No description available.

Aging is associated with attenuated sweat gland function, which has been suggested to occur in a peripheral-to-central manner. However, evidence supporting this hypothesis remains equivocal. We therefore revisited this hypothesis by evaluating sweat rate across the limbs and trunk in young and older men during whole-body, passive heating. A water-perfused suit was used to raise and clamp esophageal temperature at 0.6°C (low-heat strain) and 1.2°C (moderate-heat strain) above baseline in 14 young (24 [SD 5] years) and 15 older (69 [4] years) men. Sweat rate was measured at multiple sites on the trunk (chest, abdomen) and limbs (biceps, forearm, quadriceps, calf) using ventilated capsules (3.8 cm²). Sweat rates, expressed as the average of 5 min of stable sweat rate at low- and moderate-heat strain, were compared between groups (young, older) and regions (trunk, limbs) within each level of heat strain using a linear mixed-effects model with nested intercepts (sites nested within region nested within participant). At low-heat strain, the age-related reduction in sweat rate (older-young values) was greater at the trunk (0.65 mg/cm²/min [95% CI 0.44, 0.86]) compared to the limbs (0.42 mg/cm²/min [0.22, 0.62]; interaction: p=0.010). At moderate-heat strain, sweat rate was lower in the older compared to young (main effect: p=0.025), albeit that reduction did not differ between regions (interaction: p=0.888). We conclude that, contrary to previous suggestions, the agerelated decline in sweat rate was greater at the trunk compared to the limbs at lowheat strain, with no evidence of regional variation in that age-related decline at moderate-heat strain.

No description available.

Pressure ischemia is a medical condition characterised by the necrosis of the skin and underlying tissues in body areas exposed to prolonged pressure. This condition leads to the development of bedsores and affects 9% of hospitalised patients, costing the NHS between £1.4 and £2.1 billion per year. The severity of pressure ischemia has been linked to the concentration of sweat lactate, a product of sweat gland metabolism under anaerobic conditions, such as hypoxia. Normal levels of lactate in human sweat are 20±7 mM, but under ischemic conditions these can rise up to approximately 70 mM. This project presents the development of a novel flexible electrochemical enzyme-based biosensor for the continuous and non-invasive monitoring of sweat lactate with the potential for becoming a body-worn device for the early detection of pressure ischemia onset. The core of the recognition system is a flexible laminate, comprising two highly porous polycarbonate membranes, which provide support for the lactate oxidase enzyme, immobilised via covalent cross-linking. Oxidation of lactate produces H2O2, which is subsequently determined electrochemically. The transducer comprises a two-electrode system on a single flexible polycarbonate membrane, sputter-coated with gold (CE/RE) and platinum (WE) to render it conductive. The developed design has been improved through investigation into different factors regarding the immobilisation method of the enzyme in the laminate and the lowering of interferences from oxidising compounds present in sweat. The sensing system exhibits lactate selectivity at physiologically relevant concentrations in sweat for pressure ischemia (0–70 mM), with good reproducibility (7.2–12.2% RSD) for a hand-manufactured device. The reliability of the sensor’s performance and the capability to detect lactate fluctuations on human sweat samples has been demonstrated. The sensing system showed excellent operational and mechanical stability. The application of Nafion® on the WE lowered interferences from ascorbic acid and uric acid by 96.7 and 81.7% respectively. These results show promise towards the further development of a body-­‐worn monitoring device for determining lactate levels in undiluted human sweat samples in a reproducible, fast and accurate manner.

Ventilated capsules (i.e. hygrometry) are widely used to measure time dependent changes in local sweat rate. Despite this, understanding of the reliability (consistency) of local sweat rate is limited to the forearm during mild hyperthermia. Further, extensive regional heterogeneity in sweating may render some regions more reliable than others. Knowledge of reliability has important implications for experimental design, statistical analysis and interpretation, yet it is relatively unknown. The purpose of this study was to determine local sweat rate across various regions of the body and the reliability of these responses, during increasing levels of hyperthermia. On three separate instances, fourteen young men (age: 24 [SD 5] years) donned a whole-body water perfusion suit to raise and clamp esopogheal temperature at elicit low (+0.6°C), moderate (+1.2°C) and high (+1.8°C) levels of heat strain. Local sweat rate was measured at the forehead, chest, abdomen, bicep, forearm, hand, quadriceps, calf, and foot via ventilated capsules (3.8 cm2). Absolute reliability was assessed using coefficient of variation (CV%) which quantifies the amount of error in a given measurement. Relative reliability was evaluated via the intraclass correlation coefficient (ICC); the consistency of an individual’s rank within a group during repeated measurements. At low heat strain, most sites demonstrated acceptable relative (ICC ≥0.70), and moderate absolute reliability (CV <25%). At moderate-heat strain, the abdomen, hand, quadriceps, calf and foot had acceptable relative reliability while the forehead, abdomen, forearm, hand and quadriceps had moderate absolute reliability. At high-heat strain, relative reliability was acceptable at the abdomen, quadriceps, calf, foot and absolute reliability was moderate at the chest, abdomen, forearm, hand, quadriceps, calf and foot. Our findings indicate that reliability of local sweat rate is dependent on both measurement site and level of hyperthermia. Researchers should consider this in their experimental design to increase the likelihood of detecting an effect of an intervention if one exists.

