Provider networks and health plan premium variation

ObjectiveTo examine how plan premiums are associated with physician network breadth, hospital network breadth, and hospital network quality on the Affordable Care Act''s Health Insurance Marketplaces in all 50 states and the DC in 2016.Data SourcesData on plan premiums and characteristics came from 2016 Robert Wood Johnson Foundation Health Insurance Exchange (HIX) Compare. Provider network information was obtained from Vericred. Hospital characteristics were obtained from CMS Hospital Compare and the American Hospital Association (AHA) survey.Study DesignWe analyzed how plan premiums were associated with variations in physician network breadth, hospital network breadth, and hospital network quality using ordinary least square regressions with state‐rating area fixed effects and carrier fixed effects.Principal FindingsPlan premiums were positively associated with physician network breadth and hospital network breadth. We find the following statistically significant results: a one standard deviation increase in physician network breadth was linked to a premium increase of 2.8 percent or $101 per year; a one standard deviation increase in hospital network breadth was linked to a premium increase of 2.4 percent or $86 per year. There was no significant association between premiums and hospital network quality, as measured by hospital star ratings and the inclusion of teaching hospitals or the top‐20 hospitals nationwide.ConclusionsPhysician network breadth and hospital network breadth contributed positively to plan premiums. The roles of the two types of provider network breadth are quantitatively similar. Premiums appear to be insensitive to hospital network quality.     

抗心磷脂抗体与反复流产及宫内死胎关系

目的　探讨反复流产、宫内死胎、孕中、晚期孕妇与抗磷脂自身抗体的关系。方法　采用ELISA对44 2例患者进行ACA IgG、ACA IgM抗体测定。结果　表明反复流产患者血中ACA阳性检出率最高达 44 % ,宫内死胎阳性率 30 % ,正常妊娠妇女阳性率为 3.6 % ,检出阳性者多为宫内发育迟缓及轻度妊高症。结论　ACA阳性与反复流产及宫内死胎、宫内发育迟缓有密切关系。     

头孢噻呋钠的制备

目的 头孢噻呋钠制备工艺的研究。方法 7-ACA与2-呋喃甲硫羟酸缩合后，与AE活性酯反应得头孢噻呋酸，然后依次将之转化为头孢噻呋盐酸盐及头孢噻呋钠。结果 以7-ACA计算，总重量收率为78．9％。结论 此方法收率高，产品纯度好，适合工业化生产。     

Characterization and Management of Arrhythmic Events in Young Patients With Brugada Syndrome

Background

Information on young patients with Brugada syndrome (BrS) and arrhythmic events (AEs) is limited.

Long QT syndrome

The hereditary long QT syndrome (LQTS) is a genetic channelopathy with variable penetrance that is associated with increased propensity to syncope, polymorphous ventricular tachycardia (torsades de pointes), and sudden arrhythmic death. This inherited cardiac disorder constitutes an important cause of malignant ventricular arrhythmias and sudden cardiac death in young individuals with normal cardiac morphology. Risk assessment in affected LQTS patients relies upon a constellation of electrocardiographic, clinical, and genetic factors. Administration of beta-blockers is the mainstay therapy in affected patients, and primary prevention with an implantable cardioverter defibrillator or left cervicothoracic sympathetic denervation are therapeutic options in patients who remain symptomatic despite beta-blocker therapy. Accumulating data from the International LQTS Registry have recently facilitated a comprehensive analysis of risk factors for aborted cardiac arrest or sudden cardiac death in pre-specified age groups, including the childhood, adolescence, adulthood, and post-40 periods. These analyses have consistently indicated that the phenotypic expression of LQTS is time dependent and age specific, warranting continuous risk assessment in affected patients. Furthermore, the biophysical function, type, and location of the ion-channel mutation are currently emerging as important determinants of outcome in genotyped patients. These new data may be used to improve risk stratification and for the development of gene-specific therapies that may reduce the risk of life-threatening cardiac events in patients with this inherited cardiac disorder.     

Surface-displayed glyceraldehyde 3-phosphate dehydrogenase and galectin from Dirofilaria immitis enhance the activation of the fibrinolytic system of the host

Cardiopulmonary dirofilariosis is a cosmopolitan disease caused by Dirofilaria immitis, a filaroid parasite whose adult worms live for years in the vascular system of its host. Previous studies have shown that D. immitis can use their excretory/secretory (ES) and surface antigens to enhance fibrinolysis, which could limit the formation of clots in its surrounding environment. Moreover, several isoforms of the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and galectin (GAL) were identified in both antigenic extracts as plasminogen-binding proteins. The aim of this work is to study the interaction of the GAPDH and GAL of D. immitis with the fibrinolytic system of the host. This study includes the cloning, sequencing and expression of the recombinant forms of the GAPDH and GAL of D. immitis (rDiGAPDH and rDiGAL) and the analysis of their capacity as plasminogen-binding proteins. The results indicate that rDiGAPDH and rDiGAL are able to bind plasminogen and stimulate plasmin generation by tissue plasminogen activator (tPA). This interaction needs the involvement of lysine residues, many of which are located externally in both proteins as have been shown by the molecular modeling of their secondary structures. In addition, we show that rDiGAPDH and rDiGAL enhance the expression of the urokinase-type plasminogen activator (uPA) on canine endothelial cells in culture and that both proteins are expressed on the surface of D. immitis in close contact with the blood of the host. These data suggest that D. immitis could use the associated surface GAPDH and GAL as physiological plasminogen receptors to shift the fibrinolytic balance towards the generation of plasmin, which might constitute a survival mechanism to avoid the clot formation in its intravascular habitat.