tbuckley/cabot-search huggingface dataset:
Strong Artificial Selection in Domestic Mammals Did Not Result in an Increased Recombination Rate
Authors: Violeta Muñoz-Fuentes, Marina Marcet-Ortega, Gorka Alkorta-Aranburu, Catharina Linde Forsberg, Jane M. Morrell, Esperanza Manzano-Piedras, Arne Söderberg, Katrin Daniel, Adrian Villalba, Attila Toth, Anna Di Rienzo, Ignasi Roig, Carles Vilà
Journal: Molecular Biology and Evolution (2014)

Recombination rates vary in intensity and location at the species, individual, sex and chromosome levels. Despite the fundamental biological importance of this process, the selective forces that operate to shape recombination rate and patterns are unclear. Domestication offers a unique opportunity to study the interplay between recombination and selection. In domesticates, intense selection for particular traits is imposed on small populations over many generations, resulting in organisms that differ, sometimes dramatically, in morphology and physiology from their wild ancestor. Although earlier studies suggested increased recombination rate in domesticates, a formal comparison of recombination rates between domestic mammals and their wild congeners was missing. In order to determine broad-scale recombination rate, we used immunolabeling detection of MLH1 foci as crossover markers in spermatocytes in three pairs of closely related wild and domestic species (dog and wolf, goat and ibex, and sheep and mouflon). In the three pairs, and contrary to previous suggestions, our data show that contemporary recombination rate is higher in the wild species. Subsequently, we inferred recombination breakpoints in sequence data for 16 genomic regions in dogs and wolves, each containing a locus associated with a dog phenotype potentially under selection during domestication. No difference in the number and distribution of recombination breakpoints was found between dogs and wolves. We conclude that our data indicate that strong directional selection did not result in changes in recombination in domestic mammals, and that both upper and lower bounds for crossover rates may be tightly regulated.
Vasodilator Response Assessment in Porcine Myocardium With Magnetic Resonance Relaxometry
Authors: Warren D. Foltz, Hong Huang, Stephen Fort, Graham A. Wright
Journal: Circulation (2002)

Background— This research describes an early preclinical study of the biophysical mechanisms governing changes in myocardial T 2 during vasodilation in normal myocardium. Methods and Results— Theoretical modeling and experimental studies in an instrumented pig model (n=7) provided measures of changes in myocardial T 2 , relative blood volume (BV), and microcirculation oxygen levels (%O 2 ) during intracoronary adenosine infusion. Intracoronary adenosine increases perfusion without increasing blood volume or cardiac metabolic rate; thus, T 2 elevations should reflect elevated microcirculation oxygen levels. Robust strategies were used for magnetic resonance imaging (MRI) data collection. Measures of myocardial and vascular T 1 before and after Clariscan (Amersham Health) injection provided blood volume assessment. Changes in microcirculation oxygen levels were estimated via direct blood sampling from the left anterior descending (LAD) coronary vein. Perfusion changes were monitored using a Doppler flow wire within the left main coronary artery. Myocardial T 2 elevations (ΔT 2 =17±8%) within the LAD arterial perfusion bed were related to elevations in perfusion (coronary velocity reserve=3.2±0.4) and coronary venous %O 2 [Δ(LAD CV%O 2 ) =56±11%], whereas blood volume (ΔBV=0 ±2%) and cardiac metabolic rate [Δ(heart rate x blood pressure) = −4±11%] remained constant. Conclusions— Myocardial T 2 elevation during intracoronary adenosine infusion was significant and repeatable, caused by increases in microcirculation oxygen levels. Changes in microcirculation oxygen levels of approximately 40%O 2 should be detectable by this technique. This sensitivity should suffice for differentiating normal from abnormal myocardium via measurement of myocardial perfusion reserve.
Effect of Pharmacological Treatment of Depression on A1C and Quality of Life in Low-Income Hispanics and African Americans With Diabetes
Authors: Diana Echeverry, Petra Duran, Curley Bonds, Martin Lee, Mayer B. Davidson
Journal: Diabetes Care (2009)

