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Permeability Barrier (permeability + barrier)
Terms modified by Permeability Barrier Selected AbstractsFunctional skin adaptation in infancy , almost complete but not fully competentEXPERIMENTAL DERMATOLOGY, Issue 6 2010Joachim W. Fluhr Please cite this paper as: Functional skin adaptation in infancy , almost complete but not fully competent. Experimental Dermatology 2010; 19: 483,492. Abstract:, Early postnatal life is a period of active functional reorganization and cutaneous physiological adaptation to the extrauterine environment. Skin as the outermost organ of mammalians is endowed of multiple functions such as protection, secretion, absorption and thermoregulation. Birth stimulates the epidermal barrier maturation and the skin surface acidification especially in premature infants. In full-term infants the developed stratum corneum accomplishes competent barrier function, in contrast to prematures. Complete barrier maturation in preterm infants is fulfilled by 2,4 weeks of the postnatal life. However, in preterms with 23,25 weeks gestational age this process takes longer. Versatile regulatory mechanisms, namely skin surface acidity, calcium ion gradient and nuclear hormone receptors/ligands are interrelated in the complex postnatal newborn adaptation. The skin of newborns is adjusting quickly to the challenging environmental conditions of the postpartum. However, certain functions, for example, microcirculation, continue to develop even beyond the neonatal period, that is, up to the age of 14,17 weeks. Different environmental factors (for instance, dry and cold climate, diapers and cosmetic care procedures) influence the postnatal development of skin functional parameters such as stratum corneum hydration and the permeability barrier especially in premature infants. The aim of this article is to summarize the current knowledge on skin physiology in newborn and infants with a practical approach and to discuss the possible clinical consequences. This review offers the readership a critical and practical overview of skin physiology in newborns and infants. It emphasizes possible new research fields in neonatal and infantile skin physiology. [source] N-Palmitoyl-4-Hydroxy- L -Proline Palmityl Ester: A Pseudoceramide that Provides Efficient Skin Barrier Repair and ProtectionINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 1 2006G. Vielhaber Ceramides are the main constituents of the epidermal permeability barrier, and it has been demonstrated that the application of ceramide enriched creams promotes epidermal barrier repair. However, nature-identical ceramides are extremely expensive and difficult to formulate. We therefore developed a new pseudoceramide, N-palmitoyl-4-hydroxy- l -proline palmityl ester (BIO391). Due to its low melting point of £60°C the pseudoceramide BIO391 can easily be incorporated into cosmetic formulations. In addition, it is very safe for use in cosmetics. The efficacy of the pseudoceramide BIO391 was investigated in vivo in a model for detergent-induced barrier disruption. Trans-epidermal water loss, redness, and skin hydration were recorded before and after barrier disruption as well as during the subsequent 9-day treatment with the test products. Barrier repair of skin treated with the pseudoceramide BIO391 was accomplished earlier than that of untreated and vehicle treated skin. Optimum barrier repair was achieved with 1.0% pseudoceramide BIO391 and optimum erythema reduction with 0.5% pseudoceramide BIO391. The optimum dosage could be reduced to 0.1% pseudo-ceramide by synergistic combination with 0.1% (-)-a-bisabolol. In addition, the pseudoceramide BIO391 proved to be as effective as nature-identical ceramides 2 and 3. In summary, N-palmitoyl-4-hydroxy- l -proline palmityl ester is a highly efficient barrier repair agent with efficacy equivalent to that of nature-identical ceramides, and it has excellent formulation properties. [source] Basis of occlusive therapy in psoriasis: correcting defects in permeability barrier and calcium gradientINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 3 2001Sang Min Hwang MD Background Although occlusive dressings have great potential in the management of psoriasis vulgaris, the therapeutic mechanism is not completely understood. Occlusion artificially restores and corrects the defective barrier in psoriasis plaques. Additionally, occlusion is know to normalize the epidermal calcium gradients in hyperproliferative murine skin models. Methods To investigate the basis of the therapeutic effect of occlusion on psoriatic plaques, we investigated the ultrastructural morphology of intercorneocyte lipid layers, lamellar bodies, and calcium gradient in chronic plaque-type psoriasis after occlusion with a water vapor-impermeable membrane. The specimens were processed for electron microscopy using: (i) ruthenium tetroxide postfixation; and (ii) ion-capture cytochemistry for calcium localization. Results Occlusion for 7 days resulted in a nearly mature pattern of intercellular multilamellar structures, re-establishment of the near-normal epidermal calcium gradient, and disappearance of calcium precipitates from the stratum