Background The potential effects of pre-pregnancy body mass (BMI) and gestational weight gain (GWG) on pregnancy outcomes remain unclear. Thus, we investigated socio-demographic characteristics that affect pre-pregnancy BMIs and GWG and the effects of pre-pregnancy BMI and GWG on Chinese maternal and infant complications. Methods 3172 women were enrolled in the Chinese Pregnant Women Cohort Study-Peking Union Medical College from July 25, 2017 to July 24, 2018, whose babies were delivered before December 31, 2018. Regression analysis was employed to evaluate the socio-demographic characteristics affecting pre-pregnancy BMI and GWG values and their effects on adverse maternal and infant complications. Results Multivariate logistic regression analysis revealed that age groups < 20 years (OR: 1.97), 25–30 years (OR: 1.66), 30–35 years (OR: 2.24), 35–40 years (OR: 3.90) and ≥ 40 years (OR: 3.33) as well as elementary school or education below (OR: 3.53), middle school (OR: 1.53), high school (OR: 1.40), and living in the north (OR: 1.37) were risk factors in maintaining a normal pre-pregnancy BMI. An age range of 30–35 years (OR: 0.76), living in the north (OR: 1.32) and race of ethnic minorities (OR: 1.51) were factors affecting GWG. Overweight (OR: 2.01) and inadequate GWG (OR: 1.60) were risk factors for gestational diabetes mellitus (GDM). Overweight (OR: 2.80) and obesity (OR: 5.42) were risk factors for gestational hypertension (GHp). Overweight (OR: 1.92), obesity (OR: 2.48) and excessive GWG (OR: 1.95) were risk factors for macrosomia. Overweight and excessive GWG were risk factors for a large gestational age (LGA) and inadequate GWG was a risk factor for low birth weights. Conclusions Overweight and obesity before pregnancy and an excessive GWG are associated with a greater risk of developing GDM, GHp, macrosomia and LGA. The control of body weight before and during the course of pregnancy is recommended to decrease adverse pregnancy outcomes, especially in pregnant women aged < 20 or > 25 years old educated below university and college levels, for ethnic minorities and those women who live in the north of China. Trial registration Registered at Clinical Trials (NCT03403543), September 29, 2017.

Background: Phosphatidylserine (PS) appears on the outer membrane leaflet of cells undergoing programmed cell death and marks those cells for clearance by macrophages. Macrophages secrete lactadherin, a PS-binding protein, which tethers apoptotic cells to macrophage integrins. Methods: We utilized fluorescein-labeled lactadherin together with the benchmark PS Probe, annexin V, to detect PS exposure by flow cytometry and confocal microscopy. Immortalized leukemia cells were treated with etoposide, and the kinetics and topology of PS exposure were followed over the course of apoptosis. Results: Costaining etoposide-treated leukemoid cells with lactadherin and annexin V indicated progressive PS exposure with dim, intermediate, and bright staining. Confocal microscopy revealed localized plasma membrane staining, then diffuse dim staining by lactadherin prior to bright generalized staining with both proteins. Annexin V was primarily localized to internal cell bodies at early stages but stained the plasma membrane at the late stage. Calibration studies suggested a PS content .2.5%-8% for the membrane domains that stained with lactadherin but not annexin V. Conclusions: Macrophages may utilize lactadherin to detect PS exposure prior to exposure of sufficient PS to bind annexin V. The methodology enables detection of PS exposure at earlier stages than established methodology. Key terms: lactadherin; phosphatidylserine; apoptosis; leukemia; annexin V Phosphatidylserine (PS) appears on the outer membrane leaflet of cells undergoing programmed cell death (1-3) and marks those cells for clearance by macrophages (1). Transient exposure of PS on viable cells accompanies sperm capacitation (4), phagocytosis of apoptotic cells (5), myotube formation (6), and neutrophil (7) and platelet stimulation (8). On stimulated platelets, exposed PS supports procoagulant reactions, and on lymphocytes PS externalization appears mechanistically coupled to the function of ion channels and the multidrug resistance protein in lymphocytes (9). However, in spite of the essential relationship of PS exposure to cellular function, the topology and kinetics of PS exposure remain only partially characterized.PS exposure is frequently detected through binding of fluorescence-labeled annexin V (3). The extent to which annexin V binds to a membrane is a complex function related to the free annexin V concentration, membrane PS content, phosphatidylethanolamine content, and ambient Ca 11 concentration (10-15). Indeed, recent reports indicate that the cooperative interaction of annexin V on the plasma membrane drives a mechanism whereby invagination of the plasma membrane is followed by internal vesiculation (16).The complexity of annexin V binding and the internalization of annexin V by stressed cells leaves uncertainty about the extent to which annexin V fluorescence represents plasma membrane PS exposure in early apoptosis.Lactadherin is also a PS-binding protein and has a domain structure that includes two epithelial growth factorlike domains and two le...

HRiM normative data of both liquid and viscous swallows from healthy Chinese volunteers were established. The IRP and CFV were significantly decreased in the viscous swallows compared with those of the liquid swallows.