OBJECTIVE To determine whether pharmacological treatment of depression in low-income minorities with diabetes improves A1C and quality of life (QOL). RESEARCH DESIGN AND METHODS This was a 6-month, randomized, double-blind, placebo-controlled trial. Patients were screened for depression using Whooley's two-question tool at a county diabetes clinic. Depression was confirmed (or not) with the Computerized Diagnostic Interview Survey (CDIS) software program, and the severity of depression was assessed monthly by the Hamilton Depression Scale (HAM-D). Depressed subjects with A1C levels ≥8.0% were randomly assigned to receive either sertraline or placebo. Diabetes care was provided by nurses following detailed treatment algorithms who were unaware of therapy for depression. RESULTS A total of 150 subjects answered positively to at least one question on Whooley's questionnaire. The positive predictive value for depression diagnosed by CDIS was 69, 67, and 84% for positive answers to question 1 only, question 2 only, or both, respectively. Of the 89 subjects who entered the study, 75 completed. An intention-to-treat analysis revealed significant differences between baseline and 6 months in HAM-D and pain scores, QOL, and A1C and systolic blood pressure levels in both groups, with no differences between groups for the first three but a significantly greater decrease with sertraline in A1C and systolic blood pressure levels. Changes in HAM-D scores and A1C levels were significantly correlated in all subjects (P = 0.45 [P &amp;lt; 10−6]). CONCLUSIONS In this low-income minority population, pharmacological treatment of depression significantly improved A1C and systolic blood pressure levels compared with placebo.
Lichen planopilaris following hair transplantation and face-lift surgery
Authors: Y.Z. Chiang, A. Tosti, I.H. Chaudhry, L. Lyne, B. Farjo, N. Farjo, D. Cadore de Farias, C.E.M. Griffiths, R. Paus, M.J. Harries
Journal: British Journal of Dermatology (2011)

Journal Article Lichen planopilaris following hair transplantation and face‐lift surgery Get access Y.Z. Chiang, Y.Z. Chiang The Dermatology Centre, The University of Manchester, Salford NHS Foundation Trust, Manchester M6 8HD, U.K Search for other works by this author on: Oxford Academic Google Scholar A. Tosti, A. Tosti Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami, Miami, FL, U.S.A Search for other works by this author on: Oxford Academic Google Scholar I.H. Chaudhry, I.H. Chaudhry Department of Pathology, Manchester Royal Infirmary, Manchester, U.K Search for other works by this author on: Oxford Academic Google Scholar L. Lyne, L. Lyne Department of Pathology, Manchester Royal Infirmary, Manchester, U.K Search for other works by this author on: Oxford Academic Google Scholar B. Farjo, B. Farjo The Farjo Centre, Manchester, U.K Search for other works by this author on: Oxford Academic Google Scholar N. Farjo, N. Farjo The Farjo Centre, Manchester, U.K Search for other works by this author on: Oxford Academic Google Scholar D. Cadore de Farias, D. Cadore de Farias Dermatologic Clinic, University Hospital of Federal University of Santa Catarina, Florianópolis, SC, Brazil Search for other works by this author on: Oxford Academic Google Scholar C.E.M. Griffiths, C.E.M. Griffiths The Dermatology Centre, The University of Manchester, Salford NHS Foundation Trust, Manchester M6 8HD, U.KUniversity of Manchester, Manchester Academic Health Science Centre, Manchester, U.K Search for other works by this author on: Oxford Academic Google Scholar R. Paus, R. Paus University of Manchester, Manchester Academic Health Science Centre, Manchester, U.KDepartment of Dermatology, University of Lübeck, D‐23538 Lübeck, Germany Search for other works by this author on: Oxford Academic Google Scholar M.J. Harries M.J. Harries The Dermatology Centre, The University of Manchester, Salford NHS Foundation Trust, Manchester M6 8HD, U.KUniversity of Manchester, Manchester Academic Health Science Centre, Manchester, U.K Matthew Harries. E‐mail: mjharries@doctors.org.uk Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 166, Issue 3, 1 March 2012, Pages 666, https://doi.org/10.1111/j.1365-2133.2011.10692.x Published: 01 March 2012 Article history Accepted: 25 September 2011 Published: 01 March 2012
Enolase-1 promotes plasminogen-mediated recruitment of monocytes to the acutely inflamed lung
Authors: Malgorzata Wygrecka, Leigh M. Marsh, Rory E. Morty, Ingrid Henneke, Andreas Guenther, Juergen Lohmeyer, Philipp Markart, Klaus T. Preissner
Journal: Blood (2009)
Detection of a second t(14;18) breakpoint cluster region in human follicular lymphomas.
Authors: M L Cleary, N Galili, J Sklar
Journal: The Journal of Experimental Medicine (1986)

