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PubMed1999

A collection method and high-sensitivity enzyme immunoassay for sweat pyridinoline and deoxypyridinoline cross-links.

BACKGROUND: Collagen cross-link molecules such as pyridinoline (PYD), deoxypyridinoline (DPD), and N-terminal cross-linked peptides (NTX) have been measured in urine as indices of bone resorption. However, very little is known regarding the excretion of pyridinolines into other biological fluids. We report a collection device, normalizing analyte, and high-sensitivity immunoassay for quantitative analysis of free pyridinoline cross-links in sweat. METHODS: Flame atomic emission and ion-selective electrode techniques were used to measure potassium as a sweat volume marker. The Pyrilinks immunoassay for urine free pyridinolines was optimized to increase sensitivity for measurements in sweat. The precision, accuracy, and detection limit of this assay were characterized. To assess values and variability of sweat pyridinolines in human subjects, a nonocclusive skin patch was used to collect sweat samples from a reference group and from a mixed group experiencing accelerated bone resorption, postmenopausal women and men receiving gonadotropin-releasing hormone for prostate cancer. RESULTS: The immunoassay intra- and interassay variations were </=10% and <16%, respectively, with a detection limit of 309 pmol/L. Linearity upon dilution and analytical recovery ranged from 93% to 109% and 85% to 122%, respectively. Sweat PYD values normalized to potassium output yielded a weekly intraindividual biological variability of 14.7%. The mean increase in the population experiencing increased bone resorption vs the reference group was 36% (P <0.05) for sweat PYD/K vs 23-40% (P <0.05) for urinary PYD/Cr, DPD/Cr, and NTX/Cr. CONCLUSION: We conclude that this new platform sweat collection technology and PYD immunoassay show potential as an indicator of bone resorption.

Amino Acids↗

PubMed1991

[The effect of ageing on the active sweat gland density in the dorsum of foot].

Focal sweating in the dorsum of foot induced by iontophoresis of 1% pilocarpine was quantitatively evaluated using silastic impression mold technique in 111 control subjects (71 men & 40 women), aged 14 to 89 years, to reveal the effect of aging on the density of active sweat glands. The subjects were divided into four groups (group I: aged 14 to 29 years, group II: aged 30 to 49 years, group III: aged 50 to 69 years, group IV: aged 70 to 89 years), and the difference of the density of active sweat glands was evaluated among the groups with Wilcoxon's rank sum test. It was statistically significant (p less than 0.001) between group II and III, and between group III and IV, but not significant between group I and II. Therefore, it was concluded that the density of active sweat glands decreases prominently after 50 years of age. The density of active sweat glands was not significantly different between man and woman in each group. In the regression analysis of the density of active sweat glands on age, the relationship (Density = -0.0178.Age2 + 232.6 (R2 = 0.54), p less than 0.0001) was obtained. Based on such relationship, the predicted density and the upper and lower limits of 95% confidence interval of the predicted density for each age were obtained. These results indicate that decrease of the density of active sweat glands due to ageing should be taken into consideration in the evaluation of the density of active sweat glands in the dorsum of foot among the patients with various neurological diseases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMedDate not supplied

[Excretion of nitrogen compounds in sweat during a sauna].

The aim of the study was to determine a loss of nitrogen compounds with sweat in sauna and to estimate their plasma concentration. Sweat was collided during 30 min stay in sauna. Blood was taken before and immediately after the sauna. Concentrations of ammonia, urea, creatinine and uric acid were determined in the both fluids. It has been found, that the concentration of ammonia in sweat exceeds, that in plasma by 77 times. Ammonia plasma concentration following sauna increased by about 60%. Sweat urea concentration exceeded that in plasma by 3.5 times. Plasma urea concentration was significantly reduced after sauna. Sweat creatinine concentration was about two times higher than that in plasma. No uric acid was detected in sweat. Sweating did not affect plasma creatinine and uric acid concentrations. Results indicate that considerable amount of nitrogen is lost with sweat during sauna.

