Linear IgA bullous dermatosis: a rare side effect of vancomycin.

Following a motor vehicle accident, a 70-year-old white female was admitted with lower limb fractures that required operative repair. The postoperative course was complicated by sepsis. Vancomycin and piperacillin/tazobactam were initiated empirically.

Nicotine exacerbates brain edema during in vitro and in vivo focal ischemic conditions.

We have previously shown that nicotine, the addictive component of tobacco products, alters the blood-brain barrier (BBB) Na(+),K(+),2Cl(-) cotransporter (NKCC) during in vitro hypoxia-aglycemia exposure. Attenuation of abluminal NKCC suggests that accumulation of ions in the brain extracellular fluid would result in an increase of fluid or cytotoxic edema in the brain during hypoxia-aglycemia or stroke conditions. To further investigate whether nicotine products have the potential to worsen stroke outcome by increasing edema formation, two separate models to mimic stroke conditions were utilized to decipher the effects of short-term and long-term administrations of nicotine products on brain edema following stroke.

Pivotal role for beta-1 integrin in neurovascular remodelling after ischemic stroke.

beta1 integrin is a cell surface molecule that is critical for endothelial cell adhesion, migration and survival during angiogenesis. In the present study we employed in vivo and in vitro models to elucidate the role of beta1 integrin in vascular remodelling and stroke outcomes. At 24 h after cerebral ischemia and reperfusion (I/R), the ischemic cortex (ipsilateral area) exhibited modest beta1 integrin immunoreactivity and a robust increase was observed at 72 h.

Toll-like receptor 3 is a negative regulator of embryonic neural progenitor cell proliferation.

Toll-like receptors (TLRs) play important roles in innate immunity. Several TLR family members have recently been shown to be expressed by neurons and glial cells in the adult brain, and may mediate responses of these cells to injury and infection. To address the possibility that TLRs play a functional role in development of the nervous system, we analyzed the expression of TLRs during different stages of mouse brain development and assessed the role of TLRs in cell proliferation.

Toll-like receptor-4 mediates neuronal apoptosis induced by amyloid beta-peptide and the membrane lipid peroxidation product 4-hydroxynonenal.

The innate immune system senses the invasion of pathogenic microorganisms and tissue injury through Toll-like receptors (TLR), a mechanism thought to be limited to immune cells. We recently found that neurons express several TLRs, and that the levels of TLR2 and TLR4 are increased in neurons in response to energy deprivation. Here we report that TLR4 expression increases in neurons when exposed to amyloid beta-peptide (Abeta1-42) or the lipid peroxidation product 4-hydroxynonenal (HNE).

Targeting ischemic brain injury with intravenous immunoglobulin.

Background: Intravenous immunoglobulin (IVIG) is a therapeutic modality approved for the treatment of autoimmune disorders.

Objective: This review discusses how IVIG can prevent brain damage following ischemic stroke and discuss the potential mechanisms of action.

Methods: Medline and the world wide web were searched and the relevant literature was classified under the following categories: IVIG, IVIG mechanism of action, and ischemic stroke injury mechanisms.