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Context

The number of patients discharged from acute care hospitals to skilled nursing facilities (SNFs) is rising. These patients have increasingly complex needs and many experience poor outcomes while under SNF care, including hospital readmissions. Patients' goals of care (GoC) are viewed as a factor contributing to unplanned hospital readmissions from SNFs. However, clinicians' perspectives of GoC for hospitalized patients discharged to SNFs are not well-described.

Objectives

To explore how clinicians view GoC for hospitalized patients discharged to SNFs.

Methods

Qualitative study using semi-structured interviews and thematic analysis.

Results

Forty-one clinicians from one acute care hospital and two SNFs completed interviews ranging in length from 14 to 52 minutes (mean = 32 minutes). Of the sample, 22% were nurses, 20% physicians, 15% were from care management, and 15% were from social services. Respondents viewed patients' GoC for continuing treatment at the SNF as important, but acknowledged that they were infrequently discussed during hospitalization. Many respondents felt that patients and families had unrealistic GoC for SNF care. Factors that contributed to unrealistic GoC included patients' limited knowledge of disease processes, prognosis, and treatment options; and inconsistent or insufficient communication of GoC among hospital and SNF clinicians, the patient, and family members. Respondents associated a lack of GoC or unrealistic GoC with patients' dissatisfaction with SNF care, unplanned transitions to hospice, and hospital readmissions.

Conclusions

Respondents reported that GoC conversations infrequently occurred during hospitalization, contributing to unrealistic patient and family expectations for SNF care and poor patient outcomes. Interventions are needed that facilitate timely, accurate, and consistent GoC discussions across care continuums.  相似文献   
84.

Background:

Studies evaluating the impact of passive cost visibility tools on antibiotic prescribing are lacking.

Objective:

The objective of this study was to evaluate whether the implementation of a passive antibiotic cost visibility tool would impact antibiotic prescribing and decrease antibiotic spending.

Methods:

An efficiency and effectiveness initiative (EEI) was implemented in October 2012. To support the EEI, an antibiotic cost visibility tool was created in June 2013 displaying the relative cost of antibiotics. Using an observational study of interrupted time series design, 3 time frames were studied: pre EEI, post EEI, and post cost visibility tool implementation. The primary outcome was antibiotic cost per 1,000 patient days. Secondary outcomes included case mix index (CMI)–adjusted antibiotic cost per 1,000 patient days and utilization of the cost visibility tool.

Results:

Initiation of the EEI was associated with a $4,675 decrease in antibiotic cost per 1,000 patient days (P = .003), and costs continued to decrease in the months following EEI (P = .009). After implementation of the cost visibility tool, costs remained stable (P = .844). Despite CMI increasing over time, adjustment for CMI had no impact on the directionality or statistical significance of the results.

Conclusion:

