Skin diseases in the alpaca (Vicugna pacos): a literature review and retrospective analysis of 68 cases (Cornell University 1997-2006).

This retrospective study describes 68 alpacas with skin diseases investigated from 1997 through 2006 at Cornell University. During this time period, 40 of 715 (5.6%) alpacas presented to the university hospital had dermatological diseases.

The microanatomy of healthy skin from alpacas (Vicugna pacos).

The microanatomy of healthy skin from 12 different body sites was investigated in 14 alpacas (Vicugna pacos). The microanatomy of alpaca skin is typical of domestic animal skin in general, and closely resembles that from llamas.

Fine mapping of murine asthma quantitative trait loci and analyses of Ptgs1 and Mrc1 as positional candidate genes.

Asthma is a common respiratory disease that is driven by both genetic and environmental factors. Identification of the genes underlying asthma will provide insight into the mechanisms and treatment of this important disease. Previous studies in this laboratory identified two distinct quantitative trait loci for the asthma-related parameter, allergen-induced airway hyperresponsiveness, in a murine model by means of a genome-wide linkage analysis.

HIV-1 Nef disrupts antigen presentation early in the secretory pathway.

Human immunodeficiency virus, type 1 Nef disrupts viral antigen presentation and promotes viral immune evasion from cytotoxic T lymphocytes. There is evidence that Nef acts early in the secretory pathway to redirect major histocompatibility complex class I (MHC-I) from the trans-Golgi network to the endolysosomal pathway. However, a competing model suggests that Nef acts much later by accelerating MHC-I turnover at the cell surface.

Direct binding of human immunodeficiency virus type 1 Nef to the major histocompatibility complex class I (MHC-I) cytoplasmic tail disrupts MHC-I trafficking.

Nef, an essential pathogenic determinant for human immunodeficiency virus type 1, has multiple functions that include disruption of major histocompatibility complex class I molecules (MHC-I) and CD4 and CD28 cell surface expression. The effects of Nef on MHC-I have been shown to protect infected cells from cytotoxic T-lymphocyte recognition by downmodulation of a subset of MHC-I (HLA-A and -B). The remaining HLA-C and -E molecules prevent recognition by natural killer (NK) cells, which would otherwise lyse cells expressing small amounts of MHC-I.