tbuckley/cabot-search huggingface dataset:
Randomised controlled trial of home based motivational interviewing by midwives to help pregnant smokers quit or cut down
Authors: D M Tappin, M A Lumsden, W H Gilmour, F Crawford, D McIntyre, D H Stone, R Webber, S MacIndoe, E Mohammed
Journal: BMJ (2005)

<h3>Abstract</h3> <b>Objective</b> To determine whether motivational interviewing—a behavioural therapy for addictions—provided at home by specially trained midwives helps pregnant smokers to quit. <b>Design</b> Randomised controlled non-blinded trial analysed by intention to treat. <b>Setting</b> Clinics attached to two maternity hospitals in Glasgow. <b>Participants</b> 762<b>/</b>1684 pregnant women who were regular smokers at antenatal booking: 351 in intervention group and 411 in control group. <b>Interventions</b> All women received standard health promotion information. Women in the intervention group were offered motivational interviewing at home. All interviews were recorded. <b>Main outcome measures</b> Self reported smoking cessation verified by plasma or salivary cotinine concentration. <b>Results</b> 17/351 (4.8%) women in the intervention group stopped smoking (according to self report and serum cotinine concentration &lt; 13.7 ng/ml) compared with 19/411(4.6%) in the control group. Fifteen (4.2%) women in the intervention group cut down (self report and cotinine concentration less than half that at booking) compared with 26 (6.3%) in the control group. Fewer women in the intervention group reported smoking more (18 (5.1%) <i>v</i> 44 (10.7%); relative risk 0.48, 95% confidence interval 0.28 to 0.81). Birth weight did not differ significantly (mean 3078 g <i>v</i> 3048 g). <b>Conclusion</b> Good quality motivational interviewing did not significantly increase smoking cessation among pregnant women.
Empirical Validation of the Information–Motivation–Behavioral Skills Model of Diabetes Medication Adherence: A Framework for Intervention
Authors: Lindsay S. Mayberry, Chandra Y. Osborn
Journal: Diabetes Care (2014)

Suboptimal adherence to diabetes medications is prevalent and associated with unfavorable health outcomes, but it remains unclear what intervention content is necessary to effectively promote medication adherence in diabetes. In other disease contexts, the Information-Motivation-Behavioral skills (IMB) model has effectively explained and promoted medication adherence and thus may have utility in explaining and promoting adherence to diabetes medications. We tested the IMB model's hypotheses in a sample of adults with type 2 diabetes.Participants (N = 314) completed an interviewer-administered survey and A1C test. Structural equation models tested the effects of diabetes medication adherence-related information, motivation, and behavioral skills on medication adherence and the effect of medication adherence on A1C.The IMB elements explained 41% of the variance in adherence, and adherence explained 9% of the variance in A1C. As predicted, behavioral skills had a direct effect on adherence (β = 0.59; P < 0.001) and mediated the effects of information (indirect effect 0.08 [0.01-0.15]) and motivation (indirect effect 0.12 [0.05-0.20]) on adherence. Medication adherence significantly predicted glycemic control (β = -0.30; P < 0.001). Neither insulin status nor regimen complexity was associated with adherence, and neither moderated associations between the IMB constructs and adherence.The results support the IMB model's predictions and identify modifiable and intervenable determinants of diabetes medication adherence. Medication adherence promotion interventions may benefit from content targeting patients' medication adherence-related information, motivation, and behavioral skills and assessing the degree to which change in these determinants leads to changes in medication adherence behavior.
A phase II trial of S-1 and cisplatin in patients with metastatic or relapsed biliary tract cancer
Authors: Y.J. Kim, S.-A. Im, H.G. Kim, S.Y. Oh, K.W. Lee, I.S. Choi, D.Y. Oh, S.H. Lee, J.H. Kim, D.W. Kim, T.Y. Kim, S.W. Kim, D.S. Heo, Y.B. Yoon, Y.J. Bang
Journal: Annals of Oncology (2007)
Clinical and Biomarker Correlates of Androgen-Independent, Locally Aggressive Prostate Cancer with Limited Metastatic Potential
Authors: Vasily J. Assikis, Kim-Anh Do, Sijin Wen, Xuemei Wang, Jeong Hee Cho-Vega, Shawn Brisbay, Remigio Lopez, Christopher J. Logothetis, Patricia Troncoso, Christos N. Papandreou, Timothy J. McDonnell
Journal: Clinical Cancer Research (2004)

