The actual value of in human amniotic fluid

Bejar, Raul; Giussi, Gustavo; Casaguberta, C.; Curbelo, Violeta; Caldeyro-Barcia, R.

doi:10.1016/0028-2243(71)90020-7

Cited by 6 publications

(2 citation statements)

References 7 publications

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“…However, the mechanisms by which low O 2 tension is maintained in the epidermis are poorly understood. Possible causes of O 2 deprivation in the superficial epidermis include the absence of vascularization as well as low O 2 saturation in amniotic fluid ( Bejar et al 1971 ). Additionally, non-O 2 -dependent processes such as PI3K/AKT signaling or the generation of reactive oxygen species in proliferating keratinocytes may contribute to HIF stabilization in the basal epidermis.…”

Section: Resultsmentioning

confidence: 99%

Hypoxia-Inducible Factors Regulate Filaggrin Expression and Epidermal Barrier Function

Wong

Richardson

Seykora

et al. 2015

Journal of Investigative Dermatology

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A functional epidermal skin barrier requires the formation of a cornified envelope from terminally differentiating keratinocytes. During this process, multiple genetic and environmental signals coordinately regulate protein expression and tissue differentiation. Here we describe a critical role for hypoxia-inducible factors (HIFs) in the regulation of filaggrin expression and skin barrier formation. Similar to other mammalian tissues, fetal epidermis in mice is normally O2-deprived. Simultaneous deletion of Hif1a and Hif2a in murine epidermis revealed defects in keratinocyte terminal differentiation and epidermal barrier formation. Mice lacking Hif1a and Hif2a in the epidermis exhibited dry flaky skin, impaired permeability barrier, and enhanced sensitivity to cutaneous allergens. These defects were correlated with stratum granulosum attenuation and reduced filaggrin expression. Hypoxic treatment of primary keratinocytes induced filaggrin (Flg) gene expression in a HIF1α- and HIF2α-dependent manner, suggesting that one mechanism by which Hif1a and Hif2a loss causes epidermal barrier defects in mice lies in Flg dysregulation. Therefore, low O2 tension is an essential component of the epidermal environment that contributes to skin development and function.

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Section: Resultsmentioning

confidence: 99%

Hypoxia-Inducible Factors Regulate Filaggrin Expression and Epidermal Barrier Function

Wong

Richardson

Seykora

et al. 2015

Journal of Investigative Dermatology

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“…Furthermore, bacteria such as vaginalis and anaerobic bacteria are capable of producing phospholipase A2 in large quantity compared to other bacteria (Bejar, 1981). Phospholipase A2 promotes of prostaglandins; which is capable of liberating the arachidonic acid molecule of the embryonic membrane, which in turn increase the rate of contraction resulting to preterm labour and/or PPROM (Bejar, et 1981;Bolton,et al, 2012;Liu, Lorie, et al, 2002 and Nelson,et al 92 chorioamnionitis membranes then triggers the re rupture of the membranes and weakening of the cervix collagen (Nelson, et In addition to this, evidence has also showed that increase in the production of cytokine followed by endometrial inflammation increased the incidence of premature rupture of membranes and preterm birth in bacterial et al, 2009). Another physiological activity that occurred in the presence of myometrium infection is the expression of tumour necrosis factor α (TNF-α), which triggered the production of oxytocin receptor, prostaglandin receptors, and other (Liu, et al, The stimulation of these factors results…”

Section: Mechanism Of Microbial Infection In Preterm Labourmentioning

confidence: 99%

The Role of Infections in Preterm Labour and It’s Control: A Review

Ummasalma Aliyu Saulawa,

Fatima Muktar,

Kamaluddeen Kabir

2017

UJMR

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Preterm labour (PTL) is described as the premature contraction of the uterus before 37 weeks of the gestation cycle, which could results in preterm premature rupture of the membranes (PPROM) and in most cases may lead to preterm birth. Preterm labour that results in preterm birth is a leading precursor of neonatal morbidity and mortality. Infection in the uterus occurs by the aptness of pathogenic microbes to ascend from the female genital area to the uterus. Lactobacilli species constitute about 95% of the female genital normal flora. But the invasion and colonisation of the genital area by gram-negative anaerobes has endangered the female genital area and exposed it to infection. Pathogens such as Neisseria gonorrhoeae, Candida albican, adenovirus and many more are indicated to play a role in preterm labour.The symptoms and clinical diagnosis of infections in the female genital area include itching and inflammation of the vaginal area, heavy, copious yellow-grey, fishy smell discharge etc. Routine clinical investigations from the first trimester of gestation cycle and the administration of probiotics, antibiotics as well as proper toiletry hygiene have contributed to reducing the prevalence of preterm labour.

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