Consensual Qualitative Research: An Update

The authors reviewed the application of consensual qualitative research (CQR) in 27 studies published since the method’s introduction to the field in 1997 by C. E. Hill, B. J. Thompson, and E. N. Williams (1997). After first describing the core components and the philosophical underpinnings of CQR, the authors examined how it has been applied in terms of the consensus process, biases, research teams, data collection, data analysis, and writing up the results and discussion sections of articles. On the basis of problems that have arisen in each of these areas, the authors made recommendations for modifications of the method. The authors concluded that CQR is a viable qualitative method and suggest several ideas for research on the method itself

Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass

The apelin receptor (Aplnr) and its ligands, Apelin and Apela, contribute to metabolic control. The insulin resistance associated with pregnancy is accommodated by an expansion of pancreatic β-cell mass (BCM) and increased insulin secretion, involving the proliferation of insulin-expressing, glucose transporter 2-low (Ins+Glut2LO) progenitor cells. We examined changes in the apelinergic system during normal mouse pregnancy and in pregnancies complicated by glucose intolerance with reduced BCM. Expression of Aplnr, Apelin and Apela was quantified in Ins+Glut2LO cells isolated from mouse pancreata and found to be significantly higher than in mature β-cells by DNA microarray and qPCR. Apelin was localized to most β-cells by immunohistochemistry although Aplnr was predominantly associated with Ins+Glut2LO cells. Aplnr-staining cells increased three- to four-fold during pregnancy being maximal at gestational days (GD) 9–12 but were significantly reduced in glucose intolerant mice. Apelin-13 increased β-cell proliferation in isolated mouse islets and INS1E cells, but not glucose-stimulated insulin secretion. Glucose intolerant pregnant mice had significantly elevated serum Apelin levels at GD 9 associated with an increased presence of placental IL-6. Placental expression of the apelinergic axis remained unaltered, however. Results show that the apelinergic system is highly expressed in pancreatic β-cell progenitors and may contribute to β-cell proliferation in pregnancy

Influenza vaccination coverage among an urban pediatric asthma population: Implications for population health

Introduction Asthma is the most common chronic disease in children. Children with asthma are at high risk for complications from influenza; however annual influenza vaccination rates for this population are suboptimal. The overall aim of this study was to describe the characteristics of a high-risk population of children with asthma presenting to an urban pediatric emergency department according to influenza vaccination status. Methods The study was a retrospective chart review of 4355 patients aged 2 to 18 years evaluated in a Michigan pediatric emergency department (PED) between November 1, 2017 and April 30, 2018 with an ICD-10-CM code for asthma (J45.x). Eligible patient PED records were matched with influenza vaccination records for the 2017–2018 influenza season from the Michigan Care Improvement Registry. Geospatial analysis was employed to examine the distribution of influenza vaccination status. Results 1049 patients (30.9%) with asthma seen in the PED had received an influenza vaccine. Influenza vaccination coverage varied by Census Tract, ranging from 10% to \u3e 99%. Most vaccines were administered in a primary care setting (84.3%) and were covered by public insurance (76.8%). The influenza vaccination rate was lowest for children aged 5–11 years (30.0%) and vaccination status was associated with race (p\u3c0.001) and insurance type (p\u3c0.001). Conclusions Identification of neighborhood Census Tract and demographic groups with suboptimal influenza vaccination could guide development of targeted public health interventions to improve vaccination rates in high-risk patients. Given the morbidity and mortality associated with pediatric asthma, a data-driven approach may improve outcomes and reduce healthcare-associated costs for this pediatric population

The Influence of Motion and Stress on Optical Fibers

We report on extensive testing carried out on the optical fibers for the VIRUS instrument. The primary result of this work explores how 10+ years of simulated wear on a VIRUS fiber bundle affects both transmission and focal ratio degradation (FRD) of the optical fibers. During the accelerated lifetime tests we continuously monitored the fibers for signs of FRD. We find that transient FRD events were common during the portions of the tests when motion was at telescope slew rates, but dropped to negligible levels during rates of motion typical for science observation. Tests of fiber transmission and FRD conducted both before and after the lifetime tests reveal that while transmission values do not change over the 10+ years of simulated wear, a clear increase in FRD is seen in all 18 fibers tested. This increase in FRD is likely due to microfractures that develop over time from repeated flexure of the fiber bundle, and stands in contrast to the transient FRD events that stem from localized stress and subsequent modal diffusion of light within the fibers. There was no measurable wavelength dependence on the increase in FRD over 350 nm to 600 nm. We also report on bend radius tests conducted on individual fibers and find the 266 microns VIRUS fibers to be immune to bending-induced FRD at bend radii of R > 10cm. Below this bend radius FRD increases slightly with decreasing radius. Lastly, we give details of a degradation seen in the fiber bundle currently deployed on the Mitchell Spectrograph (formally VIRUS-P) at McDonald Observatory. The degradation is shown to be caused by a localized shear in a select number of optical fibers that leads to an explosive form of FRD. In a few fibers, the overall transmission loss through the instrument can exceed 80%.Comment: 19 pages, 22 figure

A Summary of the Lateral Cutoff Analysis and Results from Nasa's Farfield Investigation of No-Boom Thresholds

In support of the ongoing effort by the National Aeronautics and Space Administration (NASA) to bring supersonic commercial travel to the public, NASA, in partnership with other industry organizations, conducted a flight research experiment to analyze acoustic propagation at the lateral edge of the sonic boom carpet. The name of the effort was the Farfield Investigation of No-boom Thresholds (FaINT). The research from FaINT determined an appropriate metric for sonic boom waveforms in the transition and shadow zones called Perceived Sound Exposure Level, established a value of 65 dB as a limit for the acoustic lateral extent of a sonic boom's noise region, analyzed change in sonic boom levels near lateral cutoff, and compared between real sonic boom measurements and numerical predictions

Altered pancreas remodeling following glucose intolerance in pregnancy in mice

Gestational diabetes mellitus increases the risk of dysglycemia postpartum, in part, due to pancreatic β-cell dysfunction. However, no histological evidence exists comparing endocrine pancreas after healthy and glucose-intolerant pregnancies. This study sought to address this knowledge gap, in addition to exploring the contribution of an inflammatory environment to changes in endocrine pancreas after parturition. We used a previously established mouse model of gestational glucose intolerance induced by dietary low protein insult from conception until weaning. Pancreas and adipose samples were collected at 7, 30 and 90 days postpartum for histomorphometric and cytokine analyses, respectively. Glucose tolerance tests were performed prior to euthanasia and blood was collected via cardiac puncture. Pregnant female mice born to dams fed a low protein diet previously shown to develop glucose intolerance at late gestation relative to controls continued to be glucose intolerant until 1 month postpartum. However, glucose tolerance normalized by 3 months postpartum. Glucose intolerance at 7 days postpartum was associated with lower beta- and alpha-cell fractional areas and higher adipose levels of pro-inflammatory cytokine, interleukin-6. By 3 months postpartum, a compensatory increase in the number of small islets and a higher insulin to glucagon ratio likely enabled euglycemia to be attained in the previously glucose-intolerant mice. The results show that impairments in endocrine pancreas compensation in hyperglycemic pregnancy persist after parturition and contribute to prolonged glucose intolerance. These impairments may increase the susceptibility to development of future type 2 diabetes