Adult↗

PubMed1985

Promotion of palmar sweating with oral phosphatidylcholine.

Since acetylcholine is the main neurotransmitter of eccrine sweating, phosphatidylcholine ingestion might increase sweating. In 10 adults mid-palmar sweating was measured 12 hours after ingestion of a high and a low phosphatidylcholine supper. In a double blind, crossover study, mid-palmar sweating was measured in 11 consenting adults 12 hours after a low phosphatidylcholine supper taken with either lecithin or placebo. Five minutes after cleaning the palm and drying, sweat was captured in a quick-drying plastic film. The film was removed with cellophane tape and placed on a glass slide. Mean "droplet" diameter was measured by averaging the greatest diameter of 25 "droplets." Ten of 10 subjects (100%) produced more sweat with a high phosphatidylcholine meal than with a low one. Compared to placebo, 10 of 11 subjects (91%) given lecithin had significantly increased sweat secretion (p less than 0.01). It remains to be confirmed that this phosphatidylcholine-induced sweating increase is clinically significant.

Adult↗

PubMed1989

[Sweating deficiency in myotonic dystrophy].

We evaluated local sweating function quantitatively in nine cases of myotonic dystrophy (MyD) aged 26 to 61 years (mean, 45.4 years) and 25 control subjects aged 24 to 71 years (mean, 50.1 years). MyD subjects were grouped into three clinical classes according to their severity (three mild cases; class 1, three moderate; class 2 and three severe; class 3). 10 mg of acetylcholine was injected intradermally on the dorsum of the foot. After stimulation the impressions of sweat droplets were obtained using vinyl silicon impression material and the number of sweat droplet impressions per square centimeter was counted and the diameter of each droplet was measured by an image processor using a microcomputer. The result showed statistically significant decrease in the number of sweat droplets in class 2 and 3 as compared with control group and class 1. The histogram of sweat droplet diameter disclosed tendency of progressive deficit in diameter in all three clinical classes of MyD. Various kinds of autonomic function test, besides sweat tests, and nerve conduction study done on class 2 and 3 failed to show any significant abnormalities. Skin biopsy study done on lower leg on four subjects of class 2 and 3 revealed atrophy of eccrine sweat glands. These results suggests that local sweating deficiency develops in MyD as the disease progresses and that this deficiency is caused by dysfunction of eccrine glands, and not of postganglionic autonomic nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

[Immunohistochemical detection of carcinoembryonic antigen and protein S-100 in sweat gland tumors].

Carcinoembryonic antigen (CEA) and S 100 protein (S 100) have been demonstrated in formalin-fixed paraffin sections of eccrine and apocrine sweat glands, and tumors of the sweat glands, as well as, for comparison, in a variety of tumors deriving from epidermal and follicular structures using the peroxidase-antiperoxidase technique. CEA is detectable, as a membrane antigen, in the normal coil of eccrine sweat glands and in the cytoplasm of luminal cells in eccrine and apocrine sweat ducts up to the horny layer. Nearly all tumors of the sweat glands contain variable amounts of CEA. S 100 is localized in the cytoplasm of eccrine coils and secreted with the sweat. Apparently it is only found in tumors derived from the eccrine and apocrine sweat gland coils. Immunohistochemical demonstration of CEA and S 100 thus facilitates the diagnosis of tumors of the sweat glands and their differentiation from epidermal and follicular tumors.

Apocrine Glands↗

PubMed1985

Sign of complete sympathetic blockade: sweat test or sympathogalvanic response?

The sensitivity, specificity, and accuracy of the cobalt blue and ninhydrin sweat tests were compared with the sympathogalvanic response (SGR) in assessment of complete sympathetic blockade. Patients were randomly assigned to receive epidural administration of either preservative-free physiologic saline solution and 80 mg methylprednisolone (group I, control group, 9 patients) or 1.5% lidocaine with 80 mg methylprednisolone (group II, sympathetic blocked group, 10 patients). In group I, there was one false positive SGR (absence of SGR) before the block and there were four false positive SGRs after the block. In comparison, there were no false positive sweat tests (absence of sweating) before and after injection in group I. In group II, there were three false positive SGRs and no false positive sweat test before injection. After injection, one patient with an upper level of sensory blockade at T5 had persistent SGRs and positive sweat tests (false negative results). The study showed the sensitivity of the SGR and the sweat tests to be 90%. The specificity of the SGR was 56% compared to 100% for the sweat tests. The accuracy of the SGR was 74% compared to 95% for the sweat tests.

Adult↗

PubMed1971

The discharge of sweat in Welsh mountain sheep.

1. Experiments were done on Welsh Mountain sheep to determine whether the sheep can be caused to discharge sweat continuously.2. On administration of sequences of four to eighteen I.V. injections of adrenaline or noradrenaline (200 mug), sheep responded to the first 4-5 injections with decreasing amounts of sweat discharge. Thereafter, the responses were fairly constant at about 10% of the first discharge. Occasionally one injection within a series elicited no sweat discharge but on other isolated occasions large discharges of sweat were induced. The blood pressure response to repeated I.V. injections of adrenaline remained constant.3. Inhalation of amyl nitrite or rebreathing of expired air during I.V. adrenaline injections had little effect on the pattern of intermittent sweat discharges and did not induce a continuous outflow of fluid from the sweat glands.4. Continuous infusions of adrenaline and of carbachol did not cause a change in the rate of continuous water vapour loss from the skin but possibly increased the frequency of intermittent sweat discharges.5. Electrical stimulation of the cervical sympathetic nerve for short (0.5-2 min) or long (20-30 min) periods caused only transient (3-6 min) increases in water vapour loss from the cheek skin.6. None of these experiments indicated that the sweat glands of the sheep can be induced to discharge fluid continuously.

Amyl Nitrite↗

PubMed1994

[Band patterns of human sweat proteins carrying ABO-blood-group antigens tested by SDS-polyacrylamide gel electrophoresis].

Sweats were obtained from healthy 27 male and 5 female adults (A.Se: 11, A.se:1, B.Sc:5, B.Se:5, AB.Se:2 and O.Se:8 cases) in a sauna. Human sweat proteins carrying ABO-blood-group antigens were examined by SDS-polyacrylamide gel electrophoresis followed by immunoblotting with monoclonal anti-A and anti-B antibodies. Electrophoretic bands of the sweats were generally demonstrated as follows: A band in the region of a higher molecular weight than 116,000 Da, a band in each of the regions of 96,000, 82,000, 71,000, 50,000, 43,000 and from 34,000 to 30,000 Da, and several bands (2-6 bands) in region from 28,000 to 19,000 Da. There were many protein fractions carrying ABO-blood-group antigens in the sweats, regardless of the blood groups. Individual variations of the band patterns in the number and the color depth of immunoblotting were observed. The band in the sweats from the nonsecretors did not appear clearly. A band in the region between 34,000 and 30,000 Da, and several bands in the region between 28,000 and 19,000 Da were stained with PAS. These bands are probably glycoproteins with a blood group activity in sweats. Proteins carrying ABO-blood-group antigens in human erythrocyte membranes and saliva were also tested. In erythrocyte membranes, many bands ranged widely from high to low molecular weight regions were demonstrated, and several bands with higher molecular weights than 43,000 Da were shown in saliva. The band patterns of the sweats, erythrocyte membranes and saliva differed from one another, therefore, it was considered that there are proper proteins carrying ABO-blood-group antigens in sweats, erythrocyte membranes and saliva.

ABO Blood-Group System↗

PubMed1993

[Hormones regulating volume and electrolytes of sweat in patients with essential hypertension. Effect of thermal dehydration and treatment with captopril].