corneum interstices. Conclusions The normalization of the permeability barrier and epidermal calcium gradient may play important roles in the therapeutic effects of occlusive dressings in chronic plaque-type psoriasis. [source] Treatment with oxidizing agents damages the inner membrane of spores of Bacillus subtilis and sensitizes spores to subsequent stressJOURNAL OF APPLIED MICROBIOLOGY, Issue 4 2004D.E. Cortezzo Abstract Aims:, To determine if treatment of Bacillus subtilis spores with a variety of oxidizing agents causes damage to the spore's inner membrane. Methods and Results:, Spores of B. subtilis were killed 80,99% with wet heat or a variety of oxidizing agents, including betadine, chlorine dioxide, cumene hydroperoxide, hydrogen peroxide, OxoneTM, ozone, sodium hypochlorite and t-butylhydroperoxide, and the agents neutralized and/or removed. Survivors of spores pretreated with oxidizing agents exhibited increased sensitivity to killing by a normally minimal lethal heat treatment, while spores pretreated with wet heat did not. In addition, spores treated with wet heat or the oxidizing agents, except sodium hypochlorite, were more sensitive to high NaCl in plating media than were untreated spores. The core region of spores treated with at least two oxidizing agents was also penetrated much more readily by methylamine than was the core of untreated spores, and spores treated with oxidizing agents but not wet heat germinated faster with dodecylamine than did untreated spores. Spores of strains with very different levels of unsaturated fatty acids in their inner membrane exhibited essentially identical resistance to oxidizing agents. Conclusions:, Treatment of spores with oxidizing agents has been suggested to cause damage to the spore's inner membrane, a membrane whose integrity is essential for spore viability. The sensitization of spores to killing by heat and to high salt after pretreatment with oxidizing agents is consistent with and supports this suggestion. Presumably mild pretreatment with oxidizing agents causes some damage to the spore's inner membrane. While this damage may not be lethal under normal conditions, the damaged inner membrane may be less able to maintain its integrity, when dormant spores are exposed to high temperature or when germinated spores are faced with osmotic stress. Triggering of spore germination by dodecylamine likely involves action by this agent on the spore's inner membrane allowing release of the spore core's depot of dipicolinic acid. Presumably dodecylamine more readily alters the permeability of a damaged inner membrane and thus more readily triggers germination of spores pretreated with oxidizing agents. Damage to the inner spore membrane by oxidizing agents is also consistent with the more rapid penetration of methylamine into the core of treated spores, as the inner membrane is likely the crucial permeability barrier to methylamine entry into the spore core. As spores of strains with very different levels of unsaturated fatty acids in their inner membrane exhibited essentially identical resistance to oxidizing agents, it is not through oxidation of unsaturated fatty acids that oxidizing agents kill and/or damage spores. Perhaps these agents work by causing oxidative damage to key proteins in the spore's inner membrane. Significance and Impact of the Study:, The more rapid heat killing and germination with dodecylamine, the greater permeability of the spore core and the osmotic stress sensitivity in outgrowth of spores pretreated with oxidizing agents is consistent with such agents causing damage to the spore's inner membrane, even if this damage is not lethal under normal conditions. It may be possible to take advantage of this phenomenon to devise improved, less costly regimens for spore inactivation. [source] Temperature shock, injury and transient sensitivity to nisin in Gram negativesJOURNAL OF APPLIED MICROBIOLOGY, Issue 4 2001I.S. Boziaris Aims:,The effect of thermal stresses on survival, injury and nisin sensitivity was investigated in Salmonella Enteritidis PT4, PT7 and Pseudomonas aeruginosa. Methods and Results:,Heating at 55°C, rapid chilling to 0·5°C or freezing at ,20°C produced transient sensitivity to nisin. Cells were only sensitive if nisin was present during stress. Resistance recovered rapidly afterwards, though some cells displayed residual injury. Injury was assessed by SDS sensitivity, hydrophobicity changes, lipopolysaccharide release and NPN uptake. LPS release and hydrophobicity were not always associated with transient nisin sensitivity. Uptake of NPN correlated better but persisted longer after treatment. Conclusions:,Thermal shocks produce transient injury to the outer membrane, allowing nisin access. After treatment, the permeability barrier is rapidly restored by a process apparently involving reorganization rather than biosynthetic repair. Significance and Impact of the Study:,Inclusion of nisin during food treatments that impose sub-lethal stress on Gram negatives could increase process lethality, enhancing microbiological safety and stability. [source] OPTIMIZATION OF PERMEABILIZATION PROCESS FOR LACTOSE HYDROLYSIS IN WHEY USING RESPONSE SURFACE METHODOLOGYJOURNAL