tbuckley/cabot-search huggingface dataset:
Defense mechanisms in risk of suicide and risk of violence
Authors: A Apter, R Plutchik, S Sevy, M Korn, S Brown, H van Praag
Journal: American Journal of Psychiatry (1989)

This paper reports on an empirical study of defense mechanisms in 60 psychiatric inpatients. Eight defenses--compensation, denial, displacement, intellectualization, projection, reaction formation, regression, and repression--were studied in the context of a two-stage model of suicidal and violent behavior. The results showed that use of regression as a defense differentiated suicidal from nonsuicidal patients, and use of displacement differentiated violent from nonviolent patients. Repression tended to turn aggression inward, and projection and denial turned aggression outward.
Clinical profile and prognostic significance of natriuretic peptide trajectory following hospitalization for worsening chronic heart failure: findings from the ASTRONAUT trial
Authors: Stephen J. Greene, Aldo P. Maggioni, Gregg C. Fonarow, Scott D. Solomon, Michael Böhm, Albert Kandra, Margaret F. Prescott, Bernard Reimund, Tsushung A. Hua, Anastasia Lesogor, Faiez Zannad, Mihai Gheorghiade
Journal: European Journal of Heart Failure (2015)
Abstract 14674: Cardiovascular Events Associated with Lymphotoxin Alpha and its Polymorphism After the Onset of Myocardial Infarction
Authors: Shinichiro Suna, Yasuhiko Sakata, Daisaku Nakatani, Masaya Usami, Sen Matsumoto, Masahiko Hara, Keiji Okuda, Kouichi Ozaki, Seiji Takashima, Tetsuo Minamino, Hiroshi Sato, Toshihiro Tanaka, Issei Komuro
Journal: Circulation (2011)

Background. Lymphotoxin (LT) α is a member of the tumor necrosis factor family that plays a critical role in inflammation. We recently reported that the single nucleotide polymorphisms (SNPs) of th...
Neuroelectronics and Biooptics
Authors: Esther Krook-Magnuson, Jennifer N. Gelinas, Ivan Soltesz, György Buzsáki
Journal: JAMA Neurology (2015)

Brain-implanted devices are no longer a futuristic idea. Traditionally, therapies for most neurological disorders are adjusted based on changes in clinical symptoms and diagnostic measures observed over time. These therapies are commonly pharmacological or surgical, requiring continuous or irreversible treatment regimens that cannot respond rapidly to fluctuations of symptoms or isolated episodes of dysfunction. In contrast, closed-loop systems provide intervention only when needed by detecting abnormal neurological signals and modulating them with instantaneous feedback. Closed-loop systems have been applied to several neurological conditions (most notably epilepsy and movement disorders), but widespread use is limited by conceptual and technical challenges. Herein, we discuss how advances in experimental closed-loop systems hold promise for improved clinical benefit in patients with neurological disorders.
Effect of inhaled vilanterol trifenatate/fluticasone furoate on breathing pattern, dyspnea and respiratory muscle function in severe COPD
Authors: Paul Easton, Jenny Jagers, Michael Ji, Kurt Olson, Malcolm Johnson, Eric Wilde
Journal: European Respiratory Journal (2014)

Beta agonists have been shown to change ventilation and chest wall activity in COPD (Chest 2010 137:558-65). We studied the new ultra long acting beta 2   agonist-steroid combination, vilanterol trifenatate/fluticasone furoate (Relvar, VFF) to determine its effects on breathing pattern, dyspnea and respiratory muscle function in severe COPD. We studied 6 subjects with severe COPD (mean FEV 1  0.68), very minimally reversible, implanted with fine-wire EMG in parasternal (PARA) muscles, at baseline and 2hr after 2 puffs VFF. We measured: breathing pattern, dyspnea scores (BORG), PARA activity, sniff inspiratory nasal pressure (SNIP), and pulmonary function tests. Minute ventilation, frequency and mean inspiratory flow decreased (pl0.01). This breathing pattern was associated with much lower dyspnea scores (pl0.01). Mean PARA also decreased after VFF, while SNIP increased (pl0.01). We conclude that inhaled vilanterol trifenatate/fluticasone furoate (Relvar) induces a significant change in breathing pattern, which is associated with less dyspnea and increased global respiratory muscle function.
Abstract 14193: Dynamin-Related Protein 1 (DRP1)-Mediated Mitochondrial Fission Promotes Smooth Muscle Cell Hyperproliferation in Human and Experimental Pulmonary Hypertension Which Can be Therapeutically Targeted by the Fission Inhibitor MDIVI-1
Authors: Glenn Marsboom, Peter T Toth, Zhigang Hong, Xichen Wu, Yong-Hu Fang, Thenappan Thenappan, Hannah J Zhang, Peter Bache-Wiig, Jennifer Pogoriler, Yimei Chen, E Kenneth Weir, Jalees Rehman, Stephen L Archer
Journal: Circulation (2011)