The present study aimed to answer the following questions: 1. do secretion of volume related hormones in patients with EH pre and post treatment with captopril differ from normotensive subjects if examined in thermal dehydration conditions; 2. is the electrolyte composition of thermal sweat related to the plasma profile of volume related hormones? and 3. does treatment by captopril influence sweat electrolytes in EH patients. In 16 patients with EH and in 20 healthy subjects a thermal dehydration test was performed. In patients with EH this test was done twice: before treatment and after 6 weeks of captopril therapy. In all subjects plasma renin activity (PRA), aldosterone (Ald) AVP and ANP were measured before and after thermal dehydration. In sweat samples collected after 15' and 45' of thermal dehydration the concentration of Na, K and Cl was assessed. In hypertensive patients before captopril treatment significantly higher values of PRA, ALD and ANP were found, while sweat concentrations of Na and Cl were significantly lower than in controls. After captopril treatment sweat electrolytes concentrations showed a tendency to normalize. No significant correlation was found between the plasma hormonal profile and sweat Na, K and Cl concentrations respectively both in controls and patients with EH pretreatment. A significant positive correlation was noticed only in hypertensive patients post-treatment between plasma aldosterone and sweat Na and Cl concentration respectively. Results obtained in this study show, that volume related hormones (Ald, AVP, ANP) do not seem to influence markedly the electrolyte composition of thermal sweat both in healthy subjects and in hypertensive patients.

Adult↗

PubMed1953

The permeability of human sweat glands to a series of sulfonamide compounds.

A series of sulfonamide compounds, para-aminohippurate, and inulin were used to study the permeability of the epithelium of human sweat glands. Inulin was not excreted in the sweat. The ratios of the concentrations in sweat to the concentrations in plasma, S/P, of sulfanilamide, sulfapyridine, sulfathiazole, sulfadiazine, and para-aminohippurate were found to be 0.69, 0.58, 0.13, 0.11, and 0.02 respectively, independent of the plasma concentrations and the sweating rates. The fact that the S/P ratios are thus unaffected by the absolute number of molecules transported suggests that these compounds enter into the sweat by simple diffusion and not via a specific secretory mechanism which could become saturated by increasing load. If this is so, the difference in the S/P ratios must be explained by an unequal permeability of the epithelium of the sweat gland to the various compounds and some explanation for these differences in the rate of excretion must exist in terms of physicochemical properties of the compounds. A comparison between the S/P ratios and the pK values of the various sulfonamides indicates that the differences in their rates of excretion in the sweat depend upon the degree of ionization of the various compounds at the physiological pH. Compounds which are mainly non-ionized are excreted with high S/P ratios, whereas ionized compounds appear with low ratios. A quantitative relationship was shown to exist between the S/P ratio for each compound and the percentage of the compound which is non-ionized at pH 7.4.

Humans↗

PubMed2006

Immunohistochemical differentiation and localization analysis of sweat glands in the adult human axilla.

BACKGROUND: The classic concept of axillary glands differentiates between eccrine glands, producing abundant clear, nonodorous sweat; and apocrine glands, excreting small amounts of turbid, odorous milky sweat. A third type of sweat glands, the "apoeccrine" glands, were recently identified. To define the different types of sweat glands and their location and number, the authors carried out a prospective histologic study on adult human axillary skin, including various immunohistochemical markers. METHODS: Forty-three consecutive Caucasian, subjectively normhidrotic patients, who underwent a surgical procedure in the axilla unrelated to the axillary glands, were included in the study. For verification of normhidrosis, the gravimetric test was carried out by measuring the amount of sweat secretion per minute. Then, a 1 x 1-cm measuring piece of skin and subcutaneous tissue was excised in the apex of the axilla, divided into three samples--altogether, 129 samples--and processed for histologic examination. RESULTS: In the dermis, the authors found only very few eccrine (average, 0.3 gland/cm in only 12 percent of all patients) and apocrine glands (average, 0.1 gland/cm in only 4.7 percent of patients), and no apoeccrine glands in any patient. In the subcutaneous tissue, the mean number of glands per centimeter squared was 10 for the eccrine glands, nine for the apocrine glands, and six for the apoeccrine glands. CONCLUSIONS: In the authors' Caucasian subjects, all or most of the sweat glands were found in the subcutaneous tissue near the border to the dermis and not in the dermis. For extremely hyperfunctioning sweat glands, the authors recommend less radical surgical methods, with the preservation of skin, based on the knowledge that most glands are localized in the subcutaneous tissue.