Abstract Purpose: We have identified a subset of patients exhibiting extended survival with metastases from androgenindependent prostate cancer of which the principal site of progression was the tumor primary. The purpose of this study was to evaluate the expression of selected biomarkers to characterize this subset of prostate cancer patients. Experimental Design: A 105 core tissue microarray was constructed from primary tumor samples from 16 patients, with matched lymph node metastases in 5 cases. Immunohistochemistry was used to evaluate selected biomarkers associated with prostate cancer progression. Standard statistical methodologies were used to compute the distribution of time to progression and overall survival associations between pairs of biomarkers. Hierarchical clustering was done between groups of biomarkers, and we devised new methods to assess homogeneity of biomarker expression. Results: The median interval from diagnosis to salvage surgery was 65 months. The profile of biomarker expression was notable for virtual absence of neuroendocrine features, high CD10, low matrix metalloproteinase (MMP)-9, high E-cadherin expression, and high membranous β-catenin. The mean proliferative index was 12.1 ± 10.1%, and the mean apoptotic index was 3.48 ± 2.22%, and there was a significant correlation between these indices. Expression of the epidermal growth factor receptor was associated with phospho-AKT and proliferative index but inversely associated with phospho-STAT3. Conclusions: The cohort of prostate cancer patients, characterized by locally aggressive disease rather than lethal metastatic progression, was associated with a distinctive biomarker signature. The biomarker profile was, in general, more consistent with low-grade prostate cancer exhibiting local growth rather than metastatic progression. Ongoing studies will establish whether this unique subset of patients can be identified prospectively.
CD82 Restrains Pathological Angiogenesis by Altering Lipid Raft Clustering and CD44 Trafficking in Endothelial Cells
Authors: Quan Wei, Feng Zhang, Mekel M. Richardson, Nathan H. Roy, William Rodgers, Yuechueng Liu, Wenyuan Zhao, Chenying Fu, Yingjun Ding, Chao Huang, Yuanjian Chen, Yao Sun, Lexi Ding, Yang Hu, Jian-Xing Ma, Michael E. Boulton, Satish Pasula, Jonathan D. Wren, Satoshi Tanaka, Xiaolin Huang, Markus Thali, Günter J. Hämmerling, Xin A. Zhang
Journal: Circulation (2014)

Angiogenesis is crucial for many pathological processes and becomes a therapeutic strategy against diseases ranging from inflammation to cancer. The regulatory mechanism of angiogenesis remains unclear. Although tetraspanin CD82 is widely expressed in various endothelial cells (ECs), its vascular function is unknown.Angiogenesis was examined in Cd82-null mice with in vivo and ex vivo morphogenesis assays. Cellular functions, molecular interactions, and signaling were analyzed in Cd82-null ECs. Angiogenic responses to various stimuli became markedly increased upon Cd82 ablation. Major changes in Cd82-null ECs were enhanced migration and invasion, likely resulting from the upregulated expression of cell adhesion molecules such as CD44 and integrins at the cell surface and subsequently elevated outside-in signaling. Gangliosides, lipid raft clustering, and CD44-membrane microdomain interactions were increased in the plasma membrane of Cd82-null ECs, leading to less clathrin-independent endocytosis and then more surface presence of CD44.Our study reveals that CD82 restrains pathological angiogenesis by inhibiting EC movement, that lipid raft clustering and cell adhesion molecule trafficking modulate angiogenic potential, that transmembrane protein modulates lipid rafts, and that the perturbation of CD82-ganglioside-CD44 signaling attenuates pathological angiogenesis.
A comparative histological study of pulmonary vascular lesions in lungs of patients With idiopathic or heritable PAH
Authors: Maria Rosa Ghigna, Christophe Guignabert, Marc Humbert, Peter Dorfmuller
Journal: European Respiratory Journal (2013)

Although patients with pulmonary arterial hypertension (PAH) carrying a bone morphogenetic protein receptor type 2 (BMPR2) mutation present with symptoms approximately 10 years earlier than noncarriers and show more severely hampered hemodynamics at diagnosis, their histological features have never been investigated in detail and compared with idiopathic PAH. The aim of this work was to explore and compare the histology and morphology of pulmonary vascular lesions between BMPR2 mutation carriers and noncarriers.  Five random sections of lung parenchyma from 28 patients, including 15 BMPR2 mutation carriers and 13 noncarriers, were histologically re-evaluated blindly by two experienced pathologists. Density (n/cm2) and appearance of plexiform lesions (Pls) (“atypical Pls”/ typical Pls), inflammation score and arterial thickening were analysed. Our findings revealed a positive trend of Pls density in BMPR2 mutation carriers as compared to noncarriers. So called “atypical Pls” (histologically identified as larger angiodysplastic arterial lesions) were almost exclusively found in the group of BMPR2 mutation carriers.  Differences in arterial thickening between mutation carriers and non-carriers did not reach statistical significance. No difference in the score of perivascular inflammation was observed between both groups.  Our results reveal, for the first time, the existence of distinctive morphologic patterns between lungs with BMPR2-related hPAH and idiopathic PAH. A precise definition of specific histological features may lead to a better understanding of PAH pathogenesis.
Altered Expression of c-IAP1, Survivin, and Smac Contributes to Chemotherapy Resistance in Thyroid Cancer Cells
Authors: Elena Tirrò, Maria Letizia Consoli, Michele Massimino, Livia Manzella, Francesco Frasca, Laura Sciacca, Luisa Vicari, Giorgio Stassi, Luigi Messina, Angelo Messina, Paolo Vigneri
Journal: Cancer Research (2006)

