Cost-benefit analysis of outcomes from the use of fibrin sealant for fixation of skin grafts in small-size burns compared to staples as historical controls: a retrospective review.

Introduction: Historically, split-thickness skin grafts have been fixed onto the recipient site by suture and/or staples. Fibrin sealants have become available for the fixation in the past 10 years. Fibrin sealants have been shown to be at least as effective as staples, and recent reports show them to cause less pain.

Monitoring immune cells trafficking fluorescent prion rods hours after intraperitoneal infection.

Presence of an abnormal form a host-encoded prion protein (PrPC) that is protease resistant, pathologic and infectious characterizes prion diseases such as Chronic Wasting Disease (CWD) of cervids and scrapie in sheep. The Prion hypothesis asserts that this abnormal conformer constitutes most or all of the infectious prion. The role of the immune system in early events in peripheral prion pathogenesis has been convincingly demonstrated for CWD and scrapie.

Protection against pneumonic plague following oral immunization with a non-replicating vaccine.

Yersinia pestis is a dangerous bacterial pathogen that when inhaled can rapidly induce fatal pneumonic plague. Thus, there is a need for stable, safe, and easily administered mucosal vaccines capable of eliciting effective protection against pulmonary Y. pestis infections.

Metabolic flexibility permits mesenchymal stem cell survival in an ischemic environment.

The application of mesenchymal stem cells (MSCs) for myocardial repair following ischemic injury is of strong interest, but current knowledge regarding the survival and retention of differentiation potency of stem cells under ischemic conditions is limited. The present study investigated the effects of ischemia and its components (hypoxia and glucose depletion) on MSC viability and multipotency. We demonstrate that MSCs have a profoundly greater capacity to survive under conditions of ischemia compared with cardiomyocytes, measured by detecting changes in cellular morphology, caspase activity and phosphatidylserine exposure.

ER stress contributes to ischemia-induced cardiomyocyte apoptosis.

Myocardial ischemia is a severe stress condition that leads to loss of cardiomyocytes. The cell loss is attributed to apoptosis, although the exact mechanisms involved are only partially defined, which limits therapeutic opportunities. Here, we show caspase activation and apoptosis in neonatal rat cardiomyocyte cultures subjected to simulated ischemia by serum, glucose, and oxygen deprivation (SGO).

Differential regulation of iron- and manganese-specific MtsABC and heme-specific HtsABC transporters by the metalloregulator MtsR of group A Streptococcus.

The genome of the human pathogen group A Streptococcus (GAS) encodes the transporters MtsABC, FtsABCD, and HtsABC to take up ferric and manganese ions, ferric ferrichrome, and heme, respectively. The GAS genome also encodes two metalloregulators PerR and MtsR. To understand the regulation of the expression of these transporters, the mtsR and perR deletion mutants of a GAS serotype M1 strain were generated, and the effects of the deletions and Fe(3+), Mn(2+), and Zn(2+) on the expression of mtsA, htsA, and ftsB were examined.

Don't lose heart--therapeutic value of apoptosis prevention in the treatment of cardiovascular disease.

Cardiovascular disease is a leading cause of death worldwide. Loss of function or death of cardiomyocytes is a major contributing factor to these diseases. Cell death in conditions such as heart failure and myocardial infarction is associated with apoptosis.

A novel gene delivery system for mammalian cells.

Although gene therapy holds great promise for the treatment of both acquired and genetic diseases, its development has been limited by practical considerations. Non-viral efficacy of delivery remains quite poor. We are investigating the feasibility of a novel lipid-based delivery system, cochleates, to deliver transgenes to mammalian cells.

Cyclooxygenase isoforms and platelet vessel wall interactions in the apolipoprotein E knockout mouse model of atherosclerosis.

Background: Cyclooxygenase (COX) activity is induced in human atherosclerosis, and the products formed may modify the disease directly or through an effect on platelets. We examined the role of COX-1 and -2 on platelet vessel wall interactions and development of atherosclerosis in a murine model.

Methods And Results: Apolipoprotein E-deficient (apoE-/-) mice fed a 1% cholesterol diet were treated with a selective COX-1 inhibitor (SC-560), a selective COX-2 inhibitor (SC-236), or vehicle.