Patterns of symptomatology of adult women incest survivors.
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Adult↗
Biomedical subjects
B E Brown
Publications and source records attributed to B E Brown.
Avian epidermal differentiation. II. Adaptive response of permeability barrier to water deprivation and replenishment.
Zebra Finches are the epitome of desert-adapted avian species; i.e. they are able to survive without drinking water for over a year. Whereas transepidermal water loss (TEWL) in naked Zebra Finch nestlings is lower than in adults, and desert adaptation is accompanied by intercellular deposition of epidermal multigranular body (MGB) contents, MGB secretion is reduced as nestlings mature into feathered adults, indicative of less stringent barrier requirements. Here, removal of drinking water resulted in increased intercellular deposition of MGB contents, and TEWL progressively decreased. In contrast, MGB intercellular deposition decreased when birds were rehydrated, with TEWL returning towards normal within 5 days of rehydration. Finally, water-deprivation caused significant changes in epidermal lipid composition that returned toward control levels with rehydration. These studies show that adult Zebra Finches adapt to xeric stress by increased secretion of multigranular bodies resulting in reduced TEWL.
Adaptation, Physiological↗
Antimicrobial activity of stratum corneum lipids from normal and essential fatty acid-deficient mice.
Among the cutaneous effects of an essential fatty acid deficient (EFAD) diet are hyperdesquamation, increased transepidermal water loss (TEWL), and altered lipid profiles, characteristics also common to inflammatory dermatoses. Because fatty acids are antimicrobial, we examined the indigenous skin flora of normal and EFAD hairless mice, and compared the antimicrobial efficacy of lipids extracted from their stratum corneum. EFAD mice supported 100-fold more bacteria than normal mice, and were the only group from which Staphylococcus aureus were routinely isolated. Despite this greater carriage, in vitro experiments demonstrated that EFAD lipids are more lethal than normal lipids against Streptococcus pyogenes, S. aureus, S. epidermidis, Micrococcus sp., and a coryneform. Skin fungi were equally susceptible to both extracts. After thin layer chromatography, the most active fractions were found to be glycosphingolipids and phospholipids. EFAD extracts had 35% more free fatty acids and 75% more glycosphingolipids; normal extracts had more triglycerides and phospholipids. S. aureus strain 502A survived equally well on EFAD as on normal mice. Normal lipids applied on EFAD mice had no additional effect, but EFAD lipids on normal mice brought about a 35% reduction of the inoculated bacteria. If the mice were pretreated with alcohol, carriage of strain 502A was reduced by 71%. If instead the mice were previously washed with acetone to increase TEWL, a 97% reduction of the staphylococcus occurred. The application of normal flora to such acetone-washed mice decreased the efficacy to 76%. EFAD and normal lipids on human subjects were equally ineffective in eliminating strain 502A.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Lipid content and metabolism of human keratinocyte cultures grown at the air-medium interface.
The differentiation of human keratinocytes in most culture systems is incomplete; e.g., lamellar bodies, the characteristic lipid-delivery organelles of epidermis, are not present. Moreover, their lipid profile does not reflect the distinctive composition found in cornifying epidermis. In contrast, keratinocytes that grow at an air-medium interface exhibit more complete differentiation. In this study, we compared the elaboration of lamellar bodies, the lipid content, and the lipid metabolism of human keratinocytes, cultured both under standard immersed conditions and after lifting to an air-medium interface. Whereas submerged cultures neither elaborated lamellar bodies nor displayed a lipid distribution characteristic of cornifying epidermis, lifted cultures displayed advanced cornification, elaborated lamellar bodies which were deposited in intercellular domains, and a lipid profile more typical of cornifying epidermis. Moreover, lipid biosynthesis was 5-10-fold more active in lifted than in immersed cultures, and was not inhibited by exogenous lipoproteins. These findings are consistent with recent studies that demonstrate both high rates of lipogenesis in differentiating layers of the epidermis as well as autonomy of lipogenesis from the influence of circulating lipoproteins. Thus, the lipid content and metabolism of human keratinocyte cultures, grown at an air-medium interface, demonstrate features that simulate the epidermis.
