1,633 research outputs found

    Mediating Multiculturally: Culture and the Ethical Mediator

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    This commentary on mediating multiculturally in a chapter of Mediation Ethics (edited by Ellen Waldman) suggests there are times when mediators should not mediate, because of their own ethical commitments. Commenting on a hypothetical divorce scenario (of Ziba, a 17 year old from her 44 year old husband, with two children aged 3 and 2, where the parties claim to want Shari’a principles to apply), the author (Carrie Menkel-Meadow) suggests that she would not mediate a case which might violate formal laws (American marriage and divorce laws) or infringe on rights that one of the parties might not be fully aware of. A variety of sources of ethics, including formal law, legal and mediation ethical rules, and personal ethical commitments may structure how mediators choose whether to take a case, educate the parties about their rights, make a referral, or how to mediate if complex (and different for each of the parties and/or the mediator) legal, moral, religious and cultural values are at stake. The chapter contains contrasting views expressed by two different mediators, with summary and commentary by the book’s editor

    Transplantation of gut microbiota from old mice into young healthy mice reduces lean mass but not bone mass

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    Aging is associated with low bone and lean mass as well as alterations in the gut microbiota (GM). In this study, we determined whether the reduced bone mass and relative lean mass observed in old mice could be transferred to healthy young mice by GM transplantation (GMT). GM from old (21-month-old) and young adult (5-month-old) donors was used to colonize germ-free (GF) mice in three separate studies involving still growing 5- or 11-week-old recipients and 17-week-old recipients with minimal bone growth. The GM of the recipient mice was similar to that of the donors, demonstrating successful GMT. GM from old mice did not have statistically significant effects on bone mass or bone strength, but significantly reduced the lean mass percentage of still growing recipient mice when compared with recipients of GM from young adult mice. The levels of propionate in the cecum of mice receiving old donor GM were significantly lower than those in mice receiving young adult donor GM

    Utilizing the Boston Syncope Observation Management Pathway to Reduce Hospital Admission and Decrease Adverse Outcomes

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    Introduction: In an age of increasing scrutiny of each hospital admission, emergency department (ED) observation has been identified as a low-cost alternative. Prior studies have shown admission rates for syncope in the United States to be as high as 70%. However, the safety and utility of substituting ED observation unit (EDOU) syncope management has not been well studied. The objective of this study was to evaluate the safety of EDOU for the management of patients presenting to the ED with syncope and its efficacy in reducing hospital admissions. Methods: This was a prospective before-and-after cohort study of consecutive patients presenting with syncope who were seen in an urban ED and were either admitted to the hospital, discharged, or placed in the EDOU. We first performed an observation study of syncope management and then implemented an ED observation-based management pathway. We identified critical interventions and 30-day outcomes. We compared proportions of admissions and adverse events rates with a chisquared or Fisher’s exact test. Results: In the “before” phase, 570 patients were enrolled, with 334 (59%) admitted and 27 (5%) placed in the EDOU; 3% of patients discharged from the ED had critical interventions within 30 days and 10% returned. After the management pathway was introduced, 489 patients were enrolled; 34% (p\u3c0.001) of pathway patients were admitted while 20% were placed in the EDOU; 3% (p=0.99) of discharged patients had critical interventions at 30 days and 3% returned (p=0.001). Conclusion: A focused syncope management pathway effectively reduces hospital admissions and adverse events following discharge and returns to the ED. [West J Emerg Med. 2019;20(2)250–255.

    Zinc supplementation alters airway inflammation and airway hyperresponsiveness to a common allergen

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    <p>Abstract</p> <p>Background</p> <p>Zinc supplementation can modulate immunity through inhibition of NF-κB, a transcription factor that controls many immune response genes. Thus, we sought to examine the mechanism by which zinc supplementation tempers the response to a common allergen and determine its effect on allergic airway inflammation.</p> <p>Methods</p> <p>Mice were injected with zinc gluconate prior to German cockroach (GC) feces (frass) exposure and airway inflammation was assessed. Primary bone marrow-derived neutrophils and DMSO-differentiated HL-60 cells were used to assess the role of zinc gluconate on tumor necrosis factor (TNF)α expression. NF-κB:DNA binding and IKK activity were assessed by EMSA and <it>in vitro </it>kinase assay. Protein levels of A20, RIP1 and TRAF6 were assessed by Western blot analysis. Establishment of allergic airway inflammation with GC frass was followed by administration of zinc gluconate. Airway hyperresponsiveness, serum IgE levels, eosinophilia and Th2 cytokine production were assessed.</p> <p>Results</p> <p>Administration of zinc gluconate prior to allergen exposure resulted in significantly decreased neutrophil infiltration and TNFα cytokine release into the airways. This correlated with decreased NF-κB activity in the whole lung. Treatment with zinc gluconate significantly decreased GC frass-mediated TNFα production from bone-marrow derived neutrophils and HL-60 cells. We confirmed zinc-mediated decreases in NF-κB:DNA binding and IKK activity in HL-60 cells. A20, a natural inhibitor of NF-κB and a zinc-fingered protein, is a potential target of zinc. Zinc treatment did not alter A20 levels in the short term, but resulted in the degradation of RIP1, an important upstream activator of IKK. TRAF6 protein levels were unaffected. To determine the application for zinc as a therapeutic for asthma, we administered zinc following the establishment of allergic airway inflammation in a murine model. Zinc supplementation decreased airway hyperresponsiveness and serum IgE levels, but had no effect on Th2 cytokine expression.</p> <p>Conclusions</p> <p>This report suggests that the mechanism by which zinc supplementation alters NF-κB activity is via the alteration of A20 activity. In addition, this study provides evidence that supplementation of zinc to asthmatics may alter airway reactivity and serum IgE levels, suggesting zinc supplementation as a potential treatment for asthmatics.</p

    Potential Impact of miR-137 and Its Targets in Schizophrenia

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    The significant impact of microRNAs (miRNAs) on disease pathology is becoming increas- ingly evident. These small non-coding RNAs have the ability to post-transcriptionally silence the expression of thousands of genes. Therefore, dysregulation of even a single miRNA could confer a large polygenic effect. Schizophrenia is a genetically complex illness thought to involve multiple genes each contributing a small risk. Large genome-wide association studies identified miR-137, a miRNA shown to be involved in neuronal maturation, as one of the top risk genes. To assess the potential mechanism of impact of miR-137 in this disorder and identify its targets, we used a combination of literature searches, ingenuity pathway analysis (IPA), and freely accessible bioinformatics resources. Using TargetScan and the schizophrenia gene resource (SZGR) database, we found that in addition to CSMD1, C10orf26, CACNA1C, TCF4, and ZNF804A, five schizophrenia risk genes whose transcripts are also validated miR-137 targets, there are other schizophrenia-associated genes that may be targets of miR-137, including ERBB4, GABRA1, GRIN2A, GRM5, GSK3B, NRG2, and HTR2C. IPA analyses of all the potential targets identified several nervous system (NS) functions as the top canonical pathways including synaptic long-term potentiation, a process implicated in learning and memory mechanisms and recently shown to be altered in patients with schizophrenia. Among the subset of targets involved in NS development and function, the top scoring pathways were ephrin receptor signaling and axonal guidance, processes that are critical for proper circuitry formation and were shown to be disrupted in schizophrenia. These results suggest that miR-137 may indeed play a substantial role in the genetic etiology of schizophrenia by regulating networks involved in neural development and brain function
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