The Responses of Arterial Stiffness Parameter Beta-Derived Index of the Aorta and Illiac-Femoral Artery to Acute Hypovolemia in Rabbits.

Introduction: Acute hemorrhage decreases blood pressure (BP) and sometimes causes hypovolemic shock. At this time, peripheral arteries are supposed to contract and increase peripheral vascular resistance to raise BP. However, there has not been an adequate index of a degree of arterial stiffness.

Arterial stiffness of the aorta and iliofemoral artery and their responses to nitroglycerin administration in myocardial infarction-prone Watanabe heritable hyperlipidemic rabbits.

Objectives: The role of hypercholesterolemia in arterial stiffness, which usually reflects the progression of atherosclerosis has not been fully investigated. To clarify the meaning of arterial stiffness in hypercholesterolemia, we evaluated arterial stiffness in myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHLMI) rabbits by using new arterial stiffness indices of the aorta and common iliac to femoral artery. The new arterial stiffness indices of both arteries were determined by the application of the theory of cardio-ankle vascular index (CAVI) to the aorta (aBeta) and ilio-femoral artery (ifBeta).

Utility of a novel wearable electrode embedded in an undershirt for electrocardiogram monitoring and detection of arrhythmias.

Background: A 12-lead electrocardiogram (ECG) and Holter ECG have been established as gold standards for detection of arrhythmias. Recently, wearable ECG monitoring devices have been available. Our purpose of the present study was to investigate whether a novel wearable electrode embedded in an undershirt is useful for ECG monitoring and detection of arrhythmias.

Renal Venous Stasis Index Reflects Renal Congestion and Predicts Adverse Outcomes in Patients With Heart Failure.

Background: It has been recently reported that the renal venous stasis index (RVSI) assessed by renal Doppler ultrasonography provides information to stratify pulmonary hypertension that can lead to right-sided heart failure (HF). However, the clinical significance of RVSI in HF patients has not been sufficiently examined. We aimed to examine the associations of RVSI with parameters of cardiac function and right heart catheterization (RHC), as well as with prognosis, in patients with HF.

Opposing Responses of the Calcium Channel Blocker Nicardipine to Vascular Stiffness in the Elastic and Muscular Arteries in Rabbits.

Aim: The cardio-ankle vascular index (CAVI) consists of intrinsic and functional arterial stiffness mainly regulated by vasoactive compounds. A new stiffness index of the aorta (aBeta) and iliac-femoral arteries (ifBeta) was determined by applying the CAVI theory to the whole aorta and iliac-femoral arteries. We investigated the changes in aBeta and ifBeta in response to decreased blood pressure (BP) induced by the Ca channel blocker nicardipine to elucidate the involvement of Ca in aBeta and ifBeta.

Different Responses of Arterial Stiffness between the Aorta and the Iliofemoral Artery during the Administration of Phentolamine and Atenolol in Rabbits.

Aim: The mechanism underlying the stiffness of the aorta and iliofemoral artery that is required to maintain blood pressure (BP) is unclear. A new stiffness index of the aorta (aBeta) and iliac-femoral arteries (ifBeta) was defined by applying the cardio-ankle vascular index (CAVI). We compared changes in stiffness of the two arteries in response to reduced BP, due to the non-selective α adrenergic blocker phentolamine and the β adrenergic blocker atenolol, in rabbits.

BACE1 inhibition reduces endogenous Abeta and alters APP processing in wild-type mice.

Accumulation of amyloid beta peptide (Abeta) in brain is a hallmark of Alzheimer's disease (AD). Inhibition of beta-site amyloid precursor protein (APP)-cleaving enzyme-1 (BACE1), the enzyme that initiates Abeta production, and other Abeta-lowering strategies are commonly tested in transgenic mice overexpressing mutant APP. However, sporadic AD cases, which represent the majority of AD patients, are free from the mutation and do not necessarily have overproduction of APP.

Arundic Acid ameliorates cerebral amyloidosis and gliosis in Alzheimer transgenic mice.