Cell Differentiation↗
Membrane structural alterations in murine stratum corneum: relationship to the localization of polar lipids and phospholipases.
During the formation of the mammalian epidermal permeability barrier, lipids are sequestered in the stratum corneum intercellular spaces, transforming from a relatively polar lipid mixture to predominantly nonpolar species. Certain lipid catabolic enzymes, which co-localize with these lipids, may regulate this process. In order to localize the sites within the outer epidermis where polar lipids are catabolized, and their relationship to the alterations in membrane structure that occur in these layers, we compared the biochemical localization of polar lipids, the ultrastructure, and freeze-fracture morphology, as well as the localization of phospholipases within the outer epidermis. Both histochemical staining of frozen sections and biochemical studies of protease- and tape-stripped whole stratum corneum demonstrated small amounts of polar lipids in the stratum compactum, while in contrast, the stratum disjunctum was devoid of both phospholipids and glycosphingolipids. Phospholipase activity was present within lamellar bodies, among secreted lamellar body disks at the granular-cornified layer interface, and within the intercellular spaces of the stratum compactum. Both the depletion of polar lipids from the stratum compactum and deletion of these substances from the stratum disjunctum correlated with sequential changes in membrane structure observed by transmission electron microscopy and freeze-fracture. Thus, a phospholipase-mediated attack on phospholipids (with a parallel assault by other lipid catabolic enzymes on other polar species), may induce both the initial fusion and elongation of lamellar body disks and the subsequent formation of the hydrophobic membrane bilayers found in the mid-to-outer stratum corneum. These studies also may require modification of traditional views of the stratum corneum as a metabolically inert tissue, revealing its intercellular lipid domains to be partially in an active state of flux.
Animals↗
Family violence. Development of a master's level specialty track in family abuse.
Family violence is a societal reality. It will not disappear if society closes its eyes and fails to recognize its existence. When this is done, the abusive cycle is perpetuated. The specialty track described in this article was the nation's first graduate nursing educational program in the area of Family Violence. This program demonstrates nursing's potential contribution to the development of competent professionals with the expertise necessary to intervene in the abusive cycle.
Adult↗
Community health and home health nursing: keeping the concepts clear.
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Community Health Nursing↗
Localization of sites of lipid biosynthesis in mammalian epidermis.
The end-product of epidermal differentiation is a stratified layer of corneocytes whose extracellular lipid bilayers provide a permeability barrier. It is generally accepted that the epidermis synthesizes most if not all of the lipids found in this tissue and that extra-epidermal tissues contribute very little to this lipid content. Moreover, the individual epidermal strata in which epidermal lipid biosynthesis occurs are not known. To address this question, we examined [3H]H2O incorporation into nonsaponifiable and saponifiable lipids in individual epidermal cell layers 3 hr after intraperitoneal injection into neonatal mice, and compared this to protein and DNA synthesis using intraperitoneal [3H]leucine and [3H]thymidine incorporation, respectively. Lipid biosynthesis was also assessed by [14C]acetate incorporation into lipid fractions in organ cultured skin and in epidermal subpopulations. The in vivo studies demonstrated that the biosynthetic activity of both saponifiable and nonsaponifiable lipids was comparable to, if not greater, in the stratum granulosum (SG) than in basal/spinous (SB + SS) layer, despite significantly lower levels of both protein and DNA synthesis in the SG. On a mass basis, the SG accounts for about four times the biosynthetic activity of the combined SB + SS layers. The lipid biosynthetic activity in vitro also was two- to fivefold higher in the SG, regardless of whether the epidermis was separated into individual cell layers before or after incubations with radiolabel. Moreover, this difference could not be ascribed to increased acetate pools or to elevated metabolism in the SG versus the SB + SS since the rates of CO2 production were much lower in the SG fraction. The increase in lipid biosynthesis in SG over SB + SS was greatest for phospholipids, followed by glycosphingolipids, and free sterols but was observed in almost all lipid classes. These studies show not only that mammalian epidermis is an active site of de novo lipid biosynthesis, but also that this activity remains high in the stratum granulosum, while other forms of metabolic activity are diminishing. These observations are consistent with the knowledge that lipids extruded from the stratum granulosum layer provide the hydrophobic permeability barrier, and further suggest that elevated synthetic activity in the stratum granulosum would allow rapid replenishment in the event that the barrier is damaged.
Animals↗
Avian sebokeratocytes and marine mammal lipokeratinocytes: structural, lipid biochemical, and functional considerations.
In terrestrial mammals, stratum corneum lipids derive from two sources: deposition of lamellar body lipids in stratum corneum interstices and excretion of sebaceous lipids onto the skin surface, resulting in a two-compartment ("bricks and mortar") system of lipid-depleted cells surrounded by lipid-enriched intercellular spaces. In contrast, intracellular lipid droplets, normally not present in the epidermis of terrestrial mammals, are prominent in avian and marine mammal epidermis (cetaceans, manatees). We compared the transepidermal water loss, ultrastructure, and lipid biochemistry of the viable epidermis and stratum corneum of pigeon apterium, fledgling (featherless) zebra finches, painted storks, cetaceans, and manatees to those of humans and mice. Marine mammals possess an even more extensive lamellar-body secretory system than do terrestrial mammals; and lamellar-body contents, as in terrestrials, are secreted into the stratum corneum interstices. In cetaceans, however, glycolipids, but not ceramides, persist into the stratum corneum; whereas in manatees, glycolipids are replaced by ceramides, as in terrestrial mammals. Acylglucosylceramides, thought to be critical for lamellar-body deposition and barrier function in terrestrial mammals, are present in manatees but virtually absent in cetaceans, a finding that indicates that they are not obligate constituents of lamellar-body-derived membrane structures. Moreover, cetaceans do not elaborate the very long-chain, saturated N-acyl fatty acids that abound in terrestrial mammalian acylglucosylceramides. Furthermore, cold-water marine mammals generate large, intracellular neutral lipid droplets not found in terrestrial and warm-water marine mammals; these lipid droplets persist into the stratum corneum, suggesting thermogenesis, flotation, and/or cryoprotectant functions. Avians generate distinctive multigranular bodies that may be secreted into the intercellular spaces under xerotic conditions, as in zebra fledglings; ordinarily, however, the internal lamellae and limiting membranes deteriorate, generating intracellular neutral lipid droplets. The sphingolipid composition of avian stratum corneum is intermediate between terrestrials and cetaceans (approximately equal to 50% glycolipids), with triglycerides present in abundance. In the midstratum corneum of avians, neutral lipid droplets are released into the interstices, forming a large extracellular, lipid-enriched compartment, surrounding wafer-thin corneocytes, with a paucity of both lipid and keratin ("plates-and-mortar" rather than the "bricks-and-mortar" of mammals).(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Lipokeratinocytes of the epidermis of a cetacean (Phocena phocena). Histochemistry, ultrastructure, and lipid composition.
Biochemical and ultrastructural analysis of epidermis from the porpoise, Phocena phocena, revealed certain similarities and differences between cetaceans and terrestrial mammals. The predominant cell of cetacean epidermis, not found in normal terrestrial mammals, is a lipokeratinocyte, which elaborates not only keratin filaments, but also two types of lipid organelles: first, lamellar bodies, morphologically identical to those of terrestrial mammals, are elaborated in great abundance in all suprabasal epidermal layers, forming intercellular lipid bilayers in the stratum corneum interstices: and second, non-membrane-bounded droplets appear and persist in all epidermal layers. Although the porpoise lipokeratinocyte morphologically resembles the sebokeratocyte of avians in certain respects, non-membrane-bounded lipid droplets are not released into the intercorneocyte space as they are in avian stratum corneum. Whereas phospholipid/neutral lipid gradients are similar in porpoise and terrestrial mammals, PAS-positive glycoconjugates, specifically glycosphingolipids, are retained in porpoise stratum corneum, but lost from these layers in terrestrials. The novel, non-polar acylglucosyl-ceramides, which also are lost during cornification in terrestrial mammals, are retained in porpoise stratum corneum. The lipid components of porpoise lipokeratinocytes appear to subserve not only barrier function in a hypertonic milieu, but also underlie the unique buoyancy, streamlining, insulatory, and caloric properties exhibited as adaptations to the cetacean habitat.
