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At least 775 records · Page 43Linked to original sources
PubMed1995

Time course of appearance of cotinine in human beard hair after a single dose of nicotine.

The time course of appearance of cotinine in saliva and in daily collections of beard clippings was monitored by gas chromatography with mass spectrometry in six volunteers who were nonsmokers following a single 30-min buccal administration of nicotine as a chewing gum. Salivary cotinine concentrations reached a plateau after 1.5 h and were nondetectable (< 0.3 ng/ml) 24 h after drug administration. Cotinine was detected in extracts of sodium hydroxide digests of beard hair in all subjects on the third day after drug administration. Mean concentrations in beard peaked on day 5, and cotinine was not detected (< 0.03 ng/mg) after day 7. The data indicate the main route for cotinine incorporation into beard is during hair growth. Transfer into beard from sweat is of little importance. A role for transfer via sebum is equivocal.

Adult↗
PubMed1996

Mechanisms of drug incorporation into hair.

Hair testing for drugs of abuse is a developing technology that offers the possibility of longer detection times than is commonly obtained with urine or blood analysis. There are many uncertainties concerning how drugs enter hair and factors that affect drug deposition and residence in hair. Possible routes of drug entry include diffusion from blood, sweat, sebum, and skin and entry from the environment. Evidence is reviewed regarding the importance of each of these routes as possible contributors to drug deposition in hair. Binding to specific sites in hair may involve both electrostatic forces and weaker attractions, such as van der Waals forces. Melanin and protein constituents of hair may serve as binding sites. Recent in vitro studies suggest that the color of hair or melanin content may be the major determinant of cocaine binding and, consequently, may result in color or ethnic bias in hair testing.

Hair↗
PubMed1982

Maintenance of the normal flora of human skin grafts transplanted to mice.

Full-thickness human cadaver skin was maintained on the dorso-lateral thoracic region of hairless mice whose immune rejection mechanism was suppressed using anti-mouse-thymocyte globulin. The bacterial profile of the pregrafted skin did not differ significantly from the normal human microflora. In contrast, the murine skin exhibited quantitative and qualitative differences from the human flora, in particular by the complete absence of Propionibacterium acnes, the dominant bacterium on sebum-rich areas of human skin. The normal microbial profile of the human grafts was maintained throughout the experimental period despite the novel environmental milieu. There was little contamination of the grafts from the normal murine flora. It was concluded that the grafted human skin would provide a realistic model for studying the ecology of human cutaneous micro-organisms.

Animals↗
PubMed1985

Sebaceous gland hyperplasia on rabbit pinna induced by tetradecane.

To investigate the pathologic changes of sebaceous glands during comedo formation induced by topically applied substances in a rabbit pinna model, purified tetradecane was inuncted on the ventral aspect of the rabbit pinnas once a day for a week. Histologically, a marked hyperplasia of sebaceous glands, epidermis, and follicular epithelium was seen. These remarkably enlarged sebaceous glands were examined histochemically and ultrastructurally. The acinus size and cell population of the hyperplastic sebaceous gland were significantly increased over those of the normal sebaceous gland. By N-(7-dimethylamino-4-methyl-3-coumarinyl)maleimide staining, normal distribution patterns of sulfhydryl (SH) and disulfide (SS) were seen in the peripheral to differentiating layers in the hyperplastic sebaceous glands. In the terminally differentiated layer, the brilliant SH fluorescence was gradually decreased and the SS fluorescence was gradually increased in intensity, indicating that most SH groups in the sebaceous cells were converted to SS linkages before holocrine secretion. By transmission electron microscopy, several cell layers of undifferentiated sebaceous cells were observed at the periphery of the large sebaceous gland. The differentiating sebaceous cells produced a large number of lipid droplets, which were produced in either rough or smooth endoplasmic reticulum. These cells were abruptly converted into homogeneously electron-dense cells which formed several layers. These homogeneous cells gradually lost their electron density before holocrine secretion. These findings indicate that the sebaceous cells in the hyperplastic sebaceous glands undergo a magnified step-by-step cell differentiation and play a role in slightly modified lipid formation, and that there may be an increased production of sebum in the rabbit pinna model. This is the first report of sebaceous hyperplasia induced by a topically applied substance on skin surface, except for androgens. The hyperplastic sebaceous glands could serve as a model for investigations of sebaceous cell differentiation and lipid formation.

