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Purpose Patient-reported outcomes and experiences (PRO) data are an integral component of health care quality measurement and PROs are now being collected by many healthcare systems. However, hospital organizational capacity-building for the collection and sharing of PROs is a complex process. We sought to identify the factors that facilitated capacity-building for PRO data collection in a nascent quality improvement learning collaborative of 16 hospitals that has the goal of improving the childbirth experience. Description We used standard qualitative case study methodologies based on a conceptual framework that hypothesizes that adequate organizational incentives and capacities allow successful achievement of project milestones in a collaborative setting. The 4 project milestones considered in this study were: (1) Agreements; (2) System Design; (3) System Development and Operations; and (4) Implementation. To evaluate the success of reaching each milestone, critical incidents were logged and tracked to determine the capacities and incentives needed to resolve them. Assessment The pace of the implementation of PRO data collection through the 4 milestones was uneven across hospitals and largely dependent on limited hospital capacities in the following 8 dimensions: (1) Incentives; (2) Leadership; (3) Policies; (4) Operating systems; (5) Information technology; (6) Legal aspects; (7) Cross-hospital collaboration; and (8) Patient engagement. From this case study, a trajectory for capacity-building in each dimension is discussed. Conclusion The implementation of PRO data collection in a quality improvement learning collaborative was dependent on multiple organizational capacities for the achievement of project milestones., Author(s): Samia Saeb [sup.1] , Lisa M. Korst [sup.2] , Moshe Fridman [sup.2] , Jeanette McCulloch [sup.3] , Naomi Greene [sup.1] , Kimberly D. Gregory [sup.1] Author Affiliations: (1) grid.50956.3f, [...]

Objectives The goals of interconception care are to optimize women's health and encourage adequate spacing between pregnancies. Our study calculated trends in interpregnancy interval (IPI) patterns and measured the association of differing intervals with birth outcomes in California. Methods Women with 'non-first birth' deliveries in California hospitals from 2007 to 2009 were identified in a linked birth certificate and patient discharge dataset and divided into three IPI birth categories:, Author(s): Flojaune Griffin Cofer[sup.1] , Moshe Fridman[sup.2] , Elizabeth Lawton[sup.1] , Lisa M. Korst[sup.3] , Lisa Nicholas[sup.5] , Kimberly D. Gregory[sup.4] [sup.5] [sup.6] Author Affiliations: (1) Maternal, Child and Adolescent [...]

The tracking of elective deliveries (ED) prior to 39 gestational weeks has become a mandatory requirement for all hospitals with [greater than or equal to]1,100 deliveries for accreditation by The Joint Commission (TJC); however, the feasibility and accuracy of monitoring efforts remain problematic for many hospitals. Here, we evaluated the feasibility of three operational approaches to tracking ED. We used mixed methods to evaluate the feasibility of 3 different approaches to tracking ED: (1) using administrative data, (2) using electronic medical record (EMR) data, and (3) using targeted data collection in a county-wide quality improvement (QI) effort. For (1), we analyzed data from the California 2009 linked birth cohort dataset, and calculated hospital rates of ED using TJC technical specifications. For (2), we performed a case study of a project that recruited hospitals to provide EMR data for the TJC measure calculation. For (3), we performed a case study of a project that recruited hospitals to prospectively track elective inductions of labor. For (1), hospital discharge data were insufficient without supplementation from the EMR or birth certificate. For (2), legal and operational issues surrounding data sharing, and non-standardized data elements prohibited hospital participation. For (3), the QI approach successfully established policies and data collection systems yet lacked infrastructure to assure sustainability at a hospital or regional level. In summary, ED tracking required the coordination and support of multiple resources to enable hospitals to satisfactorily report on this measure. Electronic supplementary material The online version of this article (doi:10.1007/s10995-015-1725-y) contains supplementary material, which is available to authorized users., Author(s): Lisa M. Korst[sup.1] , Moshe Fridman[sup.2] , Melanie Estarziau[sup.3] , Kimberly D. Gregory[sup.4] [sup.5] , Connie Mitchell[sup.6] Author Affiliations: (1) Childbirth Research Associates, North Hollywood, CA, USA (2) AMF [...]