Adaptation, Physiological↗
Avian epidermal differentiation: role of lipids in permeability barrier formation.
Though avian skin is known to possess a highly lipogenic epidermis, little is known about its permeability barrier function. We correlated epidermal barrier function, fine structure and lipid biochemistry in the pigeon, Columbia livia, and compared these features with terrestrial mammalian systems. Whereas barrier function, as assessed by transepidermal water loss was not as efficient as in mammals, both groups shared certain morphological features including substantial compartmentalization of lipids in stratum corneum intercellular domains. Avian intercellular lipids derive from extrusion of intracellular non-membrane-bound droplets from lowermost corneocytes, rather than by secretion of lamellar discs from multigranular bodies, as previously reported in some avians, and in mammals. Instead, both the internal lamellae and the limiting membranes of multigranular bodies appear to degenerate, leading to the formation of non-membrane-bound droplets. The lipid content of avian epidermis and stratum corneum demonstrates important similarities to terrestrial mammals, i.e. abundant sphingolipids, a paucity of phospholipids, and abundant neutral lipids, but also certain striking differences, i.e. persistence of glycosphingolipids and triglycerides into the stratum corneum. Thus, avian stratum corneum forms a two-compartment system of lipid-depleted cells embedded in non-polar-lipid enriched intercellular domains, analogous to mammals. But, in contrast to mammals, the highly attenuated corneocytes of avians, which results from a paucity of keratin filaments, produce a 'straws-and-mortar' tissue, rather than the 'bricks-and-mortar' tissue of mammals.
Animals↗
Effect of essential fatty acid deficiency on cutaneous sterol synthesis.
The fact that the skin is a major site of total body sterologenesis, coupled both with the apparent absence of low density lipoprotein receptors on keratinocytes and with the lack of influence of serum cholesterol on epidermal sterologenesis, has created the impression that epidermal lipid synthesis might be autonomous, i.e., nonregulatable. Recent studies have shown, however, that disruption of cutaneous barrier function with acetone or detergents stimulates epidermal sterologenesis (J Lipid Res 26:418-427, 1985). To correlate further sterologenesis with barrier function, we measured de novo synthesis of cholesterol and total nonsaponifiable lipids in essential fatty acid-deficient (EFAD) hairless mice. Animals with defective barrier function, manifested by abnormal transepidermal water loss, demonstrated a 2-fold increase in epidermal cholesterol and total nonsaponifiable lipid synthesis over controls while synthesis in the dermis was unchanged. Epidermal sterologenesis in EFAD animals, repleted with linoleic acid either systematically or topically, returned toward normal as barrier function improved. Moreover, plastic occlusion of EFAD mouse skin normalized epidermal sterologenesis at 1 and 3 days. These results provide further evidence that epidermal sterologenesis is not entirely autonomous, and can be regulated by water barrier requirements.
Animals↗
Histochemical and morphological studies on mammalian epidermal peridermal granules.
We performed morphological studies on the epidermal peridermal granules (PG) of newborn mice using histological, fluorescent and electron microscopic methods. PG appeared during the 17th to 18th day of foetal life, and remained in the outermost epidermal layers until 5 days after birth. PG were evenly distributed over the entire cutaneous surface of the mouse, except the tail. PG were found to contain protein and corresponded to sites of transglutaminase activity, but they were devoid of lipids and nucleic acids. They could be differentiated clearly from keratohyalin granules. Together, these studies suggest that PG represent a unique epidermal protein product that serves as a marker of late foetal development.
Animals↗
Who's the boss? Power struggles.