Glenn Marsboom, 2011 Finalist and Presenting Author
Abstract 18587: Downregulation of Pulmonary Artery Endothelial Catechol-o-methyltransferase Activity by Aldosterone Increases Norepinephrine Levels in Pulmonary Arterial Hypertension
Authors: Samantha Torquato, Kiyotake Ishikawa, Jaume Aguerro, Bradley A Maron, Joseph Loscalzo, Roger J Hajjar, Jane A Leopold
Journal: Circulation (2014)

Elevated levels of norepinephrine (NE) occur in pulmonary arterial hypertension (PAH) and are determined, in part, by the activity of catechol- O -methyltransferase (COMT). COMT degrades catecholamines, is negatively regulated by calcium, and is expressed by pulmonary artery endothelial cells (PAEC). As hyperaldosteronism occurs in PAH and aldosterone (ALDO) influences calcium levels, we hypothesized that ALDO decreases COMT activity to increase NE levels in PAH. Accordingly, human PAEC were treated with ALDO (10 -7 mol/L), a level that is achieved clinically in PAH, for up to 72 h. Compared to vehicle-treated PAEC, ALDO decreased COMT activity by 59.2 ± 6.2% (p&lt;0.01) to increase NE levels in the medium (122.4 ± 11.8 vs. 210.7 ± 15.5 pg/mL/mg protein, p&lt;0.01). This occurred as a result of an ALDO-mediated decrease in COMT protein expression by 52.6 ± 9.3% (p&lt;0.01) as well as an increase in intracellular calcium levels (102.9 ± 21.0 vs. 167.7 ± 17.8 nmol/L, p&lt;0.05) to inhibit activity. These effects were abrogated by coincubation with spironolactone. To determine the in vivo relevance of these findings, COMT was examined in the rat monocrotaline model of PAH with confirmed hyperALDO. COMT was decreased (47.6 ± 10.2 %control, p&lt;0.05) in remodeled pulmonary arterioles with a concomitant increase in lung NE levels (432.8 ± 44.5 vs. 899.7 ± 34.2 pg/mL, p&lt;0.01) compared to control rats. In the porcine pulmonary vein banding model of pulmonary hypertension (PH-pigs) with elevated mean pulmonary artery pressure (15[13-15] vs. 35[27-43], p&lt;0.01) and pulmonary vascular resistance (PVR) index (1.97[1.74-2.28] vs. 5.78[2.61-8.75], p &lt;0.05), ALDO levels were also increased (27.1 ± 5.1 vs. 60.8 ± 10.6 pg/mL, p&lt;0.03) in advance of right heart failure as compared to sham controls. PH-pigs demonstrated a 48.3 ± 9.9% (p&lt;0.02) decrease in pulmonary vascular COMT expression and an increase in NE levels (114.6 ± 20.2 vs. 1,622.6 ± 489.2 pg/mL, p&lt;0.02) that correlated positively with ALDO levels (R 2 =0.58, p&lt;0.02). These findings were confirmed in patients with PAH. Together, these data indicate that there is crosstalk in the pulmonary vasculature between ALDO and the sympathetic nervous system to regulate NE levels in PAH, and thus, have implications for therapeutic interventions.
Abstract 11268: Fasting Low Density Lipoprotein Cholesterol (LDL-C) Levels Stratified by Fasting Time Do Not Have Significant Improvement in Prognostic Value versus Non-fasting LDL-C
Authors: Bethany Doran, Yu Go, Xinfeng Xu, Howard Weintraub, Samia Mora, Sripal Bangalore
Journal: Circulation (2014)

Introduction: National guidelines recommend patients obtain fasting lipid panels for risk stratification. No studies have examined whether specific fasting time cut-points provide better prognostic ability for cardiovascular (CV) events in a national sample.

Hypothesis: We tested the hypothesis that fasting and non-fasting prognostic ability for all-cause and CV mortality is different within groups stratified by length of fast definition (4, 8, or 12 hours).

