Keeping your cool: thermoregulatory performance and plasticity in desert cricetid rodents.

Small mammals in hot deserts often avoid heat via nocturnality and fossoriality, and are thought to have a limited capacity to dissipate heat using evaporative cooling. Research to date has focused on thermoregulatory responses to air temperatures (Ta) below body temperature (Tb). Consequently, the thermoregulatory performance of small mammals exposed to high Ta is poorly understood, particularly responses across geographic and seasonal scales.

Plump endothelial cells integrated into pre-existing venules contribute to the formation of 'mother' and 'daughter' vessels in pyogenic granuloma: possible role of galectin-1, -3 and -8.

Introduction: Pyogenic granuloma (PG) is a reactive inflammatory vascular lesion of the skin and mucous membranes, characterised by the presence of enlarged venules and seamed and seamless capillaries with plump endothelial cells (EC), and numerous macrophages. EC activation upregulates the synthesis of galectins and induces their translocation to the EC surface promoting angiogenesis and lymphangiogenesis, particularly galectin-1 (Gal-1), Gal-3 and Gal-8. However, the presence and distribution of Gal-1, -3 and -8, as well as their implications in the pathogenesis of PG, has not been considered.

Galectin-1 and Galectin-3 and Their Potential Binding Partners in the Dermal Thickening of Keloid Tissues.

Keloids are defined histopathologically as an inflammatory disorder characterized by exhibiting numerous fibroblasts, abnormal vascularization, increased number of proinflammatory immune cells as well as uncontrolled cell proliferation, and exacerbated and disorganized deposition of extracellular matrix (ECM) molecules. Importantly, many of these ECM molecules display N- and O-linked glycan residues and are considered as potential targets for galectin-1 (Gal-1) and galectin-3 (Gal-3). Nevertheless, the presence and localization of Gal-1 and Gal-3 as well as the interactions with some of their binding partners in keloid tissues have not been considered.

Comparison of Psychological and Physiological Responses to Imposed vs. Self-selected High-Intensity Interval Training.

Kellogg, E, Cantacessi, C, McNamer, O, Holmes, H, von Bargen, R, Ramirez, R, Gallagher, D, Vargas, S, Santia, B, Rodriguez, K, and Astorino, TA. Comparison of psychological and physiological responses to imposed vs. self-selected high-intensity interval training.

Mucin1 expression in focal epidermal dysplasia of actinic keratosis.

Background: Actinic keratoses (AKs) are generally considered as premalignant skin lesions that can progress into squamous cell carcinoma (SCC) in situ and invasive SCC. However, its progression to SCC is still matter of debate. A transmembrane glycoprotein that contributes to the progression of certain premalignant and malignant lesions is mucin1 (MUC1).

Presence of MUC1 in the epidermal thickening of psoriatic plaques.

Mucin 1 (MUC1) is a transmembrane glycoprotein that protects epithelial cells from injury caused by external stimuli. In addition to this role, MUC1 is involved in cell-cell adhesion, proliferation, motility, invasion and survival. In epithelial cells, MUC1 expression is regulated by binding of TNFα to TNFR1 and activation of the NFκB pathway.

Endothelial-mesenchymal transition occurs during embryonic pulmonary artery development.

Pulmonary vascular remodeling is a process generally associated with pulmonary hypertension that involves intimal thickening, medial hyperthrophy, and plexiform lesions. Morphological studies during pulmonary hypertension have indicated that intimal thickening consists of immature smooth muscle cells (SMCs) associated with determined extracellular matrix components, suggesting an important role for these cells in vascular lesions. Controversy exists regarding the nature and origin of the cells conforming the intimal thickenings.

CD40 and CD40L expression in the chicken embryo aorta: possible role in the endothelial-mesenchymal transdifferentiation process.

Endothelial-mesenchymal transdifferentiation (EMT) is believed to play a crucial role in embryonic vascular development and intimal thickening, which contributes to the pathogenesis of atherosclerotic lesions. However, the mechanisms by which it occurs, as well as the signals that control it, have not yet been elucidated. Given the important role played by the CD40-CD40 ligand (CD40L) system during the initiation and progress of atherosclerosis, we investigated whether both CD40 and CD40L were present in the aortic wall during EMT and the advanced stages of chicken embryo development.