SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
The sweat concentration of sodium was found to be inversely correlated with the amount of sweat obtained after a sweat test according to the method of Gibson & Cook in children without and with cystic fibrosis. Reference intervals for sweat sodium overlapped for the two groups but two-dimensional reference distributions for the amount of sweat (range 20-440 mg) correlated with its sodium content were completely separated. The establishment of similar distributions in centres carrying out sweat tests could serve to assess the performance of this investigation at local level.
Localizations of 18 antigens in normal sweat glands were analyzed. The antigens were roughly classified into 8 antigens: 1) distributed throughout the epithelial cells; 2) localized in whole sweat glands; 3) localized only in the secretory portion of sweat glands; 4) localized only in the inner cells of ductal portion of sweat glands; 5) localized in the myoepithelial cells; 6) localized only in the outer cells of dermal ducts of eccrine glands; 7) localized only seen in some of apocrine glands; 8) seen in the inflamed sweat glands. Based on these findings, I discussed about the forms and meanings of localization of those antigens.
Localizations of 18 antigens were analyzed in 41 cases with benign sweat gland tumors (13 with eccrine acrospiroma, 4 with eccrine spiradenoma, 2 with hidroacanthoma simplex, 9 with chondroid syringoma, 4 with syringocystadenoma papilliferum, 1 with tubular apocrine adenoma, 1 with papillary eccrine adenoma, 1 with apocrine cystadenoma, 1 with cylindroma, 5 with syringoma), 14 with malignant sweat gland tumors (7 with eccrine porocarcinoma, 3 with eccrine duct carcinoma, 3 with apocrine gland carcinoma, 1 with mucinous carcinoma) and 13 with extramammary Paget's disease. The results I obtained were compared with those in the normal sweat glands for determination of a differentiation of each tumor.
Explore the source record for details and available documents.
We studied pilocarpine-induced cholinergic sweating, emotional sweating and sympathetic reflex sweating in atopic dermatitis (AD) patients. Secreted sweat was measured both with equipment that continuously records sweat rate and with a filter paper method that measures sweat weight absorbed. Comparison of the two methods revealed that the filter paper method underestimated the sweat secretion in AD patients. While AD patients showed no significant abnormalities in emotional sweating and sympathetic reflex sweating, the duration of pilocarpine-induced sweating was prolonged. The time from the maximal sweat rate until the sweat rate fell to half of the maximal rate was significantly longer in AD patients than in control subjects. In contrast, the time from the beginning of sweat secretion until the maximal sweat rate was not significantly different between AD patients and control subjects. There was no significant difference between AD patients and control subjects in sweat volume secreted in 20 min after pilocarpine iontophoresis. In AD patients, the total sweat volume secreted after pilocarpine iontophoresis was greater than in control subjects, although not significantly. These results suggest that the system of deactivation of pilocarpine-induced sweat secretion is impaired in AD patients whereas the activation system is not altered.
Although cysteine proteinases have been reported to be present in human eccrine sweat, their endogenous inhibitors, cysteine proteinase inhibitors (CPIs), have remained unstudied. We now present evidence that CPIs are indeed a true ingredient of human eccrine sweat. Sweat induced in sauna was collected over a Vaseline barrier placed on the skin to minimize epidermal contamination. The absence of major epidermal contamination of the sweat was further ensured by monitoring an epidermal marker, high-molecular-mass aminopeptidase. Sweat CPI was purified sequentially by chromatography with Sephacryl S-200, carboxymethylated papain-Sepharose, and anion-exchange Mono Q fast-protein liquid chromatography columns. Sweat CPI has a molecular mass of approximately 15 kDa, is stable for temperature (up to 80 degrees C) and pH (from 3 to 10), and inhibits papain, ficin, and sweat cathepsin B- and H-like enzymes. Sweat CPI may be of sweat gland origin because 1) the rate of CPI output in sweat (CPI concentration x sweat rate) is constant over 45 min; 2) antibody against epidermal CPI, which cross-reacts with sweat CPI, localized immunoreactivity in the sweat duct; 3) CPI activity was present in the glandular extracts of control and methacholine-stimulated (for 1 h in vitro) human sweat glands; and 4) the peaks of CPI activity in the glandular extract and sweat CPI were both eluted (by high-pressure liquid chromatography) at around 15 kDa. Sweat CPI may be very similar to epidermal CPI (which belongs to the stefin family of CPIs) because of many shared characteristics. The identity and function of sweat CPI remain to be studied.
Explore the source record for details and available documents.