Methods: 16,161 individuals enrolled in the National Health and Nutrition Survey III linked to the National Death Index were stratified based on fasting status (<4 hours vs. ≥4 hours, <8 hours vs. ≥8 hours, <12 hours vs. ≥12 hours). CV and all-cause mortality were assessed after a mean of 14.0 (+/- 0.22) year follow-up. Risk of outcomes as a function of LDL-C and fasting status were stratified by cut-point and assessed using receiver operating characteristic (ROC) curves. Propensity score matching was performed after controlling for covariables in the 8 hour cut-point.

Results: For cardiovascular mortality, fasting LDL-C with a cut-point of 4 hours yielded similar prognostic value as that of non-fasting LDL-C (C statistics = 0.62 [95% CI 0.60-0.64] vs. C statistics = 0.65 [95% CI 0.59-0.70]; P=0.34), as did a cut-point of 8 hours (C-statistics = 0.62 [95% CI 0.60-0.64] vs. 0.62 [95% CI 0.59-0.64]; P=0.8) and 12 hours (C statistics = 0.61 [95% CI 0.59-0.63] vs. C statistics = 0.63 [95% CI 0.61-0.65]; P=0.27). Similar results were seen for the primary outcome for all cut-points. Propensity score matched models failed to reveal a significant difference between fasting and non-fasting cohorts.

Conclusions: This study shows similar prognostic value of fasting vs. non-fasting LDL-C on long-term mortality in a nationally representative U.S. cohort. National and international agencies should consider re-evaluating the recommendation that patients fast before obtaining a lipid panel.

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SAT0576-HPR Hand Pains and General Pain in Women and Men in Early RA, a One Year Follow Up after Diagnosis in the Tira-2 Cohort
Authors: I. Thyberg, Ö. Dahlström, M. Björk, B. Stenström, J. Adams
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Pain in Rheumatoid arthritis (RA) is more prevalent in women than men. Hand involvement in RA is associated with hand pain, low grip force and reduced grip ability. Hand pain related to hand activity and possible differences between sexes have not yet been reported in early RA. <h3>Objectives</h3> To analyze hand pain during activity, hand pain at rest and general pain during the first year of RA for women and men. <h3>Methods</h3> 454 patients were recruited into the Swedish early RA project “TIRA” during 2006-2009. The 373 patients (67 % women) that remained at 12 months follow up are reported here. Data for disease activity (DAS-28), general pain (VAS), hand pain during rest (VAS) and hand pain during activity (VAS) was registered at inclusion and at the follow-ups after 3 (M3), 6 (M6), and 12 (M12) months respectively. Hand pain during activity was related to test of grip force as measured by Grippitä. Prescribed disease-modifying anti-inflammatory drugs (DMARDs) and hand dominance was registered. Differences in mean values were analysed using ANOVA and differences in medication were analysed using chi-square tests. <h3>Results</h3> Women had slightly higher proportions of DMARDs than men throughout the study (84% to 93 % vs 75% to 92%) although the differences were significant only at M3 (p=.022; 85% vs 75%). Disease activity was high at inclusion (mean=5.12) and decreased significantly (p&lt;.001) at M3 and M6, but not between M6 and M12. Women had higher DAS than men at all follow-ups but the difference were not significant. 86% reported right-hand dominance. Women reported higher overall pain than men (p=.007) and overall pain was higher at inclusion than at the follow-ups (p&lt;.001). The paintypes were significantly different (p&lt;.001), general pain was highest and hand pain at rest was lowest. A significant interaction between pain-type and follow-up (p&lt;.001) showed that the three paintypes differed at each follow-up but for general pain and hand pain during activity at M3. There were no significant differences in hand pain between dominant and nondominant hand or between right and left hand. <h3>Conclusions</h3> Women had higher DAS and pain than men despite somewhat more women than men prescribed DMARD:s. Hand pain in activity was higher than pain during rest, strongly indicating that hand pain is closely related to performing hand activities in general in early RA. <h3>Disclosure of Interest</h3> None Declared
Vitamin K Deficiency and Hepatocellular Carcinoma—Reply
Authors: Daiki Habu, Susumu Shiomi, Takashi Tanaka, Shuhei Nishiguchi
Journal: JAMA (2004)

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Gender differences in hospitalized patients with acute exacerbation of COPD
Authors: Esra Uzaslan, Ezgi Cetindogan, Asli Gorek Dilektasli, Funda Coskun, Dane Ediger, Ercument Ege
Journal: European Respiratory Journal (2013)

