tbuckley/cabot-search huggingface dataset:
Measuring Coverage in MNCH: Indicators for Global Tracking of Newborn Care
Authors: Allisyn C. Moran, Kate Kerber, Deborah Sitrin, Tanya Guenther, Claudia S. Morrissey, Holly Newby, Joy Fishel, P. Stan Yoder, Zelee Hill, Joy E. Lawn
Journal: PLoS Medicine (2013)

Neonatal mortality accounts for 43% of under-five mortality. Consequently, improving newborn survival is a global priority. However, although there is increasing consensus on the packages and specific interventions that need to be scaled up to reduce neonatal mortality, there is a lack of clarity on the indicators needed to measure progress. In 2008, in an effort to improve newborn survival, the Newborn Indicators Technical Working Group (TWG) was convened by the Saving Newborn Lives program at Save the Children to provide a forum to develop the indicators and standard measurement tools that are needed to measure coverage of key newborn interventions. The TWG, which included evaluation and measurement experts, researchers, individuals from United Nations agencies and non-governmental organizations, and donors, prioritized improved consistency of measurement of postnatal care for women and newborns and of immediate care behaviors and practices for newborns. In addition, the TWG promoted increased data availability through inclusion of additional questions in nationally representative surveys, such as the United States Agency for International Development–supported Demographic and Health Surveys and the United Nations Children's Fund–supported Multiple Indicator Cluster Surveys. Several studies have been undertaken that have informed revisions of indicators and survey tools, and global postnatal care coverage indicators have been finalized. Consensus has been achieved on three additional indicators for care of the newborn after birth (drying, delayed bathing, and cutting the cord with a clean instrument), and on testing two further indicators (immediate skin-to-skin care and applications to the umbilical cord). Finally, important measurement gaps have been identified regarding coverage data for evidence-based interventions, such as Kangaroo Mother Care and care seeking for newborn infection.
TWEAK-Fn14 interaction enhances plasminogen activator inhibitor 1 and tissue factor expression in atherosclerotic plaques and in cultured vascular smooth muscle cells
Authors: B. Munoz-Garcia, J. Madrigal-Matute, J. A. Moreno, J. L. Martin-Ventura, O. Lopez-Franco, C. Sastre, L. Ortega, L. C. Burkly, J. Egido, L. M. Blanco-Colio
Journal: Cardiovascular Research (2010)

atherosclerotic plaque development can conclude with a thrombotic acute event triggered by plaque rupture/erosion. Tumour necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of the tumour necrosis factor superfamily that, through its receptor, fibroblast growth factor-inducible 14 (Fn14), participates in vascular remodelling, increasing vascular inflammatory responses and atherosclerotic lesion size in ApoE knockout mice. However, the role of the TWEAK-Fn14 axis in thrombosis has not been previously investigated.we have examined whether TWEAK regulates expression of prothrombotic factors such as tissue factor (TF) and plasminogen activator inhibitor 1 (PAI-1) in atherosclerotic plaques as well as in human aortic vascular smooth muscle cells (hASMCs) in culture. Expression of TF and PAI-1 was colocalized and positively correlated with Fn14 in human carotid atherosclerotic plaques. In vitro, TWEAK increased TF and PAI-1 mRNA, protein expression and activity in hASMCs. All these effects were reversed using blocking anti-TWEAK monoclonal antibody, anti-Fn14 antibody or Fn14 small interfering RNA, indicating that TWEAK increased the prothrombotic state through its receptor, Fn14. Finally, ApoE(-/-) mice were fed a hyperlipidaemic diet for 10 weeks, then randomized and treated with saline (controls), TWEAK (10 microg/kg/day), anti-TWEAK neutralizing monoclonal antibody (1000 µg/kg/day), or non-specific immunoglobulin G (1000 microg/kg/day) daily for 9 days. Systemic TWEAK injection increased TF and PAI-1 protein expression in the aortic root of ApoE(-/-) mice. Conversely, TWEAK blocking antibodies diminished both TF and PAI-1 protein expression compared with non-specific immunoglobulin G-treated mice.our results indicate that the TWEAK-Fn14 axis can regulate activation of TF and PAI-1 expression in vascular cells. TWEAK-Fn14 may be a therapeutic target in the prothrombotic complications associated with atherosclerosis.
Predictive Factors, Management, and Clinical Outcomes of Coronary Obstruction Following Transcatheter Aortic Valve Implantation
Authors: Henrique B. Ribeiro, John G. Webb, Raj R. Makkar, Mauricio G. Cohen, Samir R. Kapadia, Susheel Kodali, Corrado Tamburino, Marco Barbanti, Tarun Chakravarty, Hasan Jilaihawi, Jean-Michel Paradis, Fabio S. de Brito, Sergio J. Cánovas, Asim N. Cheema, Peter P. de Jaegere, Raquel del Valle, Paul T.L. Chiam, Raúl Moreno, Gonzalo Pradas, Marc Ruel, Jorge Salgado-Fernández, Rogerio Sarmento-Leite, Hadi D. Toeg, James L. Velianou, Alan Zajarias, Vasilis Babaliaros, Fernando Cura, Antonio E. Dager, Ganesh Manoharan, Stamatios Lerakis, Augusto D. Pichard, Sam Radhakrishnan, Marco Antonio Perin, Eric Dumont, Eric Larose, Sergio G. Pasian, Luis Nombela-Franco, Marina Urena, E. Murat Tuzcu, Martin B. Leon, Ignacio J. Amat-Santos, Jonathon Leipsic, Josep Rodés-Cabau
Journal: Journal of the American College of Cardiology (2013)
Human herpesvirus 6 involvement in paediatric drug hypersensitivity syndrome
Authors: V. Descamps
Journal: British Journal of Dermatology (2015)

