Survey data on orientations, boot camps, and pre-matriculation programs in schools/colleges of pharmacy.

A survey about orientations, boot camps, and pre-matriculation programs in schools/colleges of pharmacy was approved by the South College Institutional Review Board (IRB). The survey was sent electronically to Assistant/Associate Deans of Academic Affairs or administrators in similar positions at schools/colleges of pharmacy in October 2016. The survey was closed two months later, in December, with 50 responses.

Implementation, Revisions, and Student Perceptions of a Pre-Matriculation Program in a School of Pharmacy.

To characterize the development, revision, and student perceptions of a pre-matriculation program entitled Pharmacy Readiness and Enrichment Program (PREP) in a school of pharmacy. The program was first implemented in June 2013 for the incoming class of 2016. The main components of PREP were curriculum and scientific content review, professionalism, time management, critical thinking, and personal interactions.

α1-Acid glycoprotein induced effects in rat brain microvessel endothelial cells.

α1-Acid glycoprotein (AGP) is a positive acute phase protein which is elevated 1-10 times during inflammation. Whereas AGP has been reported to have immunomodulatory properties, other biological functions of this protein such as its effects on the blood-brain barrier (BBB) endothelium are unknown. Tight junction (TJ) proteins (ZO-1 and occludin) are crucial in maintaining BBB integrity and brain homeostasis.

Reoxygenation stress on blood-brain barrier paracellular permeability and edema in the rat.

The blood-brain barrier (BBB) serves as a critical regulator of brain homeostasis. Following hypoxia (i.e.

Hypoxia-inducible factor and nuclear factor kappa-B activation in blood-brain barrier endothelium under hypoxic/reoxygenation stress.

This investigation focuses on transcription factor involvement in blood-brain barrier (BBB) endothelial cell-induced alterations under conditions of hypoxia and post-hypoxia/reoxygenation (H/R), using established in vivo/ex vivo and in vitro BBB models. Protein/DNA array analyses revealed a correlation in key transcription factor activation during hypoxia and H/R, including NFkappaB and hypoxia-inducible factor (HIF)1. Electrophoretic mobility shift assays confirmed NFkappaB and HIF1 binding activity ex vivo and in vitro, under conditions of hypoxia and H/R.

Protection against hypoxia-induced blood-brain barrier disruption: changes in intracellular calcium.

Tissue damage after stroke is partly due to disruption of the blood-brain barrier (BBB). Little is known about the role of calcium in modulating BBB disruption. We investigated the effect of hypoxic and aglycemic stress on BBB function and intracellular calcium levels.

Nitric oxide mediates hypoxia-induced changes in paracellular permeability of cerebral microvasculature.

Ischemic stroke from a reduction in blood flow to the brain microvasculature results in a subsequent decreased delivery of oxygen (i.e., hypoxia) and vital nutrients to endothelial, neuronal, and glial cells.

Effects of hypoxia-reoxygenation on rat blood-brain barrier permeability and tight junctional protein expression.

Cerebral microvessel endothelial cells that form the blood-brain barrier (BBB) have tight junctions (TJs) that are critical for maintaining brain homeostasis. The effects of initial reoxygenation after a hypoxic insult (H/R) on functional and molecular properties of the BBB and TJs remain unclear. In situ brain perfusion and Western blot analyses were performed to assess in vivo BBB integrity on reoxygenation after a hypoxic insult of 6% O2 for 1 h.

Protection against hypoxia-induced increase in blood-brain barrier permeability: role of tight junction proteins and NFkappaB.

Co-culture with glial cells and glia-conditioned media can induce blood-brain barrier properties in microvessel endothelial cells and protect against hypoxia-induced blood-brain barrier breakdown. We examined the effect of two types of glia-conditioned media on brain microvessel endothelial cell permeability and tight junction protein expression, and studied potential mechanisms of action. We found that C6-glioma-conditioned media, but not rat astrocyte-conditioned media, protected against an increase in permeability induced by exposure to 1% oxygen for 24 hours.

Nicotine and cotinine modulate cerebral microvascular permeability and protein expression of ZO-1 through nicotinic acetylcholine receptors expressed on brain endothelial cells.

The blood-brain barrier (BBB) adapts to a variety of pathological processes. Little is known about the effects of nicotine exposure on BBB function and the ability to adapt to stroke conditions. We have demonstrated, using a well-characterized in vitro BBB model, bovine brain microvessel endothelial cells (BBMEC) model, that nicotine and its major metabolite, cotinine, modulate BBB integrity by opening the paracellular route of solute entry into the brain.

Viability of microvascular endothelial cells to direct exposure of formalin, lambda-carrageenan, and complete Freund's adjuvant.

We investigated three inflammatory agents to establish if these substances elicit a direct effect on the functional and structural integrity of the blood-brain barrier. Cellular cytotoxicity and paracellular permeability were assessed in vitro using primary bovine brain microvascular endothelial cells exposed to formalin, lambda-carrageenan, or complete Freund's adjuvant for 1, 3, or 72 h, respectively. Results showed that only the highest concentration (0.

Cerebral microvascular changes in permeability and tight junctions induced by hypoxia-reoxygenation.

Cerebral microvessel endothelial cells that form the blood-brain barrier (BBB) have tight junctions (TJ) that are critical for maintaining brain homeostasis and low permeability. Both integral (claudin-1 and occludin) and membrane-associated zonula occluden-1 and -2 (ZO-1 and ZO-2) proteins combine to form these TJ complexes that are anchored to the cytoskeletal architecture (actin). Disruptions of the BBB have been attributed to hypoxic conditions that occur with ischemic stroke, pathologies of decreased perfusion, and high-altitude exposure.