tbuckley/cabot-search huggingface dataset:
THU0591-HPR The Longitudinal Impact of Persistent Depression on Physical Health Outcomes in Rheumatoid Arthritis: Table 1.
Authors: F. Matcham, S. Norton, D.L. Scott, S. Steer, M. Hotopf
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Depression is highly prevalent in RA and is associated with increased mortality, disability and healthcare costs [1, 2]. There is limited evidence assessing the longitudinal impact of depression on RA outcomes, particularly objectively-reported clinical outcomes. <h3>Objectives</h3> To assess the impact of persistent depression on physical health outcomes over a 2-year follow-up period. <h3>Methods</h3> A secondary data analysis of a clinical trial (CARDERA) was performed [3]. Depression and physical health outcomes were measured at baseline and 6-montly intervals for 2-years. Depression was measured using the EQ-5D, and patients were categorised into 4 groups: 1) never depressed; 2) depressed at &lt;50% of time-points; 3) depressed at &gt;50% of time-points; and 4) depressed at every time-point. Physical health outcomes were: Larsen score; tender joint count (TJC); swollen joint count (SJC); ESR; assessor and patient global assessments (AGA/PGA); HAQ; pain; and DAS-28. <h3>Results</h3> Data was available for 379 patients. Patients9 mean age was 54.1 (12.3), and 68.3% of the sample were female. In total, 25.9% were never depressed, 36.9% were depressed &lt;50% of the time, 27.4% were depressed &gt;50% of the time, and 15.8% were depressed at every time-point. <h3>Conclusions</h3> Increasing persistence of depression over time tends to be associated with poor physical health outcomes, with discordance between subjectively and objectively measured outcomes. These findings have significant implications: mental health should be measured and monitored throughout the course of treatment [4]; DAS-28 scores may be inflated in depressed patients, which needs to be considered when making treatment decisions. <h3>References</h3> Matcham F et al. The prevalence of depression in Rheumatoid Arthritis: A systematic review and meta-analysis. Rheumatology 2013; 52: 2136-48. Bruce T. Comorbid depression in rheumatoid arthritis: Pathophysiology and clinical implications. Current Psychiatry Reports 2008; 10: 258-64. Choy EHS et al. Factorial randomised controlled trial of glucocorticoids and combination disease modifying drugs in early rheumatoid arthritis. Ann Rheum Dis 2008; 67: 656-63. Rayner L et al. Embedding integrated mental health assessment and management in general hospital settings: feasibility, acceptability and the prevalence of common mental disorder. Gen Hosp Psychiatr (in press), doi: 10.1016/j.genhosppsych.2013.12.004. <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2878
Demonstration of an Adhering-Junction Molecule (Plakoglobin) in the Autoantigens of Pemphigus Foliaceus and Pemphigus Vulgaris
Authors: Neil J. Korman, Russell W. Eyre, Vera Klaus-Kovtun, John R. Stanley
Journal: New England Journal of Medicine (1989)

Pemphigus foliaceus and pemphigus vulgaris are skin diseases in which antibodies against the cell surface of keratinocytes destroy the adhesion between epidermal cells, producing blisters. Patients with pemphigus foliaceus have antibodies to a complex of three polypeptides of 260, 160, and 85 kd (the foliaceus complex), whereas patients with pemphigus vulgaris have antibodies to a complex of 210-kd, 130-kd, and 85-kd polypeptides (the vulgaris complex). The 160-kd polypeptide of the foliaceus complex has been identified as desmoglein, a desmosomal glycoprotein. We suspected that the 85-kd component in both these antigenic complexes might be plakoglobin, another molecule in the adhering junctions of cells. To characterize these antigenic complexes, we used the serum of five patients with pemphigus foliaceus, that of four patients with pemphigus vulgaris, and monoclonal antiplakoglobin antibodies. We found that monoclonal antibodies to plakoglobin immunoprecipitated the 85-kd polypeptide from the dissociated foliaceus and vulgaris complexes and precipitated both complexes from epidermal extracts. Serum from patients with pemphigus foliaceus or pemphigus vulgaris (but not from four normal controls) bound desmoglein and the 130-kd polypeptide, respectively, showing that these peptides (and not plakoglobin) are the antigenic binding sites in these disorders. We conclude that plakoglobin, a protein of the adhering junctions of epidermal cells, is the 85-kd molecule in the antigenic complexes found in both pemphigus foliaceus and pemphigus vulgaris, although it is not the binding site in either disorder.
Abstract 747: p53 activation through stress induction mediates differential regulation of target genes.
Authors: Shilpi Mittal, Rama Kadamb, Nidhi Bansal, Daman Saluja
Journal: Cancer Research (2013)

