Unveiling Patient Satisfaction: Exploring Demographics, Interactions, and Health-Seeking Behavior

Objective: This study examined the social context of the patient visit (demographics, waiting room experience, patient-provider interaction) and their relationship to satisfaction with the quality of care when seeking medical treatment. It also examined satisfaction as a predictor variable for its effect on three patient behavioral outcomes. Methods: The study was implemented using a cross-sectional quantitative design among adults aged 18 and older. One hundred fifty-eight participants responded to the survey, and the final sample size was n = 147. We employed advanced data analysis, hierarchical regression, three-way ANOVA, linear regression, and logistic regression to examine four outcome variables. Results: Our hierarchical regression found that satisfaction with the quality of care was significantly associated with age, perceptions of rude treatment in the waiting room, the perceived helpfulness of the prescribed treatment, and the provider\u27s friendliness. Linear and logistic regression demonstrated that patient satisfaction strongly predicted whether patients would delay healthcare visits, recommend their current provider to family and friends, and look for a new provider. Conclusions: Factors influencing patient satisfaction appear to differ between older patients and younger adult patients, as demonstrated in this study. Addressing modifiable factors in the waiting room and within the patient-provider interaction may positively affect patient satisfaction, increase healthcare utilization, produce better patient health outcomes, and contribute to organizational success

The Grizzly, November 13, 2008

Berman Expands to Envelop Art and Imagination • Election Night Brings Cheer to Liberal Ursinus College • Changes Expected for This Year\u27s New Member Education • Passage of Prop 8 Leaves Same-Sex Couples Concerned • Days After Election: Obama Gets to Work • Forensics: Not the Science, but the Ursinus Debate Team • Escape Velocity\u27s Eternalmotion Strikes a Chord at UC • Finding the Phillies Parade: An Unforgettable Adventure • History Attached to a Philly Row Home • Opinions: Barack Obama: Our Next President • Kait Sutherland Finishes Out Hockey Reign at Ursinushttps://digitalcommons.ursinus.edu/grizzlynews/1775/thumbnail.jp

The PLATO mission

PLATO (PLAnetary Transits and Oscillations of stars) is ESA’s M3 mission designed to detect and characterise extrasolar planets and perform asteroseismic monitoring of a large number of stars. PLATO will detect small planets (down to <2REarth) around bright stars (<11 mag), including terrestrial planets in the habitable zone of solar-like stars. With the complement of radial velocity observations from the ground, planets will be characterised for their radius, mass, and age with high accuracy (5%, 10%, 10% for an Earth-Sun combination respectively). PLATO will provide us with a large-scale catalogue of well-characterised small planets up to intermediate orbital periods, relevant for a meaningful comparison to planet formation theories and to better understand planet evolution. It will make possible comparative exoplanetology to place our Solar System planets in a broader context. In parallel, PLATO will study (host) stars using asteroseismology, allowing us to determine the stellar properties with high accuracy, substantially enhancing our knowledge of stellar structure and evolution. The payload instrument consists of 26 cameras with 12cm aperture each. For at least four years, the mission will perform high-precision photometric measurements. Here we review the science objectives, present PLATO‘s target samples and fields, provide an overview of expected core science performance as well as a description of the instrument and the mission profile towards the end of the serial production of the flight cameras. PLATO is scheduled for a launch date end 2026. This overview therefore provides a summary of the mission to the community in preparation of the upcoming operational phases

Immunological alterations in murine systemic lupus erythematosus following α7-nicotinic acetylcholine receptor antagonism

Research Appreciation Day Award Winner - 2021 Texas College of Osteopathic Medicine, 2021 Medical Student Government Association Best in Fourth Year Class - 1st PlaceSystemic lupus erythematosus (SLE) is an autoimmune disease associated with pathology of multiple organs and the morbidity and mortality that ensues can be reduced with anti-inflammatory strategies. The cholinergic anti-inflammatory pathway, is an endogenous neuroimmune reflex that inhibits pro-inflammatory cytokine release through stimulation of α7 nicotinic acetylcholine receptors (α7nAChR) on splenic immune cells. Our published studies demonstrate anti-inflammatory capability of α7nAChR activation via nicotine, but loss-of-function studies are needed to further delineate the role of this receptor in SLE. Thus, we hypothesized that α7-nicotinic receptor antagonism with methyllycaconitine would exacerbate SLE's inflammatory cascade. Female SLE (NZBWF1) mice were administered methyllylcaconitine (MLA; 10 mg/kg/day IP) or saline for 14 consecutive days starting at 33 weeks of age and were then euthanized with their spleen and bone marrow processed for flow cytometry (n = 4/group). The percentage of splenic CD3+CD8+ T cells was higher in SLE mice treated with MLA (27.9±4.8 vs. 20.4±3.5%; P=NS), but CD3+CD4+ T cells (66.6±4.3 vs. 73.8±3.2%; P=NS) and CD11c dendritic cells (1.9±4.8 vs. 9.2±5.0%; P=NS) were lower in MLA-treated compared to saline-treated SLE mice. CD3+CD8+ T cells were also higher in the bone barrow of MLA-treated SLE (21.3±0.3% vs. 13.9±3.9 %; P=NS). Although not significant, these results suggest blockade of α7nAChRs potentiates the cytotoxic inflammatory profile in SLE mice. Future work will confirm the role of the α7nAChR in potentiating inflammation and end organ damage in SLE.Supported by the Lupus Research Alliance 550778 and NIH K01HL13986

Abstract 075: Sex Differences in the Development of Autoimmune-Associated Hypertension

Systemic lupus erythematosus (SLE) is an autoimmune disorder with prevalent hypertension and is a novel disease model to study the link between chronic inflammation and hypertension. Because SLE is female-dominant, studies are usually conducted in female NZBWF1 mice, a well-established model of SLE. However, men are also diagnosed with SLE and the late onset and different clinical features draws interest. We hypothesize that sex differences exist in SLE and that female SLE mice have heightened disease, hypertension, and renal injury earlier than males. Female and male SLE and control ( NZW ) mice were monitored for albuminuria starting at 30 weeks of age and then at 35 weeks implanted with vascular catheters to allow measurement of blood pressure in conscious mice. At 30 weeks, female SLE mice had elevated plasma dsDNA autoantibodies, the hallmark of SLE, compared to male SLE (4.6e5 ± 1.3e5 vs. 6.3e4 ± 2.7e4 U/mL; n=3-5; all p&lt;0.05), female controls (8.9e4 ± 3.3e4), and male controls (4.8e4 ± 9.3e3). At this same time point, 32% (7 out of 22) of female SLE mice had albuminuria versus 5% (1 out of 20) of male SLE, 5% (1 out of 22) of female controls, and no male controls. Although male SLE mice did not reach similar levels of dsDNA autoantibodies as SLE females (2.0e5 ± 4.6e4 vs. 3.9e5 ± 4.3e4; n=8-13; p=0.015), by 35 weeks, the autoantibodies were increasing in SLE males (2.0e5 ± 4.6e4 vs. 6.3e4 ± 2.7e4; p=0.157) and higher than male controls (4.3e4 ± 9.3e3; p=0.046). At 35 weeks, 63% (10 out of 16) of female SLE mice had albuminuria versus 5% (1 out of 19) of male SLE, 5% (1 out of 22) of female controls, and no male controls. Importantly, both female and male SLE mice were hypertensive at 35 weeks: blood pressure was higher in female SLE than female controls (152 ± 5 vs. 126 ± 3 mmHg; n=6-8; p=0.003) and in male SLE compared to male controls (152 ± 4 vs. 136 ± 4 mmHg; n=6-11; p=0.041). These data confirm the development of hypertension and renal injury in female SLE mice and suggest that male SLE mice develop hypertension with no renal involvement. Future studies will allow us to investigate the divergent mechanisms involved in autoimmune-induced hypertension in female and male mice, which will ultimately provide clues in sex differences in hypertensive humans with underlying chronic inflammation. </jats:p

Abstract MP24: Selective Activation Of DMV Neurons Improves Renal Injury In Systemic Lupus Erythematosus

The cholinergic anti-inflammatory pathway is a vagally-mediated mechanism that controls inflammation. Our published data suggest that an impaired cholinergic anti-inflammatory pathway contributes to hypertension and renal disease in female mice with systemic lupus erythematosus (SLE), since pharmacological potentiation of the efferent vagus via administration of galantamine reduces renal inflammation, mean arterial pressure (MAP) and glomerulosclerosis. The aim of the current study is to selectively target neurons within the dorsal motor nucleus of the vagus (DMV) to stimulate the efferent vagus and the cholinergic anti-inflammatory pathway using designer receptors exclusively activated by designer drugs (DREADDs). We hypothesized that selective activation of DMV neurons would reduce inflammation, eliminating the associated end organ damage in SLE. To study this, female SLE ( NZBWF1 ) and parental control ( NZW ) mice received bilateral microinjections of pAAV-hSyn-hM3D(Gq)-mCherry or pAAV-hSyn-mCherry (control virus) into the DMV at 31 weeks of age using the following coordinates with calamus as reference: 0 mm caudal, 0.25 mm lateral and 0.48 mm ventral. Two weeks post-microinjection, DREADD agonist CNO (3mg/kg) was administered subcutaneously for 2 weeks starting at 33 weeks. At 35 weeks, mice were housed in metabolic cages for urine collection and catheters were implanted in the carotid artery for MAP measurement. Mice were subsequently euthanized and the brain collected to confirm the site of virus microinjection. Selective activation of DMV neurons decreased the incidence of albuminuria [&gt; 300 mg/dL; 66% (4 out of 6) vs. 0% (0 out of 7)], urinary leukocytes [62.5% (5 out of 8) vs. 50% (3 out of 6)] and blood in the urine [50% (4 out of 8) vs. 16% (1 out of 6)] in SLE mice. MAP did not significantly change with the chemogenetic activation of DMV neurons in SLE mice or parental controls (SLE/control virus: 146 ± 6, n=7; SLE/Gq DREADD: 142 ± 3, n=6; NZW/control virus: 126 ± 4, n=4; NZW/Gq DREADD: 132 ± 2, n=5). These results suggests that this timeline of selective activation of DMV neurons in SLE mice reduces renal injury without altering blood pressure, but future studies will confirm the effect on hypertension and renal inflammation in SLE mice </jats:p

Sex Differences in the Development of Hypertension in the Setting of Autoimmunity

Purpose: Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease associated with high risks of hypertension. We previously confirmed the disease develops later in life in male SLE mice compared to females (35 vs.< 30 weeks). We also found that both male and female SLE mice are hypertensive by 35 weeks and that this hypertension is linked to renal injury in females but not males; therefore, we aimed to investigate potential contributors to the latent sex difference. Toll-like receptor 7 (TLR7) is an immune mediator active in autoimmunity that instigates widespread tissue damage. We hypothesized that increased TLR7 promotes renal injury in female SLE mice and a different mechanism, potentially increased renal vascular resistance (RVR), is responsible for the hypertension in male SLE mice. Methods: Renal cortical expression of TLR7 was assessed via Western blot in male and female SLE mice (NZBWF1) at 35 weeks. Renal blood flow and mean arterial pressure were measured in anesthetized male and female SLE mice to determine RVR. Results: Female SLE mice had higher (p< 0.05) expression of TLR7 (2.6e6 ±5.4e5; normalized to total protein) than males (1.7e6 ± 3.3e5). Male SLE mice had lower RVR than females (5.15 ±0.60 vs. 10.07 ±1.23 mmHg·min·kg·mL-1). Conclusion: Our data suggest that while the hypertension in female SLE mice may be due to renal mechanisms, male SLE mice develop hypertension through other mechanisms. Future studies will continue to dissect sex-specific factors that should be considered when treating hypertensive patients with underlying chronic inflammation

Effect of selective ganglion stimulation on hypertension in systemic lupus erythematosus

Effect of selective ganglion stimulation on hypertension in systemic lupus erythematosus Keanna K. Johnson1, Viet Dinh2, Cassandra M. Young-Stubbs2, Caroline G. Shimoura2, Sarika Chaudhari2, Keisa W. Mathis2 1School of Public Health,2Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, Texas Purpose: Systemic lupus erythematous (SLE) is a female-dominant autoimmune disease that causes widespread inflammation in various organs. Inflammation precedes the prevalent hypertension in the disease. The cholinergic anti-inflammatory pathway (CAP) is an endogenous neuroimmune pathway that reduces inflammation upon stimulation. We hypothesize that stimulation of the CAP by selective activation of the superior cervical ganglion will halt disease progression and hypertension in SLE. Methods: Female SLE (NZBWF1) and control (NZW) mice received unilateral microinjections of pAAV-hSyn-hM3D(Gq)-mCherry, a designer receptor exclusively activated by designer drug (DREADD), or pAAV-hSyn-mCherry (vehicle) at the superior cervical ganglion (SCG) at 32 weeks of age. SCG DREADD injections generate muscarinic receptors on SCG neurons that are activated by the designer drug, clozapine N-oxide (CNO), ultimately leading to neuronal stimulation and potentially activation of the CAP. At 33 weeks of age, mice with SCG DREADD received a daily s.c. injection of CNO (3mg/kg) for two weeks. At 35 weeks, mice received a catheter implant in the carotid artery to measure mean arterial pressure (MAP) for two consecutive days followed by euthanasia and tissue collection. Plasma was collected biweekly via retro-orbital bleeding. Plasma samples were used to quantify double-stranded (ds) DNA autoantibodies. Results: dsDNA autoantibodies were higher in SLE than control mice (8.6e5 ± 1.8e5 vs. 5.1e4 ± 1.1e4 U/mL; p=0.0002; n=13). SCG DREADD did not change dsDNA autoantibody levels in SLE mice (1.1e6 ± 2.6e5 U/mL; p=0.1410; n=6) or control mice (5.4e4 ± 1.5e4 U/mL; p=0.6549; n=9). MAP was significantly higher in SLE mice compared to control mice (150 ± 9 vs. 122 ± 3 mmHg; p=0.0009; n=5–9). SCG DREADD did not change MAP in SLE mice (137 ± 2 mmHg; p=0.2572; n=6) or controls (127 ± 3 mmHg; p=0.7678; n=9). Conclusion: These data suggest that selective activation of the CAP at the level of the SCG using DREADD did not significantly alter disease severity or blood pressure in female SLE mice with advanced disease. Future studies will determine the effect of selective ganglion stimulation on inflammatory outcomes. Funding: Research reported in this abstract was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under Award Number R25HL125447. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.National Heart, Lung, and Blood Institute of the National Institutes of Health under Award Number R25HL12544