Administration, Topical↗
PubMed1986

Effect of a new topically active antiandrogen (RU 38882) on the rat sebaceous gland: comparison with cyproterone acetate.

RU 38882 is a new antiandrogen. When given by subcutaneous or oral route, RU 38882 is about 25 times less potent than cyproterone acetate. However, when applied topically to the intact rat skin, RU 38882 (0.25-25 mg/rat/day for 5 days or 3 weeks) decreases, in a dose-related manner, the volume density of the smooth endoplasmic reticulum vesicles of the differentiating cells of the sebaceous gland, a structure directly involved in sebum lipid synthesis. Under these conditions RU 38882 is about 100 times more potent than cyproterone acetate and unlike cyproterone acetate, does not modify the prostate weight. The lack of efficacy of cyproterone acetate on the sebaceous gland could be due to its partial androgenic activity while RU 38882, under these conditions, acts as a pure antiandrogen which inhibits the nuclear androgen-receptor translocation.

Administration, Topical↗
PubMed1988

Fatty acids of acylceramides from comedones and from the skin surface of acne patients and control subjects.

Comedonal lipids and skin surface lipids were collected from six acne patients and surface lipids were collected from sex- and age-matched controls without acne. Six series of ceramides were found in each sample, the relative amounts of which were determined by thin-layer chromatography/photodensitometry. Acylceramides (ceramide 1) were isolated by preparative thin-layer chromatography and their ester-linked fatty acids were analyzed by gas-liquid chromatography. The comedonal acylceramides contained higher proportions of 16:0, 16:1 delta 6, and 18:1 delta 6 + delta 8 and much less linoleate (18:2 delta 9,12) than the acylceramides from the skin surface. In the surface lipids from legs, acylceramides from the acne patients contained less linoleate than the acylceramides from control subjects. Free fatty acids from the comedones were also isolated and analyzed, and had a composition very similar to the esterified fatty acids of comedonal acylceramides. The results confirm that fatty acids derived from sebum become incorporated into comedonal acylceramides, displacing linoleate, and show that this process even affects the acylceramides of surface epidermis, more so in acne patients than in normal subjects.

Acne Vulgaris↗
PubMed1983

Localization of de novo sterologenesis in mammalian skin.

Previous studies have demonstrated that the skin is an important site of de novo sterol synthesis and that there is a sex difference in cutaneous sterologenesis with male animals synthesizing more sterols than females. The aim of the present study was to localize the major sites of sterol synthesis within the skin and to determine which of these sites accounted for the sex differences in sterologenesis. In male and female rats whose dermal and epidermal layers are separated by dithiothreitol treatment, the dermis is the major site of skin sterologenesis (males 86% of total, females 82% of total). Moreover, the sex difference in skin sterol synthesis is quantitatively localized primarily within the dermal layer (approximately 2.5-fold greater in the dermis of males). Sterol synthesis is also increased in the epidermis of males. To rule out the possibility that sebaceous gland production accounted for our observations, we treated animals with isotretinoin (13-cis-retinoic acid), a drug that suppresses sebaceous gland sebum production. Sterol synthesis in the skin of both male and female rats is not significantly altered by isotretinoin administration and the sex difference in skin sterologenesis is unaffected. To further localize the sites of sterol synthesis within the skin, studies of hairless mice whose skin was split by DTT were initiated. In hairless mice, DTT separates the epidermis into upper (stratum corneum and granulosum) and lower (basal and spinous cells) strata. The basal layer was separated from the dermis by gentle scraping. As in rats, the dermis is the chief site of sterol synthesis in the skin. In addition, the lower layer of the epidermis (basal and spinous cells) is also a very active site of sterologenesis, accounting for 20% of total skin nonsaponifiable lipid synthesis. The upper epidermis accounted for only a small portion of total skin synthesis. It is highly likely that the bulk of cutaneous sterol synthesis occurs in the pilosebaceous epithelium.

Animals↗
PubMed1981

Differential effect of 13-cis-retinoic acid and an aromatic retinoid (Ro 10-9359) on the sebaceous glands of the hamster flank organ.

