Explore the vast range of titles available.

Current research on sexual minority youth tends to be concentrated in the fields of public health, social work, and psychology with a focus on psycho-social health risks that often rely on sexuality as a fixed unit of analysis. A sociological understanding of the processes that drive an individual to identify as gay in the first place makes an important contribution to this existing body of literature, allowing an opportunity to understand not just how sexual minority youth are vulnerable, but why. Drawing on my ethnographic research with adolescent males who frequent a lesbian, gay, bisexual, and transgender youth drop-in center, I demonstrate how sexuality gets constructed through four processes: violating compulsory heterosexuality, seeking an explanation, exploring sexuality, and negotiating identity. I will show how individuals make meaning of their sexual selves within the context of a patriarchal, heteronormative structural system, where symbols of homophobia and masculinity inform their identity development, and how that reiterates heteronormative development. I conclude by drawing attention to how the shifting boundaries of queerness should inform efforts to improve conditions for sexual minority youth and inform future research.

As norms around sexual and gender identity shift, there has been an increase in the number of adolescents coming out as LGBT. A relatively new phenomenon, the study of LGBT-identified youth has largely been centered around risk and harm experienced by these vulnerable young people. Yet much of the research is focused on the experiences of LGBT-identified people whose identities are already understood as a given. Therefore, this dissertation aims to understand how a person becomes LGBT-identified and examines how sexual and gender identities are social and historical formations, not biological facts. By exploring how adolescents in particular come to understand themselves as sexual and gendered beings, this work contributes to a larger understanding of the sociology of sexuality. Using a feminist ethnographic approach, I conducted participant observation at an LGBT youth drop-in center and 34 life-history interviews with LGBT-identified youths. By applying a queer theoretical framework to sociological concepts of identity formation, this research contributes to a more complex understanding of how compulsory heterosexuality and heteronormativity are powerful forms of social control in society. Themes include understanding the role gender atypicality plays in the formation of a gay identity, how processes of gender attribution shore up a binary gender order, how sexual minority youths pursue sexuality education that is representative of their experience via alternative forms of media, and how the queering of the family may result in positive coming out experiences for youth. Ultimately this research acknowledges the formation of boundaries between normal and queer and how these boundaries contribute to the sexual development of particular young people.

Robertson reviews Coming Out: The New Dynamics by Nicholas A Guittar.

Background Mitigation of climate change requires that new routes for the production of fuels and chemicals be as oil-independent as possible. The microbial conversion of lignocellulosic feedstocks into terpene-based biofuels and bioproducts represents one such route. This work builds upon previous demonstrations that the single-celled carotenogenic basidiomycete, Rhodosporidium toruloides, is a promising host for the production of terpenes from lignocellulosic hydrolysates. Results This study focuses on the optimization of production of the monoterpene 1,8-cineole and the sesquiterpene α-bisabolene in R. toruloides. The α-bisabolene titer attained in R. toruloides was found to be proportional to the copy number of the bisabolene synthase (BIS) expression cassette, which in turn influenced the expression level of several native mevalonate pathway genes. The addition of more copies of BIS under a stronger promoter resulted in production of α-bisabolene at 2.2 g/L from lignocellulosic hydrolysate in a 2-L fermenter. Production of 1,8-cineole was found to be limited by availability of the precursor geranylgeranyl pyrophosphate (GPP) and expression of an appropriate GPP synthase increased the monoterpene titer fourfold to 143 mg/L at bench scale. Targeted mevalonate pathway metabolite analysis suggested that 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGR), mevalonate kinase (MK) and phosphomevalonate kinase (PMK) may be pathway bottlenecks are were therefore selected as targets for overexpression. Expression of HMGR, MK, and PMK orthologs and growth in an optimized lignocellulosic hydrolysate medium increased the 1,8-cineole titer an additional tenfold to 1.4 g/L. Expression of the same mevalonate pathway genes did not have as large an impact on α-bisabolene production, although the final titer was higher at 2.6 g/L. Furthermore, mevalonate pathway intermediates accumulated in the mevalonate-engineered strains, suggesting room for further improvement. Conclusions This work brings R. toruloides closer to being able to make industrially relevant quantities of terpene from lignocellulosic biomass.

