Sex workers perspectives on strategies to reduce sexual exploitation and HIV risk: a qualitative study in Tijuana, Mexico.

Globally, female sex workers are a population at greatly elevated risk of HIV infection, and the reasons for and context of sex industry involvement have key implications for HIV risk and prevention. Evidence suggests that experiences of sexual exploitation (i.e., forced/coerced sex exchange) contribute to health-related harms. However, public health interventions that address HIV vulnerability and sexual exploitation are lacking. Therefore, the objective of this study was to elicit recommendations for interventions to prevent sexual exploitation and reduce HIV risk from current female sex workers with a history of sexual exploitation or youth sex work. From 2010-2011, we conducted in-depth interviews with sex workers (n = 31) in Tijuana, Mexico who reported having previously experienced sexual exploitation or youth sex work. Participants recommended that interventions aim to (1) reduce susceptibility to sexual exploitation by providing social support and peer-based education; (2) mitigate harms by improving access to HIV prevention resources and psychological support, and reducing gender-based violence; and (3) provide opportunities to exit the sex industry via vocational supports and improved access to effective drug treatment. Structural interventions incorporating these strategies are recommended to reduce susceptibility to sexual exploitation and enhance capacities to prevent HIV infection among marginalized women and girls in Mexico and across international settings

Targeting reperfusion injury in patients with ST-segment elevation myocardial infarction : trials and tribulations

Altres ajuts: D.J.H. and D.M.Y. are funded by the British Heart Foundation and the Rosetrees Trust, and are supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre of which D.M.Y. is a senior investigator. G.H. is supported by the German Research Foundation (He 1320/18-3; SFB 1116 B8)

Targeting reperfusion injury in patients with ST-segment elevation myocardial infarction: trials and tribulations

D.J.H. and D.M.Y. are funded by the British Heart Foundation and the Rosetrees Trust, and are supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre of which D.M.Y. is a senior investigator. D.G.-D. is funded by the Cardiovascular Research Network of the Spanish Institute of Health Instituto de Salud Carlos III (ISCiii RETICS-RIC, RD12/0042/0021). G.H. is supported by the German Research Foundation (He 1320/18-3; SFB 1116 B8). B.I. is funded by the Carlos III Institute of Health and European Regional Development Fund (ERDF/FEDER) (PI13/01979), and the ISCiii Cardiovascular Research Network (RD12/0042/0054). Funding to pay the Open Access publication charges for this article was provided by Red de Investigacion Cardiovascular del Instituto de Salud Carlos III, grupo Hospital Universitari Vall d'Hebron (RETICS 2012 RD12/0042/0021).S

A novel chromosomal inversion at 11q23 in infant acute myeloid leukemia fuses MLL to CALM, a gene that encodes a clathrin assembly protein

Rearrangements involving the MLL gene at chromosome band 11q23 are common in infant acute myeloid leukemias (AMLs). We recently encountered an infant patient with rapidly progressive AML whose leukemic cells harbored a previously undescribed MLL rearrangement involving an inversion of 11q [inv(11)(q14q23)]. We used panhandle PCR to determine that this rearrangement juxtaposed the MLL ( M ixed- L ineage L eukemia) gene to the CALM ( C lathrin A ssembly L ymphoid M yeloid leukemia) gene at 11q14–q21. The CALM protein participates in recruitment of clathrin to internal membrane surfaces, thereby regulating vesicle formation in both endocytosis and intracellular protein transport. Intriguingly, CALM has been identified in other cases of AML as a translocation partner for the AF10 gene, which has independently been found to be an MLL partner in AML. We identified the MLL - CALM fusion transcript (but not the reciprocal CALM - MLL transcript) in leukemia cell RNA by RT-PCR. The predicted 1803 amino acid MLL-CALM fusion protein includes amino-terminal MLL domains involved in transcriptional repression, and carboxy-terminal CALM-derived clathrin-binding domains. The genomic breakpoint in MLL is in the 7th intron (within the breakpoint cluster region); the corresponding CALM breakpoint is in the 7th CALM intron. In contrast, breakpoints in CALM - AF10 translocations lie in the 17th–19th CALM introns (30 kb downstream); also, in these translocations, CALM provides the 5′ end of the fusion transcript. Together with its previously recognized association with AF10 in AML, the identification of CALM as an MLL fusion partner suggests that interference with clathrin-mediated trafficking pathways may be an underappreciated mechanism in leukemogenesis. © 2002 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/35133/1/10136_ftp.pd

Challenges and strategies of children and adolescents with inflammatory bowel disease: a qualitative examination

© 2007 Nicholas et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Abrupt climatic events during the last glacial-interglacial transition in Alaska

Evidence is mounting that abrupt climatic shifts occurred during the last glacial-interglacial transition (LGIT) in the North Atlantic and other regions. However, few high-resolution climatic records of the LGIT exist from the high latitudes of the North Pacific rim. We analyzed lake sediments from southwestern Alaska for biogenic silica, organic carbon, organic nitrogen, diatom assemblages, and compound-specific hydrogen isotopes. Results reveal climatic changes coincident with the Younger Dryas, Intra-Allerod Cold Period, and Pre-Boreal Oscillation. However, major discrepancies exist in the paleoclimate patterns of the Bolling-Allerod interstadial between our data and the GISP2 18O record from Greenland, and causes are uncertain. These data suggest that the North Pacific and North Atlantic experienced similar reversals during climatic warming of the LGIT but that the Bolling-Allerod cooling trend in the GISP2 18O record is probably not a hemispheric or global pattern

RNAseq Analyses Identify Tumor Necrosis Factor-Mediated Inflammation as a Major Abnormality in ALS Spinal Cord

ALS is a rapidly progressive, devastating neurodegenerative illness of adults that produces disabling weakness and spasticity arising from death of lower and upper motor neurons. No meaningful therapies exist to slow ALS progression, and molecular insights into pathogenesis and progression are sorely needed. In that context, we used high-depth, next generation RNA sequencing (RNAseq, Illumina) to define gene network abnormalities in RNA samples depleted of rRNA and isolated from cervical spinal cord sections of 7 ALS and 8 CTL samples. We aligned \u3e50 million 2X150 bp paired-end sequences/sample to the hg19 human genome and applied three different algorithms (Cuffdiff2, DEseq2, EdgeR) for identification of differentially expressed genes (DEG’s). Ingenuity Pathways Analysis (IPA) and Weighted Gene Co-expression Network Analysis (WGCNA) identified inflammatory processes as significantly elevated in our ALS samples, with tumor necrosis factor (TNF) found to be a major pathway regulator (IPA) and TNFα-induced protein 2 (TNFAIP2) as a major network “hub” gene (WGCNA). Using the oPOSSUM algorithm, we analyzed transcription factors (TF) controlling expression of the nine DEG/hub genes in the ALS samples and identified TF’s involved in inflammation (NFkB, REL, NFkB1) and macrophage function (NR1H2::RXRA heterodimer). Transient expression in human iPSC-derived motor neurons of TNFAIP2 (also a DEG identified by all three algorithms) reduced cell viability and induced caspase 3/7 activation. Using high-density RNAseq, multiple algorithms for DEG identification, and an unsupervised gene co-expression network approach, we identified significant elevation of inflammatory processes in ALS spinal cord with TNF as a major regulatory molecule. Overexpression of the DEG TNFAIP2 in human motor neurons, the population most vulnerable to die in ALS, increased cell death and caspase 3/7 activation. We propose that therapies targeted to reduce inflammatory TNFα signaling may be helpful in ALS patients