Background Many providers ignore hypertensive blood pressures (BPs) during epidural placement, attributing them to patient pain or malposition. We aimed to determine if an elevated BP during epidural placement was associated with increased risk for developing a hypertensive disorder of pregnancy (HDP). Methods Cohort study of previously normotensive nulliparous, singleton, term patients who received neuraxial analgesia and delivered at our institution in 2016. Primary exposure was BP during epidural window (one hour before and after epidural procedure start time). Primary outcome was HDP (gestational hypertension, preeclampsia, eclampsia, or HELLP syndrome) prior to discharge. Statistics included χ², t-test, and multivariable logistic regression; α = 0.05. Results One thousand and eight hundred patients met study criteria. Patients with elevated BP during epidural window (n = 566, 31.4%) were more likely to develop HDP than patients who remained normotensive during epidural window (20.1% vs. 6.4%, adjusted OR 3.57 [95% CI 2.61–4.89]). The incidence of HDP increased in association with BP severity during epidural window: 7.3% for maximum systolic blood pressure (SBP) <140 mmHg; 18.4% for maximum SBP 140–159 mmHg (OR 2.9, 95% CI 2.0–4.0); and 29.9% for maximum SBP ≥160 mmHg (OR 5.4, 95% CI 2.9–9.8). The trend was similar for maximum diastolic BP. The magnitude of increased odds for HDP was highest for Black patients with elevated BP during epidural window (40.9% vs. 10.1%, OR 6.1, 95% CI 2.4–16). Conclusions Previously normotensive patients with an elevated BP during labor epidural placement are significantly more likely to develop HDP than patients who remain normotensive. Elevated BP during epidural placement should not be disregarded to ensure timely diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Description: The Women's Preventive Services Initiative (WPSI), a national coalition of women's health professional organizations and patient advocacy representatives, developed a recommendation for counseling midlife women aged 40 to 60 years with normal or overweight body mass index (BMI; 18.5 to 29.9 kg/m2) to maintain weight or limit weight gain to prevent obesity with the long-term goals of optimizing health, function, and well-being. This recommendation is intended to guide clinical practice and coverage of clinical preventive health services for the Health Resources and Services Administration and other stakeholders. Clinicians providing preventive health care to women in primary care settings are the target audience for this recommendation.Methods: The WPSI developed this recommendation after evaluating results of a systematic review of the effectiveness and harms of interventions to prevent weight gain and obesity in women aged 40 to 60 years without obesity. Seven randomized clinical trials including 51 638 participants and using various counseling and behavioral interventions were included. Trials indicated favorable weight changes with interventions that were statistically significantly different from control groups in 4 of 5 trials of counseling, but not in 2 trials of exercise. Few harms were reported.Recommendation: The WPSI recommends counseling midlife women aged 40 to 60 years with normal or overweight BMI (18.5 to 29.9 kg/m2) to maintain weight or limit weight gain to prevent obesity. Counseling may include individualized discussion of healthy eating and physical activity. [ABSTRACT FROM AUTHOR]

Depressed cardiac Ca cycling by the sarcoplasmic reticulum (SR) has been associated with attenuated contractility, which can progress to heart failure. The histidine-rich Ca-binding protein (HRC) is an SR component that binds to triadin and may affect Ca release through the ryanodine receptor. HRC overexpression in transgenic mouse hearts was associated with decreased rates of SR Ca uptake and delayed relaxation, which progressed to hypertrophy with aging. The present study shows that HRC may mediate part of its regulatory effects by binding directly to sarco(endo)plasmic reticulum Ca-ATPase type 2 (SERCA2) in cardiac muscle, which is confirmed by coimmunostaining observed under confocal microscopy. This interaction involves the histidine- and glutamic acid-rich domain of HRC (320-460 aa) and the part of the [NH.sub.2]-terminal cation transporter domain of SERCA2 (74-90 aa) that projects into the SR lumen. The SERCA2-binding domain is upstream from the triadin-binding region in human HRC (609-699 aa). Specific binding between HRC and SERCA was verified by coimmunoprecipitation and pull-down assays using human and mouse cardiac homogenates and by blot overlays using glutathione S-transferase and maltose-binding protein recombinant proteins. Importantly, increases in Ca concentration were associated with a significant reduction of HRC binding to SERCA2, whereas they had opposite effects on the HRC-triadin interaction in cardiac homogenates. Collectively, our data suggest that HRC may play a key role in the regulation of SR Ca cycling through its direct interactions with SERCA2 and triadin, mediating a fine cross talk between SR Ca uptake and release in the heart. triadin; calcium cycling