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Authoritarianism↗
The educational accountability model.
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Clinical Competence↗
An educator's perspective: discharge planning model.
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Continuity of Patient Care↗
De novo sterologenesis in the skin. II. Regulation by cutaneous barrier requirements.
Recent studies suggest: that the epidermis and pilosebaceous epithelium are important sites of de novo sterol synthesis, and that the rate of cutaneous cholesterol synthesis does not change with alterations in circulating sterol levels. Since cutaneous sterols may be important for permeability barrier function, we studied the effect of experimentally altered barrier function on de novo sterologenesis in the epidermal and dermal layers of the skin. Epidermal sterologenesis appeared to be modulated by the skin's barrier requirements because topical detergent and acetone treatment stimulated de novo synthesis of nonsaponifiable lipids in the epidermis, but not in the dermis. Synthetic activity paralleled both the return of barrier function toward normal and the extent of prior damage to the barrier. Moreover, plastic-wrap occlusion of solvent-treated sites simultaneously corrected both the barrier abnormality and normalized sterol synthesis, further linking increased epidermal sterologenesis to barrier requirements. Whereas topical applications of a variety of other topical lipids did not down-regulate synthesis, epicutaneously applied 25-hydroxycholesterol appeared to diminish synthesis. These results suggest that maintenance of barrier function is one purpose of epidermal de novo nonsaponifiable lipid synthesis, and demonstrate further that, despite a lack of low density lipoprotein receptors, epidermis can regulate its lipid-synthetic apparatus in response to certain specific requirements.
Acetone↗
Stratum corneum lipids in disorders of cornification. Steroid sulfatase and cholesterol sulfate in normal desquamation and the pathogenesis of recessive X-linked ichthyosis.
The pathological scaling in recessive x-linked ichthyosis is associated with accumulation of abnormal quantities of cholesterol sulfate in stratum corneum (J. Clin. Invest. 68:1404-1410, 1981). To determine whether or not cholesterol sulfate accumulates in recessive x-linked ichthyosis as a direct result of the missing enzyme, steroid sulfatase, we quantitated both steroid sulfatase and its substrate, we quantitated both steroid sulfatase and its substrate, cholesterol sulfate, in different epidermal strata, as well as within stratum corneum subcellular fractions obtained from normal human and neonatal mouse epidermis and from patients with recessive x-linked ichthyosis. In normal human and mouse epidermis, steroid sulfatase activity peaked in the stratum granulosum and stratum corneum, and negligible activity was detectable in lower epidermal layers. In contrast, in recessive x-linked ichthyosis epidermis, enzyme levels were virtually undetectable at all levels. In normal human stratum corneum, up to 10 times more steroid sulfatase activity was present in purified peripheral membrane preparations than in the whole tissue. Whereas in normal human epidermis cholesterol sulfate levels were lowest in the basal/spinous layer, and highest in the stratum granulosum, in recessive x-linked ichthyosis the levels were only slightly higher in the lower epidermis, but continued to climb in the stratum corneum. In both normal and in recessive x-linked ichthyosis stratum corneum, cholesterol sulfate appeared primarily within membrane domains, paralleling the pattern of steroid sulfatase localization. Finally, the role of excess cholesterol sulfate in the pathogenesis of recessive x-linked ichthyosis was directly tested by topical applications of this substance, which produced visible scaling in hairless mice in parallel to an increased cholesterol sulfate content of the stratum corneum. These results demonstrate an intimate relationship between steroid sulfatase and cholesterol sulfate in normal epidermis: both are concentrated in the outer epidermis (stratum corneum and stratum granulosum), and both are localized to membrane domains. Presumably, as a result of this distribution pattern, continued enzymatic degradation of substrate occurs in normal epidermis, thereby preventing excessive accumulation of cholesterol sulfate. In contrast, in recessive x-linked ichthyosis, degradation of cholesterol sulfate does not occur and cholesterol sulfate accumulates specifically in the stratum corneum, where it produces visible scale.
Administration, Topical↗