scholarly journals Wilson protein expression, copper excretion and sweat production in sweat glands of Wilson disease patients and controls

2008 ◽  
Vol 8 (1) ◽  
Author(s):  
Mark Schaefer ◽  
Mavi Schellenberg ◽  
Uta Merle ◽  
Karl Heinz Weiss ◽  
Wolfgang Stremmel
1979 ◽  
Vol 92 (2) ◽  
pp. 511-512 ◽  
Author(s):  
A. K. Rai ◽  
B. S. Mehta ◽  
M. Singh

Although sheep combat thermal stress mainly by panting, a sizeable amount (40%) of total evaporative heat loss, is from sources other than panting (Hales & Brown, 1974). The frequency of sporadic discharge of sweat glands increases with increase in ambient temperature and is accompanied by a decline in respiration rate (Bligh, 1961). The wool coat can reduce evaporative cooling but sweating may have cooling value in sheep breeds with open fleeces (Rai, Singh & More, 1978). In sheep, the number and size of the sweat glands (Waites & Voglmayr, 1962) and the quantum of sweat production in a particular time period (Ghoshal et al. 1977) varies in different body regions. In view of the possible significance of surface evaporative cooling, thermal sweating in different body regions of sheep was investigated.


1988 ◽  
Vol 65 (2) ◽  
pp. 811-814 ◽  
Author(s):  
M. J. Buono ◽  
N. T. Sjoholm

The purpose of this study was to determine the in vivo secretory activity of sweat glands from sedentary and trained subjects. Peripheral sweat production was determined using pilocarpine iontophoresis in 40 volunteers (10 sedentary men, 10 endurance-trained men, 10 sedentary women, 10 endurance-trained women). Peripheral sweat rate was significantly (P less than 0.05) greater in trained men [6.9 +/- 0.6 (SE) g.m2.min-1] and women (6.1 +/- 0.7) compared with sedentary men (3.1 +/- 0.5) and women (2.5 +/- 0.4). Furthermore, peripheral sweat rate was significantly correlated (r = 0.73) with maximal O2 uptake. The above two findings would suggest that physical training improves the secretory activity of the human sweat gland. Such a result supports previous findings that have suggested that the potentiation in sweating seen after training is achieved via a peripheral mechanism. In addition, several gender-related differences were found in the sudorific response of men and women. Specifically, women have a significantly greater sweat gland density, whereas men have a greater sweat production per gland.


2010 ◽  
Vol 42 ◽  
pp. S373
Author(s):  
G. Ranucci ◽  
E. Nicastro ◽  
C. Della Corte ◽  
M. Tufano ◽  
P. Vajro ◽  
...  

2012 ◽  
Vol 53 (6) ◽  
pp. 961-968 ◽  
Author(s):  
R. Bahde ◽  
S. Kapoor ◽  
K. K. Bhargava ◽  
M. L. Schilsky ◽  
C. J. Palestro ◽  
...  

2009 ◽  
Vol 297 (4) ◽  
pp. R1082-R1085 ◽  
Author(s):  
Michael J. Buono ◽  
Travis R. Numan ◽  
Ryan M. Claros ◽  
Stephanie K. Brodine ◽  
Fred W. Kolkhorst

We investigated whether the eccrine sweat glands must actively produce sweat during heat acclimation if they are to adapt and increase their capacity to sweat. Eight volunteers received intradermal injections of BOTOX, to prevent neural stimulation and sweat production of the sweat glands during heat acclimation, and saline injections as a control in the contralateral forearm. Subjects performed 90 min of moderate-intensity exercise in the heat (35°C, 40% relative humidity) on 10 consecutive days. Heat acclimation decreased end-exercise heart rate (156 ± 22 vs. 138 ± 17 beats/min; P = 0.0001) and rectal temperature (38.2 ± 0.3 vs. 37.9 ± 0.3°C; P = 0.0003) and increased whole body sweat rate (0.70 ± 0.29 vs. 1.06 ± 0.50 l/h; P = 0.030). During heat acclimation, there was no measurable sweating in the BOTOX-treated forearm, but the control forearm sweat rate during exercise increased 40% over the 10 days ( P = 0.040). Peripheral sweat gland function was assessed using pilocarpine iontophoresis before and after heat acclimation. Before heat acclimation, the pilocarpine-induced sweat rate of the control and BOTOX-injected forearms did not differ (0.65 ± 0.20 vs. 0.66 ± 0.22 mg·cm−2·min−1). However, following heat acclimation, the pilocarpine-induced sweat rate in the control arm increased 18% to 0.77 ± 0.21 mg·cm−2·min−1 ( P = 0.021) but decreased 52% to 0.32 ± 0.18 mg·cm−2·min−1 ( P < 0.001) in the BOTOX-treated arm. Using complete chemodenervation of the sweat glands, coupled with direct cholinergic stimulation via pilocarpine iontophoresis, we demonstrated that sweat glands must be active during heat acclimation if they are to adapt and increase their capacity to sweat.