Our results indicate that there are two major breakpoint cluster regions in chromosome 18 DNA for t(14;18) translocations in follicular lymphomas. The absence of a pFL-1 homologous transcript in a cell line containing a pFL-2-detectable translocation suggests that there may be two different pathogenetic consequences of t(14;18) translocations. One possibility is that, despite the distances between them (greater than 20 kb), breakpoints in the two cluster regions in some way affect transcription of the same gene product, which has not yet been identified. Alternatively, two separate transcriptional units may be involved. The availability of DNA probes for each of the two t(14;18) breakpoint cluster regions will allow further studies regarding the biologic significance of these two genetically distinct classes of t(14;18) translocations.
Formation of the Collateral Circulation Is Regulated by Vascular Endothelial Growth Factor-A and A Disintegrin and Metalloprotease Family Members 10 and 17
Authors: Jennifer L. Lucitti, Jessica K. Mackey, Jeffrey C. Morrison, Jody J. Haigh, Ralf H. Adams, James E. Faber
Journal: Circulation Research (2012)

Rationale: The density of native (preexisting) collaterals varies widely and is a significant determinant of variation in severity of stroke, myocardial infarction, and peripheral artery disease. However, little is known about mechanisms responsible for formation of the collateral circulation in healthy tissues. Objective: We previously found that variation in vascular endothelial growth factor (VEGF) expression causes differences in collateral density of newborn and adult mice. Herein, we sought to determine mechanisms of collaterogenesis in the embryo and the role of VEGF in this process. Methods and Results: Pial collaterals begin forming between embryonic day 13.5 and 14.5 as sprout-like extensions from arterioles of existing cerebral artery trees. Global VEGF-A overexpressing mice ( Vegf hi/+ ) formed more, and Vegf lo/+ formed fewer, collaterals during embryogenesis, in association with differences in vascular patterning. Conditional global reduction of Vegf or Flk1 only during collaterogenesis significantly reduced collateral formation, but now without affecting vascular patterning, and the effects remained in adulthood. Endothelial-specific Vegf reduction had no effect on collaterogenesis. Endothelial-specific reduction of a disintegrin-and-metalloprotease-domain-10 ( Adam10 ) and inhibition of γ-secretase increased collateral formation, consistent with their roles in VEGF-induced Notch1 activation and suppression of prosprouting signals. Endothelial-specific knockdown of Adam17 reduced collateral formation, consistent with its roles in endothelial cell migration and embryonic vascular stabilization, but not in activation of ligand-bound Notch1. These effects also remained in adulthood. Conclusions: Formation of pial collaterals occurs during a narrow developmental window via a sprouting angiogenesis-like mechanism, requires paracrine VEGF stimulation of fetal liver kinase 1-Notch signaling, and adult collateral number is dependent on embryonic collaterogenesis.
QUANTITATIVE INVESTIGATIONS OF IDIOTYPIC ANTIBODIES
Authors: Bruce W. Brient, Alfred Nisonoff
Journal: The Journal of Experimental Medicine (1970)

Rabbit anti-idiotypic antibodies were prepared by injection of specifically purified anti-p-azobenzoate antibodies (D) from individual donor rabbits. Benzoate derivatives were found to be strong inhibitors of the reactions of D with anti-D antisera. There was a close correlation between the combining affinities of the benzoate derivatives used and their effectiveness as inhibitors. Compounds tested that are chemically unrelated to benzoate were ineffective. The results indicate either that the combining site of anti-benzoate antibody is part of an important idiotypic determinant, which is sterically blocked by hapten, or that the hapten induces a conformational change which alters idiotypic determinants not involving the active site. Such conformational changes, if they occur, must be restricted since hapten has little effect on the reactions of F(ab')(2) fragments of anti-benzoate antibodies with antisera directed to rabbit fragment Fab and no detectable effect on reactions with antibodies directed to allotypic determinants.
The role of concomitant respiratory diseases on the rate of decline in FEV<sub>1</sub>among adult asthmatics
Authors: D. Sherrill, S. Guerra, A. Bobadilla, R. Barbee
Journal: European Respiratory Journal (2003)