Abstract p53 is a sequence specific transcription factor that gets up regulated in response to stress such as DNA damage, microtubule disruption or oxidative stress. p53 protein gets stabilized upon stress induction and functions by activating and repressing large number of downstream genes involved in varying functions like cell cycle, DNA repair, apoptosis or senescence depending upon type of stress. Gene activation and repression is crucial for p53 to perform its functions in the cell. p53 mediates its activation functions through its ability to bind to cis-acting DNA elements within regulatory regions. However, p53 regulates negative expression of genes either through direct recruitment on the promoter or through indirect mechanisms. Studies show that genotoxic as well as nongenotoxic stress leads to accumulation of p53 protein in cell, though the downstream effects vary under both conditions. The various cellular mechanisms that take place in the cell following DNA damage are well studied; however less is characterized about agents that disrupt microtubule assembly. To put an insight into such differential regulation mechanism, we focused to study the difference in cellular fate upon genotoxic and non genotoxic stress. In the present study, we observed that two varying stresses that include DNA damage caused by bleomycin and microtubule disruption by colchicine mediate cell cycle arrest and increased levels of p53. At the gene level, it was observed that upon bleomycin treatment, Sin3/HDAC corepressor complex is docked onto the promoters of p53 target genes whereas colchicine treatment results in dissociation of Sin3/HDAC complex from the same promoters. Moreover, recruitment of Sin3/HDAC complex is reflective of downregulation of p53 target genes and dissociation of this complex from the promoter brings about transactivation of the same genes. Therefore, our studies highlight that mere activation of p53 in varying kind of stress is not a decisive factor in gene regulation, rather interaction of p53 with corepressor or coactivator directs succeeding processes depending upon the type of stress. Citation Format: Shilpi Mittal, Rama Kadamb, Nidhi Bansal, Daman Saluja. p53 activation through stress induction mediates differential regulation of target genes. [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 747. doi:10.1158/1538-7445.AM2013-747
P363Antibody-based selective isolation of atrial and ventricular cardiomyocytes from neonatal mouse heart
Authors: D Eckardt, AM Wiencierz, M Kernbach, J Riesen, S Tomiuk, P Christalla, A Bosio
Journal: Cardiovascular Research (2014)

The mammalian heart comprises mainly cardiomyocytes, fibroblasts, endothelial cells, and smooth muscle cells. Cardiomyocyte subtypes are characterized by differential expression of intracellular proteins like MLC-2a, Cx40 or ANF in atrial cardiomyocytes as well as MLC-2v, Hey2 or Irx4 in ventricular cardiomyocytes. Nevertheless, to date the expression of chamber-specific intracellular proteins could not be correlated to corresponding cell surface markers. Therefore, the selective, surface marker-based enrichment of atrial or ventricular cardiomyocytes from whole-heart preparations is currently not possible.
TCTAP A-133 Treatment Delay in Door-to-Balloon Time in South-East Asian Patients Undergoing Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction: A Key Process Analysis of Patient Factors
Authors: Eran Wen Jun Sim, An Shing Ang, Mae Chyi Tan, Kevin Kien Hong Quah, David Foo, Paul J.L. Ong, Hee Hwa Ho
Journal: Journal of the American College of Cardiology (2015)
Abstract 1860: 15-Deoxy-Δ12,14-prostaglandin J2 induces 15-hydroxyprostaglandin dehydrogenase expression through activation of Elk-1 in human breast cancer cells
Authors: Ha-Na Lee, Hye-Rim Kim, Jong-Min Park, Young-Joon Surh, Hye-Kyung Na
Journal: Cancer Research (2011)

