Intelligent cholinergic white matter pathways algorithm based on U-net reflects cognitive impairment in patients with silent cerebrovascular disease.

Background And Objective: The injury of the cholinergic white matter pathway underlies cognition decline in patients with silent cerebrovascular disease (SCD) with white matter hyperintensities (WMH) of vascular origin. However, the evaluation of the cholinergic white matter pathway is complex with poor consistency. We established an intelligent algorithm to evaluate WMH in the cholinergic pathway.

U-fiber analysis: a toolbox for automated quantification of U-fibers and white matter hyperintensities.

Background: Whether white matter hyperintensities (WMHs) involve U-fibers is of great value in understanding the different etiologies of cerebral white matter (WM) lesions. However, clinical practice currently relies only on the naked eye to determine whether WMHs are in the vicinity of U-fibers, and there is a lack of good neuroimaging tools to quantify WMHs and U-fibers.

Methods: Here, we developed a multimodal neuroimaging toolbox named U-fiber analysis (UFA) that can automatically extract WMHs and quantitatively characterize the volume and number of WMHs in different brain regions.

White matter integrity mediates the associations between white matter hyperintensities and cognitive function in patients with silent cerebrovascular diseases.

Objective: To evaluate the relationships between cognitive function and white matter hyperintensity volume (WMHV) in patients with silent cerebrovascular disease and to investigate whether white matter integrity or brain atrophy play a role in this association.

Methods: Automated Fiber Quantification and Voxel- based morphometry were used to track and identify the integrity of 20 well-defined white matter tracts and to measure the gray matter volume (GMV). A linear regression model was applied for examining the associations between cognitive function and WMHV and mediation analysis was used to identify the roles of white matter integrity or GMV in the influence of WMHV on cognitive function.

Vascular Remodeling, Oxidative Stress, and Disrupted PPAR Expression in Rats of Long-Term Hyperhomocysteinemia with Metabolic Disturbance.

Hyperhomocysteinemia, a risk factor for vascular disease, is associated with metabolic syndrome. Our study was aimed at exploring the effect of long-term hyperhomocysteinemia with metabolic disturbances on vascular remodeling. We also studied oxidative stress and expression of PPAR in the coronary arteriole as a possible mechanism underlying vascular remodeling.

Mild hypothermia protects rat neuronal injury after intracerebral hemorrhage via attenuating endoplasmic reticulum response induced neuron apoptosis.

Background And Purpose: Mild hypothermia has been proved to reduce global and focal cerebral ischemic injury in rodents by preventing cellular apoptosis through several pathways. However, whether hypothermia will be beneficial for intracerebral hemorrhage (ICH) and its underlying mechanisms haven't reached a consensus. It has been implicated that endoplasmic reticulum (ER) stress plays a role in the secondary injury after ICH in rats.

Acute phase homocysteine related to severity and outcome of atherothrombotic stroke.

Background: Homocysteine (HCY) is associated with risk of stroke, but whether HCY affects stroke severity and prognosis remains controversial. We hypothesized HCY has an impact on atherothrombosis and this prospective study was aimed to explore the association between acute phase HCY with stroke severity and outcome in patients with atherothrombosis.

Methods: Patients <72 h after symptom onset were categorized by the modified Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification and those typed as atherothrombosis were included.