Journal Article Human herpesvirus 6 involvement in paediatric drug hypersensitivity syndrome Get access V. Descamps V. Descamps Department of Dermatology Bichat Hospital 46 rue Henri Huchard, 75018 Paris France Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 172, Issue 4, 1 April 2015, Pages 858–859, https://doi.org/10.1111/bjd.13592 Published: 01 April 2015
Molecular evolution of cytochrome c oxidase: rate variation among subunit VIa isoforms
Authors: T. R. Schmidt, S. A. Jaradat, M. Goodman, M. I. Lomax, L. I. Grossman
Journal: Molecular Biology and Evolution (1997)

Cytochrome c oxidase (COX) consists of 13 subunits, 3 encoded in the mitochondrial genome and 10 in the nucleus. Little is known of the role of the nuclear-encoded subunits, some of which exhibit tissue-specific isoforms. Subunit VIa is unique in having tissue-specific isoforms in all mammalian species examined. We examined relative evolutionary rates for the COX6A heart (H) and liver (L) isoform genes along the length of the molecule, specifically in relation to the tissue-specific function(s) of the two isoforms. Nonsynonymous (amino acid replacement) substitutions in the COX6AH gene occurred more frequently than in the ubiquitously expressed COX6AL gene. Maximum-parsimony analysis and sequence divergences from reconstructed ancestral sequences revealed that after the ancestral COX6A gene duplicated to yield the genes for the H and L isoforms, the sequences encoding the mitochondrial matrix region of the COX VIa protein experienced an elevated rate of nonsynonymous substitutions relative to synonymous substitutions. This is expected for relaxed selective constraints after gene duplication followed by purifying selection to preserve the replacements with tissue-specific functions.
Surveillance Testing Among Survivors of Early-Stage Breast Cancer
Authors: Nancy L. Keating, Mary Beth Landrum, Edward Guadagnoli, Eric P. Winer, John Z. Ayanian
Journal: Journal of Clinical Oncology (2007)

Purpose Guidelines recommend against routine surveillance testing for women who have had breast cancer. We described follow-up care for breast cancer survivors, examined how surveillance testing varies by the types of physicians seen, and assessed changes in testing rates over time. Methods Using Surveillance, Epidemiology, and End Results–Medicare data, we studied a population-based cohort of 44,511 women age ≥ 65 years diagnosed with stage I/II breast cancer during 1992 to 1999 and observed through 2001. We measured bone scans, tumor antigen tests, chest x-rays, and other chest/abdominal imaging during 3 consecutive surveillance years. We described physicians seen in follow-up and used repeated-measures logistic regression to assess the relationship with testing and to assess testing trends over time. Results Nearly half of breast cancer survivors saw a medical oncologist in surveillance year 1, but only 27% saw a medical oncologist annually for 3 years. In adjusted analyses, women seeing medical oncologists had more bone scans, tumor antigen testing, chest x-rays, and chest/abdominal imaging than other women (all P &lt; .001). Nevertheless, rates of testing decreased over time (all P &lt; .001). Rates of tumor antigen testing and chest x-rays decreased faster and chest/abdominal imaging increased slower among women seeing medical oncologists than among other women (all P &lt; .05). Conclusion Nonrecommended testing for early-stage breast cancer patients has decreased over time. Although most breast cancer survivors did not see oncologists annually, those who did had substantially higher rates of testing than others; whether such testing in this low-risk population was due to more symptoms or excessive surveillance is an important question for additional study.
Effect of dietary sodium on the severity of bronchial asthma.
Authors: T C Beard
Journal: Thorax (1993)