We wished to establish the presence of interleukin-1 (IL-1) in human sweat (5) and clarify its origin and mechanism of secretion. IL-1 alpha concentration ([IL-1 alpha]) in clean sweat from the back increased with the sweat rate, plateauing at the maximal sweat rate ([IL-1 alpha]max). The mean [IL-1 alpha]max was 545 pg/ml (n = 17) for men and 1,324 pg/ml for women in back sweat. The mean [IL-1 alpha]max for axillary sweat in men was 1,568 (n = 6). Palmar sweat was 9.2 ng/ml (n = 5) for IL-1 alpha and 7.9 ng/ml for IL-1 beta. [IL-1 alpha]max decreased to one-third that of the first sweat test, when second sauna sweat tests were conducted after 2 h of continuous sweating on the same day. Western blot analysis of the purified sweat IL-1 alpha fraction revealed bands at 17, 29, and 33 kDa. Immunoreactive IL-1 alpha was localized mainly in the secretory coil lumen, intercellular canaliculi, cytoplasm, mitochondria, and near plasma membranes. Polymerase chain reaction revealed the presence of IL-1 alpha mRNA in the sweat gland and in cultured human eccrine secretory coil cells. Both sweat IL-1 alpha and human recombinant IL-1 alpha at 500 pg/ml strongly stimulated interleukin-6 and interleukin-8 production in cultured fibroblasts. We conclude that the IL-1 alpha-like immunoreactive substance in sweat is IL-1 alpha itself, is derived from the sweat gland, and is biologically active at concentrations normally present in fresh sweat.
1. Sweat output has been measured continuously from four Welsh Mountain sheep exposed on several occasions for periods of 8 hr to air temperatures of 20, 30 and 40 degrees C. At all temperatures sweat was discharged intermittently. Discharges occurred more frequently at high air temperatures and when the animals were shorn, but not at consistently different frequencies in summer and winter.2. At 40 degrees C T(a), sweat discharges were initially large, decreased in size during the first 1-3 hr, and then continued at regular intervals and at an approximately constant size for the remainder of the experiments. Most, and probably all, sweat glands in the skin were active at each discharge.3. The volumes of sweat glands, determined histologically, decreased after prolonged activity in the heat. Comparison of the changes in sweat gland volumes with the amounts of sweat discharged led to conclusions that the decline in sweat output seen on initial exposure to heat was probably due to depletion of secretory fluid from storage within the gland and that the subsequent regular discharge of small amounts of sweat was due to expulsion of newly formed secretion.4. Examination of serial sections of midside skin revealed that in these sheep sweat glands consisted of a superficial non-convoluted duct separated from a large ampulla by a region in which the gland was convoluted. After long periods of sweating, the glands decreased in diameter in both the convoluted and non-convoluted regions but were never found to be empty.5. The pattern of sweat output from sheep during prolonged exposure to heat appears to be determined not only by processes of secretion and intermittent expulsion but also by the amount and rate of depletion of preformed sweat stored in the gland lumen.
Identification of body fluids is a common task in medico-legal practice, but specific markers for sweat have not been identified to date. To develop a method for identification of sweat, we identified a sweat-specific protein and produced monoclonal antibodies by immunizing mice with sweat proteins fractionated by anion-exchange chromatography. Among many sweat-reactive monoclonal antibodies obtained, one monoclonal antibody (G-81) was selected because of its unique specificity. G-81 reacted to sweat but not to other body fluids (e.g. serum, saliva, semen, milk, urine and tears) in ELISA. G-81 specifically stained the eccrine sweat gland and did not stain any other tissue including the apocrine sweat gland. In western blotting, G-81 reacted strongly to a 7 kDa band and faintly to 20, 27 and 33 kDa bands of sweat protein. The N-terminal amino acid sequence (18 amino acids) of G-81-reactive peptides was determined, and an identical sequence was found in an antibiotic peptide dermcidin (110 amino acids) reported recently, suggesting that G-81 recognized a fragment of dermcidin. The G-81-reactive peptide could be detected in 8,192-fold dilutions of sweat by ELISA and could be detected in 200-fold diluted sweat samples ( n=26) independent of the protein concentration. The G-81-reactive peptide was very stable and was able to detect sweat stains left for at least 11 weeks at room temperature without substantial loss of reactivity. These facts suggest that G-81 is a very useful tool for sweat identification in medico-legal practice.
