Objective To investigate the value of high-resolution magnetic resonance imaging (HR-MRI) of arterial walls in the diagnosis of cerebral artery dissection (CAD).Methods The patients diagnosed as CAD and completed computed tomography angiography (CTA),magnetic resonance angiography (MRA),digital subtraction angiography (DSA),and HR-MRI were enrolled retrospectively.The detection rate and diagnostic value of the 4 imaging techniques were compared and analyzed.Results A total of 15 patients were enrolled,5 had internal carotid artery dissection,7 had vertebral artery dissection,2 had middle cerebral artery dissection,and 1 had basilar artery dissection.HR-MRI revealed 11 intramural hematoma,9 intimal flap,3 double lumen sign,and 2 pseudoaneurysm.A total of 18 CADs were detected in 15 patients,17 (94.44％),14 (77.78％),5 (27.78％) and 6 (33.33％) were detected with HR-MRI,DSA,CTA and MRA,respectively.There were significant difference in CAD detection rates of HR-MRI,DSA,CTA and MRA (x2 =24.939,P ＜ 0.001).The CAD detection rate of HR-MRI and DSA were significantly higher than those of CTA and MRA (all P ＜ 0.01 for HR-MRI,all P ＜ 0.05 for DSA),but there was no significant difference in CAD detection rate between HR-MRI and DSA.Conclusion HR-MRI is a diagnostic method for CAD with higher sensitivity.

Objective To investigate the metabolic changes and the metabolites distribution of different hippocampal regions (head,body and tail)in patients with Alzheimer’s disease (AD)using 1 H-MRS for early diagnosis.Methods The hippocampal multivoxel 1H-MRS at 3.0 T was scanned in 30 patients with AD and other 30 normal cognitive elders (NC)as contrast.The data obtained were processed at a workstation.The hippocampus was divided into 3 parts (head,body and tail),and the ratios of N-acetylaspartate (NAA)/creatine (Cr),myoinositol (MI)/Cr and MI/NAA were calculated respectively.The metabolite ratios and distribution changes were compared between group AD and NC.Results Compared with the group NC,the NAA/Cr in group AD in bilateral hippocampal body and tail was decreased,whereas the MI/Cr and MI/NAA in bilateral body and tail,MI/NAA in left head were opposite (P<0.01).In group NC,the NAA/Cr was gradually decreased from the bilateral hippocampal heads to tails (P<0.01),however,the MI/NAA was opposite (P<0.01).No distribution differences in every metabolic ratios of bilateral hippocam-pus were found in AD group (P>0.05).Conclusion Metabolic changes and disappearance of the normal distribution in different hippocampal regions detected by 1 H-MRS provide helpful clues for early diagnosis of the AD.

Objective To analyze the patterns of cortical atrophy of the two subtypes of frontotemporal lobar degeneration (FTLD ),behavioural-vsriant frontotemporal dementia (bvFTD ) and primary progressive aphasia (PPA).And to compare them with that of Alzheimer disease (AD) to provide an objective basis for early diagnosis and differential diagnosis.MethodsA total of 83 patients were enrolled in this study and there were 30 patients with cognitively normal controls (CN),30 with AD and 23 with FTLD (10 with bvFTD,13 with PPA).Philips 3.0 T TX scanner and 8 channel head coil was employed.Three dimensional turbo fast echo(3D-TFE)T1WI sequence with high resolution was used to collect the volume data of gray matter.3D-TFE T1 WI images were normalized and segmented into gray matter map for statistical analysis by SPM 8 and VBM 8.The false discovery rate (FDR) was adopted in P value adjustment,P ＜ 0.001,and the cluster size was set at 5.The full width at half maximum (FWHM ) was set at 4 mm for the smoothing.Paired t test was used for statistics.ResultsIn bvFTD,PPA and AD groups,there were diffuse regions with reduced volume in cerebral cortex and subcortical structures (such as the hippocampus,the amygdala,the caudate nuclei,et al).The most obvious atrophic region in bvFTD and PPA group was found in the frontotemporal.Compared with AD,gray matter atrophy in bvFTD was found in brain regions including bilateral temporal lobes,bilateral superior temporal pole gyri,bilateral middle temporal pole gyri,right fusiform gyrus and bilateral frontal lobes.Among them,temporal and frontal lobes atrophy had obvious right partial lateralizing,with 14 301 voxels in right temporal lobe and 5105 in left (t =-5.03,P＜0.05).The number of atrophy voxels in right and left frontal lobe were 1344 and 125 (t =3.45,P ＜0.05).The left temporooccipital lobe atrophy was more obvious than the right in PPA,with 15 637 voxels in left and 10 723 in right ( t =- 2.65,P ＜ 0.05 ).ConclusionsThere are different brain gray matter atrophy patterns in bvFD,PPA and AD.Among them,bvFTD has asymmetric right frontal and temporal lobe atrophy,which may be related to characteristic personality changes.On the other hand,the asymmetric atrophy in left temporooccipital lobe may be responsible for the aphasis of patients with PPA.

Hemorrhagic shock, a life-threatening organ hypoperfusion caused by rapid, massive blood loss, is the leading cause of traumatic death in peacetime and wartime. The vascular endothelial glycocalyx (vEG) plays an important role in maintaining microcirculatory homeostasis. Severe ischemia and hypoxia of hemorrhagic shock can damage the vEG, leading to endothelial dysfunction and exacerbated microcirculatory and organ impairments. Therefore, early prevention and treatment of vEG damage in hemorrhagic shock can improve microcirculation dysfunction, which is of paramount importance for therapeutic efficacies and outcomes. There have been many studies on the prevention and treatment of vEG damage in hemorrhagic shock, but none is based on the management of vEG damage. The authors reviewed the progress on the mechanism and preventive and therapeutic strategies of vEG damage caused by hemorrhagic shock, hoping to provide reference for the further research of hemorrhagic shock-induced vEG damage.

Hemorrhagic shock (HS) is one of the leading causes of death among young adults worldwide. Multiple organ dysfunction in HS is caused by an imbalance between tissue oxygen supply and demand, which is closely related to the poor prognosis of patient. Mitochondrial dysfunction is one of the key mechanisms contributing to multiple organ dysfunction in HS, while mitochondrial quality control regulates mitochondrial function through a series of processes, including mitochondrial biogenesis, mitochondrial dynamics, mitophagy, mitochondrial-derived vesicles, and mitochondrial protein homeostasis. Modulating mitochondrial quality control can improve organ dysfunction. This review aims to summarize the effects of mitochondrial dysfunction on organ function in HS and discuss the potential mechanisms of mitochondrial quality control, providing insights into the injury mechanisms underlying HS and guiding clinical management.