Isolation of hair follicle bulge stem cells from YFP-expressing reporter mice.

In this article we provide a method to isolate hair follicle stem cells that have undergone targeted gene inactivation. The mice from which these cells are isolated are bred into a Rosa26-yellow fluorescent protein (YFP) reporter background, which results in YFP expression in the targeted stem cell population. These cells are isolated and purified by fluorescence-activated cell sorting, using epidermal stem cell-specific markers in conjunction with YFP fluorescence.

Essential role of integrin-linked kinase in regulation of phagocytosis in keratinocytes.

Phagocytic melanosome uptake by epidermal keratinocytes is a central protective mechanism against damage induced by ultraviolet radiation. Phagocytosis requires formation of pseudopodia via actin cytoskeleton rearrangements. Integrin-linked kinase (ILK) is an important modulator of actin cytoskeletal dynamics.

Targeted inactivation of integrin-linked kinase in hair follicle stem cells reveals an important modulatory role in skin repair after injury.

Integrin-linked kinase (ILK) is key for normal epidermal morphogenesis, but little is known about its role in hair follicle stem cells and epidermal regeneration. Hair follicle stem cells are important contributors to newly formed epidermis following injury. We inactivated the Ilk gene in the keratin 15--expressing stem cell population of the mouse hair follicle bulge.

Modulation of integrin-linked kinase nucleo-cytoplasmic shuttling by ILKAP and CRM1.

Integrin-linked kinase (ILK) plays key roles in a variety of cell functions, including cell proliferation, adhesion and migration. Within the cell, ILK localizes to multiple sites, including the cytoplasm, focal adhesion complexes that mediate cell adhesion to extracellular substrates, as well as cell-cell junctions in epidermal keratinocytes. Central to understanding ILK function is the elucidation of the mechanisms that regulate its subcellular localization.

RIG-I mediates the co-induction of tumor necrosis factor and type I interferon elicited by myxoma virus in primary human macrophages.

The sensing of pathogen infection and subsequent triggering of innate immunity are key to controlling zoonotic infections. Myxoma virus (MV) is a cytoplasmic DNA poxvirus that in nature infects only rabbits. Our previous studies have shown that MV infection of primary mouse cells is restricted by virus-induced type I interferon (IFN).

M135R is a novel cell surface virulence factor of myxoma virus.

Myxoma virus (MV) encodes a cell surface protein (M135R) that is predicted to mimic the host alpha/beta interferon receptor (IFN-alpha/beta-R) and thus prevent IFN-alpha/beta from triggering a host antiviral response. This prediction is based on sequence similarity to B18R, the viral IFN-alpha/beta-R from vaccinia virus (VV), which has been demonstrated to bind and inhibit type I interferons. However, M135R is only half the size of VV B18R.

Platypnoea orthodeoxia in a patient with aortic root dilatation and a patent foramen ovale.

Platypnoea orthodeoxia syndrome is a rare condition in which shortness of breath and hypoxaemia occur when upright and resolve when prone. The hypoxaemia results from increased right to left shunting of deoxygenated blood, when standing, through a patent foramen ovale (PFO), atrial septal defect (ASD) or other right to left shunt, in the absence of raised right-heart pressure. We present the case of a patient with platypnoea orthodeoxia with marked shunting through a large PFO, evaluated by transesophageal and transthoracic echo.

Myxoma virus M11L blocks apoptosis through inhibition of conformational activation of Bax at the mitochondria.

Many viruses inhibit or retard apoptosis, a strategy that subverts one of the most ancient antiviral mechanisms. M11L, a myxoma virus-encoded antiapoptotic protein, has been previously shown to localize to mitochondria and block apoptosis of virus-infected cells (H. Everett, M.

Real-time 3-dimensional echocardiography for quantification of the difference in left ventricular versus right ventricular stroke volume in a chronic animal model study: Improved results using C-scans for quantifying aortic regurgitation.

Objective: The purpose of our study was to test the applicability of calculating the difference between left ventricular (LV) and right ventricular (RV) stroke volume (SV) for assessing the severity of aortic (Ao) regurgitation (AR) using a real-time 3-dimensional (3D) echocardiographic (RT3DE) imaging system.

Methods: The Ao valve was incised in 5 juvenile sheep, 6 to 10 weeks before the study, to produce AR (mean regurgitant fraction = 0.50).

A new dynamic three-dimensional digital color doppler method for quantification of pulmonary regurgitation: validation study in an animal model.

Objectives: The purpose of the present study was to validate a newly developed three-dimensional (3D) digital color Doppler method for quantifying pulmonary regurgitation (PR), using an animal model of chronic PR.

Background: Spectral Doppler methods cannot reliably be used to assess pulmonary regurgitation.

Methods: In eight sheep with surgically created PR, 27 different hemodynamic states were studied.

Direct quantification of transmitral flow volume with dynamic 3-dimensional digital color Doppler: a validation study in an animal model.

Accurately quantifying transmitral flow volume is clinically important not only as a measure of cardiac output, but also as a value from which to subtract aortic flow, for determining the severity of mitral regurgitation. However, controversy exists over the accuracy of pulsed Doppler for mitral flow quantification because of the complexity of mitral flow geometry and dynamic changes in flow profile and flow area. To explore the feasibility of directly quantifying transmitral flow volume with a newly developed dynamic 3-dimensional digital color Doppler technique, this in vivo experimental study was conducted to validate the method.