Abstract Overproduction of prostaglandin E2 (PGE2) has been reported to be implicated in carcinogenesis. The intracellular level of PGE2 is regulated not only by its biosynthesis, but also by its degradation process. The key enzyme responsible for the biological inactivation of PGE2 is NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH). This enzyme catalyzes NAD+-linked oxidation of 15(S)-hydroxyl group of prostaglandins to 15-keto metabolites, thereby inactivating PGE2. In the present study, we have found that 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), one of the terminal products of cyclooxygenase-2 (COX-2), upregulates 15-PGDH expression at both protein and mRNA levels in human breast cancer (MDA-MB-231) cells. The catalytic activity of 15-PGDH was also increased by 15d-PGJ2 treatment. By using deletion constructs of 15-PGDH promoter, we found that Ets is the most essential determinant for 15-PGDH induction. Elk-1, one of Ets transcription factor family members, was phosphorylated by 15d-PGJ2 treatment as determined by Western blot and immunocytochemical analyses. siRNA knockdown of Elk-1 suppressed 15-PGDH expression, indicating that Elk-1 plays a key role in 15-PGDH induction. We also observed that a pharmacological inhibition of ERK1/2 with U0126 abrogated the 15-PGJ2-induced activation of Elk1 and expression of 15-PGDH. Like 15d-PGJ2, its non-electrophilic analog 9,10-dihydro-15d-PGJ2 induced 15-PGDH, suggesting that the α,β-unsaturated carbonyl group of 15d-PGJ2 is not essential for its upregulation of 15-PGDH induction. The induction of Elk-1-mediated 15-PGDH expression by 15d-PGJ2 may account, in part, for its anti-inflammatory and anti-carcinogenic properties of this cyclopentenone prostaglandin. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1860. doi:10.1158/1538-7445.AM2011-1860
FRI0218 Normalization of c-reactive protein within the first 8 weeks is a predictive factor for the effectiveness of subcutaneous tocilizumab monotherapy in japanese rheumatoid arthritis patients: results from the musashi study
Authors: A. Ogata
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The effectiveness and safety of subcutaneous tocilizumab 162 mg every other weeks (TCZ-SC) monotherapy were shown to be comparable to those of intravenous tocilizumab 8 mg/kg every 4 weeks (TCZ-IV) monotherapy in Japanese patients with rheumatoid arthritis (RA) in a double-blind, parallel-group, phase III non-inferiority study (MUSASHI study)<sup>1)</sup>. In the presence of serum trough TCZ level of ≥1 µg/mL, adequate suppression of IL-6 signalling during TCZ-IV treatment results in normalization of serum CRP levels.<sup>2)</sup> <h3>Objectives</h3> To investigate whether patients with normalization of serum CRP level by 12 weeks during administration of TCZ-SC achieved a clinical response at Week 24. <h3>Methods</h3> This was a post hoc analysis from the MUSASHI study. Patients with RA who had responded inadequately to any synthetic or biologic DMARD were randomized to receive 162 mg TCZ-SC every 2 weeks (TCZ-SC group) or 8 mg/kg TCZ-IV every 4 weeks without any concomitant DMARDs. Week 24 efficacy endpoints including rates of ACR response and DAS28/CDAI remission were assessed and stratified by normalization of serum CRP level (≤0.3 mg/dL) at Week 4, 8, and 12 in the TCZ-SC group. <h3>Results</h3> The efficacy analyses included 159 patients who were eligible for the per protocol analysis in the TCZ-SC group. At Week 24, 79.2% of patients in the TCZ-SC group achieved ACR20, 63.5% achieved ACR50, 37.1% achieved ACR70, 49.7% achieved DAS28 remission, and 16.4% achieved CDAI remission. Serum CRP level was normalized (≤0.3 mg/dL) in most patients (90.6%, 144/159)at Week 24. Serum CRP level was normalized in 99.2% (1679/1693 points) in the presence of serum trough TCZ level of ≥1 µg/mL. ACR20 response rate at Week 24 was 84.7% (122/144) in the patients with normalized CRP <i>vs.</i> 26.7% (4/15) in the patients without normalized CRP at Week 24. The groups with normalized CRP at Weeks 4, 8, or 12 had higher ACR response rates and DAS28/CDAI remission rates at Week 24 than the groups without normalized CRP (Table). No patients without normalized CRP at Week 8 or later achieved DAS28/CDAI remission at Week 24. <h3>Image/graph</h3> <h3>Conclusions</h3> Serum CRP level was normalized in most points with serum trough TCZ level of ≥1 µg/mLduring TCZ-SC treatment. In this TCZ-SC monotherapy setting, patients who had normalized CRP by Week 12 achieved higher rates of DAS28/CDAI remission and ACR response at Week 24 than the patients without normalized CRP. The efficacy at Week 24 was predictable by CRP normalization at Week 4. Patients whose CRP has not normalized despite 8 weeks of TCZ-SC treatment will possibly not achieve an adequate response. <h3>References</h3> Ogata A. Ann Rheum Dis 2012;71(Suppl3):373 Nishimoto N et al. Blood. 2008;112(10):3959-64. <b>Disclosure of Interest</b>: A. Ogata Consultant for: Chugai pharmceuticals
PWE-278 Does N-acetyl cysteine modulate renal function after major hepatectomy?
Authors: R Lochan, A Boukas, S Robinson, R Saif, D Manas, S White
Journal: Gut (2012)

<h3>Introduction</h3> Acute kidney injury or deterioration in pre-existing renal dysfunction following major hepatectomy is an important cause of morbidity and mortality. N-acetyl cysteine has been extensively utilised as a reno-protective agent to ameliorate contrast induced nephropathy. The aim of this study was to investigate its potential use for preserving renal function following major hepatectomy. <h3>Methods</h3> A prospective study to compare the impact of N-Acetyl cysteine (NAC) on liver function after hepatectomy was undertaken in our Unit from 2004 to 2010. A cohort of 44 patients received peri-operative NAC (10 g/24 h) for 5 days and were compared to a further cohort of 44 patients (matched for the extent of liver resection—all more than three segments), gender, age and chemotherapy use) who did not. Post-operative renal function was evaluated. Other variables known to influence renal function included associated co-morbidity, drugs, intra-operative parameters (eg, CVP and blood loss). In addition to calculating the renal risk index as described by Clavien <i>et al.</i> We also examined other outcome measures such as duration of renal support and long-term renal specific outcomes. <h3>Results</h3> There were three patients with known CKD in the NAC group as compared to one in the control group. Mean (SD) pre-operative creatinine levels [93.9 (20.5), 92.5 (19.3) p=0.7], BMI [26.9 (14.5), 28.9 (13.1) p=0.3], operating time (h) [6 (1.9), 5.5 (1.7), p=0.9]. The mean renal risk index were also similar between the NAC and control group. Mean (SD) creatinine rise (delta creatinine) between days 1 and 5 in the post-operative period, were also similar between the 2 groups [NAC 43.8 (82.9) vs Control 49.2 (63.5), p=0.72]. Renal support in the form of CVVH was needed in three patients in the study group vs one in the control group (all known to have pre-existing CKD). All these patients went back to their pre-operative renal status at 3-months follow-up. <h3>Conclusion</h3> In this study NAC does not appear to be reno-protective in patients with known renal impairment who require a major liver resection. Its presumed renoprotective role in those at “high risk” needs to be further assessed in an adequately powered RCT. <h3>Competing interests</h3> None declared.
Left Ventricular Dilatation and the Risk of Congestive Heart Failure in People without Myocardial Infarction
Authors: Ramachandran S. Vasan, Martin G. Larson, Emelia J. Benjamin, Jane C. Evans, Daniel Levy
Journal: New England Journal of Medicine (1997)

Left ventricular dilatation is a well-recognized precursor of ventricular dysfunction and congestive heart failure after myocardial infarction. The effect of left ventricular dilatation on the risk of heart failure in people initially free of myocardial infarction is not known.
Disorders of Aldosterone Biosynthesis and Action
Authors: Franklin H. Epstein, Perrin C. White
Journal: New England Journal of Medicine (1994)

Patients with Addison's disease excrete excessive amounts of sodium in the urine but retain potassium, thus becoming hyponatremic and hyperkalemic. Early studies demonstrated that the problems could be ameliorated in humans and animals by administering extracts from adrenal glands1,2. These extracts were presumed to contain hormones with sodium-retaining, or mineralocorticoid, properties. The existence of distinct mineralocorticoids was, however, not proved until a novel steroid with potent mineralocorticoid activity was isolated3. This hormone was named aldosterone to acknowledge its unique structural feature, an aldehyde group at C18.This article reviews conditions of mineralocorticoid deficiency or excess, concentrating on . . .
Abstract LB-64: Hitting Testicular Cancer Where It Hurts: Through Public Awareness and Post-Treatment Support
Authors: Timothy Buckland
Journal: Cancer Research (2011)

