Alpha and beta adrenergic receptors modulate keratinocyte migration.

Keratinocyte migration into skin wounds is the step of the healing process that correlates with the wound closure rate. Keratinocyte migration, and wound epithelialization are decreased when beta 2-adrenergic receptors (B2AR) are activated by 1 µM epinephrine/adrenaline, resulting in delayed wound healing in human and mouse skin. In the present study, we found paradoxically, that in a subset of keratinocyte strains exposure to low concentrations of epinephrine (0.1 nM) increased, rather than decreased, their migratory rate. We find that both the alpha- and the beta-adrenergic receptors are expressed in human keratinocytes, and expression of alpha-2 AR subtypes demonstrated for the first time. Therefore, we tested if the alpha-AR could be modulating the increased migratory response observed in these cell strains. By using specific inhibitors to alpha-AR, we demonstrated that blocking A2B-AR could reverse the rapid cell migration induced by the 0.1 nM epinephrine. Phosphorylation of ERK was elevated after 1-10 minutes of the low epinephrine treatment and the A2B-AR inhibitor blocked the ERK phosphorylation. The results suggest that both the A2B-AR and B2AR mediate keratinocyte migration, in which with a low level of epinephrine treatment, A2B-AR could alter the B2AR signals and regulate the migration rate.

Cerebral Aneurysm from Cardiobacterium hominis Endocarditis.

A 43-year-old male with a history of bioprosthetic aortic valve replacement and tricuspid valve annuloplasty presented with vertigo and was found to have an acute infarct in the left superior cerebellum, as well as a left-middle cerebral artery mycotic aneurysm. Blood cultures grew Cardiobacterium hominis and bioprosthetic aortic valve vegetation was found on transthoracic echocardiogram.

Lipoid Pneumonia and Sarcoidosis.

INTRODUCTION: Lipoid pneumonia is a rare, underdiagnosed disorder, and its combined presentation with sarcoidosis is even more unusual. METHODS: This paper presents a case in which both lipoid pneumonia and sarcoidosis were present, and includes the relevant literature review on lipoid pneumonia. RESULTS: Lipoid pneumonia may be acute or chronic in its presentation, resulting from exogenous or endogenous factors, or classified as idiopathic, with its precise incidence unknown. Radiographic changes maybe variable, but typically include lower lobe consolidation. Pathologic changes consist of an inflammatory giant cell reaction around lipid-related empty vacuoles and giant cell granulomas. Treatment in the case of exogenous lipoid pneumonia consists of removal of the offending oil ingestion. However, in endogenous lipoid pneumonia, treatment is aimed at the underlying cause, as there is no standard treatment. Repeated bronchoalveolar lavage, corticosteroids, and surgical resection have been used as therapies. The course of the disease is usually not progressive.