The effect of subcutaneously administered 13-cis-retinoic acid and an aromatic retinoid (Ro 10-9359) on the sebaceous glands of the hamster flank organ were compared. As previously reported, 13-cis-retinoic acid caused a marked diminution of sebaceous gland size without affecting other androgen dependent structures. The aromatic retinoid derivative showed no effect upon any of the flank organ components. Studies utilizing androgen stimulated female confirmed our previous finding that 13-cis-retinoic acid prevented the growth of sebaceous glands without affecting the development of dermal pigmentation or large pigmented hair follicles. The aromatic retinoid derivative showed slight, if any, effect upon sebaceous gland size and no effect upon pigmentation or pigmented follicle development. The findings with this model system suggest that any efficacy of Ro 10-9359 in the treatment of acne would be by some mode other than the inhibition of sebum production.

Animals↗
PubMed1978

Skin surface glycerol levels in acne vulgaris.

Free glycerol would be expected from biochemical considerations to be an end product of lipolysis of sebum triglycerides. Glycerol was measured in skin surface washings of acne vulgaris patients, in acne vulgaris patients treated for at least 3 mo with oral tetracycline and in control subjects. Surface glycerol in untreated acne subjects was significantly less than that expected theoretically, whereas the amounts of such glycerol in treated acne patients and in control subjects closely approached the theoretically expected values. It is suggested that glycerol may be an in vivo substrate for Propionibacterium acnes.

Acne Vulgaris↗
PubMed1975

Age-related changes in the resident bacterial flora of the human face.

Quantitative levels of resident aerobic and anaerobic bacteria of the face, show a characteristic age-related pattern. The density of anaerobic diptheroids and surface aerobic micrococci is higher in infancy than in early childhood. At puberty the quantity of organisms increases, with significantly higher levels achieved in late adolescence. Maximum counts are attained in early adulthood and remain constant until old age when a trend toward lower numbers occurs. These changes seem to correlate with the production of sebum.

Adolescent↗
PubMed1989

Immunohistochemical demonstration of immunoglobulin A in human sebaceous and sweat glands.

Immunoglobulin A (IgA) mediated humoral defense mechanisms have been detected on all mucous membrane surfaces. There are only a few papers about the presence of IgA in human skin. In order to demonstrate the occurrence of IgA in sebaceous and sweat glands, biopsies of normal human skin were investigated and compared to intestinal mucosa. Two different commercially available anti-IgA antibodies were used. For light microscopy peroxidase-anti-peroxidase (PAP) or avidin-biotin complex (ABC) staining was used, and for electron microscopy protein-A-gold (PAG) labeling was performed on tissue sections. Specifically decorated IgA was found in sebaceous glands as well as in various portions of eccrine glands. In sebaceous glands, the maximum of IgA concentration was seen near the mouth of pilosebaceous ducts. Sweat ducts exhibited a continuous coat of IgA, whereas secretory portions contained only singular scattered IgA positive cells. Immunoelectron microscopy suggests endocytotic uptake and processing of IgA in the glandular cells. These results indicate strongly that IgA are secreted by normal human sebaceous and sweat glands. Because it is well known that IgA plays an important role in inactivation of invading viruses, bacteria, and other antigenic structures on mucous membranes, it appears that IgA in sebum and sweat fulfil a similar function on the outer body surface.

Adolescent↗
PubMed2005

Augmentation of lipogenesis by 15-deoxy-Delta12,14-prostaglandin J2 in hamster sebaceous glands: identification of cytochrome P-450-mediated 15-deoxy-Delta12,14-prostaglandin J2 production.

