tbuckley/cabot-search huggingface dataset:
Sport psychology and concussion: new impacts to explore
Authors: G A Bloom, A S Horton, P McCrory, K M Johnston
Journal: British Journal of Sports Medicine (2004)

In recent years, there has been great interest in examining the psychological effects of athletic injuries. This has also extended to interventions in which coping strategies have been suggested to enhance recovery. Concussive injuries, which are common to many sports, hold particular problems in this regard. For example, a concussed athlete may be prone to experience isolation, pain, anxiety, and disruption of daily life as a result of the injury. This may be a problem for individual sport athletes—for example, professional skiers—who do not have the support of team mates to help them through their rehabilitation and recovery, as well as team sport athletes whose team mates may inadvertently pressure them to return to play.

Besides the physical loss resulting from an injury, there may also be psychological distress. Commonly reported emotion responses resulting from athletic injury have included anger, denial, depression, distress, bargaining, shock, and guilt.1–5 These are particularly seen in career ending injuries. Such emotional distress can negatively affect the athletes’ recovery process.

“…concussed athletes in team sports seem to have fewer long term problems” 

Injured athletes have also reported feelings of isolation and loneliness. Researchers found that athletes prevented from participating in their activity have lost contact with their team, coach, and friends.6,7 For example, Gould et al 6 examined the emotional reactions of US national team skiers to season ending injuries and found that 66.6% cited lack of attention and isolation as a source of stress during their injury. …
Associations between brain microstructures, metabolites, and cognitive deficits during chronic HIV-1 infection of humanized mice
Authors: Michael D Boska, Prasanta K Dash, Jaclyn Knibbe, Adrian A Epstein, Sidra P Akhter, Natasha Fields, Robin High, Edward Makarov, Stephen Bonasera, Harris A Gelbard, Larisa Y Poluektova, Howard E Gendelman, Santhi Gorantla
Journal: Molecular Neurodegeneration (2014)

Host-species specificity of the human immunodeficiency virus (HIV) limits pathobiologic, diagnostic and therapeutic research investigations to humans and non-human primates. The emergence of humanized mice as a model for viral infection of the nervous system has overcome such restrictions enabling research for HIV-associated end organ disease including behavioral, cognitive and neuropathologic deficits reflective of neuroAIDS. Chronic HIV-1 infection of NOD/scid-IL-2Rgcnull mice transplanted with human CD34+ hematopoietic stem cells (CD34-NSG) leads to persistent viremia, profound CD4+ T lymphocyte loss and infection of human monocyte-macrophages in the meninges and perivascular spaces. Murine cells are not infected with virus.Changes in mouse behavior were measured, starting at 8 weeks after viral infection. These were recorded coordinate with magnetic resonance spectroscopy metabolites including N-acetylaspartate (NAA), creatine and choline. Diffusion tensor magnetic resonance imaging (DTI) was recorded against multispectral immunohistochemical staining for neuronal markers that included microtubule associated protein-2 (MAP2), neurofilament (NF) and synaptophysin (SYN); for astrocyte glial fibrillary acidic protein (GFAP); and for microglial ionized calcium binding adaptor molecule 1 (Iba-1). Oligodendrocyte numbers and integrity were measured for myelin associated glycoprotein (MAG) and myelin oligodendrocyte glycoprotein (MOG) antigens.Behavioral abnormalities were readily observed in HIV-1 infected mice. Longitudinal open field activity tests demonstrated lack of habituation indicating potential for memory loss and persistent anxiety in HIV-1 infected mice compared to uninfected controls. End-point NAA and creatine in the cerebral cortex increased with decreased MAG. NAA and glutamate decreased with decreased SYN and MAG. Robust inflammation reflected GFAP and Iba-1 staining intensities. DTI metrics were coordinate with deregulation of NF, Iba-1, MOG and MAG levels in the whisker barrel and MAP2, NF, MAG, MOG and SYN in the corpus callosum.The findings are consistent with some of the clinical, biochemical and pathobiologic features of human HIV-1 nervous system infections. This model will prove useful towards investigating the mechanisms of HIV-1 induced neuropathology and in developing novel biomarkers and therapeutic strategies for disease.
Health in All Policies—The Finnish Initiative: Background, Principles, and Current Issues
Authors: Pekka Puska, Timo Ståhl
Journal: Annual Review of Public Health (2010)