Controversy exists regarding the timing and technique of total correction of traumatic intracardiac lesions. Five patients with penetrating wounds of the heart received emergency treatment aimed at securing normal haemodynamics. No attempt was made to identify intracardiac lesions at this stage. Cineangiography two months to seven years later showed aorto-right ventricular fistulae in all patients, associated in two with aortic cusp laceration and in one with an aorto-left atrial fistula. The surgical approach for aorto-right ventricular fistula was through the right ventricle or aorta. Valvar injuries were treated by plastic reconstruction. All patients showed good clinical results when seen four to 11 years later. Traumatic intracardiac lesions in patients with stable haemodynamics after initial treatment should be operated on electively. The aortic approach is preferable for aorto-right ventricular fistulae. Conservative plastic repair of valvar injuries achieves long-term competence thus avoiding prosthetic replacement.
PUBLIC HEALTH IN CENTRAL AND EASTERN EUROPE AND THE ROLE OF ENVIRONMENTAL POLLUTION
Authors: R. E. Little
Journal: Annual Review of Public Health (1998)

▪ Abstract The central and eastern European countries that composed the former Eastern Bloc have experienced an alarming decline in public health since the dissolution of the Soviet Union. Death rates have increased in most age groups. Life expectancy, especially among males, has decreased in many countries; in Russia, male life expectancy dropped by six years between 1989 and 1994. By 2020, these countries are projected to have smaller increases in life expectancy than any other geographic region. The conditions responsible for the excess mortality are cardiovascular disease, cancer, and injuries among adults. The major factors in the sharp increase are poverty, social disintegration, and crime, overlaid on historically high rates of smoking, alcohol use, and psychosocial stress. Environmental pollution, although common and sometimes severe in the former Eastern Bloc, is another, albeit not the chief, cause of the sharp decline in public health since 1989.
Improved access and targeting of musculoskeletal services in northwest Wales: targeted early access to musculoskeletal services (TEAMS) programme
Authors: Peter Maddison, Jeremy Jones, Anne Breslin, Craig Barton, Joyce Fleur, Rhian Lewis, Luke McSweeney, Carys Norgain, Sara Smith, Carolyn Thomas, Chris Tillson
Journal: BMJ (2004)

We developed a method for single-cell resolution longitudinal bioluminescence imaging of PERIOD (PER) protein and TIMELESS (TIM) oscillations in cultured male adult <i>Drosophila</i> brains that captures circadian circuit-wide cycling under simulated day/night cycles. Light input analysis confirms that CRYPTOCHROME (CRY) is the primary circadian photoreceptor and mediates clock disruption by constant light, and that eye light input is redundant to CRY. 3hr light phase delays (Friday) followed by 3hr light phase advances (Monday morning) simulate the common practice of staying up later at night on weekends, sleeping in later on weekend days then returning to standard schedule Monday morning (weekend light shift, WLS). PER and TIM oscillations are highly synchronous across all major circadian neuronal subgroups in unshifted light schedules for 11 days. In contrast, WLS significantly dampens PER oscillator synchrony and rhythmicity in most circadian neurons during and after exposure. Lateral ventral neuron (LNv) oscillations are the first to desynchronize in WLS and the last to resynchronize in WLS. Surprisingly, the dorsal neuron group-3 (DN3s), increase their within-group synchrony in response to WLS. <i>In vivo</i>, WLS induces transient defects in sleep stability, learning, and memory that temporally coincide with circuit desynchrony. Our findings suggest that WLS schedules disrupt circuit-wide circadian neuronal oscillator synchrony for much of the week, thus leading to observed behavioral defects in sleep, learning, and memory. <b>SIGNIFICANCE STATEMENT</b> The circadian clock controls numerous aspects of daily animal physiology, metabolism and behavior. Much of our understanding of circadian circuit-level oscillations stem from <i>ex vivo</i> imaging of mammalian suprachiasmatic nucleus (SCN) brain slices. Humans regularly subject themselves to weekday/weekend light shifts but the effects of phase-shifting light signals cannot be measured in SCN. We measured circuit-level circadian responses to a weekday/weekend light shift (WLS) protocol in light-sensitive <i>ex vivo Drosophila</i> whole-brain preparation that shows temporal coincidence to circadian behavioral events. Robust sub-circuit-specific oscillator desynchrony/resynchrony responses to light coincide with functional defects in learning and memory, and sleep pattern disruption <i>in vivo</i>. Our results reflect that WLS causes circadian-circuit desynchronization and correlates with disrupted cognitive and sleep performance.
Gain of glycosylation in integrin α3 causes lung disease and nephrotic syndrome
Authors: Nayia Nicolaou, Coert Margadant, Sietske H. Kevelam, Marc R. Lilien, Michiel J.S. Oosterveld, Maaike Kreft, Albertien M. van Eerde, Rolph Pfundt, Paulien A. Terhal, Bert van der Zwaag, Peter G.J. Nikkels, Norman Sachs, Roel Goldschmeding, Nine V.A.M. Knoers, Kirsten Y. Renkema, Arnoud Sonnenberg
Journal: Journal of Clinical Investigation (2012)