Prostaglandins (PGs) play important roles in the regulation of cutaneous cell functions under physiological and pathological conditions. In this study, we examined the involvement of PGs in sebocyte lipogenesis using non-steroidal anti-inflammatory drugs in vivo and in vitro. Hamster auricle sebocytes spontaneously differentiated to accumulate intracellular triacylglycerol (TG), under which the relative levels of 15-deoxy-Delta(12,14)-PGJ2 (15d-PGJ2) to PGF(2alpha) and PGE2 increased. 15d-PGJ2 was found to augment the formation of lipid droplets, which was because of an increase of TG synthesis by diacylglycerol acyltransferase (DGAT). Furthermore, sebocytes constitutively produced cyclooxygenase 2 (COX-2), but not COX-1, in vivo and in vitro. When sebocytes were treated with COX inhibitors such as indomethacin, diclofenac, or NS-398, the production of PGF(2alpha) and PGE2 decreased. The production of 15d-PGJ2, however, was increased in these inhibitor-treated sebocytes. In addition, indomethacin, diclofenac, and NS-398 augmented the synthesis of TG along with the increase in DGAT activity. Similarly, topical administration of indomethacin to hamster auricles caused the development of sebaceous glands with the augmentation of sebum deposition in vivo. Furthermore, indomethacin and NS-398-augmented 15d-PGJ2 production and TG synthesis were suppressed by a non-selective cytochrome P-450 (CYP) inhibitor, SKF-525A. A ligand activator of peroxisome proliferation activating receptor gamma (PPARgamma), troglitazone-induced synthesis of TG, however, was not altered even in the presence of SKF-525A. These results suggest that 15d-PGJ2 is a crucial stimulator of sebocyte lipogenesis by augmenting DGAT-mediated synthesis of TG. In addition to the COX-2-dependent pathway of PG synthesis, our findings suggest a sebocyte-specific pathway of 15d-PGJ2 production by CYP, the activity of which may be evoked by inhibiting COX-2.

Animals↗
PubMed2005

Allergic contact dermatitis from iodine preparations: a conundrum.

Iodine preparations are widely used antiseptics, yet limited information exists on their irritant potential and threshold for diagnostic patch testing. We examine this issue by using iodine in different preparations and concentrations. A total of 24 fair-skinned, healthy volunteers without a history of iodine allergy, ranging in age from 18 to 65 years (mean age 49.5 + 10.7 SD), were recruited. Concentrations of 0.5%, 1%, 5% and 10% iodine in petrolatum (pet.), 0.5%, 0.75% and 1% iodine in 70% isopropyl alcohol (IPA) and 1%, 5%, 7.5% and 10% of povidone-iodine (PVP-I) were applied for 2 days to the intrascapular area on the back or to the volar forearm between cubital fossa and wrist using Finn Chambers on Scanpor. Test sites were read 2 days (D2) and 4 days (D4) after patch application. Skin reactions were graded according to the following scheme: 0 = no reaction, + = questionable erythema, 1 = definite erythema, 2 = erythema and induration and 3 = vesiculation. Mild-to-moderate reactions (+ to 2) were observed in 75% of the subjects patched with 5% iodine in pet. at 2-4 days after application. Almost all subjects reacted to 10% iodine at D2 and D4, with 65% exhibiting erythema and induration or vesiculation. A large number (33%) of the subjects developed some reactions to the low concentration (0.5%) of iodine in 70% IPA at D2. Vesicles were seen in 54% of the subjects patched with 1% iodine in 70% IPA at D4. Only 1 subject reacted to 7.5% and 10% PVP-I. Iodine can be irritant to normal skin in pet. and in 70% IPA. Pet. possibly enhances skin contact with iodine, thus increasing its irritant capacity. Alcohol removes sebum from the skin surface, and it might increase iodine penetration into the skin, causing a higher degree of irritation. PVP-I is relatively non-irritant, because its iodine is complexed in an iodophor. For diagnostic patch testing, we recommend using iodine at less than 1% in pet. and at less than 0.5% in 70% IPA. For PVP-I, 10% appears non-irritant. With the variation in patch-test irritant response, interpretation of the patch-test response in the light of clinical history is mandatory.

2-Propanol↗
PubMed2005

What is the pathogenesis of acne?

For a long time, the mantra of acne pathogenesis debates has been that acne vulgaris lesions develop when (supposedly largely androgen-mediated) increased sebum production, ductal hypercornification, and propionibacteria come together with local inflammatory process in the unlucky affected individual. And yet, the exact sequence, precise interdependence, and choreography of pathogenic events in acne, especially the 'match that lights the fire' have remained surprisingly unclear, despite the venerable tradition of acne research over the past century. However, exciting recent progress in this--conceptually long somewhat stagnant, yet clinically, psychologically, and socioeconomically highly relevant--everyday battlefield of skin pathology encourages one to critically revisit conventional concepts of acne pathogenesis. Also, this provides a good opportunity for defining more sharply key open questions and intriguing acne characteristics whose underlying biological basis has far too long remained uninvestigated, and to emphasize promising new acne research avenues off-the-beaten-track--in the hope of promoting the corresponding development of innovative strategies for acne management.

