Physical activity and arterial stiffness: is body fat a mediator?

Purpose: Physical activity (PA) and body fat percentage (%BF) are independently associated with arterial stiffness, but it has not been explored if there is an associative pathway among these variables. This study examined whether %BF mediates the relationship between PA or sedentary behavior levels with arterial stiffness.

Methods: Fifty adults (1:1 men:women; age 28 ± 11 year) had carotid-femoral pulse wave velocity (CF-PWV) measured by applanation tonometry, %BF by bioelectrical impedance, and PA levels by accelerometry.

Mast Cell Proteases Cleave Prion Proteins and a Recombinant Ig against PrP Can Activate Human Mast Cells.

IgE Abs, best known for their role in allergic reactions, have only rarely been used in immunotherapies. Nevertheless, they offer a potential alternative to the more commonly used IgGs. The affinity of IgE Ag binding influences the type of response from mast cells, so any immunotherapies using IgEs must balance Ag affinity with desired therapeutic effect.

High Dose and Delayed Treatment with Bile Acids Ineffective in RML Prion-Infected Mice.

Prion diseases are a group of neurodegenerative diseases associated with the misfolding of the cellular prion protein (PrP) into the infectious form (PrP). There are currently no treatments for prion disease. Bile acids have the ability to protect hepatocytes from apoptosis and are neuroprotective in animal models of other protein-folding neurodegenerative diseases, including Huntington's, Parkinson's, and Alzheimer's disease.

Bile Acids Reduce Prion Conversion, Reduce Neuronal Loss, and Prolong Male Survival in Models of Prion Disease.

Unlabelled: Prion diseases are fatal neurodegenerative disorders associated with the conversion of cellular prion protein (PrPC) into its aberrant infectious form (PrPSc). There is no treatment available for these diseases. The bile acids tauroursodeoxycholic acid(TUDCA) and ursodeoxycholic acid (UDCA) have been recently shown to be neuroprotective in other protein misfolding disease models, including Parkinson’s, Huntington’s and Alzheimer’s diseases, and also in humans with amyotrophic lateral sclerosis.

Transcriptional profiling in rat hair follicles following simulated Blast insult: a new diagnostic tool for traumatic brain injury.

With wide adoption of explosive-dependent weaponry during military activities, Blast-induced neurotrauma (BINT)-induced traumatic brain injury (TBI) has become a significant medical issue. Therefore, a robust and accessible biomarker system is in demand for effective and efficient TBI diagnosis. Such systems will also be beneficial to studies of TBI pathology.

Toxicity of the azo dyes Acid Red 97 and Bismarck Brown Y to Western clawed frog (Silurana tropicalis).

Azo compounds are used in a variety of industrial applications, such as textile colorant. Azo dyes have been found to contaminate aquatic environments and it has been shown that these compounds could potentially be toxic or induce endocrine disruption in aquatic organisms. However, there are few data available on the toxicity of these dyes, specifically Acid Red 97 (AR97) and Bismarck Brown Y (BBY).

Evidence for a second messenger function of dUTP during Bax mediated apoptosis of yeast and mammalian cells.

The identification of novel anti-apoptotic sequences has lead to new insights into the mechanisms involved in regulating different forms of programmed cell death. For example, the anti-apoptotic function of free radical scavenging proteins supports the pro-apoptotic function of Reactive Oxygen Species (ROS). Using yeast as a model of eukaryotic mitochondrial apoptosis, we show that a cDNA corresponding to the mitochondrial variant of the human DUT gene (DUT-M) encoding the deoxyuridine triphosphatase (dUTPase) enzyme can prevent apoptosis in yeast in response to internal (Bax expression) and to exogenous (H(2)O(2) and cadmium) stresses.

Anti-apoptosis and cell survival: a review.

Type I programmed cell death (PCD) or apoptosis is critical for cellular self-destruction for a variety of processes such as development or the prevention of oncogenic transformation. Alternative forms, including type II (autophagy) and type III (necrotic) represent the other major types of PCD that also serve to trigger cell death. PCD must be tightly controlled since disregulated cell death is involved in the development of a large number of different pathologies.