Diffusion in liquid mixtures.

The understanding of transport and mixing in fluids in the presence and in the absence of external fields and reactions represents a challenging topic of strategic relevance for space exploration. Indeed, mixing and transport of components in a fluid are especially important during long-term space missions where fuels, food and other materials, needed for the sustainability of long space travels, must be processed under microgravity conditions. So far, the processes of transport and mixing have been investigated mainly at the macroscopic and microscopic scale. Their investigation at the mesoscopic scale is becoming increasingly important for the understanding of mass transfer in confined systems, such as porous media, biological systems and microfluidic systems. Microgravity conditions will provide the opportunity to analyze the effect of external fields and reactions on optimizing mixing and transport in the absence of the convective flows induced by buoyancy on Earth. This would be of great practical applicative relevance to handle complex fluids under microgravity conditions for the processing of materials in space.

Self-Pinning on a Liquid Surface.

We report on the first experimental evidence of a self-pinning liquid drop on a liquid surface. This particular regime is observed for a miscible heavier oil drop (dichloromethane) deposited on an aqueous solution laden by an ionic surfactant (hexadecyltrimethylammonium bromide). Experimental characterization of the drop shape evolution coupled to particle image velocimetry points to the correlation between the drop profile and the accompanying flow field. A simple model shows that the observed pinned stage is the result of a subtle competition between oil dissolution and surfactant adsorption.

Health-care workers and latex allergy.

Latex hypersensitivity can pose a threat to anyone, but health-care providers are among the high-risk groups for developing latex hypersensitivity. Latex hypersensitivity likely results from health-care workers' increased use of gloves following implementation of universal precautions. It is also believed that the antigenic load of latex gloves causes an increase in latex hypersensitivity resulting from massive production of gloves. Although there are many studies on the prevalence of latex hypersensitivity among health-care workers, there appear to be discrepancies, which may affect the different apparent prevalence. Testing for latex hypersensitivity raises another problem. Latex allergens cannot be identified specifically; therefore, there is no standard test or testing solution that can identify hypersensitive persons. Although latex glove hypersensitivity was first identified in the late 1970s, there remain many uncertainties associated with it; as a result, there is a growing concern among health-care providers. The authors offer several precautions to avoid the development of latex hypersensitivity.

The essentials of the complete skin examination.

The skin is unique among organs in that it is entirely exposed. Complete examination is thus possible and, when done well, incorporates input from a variety of the senses. A dermatologist's thoughts regarding the essential aspects of the complete skin examination are presented.

Contact allergens and epidermal proinflammatory cytokines modulate Langerhans cell E-cadherin expression in situ.

After exposure to antigen, Langerhans cells (LC) migrate from the epidermis to lymph nodes, where they initiate primary immune responses in T cells. The adhesion molecule E-cadherin mediates adhesion of LC to keratinocytes in vitro and may be responsible for localization of LC in epidermis. To determine if levels of LC E-cadherin are modulated during LC emigration from epidermis, we utilized flow cytometry to evaluate E-cadherin expression on BALB/c LC exposed in situ to the contact allergen 2,4,6-trinitrochlorobenzene (TNCB). TNCB induced increased I-A/E antigen and decreased E-cadherin expression on a subpopulation of LC as early as 12 h, and as late as 48 h, after application. At 24 h, approximately 30% of LC in TNCB-treated skin expressed increased I-A/E antigens; of these activated LC, approximately 40% expressed decreased levels of E-cadherin. E-cadherin levels on this latter subset were approximately 15% of those expressed by LC in normal skin, and were similar to levels on cultured LC and LC that migrated from skin explants. The effect was specific for allergens; no changes occurred in LC following treatment with several contact irritants or the tolerogen dinitrothiocyanobenzene. To determine if cytokines modulated LC E-cadherin expression, we introduced various cytokines into BALB/c ear skin and assayed I-A/E antigen and E-cadherin levels. Of the cytokines tested, only interleukin-1 and tumor necrosis factor alpha reproduced the effects of TNCB. We propose that downmodulation of E-cadherin expression occurs as a consequence of local cytokine production during antigen-induced LC activation, facilitating LC emigration and the initiation of immune responses against antigens encountered in epidermis.

Expression of E-cadherin by murine dendritic cells: E-cadherin as a dendritic cell differentiation antigen characteristic of epidermal Langerhans cells and related cells.

Murine epidermal Langerhans cells (LC) synthesize and express E-cadherin, a homophilic adhesion molecule that mediates adhesion of LC to keratinocytes in vitro. To determine if E-cadherin expression is characteristic of LC or is a feature of all dendritic cells (DC), we studied DC from various lymphoid tissues and peripheral blood for reactivity with anti-E-cadherin monoclonal antibody. By flow cytometry, DC prepared from skin-associated lymph nodes (LN) expressed E-cadherin, whereas DC prepared from gut-associated LN and spleen did not. However, direct comparison revealed that levels of E-cadherin expressed by DC from skin-associated LN were approximately fivefold lower than those expressed by freshly-prepared LC. Immunohistochemical studies confirmed that E-cadherin was expressed by DC in skin-associated LN in situ, and demonstrated that the number of E-cadherin+ DC in LN draining skin previously treated with the contact allergen 2,4,6-trinitrochlorobenzene was increased relative to the number of E-cadherin+ DC present in LN draining normal skin. DC propagated from the blood of cyclophosphamide-treated mice in granulocyte/macrophage-colony stimulating factor-supplemented media also expressed E-cadherin. E-cadherin immunoprecipitated from DC co-migrated in SDS polyacrylamide gels with that from fibroblasts transfected with murine E-cadherin cDNA, and mRNA encoding extracellular and intracellular regions of E-cadherin was present in DC propagated from blood. These results indicate that E-cadherin expressed by murine dendritic cells is identical to E-cadherin expressed by epithelial cells, and suggest that E-cadherin represents a DC differentiation antigen characteristic of LC and lineage-related cells (skin-associated LN DC).