Abstract The American Cancer Society estimated that in 2010 there were 8480 American men diagnosed with testicular cancer. Within this population, the vast majority of those diagnosed were young males between the ages of 15 and 29. Although treatment of this disease has been highly effective, there are two key areas where support is lacking: public awareness and post-treatment care. Many young males that notice something wrong do not seek immediate medical attention due to a lack of education regarding the signs and symptoms of testicular cancer, as well as the embarrassing stigma of this disease. As in all cancer cases, finding and treating this disease early is crucial. Although this group has a high survival rate (bordering on 95%), the goal of early detection is to minimize exposure to harmful treatments and promote survival of all patients. Through the work of The Canadian Testicular Cancer Association, increasing awareness is being addressed in Canada. The goals of this Ontario-based organization are to make people aware of the early warning signs of testicular cancer and to encourage males that suspect something is wrong to seek medical attention. A recent campaign designed to combat these issues occurred last January. ‘Manuary’ is a month-long nationwide awareness campaign, with events occurring throughout the month. The second underrepresented area of support for testicular cancer patients is in post-treatment care. As can be said for many young adult cancers, when patients are diagnosed, their lives are in a stage of transition. This fast-paced transitionary phase can be abruptly stalled with administration of treatment, creating a gap between a patient's pre-cancer life and where they have been left. Many young testicular cancer patients have trouble coping with this issue, creating feelings of isolation and depression. From a patient's stand point, there is a significant lack of support from the health care system in helping them deal with these issues. By creating support groups and making them nationally or even internationally available, the goal is to empower patients to see that they are not alone and develop strategies to overcome these emotions. Through connections within The Canadian Testicular Cancer Association, one-on-one patient interactions have been established. Mr. Buckland's goal is to make these resources easily accessible to all testicular cancer patients in any support group. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-64. doi:10.1158/1538-7445.AM2011-LB-64
SAT0082 Physical Activity and Rheumatoid Arthritis: Results from QUEST-RA Moroccan Study
Authors: S. El Kabbaj, H. rkain, I. Benslama, T. lakhdar, F. Znat, L. Benbrahim, B. Benchekroun, F. Allali, N. Hajjaj-Hassouni
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Regular physical activity is associated with decreased morbidity and mortality. Traditionally, patients with rheumatoid arthritis (RA) have been advised to limit physical exercise. <h3>Objectives</h3> to Assess the impact of rheumatoid arthritis on physical activity. <h3>Methods</h3> The Questionnaires in Standard Monitoring of Patients with Rheumatoid Arthritis (QUEST-RA) is a cross-sectional study that includes a self-report questionnaire and clinical assessment of non selected consecutive outpatients with RA who are receiving usual clinical care. Frequency of physical exercise (&gt;or=30 minutes with at least some shortness of breath, sweating) is queried with 4 response options: &gt;or=3 times weekly, 1-2 times weekly, 1-2 times monthly, and no exercise. <h3>Results</h3> The total of 1129 patients were enrolled: 87,3% were women, the mean age was 48 years, and the mean disease duration was 6 years. Only 2,8% of all patients reported physical exercise&gt;or=3 times weekly. The majority of the patients were physically inactive with no regular weekly exercise: &gt;80. Physical inactivity was associated with disease duration, higher levels of disease activity, pain, morning stiffness and fatigue. <h3>Conclusions</h3> This study provided the evidence that the physical inactivity rates remain high among people with RA during this millennium. The rheumatologist should motivate patients to increase physical activity levels. <h3>Disclosure of Interest</h3> None Declared
Varicella zoster gastritis in an immunocompetent adult woman
Authors: D. Kim, W. Moon, C. Lim
Journal: Endoscopy (2012)

A 42-year-old Korean woman presented to the emergency room with severe epigastric pain and anorexia lasting for 7 days. She had developed a papulovesicular skin rash that began on the trunk and then spread to the face and limbs, accompanied by 3 days of fever and myalgia, 7 days prior to presentation. The woman had been diagnosed with chickenpox and treated with intravenous acyclovir (started on the first day of skin eruption) for 7 days at an outside clinic. Her medical history was not significant for immune abnormalities, disruption of mucosal integrity, or immunosuppressant medication, including non-steroidal anti-inflammatory drugs. Her vital signs were stable and an abdominal and chest examination normal except for the generalized papular rash that had crusted over ([Fig. 1]). Laboratory tests and a simple abdominal X-ray were normal. Upper gastrointestinal endoscopy revealed multiple round to oval discrete or confluent erosive lesions, approximately 0.3 – 0.8 cm in size, with slightly raised erythematous margins, involving the whole antrum, the lesser curvature side of the mid-body, and the fundus ([Fig. 2]). A rapid urease test for Helicobacter pylori was negative.