tbuckley/cabot-search huggingface dataset:
Higher Crash and Near-Crash Rates in Teenaged Drivers With Lower Cortisol Response
Authors: Marie Claude Ouimet, Thomas G. Brown, Feng Guo, Sheila G. Klauer, Bruce G. Simons-Morton, Youjia Fang, Suzanne E. Lee, Christina Gianoulakis, Thomas A. Dingus
Journal: JAMA Pediatrics (2014)

Road traffic crashes are one of the leading causes of injury and death among teenagers worldwide. Better understanding of the individual pathways to driving risk may lead to better-targeted intervention in this vulnerable group.To examine the relationship between cortisol, a neurobiological marker of stress regulation linked to risky behavior, and driving risk.The Naturalistic Teenage Driving Study was designed to continuously monitor the driving behavior of teenagers by instrumenting vehicles with kinematic sensors, cameras, and a global positioning system. During 2006-2008, a community sample of 42 newly licensed 16-year-old volunteer participants in the United States was recruited and driving behavior monitored. It was hypothesized in teenagers that higher cortisol response to stress is associated with (1) lower crash and near-crash (CNC) rates during their first 18 months of licensure and (2) faster reduction in CNC rates over time.Participants' cortisol response during a stress-inducing task was assessed at baseline, followed by measurement of their involvement in CNCs and driving exposure during their first 18 months of licensure. Mixed-effect Poisson longitudinal regression models were used to examine the association between baseline cortisol response and CNC rates during the follow-up period.Participants with a higher baseline cortisol response had lower CNC rates during the follow-up period (exponential of the regression coefficient, 0.93; 95% CI, 0.88-0.98) and faster decrease in CNC rates over time (exponential of the regression coefficient, 0.98; 95%, CI, 0.96-0.99).Cortisol is a neurobiological marker associated with teenaged-driving risk. As in other problem-behavior fields, identification of an objective marker of teenaged-driving risk promises the development of more personalized intervention approaches.
The frequency and prognostic impact of dic(9;20)(p13.2;q11.2) in childhood B-cell precursor acute lymphoblastic leukemia: results from the NOPHO ALL-2000 trial
Authors: V. Zachariadis, F. Gauffin, E. Kuchinskaya, M. Heyman, J. Schoumans, E. Blennow, B. Gustafsson, G. Barbany, I. Golovleva, Hans Ehrencrona, L. Cavelier, Linda Palmqvist, G. Lonnerholm, M. Nordenskjold, Bertil Johansson, E. Forestier, Agneta Nordgren
Journal: Leukemia (2011)
Diverse novel functions of neutrophils in immunity, inflammation, and beyond
Authors: Attila Mócsai
Journal: The Journal of Experimental Medicine (2013)

Neutrophils have long been considered simple suicide killers at the bottom of the hierarchy of the immune response. That view began to change 10–20 yr ago, when the sophisticated mechanisms behind how neutrophils locate and eliminate pathogens and regulate immunity and inflammation were discovered. The last few years witnessed a new wave of discoveries about additional novel and unexpected functions of these cells. Neutrophils have been proposed to participate in protection against intracellular pathogens such as viruses and mycobacteria. They have been shown to intimately shape the adaptive immune response at various levels, including marginal zone B cells, plasmacytoid dendritic cells and T cell populations, and even to control NK cell homeostasis. Neutrophils have been shown to mediate an alternative pathway of systemic anaphylaxis and to participate in allergic skin reactions. Finally, neutrophils were found to be involved in physiological and pathological processes beyond the immune system, such as diabetes, atherosclerosis, and thrombus formation. Many of those functions appear to be related to their unique ability to release neutrophil extracellular traps even in the absence of pathogens. This review summarizes those novel findings on versatile functions of neutrophils and how they change our view of neutrophil biology in health and disease.
Breast-Feeding and Alcoholism: The Trotter Hypothesis
Authors: Donald W. Goodwin, William F. Gabrielli, Elizabeth C. Penick, Elizabeth J. Nickel, Sunil Chhibber, Joachim Knop, Per Jensen, Fini Schulsinger
Journal: American Journal of Psychiatry (1999)

