tbuckley/cabot-search huggingface dataset:
Resuscitation Practices Associated With Survival After In-Hospital Cardiac Arrest
Authors: Paul S. Chan, Sarah L. Krein, Fengming Tang, Theodore J. Iwashyna, Molly Harrod, Mary Kennedy, Jessica Lehrich, Steven Kronick, Brahmajee K. Nallamothu
Journal: JAMA Cardiology (2016)

Although survival of patients with in-hospital cardiac arrest varies markedly among hospitals, specific resuscitation practices that distinguish sites with higher cardiac arrest survival rates remain unknown.To identify resuscitation practices associated with higher rates of in-hospital cardiac arrest survival.Nationwide survey of resuscitation practices at hospitals participating in the Get With the Guidelines-Resuscitation registry and with 20 or more adult in-hospital cardiac arrest cases from January 1, 2012, through December 31, 2013. Data analysis was performed from June 10 to December 22, 2015.Risk-standardized survival rates for cardiac arrest were calculated at each hospital and were then used to categorize hospitals into quintiles of performance. The association between resuscitation practices and quintiles of survival was evaluated using hierarchical proportional odds logistic regression models.Overall, 150 (78.1%) of 192 eligible hospitals completed the study survey, and 131 facilities with 20 or more adult in-hospital cardiac arrest cases comprised the final study cohort. Risk-standardized survival rates after in-hospital cardiac arrest varied substantially (median, 23.7%; range, 9.2%-37.5%). Several resuscitation practices were associated with survival on bivariate analysis, although only 3 were significant after multivariable adjustment: monitoring for interruptions in chest compressions (adjusted odds ratio [OR] for being in a higher survival quintile category, 2.71; 95% CI, 1.24-5.93; P = .01), reviewing cardiac arrest cases monthly (adjusted OR for being in a higher survival quintile category, 8.55; 95% CI, 1.79-40.00) or quarterly (OR, 6.85; 95% CI, 1.49-31.30; P = .03), and adequate resuscitation training (adjusted OR, 3.23; 95% CI, 1.21-8.33; P = .02).Using survey information from acute care hospitals participating in a national quality improvement registry, we identified 3 resuscitation strategies associated with higher hospital rates of survival for patients with in-hospital cardiac arrest. These strategies can form the foundation for best practices for resuscitation care at hospitals given the high incidence and variation in survival for in-hospital cardiac arrest.
P667Impaired chronic hypoxic response in type 2 diabetic hearts is associated with inability to downregulate PPARa
Authors: L Mansor, CA Carr, L Le Page, T Lund, E Aasum, K Clarke, D Tyler, L Heather
Journal: Cardiovascular Research (2014)

Cardiovascular disease is the leading cause of mortality in type 2 diabetic patients. Metabolic changes and abnormal hypoxia signalling in the diabetic heart are hypothesised to decrease recovery following a myocardial infarction. Therefore the aim of this study was to investigate the cardiac metabolic adaptation to physiological hypoxia in diabetic rats. Type 2 diabetes was generated in rats using a high fat diet and low dose streptozotocin. Both control and diabetic rats were housed in hypoxia (11% oxygen) or normoxia for three weeks. Following hypoxia, control hearts had upregulated anaerobic glycolysis, increased glycogen content and suppressed fatty acid oxidation. Conversely, these hypoxia-induced metabolic changes were decreased in diabetic hearts, in that glycolysis and glycogen content remained lower, while fatty acid oxidation rates remained higher than in control hearts. Peroxisome proliferator-activated receptor α (PPARα) is a transcription factor that positively regulates fatty acid metabolism, and PPARα-regulated targets were downregulated following hypoxia in the control hearts. PPARα target proteins were upregulated in normoxic diabetic rat hearts and remained elevated following hypoxia. We found that cardiac mRNA expression of the hypoxia-inducible factor (HIF) target genes prolyl hydroxylase 3, heme oxygenase 1 and VEGF were regulated in control and diabetic hearts to the same extent, showing that there were no defects in hypoxia signalling or HIF in diabetic hearts. In conclusion, the abnormal metabolic adaptation to hypoxia in diabetes is associated with an inability of hypoxia to suppress PPARα activation, and occurs independently of changes in hypoxia and HIF signalling pathways. Thus fat metabolism is maintained to the detriment of glucose metabolism.
P282 An Integrated IT System For COPD Between Primary, Secondary and Community Care Using SystmOne
Authors: DJ Powrie, R Goodwin, D Allan-Smith, E Paddison, M Ali, S Ansari, KG Lingam, AG Davison
Journal: Thorax (2012)

<h3></h3> Southend Hospital and South Essex PCT have been developing an integrated COPD service for over a decade. Information sharing between providers remained a barrier to improved services. SystmOne is a medical management system used by 70% of practises in our area and utilised by community services. We decided to develop a COPD system for primary, secondary and community care using SystmOne. <h3>Development</h3> A business case was developed and agreed by the IT strategy groups of the PCT, hospital trust and community trust. A project manager was appointed who worked with clinical leads from the hospital and PCT. The clinicians who would utilise the system including hospital consultants, respiratory nurse specialists, GPs, community matrons, community oxygen team and early supported discharge team all contributed to the design of the template. The system records demographic information, respiratory and smoking history, pertinent respiratory investigations such as spirometry and blood gases as well as whether the patient has been referred for pulmonary rehabilitation, smoking cessation or has a self management plan. At each clinical consultation symptoms and management changes are recorded. Tasks can be sent between members of the team for example allowing community matrons to send queries to hospital consultants. <h3>Implementation</h3> All GPs agreed to participate in the scheme. Patients were required to sign a form consenting to sharing of clinical information. The project manager undertook training of all the clinical groups involved as well as hospital secretarial and clinic staff. Community staff were provided with laptops enabling remote access. After a training period of 5 months the system went live in March 2011. We now have 1522 patients registered on the system. 13 patients refused consent to the sharing of information. <h3>Benefits</h3> The system has allowed improved communication between members of the team. The template has served as a management checklist ensuring that important components of COPD care are not forgotten. The system has been used to identify patients with very severe disease for discussion at a severe disease MDT and been associated with a 5% reduction in outpatient attendances.
Gene Therapy Review Finds Few Complications
Authors: S. Jenks
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Gene Therapy Review Finds Few Complications Get access Susan Jenks Susan Jenks Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 15, 4 August 1993, Pages 1188–1190, https://doi.org/10.1093/jnci/85.15.1188 Published: 04 August 1993
In Vivo Antigenic Modification of Tumor Cells. I. Introduction of Murine Leukemia Virus Antigens on Non-Virus-Producing Murine Sarcomas&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: J D Iglehart, E C Ward, K Thiel, G Huper, S S Geier, D P Bolognesi
Journal: JNCI Journal of the National Cancer Institute (1981)

Murine oncovirus antigens represent excellent targets for immune recognition, and virus-associated tumors are generally susceptible to various immunotherapy protocols. Virus-negative tumors, however, are nonimmunogenic and refractory to immunologic control. Therefore, the feasibility of the introduction of antigens onto non-virus-expressing tumors in situ in inbred C57BL/6J mice by systemic administration of nononcogenic murine retroviruses was investigated. Two classes of murine fibrosarcomas were studied: a 3-methylcholanthrene-induced fibrosarcoma syngeneic to C57BL/6 mice (MCA-FS) and a Harvey murine sarcoma virus-transformed, nonproducer fibrosarcoma syngeneic to C57BL/6 mice (H-NP). Both were found to be devoid of infectious ecotropic murine leukemia virus (MuLV) or MuLV antigens. A single dose of Friend murine leukemia virus (F-MuLV) was used to superinfect MCA-FS- and H-NP-induced tumors in vivo and converted these tumors to a highly productive, virus-positive state. In vivo superinfected tumors were indistinguishable from their preinfected counterparts by competition radioimmunoassays for the virion's major envelope glycoprotein, gp71, and its group-specific antigen, p30, and by assays for infectious virus. Analysis of virus from tumor extracts proved that the antigenic specificity of the superinfected tumor was provided by F-MuLV administered systemically to the animals. Finally, an immunoperoxidase technique, applied to tumor cross sections, demonstrated the uniform appearance of viral antigens in the superinfected tumors.
Prospective Study of the Association between Sleep-Disordered Breathing and Hypertension
Authors: Paul E. Peppard, Terry Young, Mari Palta, James Skatrud
Journal: New England Journal of Medicine (2000)