Background: Recent data suggest that acidosis alone is not a good predictor of mortality in trauma patients. Little data are currently available regarding factors associated with survival in trauma patients presenting with acidosis. Aims: The aims were to characterize the outcomes of trauma patients presenting with acidosis and to identify modifiable risk factors associated with mortality in these patients. Settings and Design: This is a retrospective observational study of University of Arkansas for Medical Sciences (UAMS) trauma patients between November 23, 2013, and May 21, 2017. Methods: Data were collected from the UAMS trauma registry. The primary outcome was hospital mortality. Analyses were performed using t-test and Pearson's Chi-squared test. Simple and multiple logistic regressions were performed to determine crude and adjusted odds ratios. Results: There were 532 patients identified and 64.7% were acidotic (pH < 7.35) on presentation: 75.9% pH 7.2-7.35; 18.5% pH 7.0-7.2; and 5.6% pH ≤ 7.0. The total hospital mortality was 23.7%. Nonsurvivors were older and more acidotic, with a base deficit >−8, Glasgow Coma Scale (GCS) ≤ 8, systolic blood pressure ≤ 90, International Normalized Ratio (INR) >1.6, and Injury Severity Score (ISS) >15. Mortality was significantly higher with a pH ≤ 7.2 but mortality with a pH 7.2-7.35 was comparable to pH > 7.35. In the adjusted model, pH ≤ 7.0, pH 7.0-7.2, INR > 1.6, GCS ≤ 8, and ISS > 15 were associated with increased mortality. For patients with a pH ≤ 7.2, only INR was associated with increase in mortality. Conclusions: A pH ≤ 7.2 is associated with increased mortality. For patients in this range, only the presence of coagulopathy is associated with increased mortality. A pH > 7.2 may be an appropriate treatment goal for acidosis. Further work is needed to identify and target potentially modifiable factors in patients with acidosis such as coagulopathy.

To characterize somatic alterations in colorectal carcinoma, we conducted a genome-scale analysis of 276 samples, analysing exome sequence, DNA copy number, promoter methylation and messenger RNA and microRNA expression. A subset of these samples (97) underwent low-depth-of-coverage whole-genome sequencing. In total, 16% of colorectal carcinomas were found to be hypermutated: three-quarters of these had the expected high microsatellite instability, usually with hypermethylation and MLH1 silencing, and one-quarter had somatic mismatch-repair gene and polymerase ε ( POLE ) mutations. Excluding the hypermutated cancers, colon and rectum cancers were found to have considerably similar patterns of genomic alteration. Twenty-four genes were significantly mutated, and in addition to the expected APC , TP53 , SMAD4 , PIK3CA and KRAS mutations, we found frequent mutations in ARID1A , SOX9 and FAM123B. Recurrent copy-number alterations include potentially drug-targetable amplifications of ERBB2 and newly discovered amplification of IGF2 . Recurrent chromosomal translocations include the fusion of NAV2 and WNT pathway member TCF7L1 . Integrative analyses suggest new markers for aggressive colorectal carcinoma and an important role for MYC -directed transcriptional activation and repression. The Cancer Genome Atlas consortium reports on their genome-wide characterization of somatic alterations in colorectal cancer; in addition to revealing a remarkably consistent pattern of genomic alteration, with 24 genes being significantly mutated, the study identifies new targets for therapeutic intervention and suggests an important role for MYC-directed transcriptional activation and repression. Mutations associated with colorectal cancer The Cancer Genome Atlas consortium reports on their genome-wide characterization of somatic alterations in colorectal carcinoma. Combined analysis of exome sequence data, DNA copy number, promoter methylation, messenger RNA and microRNA expression, as well as low-coverage whole-genome sequencing reveal that 16% of these carcinomas have hypermutation. Of these, three-quarters have the expected high microsatellite instability, but the rest have somatic mismatch repair gene mutations. The data reveal a remarkably consistent pattern of genomic alteration, with 24 genes being significantly mutated. As well as identifying new biomarkers for aggressive colorectal carcinoma, the data imply an important role for MYC -directed transcriptional activation and repression.