Our study demonstrated a significant and sustained decrease in antibiotic cost per 1,000 patient days when focused medication cost reduction efforts were implemented, but passive cost visibility tool implementation was not associated with additional cost reduction. Antibiotic cost visibility tools may be of most benefit when prior medication cost reduction efforts are lacking or when an active intervention is incorporated.  相似文献   
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BACKGROUND. Measurement of cardiac norepinephrine spillover may indicate the amount of transmitter at neuroeffector sites but does not distinguish neuronal release or reuptake in determining this amount or provide information about other aspects of sympathetic function. This report examines how cardiac spillover of the norepinephrine metabolite dihydroxyphenylglycol (DHPG) provides additional distinct information about cardiac sympathetic function. METHODS AND RESULTS. Arterial and coronary venous blood samples were taken during cardiac catheterization and intravenous infusion of [3H]norepinephrine in 57 subjects. Subjects were given intravenous yohimbine or underwent mental stress, handgrip exercise, and cycling exercise to activate sympathetic nerves or were given intravenous desipramine to block norepinephrine reuptake. Cardiac DHPG spillover (601 +/- 41 pmol/min) was eightfold greater than norepinephrine spillover (78 +/- 10 pmol/min) at rest and increased during sympathetic activation by 65% of the increase of norepinephrine. This and the desipramine-sensitive cardiac production of [3H]-labeled DHPG from [3H]norepinephrine indicated that 10.5 times more endogenous norepinephrine is recaptured than escapes into plasma; that more than 90% of recaptured norepinephrine is sequestered into storage vesicles; and that under resting conditions, most cardiac spillover of DHPG and turnover of norepinephrine are from metabolism of transmitter leaking from vesicles; the latter process is independent of exocytotic transmitter release with a rate at rest over 100-fold that of norepinephrine spillover and over 10-fold that of norepinephrine reuptake. CONCLUSIONS. Cardiac spillover of DHPG provides information about processes close to or within sympathetic nerve endings that cannot be provided by measurements of norepinephrine spillover alone. This includes quantitative information about the role of neuronal uptake in terminating the actions of norepinephrine at neuroeffector sites and the importance of vesicular-axoplasmic exchange of norepinephrine as a dynamic process contributing to norepinephrine turnover.  相似文献   
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To assess the role of different factors on the long-term antihypertensive effect of regular exercise we examined the time course of changes in haemodynamics, oxygen consumption and plasma noradrenaline in 10 normal healthy subjects. For 12 weeks, subjects performed alternating months of training and detraining in a random order. Training involved 40 min of bicycle exercise three times per week at 60-70% of maximum work. Steady-state changes at the end of 1 month's exercise were: (1) falls in resting blood pressure when supine and erect by 8/5 and 10/6 mmHg, respectively (P less than 0.01); (2) a reduction in the total peripheral resistance index of 14%; (3) an increase in maximum oxygen consumption of 14% (P less than 0.005); and (4) a fall in plasma noradrenaline of 21% (P less than 0.05). A significant fall in blood pressure occurred at the third training bout (P less than 0.005), at the beginning of the second week, and no further reduction occurred beyond the fourth bout of exercise. The reduction in plasma noradrenaline concentration was confined to the second half of the month in which exercise took place and lagged behind the blood pressure changes. There were significant differences between the rates of the initial fall of blood pressure and noradrenaline, and the times taken for the maximum changes to occur (P less than 0.05). During detraining, blood pressure remained low for 1-2 weeks after cessation of exercise, as did plasma noradrenaline. Both then rose gradually towards the initial sedentary levels.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   
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Endogenous plasma prolactin and baseline corticosterone concentrations were measured in Dark-eyed Juncos (Junco hyemalis, n=27) photostimulated into migratory condition to look at how these hormones may be linked to the development of migratory condition. In addition to the commonly used assay for corticosterone, a recombinant-derived European starling prolactin assay validated for Dark-eyed juncos was used to measure endogenous prolactin in order to detect small but significant changes in plasma prolactin levels. In response to transfer from short (10.5L:13.5D) to long (18L:6D) days, the birds increased in body mass, fat score, daily food intake, and nocturnal migratory locomotor activity (Zugunruhe). On short-days, both hormones were low (corticosterone mean=2.89ng/mL+/-0.48 SE; prolactin mean=6.43ng/mL+/-1.31 SE). But, within 14 days of photostimulation both hormones increased significantly (Day 14: corticosterone mean=5.71ng/mL+/-0.77 SE; prolactin mean=19.67ng/mL+/-2.81 SE), rising further by Day 48 (corticosterone mean=8.41ng/mL+/-0.72; prolactin mean=112.67ng/mL+/-9.18 SE). On Day 48, birds with the most fat (fat score=3) had significantly higher corticosterone levels than those with less fat (fat score=2). This pattern, albeit not statistically significant, was similar for prolactin. These results illustrate that, independent of the seasonal peak in prolactin associated with the onset of photorefractoriness, plasma prolactin levels can rise, in concert with corticosterone, as birds come into spring migratory condition, providing some support for earlier hypotheses that these two hormones play an integral role in the development of migratory condition. Whether similar changes in plasma prolactin occur with respect to autumn migration, as does baseline corticosterone, has yet to be determined.  相似文献   
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The alpha4 laminin subunit is a component of the basement membrane of blood vessels where it codistributes with the integrins alphavbeta3, alpha3beta1, and alpha6beta1. An antibody against the G domain (residues 919-1207; G(919-1207)) of the alpha4 laminin subunit inhibits angiogenesis in a mouse-human chimeric model, indicating the functional importance of this domain. Additional support for the latter derives from the ability of recombinant G(919-1207) to support endothelial cell adhesion. In particular, endothelial cell adhesion to G(919-1207) is half-maximal at 1.4 nM, whereas residues 919-1018 and 1016-1207 of the G domain are poor cellular ligands. Function blocking antibodies against integrins alphavbeta3 and beta1 and a combination of antibodies against alpha3 and alpha6 integrin subunits inhibit endothelial cell attachment to G(919-1207). Moreover, both alphavbeta3 and alpha3beta1 integrin bind with high affinity to G(919-1207). Together, our studies demonstrate that the G domain of laminin alpha4 chain is a specific, high affinity ligand for the alphavbeta3 and alpha3beta1 integrin heterodimers and that these integrins, together with alpha6beta1, function cooperatively to mediate endothelial cell-alpha4 laminin interaction and hence blood vessel development. We propose a model based on these data that reconcile apparent discrepancies in the recent literature with regard to the role of the alphavbeta3 integrin in angiogenesis.  相似文献   
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