Objective To investigate the early changes of cardiac output and vital signs in term neonates shortly after born from gestational diabetic women.Methods From January 2015 to April 2015, 22 term neonates of gestational diabetes mellitus (GDM) women with euglycemia during pregnancy (GDM group) and 20 term neonates of non complicated gravidas (control group) in Shanghai First Maternity and Infant Hospital were enrolled.Neonates in both groups were measured by ultrasonic cardiac output monitor (USCOM) for cardiac hemodynamics index, including aortic peak flow velocity, pulmonary artery peak flow velocity, left cardiac output, right cardiac output and Smith Madigan inotropy index at one and two hours after birth.Vital signs including heart rate, respiratory rate, blood pressure and peripheral blood glucose were measured as well.Two independent sample t-test and Chi square test were used for statistical analysis.Results The peripheral blood glucose of neonates in GDM group was significantly lower than that of the control [(3.0±0.4) vs (4.0± 0.4) mmol/L, t=8.400, P ＜ 0.01), but all within normal range.Vital signs including heart rate, respiratory rate, mean blood pressure showed no differences between the groups (all P ＞ 0.05).In GDM group, aortic peak flow velocity were (1.230±0.160) and (1.210±0.220) m/s, left ventricle cardiac output was (0.867±0.196) and (0.859±0.193) L/min, Smith Madigan inotropy index was (0.846±0.180) and (0.823±0.189) W/m2 at one and two hours after birth, respectively, which were significantly higher than those in the control group [aortic peak flow velocity: (1.080±0.130) and (1.090± 0.120) m/s;left ventricle cardiac output: (0.754±0.098) and (0.757 ± 0.099) L/min;Smith Madigan inotropy index: (0.746 ± 0.097) and (0.725 ± 0.086) W/m2;t=3.464, 2.265, 2.296, 2.187, 2.263 and 2.202, respectively, all P ＜ 0.05].But no statistically significant differences was found on pulmonary artery peak flow velocity and right cardiac output between the two groups.Cardiac hemodynamics index had no difference between one and two hours within each group (all P ＞ 0.05).Conclusion The left ventricular contractility and left cardiac work are increased in neonates of gestational diabetes mellims women with good sugar control during pregnancy.

To compare the performance of self-inflating bag (SIB) with T-piece resuscitator (TPR) in neonatal resuscitation.Methods:This study involved the trainees participating in a Neonatal Resuscitation Simulation Camp (NRSC) organized by Shanghai First Maternity and Infant Hospital in December 2019. They were trained to provide positive pressure ventilation with the two devices on artificial lungs. Ventilation parameters including peak inspiratory pressure (PIP), positive end-expiratory pressure (PEEP), PIP in pulmonary alveoli (PIP alv), mean airway pressure (MAP), frequency, inspiratory time (Ti), tidal volume and minute ventilation volume were recorded and analyzed by independent sample t-test or rank sum test. Results:The PIP alv, PIP, oxygen flow rate, tidal volume and minute ventilation volume delivered by TPR were significantly lower than those by SIB [(17.18±1.61) vs (24.05±4.29) cmH 2O (1 cmH 2O=0.098 kPa), t=－6.87; (17.91±1.35) vs (29.97±4.50) cmH 2O, t=－14.06; (3.65±0.25) vs (6.88±1.59) L/min, t=－11.33; (15.90±1.81) vs (24.02±4.29) ml/min, t=－10.99; (664.71±88.94) vs (1 069.49±205.68) ml/min, t=－9.89; all P<0.001]. However, compared with SIB, the PEEP in pulmonary alveoli, Ti, duration of ventilation, inspiratory to expiratory ratio were increased when using TPR [(4.76(4.69-5.57) vs 0.19(0.12-4.10) cmH 2O, T=1 190.00; (0.59±0.15) vs (0.43±0.09) s, t=5.01; (1.46±0.23) vs (1.36±0.11) s, t=2.15; 0.71±0.22 vs 0.47±0.13, t=5.14; all P<0.05]. Conclusion:TPR could deliver more stable and safer PIP, PEEP and tidal volume than SIB and keeping MAP at a stable level during positive pressure ventilation on artificial lungs.

Background::Pulmonary arterial hypertension (PAH) is characterized by excessive proliferation of small pulmonary arterial vascular smooth muscle cells (PASMCs), endothelial dysfunction, and extracellular matrix remodeling. G protein-coupled receptor kinase 2 (GRK2) plays an important role in the maintenance of vascular tone and blood flow. However, the role of GRK2 in the pathogenesis of PAH is unknown.Methods::GRK2 levels were detected in lung tissues from healthy people and PAH patients. C57BL/6 mice, vascular smooth muscle cell-specific Grk2-knockout mice ( Grk2?SM22), and littermate controls ( Grk2flox/flox) were grouped into control and hypoxia mice ( n = 8). Pulmonary hypertension (PH) was induced by exposure to chronic hypoxia (10%) combined with injection of the SU5416 (cHx/SU). The expression levels of GRK2 and Yes-associated protein (YAP) in pulmonary arteries and PASMCs were detected by Western blotting and immunofluorescence staining. The mRNA expression levels of Grk2 and Yes-associated protein ( YAP) in PASMCs were quantified with real-time polymerase chain reaction (RT-PCR). Wound-healing assay, 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay, and 5-Ethynyl-2′-deoxyuridine (EdU) staining were performed to evaluate the proliferation and migration of PASMCs. Meanwhile, the interaction among proteins was detected by immunoprecipitation assays. Results::The expression levels of GRK2 were upregulated in the pulmonary arteries of patients with PAH and the lungs of PH mice. Moreover, cHx/SU-induced PH was attenuated in Grk2?SM22 mice compared with littermate controls. The amelioration of PH in Grk2?SM22 mice was accompanied by reduced pulmonary vascular remodeling. In vitro study further confirmed that GRK2 knock-down significantly altered hypoxia-induced PASMCs proliferation and migration, whereas this effect was severely intensified by overexpression of GRK2. We also identified that GRK2 promoted YAP expression and nuclear translocation in PASMCs, resulting in excessive PASMCs proliferation and migration. Furthermore, GRK2 is stabilized by inhibiting phosphorylating GRK2 on Tyr86 and subsequently activating ubiquitylation under hypoxic conditions. Conclusion::Our findings suggest that GRK2 plays a critical role in the pathogenesis of PAH, via regulating YAP expression and nuclear translocation. Therefore, GRK2 serves as a novel therapeutic target for PAH treatment.