Many historical developments, such as the Alma Ata Declaration or the Ottawa Charter, have drawn attention to the need for intersectoral work and for considering the health aspects of different policy proposals. In the 1970s, Finland started broad actions to change national diets to reduce the high mortality associated with cardiovascular diseases (CVDs). This and other work in Finland have involved many sectors and policies, resulted in significant public health improvements, and paved the way for the Health in All Policies (HiAP) initiative started during the Finnish European Union (EU) presidency in 2006. The initiative and the principles have encouraged further developments in Finland and have been linked with related developments within the EU and the World Health Organization (WHO).
Colon perforation during antiangiogenic therapy for malignant glioma
Authors: Andrew D. Norden, Jan Drappatz, Abigail Slate Ciampa, Lisa Doherty, Debra Conrad LaFrankie, Santosh Kesari, Patrick Y. Wen
Journal: Neuro-Oncology (2008)

Antiangiogenic drugs have emerged as effective treatment options for patients with recurrent malignant gliomas (MGs). Though this class of drugs is generally well tolerated, rare life-threatening complications, including thromboembolism, hemorrhage, and gastrointestinal (GI) perforation, are reported. We describe six cases of GI perforation among 244 glioma patients (2.5%) during treatment with antiangiogenic agents in combination with chemotherapy and corticosteroids. Two patients succumbed to this complication, and the others recovered. Because GI perforation is a life-threatening yet treatable complication, neurooncologists must have a low threshold to consider it in patients on antiangiogenic drug therapy who present with abdominal pain and other GI complaints.
Fibrinogen-independent platelet adhesion and thrombus formation on subendothelium mediated by glycoprotein IIb-IIIa complex at high shear rate.
Authors: H J Weiss, J Hawiger, Z M Ruggeri, V T Turitto, P Thiagarajan, T Hoffmann
Journal: Journal of Clinical Investigation (1989)

Platelet adhesion and thrombus formation on subendothelium, studied at a shear rate of 2,600 s-1, were inhibited by two synthetic peptides known to interact with GPIIb-IIIa. One peptide (HHLGGAKQAGDV) corresponds to the carboxyl terminal segment of the fibrinogen gamma-chain (gamma 400-411) and the other (RGDS) contains the amino acid sequence Arg-Gly-Asp (RGD) common to fibronectin, von Willebrand factor, vitronectin and the alpha-chain of fibrinogen. Neither platelet adhesion nor thrombus formation were decreased in a patient with severe congenital fibrinogen deficiency and this was equally true when his blood was further depleted of the small amounts of fibrinogen present utilizing an anti-fibrinogen antibody. In normal subjects, adhesion and thrombus formation were inhibited by the Fab' fragments of a monoclonal anti-GPIIb-IIIa antibody (LJ-CP8), which interferes with the interaction of platelets with all four adhesive proteins in both the fluid and solid phase. However, another anti-GPIIb-IIIa antibody (LJ-P5) that had minimal effects on the interaction of platelets with fibrinogen, but inhibited to varying degrees platelet interaction with other adhesive proteins, was equally effective. The findings demonstrate that, at a shear rate of 2,600 s-1, adhesive proteins other than fibrinogen are involved in GPIIb-IIIa-mediated platelet adhesion and thrombus formation on subendothelium. In addition, since LJ-P5 inhibited the binding of soluble von Willebrand factor and vitronectin, these adhesive proteins may be involved in platelet thrombus formation. In contrast to the results obtained at a shear rate of 2,600 s-1, fibrinogen could play a role in mediating platelet-platelet interactions with weak agonists or lower shear rates.
The presence of TP53 mutation at diagnosis of follicular lymphoma identifies a high-risk group of patients with shortened time to disease progression and poorer overall survival
Authors: Derville O'Shea, Ciarán O'Riain, Claire Taylor, Rachel Waters, Emanuela Carlotti, Finlay MacDougall, John Gribben, Andreas Rosenwald, German Ott, Lisa M. Rimsza, Erlend B. Smeland, Nathalie Johnson, Elias Campo, Timothy C. Greiner, Wing C. Chan, Randy D. Gascoyne, George Wright, Louis M. Staudt, T. Andrew Lister, Jude Fitzgibbon
Journal: Blood (2008)
Gene-Expression Patterns in Drug-Resistant Acute Lymphoblastic Leukemia Cells and Response to Treatment
Authors: Amy Holleman, Meyling H. Cheok, Monique L. den Boer, Wenjian Yang, Anjo J.P. Veerman, Karin M. Kazemier, Deqing Pei, Cheng Cheng, Ching-Hon Pui, Mary V. Relling, Gritta E. Janka-Schaub, Rob Pieters, William E. Evans
Journal: New England Journal of Medicine (2004)