The authors' goal was to determine whether early termination of breast-feeding contributes to later alcohol dependence, as proposed more than 200 years ago by the British physician Thomas Trotter.In 1959-1961, a multiple-specialty group of physicians studied 9, 182 consecutive deliveries in a Danish hospital, obtaining data about prepartum and postpartum variables. The present study concentrates on perinatal variables obtained from 200 of the original babies who participated in a 30-year high-risk follow-up study of the antecedents of alcoholism.Of the 27 men who were diagnosed as alcohol dependent at age 30, 13 (48%) came from the group weaned from the breast before the age of 3 weeks; only 33 (19%) of the 173 non-alcohol-dependent subjects came from the early weaning group. When challenged by other perinatal variables in a multiple regression analysis, early weaning significantly contributed to the prediction of the severity of alcoholism at age 30.The data support the hypothesis that early weaning may be associated with a greater risk of alcohol dependence later in life.
Impact of Different Platelet Glycoprotein IIb/IIIa Receptor Inhibitors Among Diabetic Patients Undergoing Percutaneous Coronary Intervention
Authors: Marco Roffi, David J. Moliterno, Bernhard Meier, Eric R. Powers, Cindy L. Grines, Peter M. DiBattiste, Howard C. Herrmann, Michel Bertrand, Katherine E. Harris, Laura A. Demopoulos, Eric J. Topol
Journal: Circulation (2002)

Background — The platelet glycoprotein IIb/IIIa receptor inhibitor abciximab, a monoclonal antibody, has been shown to improve early and late outcomes among diabetic patients undergoing percutaneous coronary intervention (PCI). It is unknown whether small-molecule agents confer similar benefits. Methods and Results — In 18 countries, 4809 patients undergoing PCI with stent implantation were randomized to tirofiban or abciximab. At the time of enrollment, patients were stratified according to diabetes status. As compared with non-diabetic patients, patients with diabetes (n=1117) showed similar 30-day ischemic outcomes, an increased incidence of any target vessel revascularization (TVR) at 6 months (10.3% versus 7.8%; P = 0.008), and a trend toward higher 1-year mortality (2.5% versus 1.6%; P =0.056). Among diabetic patients randomized to tirofiban (n=560), the incidence of death, myocardial infarction (MI), or urgent TVR at 30 days was 6.2%, and among those randomized to abciximab (n=557) it was 5.4% (hazard ratio [HR] 1.16; P =0.540). At 6 months, the composite of death, MI, or any TVR occurred in 15.7% and in 16.9% of tirofiban and abciximab patients, respectively (HR 0.93; P =0.610). Any TVR occurred in 9.5% and 11.1%, respectively (HR 0.84; P = 0.366). The 1-year mortality was 2.1% in the tirofiban group and 2.9% in the abciximab group (HR 0.74; P = 0.436). Conclusions — Among diabetic patients undergoing PCI, tirofiban and abciximab were associated with comparable event rates, including similar rates of 6-month TVR and 1-year mortality. These findings suggest that the non-glycoprotein IIb/IIIa properties of abciximab do not translate into a discernible long-term clinical benefit among diabetic patients.
Cellular responses to hypoxia in the pulmonary circulation
Authors: S. O Brij, A. J Peacock
Journal: Thorax (1998)

Abstract Welsh, David J., and Andrew J. Peacock. Cellular responses to hypoxia in the pulmonary circulation. High Alt Med Biol 14:111–116, 2013.—Hypoxia can be defined as a reduction in available oxygen, whether in a whole organism or in a tissue or cell. It is a real life cause of pulmonary hypertension in humans both in terms of patients with chronic hypoxic lung disease and people living at high altitude. The effect of hypoxia on the pulmonary vasculature can be described in two ways; Hypoxic pulmonary vasoconstriction (HPV) (resulting from smooth muscle cell contraction) and pulmonary vascular remodelling (PVR) (resulting from pulmonary vascular cell proliferation). The pulmonary artery is made up of three resident cell types, the endothelial (intima), smooth muscle (media) and fibroblast (adventitia) cells. This review will examine the effects of hypoxia on the cells of the pulmonary vasculature and give an insight into the possible underlying mechanisms.
Insulin improves β-cell function in glucose-intolerant rat models induced by feeding a high-fat diet
Authors: Hui-qing Li, Bao-ping Wang, Xiu-Ling Deng, Jiao-yue Zhang, Yong-bo Wang, Juan Zheng, Wen-fang Xia, Tian-shu Zeng, Lu-lu Chen
Journal: Metabolism (2011)
MET and AXL Inhibitor NPS-1034 Exerts Efficacy against Lung Cancer Cells Resistant to EGFR Kinase Inhibitors Because of MET or AXL Activation
Authors: Jin Kyung Rho, Yun Jung Choi, Seon Ye Kim, Tae Won Kim, Eun Kyung Choi, Seon-Joo Yoon, Bu Man Park, Eunhye Park, Jong Hwan Bae, Chang-Min Choi, Jae Cheol Lee
Journal: Cancer Research (2013)

