Gartner_BRS Cell Biology & Histology, 9e

BRS Cell Biology and Histology

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B. Apocrine sweat glands (see Fig. 12.5) are larger simple coiled, specialized sweat glands approximately 3 mm in diameter, located in various areas of the body (eg, axilla, areola of the nipple, perianal region) and the ceruminous (wax) glands of the external auditory canal. Apocrine glands are stimulated by sympathetic innervation, usually in response to stressful conditions. 1. These glands begin to function at the onset of puberty and are responsive to hormonal influ ences ; their large coiled secretory units are positioned in the dermis and hypodermis and are enveloped by scattered myoepithelial cells. Unlike in eccrine glands, the secretory units are composed of a single cell type that secretes viscous, odorless fluids into hair follicles instead of sweat pores. Bacteria on the skin surface metabolize these secretions and produce odors that are somewhat specific to each individual. 2. These sweat glands use merocrine secretion (exocytosis) as the mode of secretion, not by re leasing a portion of the cytoplasm, as the term apocrine in the name of the gland may imply. PEARLS Axillary osmidrosis ( axillary body odor ) results from the bacterial metabolism of the fatty acid andro stenone and androstenol-containing secretions of the apocrine glands . Each individual has a distinctive odor that is so characteristic that parents can recognize their biologic children and that babies can recog nize their mothers by these olfactory cues. A particular gene, ABCC11 , originally recognized to code for multidrug-resistance protein 8, is now known to transport small molecules into and out of cells. People who present with a single nonsynonymous nucleotide polymorphism of this gene from both parents (namely, the AA allele ), that is, a point mutation in which a single guanine nucleotide is changed to an adenine, have no body odor and have dry earwax. Individuals with all other alleles, GA and GG, have wet earwax and body odor. The AA allele is widespread among Koreans and many nationalities in East Asia but is totally absent in Africans, African Americans, and most Caucasians. C. Sebaceous glands (see Fig. 12.5) are branched acinar glands that employ the holocrine mode of secretion. Clustered acini of one sebaceous gland empty into a single short duct that drains into the neck of the hair follicle. These glands are modified as the tarsal glands ( Meibomian glands ) in the eyelid. 1. Sebaceous glands are embedded in the dermis and associated with hair follicles over most of the body’s surface; they are absent from the palms and soles. They are most abundant on the face, forehead, and scalp, and they release sebum (composed of an oily secretion and degen erating epithelial cells). 2. Sebum has a number of functions, including maintaining the skin’s barrier to aqueous fluids, guarding skin from oxidative stress, shielding skin from microorganisms, and maintaining the suppleness of skin and the luster of hair. Clinical A. Hairs (hair shafts) are keratinized, thin, threadlike structures that extend for various lengths above the surface of the epidermis. Hair in mammals functions in thermal protection and, in some instances, as camouflage and sensory organs. In humans, its function is more of a tactile sensory organ because when a hair shaft is disturbed, it relays that sensory information to the nervous system. There are three types of human hairs: lanugo, present in the perinatal period only, and vellus and terminal hairs, both present throughout postnatal life. 1. Lanugo is an exceptionally fine, somewhat longish hair that covers most of the body during fetal development and falls out shortly after birth. 2. Vellus hairs are short, fine, pale, “peach fuzz”-like hairs covering most of the body. 3. Terminal hairs are the coarse, long, highly keratinized, dark hairs present on the head, eye brows, eyelashes, axilla, groin, and other areas of the body. Most of the primate body is covered by terminal hair. V. HAIR, HAIR FOLLICLE, AND ARRECTOR PILI MUSCLE (Fig. 12.6; also see Fig. 12.5)

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