Sweat rates on the forearm and on the palm were simultaneously recorded by resistance hygrometry and the mode of sweating in these areas in response to thermal and non-thermal stimuli were compared with each other. In Series A, periodic infrared irradiation (1 min on, 1 min off) was done to the back of the trunk, and reflex responses in sweat rate were recorded on both test areas. A high correlation was noted between the mean changes in the palmar sweat rate and those in the forearm one during the irradiation cycle in a majority of cases. However the magnitude of the sweat response was much less on the palm than on the forearm. These observations reveal that the central mechanism of palmar sweating may be affected to some extent by the thermoregulatory mechanism. Series B was concerned with the pattern of response in forearm sweating to various non-thermal stimuli. Careful observations showed that the forearm sweating responded diversely to various mental stimuli, unlike the palmar sweating whose response was always an increase. Mental arithmetic, mental testing and physical exercise caused an immediate increase in the palmar sweating but often elicited a transient decrease in the forearm sweating, whereas pain, noise, and emotional stimuli consistently provoked an increase of sweating on the forearm as well as on the palm. These observations suggest that the activities of higher centers, presumably involving neocortex and limbic cortex, exert various influences on the central mechanisms of palmar and generalized sweating.
This study was designed to examine whether or not the total body sweat rate can be used as a practical index for prescribing exercise. The sweat rate was experimentally studied in relation to factors such as intensity of exercise, the secretory capacity of sweating mechanism, and body temperature. After determining the maximum sweating rate on the whole body surface, regarded as the secretory capacity of the sweating mechanism, each physically trained subject was made to pedal a bicycle ergometer for 60 min at each of several kinds of mechanical work rates under fixed hot climatic conditions in summer. Total body sweat rate, rectal temperature, and RMR were measured during the experiment. The sweat secreting index (SSI), which is ratio of total body sweat rate to maximum sweat rate, was calculated, and was presumed to indicate the functioning rate of sweat secretory capacity. The total body sweat rate responded to factors such as RMR, SSI, and rectal temperature with a high correlation coefficient. From these results it was concluded that the total body sweat rate can be used as a practical index for prescribing exercise.
The basic mechanisms of sweat gland function and an updated review of some relatively common disorders of sweat secretion, are presented. Although sweat secretion and ductal absorption are basically biophysical and biologic cellular processes, a detailed description of the basic biophysical principles of membrane transport has been avoided to make the discussion more readable. The cited references will, however, help those readers primarily interested in the basic details of sweat gland function. Part I of this article includes a discussion of morphologic characteristics, central and peripheral nervous control of sweat secretion, neurotransmitters, intracellular mediators and stimulus secretion coupling, Na-K-Cl cotransport model for the ionic mechanism of sweat secretion, ingredients of sweat, ductal function, the pathogenesis of abnormal sweat gland function in cystic fibrosis, and the discovery of the apoeccrine sweat gland. Part II, to be published in the May issue of the Journal, reviews reports of all those major disorders of hyperhidrosis and hypohidrosis that have appeared in the literature during the past 10 years. It is hoped that this review will serve as a resource for clinicians who encounter puzzling disorders of sweating in their patients, as well as for investigators who wish to obtain a quick update on sweat gland function.
Functional characteristics of isolated single human axillary apoeccrine sweat glands have been studied using in vitro sweat induction methods. Sustained copious clear fluid secretion was evoked by methacholine (MCh), epinephrine (EP), isoproterenol (ISO), and phenylephrine (PL) in decreasing order in a pharmacologically specific manner. Apoeccrine glands showed a higher cholinergic sensitivity than eccrine sweat glands, as shown by the apparent association constant for MCh of 2.7 X 10(-7) M compared with 2.1 X 10(-6) M for the axillary eccrine sweat gland. The average total sweat rate of the apoeccrine gland for a 30-min period was sevenfold higher than that of the eccrine sweat gland. In contrast, isolated apocrine glands showed intermittent pulsatile turbid sweat secretion in response to MCh or EP. The Na+ and K+ concentration of apoeccrine glands was nearly isotonic, whereas those of apocrine sweat was 120-140 mM for Na+ and 10-20 mM for K+. Apoeccrine ductal Na+ absorption was also observed in the apoeccrine glands and was no more efficient than that of the axillary eccrine sweat gland. Thus apoeccrine sweat glands are functionally and pharmacologically distinct from axillary apocrine glands and significantly contribute to overall axillary sweating in humans.