Integrins are transmembrane αβ glycoproteins that connect the extracellular matrix to the cytoskeleton. The laminin-binding integrin α3β1 is expressed at high levels in lung epithelium and in kidney podocytes. In podocytes, α3β1 associates with the tetraspanin CD151 to maintain a functional filtration barrier. Here, we report on a patient homozygous for a novel missense mutation in the human ITGA3 gene, causing fatal interstitial lung disease and congenital nephrotic syndrome. The mutation caused an alanine-to-serine substitution in the integrin α3 subunit, thereby introducing an N-glycosylation motif at amino acid position 349. We expressed this mutant form of ITGA3 in murine podocytes and found that hyperglycosylation of the α3 precursor prevented its heterodimerization with β1, whereas CD151 association with the α3 subunit occurred normally. Consequently, the β1 precursor accumulated in the ER, and the mutant α3 precursor was degraded by the ubiquitin-proteasome system. Thus, these findings uncover a gain-of-glycosylation mutation in ITGA3 that prevents the biosynthesis of functional α3β1, causing a fatal multiorgan disorder.
Squamous Metaplasia in Organ Cultures of Vitamin A-Deficient Hamster Trachea: Cytokinetic and Ultrastructural Alterations&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: Dharam Chopra
Journal: JNCI Journal of the National Cancer Institute (1982)

Cytokinetic and morphologic studies were performed to elucidate the origin of epidermoid metaplasia in organ cultures of tracheas derived from vitamin A-deficient Syrian golden hamsters. Focal areas of squamous metaplasia were observed 2 days after explantation, and extensive epidermoid metaplasia and cornification were present in approximately 89% of the explants at day 10. During the first 2 days, both basal and mucous cells proliferated actively. By day 3, the total mucous cell [3H]thymidine labeling index (LI) had declined and remained at very low levels during the remaining culture period. The basal cell LI also declined from its higher level, but it remained at relatively higher levels than those of the mucous cells between days 3 and 9 after culture. In the lesions, labeled cells were generally confined to the basal layer, and the LI was about thirtyfold greater than the total basal cell LI. As the lesions progressed, the surface layer containing the mucous and ciliated cells was exfoliated as a result of population pressure from the underlying actively proliferating basal cells and subsequent epidermoid differentiation of the daughter cells. These data support the hypothesis that epidermoid metaplasia of tracheobronchial epithelium caused by vitamin A deficiency originates from the generative or basal cells.
Bayesian Inference of Species Trees from Multilocus Data
Authors: J. Heled, A. J. Drummond
Journal: Molecular Biology and Evolution (2009)

Until recently, it has been common practice for a phylogenetic analysis to use a single gene sequence from a single individual organism as a proxy for an entire species. With technological advances, it is now becoming more common to collect data sets containing multiple gene loci and multiple individuals per species. These data sets often reveal the need to directly model intraspecies polymorphism and incomplete lineage sorting in phylogenetic estimation procedures. For a single species, coalescent theory is widely used in contemporary population genetics to model intraspecific gene trees. Here, we present a Bayesian Markov chain Monte Carlo method for the multispecies coalescent. Our method coestimates multiple gene trees embedded in a shared species tree along with the effective population size of both extant and ancestral species. The inference is made possible by multilocus data from multiple individuals per species. Using a multiindividual data set and a series of simulations of rapid species radiations, we demonstrate the efficacy of our new method. These simulations give some insight into the behavior of the method as a function of sampled individuals, sampled loci, and sequence length. Finally, we compare our new method to both an existing method (BEST 2.2) with similar goals and the supermatrix (concatenation) method. We demonstrate that both BEST and our method have much better estimation accuracy for species tree topology than concatenation, and our method outperforms BEST in divergence time and population size estimation.
Emerging anti-inflammatory strategies for COPD
Authors: Mario Cazzola, Clive P. Page, Luigino Calzetta, M. Gabriella Matera
Journal: European Respiratory Journal (2012)