Several recent reports have presented evidence suggesting that adults with asthma have an accelerated rate of decline in pulmonary function compared with nonasthmatics. However, most of these studies have not taken into account the possible effect of comorbid lung disease in addition to asthma. This study was designed to determine if comorbid respiratory diseases modify or otherwise change the estimates of decline in forced expiratory volume in one second (FEV 1 ). Study subjects were White, non-Mexican, American participants, who were ≥20 yrs of age at the initial survey and had at least one pulmonary function testing. Respiratory disease status, based on self-reported questionnaires and pulmonary function tests, were assessed during 12 surveys spanning a period of up to 20 yrs. There were 2,926 subjects who met the inclusion criteria, 214 (7.3%) had physician-confirmed asthma, 325 (11.1%) chronic obstructive pulmonary disease (COPD), and 125 (4.3%) both physician-confirmed asthma and COPD. Longitudinal analysis revealed that among those with longstanding asthma, FEV 1 values were low but did not decline at a more rapid rate than normal. Likewise, subjects with both asthma and COPD had the lowest levels of FEV 1 , but also a rate of decline that was not significantly increased. Only those with COPD in the absence of asthma experienced both a low initial FEV 1 level and a significantly steeper rate of decline. Based on these findings, the authors conclude that forced expiratory volume in one second does not decline more rapidly in asthmatics or in those with asthma and chronic obstructive pulmonary disease, compared with nonasthmatics.
Serological markers predict inflammatory bowel disease years before the diagnosis
Authors: Fiona D M van Schaik, Bas Oldenburg, Andrew R Hart, Peter D Siersema, Stefan Lindgren, Olof Grip, Birgit Teucher, Rudolf Kaaks, Manuela M Bergmann, Heiner Boeing, Franck Carbonnel, Prevost Jantchou, Marie-Christine Boutron-Ruault, Anne Tjønneland, Anja Olsen, Francesca L Crowe, Petra H M Peeters, Martijn G H van Oijen, H Bas Bueno-de-Mesquita
Journal: Gut (2012)

<h3>Objective</h3> Anti-neutrophil cytoplasmic antibodies and anti-<i>Saccharomyces cerevisiae</i> mannan antibodies (ASCAs) have been detected in the serum of patients with ulcerative colitis (UC) and Crohn9s disease (CD) and their unaffected family members. The aim of this study was to establish the value of serological markers as predictors of UC and CD. <h3>Design</h3> Individuals who developed CD or UC were identified from the European Prospective Investigation into Cancer and Nutrition (EPIC) study. At recruitment, none of the participants had a diagnosis of CD or UC. For each incident case, two controls were randomly selected matched for centre, date of birth, sex, date of recruitment and time of follow-up. Serum of cases and controls obtained at recruitment were analysed for ASCA IgG, ASCA IgA, perinuclear anti-neutrophil cytoplasmic antibody (pANCA), antibodies against <i>Escherichia coli</i> outer membrane porin C (OmpC) and flagellin CBir1. Conditional logistic regression was used to determine risk of CD and UC. Receiver operating characteristic curves were constructed to test accuracy. <h3>Results</h3> A total of 77 individuals were diagnosed with CD and 167 with UC after a mean follow-up of 4.5 (SD 3.2) and 4.4 (SD 3.1) years following blood collection, respectively. Combinations of pANCA, ASCA, anti-CBir1 and anti-OmpC were most accurate in predicting incident CD and UC (area under curve 0.679 and 0.657, respectively). The predictive value of the combination of markers increased when time to diagnosis of CD or UC decreased. <h3>Conclusion</h3> A panel of serological markers is able to predict development of CD and UC in individuals from a low-risk population.
Effects of Tamoxifen on Spinal Bone Density in Women With Breast Cancer
Authors: S. Turken, E. Siris, D. Seldin, E. Flaster, G. Hyman, R. Lindsay
Journal: JNCI Journal of the National Cancer Institute (1989)

Bone densitometry (L2-L4) was performed on 10 postmenopausal women with breast cancer after 0, 6, and 12 months of tamoxifen treatment; the results were compared with data from 10 normal controls. The patients and controls differed significantly at 6 (P<.05) and 12 (P<.003) months. The tamoxifen group showed a nonsignificant mean gain in bone mineral density after 6 and 12 months of treatment (+0.024 ± 0.014 and +0.022 ± 0.018 g/cm2, respectively), whereas the controls showed a nonsignificant mean loss of bone mass at 6 months (−0.012 ± 0.018 g/cm2 and a statistically significant loss of bone density after 12 months (−0.024 ± 0.01 g/cm2). These preliminary data suggest that tamoxifen use is associated with preservation of bone mass during the first year of treatment. [J Natl Cancer Inst 81: 1086–1088, 1989]
Acetylsalicylic Acid Inhibits Cell Proliferation by Involving Transforming Growth Factor-β
Authors: Santiago Redondo, Carlos G. Santos-Gallego, Patricia Ganado, Marta García, Laura Rico, Marcela Del Rio, Teresa Tejerina
Journal: Circulation (2003)