OF FOOD PROCESS ENGINEERING, Issue 3 2009GURPREET KAUR ABSTRACT To overcome the permeability barrier and prepare whole cell biocatalysts with high activities, permeabilization of Kluyveromyces marxianus var. lactis NCIM 3566 in relation to, -galactosidase activity was optimized using cetyltrimethylammonium bromide (CTAB) as permeabilizing agent. Permeabilized whole cells can be advantageous over pure enzyme preparations in terms of cost-effectiveness and increased stability maintained by the intracellular environment. Response surface methodology (RSM) was applied to optimize concentration of CTAB, temperature and the treatment time for maximum permeabilization of yeast cells. The optimum operating conditions for permeabilization process to achieve maximum enzyme activity obtained by RSM were 0.06% (w/v) CTAB concentration, 28C temperature and process duration of 14 min. At these conditions of process variables, the maximum value of enzyme activity was found to be 1,334 IU/g. The permeabilized yeast cells were highly effective and resulted in 90.5% lactose hydrolysis in whey. PRACTICAL APPLICATION , -Galactosidase is one of the most promising enzymes, which has several applications in the food, fermentation and dairy industry. However, the industrial applications of , -galactosidase have been hampered by the costs involved in downstream processing. The present investigation was focused on developing the low-cost technology for lactose hydrolysis based on permeabilization process. Disposal of lactose in whey and whey permeates is one of the most significant problems with regard to economics and environmental impact faced by the dairy industries. Keeping this in view, lactose hydrolysis in whey has been successfully performed using permeabilized Kluyveromyces marxianus cells. Hydrolysis of lactose using , -galactosidase converts whey into a potentially very useful food ingredient, which has immense applications in food industries. Its use has increased significantly in recent years, mainly in the dairy products and in digestive preparations. Lactose hydrolysis causes several potential changes in the manufacture and marketing of dairy products, including increased solubility, sweetness and broader fermentation possibilities. [source] Uptake and Dispersion of Metformin in the Isolated Perfused Rat LiverJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 8 2000CHEN-HSI CHOU Although metformin is a widely used oral antihyperglycaemic, the exact mechanisms of its cellular uptake and action remain obscure. In this study the hepatic extraction and disposition kinetics of metformin were investigated by use of an isolated in-situ rat liver preparation. The liver was perfused in single-pass mode with protein-free Krebs bicarbonate medium at a flow rate of 20mLmin,1. During constant infusion with 1 mgL,1 metformin hydrochloride the hepatic uptake of metformin approached equilibrium within 10 min. The steady-state availability, F, determined from the ratio of outflow concentration to input concentration, was 0.99±0.02 (mean±s.d., n=4). The outflow profile of metformin resulting from a bolus injection of 25 ,g into the portal vein, had a sharp peak then a slower declining terminal phase. The mean transit time (MTT; 49.5±14.5, n = 6) and normalized variance (CV2; 4.13±0.05) of the hepatic transit times of metformin were estimated by numerical integration from the statistical moments of the outflow data. The volume of distribution of metformin in the liver (1.58±0.28 mL (g liver),1) was estimated from its MTT. The volume of distribution is greater than the water space of liver, indicating that metformin enters the hepatic aqueous space and becomes distributed among cellular components. The magnitude of CV2 for metformin is greater than for the vascular marker sucrose, suggesting that distribution of metformin into hepatic tissue is not instantaneous. In conclusion, hepatic uptake of metformin is rate-limited by a permeability barrier. Although metformin is accumulated in the liver, the organ does not extract it. [source] Barrier requirements as the evolutionary "driver" of epidermal pigmentation in humansAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 4 2010Peter M. Elias Current explanations for the development of epidermal pigmentation during human evolution are not tenable as stand-alone hypotheses. Accordingly, we assessed instead whether xeric- and UV-B-induced stress to the epidermal permeability barrier, critical to survival in a terrestrial environment, could have "driven" the development of epidermal pigmentation. (1) Megadroughts prevailed in central Africa when hominids expanded into open savannahs [,1.5,0.8 million years ago], resulting in sustained exposure to both extreme aridity and erythemogenic UV-B, correlating with genetic evidence that pigment developed ,1.2 million years ago. (2) Pigmented skin is endowed with enhanced permeability barrier function, stratum corneum integrity/cohesion, and a reduced susceptibility to infections. The enhanced function of pigmented skin can be attributed to the lower pH of the outer epidermis, likely due to the persistence of (more-acidic) melanosomes into the outer epidermis, as well as the conservation