Gender, religion, and sociopolitical issues in cross-cultural online education

Cross-cultural education is thought to develop critical consciousness of how unequal distributions of power and privilege affect people’s health. Learners in different sociopolitical settings can join together in developing critical consciousness – awareness of power and privilege dynamics in society – by means of communication technology. The aim of this research was to define strengths and limitations of existing cross-cultural discussions in generating critical consciousness. The setting was the FAIMER international fellowship program for mid-career interdisciplinary health faculty, whose goal is to foster global advancement of health professions education. Fellows take part in participant-led, online, written, task-focused discussions on topics like professionalism, community health, and leadership. We reflexively identified text that brought sociopolitical topics into the online environment during the years 2011 and 2012 and used a discourse analysis toolset to make our content analysis relevant to critical consciousness. While references to participants’ cultures and backgrounds were infrequent, narratives of political-, gender-, religion-, and other culture-related topics did emerge. When participants gave accounts of their experiences and exchanged cross-cultural stories, they were more likely to develop ad hoc networks to support one another in facing those issues than explore issues relating to the development of critical consciousness. We suggest that cross-cultural discussions need to be facilitated actively to transform learners’ frames of reference, create critical consciousness, and develop cultural competence. Further research is needed into how to provide a safe environment for such learning and provide faculty development for the skills needed to facilitate these exchanges.

Cystic Fibrosis from Laboratory to Bedside: The Role of A20 in NF-κB-Mediated Inflammation

Cystic fibrosis (CF) is a lifelong, inflammatory multi-organ disease and the most common lethal, genetic condition in Caucasian populations, with a median survival rate of 41.5 years. Pulmonary disease, characterized by infective exacerbations, bronchiectasis and increasing airway insufficiency is the most serious manifestation of this disease process, currently responsible for over 80% of CF deaths. Chronic dysregulation of the innate immune and host inflammatory response has been proposed as a mechanism central to this genetic condition, primarily driven by the nuclear factor κB (NF-κB) pathway. Chronic activation of this transcription factor complex leads to the production of pro-inflammatory cytokines and mediators such as IL-6, IL-8 and TNF-α. A20 has been described as a central and inducible negative regulator of NF-κB. This intracellular molecule negatively regulates NF-κB-driven pro-inflammatory signalling upon toll-like receptor activation at the level of TRAF6 activation. Silencing of A20 increases cellular levels of p65 and induces a pro-inflammatory state. We have previously shown that A20 expression positively correlates with lung function (FEV1%) in CF. Despite improvement in survival rates in recent years, advancements in available therapies have been incremental. We demonstrate that the experimental use of naturally occurring plant diterpenes such as gibberellin on lipopolysaccharide-stimulated cell lines reduces IL-8 release in an A20-dependent manner. We discuss how the use of a novel bio-informatics gene expression connectivity-mapping technique to identify small molecule compounds that similarly mimic the action of A20 may lead to the development of new therapeutic approaches capable of reducing chronic airway inflammation in CF. 

Comments on “Wirtinger-based integral inequality: Application to time-delay systems [Automatica 49 (2013) 2860–2866]”

In a recent paper (Automatica 49 (2013) 2860–2866), the Wirtinger-based inequality has been introduced to derive tractable stability conditions for time-delay or sampled-data systems. We point out that there exist two errors in Theorem 8 for the stability analysis of sampled-data systems, and the correct theorem is presented.

The VLT-FLAMES Tarantula Survey XXII. Multiplicity properties of the B-type stars

We investigate the multiplicity properties of 408 B-type stars observed in the 30 Doradus region of the Large Magellanic Cloud with multi-epoch spectroscopy from the VLT-FLAMES Tarantula Survey (VFTS). We use a cross-correlation method to estimate relative radial velocities from the helium and metal absorption lines for each of our targets. Objects with significant radial-velocity variations (and with an amplitude larger than 16 km s^-1) are classified as spectroscopic binaries. We find an observed spectroscopic binary fraction (defined by periods of <10^3.5 d and mass ratios >0.1) for the B-type stars, f<inf>B</inf>(obs) = 0.25 ± 0.02, which appears constant across the field of view, except for the two older clusters (Hodge 301 and SL 639). These two clusters have significantly lower binary fractions of 0.08 ± 0.08 and 0.10 ± 0.09, respectively. Using synthetic populations and a model of our observed epochs and their potential biases, we constrain the intrinsic multiplicity properties of the dwarf and giant (i.e. relatively unevolved) B-type stars in 30 Dor. We obtain a present-day binary fraction f<inf>B</inf>(true) = 0.58 ± 0.11, with a flat period distribution. Within the uncertainties, the multiplicity properties of the B-type stars agree with those for the O stars in 30 Dor from the VFTS.

TH2 and TH17 inflammatory pathways are reciprocally regulated in asthma

Increasing evidence suggests that asthma is a heterogeneous disorder regulated by distinct molecular mechanisms. In a cross-sectional study of asthmatics of varying severity (n = 51), endobronchial tissue gene expression analysis revealed three major patient clusters: TH2-high, TH17-high, and TH2/17-low. TH2-high and TH17-high patterns were mutually exclusive in individual patient samples, and their gene signatures were inversely correlated and differentially regulated by interleukin-13 (IL-13) and IL-17A. To understand this dichotomous pattern of T helper 2 (TH2) and TH17 signatures, we investigated the potential of type 2 cytokine suppression in promoting TH17 responses in a preclinical model of allergen-induced asthma. Neutralization of IL-4 and/or IL-13 resulted in increased TH17 cells and neutrophilic inflammation in the lung. However, neutralization of IL-13 and IL-17 protected mice from eosinophilia, mucus hyperplasia, and airway hyperreactivity and abolished the neutrophilic inflammation, suggesting that combination therapies targeting both pathways may maximize therapeutic efficacy across a patient population comprising both TH2 and TH17 endotypes.