159 research outputs found

    Defectors cannot be detected during"small talk" with strangers.

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    To account for the widespread human tendency to cooperate in one-shot social dilemmas, some theorists have proposed that cooperators can be reliably detected based on ethological displays that are difficult to fake. Experimental findings have supported the view that cooperators can be distinguished from defectors based on "thin slices" of behavior, but the relevant cues have remained elusive, and the role of the judge's perspective remains unclear. In this study, we followed triadic conversations among unacquainted same-sex college students with unannounced dyadic one-shot prisoner's dilemmas, and asked participants to guess the PD decisions made toward them and among the other two participants. Two other sets of participants guessed the PD decisions after viewing videotape of the conversations, either with foreknowledge (informed), or without foreknowledge (naΓ―ve), of the post-conversation PD. Only naΓ―ve video viewers approached better-than-chance prediction accuracy, and they were significantly accurate at predicting the PD decisions of only opposite-sexed conversation participants. Four ethological displays recently proposed to cue defection in one-shot social dilemmas (arms crossed, lean back, hand touch, and face touch) failed to predict either actual defection or guesses of defection by any category of observer. Our results cast doubt on the role of "greenbeard" signals in the evolution of human prosociality, although they suggest that eavesdropping may be more informative about others' cooperative propensities than direct interaction

    Membrane cholesterol regulates vascular endothelial cell viability, function, and lipid signaling

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    Membranes, including the plasma membrane, consist of phospholipids and cholesterol, which dictate their fluidity and the structural and functional integrities of the mammalian cells. Membrane cholesterol, especially the lipid raft-associated kind, has been emerging as one of the pivotal players among membrane lipids in modulating the cellular signaling cascades, which regulate normal cellular functions and pathophysiological events. Endothelial cells (ECs) of blood vessels are critical in the maintenance of the vascular tone, homeostasis of the blood vessel, and proper function of the cardiovascular system. Cholesterol of the vascular ECs is being recognized as an important element in the vascular EC signaling that dictates cellular replication and cell death. Therefore, here, we hypothesized that the membrane cholesterol would be a key player in maintaining the viability, functions, and lipid signaling of the vascular ECs. In our preliminary studies, to test our hypothesis, we had chosen three different widely used ECs in culture, including the bovine pulmonary artery ECs (BPAECs), bovine lung microvascular ECs, and human umbilical vein ECs as the model ECs. We then subjected these cells to the removal of membrane cholesterol by the treatment of two well established cholesterol-depleting agents, cyclodextrins, methyl-Ξ²-cyclodextrin (MΞ²CD) and hydroxypropyl-Ξ²-cyclodextrin (HPCD) and had chosen that the BPAECs would be used as the model ECs for the entire study. Following the treatment of BPAECs with two different widely used concentrations of MΞ²CD and HPCD (2% and 5%, wt/vol to deplete cellular cholesterol) for 15-120 min, the loss of membrane cholesterol, cell viability, and cell morphology were determined. Membrane cholesterol was determined in the cells by the spectrofluorometric method. Lactate dehydrogenase (LDH) released into the medium was determined by the spectrophotometric method. Cell morphology was examined by light microscopy. The results revealed that both MΞ²CD and HPCD caused significant and striking dose- and time-dependent loss of membrane cholesterol, loss of cell viability, and altered cell morphology in all the three chosen EC systems including the BPAECs. However, MΞ²CD appeared to cause greater loss of membrane cholesterol, cell viability, and cell morphology as compared to the extent of the same caused by HPCD, under identical conditions, in all the chosen EC systems including the BPAECs. On the other hand, filipin (1-10 ΞΌM; as positive control), a fungal natural product, which sequesters but does not remove membrane cholesterol, caused only loss of cell viability in BPAECs without inducing the loss of membrane cholesterol. In conclusion, the results of this study showed that the membrane cholesterol was an important player in maintaining the cell viability and morphology in the vascular ECs. Removal of cholesterol by cyclodextrin (especially MΞ²CD) treatment, apparently caused loss of fluidity of the cell membrane and leakage of vital cellular components, and thus caused loss of cell morphology in BPAECs. Also, the study offered a safer method of removal of cholesterol by utilizing HPCD, without causing extensive loss of cell viability as seen with the MΞ²CD treatment, for studies to investigate the role of lipid raft-associated cholesterol in cellular functions. Phospholipases play important roles in cellular signaling during normal and pathophysiological states. Phospholipase D (PLD) is one such cell signaling phospholipase, which generates potent bioactive lipids such as phosphatidic acid, diacylglycerol, and lysophosphatidic acid from the membrane phospholipids. Here, we also hypothesized that membrane cholesterol (including the raft-associated form) would also modulate the lipid signaling PLD in the vascular ECs. Hence, we tested the modulatory effects of MΞ²CD- and HPCD-assisted cholesterol removal on the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced (through protein kinase C [PKC] activation), diperoxovanadate (DPV)-induced (through protein tyrosine kinase [PTyK] activation), and oxidant (H2O2)-induced PLD activation in BPAECs. Our results revealed that the two chosen cyclodextrins (MΞ²CD and HPCD), differentially regulated the TPA-, DPV-, and oxidant-induced activation of PLD in BPAECs, suggesting that PLD responded to the differential removal of cholesterol and cellular effects (activation of upstream signaling kinases, PKC and PTyK) induced by MΞ²CD and HPCD. Overall, this study established the importance of membrane cholesterol in vascular EC integrity and lipid signaling. Advisor: Narasimham Parinandi, Ph.D.No embarg

    Controlled clinical trial of canine therapy versus usual care to reduce patient anxiety in the emergency department

