The impact of shared governance on the adverse mood of parturients with gestational hypertension and perinatal indicators of newborns

This study aimed to investigate the effect of shared governance on the adverse mood of parturients with gestational hypertension and perinatal indicators of newborns. A total of 318 patients with gestational hypertension treated in our hospital were enrolled as study subjects and were divided into a study group (200 cases) and a control group (118 cases) using double-blind, controlled and randomised methods. Before intervention, the systolic blood pressure (SBP), diastolic blood pressure (DBP), Hamilton Anxiety Rating Scale (HAMA), Hamilton Depression Rating Scale (HAMD) and Quality of Life Scale (SF-36) scores did not differ significantly between the two groups (p>.05). After intervention, the study group had lower SBP, DBP, HAMA and HAMD scores and higher SF-36 scores than the control group (p<.05). The neonates in the study group experienced a lower incidence of adverse outcomes than those in the control group (p<.05). Shared governance can regulate blood pressure and improve mood and quality of life in parturients with gestational hypertension. It can also reduce the incidence of adverse events in newborns during the perinatal period. Impact Statement What is already known on this subject? Gestational hypertension is the development of hypertension in pregnant women after 2 or 20 weeks of gestation and is characterised by headache, dizziness, nausea and swelling of the lower legs. Early intervention is key to improving maternal and neonatal prognosis. Shared governance is an emerging model of participatory decision-making in which nurses are empowered to make decisions about clinical practice standards, quality improvement, staff and professional development, and research, aiming to cultivate the patients' sense of responsibility for their health. What do the results of this study add? This study demonstrated that shared governance can regulate maternal blood pressure and improve maternal adverse mood, maternal quality of life and reduce the incidence of perinatal adverse events in the newborn, indicating the potential of shared governance and may promote the clinical application of shared governance. What are the implications of these findings for clinical practice and/or further research? This study starts with adverse mood of parturients and perinatal outcomes of newborns, and demonstrates in detail the impact of shared governance in nursing interventions on parturients with gestational hypertension and neonates. The data are detailed and reliable, providing certain clinical references for follow-up research

Activation of Notch3 promotes pulmonary arterial smooth muscle cells proliferation via Hes1/p27Kip1 signaling pathway

Activation of the Notch3 cascade is involved in the development of pulmonary arterial hypertension by stimulating the proliferation of vascular smooth muscle cells. However, the detailed molecular mechanisms underlying this effect are still unclear. The present study aims to address this issue. We demonstrated that over‐expression of intracellular domain of the Notch3 receptor (NICD3) by adenovirus transfection dramatically induced proliferation of primary cultured pulmonary artery smooth muscle cells. This was accompanied with up‐regulation of Hes1 protein and down‐regulation of p27Kip1 protein. More importantly, we observed that prior silencing of Hes1 with siRNA blocked NICD3 over‐expression‐induced p27Kip1 reduction and cell proliferation. The present study suggests that Hes1 lies downstream of NICD3 and particularly mediates Notch3 signaling‐induced proliferation of pulmonary arterial smooth muscle cells by down‐regulation of p27Kip1 expression

Hydroxyethyl starch 130/0.4 and sodium chloride injection as adjunctive therapy in patients with cerebral hypoperfusion

Abstract Background Both severe stenosis and completed occlusion in internal carotid artery or its distal branches have been considered the main reasons of cerebral hypoperfusion, which contributes to the washout disturbances of embolism in low perfusion territories distal to stenosis. An aggravated hypoperfusion state in certain brain region may induce ischemic stroke and further cognitive decline. However, the effective medication for cerebral hypoperfusion is largely unsettled. Methods/design By using computed tomography perfusion (CTP) imaging, the trial will evaluate the effectiveness, safety and tolerability of hydroxyethyl starch (HES) 130/0.4 for patients with extra-/intra-cranial artery stenosis and cerebral hypoperfusion. From 5 neurological inpatient wards, 300 patients will be randomly recruited for administered routine medications plus intravascular volume therapies using the equal volume of HES 130/0.4 or 0.9% sodium chloride solution. Cerebral hypoperfusion state after 7-day intervention is the primary outcome measure. The secondary outcome measures includes, impaired renal function, abnormal heart function, hematological changes, neurological dysfunctions and cerebrovascular events in peri-intervention period and/or 3-month follow-up. The sample size will allow the detection of a two-sided 5% significance level between groups in the endpoint with a power of 80%. Discussion The trial would provide important efficacy and safety data on the intravascular administration of HES 130/0.4 in patients with unilateral cerebral hypoperfusion. The effects on kidney function, heart function, coagulation, neurological function and cerebralvascular events will be assessed. Trial registration ClinicalTrials.gov (Identifier: NCT01192581)</p

Endothelin-1 induces hypoxia inducible factor 1 alpha expression in pulmonary artery smooth muscle cells

Chinese National Science Foundation [81070045, 8117051]; Second Affiliated Hospital of Medical College of Xi'an Jiaotong University, PR ChinaEndothelin-1 (ET-1) dose-dependently increased HIF1 alpha expression in pulmonary artery smooth muscle cells (PASMCs). Inhibition of protein synthesis did not affect ET-1-induced HIF1 alpha expression. The maximum effect of ET-1 was similar to that caused by proteasome inhibitor MG132. Further study indicates that ET-1 also dose-dependently stimulated calcineurin activation, specific calcineurin inhibitor cyclosporine A (CsA), abolished ET-1-induced HIF1 alpha elevation, and reversed ET-1-induced RACK1 (receptor of activated protein kinase C 1) de-phosphorylation. Endothelin receptor A was found to specifically mediate the effects of ET-1. To examine whether RACK1 is particularly involved in proteasome-dependent HIF1 alpha degradation, RACK1 was silenced by siRNA transfection. Cells lacking RACK1 exhibited significant elevation of HIF1 alpha protein level. Taken together, our study suggests that ET-1 suppressed proteasome-dependent HIF1 alpha degradation by calcineurin-dependent RACK1 de-phosphorylation. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved