tbuckley/cabot-search huggingface dataset:
AB0994 Clinical characteristics of elbow epicondilitis in patients with ostheoarthritis
Authors: E.R. Kirillova, N. Shamsutdinova
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Objectives</h3> The aim: To estimate clinical characteristics of elbow epicondilitis in patients with ostheoarthritis. <h3>Methods</h3> Methods: We investigated 80 patients with ostheoarthritis and epicondilitis of elbow joints. Diagnosis of elbow epicondilitis were estimated according to Southampton, 2004. Statistically datas was performed with Shapiro-Uilx, Fisher and χ<sup>2</sup> criteria <h3>Results</h3> Results. Epicondilitis was found significantly more frequent in women (54 - 67,5%) than in a men (26 - 32,5%) (d&lt;0,05). Distribution on the age was not normal. The middle age was 54 years (36-73 years). Wright-handed epicondilitis was registered in 35% patients (28 patients), left-handed epicondilitis was registered in 13,8% patients (11 patients), bilateral – in 51,2% (41 patients). Of all examined joints (160) match the criteria for epicondylitis 125 (78.1%). Among the most frequently encountered lesion both medial and lateral epicondyle - in 83 joints (66.4%). Lateral epicondylitis was found in 25 joints (20.0%), the median - in 17 (13.6%). Clinical manifestations of epicondylitis is independent of the radiographic stage of osteoarthritis. <h3>Conclusions</h3> Conclusion: bilateral epicondylitis most frequently occurs in patients with osteoarthritis with pathology of the elbow joint insertion, as well as the simultaneous destruction of the medial and lateral elbow enthesitis. Simultaneous destruction of the medial and lateral epicondyles is a characteristic feature of epicondylitis at osteoarthritis. <h3>Disclosure of Interest</h3> None Declared
PMO-009 Are dietitians' recommendations for the post-discharge support of malnourished patients carried out in the community?
Authors: D Coleman, C Baldwin, C E Weekes
Journal: Gut (2012)

<h3>Introduction</h3> Disease-related malnutrition is common and is often identified during a hospital admission. Hospital stays tend to be short and therefore it is crucial that nutritional interventions begun in hospital are continued on discharge (Elia <i>et al</i> 2010). Research has highlighted failings in nutritional care across this boundary (van Bokhorst-de van der Schueren <i>et al</i> 2005; Bavelaar <i>et al</i> 2008). The aim of this study was to evaluate the continuation of dietetic interventions across the transition from acute to community care. <h3>Methods</h3> All patients admitted to the acute medical wards and referred to a dietitian for nutrition support between 1 July and 30 September 2011 were considered eligible for this study. Patients were excluded if they died within 1-month of discharge, received enteral or parenteral nutrition, were receiving dietetic care for a long-term chronic condition or were still in hospital at 31 October 2011. Eligible patients or their carers were contacted to determine whether recommendations for their post-discharge oral nutritional support had been carried out. Data were analysed using SPSS V.17.0. <h3>Results</h3> Of 108 patients, 27 (25 %) died before contact could be made and 17 (16 %) did not meet the inclusion criteria. 64 patients were included in this study of whom 35 (56%) were recommended one or more post-discharge dietetic interventions, including consumption of oral nutritional supplements and follow-up dietetic appointments. Of the 35 patients, it was not possible to contact 14 (40 %) within the time limits of the study. Contact was made with 21 patients of whom 17 (81%) received all the interventions recommended by the dietitian. Of the four patients who did not receive the recommended interventions, in 3 (75%) this was due to patient perception that treatment was no longer required. Of the 64 patients who met the inclusion criteria no comments were included in the discharge letter from the medical team on either nutritional status or dietetic input. <h3>Conclusion</h3> In this study it was possible to contact only a small sample of eligible patients however, of those who were contacted the majority had received the post-discharge interventions recommended by the dietitian. Further studies are required to determine if dietetic recommendations are as likely to be carried out in patients who are more difficult to contact post discharge. <h3>Competing interests</h3> None declared. <h3>References</h3> 1. <b>Bavelaar JW</b>, Otter CD, van Bodegraven AA, <i>et al. Clin Nutr</i> 2008;<b>27</b>:431–8. 2. <b>Elia M</b>, Russell CA, Stratton RJ. <i>Proc Nutr Soc</i> 2010;<b>69</b>:470–6. 3. <b>van Bokhorst-de van der Schueren MAE</b>, Klinkenberg M, Thijs A. <i>Eur J Clin Nutr</i> 2005;<b>59</b>:1129–35.
Shared decision-making: enhancing the clinical relevance
Authors: Vikki A Entwistle, Alan Cribb, Ian S Watt
Journal: Journal of the Royal Society of Medicine (2012)