Abstract Resistance to chemotherapy predicts an unfavorable outcome for patients with radioiodine-insensitive thyroid cancer. To investigate the mechanisms underlying this resistance, we evaluated the expression of four different inhibitor of apoptosis proteins, and their antagonist, Smac, in thyroid cancer cells that survived 48 hours of exposure to cisplatin, doxorubicin, or taxol. We found high levels of c-IAP1 after cisplatin treatment and increased expression of survivin following exposure to doxorubicin. Cells that endured treatment with taxol showed reduced expression of Smac and released minimal amounts of this protein from the mitochondria. Down-regulation of c-IAP1 and survivin increased the cytotoxicity of cisplatin and doxorubicin, whereas overexpression of Smac improved the efficacy of taxol. Finally, thyroid cancer cells permanently resistant to doxorubicin or cisplatin showed increased expression of c-IAP1 and survivin, respectively. However, silencing of these proteins by RNA interference restored sensitivity to doxorubicin and cisplatin. Thus, in thyroid cancer cells, early resistance to chemotherapeutic agents requires high levels of c-IAP1 and survivin and low levels of Smac. Furthermore, increased expression of c-IAP1 and survivin contributes to the acquisition of permanent resistance to cytotoxic compounds. (Cancer Res 2006; 66(8): 4263-72)
In vitro schedule-dependency of myelotoxicity and cytotoxicity of Ecteinascidin 743 (ET-743)
Authors: M. Ghielmini, E. Colli, E. Erba, D. Bergamaschi, S. Pampallona, J. Jimeno, G. Faircloth, C. Sessa
Journal: Annals of Oncology (1998)
Coffee Consumption and Prostate Cancer Risk and Progression in the Health Professionals Follow-up Study
Authors: K. M. Wilson, J. L. Kasperzyk, J. R. Rider, S. Kenfield, R. M. van Dam, M. J. Stampfer, E. Giovannucci, L. A. Mucci
Journal: JNCI Journal of the National Cancer Institute (2011)

Coffee contains many biologically active compounds, including caffeine and phenolic acids, that have potent antioxidant activity and can affect glucose metabolism and sex hormone levels. Because of these biological activities, coffee may be associated with a reduced risk of prostate cancer. We conducted a prospective analysis of 47 911 men in the Health Professionals Follow-up Study who reported intake of regular and decaffeinated coffee in 1986 and every 4 years thereafter. From 1986 to 2006, 5035 patients with prostate cancer were identified, including 642 patients with lethal prostate cancers, defined as fatal or metastatic. We used Cox proportional hazards models to assess the association between coffee and prostate cancer, adjusting for potential confounding by smoking, obesity, and other variables. All P values were from two-sided tests. The average intake of coffee in 1986 was 1.9 cups per day. Men who consumed six or more cups per day had a lower adjusted relative risk for overall prostate cancer compared with nondrinkers (RR = 0.82, 95% confidence interval [CI] = 0.68 to 0.98, Ptrend = .10). The association was stronger for lethal prostate cancer (consumers of more than six cups of coffee per day: RR = 0.40, 95% CI = 0.22 to 0.75, Ptrend = .03). Coffee consumption was not associated with the risk of nonadvanced or low-grade cancers and was only weakly inversely associated with high-grade cancer. The inverse association with lethal cancer was similar for regular and decaffeinated coffee (each one cup per day increment: RR = 0.94, 95% CI = 0.88 to 1.01, P = .08 for regular coffee and RR = 0.91, 95% CI = 0.83 to 1.00, P = .05 for decaffeinated coffee). The age-adjusted incidence rates for men who had the highest (≥6 cups per day) and lowest (no coffee) coffee consumption were 425 and 519 total prostate cancers, respectively, per 100 000 person-years and 34 and 79 lethal prostate cancers, respectively, per 100 000 person-years. We observed a strong inverse association between coffee consumption and risk of lethal prostate cancer. The association appears to be related to non-caffeine components of coffee.
Evolution of HLA-DRB Genes
Authors: Gaby G.M. Doxiadis, Ilka Hoof, Nanine de Groot, Ronald E. Bontrop
Journal: Molecular Biology and Evolution (2012)