Background While many malaria-endemic countries have health management information systems that can measure and report malaria trends in a timely manner, these routine systems have limitations. Periodic community cross-sectional household surveys are used to estimate malaria prevalence and intervention coverage but lack geographic granularity and are resource intensive. Incorporating malaria testing for all women at their first antenatal care (ANC) visit (i.e., ANC1) could provide a more timely and granular source of data for monitoring trends in malaria burden and intervention coverage. This article describes a protocol designed to assess if ANC-based surveillance could be a pragmatic tool to monitor malaria. Methods This is an observational, cross-sectional study conducted in Benin, Burkina Faso, Mozambique, Nigeria, Tanzania, and Zambia. Pregnant women attending ANC1 in selected health facilities will be tested for malaria infection by rapid diagnostic test and administered a brief questionnaire to capture key indicators of malaria control intervention coverage and care-seeking behaviour. In each location, contemporaneous cross-sectional household surveys will be leveraged to assess correlations between estimates obtained using each method, and the use of ANC data as a tool to track trends in malaria burden and intervention coverage will be validated. Results This study will assess malaria prevalence at ANC1 aggregated at health facility and district levels, and by gravidity relative to current pregnancy (i.e., gravida 1, gravida 2, and gravida 3 +). ANC1 malaria prevalence will be presented as monthly trends. Additionally, correlation between ANC1 and household survey–derived estimates of malaria prevalence, bed net ownership and use, and care-seeking will be assessed. Conclusion ANC1-based surveillance has the potential to provide a cost-effective, localized measure of malaria prevalence that is representative of the general population and useful for tracking monthly changes in parasite prevalence, as well as providing population-representative estimates of intervention coverage and care-seeking behavior. This study will evaluate the representativeness of these measures and collect information on operational feasibility, usefulness for programmatic decision-making, and potential for scale-up of malaria ANC1 surveillance.

Objectives: To evaluate and analyze the efficacy of implementation of hemorrhage-control training into the formal medical school curriculum. We predict this training will increase the comfort and confidence levels of students with controlling major hemorrhage and they will find this a valuable skill set for medical and other healthcare professional students. Methods: After IRB and institutional approval was obtained, hemorrhage-control education was incorporated into the surgery clerkship curriculum for 96 third-year medical students at the University of Arkansas for Medical Sciences using the national Stop The Bleed program. Using a prospective study design, participants completed pre- and post-training surveys to gauge prior experiences and comfort levels with controlling hemorrhage and confidence levels with the techniques taught. Course participation was mandatory; survey completion was optional. The investigators were blinded as to the individual student’s survey responses. A knowledge quiz was completed following the training. Results: Implementation of STB training resulted in a significant increase in comfort and confidence among students with all hemorrhage-control techniques. There was also a significant difference in students’ perceptions of the importance of this training for physicians and other allied health professionals. Conclusion: Hemorrhage-control training can be effectively incorporated into the formal medical school curriculum via a single 2-hour Stop The Bleed course, increasing students’ comfort level and confidence with controlling major traumatic bleeding. Students value this training and feel it is a beneficial addition to their education. We believe this should be a standard part of undergraduate medical education.

Stefan Mundlos and colleagues report the identification of mutations in PYCR1 that cause autosomal recessive cutis laxa. PYCR1 encodes an enzyme involved in proline metabolism and localizes to mitochondria. Autosomal recessive cutis laxa (ARCL) describes a group of syndromal disorders that are often associated with a progeroid appearance, lax and wrinkled skin, osteopenia and mental retardation 1 , 2 , 3 . Homozygosity mapping in several kindreds with ARCL identified a candidate region on chromosome 17q25. By high-throughput sequencing of the entire candidate region, we detected disease-causing mutations in the gene PYCR1 . We found that the gene product, an enzyme involved in proline metabolism, localizes to mitochondria. Altered mitochondrial morphology, membrane potential and increased apoptosis rate upon oxidative stress were evident in fibroblasts from affected individuals. Knockdown of the orthologous genes in Xenopus and zebrafish led to epidermal hypoplasia and blistering that was accompanied by a massive increase of apoptosis. Our findings link mutations in PYCR1 to altered mitochondrial function and progeroid changes in connective tissues.