Shared decision-making is increasingly advocated to enable patients to participate in decisions that affect them, to protect patients from insufficiently individualized supply-driven care, and to reduce health care costs and waste by avoiding the provision of unwanted interventions.1–3

The concept of shared decision-making can be understood in several ways. A number of definitions and descriptive models have been offered, emphasizing different aspects of clinician-patient interaction and decision-making.4 Most definitions and models can be variously interpreted when considered in relation to the complex realities of healthcare provision. Clinicians' understandings of shared decision-making can have important implications for clinical practice.5 They can diverge, for example, over questions of whether, when and how it is appropriate to recommend a particular treatment or challenge a patient's expressed preferences.

This paper considers the practical and ethical implications of, ‘narrow’ and ‘broader’ ways of thinking about shared decision-making. It illustrates how narrow understandings of shared decision-making, which focus on informing patients so they can choose between options, can make it hard for many patients to share meaningfully in decision-making that affects them. It then outlines how broader understandings, which allow for more clinician influence and extend the relevance of shared decision-making to diverse situations, can be justified in principle and appraised for appropriateness.

Table 1 compares the key features of narrow and broader understandings of shared decision-making.



Table 1

Key features and implications of narrow and broader understandings of shared decision-making
Beta-Adrenergic–Antagonist Drugs in the Prevention of Gastrointestinal Bleeding in Patients with Cirrhosis and Esophageal Varices
Authors: T Poynard, P Calès, L Pasta, G Ideo, J P Pascal, L Pagliaro, D Lebrec
Journal: New England Journal of Medicine (1991)

Original Article from The New England Journal of Medicine — Beta-Adrenergic–Antagonist Drugs in the Prevention of Gastrointestinal Bleeding in Patients with Cirrhosis and Esophageal Varices — An Analysis of Data and Prognostic Factors in 589 Patients from Four Randomized Clinical Trials
Abstract 2425: Collapsin response mediator protein 4 promotes tumor cell invasion and lethality of pancreatic cancer
Authors: Yukihiko Hiroshima, Fumio Nakamura, Hiroshi Miyamoto, Ryutaro Mori, Koichi Taniguchi, Ryusei Matsuyama, Kazuhisa Takeda, Hirotoshi Akiyama, Kuniya Tanaka, Yasushi Ichikawa, Yoji Nagashima, Yoshio Goshima, Itaru Endo
Journal: Cancer Research (2012)

Abstract BACKGROUND: Pancreatic cancer is an aggressive malignancy with one of the worst outcomes among all cancers. Recently, Collapsin Response Mediator Proteins (CRMPs) were associated with proliferation, apoptosis, differentiation and invasion in several cancers. However, CRMPs expression and their role in pancreatic cancer have not been investigated. This study aimed to clarify the clinical significance of CRMPs in pancreatic cancer. METHODS: Pancreatic adenocarcinoma samples were obtained from 53 patients. Crmp expression in these samples was examined using realtime RT-PCR. CRMP4 protein expression was examined immunohistochemically and compared with the clinicopathological features of the tumors. Furthermore, knock down of CRMP4 expression using siRNA was examined in pancreatic cancer cell lines to determine whether CRMP4 regulates cell proliferation and invasion in vitro. RESULTS: Of all the CRMPs, the crmp4 gene was determined to be the only one differentially expressed in pancreatic cancer tissues (p = 0.008). The expression of CRMP4 was detected immunohistochemically in 34 of the 53 (64.1%) pancreatic cancer samples, and CRMP4 staining was highly correlated with poor differentiation (p = 0.003) and liver metastasis (p = 0.021). Multivariate analyses suggested that venous invasion and CRMP4 overexpression were prognostic factors for survival. CRMP4 knockdown using siRNA reduced cellular invasion, but did not affect proliferation. CONCLUSIONS: Our results suggested that CRMP4 overexpression was a strong prognostic factor for increasing pancreatic cancer invasiveness, and can be a novel therapeutic target for pancreatic cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2425. doi:1538-7445.AM2012-2425
FRECUENCIA DE COLONOSCOPIAS PREVIAS EN PACIENTES DIAGNOSTICADOS DE CANCER COLORECTAL SEGÚN SU LOCALIZACION (Colon Derecho vs. Colon Izquierdo)
Authors: S Maestro, H Nuñez, E Saracibar, RE Madrigal, A Perez-Millan, J Barcenilla, A Del Moral, F Igea
Journal: Endoscopy (2010)

Objetivos: Durante los últimos años múltiples publicaciones ponen en duda la eficacia de la colonoscopia en la prevención del cáncer de colon derecho. La tasa de fallo diagnóstico en dicha localización es superior a la del colon izquierdo. Algún trabajo pone en duda la eficacia de la colonoscopía en esta localización. Nos propusimos el presente trabajo con este objetivo: Determinar la eficacia de la colonoscopía en la prevención del cáncer de colón derecho mediante el análisis de la frecuencia de colonoscopías previas en pacientes diagnosticados de cáncer colorectal en nuestro centro.
Performing Arts: The Consulting Room
Authors: S. Knight
Journal: BMJ (1999)

The Royal London Hospital, 9, 10, 11 July

For the past 10 weeks, patients at the Royal London Hospital have been persuaded to take part in an ambitious arts project presented by the IOU theatre. While perhaps not kicking off their shoes and dancing, both staff and patients have participated in singing workshops and interviews conducted by the members of the theatre in an attempt to explore notions of illness. The resulting presentation, named “The Consulting Room,” incorporates these interviews into a 40 minute show and is the third in a series that will culminate at next year's Greenwich and …
P3-09-02: Intermittent Dietary Carbohydrate Restriction Enables Weight Loss and Reduces Breast Cancer Risk Biomarkers.
Authors: M Harvie, C Wright, M Pegington, E Mitchell, DG Evans, S Jebb, R Clarke, R Goodacre, W Dunn, M Mattson, A Howell
Journal: Cancer Research (2011)

Abstract Background: Energy restriction is a potential strategy for breast cancer prevention but is difficult to achieve and maintain. We found that intermittent energy restriction (2 days strict dieting week) is comparable to the standard approach of moderate daily restriction for weight loss and marginally better for improving insulin sensitivity, but no easier to follow1. In this follow on study we wished to test whether 2 novel intermittent low carbohydrate/low energy diets were feasible and easier to follow than a standard daily energy restriction. Design: Randomised comparison of 3 dietary types over 4 months in 115 overweight or obese (mean body mass index 31.0 [±5.3 SD] kg/m2) women at increased risk of breast cancer (lifetime risk &amp;gt; 1 in 6). Diets: 1. A restricted low carbohydrate diet (RLCD): 650 kcal and &amp;lt;50g carbohydrate / day for 2 days per week 2. Ad lib low carbohydrate diet (ALCD): &amp;lt;50g / day for 2 days per week with other food types (e.g. protein) ad lib 3. A standard daily restricted Mediterranean diet (DRMD): ∼ 1500kcal/day for 7 days per week Methods: Weight, anthropometrics, blood markers for breast cancer; insulin resistance, oxidative stress markers, leptin, adiponectin, lipids, inflammatory markers IGF-1 were assessed at baseline, 1, 3 and 4 months. Results: 88/114 completed the study (77%, drop outs 6 RLCD, 8 ALCD 12 DRMD). Last observation carried forward analyses show both intermittent low carbohydrate diets were superior to standard daily restriction for reducing weight and body fat: mean (95% confidence interval [CI]) change in body fat for RLCD was −4.3 (−5.6 to −3.0) kg, for ALCD −4.1 (−5.2 to −3.1) kg vs. −2.4 (−3.4 to −1.2) kg for DRMD (P value for difference between groups = 0.02). The intermittent groups had greater improvement in insulin resistance: mean (95% CI) change for RLCD was −22 (−35 to −11) %, ALCD −14 (−27 to −5%) % vs. −4 (−16 to 9) % for DRMD (P = 0.02). Other biomarkers are being assayed currently. Conclusion: Greater weight loss, fewer drop outs and greater reductions in insulin resistance with the novel intermittent low carbohydrate diets indicate that these are alternative approaches for energy restriction for potentially reducing risk of breast cancer and other diseases. Reference: 1Harvie MN, Pegington M, Mattson MP, Frystyk J, Dillon B, Evans G et al. The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women. Int.J Obes (Lond) 35; 714–27, 2011. This study is funded by the Genesis Breast Cancer Prevention Appeal: www.genesisuk.org Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P3-09-02.
Abstract SY14-01: Investigating MTORC1 inhibition downstream of Apc loss in vivo
Authors: Owen J. Sansom
Journal: Cancer Research (2012)