Apocrine and eccrine sweat glands are distinct in function, although they are closely related to each other developmentally and morphologically. In certain sweat gland tumors, it is difficult to differentiate between eccrine or apocrine sweat glands. Therefore, this paper reviews histochemical and immunohistochemical markers to differentiate apocrine and eccrine sweat glands with the aim of better understanding the structural and functional characteristics of these sweat glands. Specific markers for apocrine sweat glands are as follows: neuraminidase sensitive anionic sites detected by cationic colloidal gold at pH 2.0, and mitochondrion-like secretory granules that have epidermal growth factor-like antigenicity. The following antibodies react with apocrine sweat glands but not with eccrine sweat glands; the antibodies raised against 70 kDa glycoprotein purified from human milk fat globule membranes, and HMFG-1 (1.10.F3) monoclonal antibody produced by immunizing mice with defatted human milk fat globule membranes. Markers for eccrine sweat glands are as follows: dark cell granules that have chondroitinase ABC sensitive anionic sites detected by cationic gold at pH 2.0 after pretreatment with EGTA, and intercellular canaliculi with high activity of alkaline phosphatase. CEA and GCDFP-15 are expressed in both eccrine and apocrine sweat glands. Anti-EMA monoclonal antibody (E29) stains both eccrine and apocrine sweat glands.
Previous studies suggest that the sympathetic innervation of the sweat glands in the rat is initially noradrenergic and during development undergoes a transition in neurotransmitter phenotype to become cholinergic. To characterize this system and its development further, we have examined the adrenergic and cholinergic components of the secretory response in adult and immature rats and have studied the onset of sweating in the plantar sweat glands of developing rats. Stimulation of the sciatic nerve in adult rats elicited a secretory response which was completely blocked by the cholinergic antagonist, atropine, and was unaffected by adrenergic antagonists, indicating that nerve-evoked secretion was cholinergic. In adult rats, the sweat glands were quite sensitive to cholinergic agonists. In addition to acetylcholine, the mature sweat gland innervation contains vasoactive intestinal peptide (VIP). In some rats, the injection of VIP alone elicited a secretory response which was blocked by atropine, suggesting that the response to VIP was mediated cholinergically. In contrast to cholinergic agonists, the glands responded relatively infrequently and with reduced volumes of sweat to the alpha- and beta-adrenergic agonists 6-fluoronorepinephrine and isoproterenol. However, when VIP, which is a potent vasodilator, was simultaneously injected with adrenergic agonists, glands in many of the injected footpads exhibited a secretory response. The response to adrenergic agonists in combination with VIP was reduced by atropine and by phentolamine plus propranolol, but was blocked completely only by a combination of the three antagonists, indicating that both adrenergic and cholinergic mechanisms were involved. In immature rats, sweating evoked by nerve stimulation first appeared at 14 days of age in 25% of the rats tested. Both the percentage of rats sweating and the number of active glands increased rapidly. At 16 days, 50% of the rats tested exhibited some active glands, and by 21 days all rats tested exhibited a secretory response. In 16-day-old rats, nerve-evoked sweating was almost completely inhibited by local injection of 1 microM atropine, but was unaffected by phentolamine and propranolol in concentrations up to 10 microM. Similarly, the glands were sensitive to 10 microM muscarine, but they exhibited no secretory response to the alpha-adrenergic agonists, clonidine and 6-fluoronorepinephrine, nor to the beta-adrenergic agonist, isoproterenol, at concentrations up to 50 microM. The simultaneous injection of VIP with adrenergic agonists did not reveal an adrenergically mediated secretory response in 16-day-old animals.(ABSTRACT TRUNCATED AT 400 WORDS)
Secretory immunoglobulin A (sIgA) plays an important role in local immune defense mechanisms. Although skin is always exposed to external antigens, the role of local immune defenses involving sIgA in the skin has not been adequately studied. In order to evaluate the presence of sIgA in sweat, we have measured the concentration of sIgA in human sweat by enzyme immunoassay and have localized the components of sIgA in the sweat glands of human axillary skin. The concentration of sIgA in sweat was found to be 10 times higher in men than in women (13.0 +/- 0.9 micrograms/ml versus 1.6 +/- 0.9 micrograms/ml). Secretory component (SC) was localized immunohistochemically in protein synthetic organelles, such as the perinuclear spaces and Golgi complex, in cytoplasmic vesicles, and along the external surface membranes of mucous cells on the terminal segment of eccrine sweat glands. IgA and J chain were present in plasma cells in the protein synthetic organelles. The luminal aspects of eccrine sweat ducts also strongly express SC, as well as IgA and J chain. Neither SC, IgA, or J chain were identified in epithelial cells of apocrine sweat glands. These findings are consistent with the theory that J chain complexed with dimeric IgA is synthesized in plasma cells and is transported by SC-mediated endocytosis transfer across mucous cells of eccrine sweat glands and thus into sweat.