Childhood acute lymphoblastic leukemia (ALL) is curable with chemotherapy in approximately 80 percent of patients. However, the cause of treatment failure in the remaining 20 percent of patients is largely unknown.We tested leukemia cells from 173 children for sensitivity in vitro to prednisolone, vincristine, asparaginase, and daunorubicin. The cells were then subjected to an assessment of gene expression with the use of 14,500 probe sets to identify differentially expressed genes in drug-sensitive and drug-resistant ALL. Gene-expression patterns that differed according to sensitivity or resistance to the four drugs were compared with treatment outcome in the original 173 patients and an independent cohort of 98 children treated with the same drugs at another institution.We identified sets of differentially expressed genes in B-lineage ALL that were sensitive or resistant to prednisolone (33 genes), vincristine (40 genes), asparaginase (35 genes), or daunorubicin (20 genes). A combined gene-expression score of resistance to the four drugs, as compared with sensitivity to the four, was significantly and independently related to treatment outcome in a multivariate analysis (hazard ratio for relapse, 3.0; P=0.027). Results were confirmed in an independent population of patients treated with the same medications (hazard ratio for relapse, 11.85; P=0.019). Of the 124 genes identified, 121 have not previously been associated with resistance to the four drugs we tested.Differential expression of a relatively small number of genes is associated with drug resistance and treatment outcome in childhood ALL.
Extracellular Signal-Regulated Kinases 1 and 2 Regulate the Balance Between Eccentric and Concentric Cardiac Growth
Authors: Izhak Kehat, Jennifer Davis, Malte Tiburcy, Federica Accornero, Marc K. Saba-El-Leil, Marjorie Maillet, Allen J. York, John N. Lorenz, Wolfram H. Zimmermann, Sylvain Meloche, Jeffery D. Molkentin
Journal: Circulation Research (2010)

An increase in cardiac afterload typically produces concentric hypertrophy characterized by an increase in cardiomyocyte width, whereas volume overload or exercise results in eccentric growth characterized by cellular elongation and addition of sarcomeres in series. The signaling pathways that control eccentric versus concentric heart growth are not well understood.To determine the role of extracellular signal-regulated kinase 1 and 2 (ERK1/2) in regulating the cardiac hypertrophic response.Here, we used mice lacking all ERK1/2 protein in the heart (Erk1(-/-) Erk2(fl/fl-Cre)) and mice expressing activated mitogen-activated protein kinase kinase (Mek)1 in the heart to induce ERK1/2 signaling, as well as mechanistic experiments in cultured myocytes to assess cellular growth characteristics associated with this signaling pathway. Although genetic deletion of all ERK1/2 from the mouse heart did not block the cardiac hypertrophic response per se, meaning that the heart still increased in weight with both aging and pathological stress stimulation, it did dramatically alter how the heart grew. For example, adult myocytes from hearts of Erk1(-/-) Erk2(fl/fl-Cre) mice showed preferential eccentric growth (lengthening), whereas myocytes from Mek1 transgenic hearts showed concentric growth (width increase). Isolated adult myocytes acutely inhibited for ERK1/2 signaling by adenoviral gene transfer showed spontaneous lengthening, whereas infection with an activated Mek1 adenovirus promoted constitutive ERK1/2 signaling and increased myocyte thickness. A similar effect was observed in engineered heart tissue under cyclic stretching, where ERK1/2 inhibition led to preferential lengthening.Taken together, these data demonstrate that the ERK1/2 signaling pathway uniquely regulates the balance between eccentric and concentric growth of the heart.
Acute T-cell leukemias remain dependent on Notch signaling despite PTEN and INK4A/ARF loss
Authors: Hind Medyouf, Xiuhua Gao, Florence Armstrong, Samuel Gusscott, Qing Liu, Amanda Larson Gedman, Larry H. Matherly, Kirk R. Schultz, Francoise Pflumio, Mingjian James You, Andrew P. Weng
Journal: Blood (2009)
Influence of Bcl-2 Family Members on the Cellular Response of Small-Cell Lung Cancer Cell Lines to ABT-737
Authors: Stephen K. Tahir, Xiufen Yang, Mark G. Anderson, Susan E. Morgan-Lappe, Aparna V. Sarthy, Jun Chen, Robert B. Warner, Shi-Chung Ng, Stephen W. Fesik, Steve W. Elmore, Saul H. Rosenberg, Christin Tse
Journal: Cancer Research (2007)