Abstract The Apc tumour suppressor gene is mutated in up to 80% percent of colorectal cancers (CRC), therefore strategies specifically targeting Apc deficient cells in vivo may be of therapeutic relevance. Thus far most work in murine models have focussed on models of adenomas where only Apc is lacking (and not other mutations that drive progression). In my talk, I will discuss our recent work inhibiting mTOR in Apc deficient cells in vivo either via small molecules or genetically deleting critical components of mTORC1 (Raptor) and mTORC2 (Rictor). Here we show that Apc deficient cells are dependent on mTORC1 for proliferation (in a S6 kinase dependent manner). However additional mutation of KRAS or p53 renders the cells insensitive to mTORC1 inhibition. I will discuss the mechanisms underpinning this resistance and how overcoming these may allow us to target more advanced intestinal tumours in vivo. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY14-01. doi:1538-7445.AM2012-SY14-01
Abstract LB-281: Hodgkin Lymphoma requires stabilized NIK and constitutive RelB expression for survival
Authors: Stella M. Ranuncolo, Wenming Xiao, George Wright, Mones Abu-Asab, Stefania Pittaluga, Elaine S. Jaffe, Brian Lewis
Journal: Cancer Research (2012)

Abstract The REL family of transcription factors plays major roles in diverse cell processes and tumor etiology. Despite considerable evidence supporting the role of the REL members in the immune system and lymphomagenesis, it is not clear whether each REL controls unique targets in distinct subsets of B cell-derived lymphomas or whether each is redundant. We delivered specific shRNAs to knock down each REL member in representative non-Hodgkin (NHL) and Hodgkin lymphoma (HL) cell lines. All NHL and HL cell lines were dependent on RelA and c-Rel for survival but only HL cells were sensitive to RelB depletion. ChIP-seq analysis uncovered an extensive nonoverlapping REL networks and that RelB directly controlled cell cycle regulators and apoptosis inhibitors including BCL2 and BCLx. However, the RelB shRNA in HL cells does not kill these cells by apoptosis. Electron microscopy revealed intact nuclei with considerable numbers of cytosolic vacuoles, indicative of autophagy. Secondly, ATG7, a key player in the autophagosomes development, is induced. We found that HL cell lines and primary tumors stably expressed NIK and that HL cell lines are missing either TRAF2 or TRAF3 protein (negative regulators of NIK). Unexpectedly, RelB shRNA resulted in the re-expression of TRAF2 and degradation of NIK protein. Lastly, both NIK shRNA and a small molecule inhibitor of NIK had the same phenotype as the relB shRNA. These data shed light on unexplored aspects of HL biology. We found that HL is the only GC B-cell derived malignancy that relies on RelB for viability, and thus differentiates Hodgkin lymphoma from non-Hodgkin lymphomas. These data argue that each REL member has specific and unique functions and gene targets, as we predicted from the lack of similarities in their transactivation domains. Furthermore, the RelB dependency in HL suggests that NIK is an attractive therapeutic target and the possibility of targeting NIK enzymatic activity in HL patients with diminishing side effects. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-281. doi:1538-7445.AM2012-LB-281
PREVALENCE OF PLAQUE RUPTURE IS HIGHER IN PATIENTS WITH AORTIC DILATATION: FIRST OBSERVATION OF THE EARLY STAGE OF ANEURISMAL FORMATION WITH NON-OBSTRUCTIVE ANGIOSCOPY
Authors: Satoru Takahashi, Sei Komatsu, Mitsuhiko Takewa, Junichi Yoshida, Yasuhiko Kobayashi, Atsuko Imai, Hitoshi Minamiguchi, Tomoki Ohara, Kazuhisa Kodama
Journal: Journal of the American College of Cardiology (2015)
The Side Effects of Managed Care on The Drug Industry
Authors: K. Nagy
Journal: JNCI Journal of the National Cancer Institute (1995)

The Side Effects of Managed Care on The Drug Industry Get access Kate Nagy Kate Nagy Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 17, 6 September 1995, Pages 1279–1280, https://doi.org/10.1093/jnci/87.17.1279 Published: 06 September 1995
Abstract 2894: Environmentally responsive nanoparticles for the intracellular delivery of RNAi therapeutics into tumor-associated macrophages
Authors: Shann S. Yu, Cheryl M. Lau, Whitney J. Barham, Halina M. Onishko, Christopher E. Nelson, Fiona E. Yull, Craig L. Duvall, Todd D. Giorgio
Journal: Cancer Research (2012)