In non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutations, acquired resistance to EGFR-tyrosine kinase inhibitors (EGFR-TKI) can occur through a generation of bypass signals such as MET or AXL activation. In this study, we investigated the antitumor activity of NPS-1034, a newly developed drug that targets both MET and AXL, in NSCLC cells with acquired resistance to gefitinib or erlotinib (HCC827/GR and HCC827/ER, respectively). Characterization of H820 cells and evaluation of NPS-1034 efficacy in these cells were also performed. The resistance of HCC827/GR was mediated by MET activation, whereas AXL activation led to resistance in HCC827/ER. The combination of gefitinib or erlotinib with NPS-1034 synergistically inhibited cell proliferation and induced cell death in both resistant cell lines. Accordingly, suppression of Akt was noted only in the presence of treatment with both drugs. NPS-1034 was also effective in xenograft mouse models of HCC827/GR. Although the H820 cell line was reported previously to have T790M and MET amplification, we discovered that AXL was also activated in this cell line. There were no antitumor effects of siRNA or inhibitors specific for EGFR or MET, whereas combined treatment with AXL siRNA or NPS-1034 and EGFR-TKIs controlled H820 cells, suggesting that AXL is the main signal responsible for resistance. In addition, NPS-1034 inhibited cell proliferation as well as ROS1 activity in HCC78 cells with ROS1 rearrangement. Our results establish the efficacy of NPS-1034 in NSCLC cells rendered resistant to EGFR-TKIs because of MET or AXL activation or ROS1 rearrangement.
A Psychoeducational Program to Restore Hypoglycemia Awareness: The DAFNE-HART Pilot Study
Authors: Nicole de Zoysa, Helen Rogers, Marietta Stadler, Carla Gianfrancesco, Susan Beveridge, Emma Britneff, Pratik Choudhary, Jackie Elliott, Simon Heller, Stephanie A. Amiel
Journal: Diabetes Care (2013)

OBJECTIVE To develop and pilot a novel intervention addressing motivational and cognitive barriers to avoiding hypoglycemia in people with type 1 diabetes and persistent impaired awareness of hypoglycemia (IAH) despite training in flexible insulin therapy. RESEARCH DESIGN AND METHODS A 6-week intervention using motivational interviewing and cognitive behavioral techniques was designed. Diabetes educators were trained and supported in its delivery to 23 people with IAH (Gold score ≥4). RESULTS Twelve months postcourse, hypoglycemia awareness had improved (P &amp;lt; 0.001). Median (range) rates of severe hypoglycemia (SH) fell from 3 (0–104) to 0 (0–3) per person per year (P &amp;lt; 0.0001) and moderate from 14 (0–100) to 0 (0–18) per person per 6 weeks (P &amp;lt; 0.001). Worry and behavior around hyperglycemia improved. HbA1c was unchanged. CONCLUSIONS A pilot intervention targeting motivation and cognitions around hypoglycemia engaged patients with resistant IAH and recurrent SH and was associated with significant improvement, supporting the hypothesis that these factors underpin problematic hypoglycemia.
Use of Recombinant Proteins for Diagnosis of Cockroach Allergy in Patients with Asthma and/or Rhinitis Living in Brazil
Authors: A.R. Santos, M.C. Rodrigues, M. Thiesen, A.S. Zampolo, V.P.L. Ferriani, L. Arruda
Journal: Journal of Allergy and Clinical Immunology (2006)
Verbal hallucinations and language production processes in schizophrenia
Authors: Ralph E. Hoffman
Journal: Behavioral and Brain Sciences (1986)