The HLA region shows diversity concerning the number and content of DRB genes present per haplotype. Similar observations are made for the equivalent regions in other primate species. To elucidate the evolutionary history of the various HLA-DRB genes, a large panel of intron sequences obtained from humans, chimpanzees, rhesus macaques, and common marmosets has been subjected to phylogenetic analyses. Special attention was paid to the presence and absence of particular transposable elements and/or to their segments. The sharing of different parts of the same long interspersed nuclear element-2 (LINE2, L2) and various Alu insertions by the species studied demonstrates that one precursor gene must have been duplicated several times before the Old World monkey (OWM) and hominid (HOM) divergence. At least four ancestral DRB gene families appear to have been present before the radiation of OWM and HOM, and one of these even predates the speciation of Old and New World primates. Two of these families represent the pseudogenes DRB6/DRB2 and DRB7, which have been locked in the genomes of various primate species over long evolutionary time spans. Furthermore, all phylogenies of different intron segments show consistently that, apart from the pseudogenes, only DRB5 genes are shared by OWM and HOM, and they demonstrate the common history of certain DRB genes/lineages of humans and chimpanzees. In contrast, the evolutionary history of some other DRB loci is difficult to decipher, thus illustrating the complex history of the evolution of DRB genes due to a combination of mutations and recombination-like events. The selected approach allowed us to shed light on the ancestral DRB gene pool in primates and on the evolutionary relationship of the various HLA-DRB genes.
CHOLINESTERASE ACTIVITY OF HUMAN SKIN
Authors: I. A. MAGNUS, R. H. S. THOMPSON
Journal: British Journal of Dermatology (1954)

Journal Article CHOLINESTERASE ACTIVITY OF HUMAN SKIN Get access I. A. MAGNUS, I. A. MAGNUS Registrar and Junior Research Fellow, Department of Dermatology, Guy's Hospital, London Search for other works by this author on: Oxford Academic Google Scholar R. H. S. THOMPSON R. H. S. THOMPSON Professor of Chemical Pathology, Guy's Hospital Medical School, London Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 66, Issue 5, 1 May 1954, Pages 163–173, https://doi.org/10.1111/j.1365-2133.1954.tb12613.x Published: 01 May 1954
Autologous haemopoietic stem-cell transplantation followed by allogeneic or autologous haemopoietic stem-cell transplantation in patients with multiple myeloma (BMT CTN 0102): a phase 3 biological assignment trial
Authors: Amrita Krishnan, Marcelo C Pasquini, Brent Logan, Edward A Stadtmauer, David H Vesole, Edwin Alyea, Joseph H Antin, Raymond Comenzo, Stacey Goodman, Parameswaran Hari, Ginna Laport, Muzaffar H Qazilbash, Scott Rowley, Firoozeh Sahebi, George Somlo, Dan T Vogl, Daniel Weisdorf, Marian Ewell, Juan Wu, Nancy L Geller, Mary M Horowitz, Sergio Giralt, David G Maloney
Journal: The Lancet Oncology (2011)
Comparison of the depth profiles of water and water-binding substances in the stratum corneum determined in vivo by Raman spectroscopy between the cheek and volar forearm skin: effects of age, seasonal changes and artificial forced hydration
Authors: M. Egawa, H. Tagami
Journal: British Journal of Dermatology (2007)