Like microglia, reactive astrocytes produce a myriad of neurotoxic substances in various brain pathologies, such as Alzheimer's disease (AD), trauma, and cerebral ischemia. Among the numerous products of reactive astrocytes, attention has recently been directed toward the possible detrimental role of S100B, because the protein has been shown to be highly expressed along with the progression of brain damage and to exert neurotoxic effects at high concentrations. The present study aimed to examine the possible role of astrocyte-derived S100B in the progression of cerebral amyloidosis and gliosis in transgenic mice overproducing mutant amyloid precursor protein (Tg APP(sw) mice, line 2576).

Longer forms of amyloid beta protein: implications for the mechanism of intramembrane cleavage by gamma-secretase.

Gamma-cleavage of beta-amyloid precursor protein (APP) in the middle of the cell membrane generates amyloid beta protein (Abeta), and epsilon-cleavage, approximately 10 residues downstream of the gamma-cleavage site, releases the APP intracellular domain (AICD). A significant link between generation of Abeta and AICD and failure to detect AICD41-99 led us to hypothesize that epsilon-cleavage generates longer Abetas, which are then processed to Abeta40/42. Using newly developed gel systems and an N-end-specific monoclonal antibody, we have identified the longer Abetas (Abeta1-43, Abeta1-45, Abeta1-46, and Abeta1-48) within the cells and in brain tissues.

Abeta N-terminal-end specific antibody reduced beta-amyloid in Alzheimer-model mice.

Alzheimer's disease (AD) is a neurodegenerative disease with memory dysfunction that is causing serious medical problems in modern society. For the fundamental treatment of AD, an amyloid beta protein (Abeta) vaccine is considered to be the most potent candidate. To cure AD, we developed Abeta N-terminal-end specific monoclonal antibody named 82E1, which does not cross-react with full-length Abeta precursor.

Development of Abeta terminal end-specific antibodies and sensitive ELISA for Abeta variant.

Alzheimer's disease (AD) is a neurodegenerative affliction associated with memory dysfunction. Senile plaques are a pathological hallmark of AD, and amyloid beta (Abeta) peptides are a major component of these plaques. Abeta peptides are derived from proteolytic cleavage of the Abeta protein precursor (APP) by beta- and gamma-secretases to generate two principal species, Abeta1-40 and Abeta1-42.

Characteristic developmental expression of amyloid beta40, 42 and 43 in patients with Down syndrome.

We immunohistochemically studied the expression of beta-amyloid precursor protein (APP), Abeta40, Abeta42, and Abeta43 in the frontal lobes of 20 Down syndrome (DS) patients and 13 controls. The immunoreactivity for each antibody was different in the degree of intensity and the chronological pattern of expression. APP and Abeta43 immunoreactivity was increased in neurons initially, and then Abeta43 and 42 immunoreactivity appeared in diffuse plaques from 32 years of age.

Ultrastructural localization of flotillin-1 to cholesterol-rich membrane microdomains, rafts, in rat brain tissue.

There is much interest in research on cholesterol-rich membrane microdomains, rafts, in the field of neurobiology. However, no one has shown the ultrastructure of rafts in tissues. We examined the ultrastructure of rafts in rat brain tissue by pre-embedding immunoelectron microscopy using flotillin-1 antibody, which is a biochemical marker of lipid rafts, and BCtheta, which is nicked and biotinylated theta-toxin, and binds to membrane cholesterol of rafts.

Antiserum against human glucose transporter 5 is highly specific for microglia among cells of the mononuclear phagocyte system.

Human monocytes and a variety of tissue macrophages, including microglia, were studied immunohistochemically to determine the expression of a novel microglial marker, human glucose transporter 5 (hGLUT5), in these cells. The hGLUT5 was not expressed in most peripheral macrophages in the normal state, but weakly expressed in some foamy macrophages in atherosclerotic lesions. There was no hGLUT5 reactivity in blood monocytes.

Mapping of functional epitopes of osteopontin by monoclonal antibodies raised against defined internal sequences.

Osteopontin (OPN) is a secreted protein that has been implicated in diverse physiological and pathological processes. OPN can bind to integrins, via GRGDS or SVVYGLR amino acid sequences, and to other cell surface receptors, and many of OPN's functions are likely mediated via cell adhesion and subsequent signaling. Here we developed and characterized a series of five monoclonal antibodies, raised to distinct internal peptide sequences of human OPN, and have used these sequence-specific reagents, along with the previously described anti-OPN monoclonal antibody mAb53, to map functional epitopes of OPN that are important to cell adhesion and migration.