of genes associated with eumelanin synthesis and melanosome acidification (e.g., TYR, OCA2 [p protein], SLC24A5, SLC45A2, MATP) in pigmented populations. Five keratinocyte-derived signals (stem cell factor,KIT; FOXn1,FGF2; IL-1,, NGF, and p53) are potential candidates to have stimulated the sequential development of epidermal pigmentation in response to stress to the barrier. We summarize evidence here that epidermal interfollicular pigmentation in early hominids likely evolved in response to stress to the permeability barrier. Am. J. Hum. Biol., 2010. © 2010 Wiley-Liss, Inc. [source] Effects of a multilamellar emulsion on glucocorticoid-induced epidermal atrophy and barrier impairmentTHE JOURNAL OF DERMATOLOGY, Issue 2 2006Sung K. AHN ABSTRACT Skin atrophy is one of the most frequent side-effects of the topical glucocorticoid. Skin barrier impairment has also been reported as a steroid-induced side effect. Although there have been various studies on preventing or minimizing this atrophogenic effect, little has been reported about preventing barrier impairment. This study was performed to determine the effects of a multilamellar emulsion (MLE) that had a well-ordered lamellar structure on the steroid-induced barrier impairment and epidermal atrophy. To confirm these effects of MLE, 0.05% clobetasol-17-propionate (CP) and 0.05% clobetasol-17-propionate in MLE (MLE/CP) were topically applied to both flanks of hairless mice for 9 days. The topically applied CP induced a significant impairment of the epidermal permeability barrier, and MLE/CP also did not have a preventive effect on this change. However, skinfold thickness studies and histological studies showed that MLE/CP significantly reduced the steroid-induced atrophy. The topical application of MLE/CP was also shown to have a preventive effect on the steroid-induced increase of the stratum corneum (SC) surface pH. In addition, the electron microscopic findings showed relatively well-conserved lamellar bilayers in the skin treated with MLE, as compared to CP only. The results showed that the topical application of MLE immediately after CP treatment prevented the glucocorticoid-induced transepidermal water loss values increase. Light microscopy measurements showed that the skin treated with MLE immediately after CP treatment for 1 week had a slightly lower decline of skin thickness than did the CP-treated skin. These results suggest that MLE should be effective for preventing glucocorticoid-induced epidermal atrophy and for repairing the barrier impairment. [source] Mechanism of action of vitamin C in sepsis: Ascorbate modulates redox signaling in endotheliumBIOFACTORS, Issue 1 2009John X. Wilson Abstract Circulating levels of vitamin C (ascorbate) are low in patients with sepsis. Parenteral administration of ascorbate raises plasma and tissue concentrations of the vitamin and may decrease morbidity. In animal models of sepsis, intravenous ascorbate injection increases survival and protects several microvascular functions, namely, capillary blood flow, microvascular permeability barrier, and arteriolar responsiveness to vasoconstrictors and vasodilators. The effects of parenteral ascorbate on microvascular function are both rapid and persistent. Ascorbate quickly accumulates in microvascular endothelial cells, scavenges reactive oxygen species, and acts through tetrahydrobiopterin to stimulate nitric oxide production by endothelial nitric oxide synthase. A major reason for the long duration of the improvement in microvascular function is that cells retain high levels of ascorbate, which alter redox-sensitive signaling pathways to diminish septic induction of NADPH oxidase and inducible nitric oxide synthase. These observations are consistent with the hypothesis that microvascular function in sepsis may be improved by parenteral administration of ascorbate as an adjuvant therapy. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Substrate-permeable encapsulation of enzymes maintains effective activity, stabilizes against denaturation, and protects against proteolytic degradationBIOTECHNOLOGY & BIOENGINEERING, Issue 5 2001Mathieu Nasseau Abstract How can enzymes be protected against denaturation and proteolysis while keeping them in a fully functional state? One solution is to encapsulate the enzymes into liposomes, which enhances their stability against denaturation and proteases. However, the permeability barrier of the lipid membrane drastically reduces the activity of enzyme entrapped in the liposome by reducing the internal concentration of the substrate. To overcome this problem, we permeabilized the wall of the liposome by reconstitution of a porin from Escherichia coli. In this way, we recovered the full functionality of the enzyme while retaining the protection against denaturation and proteolytic enzymes. © 2001 John Wiley & Sons, Inc. Biotechnol Bioeng 75: 615,618, 2001. [source] An exhumed palaeo-hydrocarbon migration fairway in a faulted carrier system, Entrada Sandstone of SE Utah, USAGEOFLUIDS (ELECTRONIC), Issue 3 2001I. R. Garden Abstract The Moab Anticline, east-central Utah, is an exhumed hydrocarbon palaeo-reservoir which was supplied by hydrocarbons that migrated from the