedusingRMVECstreatedwithandwithouttransferAd-15-LOX-1orAd-vectorbothunderhypoxiaandnormoxiaconditionat12,24,48,72hours.Theefficacyofthegenetransferwasassessedbyimmunofluorescencestaining.CellsproliferationwasevaluatedbytheCCK-8method.RNAandproteinexpressionsof15-LOX-1,VEGF-A,VEGFR-2,eNOsandPPAR-rwereanalyzedbyreal-timereversetranscriptionpolymerasechainreaction(RT-PCR)andWesternblot.RESULTS:RoutineevaluationforFITC-markedCD31showedthatcellswerepure.Theresultsofblood-gasanalysisshowedthatwhenthecultureswereexposedtohypoxiaformorethan2hours,thePo2was4.5to5.4Kpa.WeverifiedRMVECscouldbeinfectedwithAd-15-LOX-1orAd-vectorviaFluorescencemicroscopy.CCK-8analysisrevealedthattheproliferativecapacitiesofRMVECsinhypoxicgroupweresignificantlyhigherateachtimepointthantheywereinnormoxicgroup(P<0.05).Inahypoxiccondition,theproliferativecapacitiesofRMVECsin15-LOX-1groupweresignificantlyinhibited(P<0.05).Real-timeRT-PCRanalysisrevealedthattheexpressionsofVEGF-A,VEGF-R2andeNOsmRNAincreasedinhypoxiagroupcomparedwithnormoxiagroup(P<0.01).However,theexpressionsof15-LOX-1,PPAR-rmRNAdecreasedinhypoxiagroupcomparedwithnormoxiagroup(P<0.01).Italsoshowedthatinahypoxiccondition,theexpressionsofVEGF-A,VEGF-R2andeNOsmRNAdecreasedsignificantlyin15-LOX-1groupcomparedwithhypoxiagroup(P<0.01).However,15-LOX-1andPPAR-rmRNAincreasedsigni

简介：AbstractBackground:Endothelial cells play a key role in the cytokine storm caused by influenza A virus. MicroRNA-155 (miR-155) is an important regulator in inflammation. Its role in the inflammatory response to influenza A infection, however, has yet to be elucidated. In this study, we explored the role as well as the underlying mechanism of miR-155 in the cytokine production in influenza A-infected endothelial cells.Methods:Human pulmonary microvascular endothelial cells (HPMECs) were infected with the influenza A virus strain H1N1. The efficiency of H1N1 infection was confirmed by immunofluorescence. The expression levels of proinflammatory cytokines and miR-155 were determined using real-time polymerase chain reaction. A dual-luciferase reporter assay characterized the interaction between miR-155 and sphingosine-1-phosphate receptor 1 (S1PR1). Changes in the target protein levels were determined using Western blot analysis.Results:MiR-155 was elevated in response to the H1N1 infection in HPMECs (24 h post-infection vs. 0 h post-infection, 3.875 ± 0.062 vs. 1.043 ± 0.013, P = 0.001). Over-expression of miR-155 enhanced inflammatory cytokine production (miR-155 mimic vs. negative control, all P < 0.05 in regard of cytokine levels) and activation of nuclear factor kappa B in infected HPMECs (miR-155 mimic vs. negative control, P = 0.004), and down-regulation of miR-155 had the opposite effect. In addition, S1PR1 was a direct target of miR-155 in the HPMECs. Inhibition of miR-155 enhanced the expression of the S1PR1 protein. Down-regulation of S1PR1 decreased the inhibitory effect of the miR-155 blockade on H1N1-induced cytokine production and nuclear factor kappa B activation in HPMECs.Conclusion:MiR-155 maybe modulate influenza A-induced inflammatory response by targeting S1PR1.