The epidermal barrier

Cartlidge, P. H. T.

doi:10.1053/siny.2000.0013

Cited by 139 publications

(97 citation statements)

References 17 publications

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“…The etiology of nasal injury secondary to nCPAP is that the increased pressure around the nostrils decreases the circulation of blood flow which impairs tissue perfusion, and subsequently causes ischemic lesions. [8] Thus relieving the pressure is the key factor for the prevention of nasal trauma. [11] McCoskey [15] reported the important role of positioning the neonate in preventing nasal injury with nCPAP application, and also pointed out concrete proposals by positioning the neonate in prone with the neonate's hand tucked under the chin to keep the mouth closed and less altering of the prongs or mask.…”

Section: Discussionmentioning

confidence: 99%

“…[5,6] The local pressure of nasal prongs to the nasal region is easy to cause nasal injury in the newborn due to the cutaneous vulnerability. [6,7] Besides anatomical factors, such as endvascularization of the columella and nostrils, [8] Diblasi [9] emphasized that fixation technique was also an important factor for selecting the proper hat and prongs. The lack of stabilization and, hence, excessive movement of the prongs could result in nasal injury, interface displacement, and loss of system pressure.…”

Section: Introductionmentioning

confidence: 99%

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Hydrocolloid dressing in preventing nasal trauma secondary to nasal continuous positive airway pressure in preterm infants

Xie

2014

World Journal of Emergency Medicine

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hydrocolloid dressing in preventing nasal trauma secondary to nasal continuous positive airway pressure in preterm infants

Xie

2014

World Journal of Emergency Medicine

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“…Essential fatty acids are required for normal growth and skin function, and a deficiency in these fatty acids is characterized by growth retardation, skin abnormalities, and increased transepidermal water loss (31,44,45). In addition, linoleic acid is a component of acylceramide, a lipid thought to be involved in epidermal permeability barrier function (32).…”

Section: Discussionmentioning

confidence: 99%

Lipopenia and Skin Barrier Abnormalities in DGAT2-deficient Mice

Stone

Myers

Watkins³

et al. 2004

Journal of Biological Chemistry

530

484

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The synthesis of triglycerides is catalyzed by two known acyl-CoA:diacylglycerol acyltransferase (DGAT) enzymes. Although they catalyze the same biochemical reaction, these enzymes share no sequence homology, and their relative functions are poorly understood. Gene knockout studies in mice have revealed that DGAT1 contributes to triglyceride synthesis in tissues and plays an important role in regulating energy metabolism but is not essential for life. Here we show that DGAT2 plays a fundamental role in mammalian triglyceride synthesis and is required for survival. DGAT2-deficient (Dgat2 ؊/؊ ) mice are lipopenic and die soon after birth, apparently from profound reductions in substrates for energy metabolism and from impaired permeability barrier function in the skin. DGAT1 was unable to compensate for the absence of DGAT2, supporting the hypothesis that the two enzymes play fundamentally different roles in mammalian triglyceride metabolism.Triglycerides (triacylglycerols) are the major storage form of energy in eukaryotic organisms. However, excessive deposition of triglycerides in white adipose tissue (WAT) 1 leads to obesity and in non-adipose tissues (such as pancreatic ␤ cells, skeletal muscle, and liver) is associated with tissue dysfunction referred to as lipotoxicity (1, 2). Therefore, an understanding of the processes that mediate triglyceride synthesis is of significant biomedical importance.Triglycerides are synthesized from diacylglycerol and activated forms of fatty acids (fatty acyl-CoAs) in a reaction catalyzed by acyl-CoA:diacylglycerol acyltransferase (DGAT) enzymes (3-5). The genes for two DGAT enzymes, DGAT1 and DGAT2, have been identified (6, 7). Both DGAT1 and DGAT2 are ubiquitously expressed, with the highest levels of expression found in tissues that are active in triglyceride synthesis, such as WAT, small intestine, liver, and mammary gland (6, 7). Both enzymes are intrinsic membrane proteins, although DGAT1 has 6 -12 putative transmembrane domains, whereas DGAT2 has one. Both also have similarly broad fatty acyl-CoA substrate specificities in in vitro assays (7). However, despite their ability to catalyze similar reactions, DGAT1 and DGAT2 belong to different gene families that share neither DNA nor protein sequence similarity. DGAT1 is homologous to the acylCoA:cholesterol acyltransferase enzymes, ACAT1 and ACAT2, which are involved in cholesterol ester biosynthesis (6), whereas DGAT2 shares homology with acyl-CoA:monoacylglycerol acyltransferase enzymes (8 -13). This raises the question of why two different types of DGAT enzymes have emerged from convergent evolution.Insights into the functions of DGAT1 and DGAT2 in triglyceride metabolism have been provided by studies in yeast. Through deletion and overexpression studies, several groups have demonstrated that DGA1, the yeast homologue of DGAT2, is the major DGAT enzyme contributing to triglyceride synthesis and storage in yeast (14 -16). In contrast, ARE2, a yeast homologue of DGAT1, plays a minor role in triglyceride synthesis. Intere...

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“…Here, we show that lethality of homozygous Cx43K258stop mice is caused by a defective epidermal permeability barrier. This barrier is formed by terminally differentiated keratinocytes and lipids and is crucial for survival ex utero, because it retards dehydration and inhibits invasion of microorganisms and noxious material (Cartlidge, 2000). Defects of the epidermal permeability barrier in mice are related to mutations of genes involved in terminal differentiation of keratinocytes (Segre, 2003).…”

Section: Discussionmentioning

confidence: 99%