Dose-dependent systemic and regional hemodynamic effects of calcitonin gene-related peptide.

The dose-response effects of infused calcitonin gene-related peptide (CGRP), a potent vasodilator, on systemic and regional hemodynamics in the conscious rat remain incompletely defined. The radioactive microsphere technique provided these determinations before and after the intravenous administration of vehicle or 22, 65, 220, and 2200 pmol of CGRP. Neither vehicle nor 22 pmol of CGRP significantly changed any systemic or regional hemodynamic parameter. Starting at the 65-pmol dose, CGRP significantly decreased mean blood pressure and total peripheral resistance, while increasing heart rate without changing cardiac output. CGRP produced selective regional vasodilatory effects, with the coronary circulation being unusually sensitive. In contrast, CGRP caused significant increases in blood flow to the mesenteric and cutaneous circulations only at the two highest doses. CGRP increased plasma norepinephrine, epinephrine, and renin activity significantly at only the 2200-pmol dose. In conclusion, CGRP decreases blood pressure by peripheral vasodilation, with a threshold dose occurring between 22 and 65 pmol. In addition, the coronary circulation appears to be particularly sensitive to the vasodilatory properties of CGRP.

Effect of galactose on systemic hemodynamics and blood flow rate in normal and tumor tissues in rats.

The effect of galactose on systemic hemodynamics and blood flow rate of Walker 256 carcinomas and several normal tissues of unanesthetized, unrestrained female Sprague-Dawley rats was measured, using the radioactive microsphere technique, prior to and at 30 and 60 min after galactose administration (6 g/kg body weight, i.v.). Whereas heart rate remained unchanged following injection, cardiac output (CO) and cardiac index decreased by 35% (P less than 0.05). Mean arterial pressure immediately decreased during the injection but then increased reaching a value 10% (P less than 0.05) above the baseline 30 min following injection. Stroke volume (SV) decreased by 30% (P less than 0.05) and total peripheral resistance increased by 65% (P less than 0.05). Redistribution of blood flow, expressed as %CO, among normal tissues was seen to the brain, kidneys, liver, jejunum, and hindlimb muscle and away from the pancreas, stomach, and skin. Changes in %CO to the spleen, colon, forelimb muscle, and peritumor tissue were not significant. Blood flow rate in most normal tissues either decreased or remained constant following injection. An exception was in the liver where blood flow significantly increased. Blood flow significantly decreased in the tumor (approximately 60%) and this reduction in blood flow was larger than the reduction in CO. These results suggest that (a) the effect of galactose on systemic hemodynamics and blood flow rate are similar to those produced by glucose; (b) reduction in blood flow rate in tumors is due to both systemic and local effects; and (c) changes in blood flow to normal tissues should not be disregarded when using galactose in combination with hyperthermia and/or chemotherapy for cancer treatment.

Systemic and regional hemodynamic effects of calcitonin gene-related peptide.

Calcitonin gene-related peptide, a 37-amino-acid neuropeptide, has been shown to be widely distributed in periadventitial nerves throughout the cardiovascular system, particularly in association with coronary arteries. In vivo and in vitro studies have demonstrated that calcitonin gene-related peptide possesses potent vasodilator properties. Circulating calcitonin gene-related peptide is derived primarily from periadventitial nerves, though its systemic and regional hemodynamic effects are unknown. In this study, systemic and regional hemodynamics were determined by the radioactive microsphere technique prior to and following the intravenous administration of 65-pmol and 2.2-nmol doses of calcitonin gene-related peptide and vehicle to three groups of conscious, unrestrained rats. Vehicle administration did not change any systemic or regional organ hemodynamic parameter determined. In contrast, 65 pmol and 2.2 nmol of calcitonin gene-related peptide significantly decreased mean blood pressure and total peripheral resistance and increased heart rate in a dose-dependent manner, while only slightly increasing cardiac output. Both 65-pmol and 2.2-nmol doses of calcitonin gene-related peptide significantly increased blood flow (percentage of cardiac output) to the heart. There was no difference in blood flow to the heart between the two doses. In addition, the 2.2-nmol dose of calcitonin gene-related peptide significantly increased blood flow to the stomach, liver, and skin and decreased it to the brain, kidneys, and spleen. In conclusion, calcitonin gene-related peptide infusion decreases blood pressure in a dose-dependent manner primarily by peripheral vasodilation. In addition, calcitonin gene-related peptide selectively changes regional organ blood flow, particularly to cause coronary vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)