The hallmark of chronic obstructive pulmonary disease (COPD) is an enhanced or abnormal inflammatory immune response of the lungs to inhaled particles and gases, usually from cigarette smoke, characterised by increased numbers of neutrophils, activated macrophages and activated T-lymphocytes (Tc1 and Th1 cells). Therefore, suppression of the inflammatory response is a logical approach to the treatment of COPD. Despite the inflammatory nature of COPD, currently available anti-inflammatory therapies provide little or no benefit in COPD patients and may have detrimental effects. For this reason, there is an urgent need to discover effective and safe anti-inflammatory treatments that might prevent the relentless progression of the disease. In recent years, attention has largely been focused on inhibition of recruitment and activation of inflammatory cells, and on antagonism of their products. In this review, we put together a summary of the state-of-the-art development of clearly and/or potentially useful anti-inflammatory strategies in COPD.
Alteration of Skin in Gross Leukemia. III. Quantitation of the Role of Tumor Cells&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: T. Mariani, Y. Maruyama, R. A. Good
Journal: JNCI Journal of the National Cancer Institute (1972)

Normal (C3H/Bi × DBA/2)F1 mice were transplanted with normal syngeneic skin. Twenty-four hours later, suspensions containing the following log10 titrations—1 × 106,1 × 105,1 × 104,1 × 103,1 ×102, 1 × 101, and 4 tumor Gross lymphoma cells—were injected directly into the skin graft. A high incidence of graft rejection was observed in the animals receiving more than 1 × 101 cells; tumor regularly developed at the graft site in all those receiving more than 4 cells. As the number of tumor cells injected decreased, the rejection rate also decreased, tumor development took longer, and host survival time increased. The critical point for inducing skin-graft rejection lies between 10 and 100 tumor cells. The data indicate that the rejection may be due to some response elicited by the tumor cell itself.
Long–Term Mortality and Morbidity of Transfusion–Associated Non–A, Non–B, and Type C Hepatitis: A National Heart, Lung, and Blood Institute Collaborative Study
Authors: Leonard B. Seeff, Blaine F. Hollinger, Harvey J. Alter, Elizabeth C. Wright, Casey M.B. Cain, Zelma J. Buskell, Kamal G. Ishak, Frank L. Iber, Doris Toro, Arun Samanta, Ronald L. Koretz, Robert P. Perrillo
Journal: Hepatology (2001)

Persons with non–A, non–B hepatitis (cases) identified in 5 transfusion studies in the early 1970s have been followed ever since and compared for outcome with matched, transfused, non–hepatitis controls from the same studies. Previously, we reported no difference in all–cause mortality but slightly increased liver–related mortality between these cohorts after 18 years follow–up. We now present mortality and morbidity data after approximately 25 years of follow–up, restricted to the 3 studies with archived original sera. All–cause mortality was 67% among 222 hepatitis C–related cases and 65% among 377 controls ( P = NS). Liver–related mortality was 4.1% and 1.3%, respectively ( P = .05). Of 129 living persons with previously diagnosed transfusion–associated hepatitis (TAH), 90 (70%) had proven TAH–C, and 39 (30%), non–A–G hepatitis. Follow–up of the 90 TAH–C cases revealed viremia with chronic hepatitis in 38%, viremia without chronic hepatitis in 39%, anti–HCV without viremia in 17%, and no residual HCV markers in 7%. Thirty–five percent of 20 TAH–C patients biopsied for biochemically defined chronic hepatitis displayed cirrhosis, representing 17% of all those originally HCV–infected. Clinically evident liver disease was observed in 86% with cirrhosis but in only 23% with chronic hepatitis alone. Thirty percent of non–A, non–B hepatitis cases were unrelated to hepatitis viruses A,B,C, and G, suggesting another unidentified agent. In conclusion, all–cause mortality approximately 25 years after acute TAH–C is high but is no different between cases and controls. Liver–related mortality attributable to chronic hepatitis C, though low (&lt;3%), is significantly higher among the cases. Among living patients originally HCV–infected, 23% have spontaneously lost HCV RNA.