Introduction: The prevalence and hospitalization of COPD in women are increasing in developing countries.Little is known about gender differences in acute exacerbations of COPD (AECOPD).Objective: We aimed to evaluate if gender is a risk factor that has effects on clinical characteristics of the patients with AECOPD. Methods: We included patients whom admitted and hospitalized a tertiary reference center with AECOPD between 2011-2013 years.Medical records of the study participants have been screened retrospectively for 24 months. Results :A total of 242 patients (209 males, and 33 females) hospitalized for AECOPD were included. Mean age, clinical findings and routine laboratory tests on admission did not differ between males and females.In arterial blood gas analyzes PaCO2 levels were found to be significantly higher in females than the males [53.8 mmHg (min:28.6-max:102.5) mmHg],[42.4 mmHg (min:24 - max:109.1 mmHg].Also HCO3 and pH levels of females were significantly higher than males. Percentage of the patient more than one comorbidities were significantly higher in females than the males (30% vs 11%).Diabetes mellitus (F/M: 27%/12%, p<0.05), hypertension (F/M: 36% /21%, p=0.07), and obesity (F/M: 21%/1%,p<0.05) were also more prevelant in females with AECOPD. Lung cancer was only detected in males(10%). Gender was not an effecting factor on mortality in patients with AECOPD. Conclusion:Female COPD patients were tend to be more hypercapnic than the males on admission.Although comorbidities are common in hospitalized patients, their relative distribution varies by gender. Therefore the effects of different comorbidities in gender related AECOPD hospitalization needs to be verified with further studies.
Abstract 13847: PTRF/Cavin-1 Knock-out Mice Develop a Progressive Cardiomyopathy with ERK1/2 Hyperactivation and Caveolin-3 Reduction
Authors: Takeru Kasahara, Takehiro Ogata, Naoki Maruyama, Takuya Taniguchi, Tetsuro Hamaoka, Kotaro Miyagawa, Naohiko Nakanishi, Tomomi Ueyama
Journal: Circulation (2014)

Background:  Mutations in the PTRF gene, coding for Cavin-1, cause congenital generalized lipodystrophy type 4 (CGL4) associated with myopathy. Symptoms of patients with CGL4 are more widespread comprising myopathy, smooth and skeletal muscle hypertrophy and osteopenia. In particular, patients with CGL4 due to PTRF/Cavin-1 mutations have fetal cardiac arrhythmia and long-QT syndrome. Patients with PTRF/Cavin-1 deficiency show reduction of Caveolin-3 (Cav3) whose deficiency leads to cardiac hypertrophy with loss of caveolae. However, it remains unknown whether loss of PTRF/Cavin-1 affects the phenotypic behavior cardiac myocytes in vitro. Here, we present a detailed characterization of the hearts of PTRF/Cavin-1 knock-out (KO) mice.   Methods and Results:  PTRF/Cavin-1 KO mice developed a progressive cardiomyopathic phenotype. At four months of age, PTRF/Cavin-1 KO heats displayed significant wall thickness of left ventricles and reduced fractional shortening as revealed by echocardiography. Histological analysis revealed marked cardiomyocyte hypertrophy with progressive interstitial/peri-vascular fibrosis. Hypertrophy-related fetal gene expression was also induced in PTRF/Cavin-1 KO mice. Western blotting analysis and quantitative RT-PCR revealed that Cav3 expression was significantly suppressed in PTRF/Cavin-1 KO hearts compared with wild-type hearts. Because Cav3 deletion-induced cardiac hypertrophy shows hyperactivation of p42/44 MAPK (ERK1/2) and loss of caveolae in cardiomyocytes, we assessed the ERK1/2 activity and caveolar morphology in the heart of PTRF/Cavin-1 KO mice. ERK1/2 was hyperactivated in PTRF/Cavin-1 KO hearts. Furthermore, electron microscopy displayed the absence of caveolae in cardiomyocytes of PTRF/Cavin-1 KO mice. However, small vesicles were retained in PTRF/Cavin-1 KO cardiomyocytes.   Conclusion:  PTRF/Cavin-1 KO mice develop a progressive cardiomyopathy with ERK1/2 hyperactivation. Our results suggest that this process is attributable to Cav3 reduction. Our data argue that loss of PTRF/Cavin-1 expression is sufficient to induce a molecular program leading to cardiomyocyte hypertrophy and cardiomyopathy.
Britain Divided: the Growth of Social Exclusion in the 1980s and 1990s, by Ed Alan Walker, Carol Walker
Authors: S. Iliffe
Journal: BMJ (1997)