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    Objective Test if therapy dogs reduce anxiety in emergency department (ED) patients. Methods In this controlled clinical trial (NCT03471429), medically stable, adult patients were approached if the physician believed that the patient had β€œmoderate or greater anxiety.” Patients were allocated on a 1:1 ratio to either 15 min exposure to a certified therapy dog and handler (dog), or usual care (control). Patient reported anxiety, pain and depression were assessed using a 0–10 scale (10 = worst). Primary outcome was change in anxiety from baseline (T0) to 30 min and 90 min after exposure to dog or control (T1 and T2 respectively); secondary outcomes were pain, depression and frequency of pain medication. Results Among 93 patients willing to participate in research, 7 had aversions to dogs, leaving 86 (92%) were willing to see a dog six others met exclusion criteria, leaving 40 patients allocated to each group (dog or control). Median and mean baseline anxiety, pain and depression scores were similar between groups. With dog exposure, median anxiety decreased significantly from T0 to T1: 6 (IQR 4–9.75) to T1: 2 (0–6) compared with 6 (4–8) to 6 (2.5–8) in controls (P<0.001, for T1, Mann-Whitney U and unpaired t-test). Dog exposure was associated with significantly lower anxiety at T2 and a significant overall treatment effect on two-way repeated measures ANOVA for anxiety, pain and depression. After exposure, 1/40 in the dog group needed pain medication, versus 7/40 in controls (P = 0.056, Fisher’s exact test). Conclusions Exposure to therapy dogs plus handlers significantly reduced anxiety in ED patients

    Wildfire Risk as a Socioecological Pathology

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    Wildfire risk in temperate forests has become a nearly intractable problem that can be characterized as a socioecological β€œpathology”: that is, a set of complex and problematic interactions among social and ecological systems across multiple spatial and temporal scales. Assessments of wildfire risk could benefit from recognizing and accounting for these interactions in terms of socioecological systems, also known as coupled natural and human systems (CNHS). We characterize the primary social and ecological dimensions of the wildfire risk pathology, paying particular attention to the governance system around wildfire risk, and suggest strategies to mitigate the pathology through innovative planning approaches, analytical tools, and policies. We caution that even with a clear understanding of the problem and possible solutions, the system by which human actors govern fire-prone forests may evolve incrementally in imperfect ways and can be expected to resist change even as we learn better ways to manage CNHS

    Unconditional care in academic emergency departments

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    Recent news stories have explicitly stated that patients with symptoms of COVID-19 were "turned away" from emergency departments. This commentary addresses these serious allegations, with an attempt to provide the perspective of academic emergency departments (EDs) around the Nation. The overarching point we wish to make is that academic EDs never deny emergency care to any person

    Perception of Physician Empathy Varies With Educational Level and Gender of Patients Undergoing Low-Yield Computerized Tomographic Imaging

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    Objective: Lack of empathic communication between providers and patients may contribute to low value diagnostic testing in emergency care. Accordingly, we measured the perception of physician empathy and trust in patients undergoing low-value computed tomography (CT) in the emergency department (ED). Methods: Multicenter study of ED patients undergoing CT scanning, acknowledged by ordering physicians as unlikely to show an emergent condition. Near the end of their visit, patients completed the Jefferson Scale of Patient Perception of Physician Empathy (JSPPPE), Trust in Physicians Survey (TIPS), and the Group Based Medical Mistrust Scale (GBMMS). We stratified results by patient demographics including gender, race, and education. Results: We enrolled 305 participants across 9 sites with diverse geographic, racial, and ethnic representation. The median scores (interquartile ranges) for the JSPPPE, TIPS, and GBMMS for all patients were 29 (24-33.5), 55 (47-62), and 18 (12-29). Compared with white patients, nonwhite patients had similar JSPPPE and TIPS scores but had higher (worse) GBMMS scores. Females had significantly lower JSPPPE and TIPS scores than males, and scores were lower (worse) in females with college degrees. Patients in the lowest tier of educational status had the highest (better) JSPPPE and TIPS scores. Scores were invariant with physician characteristics. Conclusion: Among patients undergoing low-value CT scanning in the ED, the degree of patient perception of physician empathy and trust varied based on the patients’ level of education and gender. Given this variation, an intervention to increase patient perception of physician empathy should contain individualized strategies to address these subgroups, rather than a one-size-fits-all approach

    Multiple Organ System Defects and Transcriptional Dysregulation in the Nipbl+/βˆ’ Mouse, a Model of Cornelia de Lange Syndrome

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    Cornelia de Lange Syndrome (CdLS) is a multi-organ system birth defects disorder linked, in at least half of cases, to heterozygous mutations in the NIPBL gene. In animals and fungi, orthologs of NIPBL regulate cohesin, a complex of proteins that is essential for chromosome cohesion and is also implicated in DNA repair and transcriptional regulation. Mice heterozygous for a gene-trap mutation in Nipbl were produced and exhibited defects characteristic of CdLS, including small size, craniofacial anomalies, microbrachycephaly, heart defects, hearing abnormalities, delayed bone maturation, reduced body fat, behavioral disturbances, and high mortality (75–80%) during the first weeks of life. These phenotypes arose despite a decrease in Nipbl transcript levels of only ∼30%, implying extreme sensitivity of development to small changes in Nipbl activity. Gene expression profiling demonstrated that Nipbl deficiency leads to modest but significant transcriptional dysregulation of many genes. Expression changes at the protocadherin beta (Pcdhb) locus, as well as at other loci, support the view that NIPBL influences long-range chromosomal regulatory interactions. In addition, evidence is presented that reduced expression of genes involved in adipogenic differentiation may underlie the low amounts of body fat observed both in Nipbl+/βˆ’ mice and in individuals with CdLS
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