Abstract How is it that many schizophrenics identify certain instances of verbal imagery as hallucinatory? Most investigators have assumed that alterations in sensory features of imagery explain this. This approach, however, has not yielded a definitive picture of the nature of verbal hallucinations. An alternative perspective suggests itself if one allows the possibility that the nonself quality of hallucinations is inferred on the basis of the experience of unintendedness that accompanies imagery production. Information-processing models of “intentional” cognitive processes call for abstract planning representations that are linked to goals and beliefs. Unintended actions - and imagery - can reflect planning disruptions whereby cognitive products do not cohere with concurrent goals. A model of schizophrenic speech disorganization is presented that postulates a disturbance of discourse planning. Insofar as verbal imagery can be viewed as inwardly directed speech, a consequence of such planning disturbances could be the production of unintended imagery. This link between the outward disorganization of schizophrenic speech and unintended verbal imagery is statistically supported by comparing the speech behavior of hallucinating and nonhallucinating schizophrenics. Studies of “borderline” hallucinations during normal, “goal-less” relaxation and drowsiness suggest that experiential unintendedness leads to a nonpathological variant of hallucinatory otherness that is correctable upon emerging from such passive cognitive states. This contrasts with the schizophrenic case, where nonconcordance with cognitive goals reinforces the unintendedness of verbal images and sustains the conviction of an external source. This model compares favorably with earlier models of verbal hallucinations and provides further evidence for a language production disorder in many schizophrenics. Short Abstract : How is it that many schizophrenics identify certain instances of verbal imagery as hallucinatory? This paper proposes that the critical feature identifying hallucinations is the experience of unintendedness. This experience is nonpathological during passive conscious states but pathological if occurring during goal-directed cognitive processing. A model of schizophrenic speech disorganization is presented that postulates a disturbance of discourse planning that specifies communicative intentions. These alterations could generate unintended verbal imagery as well. Statistical data are offered to support the model, and relevant empirical studies are reviewed.
Effects of a multidimensional anabolic steroid prevention intervention. The Adolescents Training and Learning to Avoid Steroids (ATLAS) Program
Authors: Linn Goldberg, Diane Elliot, Gregory N. Clarke, David P. MacKinnon, Esther Moe, Leslie Zoref, Christopher Green, Stephanie L. Wolf, Erick Greffrath, Daniel J. Miller, Angela Lapin
Journal: JAMA (1996)

To test a team-based, educational intervention designed to reduce adolescent athletes' intent to use anabolic androgenic steroids (AAS).Randomized prospective trial.Thirty-one high school football teams in the Portland, Ore, area.Seven hundred two adolescent football players at experimental schools; 804 players at control schools.Seven weekly, 50-minute class sessions were delivered by coaches and student team leaders, addressing AAS effects, sports nutrition and strength-training alternatives to AAS use, drug refusal role play, and anti-AAS media messages. Seven weight-room sessions were taught by research staff. Parents received written information and were invited to a discussion session.Questionnaires before and after intervention and at 9- or 12-month follow-up, assessing AAS use risk factors, knowledge and attitudes concerning AAS, sports nutrition and exercise knowledge and behaviors, and intentions to use AAS.Compared with controls, experimental subjects at the long-term follow-up had increased understanding of AAS effects, greater belief in personal vulnerability to the adverse consequences of AAS, improved drug refusal skills, less belief in AAS-promoting media messages, increased belief in the team as an information source, improved perception of athletic abilities and strength-training self-efficacy, improved nutrition and exercise behaviors, and reduced intentions to use AAS. Many other beneficial program effects remained significant at the long-term follow-up.This AAS prevention program enhanced healthy behaviors, reduced factors that encourage AAS use, and lowered intent to use AAS. These changes were sustained over the period of 1 year. Team-based interventions appear to be an effective approach to improve adolescent behaviors and reduce drug use risk factors.
Abstract B33: PKC resistance in uveal melanoma is mediated by activation of AKT and reversed by BYL719, the PI3Kα inhibitor
Authors: Elgilda Musi, Grazia Ambrosini, Gary K. Schwartz
Journal: Cancer Research (2015)

