Foot ulcers, particularly in the diabetic setting, are a major medical and socioeconomic challenge. While the effects of diabetes and its various sequelae have been extensively studied, in the wound field it is commonly assumed that the wound healing process is essentially identical between different skin types, despite the many well-known specializations in palmoplantar skin, most of which are presumed to be evolutionary adaptations for weightbearing. This article will examine how these specializations could alter the wound healing trajectory and contribute to the pathology of foot ulcers.

The published literature makes a very strong case that a wide range of disease morbidity associates with and may in part be due to epithelial barrier leak. An equally large body of published literature substantiates that a diverse group of micronutrients can reduce barrier leak across a wide array of epithelial tissue types, stemming from both cell culture as well as animal and human tissue models. Conversely, micronutrient deficiencies can exacerbate both barrier leak and morbidity. Focusing on zinc, Vitamin A and Vitamin D, this review shows that at concentrations above RDA levels but well below toxicity limits, these micronutrients can induce cell- and tissue-specific molecular-level changes in tight junctional complexes (and by other mechanisms) that reduce barrier leak. An opportunity now exists in critical care-but also medical prophylactic and therapeutic care in general-to consider implementation of select micronutrients at elevated dosages as adjuvant therapeutics in a variety of disease management. This consideration is particularly pointed amidst the COVID-19 pandemic.

UNASSIGNED: Psoriasis is a common papulosquamous disorder characterized by increased epidermal turnover resulting in excessive skin shedding and a compromised barrier function of the skin. Transepidermal water loss (TEWL) is an effective and non-invasive way to measure the barrier function in this condition.
UNASSIGNED: To measure the physiological changes in the skin barrier function in psoriasis by measuring the extent of TEWL. To study the differences in TEWL in pathologically involved and uninvolved skin in psoriasis. To compare the TEWL in skin lesions in psoriatic patients and site matched controls.
UNASSIGNED: To determine the barrier quality of the stratum corneum, we performed TEWL measurements using the closed chamber evaporation method (VapoMeter Delfin Technologies, Kuopio, Finland). The ambient temperature ranged between 21°C and 24°C, with a mean relative humidity range of 39%-50%. In total, four sites were measured for all the 50 cases, two involved plaques on the body were selected for the study of lesional psoriatic skin, and the standard sites of ankle and elbow were measured irrespective of being involved or uninvolved with psoriatic skin. TEWL measurements in controls were site matched. Statistical testing was done using SPSS ver. 17. The interval scale data were tested for normality using Shapiro-Wilk test, and between groups testing was done using Mann-Whitney test.
UNASSIGNED: The TEWL was higher among the cases in all the four measured areas compared to the controls, thus showing overall impaired skin barrier function in psoriatic skin. In addition, among the cases, the involved sites show higher TEWL in comparison to the uninvolved skin. This is highly suggestive that plaques of psoriasis have reduced water holding capacity.
UNASSIGNED: Psoriasis is a dermatosis with overall compromise of the skin barrier function exhibiting exponential TEWL in lesional skin, with increased TEWL over non-lesional skin as well. Thus, it may be concluded that TEWL is an effective, non-invasive and objective method in assessment of skin barrier function.

The appearance of multicellularity implied the adaptation of signaling networks required for unicellular life to new functions arising in this remarkable evolutionary transition. A hallmark of multicellular organisms is the formation of cellular barriers that compartmentalize spaces and functions. Here we discuss recent findings concerning the role of RhoB in the negative control of Rac1 trafficking from endosomes to the cell border, in order to induce membrane extensions to restore endothelial barrier function after acute contraction. This role closely resembles that proposed for RhoB in controlling single cell migration through Rac1, which has also been observed in cancer cell invasion. We highlight these similarities as a signaling paradigm that shows that endothelial barrier integrity is controlled not only by the formation of cell-cell junctions, but also by a balance between ancestral mechanisms of cell spreading and contraction conserved from unicellular organisms and orchestrated by Rho GTPases.