Regulation of myocardial function by histidine-rich, calcium-binding protein. Am J Physiol Heart Circ Physiol 287: H1705-H1711, 2004. First published June 10, 2004; 10.1152/ajpheart.01211.2003.--Impaired sarcoplasmic reticulum (SR) Ca release has been suggested to contribute to the depressed cardiac function in heart failure. The release of Ca from the SR may be regulated by the ryanodine receptor, triadin, junctin, calsequestrin, and a histidine-rich, Ca-binding protein (HRC). We observed that the levels of HRC were reduced in animal models and human heart failure. To gain insight into the physiological function of HRC, we infected adult rat cardiac myocytes with a recombinant adenovirus that contains the full-length mouse HRC cDNA. Overexpression (l.7-fold) of HRC in adult rat cardiomyocytes was associated with increased SR Ca load (28%) but decreased SR Ca-induced Ca release (37%). resulting in impaired Ca cycling and depressed fractional shortening (36%) as well as depressed rates of shortening (38%) and relengthening (33%). Furthermore, the depressed basal contractile and Ca kinetic parameters in the HRC-infected myocytes remained significantly depressed even after maximal isoproterenol stimulation. Interestingly, HRC overexpresssion was accompanied by increased protein levels of junctin (1.4-fold) and triadin (1.8-fold), whereas the protein levels of ryanodine receptor, calsequestrin, phospholamban, and sarco(endo)plasmic reticulum Ca-ATPase remained unaltered. Collectively, these data indicate that alterations in expression levels of HRC are associated with impaired cardiac SR Ca homeostasis and contractile function. sarcoplasmic reticulum; calcium cycling; contractility

The protein kinase C (PKC) family of serine/threonine kinases functions downstream of nearly all membrane-associated signal transduction pathways. Here we identify PKC-[alpha] as a fundamental regulator of cardiac contractility and Ca[sup.2+] handling in myocytes. Hearts of Prkca-deficient mice are hypercontractile, whereas those of transgenic mice overexpressing Prkca are hypocontractile. Adenoviral gene transfer of dominant-negative or wild-type PKC-[alpha] into cardiac myocytes enhances or reduces contractility, respectively. Mechanistically, modulation of PKC-[alpha] activity affects dephosphorylation of the sarcoplasmic reticulum Ca[sup.2+] ATPase-2 (SERCA-2) pump inhibitory protein phospholamban (PLB), and alters sarcoplasmic reticulum Ca[sup.2+] loading and the Ca[sup.2+] transient. PKC-[alpha] directly phosphorylates protein phosphatase inhibitor-1 (I-1), altering the activity of protein phosphatase-1 (PP-1), which may account for the effects of PKC-[alpha] on PLB phosphorylation. Hypercontractility caused by Prkca deletion protects against heart failure induced by pressure overload, and against dilated cardiomyopathy induced by deleting the gene encoding muscle LIM protein (Csrp3). Deletion of Prkca also rescues cardiomyopathy associated with overexpression of PP-1. Thus, PKC-[alpha] functions as a nodal integrator of cardiac contractility by sensing intracellular Ca[sup.2+] and signal transduction events, which can profoundly affect propensity toward heart failure., Author(s): Julian C Braz [1, 2]; Kimberly Gregory [2]; Anand Pathak [2]; Wen Zhao [2]; Bogachan Sahin [3]; Raisa Klevitsky [1]; Thomas F Kimball [1]; John N Lorenz [4]; Angus [...]