ABT-737 is a novel and potent Bcl-2 antagonist with single-agent activity against small-cell lung cancer (SCLC) cell lines. Here, we evaluated the contribution of Bcl-2 family members to the in vitro cellular response of several SCLC cell lines to ABT-737. Relatively higher levels of Bcl-2, Bcl-X(L), Bim and Noxa, and lower levels of Mcl-1 characterized naïve SCLC cell lines that were sensitive to ABT-737. Conversely, a progressive decrease in the relative levels of Bcl-2 and Noxa and a progressive increase in Mcl-1 levels characterized the increased resistance of H146 cells following chronic exposure to ABT-737. Knockdown of Mcl-1 with small interfering RNA sensitized two resistant SCLC cell lines H196 and DMS114 to ABT-737 by enhancing the induction of apoptosis. Likewise, up-regulation of Noxa sensitized H196 cells to ABT-737. Combination treatment with DNA-damaging agents was extremely synergistic with ABT-737 and was associated with the down-regulation of Mcl-1 and the up-regulation of Noxa, Puma, and Bim in H196 cells. Thus, SCLC cells sensitive to ABT-737 expressed the target proteins Bcl-2 and Bcl-X(L), whereas Mcl-1 and factors regulating Mcl-1 function seem to contribute to the overall resistance of SCLC cells to ABT-737. Overall, these observations provide further insight as to the mechanistic bases for ABT-737 efficacy in SCLC and will be helpful for profiling patients and aiding in the rational design of combination therapies.
P-selectin and vascular cell adhesion molecule 1 mediate rolling and arrest, respectively, of CD4+ T lymphocytes on tumor necrosis factor α-activated vascular endothelium under flow.
Authors: F W Luscinskas, H Ding, A H Lichtman
Journal: The Journal of Experimental Medicine (1995)

This report examines the adhesive interactions of human CD4+ T lymphocytes with tumor necrosis factor alpha-activated human endothelial cell monolayers in an in vitro model that mimics microcirculatory flow conditions. Resting CD4+ T cell interactions with activated endothelium consisted of initial attachment followed by rolling, stable arrest, and then spreading and transendothelial migration. P-selectin, but not E-, or L-selectin, mediated most of this initial contact and rolling, whereas beta 1-integrins (alpha 4 beta 1), interacting with endothelial-expressed vascular cell adhesion molecule 1, participated in rolling and mediated stable arrest. In contrast, beta 2-integrins were primarily involved in spreading and transmigration. These findings highlight an important role for P-selectin and suggest discrete functions for beta 1- and beta 2-integrins during lymphocyte recruitment to sites of immune-mediated inflammation.
Molecular monitoring of tumour load kinetics predicts disease progression after non-myeloablative allogeneic stem cell transplantation in multiple myeloma
Authors: M.S. Raab, F.W. Cremer, I.N. Breitkreutz, S. Gerull, T. Luft, A. Benner, M. Goerner, A.D. Ho, H. Goldschmidt, M. Moos
Journal: Annals of Oncology (2005)
Exercise training combined with angiotensin II receptor blockade limits post-infarct ventricular remodelling in rats
Authors: X. Xu, W. Wan, L. Ji, S. Lao, A. S. Powers, W. Zhao, J. M. Erikson, J. Q. Zhang
Journal: Cardiovascular Research (2008)

Our aim was to test the hypothesis that angiotensin II receptor blockade combined with exercise training after myocardial infarction (MI) could attenuate post-MI left ventricular remodelling and preserve cardiac function. Sprague–Dawley rats underwent ligation of the left descending coronary artery, resulting in MI, or a sham operation. Losartan treatment and exercise training were initiated 1 week after infarction and continued for 8 weeks, either as a single intervention or combined. Collagen volume fraction in the sedentary MI (MISed) group was significantly higher than other MI groups treated with exercise training and/or losartan. Compared with MISed group, hearts of rats receiving exercise and/or losartan treatment had lower tissue inhibitor of matrix metalloproteinase (TIMP) 1. Matrix metalloproteinase (MMP) 2 or MMP-9 did not differ among all groups. Additionally, the level of angiotensin II receptor type 1 (AT1) protein significantly decreased in response to exercise training. Furthermore, angiotensin converting enzyme (ACE) binding was markedly lower in hearts receiving exercise training than in the MISed hearts. Cardiac function was preserved in rats receiving exercise training, and the beneficial effect was further improved by exercise combined with losartan treatment in comparison to the MISed group. Our results suggest that post-MI exercise training and/or AngII receptor blockade reduces TIMP-1 expression and mitigates the expressions of ACE and AT1 receptor. These improvements, in turn, attenuate myocardial fibrosis and preserve post-MI cardiac function.
Efficacy of Escitalopram for Hot Flashes in Healthy Menopausal Women
Authors: Ellen W. Freeman
Journal: JAMA (2011)