Ed Alan Walker, Carol Walker: Child Poverty Action Group, £9.95, pp 308 ISBN 0 946744 91 2

Anyone who felt relieved but not elated at the election result on 3 May need only read this book to understand their emotional shortfall. The defeat of a party that had deliberately engineered mass unemployment as an economic and social lever, targeted the most vulnerable and politically expendable to redistribute money from poor to rich, and routinely denied responsibility for its actions should certainly make our hearts rise. The breadth and depth of poverty the Conservatives have left behind, and …
Abstract 2074: Metastasis prevention using fibroblast activation protein-targeting prodrugs at the pre-metastatic niche
Authors: Meera Murgai, Amber Giles, Miki Kasai, Yorleny Vicioso, Crystal Mackall, Rosandra Kaplan
Journal: Cancer Research (2014)

Abstract Metastasis is the major cause of cancer death, and therapies that effectively target this process are required in order to improve patient survival. Previous work by Kaplan et al demonstrated that activated resident stromal cells and recruited bone marrow derived cells (BMDCs) form an altered microenvironment at distant sites in response to the primary tumor, termed the pre-metastatic niche, that promotes metastatic progression. Current on-going studies in the laboratory focus on in-depth investigations of the role, composition and mechanism of action by which each cell population including the bone marrow-derived hematopoietic cells and the activated stromal cells within the pre-metastatic niche contribute to metastatic progression. Fibroblast activation protein (FAP) is a serine protease that is overexpressed by tumor associated stromal cells, including cancer-associated fibroblasts (CAFs) and is implicated in the suppression of tumor immunity. Using a mouse model that expresses FAP promoter-driven mCherry and luciferase, we demonstrate that FAP gene expression is up-regulated in both tumor-bearing mice in pre-metastatic tissue at pre-metastatic time-points and in non-tumor-bearing mice injected with tumor-conditioned media, suggesting that metastatic tumors secrete factors that increases the number of FAP-expressing cells at the pre-metastatic niche. The studies described herein investigate the hypothesis that FAP-expressing cells at the pre-metastatic niche promote metastasis, and FAP-targeted cytotoxic drug delivery will aid in targeting tumor colonization and inhibiting metastatic progression. Citation Format: Meera Murgai, Amber Giles, Miki Kasai, Yorleny Vicioso, Crystal Mackall, Rosandra Kaplan. Metastasis prevention using fibroblast activation protein-targeting prodrugs at the pre-metastatic niche. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2074. doi:10.1158/1538-7445.AM2014-2074
Characteristics of acute myeloid leukemia with myelodysplasia‐related changes: A retrospective analysis in a cohort of <scp>Chinese</scp> patients
Authors: Xiao‐Qian Xu, Jian‐Min Wang, Lei Gao, Hui‐Ying Qiu, Li Chen, Lin Jia, Xiao‐Xia Hu, Jian‐Min Yang, Xiong Ni, Jie Chen, Shu‐Qing Lü, Wei‐Ping Zhang, Xian‐Min Song
Journal: American Journal of Hematology (2014)

We retrospectively analyzed 449 patients with AML under the WHO classification of AML 2008 and probed implications of this classification in diagnosis and treatment of acute myeloid leukemia with myelodysplasia-related changes (AML-MRC) among them. The clinical presentations, biological features, treatments, and prognosis of patients diagnosed with AML-MRC were analyzed and compared with those of AML not otherwise specified (AML-NOS). In all patients, 115 (25.6%) were diagnosed as AML-MRC including 64 males and 51 females with median onset age of 48 years (range from 17 to 78). Their complete remission (CR) rate was 60.9% and relapse rate was 57.1%. The observed median overall survival (OS) and disease-free survival (DFS) were 10 and 5 months, respectively, which was significantly shorter than those of AML-NOS patients (P < 0.05). The prognosis of AML-MRC patients with myelodysplastic syndrome (MDS)-related cytogenetics sole was similar to those with history of MDS or myelodysplastic/myeloproliferative neoplasm (MDS/MPN). Patients with MDS-related cytogenetic abnormalities and/or history of MDS or MDS/MPN predisposed significantly shortened CR, OS, and DFS than AML-MRC patients with only multilineage dysplasia (MLD) and AML-NOS patients (P < 0.05). Multivariate analysis showed that age, cytogenetics, and history of MDS or MDS/MPN were independent prognostic factors. Patient diagnosed as AML-MRC presented distinctive clinical and biological features. Presence of MLD does not change the prognosis.