Sleep-disordered breathing is prevalent in the general population and has been linked to chronically elevated blood pressure in cross-sectional epidemiologic studies. We performed a prospective, population-based study of the association between objectively measured sleep-disordered breathing and hypertension (defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of antihypertensive medications).
P14.04 * A REVIEW OF CORRELATION OF PHENOTYPE AND GENOTYPE IN VON HIPPEL-LINDAU DISEASE
Authors: M. Ishibashi, T. Watanabe, K. Adachi, E. Nanba
Journal: Neuro-Oncology (2014)

Von Hippel-Lindau disease is an autosomal dominantly inherited and multisystic tumor syndrome caused by mutation in the VHL gene. These mutations were reported from various countries with a variety of races. Even in a country, the different genotypes and phenotypes were reported. Therefore we reviewed these correlation of genotypes and phenotypes using previously reported infinite cases and our experienced cases. Moreover, we tried establishing a classification including the information about genetic change and exhibiting tumors. Finally, We assessed whether it is possible to predict an occurence of de novo tumors and developping of VHL disease.
Abstract 2863: Long term COX-2 inhibition in the small intestine of C57BL/6J <i>Apc</i>+/+ mice altered TGFβ signaling
Authors: Adelaide M. Carothers, Jennifer S. Davids, Beatrice C. Damas, Monica M. Bertagnolli
Journal: Cancer Research (2010)

Abstract Previously, we showed that short term (3 weeks) treatment of ApcMin/+ mice with the COX-2 inhibitor, celecoxib, reduced intestinal tumorigenesis, but long term drug treatment (5 months) increased intestinal tumors, stromal myofibroblasts, fibrosis, and expression of COX-2, PGE2, and TGFβ1, 2, 3 (TGFβ). Because COX-2 inhibitors are often used in patients with chronic inflammation, we examined the effects of celecoxib in Apc+/+ mice by immunoblotting and immunohistochemistry. Short term treatment induced canonical TGFβ signaling with increased expression of TGFβ and its receptor, effector, and targeted product (TβRII, Smad4, and PAI-1). In parallel, integrin signaling was suppressed with reduced expression of β1 integrin, active Focal Adhesion Kinase (FAK-p-Y397), Integrin-Linked Kinase, and the RhoA inhibitor, p190RhoGAP. Enterocyte differentiation but not proliferation was reduced relative to controls. Although COX-2 and TGFβ expression remained higher than basal levels, long term treatment reversed the effects on canonical TGFβ and integrin signaling, resulting in increased proliferation and differentiation. These results suggest that in the normal intestine PGE2 plays a role in modulating mechanical changes in cell-matrix adhesion via crosstalk between TGFβ and integrins. The mechanism for this could depend on the ability of PGE2 to increase [cAMPi] and Protein Kinase A activity. Chronic exposure to celecoxib may promote tumorigenesis by enhancing enterocyte positive growth regulation via integrins, while suppressing its negative regulation via TGFβ. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2863.
Characterization of cis-Acting Sequences and trans-Acting Signals Regulating Early Growth Response 1 and c-fos Promoters Through the Granulocyte-Macrophage Colony-Stimulating Factor Receptor in BA/F3 Cells
Authors: Sumiko Watanabe, Hideya Kubota, Kathleen M. Sakamoto, Ken-ichi Arai
Journal: Blood (1997)
Abstract 3290: Modulation of AKT, ERK and Mcl-1 by apigenin sensitizes colon cancer cells to anti-tumor activities of ABT263.
Authors: Huanjie Shao, Kai Jing, Esraa Mahmoud, Xianjun Fang, Chunrong Yu
Journal: Cancer Research (2013)