the predominant therapy for menopausal hot flashes, but their use decreased substantially following the shifts in riskbenefit ratios that were identified in the Women's Health Initiative Estrogen plus Progestin randomized controlled trial. 1,2][5] Selective serotonin and serotonin norepinephrine reuptake inhibitors (SSRIs and SNRIs) have been investigated for hot flash treatment with mixed results [6][7][8][9][10][11] ; a pooled analysis of 7 SSRI and SNRI studies showed that decreases in hot flash scores ranged from 3% to 41% compared with placebo. 6Differences among the serotonergic antidepressants, 11 study popu-
PDGF-D induces macrophage recruitment, increased interstitial pressure, and blood vessel maturation during angiogenesis
Authors: Marko Uutela, Maria Wirzenius, Karri Paavonen, Iiro Rajantie, Yulong He, Terhi Karpanen, Marja Lohela, Helge Wiig, Petri Salven, Katri Pajusola, Ulf Eriksson, Kari Alitalo
Journal: Blood (2004)
Sequential Diagnosis by Computer
Authors: G. Anthony Gorry
Journal: JAMA (1968)

A computer program for sequential diagnosis has been developed for use in a variety of problem areas. The program employs sequential decision-making to balance the risk of making a diagnosis against the cost of further testing and the value of the evidence which can be obtained. Basically the program consists of an information structure which describes the problem area, an inference function which interprets signs and symptoms in terms of the medical knowledge in the information structure, and a test selection function which continually reevaluates the potential value of diagnostic tests in the light of increased information about the patient and the costs of tests and possible misdiagnoses.
Hepatobiliary Cancers, Version 2.2014
Authors: Al B. Benson, Michael I. D’Angelica, Thomas A. Abrams, Chandrakanth Are, P. Mark Bloomston, Daniel T. Chang, Bryan M. Clary, Anne M. Covey, William D. Ensminger, Renuka Iyer, R. Kate Kelley, David Linehan, Mokenge P. Malafa, Steven G. Meranze, James O. Park, Timothy Pawlik, James A. Posey, Courtney Scaife, Tracey Schefter, Elin R. Sigurdson, G. Gary Tian, Jean-Nicolas Vauthey, Alan P. Venook, Yun Yen, Andrew X. Zhu, Karin G. Hoffmann, Nicole R. McMillian, Hema Sundar
Journal: Journal of the National Comprehensive Cancer Network (2014)

Hepatobiliary cancers include a spectrum of invasive carcinomas arising in the liver (hepatocellular carcinoma), gall bladder, and bile ducts (cholangiocarcinomas). Gallbladder cancer and cholangiocarcinomas are collectively known as biliary tract cancers. Gallbladder cancer is the most common and aggressive type of all the biliary tract cancers. Cholangiocarcinomas are diagnosed throughout the biliary tree and are typically classified as either intrahepatic or extrahepatic cholangiocarcinoma. Extrahepatic cholangiocarcinomas are more common than intrahepatic cholangiocarcinomas. This manuscript focuses on the clinical management of patients with gallbladder cancer and cholangiocarcinomas (intrahepatic and extrahepatic).
Lack of effect of propranolol on canine coronary collateral development during progressive coronary stenosis and occlusion
Authors: M V Cohen
Journal: Cardiovascular Research (1993)

Objective: The aim was to test the effect of propranolol, a β adrenergic receptor blocking drug which diminishes myocardial ischaemia, on coronary collateral development. Methods: Dogs were chronically instrumented with a left circumflex coronary artery Doppler flow probe, ameroid constrictor, pneumatic occluder, and left atrial and aortic catheters. Haemodynamic studies and measurements of normal myocardial and collateral blood flows were performed at least weekly after surgery, or sooner if the left circumflex artery occluded spontaneously, in eight control dogs and seven animals treated with propranolol, 240 mg twice daily (a dose which successfully attenuated the chronotropic effect of a graded infusion of isoprenaline). In dogs in which the left circumflex artery occluded within the first four weeks after surgery, collateral blood flow was measured during exercise on a motorised treadmill. Results: There was no difference between the groups in the rate or pattern of coronary collateral development, magnitude of collateral flow before or after spontaneous left circumflex occlusion, and collateral vascular reserve during exercise. At the time of coronary occlusion resting collateral flow was equivalent to normal perfusion levels in both groups and averaged 87-96% of normal flows during exercise. Conclusions: Propranolol has no observable effect on coronary collateral development despite its acknowledged ability to prevent or attenuate myocardial ischaemia. Cardiovascular Research 1993;27:249-254