It takes patience and persistence to get negative feedback about patients’ experiences: a secondary analysis of national inpatient survey data

Background: Patient experience surveys are increasingly used to gain information about the quality of healthcare. This paper investigates whether patients who respond before and after reminders to a large national survey of inpatient experience differ in systematic ways in how they evaluate the care they received. Methods: The English national inpatient survey of 2009 obtained data from just under 70,000 patients. We used ordinal logistic regression to analyse their evaluations of the quality of their care in relation to whether or not they had received a reminder before they responded. Results: 33% of patients responded after the first questionnaire, a further 9% after the first reminder, and a further 10% after the second reminder. Evaluations were less positive among people who responded only after a reminder and lower still among those who needed a second reminder. Conclusions: Quality improvement efforts depend on having accurate data and negative evaluations of care received in healthcare settings are particularly valuable. This study shows that there is a relationship between the time taken to respond and patients’ evaluations of the care they received, with early responders being more likely to give positive evaluations. This suggests that bias towards positive evaluations could be introduced if the time allowed for patients to respond is truncated or if reminders are omitted

Interleukin-17A Serves a Priming Role in Autoimmunity by Recruiting IL-1β-Producing Myeloid Cells that Promote Pathogenic T Cells.

Interleukin-17A (IL-17A) is a major mediator of tissue inflammation in many autoimmune diseases. Anti-IL-17A is an effective treatment for psoriasis and is showing promise in clinical trials in multiple sclerosis. In this study, we find that IL-17A-defective mice or mice treated with anti-IL-17A at induction of experimental autoimmune encephalomyelitis (EAE) are resistant to disease and have defective priming of IL-17-secreting γδ T (γδT17) cells and Th17 cells. However, T cells from Il17a-/- mice induce EAE in wild-type mice following in vitro culture with autoantigen, IL-1β, and IL-23. Furthermore, treatment with IL-1β or IL-17A at induction of EAE restores disease in Il17a-/- mice. Importantly, mobilization of IL-1β-producing neutrophils and inflammatory monocytes and activation of γδT17 cells is reduced in Il17a-/- mice. Our findings demonstrate that a key function of IL-17A in central nervous system (CNS) autoimmunity is to recruit IL-1β-secreting myeloid cells that prime pathogenic γδT17 and Th17 cells.This work was supported by grants from Science Foundation Ireland (11/PI/1036, 16/IA/4468, and 12/RI/2340).S

Loss of the molecular clock in myeloid cells exacerbates T cell-mediated CNS autoimmune disease

Circadian controls of immune responses by the molecular clock have been reported, but the underlying mechanisms are unclear. Here the authors show that the master circadian gene, Bmal1, is essential for modulating the homeostasis of myeloid cells to control pro-inflammatory IL-17+/IFN-γ+ T cells in autoimmunity

Oxygen tension-mediated erythrocyte membrane interactions regulate cerebral capillary hyperemia.

The tight coupling between cerebral blood flow and neural activity is a key feature of normal brain function and forms the basis of functional hyperemia. The mechanisms coupling neural activity to vascular responses, however, remain elusive despite decades of research. Recent studies have shown that cerebral functional hyperemia begins in capillaries, and red blood cells (RBCs) act as autonomous regulators of brain capillary perfusion. RBCs then respond to local changes of oxygen tension (PO2) and regulate their capillary velocity. Using ex vivo microfluidics and in vivo two-photon microscopy, we examined RBC capillary velocity as a function of PO2 and showed that deoxygenated hemoglobin and band 3 interactions on RBC membrane are the molecular switch that responds to local PO2 changes and controls RBC capillary velocity. Capillary hyperemia can be controlled by manipulating RBC properties independent of the neurovascular unit, providing an effective strategy to treat or prevent impaired functional hyperemia