Acne Vulgaris↗
PubMed2005

Clinical diagnosis of common scalp disorders.

Scalp skin is unique on the body due to the density of hair follicles and high rate of sebum production. These features make it susceptible to superficial mycotic conditions (dandruff, seborrheic dermatitis, and tinea capitis), parasitic infestation (pediculosis capitis), and inflammatory conditions (psoriasis). Because these scalp conditions share similar clinical manifestations of scaling, inflammation, hair loss, and pruritus, differential diagnosis is critically important. Diagnostic techniques and effective treatment strategies for each of the above conditions will be discussed.

Adult↗
PubMed1993

Quantitative analysis of stratum corneum lipids in xerosis and asteatotic eczema.

Sphingolipids, a major constituent of intercellular lipids, are an important determinant for both water-holding and permeability barrier function in the stratum corneum. To assess the pathogenic role of sphingolipids in the stratum corneum of dry skin disorders such as xerosis and asteatotic eczema in leg skin, ceramides were quantified by thin layer chromatography after n-hexane/ethanol extraction of resin-stripped stratum corneum and evaluated as micrograms/mg stratum corneum. In healthy leg skin (n = 49), there was age-related decline in the total ceramide, whereas xerosis (n = 25) and asteatotic eczema (n = 16) suffering significantly reduced water-holding properties, exhibited no definite decrease, rather slight increase in ceramide quantity with the same composition of each individual ceramide as compared to healthy age-matched controls. These data indicate that the seemingly elevated level of ceramide is an artificial effect due to inflammatory processes which result from susceptibility to dryness. Analysis of sebum-derived lipids present in the stratum corneum revealed that there was a significant decline in free fatty acids in xerosis and asteatotic eczema as compared to age-matched healthy controls, and a similar decline in triglycerides in the above three groups when compared to younger controls. Although the observed decrease in the stratum corneum lipids may well explain the high incidence of winter dry skin in older people, the progression toward asteatotic eczema can not be accompanied solely by a decrease in ceramide quantity, suggesting that the evolution of xerotic skin is associated with other moisturizing factors and/or environmental stimuli.

Adult↗
PubMed1996

The effect of methotrexate on the expression of a cysteine protease inhibitor (type 2 cystatin) in rat sebaceous glands.

The purpose of this study was to assess whether rat cystatin S, a cysteine proteinase inhibitor, is present in rat sebaceous glands, and to measure the effects of methotrexate on the expression of cystatin in these glands. With methotrexate treatment, the number of skin sebaceous cells expressing cystatin increased from 13.9% to 34.3% (P < .05). A smaller increase (from 15.3% to 23.9%; P = .1) was observed in Zymbal sebaceous glands. Type 2 cystatin could not be detected in the major salivary glands, nor in trachea, lung, stomach, small intestine, large intestine, spleen, liver, kidney, or pancreas, in any of the rats given either saline or methotrexate. Our results suggest that type 2 cystatin is a constituent of normal sebaceous glands, and that the amount of cystatin present in these glands increases with methotrexate administration. We speculate that, in addition to the protective functions ascribed to sebaceous lipids, sebum may augment the physical barrier of skin through secretion of cysteine proteinases that may be pharmacologically modulated.

Animals↗
PubMed1976

Pilo-sebaceous duct physiology. III. Observations on the number and size of pilo-sebaceous ducts in acne vulgaris.

We have used surface microscopy to measure the pil-sebaceous duct orifices at different sites in 150 subjects. Our data have shown that there are more pilo-sebaceous units on the face compared to the back and that these exists are smaller on the face. Despite the small exit the sebum excretion rate per gland on the forehead was not significantly different from that on the back. Thus the number of pilo-sebaceous duct units and the pilo-sebaceous canal exit size are possible factors in the localization of acne.

Acne Vulgaris↗