Patient satisfaction with pain management has increasing importance with Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) scores tied to reimbursement. Previous studies indicate patient satisfaction is influenced by staff interactions. This single-group pre/post design study aimed to improve satisfaction with pain management in older adults undergoing total joint replacement. This was a single-group pre-/posttest design. Nurse (knowledge assessment) and patient (American Pain Society Patient Outcomes Questionnaire Revised [APS-POQ-R], HCAHPS) responses evaluated pre- and postimplementation of the online educational program. Nurse focus group followed intervention. Nurses' knowledge improved significantly (p < .006) postintervention. HCAHPS scores (3-month average) for items reflecting patient satisfaction improved from 70.2 ± 9.5 to 73.9 ± 6.0. APS-POQ-R scores did not change. Focus group comments indicated need for education regarding linkages between pain management and patient satisfaction. Education on linkages between patient satisfaction and pain management can improve outcomes; education on strategies to further improve practice may enhance ability to achieve benchmarks.
The expression of the negative Regulator of G protein signaling 16 (RGS16) is rapidly induced in cardiomyocytes by various stimuli. To identify the promoter of the mouse RGS16 gene, a 1.8-kb deoxyribonucleic acid fragment 5' of the RGS16-coding region was subcloned into a firefly-luciferase reporter vector and four overlapping fragments were analyzed. The luciferase production was quantified in neonatal rat cardiac myocytes (NRCM). A 0.6-kb fragment that induced a tenfold increase in luciferase activity contained the minimal promoter sequence. Its activity was twofold stimulated by fetal calf serum, endothelin-1 (ET-1), and sphingosine 1-phosphate (S1P), which stimuli also elevated the level of RGS16 protein. Stimulation of NRCM with ET-1 induced activation of the monomeric GTPases RhoA and Rac1, whereas S1P and the selective S1P1 receptor agonist SEW2871 only induced a pronounced activation of Rac1. In accordance, the treatment with the Rho-, Rac-, and Cdc42-inactivating Clostridium difficile Toxin B (TcdB) 10463 inhibited ET-1 and S1P-induced transcriptional activation. The ET-1-induced activation was insensitive to pertussis toxin but selectively suppressed by the RhoA-C-specific C2I-C3 ADP-ribosyl transferase and the ET(B) receptor antagonist BQ788. The S1P-induced activation was specifically inhibited by pertussis toxin and the Rac-inactivating TcdB 1470. All stimulated transcriptional activity was abolished by the negative transcription factor Yin Yang 1 (YY1), which binds to a consensus sequence within the minimal promoter. Taken together, our data show that most likely ET(B)- and S1P1-receptors induce RGS16 protein expression in cardiac myocytes by increasing the transcriptional activity of the rgs16 gene. This activation is mediated by heterotrimeric G proteins, Rho GTPases, and is under negative control of the transcription factor YY1.
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