Lectin-like oxidized LDL receptor 1 is involved in CRP-mediated complement activation.

Background: C-reactive protein (CRP) is purported to be a risk factor that acts independently of LDL cholesterol in predicting all-cause mortality in patients with ischemic heart disease. Lectin-like oxidized LDL receptor 1 (LOX-1) impairs endothelial function and exacerbates myocardial injury. We recently demonstrated that CRP increased vascular permeability through direct binding to LOX-1.

LOX-1 mediates vascular lipid retention under hypertensive state.

Objectives: Hypertension is a powerful independent risk factor for atherosclerotic cardiovascular diseases; however, the precise molecular mechanisms whereby hypertension promotes atherosclerotic formation remain to be determined. The interaction between oxidized low-density lipoprotein (oxLDL) and its receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a critical role in atherogenesis. To clarify how hypertension promotes atherosclerosis, we investigated specific roles of LOX-1 in acceleration of lipid deposition under a hypertensive state.

Oxidized LDL receptor LOX-1 binds to C-reactive protein and mediates its vascular effects.

Background: C-reactive protein (CRP) exerts biological activity on vascular endothelial cells. This activity may promote atherothrombosis, but the effects of this activity are still controversial. Lectin-like oxidized LDL receptor-1 (LOX-1), the oxidized LDL receptor on endothelial cells, is involved in endothelial dysfunction induced by oxidized LDL.

Blood flow regulation in the cerebral microvasculature with an arcadal network: a numerical simulation.

Blood flow regulation in the cerebral microvasculature with an arcadal network was investigated using a numerical simulation. A mathematical model for blood flow in the arcadal network, based on in vivo data of cat cerebral microvasculature and flow velocity was developed. The network model consists of 45 vessel segments and 25 branching points.

Microembolic flow disturbances in the cerebral microvasculature with an arcadal network: a numerical simulation.

Flow disturbance due to microembolism in the cerebral microvasculature with an arcadal network was studied by a numerical simulation. A mathematical model for flow in the arcadal network was developed, based on in vivo data of cat cerebral microvasculature and flow velocity. The network model consisted of 45 vessel segments, and 25 branching points.

Maturity of pericytes in cerebral neocapillaries induced by growth factors: fluorescence immuno-histochemical analysis using confocal laser microscopy.

The maturity of pericytes in cerebral neocapillaries induced by two different growth factors: basic fibroblast growth factor (bFGF) and platelet-derived growth factor (PDGF), was examined using an immunohistochemical staining technique. Cerebral angiogenesis was induced in mice by implanting a sandwich system of bFGF/PDGF gel and nylon-mesh over the exposed cortex. On 28th day after incubation, a small volume of cerebral tissue with the nylon-mesh was isolated and stained using tetramethyl rhodamine isothiocyanate (TRITC)-labeled secondary antibody to the primary antibody against NG_2 proteoglycan and fluorescein isothiocyanate (FITC)-labeled Griffonia simplicifolia (GS)-lectin.

Cerebral microvascular responses to air embolism-reperfusion in the cat using fluorescence videomicroscopy.

Cerebral microvascular changes due to air embolism-reperfusion in the cat were investigated. Air embolism-reperfusion was produced in the cerebral microvessels by an intra-carotid injection of air (0.2-0.

The effect of long-term supplementation of vitamin C on leukocyte adhesion to the cerebral endothelium in STZ-induced diabetic rats.

The effect of long-term supplementation of vitamin C on leukocyte adhesion to the cerebral endothelium was investigated in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced in male Wistar Furth rats by intravenous injection of STZ. The vitamin C, ascorbic acid, was supplemented with drinking water (1 g/l).

Cerebral microcirculatory changes in rat with a cardiopulmonary bypass using fluorescence videomicroscopy.

Cerebral microcirculatory changes in rat with a cardiopulmonary bypass (CPB) at normothermia was investigated in relation to cerebrovascular disorders caused by surgical operation with CPB. The mean arterial pressure was changed from 50 to 200 mmHg by changing the pump flow-rate. A non-pulsatile flow model was developed by stopping the cardiac beat using a fibrillator.