Adult↗

PubMed2003

Sweating dysfunction in Parkinson's disease.

We sought to determine the prevalence and nature of sweating disturbances in patients with Parkinson's disease (PD), and investigated their correlation with other clinical features and with Quality of Life (QoL) measures. A questionnaire on symptoms and consequences of sweating dysfunction was completed by 77 consecutive outpatients, from three movement disorder clinics, and 40 controls. QoL was assessed using the disease-specific Parkinson's Disease Questionnaire (PDQ)-39 and generic EuroQoL (EQ)-5D rating scales. Patients also underwent a clinical examination, including assessment with the Unified Parkinson's Disease Rating Scale and the Hoehn and Yahr staging system. Sweating disturbances, either hypohidrosis or in particular, hyperhidrosis, were reported by 64% of patients and by 12.5% of controls (P < 0.005) and were often localised or asymmetric. Complaints of sweating disturbances were not correlated with disease severity, but did correlate with other symptoms of autonomic dysfunction. Sweating problems occurred predominantly in off periods and in on periods with dyskinesias. Sweating disturbances were not correlated with overall QoL scores, but we did observe a significant correlation with the pain dimension of the PDQ-39 and the visual analogue scale of the EQ-5D. Furthermore, many patients reported physical, social, and emotional impairment due to sweating. Sweating disturbances are common and distressing symptoms of PD that are related mainly to autonomic dysfunction, off periods, and dyskinesias.

Aged↗

PubMed2000

Sweat secretion rates in growth hormone disorders.

BACKGROUND: While increased sweating is a prominent symptom in patients with active acromegaly, reduced sweating is gaining status as part of the growth hormone deficiency (GHD) syndrome. DESIGN AND SUBJECTS: Sweat secretion rate (SSR), as measured by pilocarpine iontophoresis represents the maximal capacity for stimulated sweat secretion in a localized skin area. SSR was studied in 37 patients with a history of acromegaly, 20 adult patients with GHD before and during long-term GH substitution of GHD adults, and 58 control subjects. RESULTS: Acromegaly: Patients with acromegaly had significantly higher SSR than healthy controls (Z-score + 1.9 (+/- 1.1) mean (+/- SD) (P < 0.001)). SSR was increased irrespective of current clinical disease activity. Thus, the SSR Z-scores in 16 clinically inactive patients were + 2.1 (+/- 1.2), in 10 slightly or doubtfully active patients + 1.5 (+/- 0.7) and in 11 active patients + 1.8 (+/- 1.3). There was no correlation between SSR and IGF-I. GHD: Twenty adult patients participated in an 18-month randomised, placebo controlled, double blinded study of physiological dose GH substitution, followed by 18 months of open GH treatment. SSR at baseline was reduced in male but not in female GHD patients. Mean SSR (95% confidence interval) for 11 male patients was 89.0 mg/30 minutes (51.9-126.1) as compared to 133.5 mg/30 minutes (59.2-259.9) (P = 0.01) in 24 male controls, and for 11 female patients 48.2 mg/30 minutes (25.9-70.6) as compared to 49.2 mg/30 minutes (12.6-93. 9) in 34 female controls. GH treatment in physiological substitution doses for up to 36 months had no effect on SSR. CONCLUSION: We have demonstrated that longstanding GH hypersecretion in patients with acromegaly induces irreversible changes of sweat gland function, with persistently elevated SSR despite treatment and clinical cure. In GHD patients, SSR was reduced in males but not in females, which together with the established gender difference in normal controls emphasises the role of androgen deficiency as a cofactor for reduced sweating in hypopituitary patients. Sweat gland development seems to be more susceptible to lack of hormones in childhood and adolescence than in adulthood, whereas growth hormone excess can modify sweat function later in life.

