GFR and the concentration of urine in the absence of vasopressin. Berliner-Davidson re-explored

Robert W. Berliner made many important contributions to our understanding of the urinary concentrating mechanism. Among these, one must number his demonstration that urine can be rendered hyperosmotic to plasma even when vasopressin is absent, as well as his definition of the role of the glomerular filtration rate (GFR) in the concentrating process [1, 2]—points that had also been suggested by several other investigators [reviewed in 3, 4]. In postulating how urine might be concentrated without vasopressin purely by changes occurring within the kidney [1], Dr. Berliner expressed the essence of a message, which we still tend to overlook today, namely, that “…although it is commonly stated that the function of ADH is to cause the excretion of a hypertonic urine, its more important function might be better defined as preventing the excretion of a dilute urine.”The availability of the Brattleboro rat, which has an inherited deficiency for synthesizing vasopressin [5], made it possible to further explore the mechanisms by which urine can be concentrated in the apparent absence of the hormone. We here review these experiments, paying special attention to the role of GFR in the process

A review of the design and clinical evaluation of the ShefStim array-based functional electrical stimulation system

Functional electrical stimulation has been shown to be a safe and effective means of correcting foot 12 drop of central neurological origin. Current surface-based devices typically consist of a single channel stimulator, 13 a sensor for determining gait phase and a cuff, within which is housed the anode and cathode. The cuff-mounted 14 electrode design reduces the likelihood of large errors in electrode placement, but the user is still fully responsible 15 for selecting the correct stimulation level each time the system is donned. Researchers have investigated different 16 approaches to automating aspects of setup and/or use, including recent promising work based on iterative learning 17 techniques. This paper reports on the design and clinical evaluation of an electrode array-based FES system for 18 the correction of drop foot, ShefStim. The paper reviews the design process from proof of concept lab-based study, 19 through modelling of the array geometry and interface layer to array search algorithm development. Finally, the 20 paper summarises two clinical studies involving patients with drop foot. The results suggest that the ShefStim 21 system with automated setup produces results which are comparable with clinician setup of conventional systems. 22 Further, the final study demonstrated that patients can use the system without clinical supervision. When used 23 unsupervised, setup time was 14 minutes (9 minutes for automated search plus 5 minutes for donning the 24 equipment), although this figure could be reduced significantly with relatively minor changes to the design

Evaluation of pre-game hydration status, heat stress, and fluid balance during professional soccer competition in the heat

This study evaluated initial hydration status (stadium arrival urine specific gravity), fluid balance (pre- and post-game nude body weight, fluid intake, urine collection), and core temperature changes (pre-game, half-time, post-game) during a professional soccer game. We monitored 17 male players (goalies included) between stadium arrival and game end (3h), playing at 34.9°C and 35.4% relative humidity, for an average Wet Bulb Globe Temperature (WBGT) heat stress index of 31.9°C. Data are mean ± SD (range). Initial urine specific gravity (USG) was 1.018 ± 0.008 (1.003-1.036); seven players showed USG ≥ 1.020. Over the three hours, body mass (BM) loss was 2.58 ± 0.88kg (1.08-4.17kg), a dehydration of 3.38 ± 1.11%BM (1.68-5.34%BM). Sweat loss was 4448 ± 1216mL (2950-6224mL), vs. fluid intake of 1948 ± 954mL (655-4288mL). Despite methodological problems with many players, core temperatures greater than or equal to 39.0°C were registered in four players by halftime, and in nine by game’s end. Many of these players incurred significant dehydration during the game, compounded by initial hypohydration; thermoregulation may have been impaired to an extent we were unable to measure accurately. We suggest some new recommendations for soccer players training and competing in the heat to help them avoid substantial dehydration.Gatorade Sports Science Institute//Universidad de Costa Rica VI-245-A4-303UCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias Sociales::Centro de Investigación en Ciencias del Movimiento Humano (CIMOHU

On the role of antidiuretic hormone in the inhibition of acute water diuresis in adrenal insufficiency and the effects of gluco- and mineralocorticoids in reversing the inhibition

In order to determine whether or not antidiuretic hormone (ADH) is essential to the inhibition of an acute water diuresis in adrenal insufficiency, the response to oral water loads was tested in rats with hereditary hypothalamic diabetes insipidus (DI) which lack ADH. It was found that 60 min after water loads of 3 or 5% of body weight urine flow was significantly lower and urine osmolality significantly higher in adrenalectomized DI rats than in the same DI rats before removal of their adrenal glands. The efficacy of gluco- and mineralocorticoids in reversing the inhibition was then determined in the same adrenalectomized DI rats. Prednisolone alone, administered either acutely or chronically, restored the response in urine flow to that seen in the same rats before adrenalectomy, but failed to correct the defect in urinary dilution. Aldosterone when given alone tended to correct the diluting ability but not the response in urine flow. When these two adrenal cortical hormones were given simultaneously, both the urine flow and urine osmolality were nearly identical to what they had been in the same DI rats before adrenalectomy. These studies strongly suggest (a) that ADH is not essential to the inhibition of an acute water diuresis in adrenal insufficiency, although it may abet the inhibition in individuals without diabetes insipidus, which can elaborate ADH; and (b) that both gluco- and mineralocorticoids are required in adrenal insufficiency in order to fully restore the water diuresis as judged by the dual criteria of urine flow and urine osmolality