Background: Obstructive sleep apnea (OSA) has been associated with adverse fetal outcomes in some studies. Second trimester Down syndrome screening markers reflect fetal and fetoplacental wellbeing. We aimed to compare markers of fetal and feto-placental wellbeing in women with OSA and low risk controls.
Methods: A retrospective case-control study of pregnant women with OSA and available second trimester markers was performed. Controls were screened for sleep disordered breathing (SDB) at the time of delivery using a questionnaire. Women at low risk for OSA were selected. Marker levels were adjusted for gestational age and race and reported as multiples of median and later adjusted for body mass index (BMI).
Results: Twenty-four OSA cases and 166 controls were identified. Women with OSA had a higher mean BMI when compared to controls (37.1?±?12.7 versus 24.1?±?5.1, p?=?0.03). Estriol (uE3) multiples of the median (MoM) levels were lower in women with OSA compared to controls, even after adjusting for BMI, 0.74 (interquartile range (IQR) 0.45) versus 1.06 (IQR 0.38), respectively, p?=?0.026. Once adjusted for BMI, alpha feto-protein (AFP) MoM levels were no longer significantly different in women with OSA compared to controls.
Conclusion: OSA is associated with reduced serum uE3 levels, independently of BMI, possibly indicating fetal distress. 相似文献
We describe Collinsium ciliosum from the early Cambrian Xiaoshiba Lagerstätte in South China, an armored lobopodian with a remarkable degree of limb differentiation including a pair of antenna-like appendages, six pairs of elongate setiferous limbs for suspension feeding, and nine pairs of clawed annulated legs with an anchoring function. Collinsium belongs to a highly derived clade of lobopodians within stem group Onychophora, distinguished by a substantial dorsal armature of supernumerary and biomineralized spines (Family Luolishaniidae). As demonstrated here, luolishaniids display the highest degree of limb specialization among Paleozoic lobopodians, constitute more than one-third of the overall morphological disparity of stem group Onychophora, and are substantially more disparate than crown group representatives. Despite having higher disparity and appendage complexity than other lobopodians and extant velvet worms, the specialized mode of life embodied by luolishaniids became extinct during the Early Paleozoic. Collinsium and other superarmored lobopodians exploited a unique paleoecological niche during the Cambrian explosion.Onychophorans, or velvet worms, comprise a relatively small phylum (∼180 species) of soft-bodied panarthropods constituting a minor component of modern rainforest ecosystems around the world (1). The overall organization of extant onychophorans is remarkably conserved (2), typified by a low morphological variability and homogeneous autoecologies as ambush predators of small invertebrates. An emerging fossil record, however, points to a substantially wider range of forms and habits during their early evolutionary history (3–8). Paleozoic lobopodians—a paraphyletic group of soft-bodied extinct organisms resembling worms with legs—occupy basal phylogenetic positions within the stem lineages of Onychophora, Tardigrada, and Euarthropoda (3, 6, 9), and thus offer critical insights about the early evolution and paleobiology of panarthropod phyla. Here, we describe the stem group onychophoran Collinsium ciliosum, a “superarmored” lobopodian with complex limbs, based on a large and exquisitely preserved population from the early Cambrian (Stage 3) Xiaoshiba Lagerstätte in South China (10, 11) (SI Appendix, Fig. S1). 相似文献
Mast cell activation disease (MCAD) is a term referring to a heterogeneous group of disorders characterized by aberrant release of variable subsets of mast cell (MC) mediators together with accumulation of either morphologically altered and immunohistochemically identifiable mutated MCs due to MC proliferation (systemic mastocytosis [SM] and MC leukemia [MCL]) or morphologically ordinary MCs due to decreased apoptosis (MC activation syndrome [MCAS] and well-differentiated SM). Clinical signs and symptoms in MCAD vary depending on disease subtype and result from excessive mediator release by MCs and, in aggressive forms, from organ failure related to MC infiltration. In most cases, treatment of MCAD is directed primarily at controlling the symptoms associated with MC mediator release. In advanced forms, such as aggressive SM and MCL, agents targeting MC proliferation such as kinase inhibitors may be provided. Targeted therapies aimed at blocking mutant protein variants and/or downstream signaling pathways are currently being developed. Other targets, such as specific surface antigens expressed on neoplastic MCs, might be considered for the development of future therapies. Since clinicians are often underprepared to evaluate, diagnose, and effectively treat this clinically heterogeneous disease, we seek to familiarize clinicians with MCAD and review current and future treatment approaches. 相似文献