Abstract Apigenin is an edible plant-derived flavonoid showing anti-tumor activities in vitro and in vivo. Pretreatment with apigenin resulted in cell growth arrest and/or apoptosis in various types of tumors via modulating multiple cell signaling pathways. In the present study, we evaluated interactions between apigenin and ABT263 in multiple colon cancer cell lines. We found that apigenin enhanced ABT263-induced apoptosis in colon cancer cells in a time- and dose-dependent manner. ABT263 alone only resulted in limited cell killing in association with upregulation of Mcl-1, a potential mechanism for acquired ABT263 resistance. Apigenin antagonized ABT263-induced Mcl-1 expression and dramatically enhanced ABT263-induced cell death. Apigenin also suppressed AKT and ERK activation. Inactivation of either AKT or ERK pathway by lentivirus-transduced shRNA or specific small molecule inhibitors synergized with ABT263 to induce cell death, reflecting that AKT and ERK pathways are apigenin targets. Moreover, the synergism between ABT263 and apigenin was associated with the upregulation of Bim and subsequent activation of Bax. Xenograft studies with HCT116 cells in SCID mice showed that the combination treatment with apigenin and ABT263 inhibited tumor growth up to 70% without obvious adverse effects, while either agent alone showed only about 30% inhibition. Collectively, our findings demonstrate a novel and effective strategy to treat colon cancer by combination of ABT263 and apigenin. The combined effect is mediated by apigenin downregulation of Mcl-1, Akt and ERK activities. Citation Format: Huanjie Shao, Kai Jing, Esraa Mahmoud, Xianjun Fang, Chunrong Yu. Modulation of AKT, ERK and Mcl-1 by apigenin sensitizes colon cancer cells to anti-tumor activities of ABT263. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3290. doi:10.1158/1538-7445.AM2013-3290
HIGH PLATELET REACTIVITY IS ASSOCIATED WITH VASCULAR FUNCTION IN PATIENTS AFTER PERCUTANEOUS CORONARY INTERVENTION RECEIVING CLOPIDOGREL
Authors: Gerasimos Siasos, Evangelos Oikonomou, Marina Zaromitidou, Stamatios Kioufis, Manolis Vavuranakis, Konstantinos Maniatis, Eleni Kokkou, Konstantinos Mourouzis, Sotirios Tsalamandris, Theodoros Zografos, Nikolaos Papageorgiou, Athanasios Papavassiliou, Christodoulos I Stefanadis, Dimitris Tousoulis
Journal: Journal of the American College of Cardiology (2015)
AB0540 Role of B-Lymphocyte Activating Factor (BAFF) in the Pathogenesis of Systemic Lupus Erythematosus
Authors: N. Abdelmoaty, S. Salama, N. Kamel, M. ZAmzam, M. ElTayeb, S. Maroof, H. Amer, A. Kamel
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> B-lymphocyte activating factor (BAFF) is a new member of the tumor necrosis factor family that promotes B-cell survival, acting as an antiapoptotic factor and thus contributing to the development of autoimmune disease. <h3>Objectives</h3> The aim of the study was to investigate the role of BAFF in the pathogenesis ofsystemic lupus erythematosus (SLE) by correlating its serum levels to differentclinicopathological indices of disease activity. <h3>Methods</h3> The research carried out here with human subjects was in compliance with the Helsinki Declaration. This is a prospective study that was conducted on 20 female patients with SLE. Ten healthy controls of matching age and sex were also included in this study. All patients were subjected to full history taking and clinical examination upon presentation, and the following laboratory parameters were evaluated: complete blood picture, erythrocyte sedimentation rate, serum (creatinine, blood urea nitrogen), and complete urine analysis (anti nuclear antibody, anti-dsDNA, C3, C4 in serum). Serum BAFF levels were measured by enzyme-linked immunosorbent assay in all patients. Renal biopsy was performed whenever necessary. <h3>Results</h3> Serum BAFF levels were significantly higher in patients with active SLE than in controls (Po0.05). These levels also correlated positively with systemic lupus erythematosus disease activity index (SLEDAI) in a highly significant manner (Po0.001). Correlating serum BAFF among patients with photosensitivity and symptoms of central nervous system affection proved to be highly significant (Po0.001). In addition, within this study, serum BAFF levels correlated positively with ESR levels among patients and negatively with both C3 and C4 in a significant manner (Po0.05 and 0.001, respectively). <h3>Conclusions</h3> Serum BAFF levels were significantly higher among patients with active SLE thanamong controls. It correlated in a negative manner with both C3 and C4 – significantlywith C3 and highly significantly with C4. BAFF levels also correlated with SLEDAI in ahighly significant manner, implicating B-cell immunoglobulin production and immunecomplex formation in the disease activity of lupus patients. <h3>References</h3> Yoshimoto K, Tanaka M, Kojima M, Setoyama Y, Kameda H, Suzuki K, et al. Regulatory mechanims for the production of BAFF and IL-6 are impaired in monocytes of patients with primary Sjögren9s syndrome. Arthritis Res Ther 2011. <h3>Acknowledgements</h3> We are gratefull to Ain Shams Universiy hospital manager and Head of clinical pathology for facilitating this research. There are no conflicts of interest. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.1292
Case 39-2012
Authors: Shamim H. Nejad, Pamela W. Schaefer, Ednan K. Bajwa, Felicia A. Smith
Journal: New England Journal of Medicine (2012)