Moab Fault up-dip towards the crest of the structure beneath the regional seal of the Tidwell mudstone. Iron oxide reduction in porous, high permeability aeolian sandstones records the secondary migration of hydrocarbons, filling of traps against small sealing faults and spill pathways through the Middle Jurassic Entrada Sandstone. Hydrocarbons entered the Entrada Sandstone carrier system from bends and other leak points on the Moab Fault producing discrete zones of reduction that extend for up to 400 m from these leak points. They then migrated in focused stringers, 2,5 m in height, to produce accumulations on the crest of the anticline. Normal faults on the anticline were transient permeability barriers to hydrocarbon migration producing a series of small compartmentalized accumulations. Exsolution of CO2 as local fault seals were breached resulted in calcite cementation on the up-dip side of faults. Field observations on the distribution of iron oxide reduction and calcite cements within the anticline indicate that the advancing reduction fronts were affected neither by individual slip bands in damage zones around faults nor by small faults with sand: sand juxtapositions. Faults with larger throws produced either sand: mudstone juxtapositions or sand: sand contacts and fault zones with shale smears. Shale-smeared fault zones provided seals to the reducing fluid which filled the structural traps to spill points. [source] A REVIEW OF GEOLOGICAL DATA THAT CONFLICT WITH THE PARADIGM OF CATAGENIC GENERATION AND MIGRATION OF OILJOURNAL OF PETROLEUM GEOLOGY, Issue 3 2005H. Hugh Wilson The majority of petroleum geologists today agree that the complex problems that surround the origin, generation, migration and accumulation of hydrocarbons can be resolved by accepting the geochemical conclusion that the process originates by catagenic generation in deeply-buried organically-rich source rocks. These limited source rock intervals are believed to expel hydrocarbons when they reach organic maturity in oil kitchens. The expelled oil and gas then follow migration pathways to traps at shallower levels. However, there are major geological obstacles that cast doubt upon this interpretation. The restriction of the source rock to a few organically rich levels in a basin forces the conclusion that the basin plumbing system is leaky and allows secondary horizontal and vertical migration through great thicknesses of consolidated sedimentary rocks in which there are numerous permeability barriers that are known to effectively prevent hydrocarbon escape from traps. The sourcing of lenticular traps points to the enclosing impermeable envelope as the logical origin of the trapped hydrocarbons. The lynch-pin of the catagenic theory of hydrocarbon origin is the expulsion mechanism from deeply-buried consolidated source rock under high confining pressures. This mechanism is not understood and is termed an "enigma". Assuming that expulsion does occur, the pathways taken by the hydrocarbons to waiting traps can be ascertained by computer modelling of the basin. However, subsurface and field geological support for purported migration pathways has yet to be provided. Many oilfield studies have shown that oil and gas are preferentially trapped in synchronous highs that were formed during, or very shortly after, the deposition of the charged reservoir. An unresolved problem is how catagenically generated hydrocarbons, expelled during a long-drawn-out maturation period, can have filled synchronous highs but have avoided later traps along the assumed migration pathways. From many oilfield studies, it has also been shown that the presence of hydrocarbons inhibits diagenesis and compaction of the reservoir rock. This "Füchtbauer effect" points to not only the early charging of clastic and carbonate reservoirs, but also to the development of permeability barriers below the early-formed accumulations. These barriers would prevent later hydrocarbon additions during the supposed extended period of expulsion from an oil kitchen. Early-formed traps that have been sealed diagenetically will retain their charge even if the trap is opened by later structural tilting. Diagenetic traps have been discovered in clastic and carbonate provinces but their recognition as viable exploration targets is discouraged by present-day assumptions of late hydrocarbon generation and a leaky basin plumbing system. Because there are so many geological realities that cast doubt upon the assumptions that devolve from the paradigm of catagenic generation, the alternative concept of early biogenic generation and accumulation of immature oil, with in-reservoir cracking during burial, is again worthy of serious consideration. This concept envisages hydrocarbon generation by bacterial activity in many anoxic environments and the charging of synchronous highs from adjacent sources. The resolution of the fundamental problem of hydrocarbon generation and accumulation, which is critical to exploration strategies, should be sought in the light of a thorough knowledge of the geologic factors involved, rather than by computer modelling which may be guided by questionable geochemical assumptions. [source] | ||||||||||||||||