Dermatologists and cosmetic scientists are becoming increasingly interested in stratum corneum (SC) hydration because the SC plays an important role in keeping the skin surface soft and smooth. However, conventional in vivo noninvasive methods do not provide direct information about the depth profiles of water content or SC components that hold water.To study the depth profiles of water and SC components in vivo by Raman spectroscopy, and to analyse the changes due to age, anatomical location, season and water application.In vivo Raman spectra of the skin of the cheek and the volar forearm were obtained from 50 healthy Japanese volunteers of different ages (age range 22-76 years) with a confocal Raman spectrometer. The depth-dependent profiles of water and of SC water-binding components were calculated from the respective Raman spectra.The depth profile of the SC water content was observed in a pattern ranging from around 30% (water/wet tissue) at the outermost layer of the SC to about 70% at the deeper living layer. Although the water content at a depth of 10-30 microm in the forearm skin tended to be lower in older subjects than in younger subjects, no such difference was found in the much thinner SC of the cheek. Moreover, there was no seasonal difference in depth profile of water content from the mid part of the SC to an 80-microm depth from the skin surface both in the cheek and in the forearm. The water content of all the evaluated SC components showed a gradual decrease from the surface to deeper portions. The mean amounts of lactate in the forearm skin and cholesterol in the cheek skin were significantly higher in younger subjects than in older subjects. In contrast, the levels of free amino acids and trans-urocanic acid were higher in the forearm skin of older subjects than in younger subjects. The relative amounts of urea and lactate were the highest in summer, when that of trans-urocanic acid was the lowest. Prolonged water application on the forearm skin even for 90 min resulted in a remarkable increase in water content throughout the SC, even reaching the granular layer, which was only gradually released from the upper part of the SC after discontinuation of the hydration procedure.Our present findings suggest that changes in the concentration depth profiles of water, free amino acids and lipids in the skin depend on age, anatomical site and season. These findings indicate the important roles played by various water-holding substances in the SC in the regulation of SC water content.
Low Levels of Tumor Necrosis Factor α Increase Tumor Growth by Inducing an Endothelial Phenotype of Monocytes Recruited to the Tumor Site
Authors: Bin Li, Alicia Vincent, Justin Cates, Dana M. Brantley-Sieders, D. Brent Polk, Pampee P. Young
Journal: Cancer Research (2008)

Abstract Microenvironmental cues instruct infiltrating tumor-associated myeloid cells to drive malignant progression. A subpopulation of tumor-associated myeloid cells coexpressing endothelial and myeloid markers, although rare in peripheral blood, are primarily associated with tumors where they enhance tumor growth and angiogenesis. These biphenotypic vascular leukocytes result from the endothelial differentiation of myeloid progenitors, a process regulated by tumor necrosis factor (TNF)α in vitro. An in vivo increase in tumor-derived TNFα expression promoted tumor growth and vascularity of mouse melanoma, lung cancer, and mammary tumors. Notably, tumor growth was accompanied by a significant increase in myeloid/endothelial biphenotypic populations. TNFα-associated tumor growth, vascularity, and generation of tumor vascular leukocytes in mouse melanoma tumors were dependent on intact host TNFα receptors. Importantly, TNFα-expressing tumors did not exhibit increased inflammation over control tumors, suggesting a unique action related to myeloid to endothelial differentiation. Our studies suggest that TNFα constitutes a tumor microenvironment signal that biases recruited monocytes toward a proangiogenic/provasculogenic myeloid/endothelial phenotype. [Cancer Res 2009;69(1):338–48]
The Actin Cytoskeleton in T Cell Activation
Authors: Janis K. Burkhardt, Esteban Carrizosa, Meredith H. Shaffer
Journal: Annual Review of Immunology (2008)

T cell cytoarchitecture differs dramatically depending on whether the cell is circulating within the bloodstream, migrating through tissues, or interacting with antigen-presenting cells. The transition between these states requires important signaling-dependent changes in actin cytoskeletal dynamics. Recently, analysis of actin-regulatory proteins associated with T cell activation has provided new insights into how T cells control actin dynamics in response to external stimuli and how actin facilitates downstream signaling events and effector functions. Among the actin-regulatory proteins that have been identified are nucleation-promoting factors such as WASp, WAVE2, and HS1; severing proteins such as cofilin; motor proteins such as myosin II; and linker proteins such as ezrin and moesin. We review the current literature on how signaling pathways leading from diverse cell surface receptors regulate the coordinated activity of these and other actin-regulatory proteins and how these proteins control T cell function.
MICA, a gene contributing strong susceptibility to ankylosing spondylitis
Authors: Xiaodong Zhou, Jiucun Wang, Hejian Zou, Michael M Ward, Michael H Weisman, Maribel G Espitia, Xiangjun Xiao, Effie Petersdorf, Emmanuel Mignot, Javier Martin, Lianne S Gensler, Paul Scheet, John D Reveille
Journal: Annals of the Rheumatic Diseases (2013)

The human major histocompatibility complex class I chain-related gene A (MICA) controls the immune process by balancing activities of natural killer cells, γδ T cells and αβ CD8 T cells, and immunosuppressive CD4 T cells. MICA is located near HLA-B on chromosome 6. Recent genomewide association studies indicate that genes most strongly linked to ankylosing spondylitis (AS) susceptibility come from the region containing HLA-B and MICA. While HLA-B27 is a well-known risk genetic marker for AS, the potential effect of linkage disequilibrium (LD) shields any associations of genes around HLA-B with AS. The aim of this study was to investigate a novel independent genetic association of MICA to AS.