A 55-year-old man with a history of alcoholism was admitted to this hospital because of seizures, agitation, and delirium. He required sedation and mechanical ventilation. A diagnosis and management decisions were made.
Deception through self-deception: Take a look at somatoform disorders
Authors: Alfonso Troisi
Journal: Behavioral and Brain Sciences (2011)

Abstract Patients with physical symptoms for which no organic cause can be found are distributed along a continuum of disease simulation that ranges from a sincere belief of having a serious disease to intentional presentation of false symptoms. The evolutionary hypothesis that self-deception improves the deception of others can explain such a combination of unconscious and intentional production of physical symptoms.
PWE-184 The Association of Dietician follow up with the Quality of Life in Coeliac Disease
Authors: M A Zubir, B Engel
Journal: Gut (2013)

<h3>Introduction</h3> Coeliac disease (CD) is present in 1% of the UK population however there are still many undiagnosed cases in the community. The main treatment for this condition is gluten free diet. The role of dieticians in the follow up care of CD patients is crucial especially with regards to educating CD patients about their dietary requirement as well as their role in disease monitoring. The aim of the study is to assess the association of dieticians follow up on the quality of life in CD patients. <h3>Methods</h3> CD patients who were identified on histology over a 10 years period in East Sussex were sent a socio-demographic questionnaire and the Coeliac Disease Quality of Life (CD-QOL) survey by post. The participants of the study who attend dietician follow up were then compared with those who did not. Multiple linear and logistic regression analyses were used to identify any significant relationships <h3>Results</h3> Overall, 58 participants (34%) completed and returned the questionnaires. Dietician involvement appeared to be the most important predictor (beta = –0.424, p = 0.001) for overall CDQOL score but surprisingly, the negative value indicates that dietician involvement was associated with a lower quality of life score. Increasing age seemed to have a positive impact (beta = 0.312, p = 0.011) on overall quality of life. However, a change of the recent gluten free prescription (beta = –0.246, p = 0.037) which limits the products available and having initially presented with gastrointestinal symptoms (beta = –0.24, p = 0.044) were found to have negative contributions to the overall CDQOL score. The overall model fit was moderate (R2 = 0.336). Logistic regression was used to identify the likelihood of dietician follow up and the only significant predictor identified was the overall CDQOL score (OR 0.95, p = 0.019) which indicates that those with higher quality of life score were less likely to have dietician follow up. <h3>Conclusion</h3> Dietician follow up is associated with poorer quality of life but due to the nature of this study, cause and effect cannot be established. It may be that patients who have poorer quality of life chose to see a dietician and longitudinal study is required to further assess this association. This study also suggests that the recent change to the gluten free prescription has negatively impacted the quality of life of those with CD. This fact should be taken into consideration for any future health providers dealing with local CD service provisions. <h3>Disclosure of Interest</h3> None Declared.
Coronary Risk Factors and Plaque Morphology in Men with Coronary Disease Who Died Suddenly
Authors: Allen P. Burke, Andrew Farb, Gray T. Malcom, You-hui Liang, John Smialek, Renu Virmani
Journal: New England Journal of Medicine (1997)

Cigarette smoking and abnormal serum cholesterol concentrations are risk factors for acute coronary syndromes, but the underlying mechanisms are poorly understood. We studied whether cigarette smoking and abnormal cholesterol values may precipitate acute coronary thrombosis and sudden death resulting from either rupture of vulnerable coronary plaques or erosion of plaques.