Acromegaly↗

PubMed2001

Botulinum toxin A for axillary hyperhidrosis (excessive sweating).

BACKGROUND: Treatment of primary focal hyperhidrosis is often unsatisfactory. Botulinum toxin A can stop excessive sweating by blocking the release of acetylcholine, which mediates sympathetic neurotransmission in the sweat glands. METHODS: We conducted a multicenter trial of botulinum toxin A in 145 patients with axillary hyperhidrosis. The patients had rates of sweat production greater than 50 mg per minute and had had primary axillary hyperhidrosis that was unresponsive to topical therapy with aluminum chloride for more than one year. In each patient, botulinum toxin A (200 U) was injected into one axilla, and placebo was injected into the other in a randomized, double-blind manner. (The units of the botulinum toxin A preparation used in this study are not identical to those of other preparations.) Two weeks later, after the treatments were revealed, the axilla that had received placebo was injected with 100 U of botulinum toxin A. Changes in the rates of sweat production were measured by gravimetry. RESULTS: At base line, the mean (+/-SD) rate of sweat production was 192+/-136 mg per minute. Two weeks after the first injections the mean rate of sweat production in the axilla that received botulinum toxin A was 24+/-27 mg per minute, as compared with 144+/-113 mg per minute in the axilla that received placebo (P< 0.001). Injection of 100 U into the axilla that had been treated with placebo reduced the mean rate of sweat production in that axilla to 32+/-39 mg per minute (P<0.001). Twenty-four weeks after the injection of 100 U, the rates of sweat production (in the 136 patients in whom the rates were measured at that time) were still lower than base-line values, at 67+/-66 mg per minute in the axilla that received 200 U and 65+/-64 mg per minute in the axilla that received placebo and 100 U of the toxin. Treatment was well tolerated; 98 percent of the patients said they would recommend this therapy to others. CONCLUSIONS: Intradermal injection of botulinum toxin A is an effective and safe therapy for severe axillary hyperhidrosis.

Adult↗

PubMed2000

Pancreatic function and extended mutation analysis in DeltaF508 heterozygous infants with an elevated immunoreactive trypsinogen but normal sweat electrolyte levels.

BACKGROUND: Newborn screening for cystic fibrosis (CF) with immunoreactive trypsinogen (IRT) and DeltaF508 analysis followed by sweat testing misses some infants with CF and detects more DeltaF508 carriers than expected. Some of the apparent DeltaF508 carriers may be DeltaF508 compound heterozygotes with normal sweat electrolyte levels. METHODS: Infants identified by newborn screening with an elevated IRT level, one DeltaF508 allele, and a sweat chloride level <60 mmol/L underwent CF mutation analysis, pancreatic stimulation testing, and repeat IRT analysis followed by clinical review and repeat sweat test at 12 months. RESULTS: Over a 24-month period we identified 122 DeltaF508 heterozygotes and recruited 57; 4 had borderline sweat chloride levels (40 to 60 mmol/L), 5 (8.8%, 95% CI 1.4, 16.2) had a second CF mutation (R117H), and 11 (20%, 95% CI 10, 30) had the intron 8 5T allele. Three had clinical CF at 12 months (initial sweat chloride levels: 53, 51, and 32 mmol/L). Pancreatic electrolyte secretion in the subjects with a borderline sweat chloride level was similar to that in patients with known CF. CONCLUSION: The excess of DeltaF508 heterozygotes detected by IRT/DNA screening is associated with the presence of a second mutation or the 5T allele in some infants. Screened infants with borderline sweat chloride levels almost certainly have CF, but long-term follow-up of the infants with the genotype DeltaF508/R117H and DeltaF508/5T is required to determine their outcome. In the meantime, newborn screening should be confined to severe mutations associated with classic CF.

Cystic Fibrosis↗

PubMed2005

[In vitro isolation, cultivation and identification of sebocytes and eccrine sweat gland cells from human fetal skin].