Abstract Uveal melanoma is the one of most common intraocular malignancies of the adult eye. Recently, Protein Kinase C (PKC) inhibitors have been used, as single agent and in combination, to treat GNAQ/GNA11-mutant uveal melanoma. However, patients may develop resistance to drug therapy. We have studied mechanisms of PKC resistance in uveal melanoma by exposing GNAQ/GNA11 mutant cell lines (92.1, Omm1.3 and Omm1) to increasing concentrations of the PKC inhibitor AEB071 for extended periods of time. Cell survival, as measured by cell proliferation assays, indicates IC50s of &amp;gt; 5μM, ten times higher than the sensitive parental cells. Western blot analysis indicates increased expression of p-MARCKS (the PKC substrate), p-ERK and p-AKT in the resistant cells. When treated with AEB071, there was no evidence of PKC enzyme inhibition and no suppression of p-MARCKS, p-ERK or p-AKT. Though resistant to AEB071, treatment of the resistant cells with BYL719, a PI3Kα inhibitor, shows inhibition of cell growth (IC50s between 1 and 2 μM) with inhibition of p-AKT similar to that of the parental cells. Furthermore, this effect on growth inhibition can be enhanced by combining AEB071 with BYL719 resulting in inhibition of p-ERK, p-S6 and p-AKT despite persistent activation of p-MARCKS. Analysis of p-glycoprotein (MDR) in the PKC resistant cell lines showed no differences when compared to the parental cell lines, suggesting that this effect is not due to differences in drug accumulation. These studies support the combination of AEB071 and BYL719 as a means to maintain sensitization to PKC inhibitor therapy despite the onset of drug resistance. A clinical trial with AEB071 and BYL719 will be initiated shortly. Citation Format: Elgilda Musi, Grazia Ambrosini, Gary K. Schwartz. PKC resistance in uveal melanoma is mediated by activation of AKT and reversed by BYL719, the PI3Kα inhibitor. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Melanoma: From Biology to Therapy; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(14 Suppl):Abstract nr B33.
Xenobiotic acceleration of idiopathic systemic autoimmunity in lupus-prone bxsb mice.
Authors: K M Pollard, D L Pearson, P Hultman, T N Deane, U Lindh, D H Kono
Journal: Environmental Health Perspectives (2001)

The diverse genetic backgrounds of lupus-prone murine models, which produce both quantitative and qualitative differences in disease expression, may be a valuable resource for studying the influence of environmental exposure on autoimmune disease in sensitive populations. We tested this premise by exposing autoimmune-prone BXSB and the nonautoimmune C57BL/6 mice to the heavy metal mercury. Although both strains express a nonsusceptible H-2 haplotype, exposure to mercury accelerated systemic autoimmunity in both male and female BXSB mice, whereas the C57BL/6 mice were resistant. The subclasses of antichromatin antibodies elicited in BXSB mice by mercury exposure were more consistent with the predominant Th1-type response of idiopathic disease than with the Th2-type response found in mercury-induced autoimmunity (HgIA). The appearance and magnitude of both humoral and cellular features of systemic autoimmunity correlated with the mercury dose. Furthermore, environmentally relevant tissue levels of mercury were associated with exacerbated systemic autoimmunity. These studies demonstrate that xenobiotic exposure can accelerate spontaneous systemic autoimmunity, and they support the possibility that low-level xenobiotic exposure enhances susceptibility to systemic autoimmunity in genetically susceptible individuals.
Breast Cancer Stem Cells—Ready for Their Close-up?
Authors: Kristine E. Calhoun
Journal: JAMA Surgery (2013)

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Cardiac Magnetic Resonance Imaging in Giant Cell Myocarditis
Authors: Yasumori Sujino, Fumiko Kimura, Jun Tanno, Shintaro Nakano, Eriko Yamaguchi, Michio Shimizu, Nanami Okano, Yuichi Tamura, Jun Fujita, Leslie T. Cooper, Takaaki Senbonmatsu, Toshihiro Muramatsu, Shigeyuki Nishimura
Journal: Circulation (2014)