Acetylsalicylic acid (ASA) inhibits cell proliferation. This may be mediated by transforming growth factor-beta (TGF-beta). TGF-beta directly stops cell proliferation, restrains cells in G(0), and inhibits the uptake of platelet-derived growth factor and insulin-like growth factor. These effects are identical to those observed with ASA treatment.We cultured rat thoracic aorta vascular smooth muscle cells and measured cytotoxicity, cell proliferation, cell cycle, transcription of TGF-beta1, and concentration of TGF-beta1 in supernatant medium. ASA dose-dependently restrained cells in G(0) phase with no cytotoxic effect and inhibited cell proliferation by 30.86%. Anti-TGF-beta1 reversed this inhibition by 30.21%. However, ASA treatment decreased TGF-beta1 transcription and had no significant effect on TGF-beta1 concentration.TGF-beta seems to play an important role in ASA-mediated inhibition of cell proliferation. Therefore, treatment with ASA prevents coronary disease not only by means of its antiplatelet properties but also by an important inhibition of plaque growth. This relationship between ASA and TGF-beta explains many other effects, such as cancer chemoprevention, immunomodulation, and wound healing. The aim of this study was to demonstrate this link.
Platelet–Monocyte Aggregates
Authors: Jane E. Freedman, Joseph Loscalzo
Journal: Circulation (2002)

hrombus formation within a coronary vessel is the precipitating event in unstable coronary syndromes.The angiographic severity of coronary stenoses may not predict sites of subsequent acute coronary events, inasmuch as rupture of atheromatous plaque with thrombosis in relatively mildly stenosed vessels may underlie many acute coronary syndromes.The intact endothelium normally prevents platelet activation, but the intimal injury associated with endothelial denudation and plaque rupture exposes subendothelial collagen and von Willebrand factor, which support prompt platelet adhesion and activation.Circulating platelets can adhere either directly to collagen or indirectly, via the binding of von Willebrand factor, to the glycoprotein Ib/IX complex.Local platelet activation promotes thrombus formation and additional platelet recruitment by supporting cell surface thrombin formation and releasing potent platelet agonists, such as adenosine 5Ј-diphosphate, serotonin, and thromboxane A 2 .The central role of platelet activation in acute coronary syndromes is supported by increased plateletderived thromboxane and prostaglandin metabolites detected in patients with acute coronary syndromes 1 and the clear clinical benefit of treatment with aspirin for prevention of acute coronary events.
Structural and functional plasticity of the luteinizing hormone/choriogonadotrophin receptor
Authors: Britta Troppmann, Gunnar Kleinau, Gerd Krause, Jörg Gromoll
Journal: Human Reproduction Update (2013)

In recent years it became evident that several types of the luteinizing hormone/choriogonadotrophin receptor (LHCGR) exist. In addition to the classical receptor type known in rodents, an LHCGR type containing an additional exon is present in primates and humans. This specific exon 6A introduces a hitherto unknown regulatory pathway of the LHCGR at the transcriptional level which can lead to the expression of an alternative protein covering the extracellular part only. Furthermore, an LHCGR type lacking exon 10 at the mRNA and protein levels has been described in the New World primate lineage, giving rise to an additional receptor type in which amino acids of the extracellular hinge region connecting the leucine-rich repeat domain and transmembrane domain are missing. Topic-related information was retrieved by systematic searches using Medline/PubMed. Structural homology models were retrieved from a glycoprotein hormone receptors web application and from recent publications. In a novel approach, we combine functional aspects with three-dimensional properties of the LHCGR and the different receptor types to deduce causative relationships between these two parameters. On this basis, the physiological impact and patho-physiological consequences of the different LHCGR types are inferred. The complex system of different LHCGR types and two corresponding hormones (LH and CG) represents a major challenge for future studies on selective hormone binding, signal transduction and receptor regulation. The presence of these naturally occurring LHCGR types requires re-examining of our present view on receptor function, experimental set-ups and data interpretation, but also offers new clinical approaches to interfere with LH/CG action in humans.