2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Muhammad M Ahsan ◽  
Tara Thompson ◽  
Chandralekha Ashangari ◽  
Amer Suleman

Background: Postural Orthostatic Tachycardia Syndrome (POTS) is a form of dysautonomia that is estimated to impact between 1,000,000 and 3,000,000 Americans and millions more around the world. Symptoms often include orthostatic intolerance such as dizziness, fatigue, excessive sweating and many others. The aim of this study is to determine the Q-sweat study in POTS patients. Methods: This study was a randomized, single-blind study. Patients evaluated between October 2014 to June 2015 were included. The skin on the leg and wrist is wiped with acetone, then alcohol and dried, cleaning the skin in preparation for the test. Four electrodes filled with acetylcholine are placed on three areas of the leg and one area on the wrist. A mild electrical current called iontophoresis is then applied to help the drug stimulate the sweat glands. This evokes sweating at the site, but it also allows the body to release its own acetylcholine, resulting in sweat production at nearby sites. After a stimulus (e.g. a deep breath) any deviation from the baseline is reported. If no change is seen, a stronger stimulus is applied (e.g. electrical stimulation) and if there is still no change seen, an “absent response” is reported. The onset latency and magnitude of response can be quantified, although the results are highly variable within and between subjects. The sweat response is measured Q-sweat recordings of Left proximal leg, Left distal leg and Left foot sites were analyzed. Results are categorized as Normal response, no response, hung up and prolong response. Results: A total 144 POTS patients were included, Out of 144 POTS patients 88% are females (n=127, mean age 31.93±12.37) and 12% are males (n=17, mean age 31.59±11.14), Left proximal leg site 69/144(48%) Patients had hung up, 8/144(6%) had No response, 29/144(20%) had Normal, 38/144(26%) had Prolong. Left distal leg site 72/144(50%) had hung up, 13/144(9%) had No response, 23/144(16%) had Normal, 36/144(25%) had Prolong. Left foot site 36/144(25%) had hung up, 35/144(24%) had No response, 40/144(28%) had Normal, 33/144(23%) had Prolong response. Conclusion: Postural Orthostatic Tachycardia Syndrome had a higher percentage of patients with Hung up response.


2019 ◽  
Vol 42 (2) ◽  
pp. 371-380 ◽  
Author(s):  
Jan Pfeiffenberger ◽  
Christine Marie Lohse ◽  
Daniel Gotthardt ◽  
Christian Rupp ◽  
Markus Weiler ◽  
...  

2019 ◽  
Vol 40 (2) ◽  
pp. 59-77 ◽  

Wilson disease (WD) is an autosomal recessively-inherited disorder of copper metabolism and characterised by a pathological accumulation of copper. The ATP7B gene encodes for a transmembrane copper transporter essential for biliary copper excretion. Depending on time of diagnosis, severity of disease can vary widely. Almost all patients show evidence of progressive liver disease. Neurological impairments or psychiatric symptoms are common in WD patients not diagnosed during adolescence. WD is a treatable disorder, and early treatment can prevent the development of symptoms in patients diagnosed while still asymptomatic. This is why the early diagnosis of WD is crucial. The diagnosis is based on clinical symptoms, abnormal measures of copper metabolism and DNA analysis. Available treatment includes chelators and zinc salts which increase copper excretion and reduce copper uptake. In severe cases, liver transplantation is indicated and accomplishes a phenotypic correction of the hepatic gene defect. Recently, clinical development of the new copper modulating agent tetrathiomolybdate has started and direct genetic therapies are being tested in animal models. The following review focuses especially on biochemical markers and how they can be utilised in diagnosis and drug monitoring.


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