tbuckley/cabot-search huggingface dataset:
SAT0152 Body mass index negatively influences the response to infliximab in rheumatoid arthritis
Authors: S. Ottaviani, A. Gardette, E. Quintin, K. Dawidowicz, E. Palazzo, G. Hayem, O. Meyer, P. Dieudé
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The excess of adipose tissue in obese individuals may have immunomodulating properties and pharmacokinetics consequences. Adipose tissue is potentially involved in the regulation of inflammation in rheumatoid arthritis (RA). Recently, an exploratory study suggested that body mass index (BMI) could affect infliximab (IFX) treatment responses in RA patients (1). <h3>Objectives</h3> The aim of this study was to investigate whether body mass index (BMI) affects the response to IFX in RA patients. <h3>Methods</h3> In this retrospective study were included RA patients fulfilling the ACR 1987 criteria and receiving infliximab therapy. All individuals provided informed written consent as approved by the local ethic committee board. The BMI was assessed before the initiation of IFX treatment (3 mg/kg intravenously). After 6 months of treatment, changes in disease activity (DAS28) were assessed. The primary end point was the EULAR DAS28 response. The following covariates were included for the analysis: gender, anti-CCP antibodies and RF status, mean disease duration, erythrocyte sedimentation rate (ESR), CRP level, DAS28, concomitant DMARDS therapy and corticosteroids consummation. <h3>Results</h3> A total of 73 RA patients (age: 48.5±10.5 years, 82% of females, disease duration: 8.8±6.9 years, 77% RF+, 86% anti-CCP +) were included. At M0, BMI was 27.1±6.9 kg/m<sup>2</sup>. Patients were classified in 3 distinct groups according to their BMI: normal (BMI &lt;25 kg/m<sup>2</sup>), overweight (BMI [25-30] kg/m<sup>2</sup>) and obesity (BMI &gt;30 kg/m<sup>2</sup>). At baseline no difference was observed between the 3 BMI subgroups according to the RA covariates, notably the DAS28. The EULAR non-response was found to be only influenced by 2 independent factors: a lower initial DAS28 (4.9±1.4 <i>vs</i> 5.9±1.0, <i>P</i>=0,012) and a higher BMI (29.5±8.7 vs 25.2±3.9 kg/m<sup>2</sup>, <i>P</i>=0.013). When the 3 BMI subgroups were independently analyzed, the negative influence of BMI on response to IFX was only found in obese patients (<i>P</i>=0.008, OR 5.2 [1.3-23.2]) in comparison to normal BMI group. <h3>Conclusions</h3> Our study supports the previously reported negative correlation between BMI and infliximab response in RA. Further prospective studies, including assessment of the fat mass, pharmacokinetics and adipokines dosages are mandatory to elucidate the role of obesity and the fat mass in modulating the RA IFX response. <h3>References</h3> Klaasen R, Wijbrandts CA, Gerlag DM, Tak PP. Body mass index and clinical response to infliximab in rheumatoid arthritis. Arthritis Rheum 2011. <h3>Disclosure of Interest</h3> None Declared
RECENT TRENDS IN HOSPITALIZATION FOR CORONARY ARTERY DISSECTION (NATIONWIDE INPATIENT SAMPLE, 2007-2012)
Authors: Sagar Mallikethi Lepakshi Reddy, Alexandros Briasoulis, Robert Brook, Luis Afonso, Shaun Cardozo, Melvyn Rubenfire, Cindy Grines
Journal: Journal of the American College of Cardiology (2016)
Is It Bad to Be Blue?
Authors: Ernst R. Jaffé
Journal: New England Journal of Medicine (1969)

Man is endowed with erythrocytes to contain the hemoglobin essential for the transportation of oxygen from the lungs to the tissues. This vital task requires that the iron of the heme moiety be in the ferrous state to permit reversible binding of molecular oxygen. The intracellular environment of hemoglobin is such that some oxidation from the ferrous (hemoglobin) to the ferric (methemoglobin) state might be expected, although the extent to which this really occurs during the 120-day life of the human erythrocyte is still unknown. Metabolic processes are normally active in this relatively disadvantaged, anucleate cell to protect hemoglobin against . . .
Abstract 3616: Androgen deprivation therapy and second primary lung cancer risk in prostate cancer patients in the US Veterans.
Authors: Hyunseok Kang, Rathi N. Pillai, Johann C. Brandes
Journal: Cancer Research (2013)

Abstract Background Previous observational studies have consistently reported decreased risk of lung cancers among prostate cancer patients. Recent literature suggests a role of estrogen receptor (ER) beta and aromatase, which can convert testosterone to estrogen, in development and progression of non small cell lung cancers. Second primary lung cancer risk among breast cancer patients appears to be higher in ER negative patients compared to ER positive patients probably from estrogen receptor blockade. As androgen deprivation therapy (ADT) has been well established for more than 70 years as an effective treatment modality for prostate cancer, we hypothesized the hormone modulation may decrease lung cancer risk and investigated the effect of ADT on second primary lung cancer risk among patients with prostate cancer. Methods We identified 62,589 men in VA Central Cancer Registry (VACCR) who were diagnosed with prostate cancer between 1999 and 2008, with follow-up available through 2010. The primary outcome was development of lung cancer, determined by VACCR. Descriptive statistics were used to compare basic characteristics between the groups. Cox proportional hazards model was used to assess the influence of ADT on the lung cancer incidence, adjusted for patient characteristics and prostate cancer stage. All the statistical analyses were performed using STATA 10 (Stata Corp, College Station, TX). Results Men who had ADT as part of their treatment for prostate cancer tend to be older (median age 71.3 vs 65.7, p &amp;lt; 0.01) and smoke slightly more (72.5% vs 71.4%, p=0.02). As expected, ADT group tend to have higher stage prostate cancers. There were 766 secondary lung cancers diagnosed in the cohort for the follow-up period. ADT group had significantly decreased secondary lung cancer risk by approximately 20% (HR 0.83, 95%CI=0.70-0.97) when adjusted for age, smoking status and prostate cancer stage at presentation. Conclusion Our study suggests that ADT in prostate cancer patients is associated with a decreased risk of second primary lung cancers. Independent validation studies and subgroup analyses to clarify the association is warranted. This work was supported by Veteran's Health Administration 1IK2BX001283-01 and NCI 5P50CA128613-02. Citation Format: Hyunseok Kang, Rathi N. Pillai, Johann C. Brandes. Androgen deprivation therapy and second primary lung cancer risk in prostate cancer patients in the US Veterans. [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 3616. doi:10.1158/1538-7445.AM2013-3616
IMPACT OF DEVICE LANDING ZONE CALCIFICATION ON PARAVALVULAR AORTIC REGURGITATION AFTER TRANSCATHETER AORTIC VALVE REPLACEMENT: A REAL-TIME THREE-DIMENSIONAL TRANSESOPHAGEAL ECHOCARDIOGRAPHY STUDY
Authors: Hirotsugu Mihara, Kentaro Shibayama, Kenji Harada, Javier Berdejo, Yuji Itabashi, Robert Siegel, Hasan Jilaihawi, Raj Makkar, Takahiro Shiota
Journal: Journal of the American College of Cardiology (2014)
Abstract 5289: HO-3867 inhibits cell migration, invasion and tumor growth of ovarian cancer through alterations in fatty acid synthase (FASN) and focal adhesion kinase (FAK) signaling
Authors: Karuppaiyah Selvendiran, S. Ahmed, A. Dayton, A. Bratasz, ML. Kuppusamy, BK. Rivera, K. