Reducing gender disparities in post-total knee arthroplasty expectations through a decision aid

BACKGROUND: Gender disparities in total knee arthroplasty utilization may be due to differences in perceptions and expectations about total knee arthroplasty outcomes. This study evaluates the impact of a decision aid on perceptions about total knee arthroplasty and decision-making parameters among patients with knee osteoarthritis. METHODS: Patients with moderate to severe knee osteoarthritis viewed a video about knee osteoarthritis treatments options, including total knee arthroplasty, and received a personalized arthritis report. An adapted version of the Western Ontario and McMaster Universities Osteoarthritis Index was used to assess pain and physical function expectations following total knee arthroplasty before/after the intervention. These scores were compared to an age- and gender-adjusted means for a cohort of patients who had undergone total knee arthroplasty. Decision readiness and conflict were also measured. RESULTS: At baseline, both men and women had poorer expectations about post-operative pain and physical outcomes compared with observed outcomes of the comparator group. Following the intervention, women’s mean age-adjusted expectations about post- total knee arthroplasty pain outcomes improved (Pre: 27.0; Post: 21.8 [p =0.08; 95% CI −0.7, 11.0]) and were closer to observed post-TKA outcomes; whereas men did not have a significant change in their pain expectations (Pre: 21.3; Post: 19.6 [p = 0.6; 95% CI −5.8, 9.4]). Women also demonstrated a significant improvement in decision readiness; whereas men did not. Both genders had less decision conflict after the intervention. CONCLUSIONS: Both women and men with osteoarthritis had poor estimates of total knee arthroplasty outcomes. Women responded to the intervention with more accurate total knee arthroplasty outcome expectations and greater decision readiness. Improving patient knowledge of total knee arthroplasty through a decision aid may improve medical decision-making and reduce gender disparities in total knee arthroplasty utilization. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12891-015-0473-x) contains supplementary material, which is available to authorized users

The role of membrane lipids in the induction of macrophage apoptosis by microparticles.

Microparticles are membrane-derived vesicles that are released from cells during activation or cell death. These particles can serve as mediators of intercellular cross-talk and induce a variety of cellular responses. Previous studies have shown that macrophages undergo apoptosis after phagocytosing microparticles. Here, we have addressed the hypothesis that microparticles trigger this process via lipid pathways. In these experiments, microparticles induced apoptosis in primary macrophage cells or cell lines (RAW 264.7 or U937) with up to a 5-fold increase. Preincubation of macrophages with phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)BP) reduced the microparticle-induced apoptosis in a dose-dependent manner. PtdIns(3,5)BP is a specific inhibitor of the acid sphingomyelinase and thus can block the generation of pro-apoptotic ceramides. Similarly, the pre-incubation of macrophages with PtdIns(3,5)BP prevented microparticle-induced upregulation of caspase 8, which is a major target molecule of ceramide action in the apoptosis pathway. PtdIns(3,5)BP, however, had no effect on the spontaneous rate of apoptosis. To evaluate further signaling pathways induced by microparticles, the extracellular signal regulated kinase (ERK-) 1 was investigated. This kinase plays a role in activating phospholipases A2 which cleaves membrane phospholipids into arachidonic acid; microparticles have been suggested to be a preferred substrate for phospholipases A2. As shown in our experiments, microparticles strongly increased the amount of phosphorylated ERK1/2 in RAW 264.7 macrophages in a time-dependent manner, peaking 15 min after co-incubation. Addition of PD98059, a specific inhibitor of ERK1, prevented the increase in apoptosis of RAW 264.7 macrophages. Together, these data suggest that microparticles perturb lipid homeostasis of macrophages and thereby induce apoptosis. These results emphasize the importance of biolipids in the cellular cross-talk of immune cells. Based on the fact that in clinical situations with excessive cell death such as malignancies, autoimmune diseases and following chemotherapies high levels of circulating microparticles might modulate phagocytosing cells, a suppression of the immune response might occur due to loss of macrophages

Unhappiness as an Engine of Economic Growth

1noneThe citizens of the US, China and India have experienced a significant decline in happiness, social capital and leisure in the past few decades, as well as an epidemic of social comparisons. This deep and long-standing social crisis is puzzling when we consider the sustained economic growth of these countries. Is there a relationship between social crisis and growth? The defensive growth approach argues that they may feed each other. The erosion of environmental and social assets caused by increased market activity limits their accessibility, inducing consumers and producers to search for substitutes in the marketplace. Defensive growth is a process whereby market goods and services progressively replace declining non-market sources of well-being and compensate for the negative externalities generated by the increased marketization of society. This process is a selfreinforcing loop: the externalities generated by the expansion of market activities induce households and producers to compensate by buying more goods, further expanding market activity. Because the flip side of increasing economic affluence is rising social and environmental poverty, the impact of defensive growth on happiness is disappointing. I conclude that declining social capital has boosted GDP, working hours and the decline in happiness in the US, China and India. © Springer Nature Switzerland AG 2019noneStefano BartoliniBartolini, Stefan