Abstract Tumor-associated macrophages (TAMs) represent a potentially promising therapeutic target in cancer because they have been shown to facilitate tumor growth, invasiveness, and metastasis. However, methods to specifically target therapies to TAMs are lacking. To address this problem, we designed and synthesized mannosylated micellar nanoparticles (ManNPs), composed of tri-block co-polymers. The three polymer blocks include (1) an azido-displaying block for functionalization with biomolecules via azide-alkyne ‘click’ chemistry, (2) a cationic block for the condensation of polyanions such as siRNA, and (3) a pH-responsive terpolymer block that facilitates endosomal disruption. This terpolymer is hydrophobic at pH 7.4, allowing these polymers to self-assemble into 25 nm micellar nanoparticles under physiologic conditions. However, they become protonated at lower pH ranges representative of endosomal compartments (5.8 - 6.2), leading to disassembly of the nanoparticles, and increased ability to disrupt endosomal membranes and enable cytoplasmic delivery. This pH-dependent behavior has been validated using a red blood cell hemolysis assay. This environmentally-responsive behavior facilitates improved cytoplasmic delivery of siRNA, access to the intracellular silencing machinery, and consequently, knockdown of target gene expression. Further, we demonstrate that mannosylation of these nanoparticles via ‘click’ chemistry significantly enhances their ability to deliver siRNA into murine bone marrow-derived primary macrophages (BMDMs), relative to control, untargeted nanoparticles. Targeted nanoparticle uptake is mediated specifically through the macrophage mannose receptor (CD206), as validated through competition experiments with free mannose, or by pre-incubating BMDMs with lipopolysaccharide to downregulate CD206 expression. This is particularly important for cancer applications because CD206 is upregulated in tumor-suppressed and non-activated macrophages, enabling more specific targeting of TAMs versus healthy macrophages in other tissues. The ManNPs described here present new opportunities to target TAMs in various cancers, providing an enabling technology for the modification of the immunosuppressive tumor environment by targeting TAM activity. Studies are pending to demonstrate this behavior in an in vivo murine model of metastatic breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2894. doi:1538-7445.AM2012-2894
A3.20 TNF Regulates CD3ζ Expression of T Lymphocytes Via SRC-Like Adaptor Protein-Dependent Proteasomal Degradation
Authors: Barbara Érsek, Viktor Molnár, Andrea Balogh, János Matkó, Andrew P Cope, Edit I Buzás, András Falus, György Nagy
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background and Objectives</h3> although ζ-chain downregulation of human T lymhocytes is common at sites of chronic inflammation, the precise mechanism of ζ-chain regulation is not known. Src-like adaptor protein (SLAP) is a regulator of T cell activation; earlier data have reported that SLAP regulates immunoreceptor signalling. We studied the mechanism of CD3 ζ-chain downregulation. <h3>Materials and Methods</h3> CD3ζ and SLAP protein levels of T lymphocytes were measured by Western blot. Jurkat cells were transiently transfected with siRNAs to silence SLAP, knockdown efficiency of the siRNAs was measured by real-time RT-PCR and by Western blot. For confocal microscopy experiments cells were transfected with eGFP-SLAP cDNA vector or control eGFP vector. The colocalisation between CD3ζ and SLAP were measured by laser confocal microscopy. CD3ζ mRNA was measured by quantitative real-time RT-PCR, IL-2 level was measured by ELISA. <h3>Results</h3> in vitro TNF treatment of human T cells selectively, dose dependently and reversibly downregulates CD3 ζ-chain expression and inhibits activation-induced IL-2 expression (p &lt; 0.01). Inhibition of the proteasome prevented the effect of TNF on CD3 ζ-chain expression. The colocalization of SLAP with CD3 ζ-chain and the SLAP expression were enhanced by TNF treatment (p &lt; 0.01 and p &lt; 0.05, respectively). SLAP silencing with small interfering RNA inhibited the TNF-induced ζ-chain downregulation. SLAP levels of the CD4 T cells, isolated from patients with rheumatoid arthritis were higher than that of the healthy donors’ (p &lt; 0.05). In addition, in vitro TNF treatment did not alter the SLAP expression of the CD4 lymphocytes of anti-TNF therapy-treated RA patients. <h3>Conclusions</h3> our present data suggest that TNF regulates T cell activation during inflammatory processes, by altering CD3 ζ-chain expression via a SLAP-dependent mechanism. Thereafter SLAP-dependent regulation of CD3 ζ-chain may have an important role in the fine control of TCR signalling during chronic inflammation. SLAP may have a role in the pathomechanism of RA.