OBJECTIVE: To explore the preliminary methods of in vitro isolation, culture and identification of sebocytes and eccrine sweat gland cells from human fetal skin. METHODS: Human fetal skin was digested with dispase or type II collagenase, and then by micro - sieving to isolate human sebaceous gland and eccrine sweat gland cells. DMEM/F12 (1: 1) was used as the basic culture medium, supplemented with fetal bovine serum, recombinant human epidermal growth factor, L-glutamine, Hydrocortisone, choleratoxin, penicillin and streptomycin as the medium for sebocytes, or fetal bovine serum, recombinant human epidermal growth factor, triiodothyronine, hydrocortisone, insulin, transferrin, sodium selenite to the medium for eccrine sweat gland duct cells. Primary cultures and subcultures were incubated at 37 degrees C in humidified atmosphere of 5% CO2/95% oxygen. Cell morphology was observed by inverted phase contrast microscopy, and the cultured cells were identified with cell clone efficiency determination. The cultured sebocytes were identified with oil red staining and CK4.62, Epithelia Membrane Antigen (EMA) immunohistochemistry staining. The cultured eccrine sweat gland duct cells were identified with CK7, CK19 immunohistochemistry staining. RESULTS: The isolated sebocytes and eccrine sweat gland cells from human fetal skin could grow by adhering to the wall and proliferate in vitro. The cell clone efficiency of human fetal sebocytes was 2.7%, which was obviously lower than that of human fetal keratinocytes (8.0%, P < 0.01). There was no obvious difference in the cell clone efficiency between human fetal eccrine sweat gland cells (7.3%) and human fetal keratinocytes (7.7%, P > 0.05) . The results of oil red staining indicated that a small quantity of lipid droplets in sebocytes, and immunohistochemistry staining of CK4.62, EMA were positive in subculture sebocytes. The immunohistochemistry staining of CK7, CK19 was positive in subculture eccrine sweat gland duct cells. CONCLUSION: In vitro cultured human fetal sebocytes and eccrine sweat gland duct cells displayed the markers and biological characteristics of epithelial lineage, but human fetal sebocytes proliferated more

Cell Culture Techniques↗

PubMed1996

Longitudinal effects of age on heat-activated sweat gland density and output in healthy active older men.

To investigate longitudinal effects of age on heat-activated sweat gland density and output, eight healthy active men (mean age 65-70 years) were retested after 5-years using 60-min passive heating [by placing the lower legs and feet in a 42 degrees C water bath while sitting in a warm chamber (35 degrees C and 45% relative humidity)]. Their height, body mass, surface area-to-mass ratio, mean skinfold thickness, resting systolic and diastolic blood pressures, pedometer readings and estimated maximal oxygen uptake did not differ over the 5-years. During the 60-min exposure the increase of rectal temperature was significantly greater in the second test than in the initial test (P < 0.05), although mean skin temperature, metabolic heat production and heart rate did not differ. Total body sweating rate was significantly less in the second test than in the initial test [210 (SEM 13) vs 253 (SEM 16) g.m-2.h-1, P < 0.02]. The mean body temperature at the onset of sweating on the thigh was significantly higher in the second test (P < 0.04), but not on the back. Local sweat rate (msw) had decreased significantly on the back in the second test (P < 0.001), but had not changed on the thigh where it had been smaller (compared to younger men) in the initial test. The decreased msw on the back was due to a lower sweat gland output (SGO) per gland, but not from the recruitment of fewer glands. In contrast, the sweat gland density on the thigh was less in the second test than in the initial test [72 (SEM 4) vs 86 (SEM 7) glands.cm-2, P < 0.03], but the SGO which had shown considerably smaller values in the initial test remained unchanged. These results would suggest that sweat gland function decreased over 5 years in healthy active men in their sixth and seventh decades, despite their having similar physical characteristics and exercise habits. Furthermore, the decline did not occur uniformly over the body surface and it is suggested that it may well extend from the lower limbs to the trunk.

Aged↗