No description available.

Pressure ischemia is a medical condition characterised by the necrosis of the skin and underlying tissues in body areas exposed to prolonged pressure. This condition leads to the development of bedsores and affects 9% of hospitalised patients, costing the NHS between £1.4 and £2.1 billion per year. The severity of pressure ischemia has been linked to the concentration of sweat lactate, a product of sweat gland metabolism under anaerobic conditions, such as hypoxia. Normal levels of lactate in human sweat are 20±7 mM, but under ischemic conditions these can rise up to approximately 70 mM. This project presents the development of a novel flexible electrochemical enzyme-based biosensor for the continuous and non-invasive monitoring of sweat lactate with the potential for becoming a body-worn device for the early detection of pressure ischemia onset. The core of the recognition system is a flexible laminate, comprising two highly porous polycarbonate membranes, which provide support for the lactate oxidase enzyme, immobilised via covalent cross-linking. Oxidation of lactate produces H2O2, which is subsequently determined electrochemically. The transducer comprises a two-electrode system on a single flexible polycarbonate membrane, sputter-coated with gold (CE/RE) and platinum (WE) to render it conductive. The developed design has been improved through investigation into different factors regarding the immobilisation method of the enzyme in the laminate and the lowering of interferences from oxidising compounds present in sweat. The sensing system exhibits lactate selectivity at physiologically relevant concentrations in sweat for pressure ischemia (0–70 mM), with good reproducibility (7.2–12.2% RSD) for a hand-manufactured device. The reliability of the sensor’s performance and the capability to detect lactate fluctuations on human sweat samples has been demonstrated. The sensing system showed excellent operational and mechanical stability. The application of Nafion® on the WE lowered interferences from ascorbic acid and uric acid by 96.7 and 81.7% respectively. These results show promise towards the further development of a body-­‐worn monitoring device for determining lactate levels in undiluted human sweat samples in a reproducible, fast and accurate manner.

The human eccrine sweat gland is present on most body sites and is crucial for thermoregulation. Yet, little is known on the mechanisms that govern its function and its morphogenesis. The main reason for the lack in research with regards to the human eccrine gland is the difficulty in isolation and maintenance of the glands and cells in vitro. Only one other cell line derived from the human eccrine gland has ever been reported, the NCLSG3 cell line. NCL-SG3 cells do not however, function like native eccrine secretory coil cells, and thus a better cell model was required. In this project, a human eccrine secretory coil cell line, the EC23 cell line, was developed, along with 8 clones derived from said cell line. EC23 cells and their clones express a panel of markers characteristic of the human eccrine sweat gland secretory coil cells. Furthermore, calcium fluxes can be elicited by cholinergic stimulation of the cells suggesting retention of the native secretory cell phenotype unlike NCL-SG3 cells. The EC23 cell line is also responsive to adrenergic stimuli to a higher degree than NCL-SG3 cells, especially clone 2, however all the cell lines responded significantly less than primary eccrine secretory coil cells upon isoproterenol stimulation. It was also found that the mesenchyme has a crucial effect in determining the formation of eccrine like down-growths in Matrigel organotypic models seeded with EC23 cells, where organotypics made with adult fibroblasts failed to form down-growths in comparison to neonatal fibroblasts. Furthermore, the co-culture of EC23 cell with keratinocytes enhanced the amount of downgrowth. EC23 cells have the capacity to form branching structures that resemble native eccrine glands in GFR Matrigel supplemented with EGF and EDA, and to a lesser extent BMP4. In conclusion it was demonstrated that the EC23 cells can be used as a model to study the human eccrine gland, in particular the secretory coil.

No description available.

No description available.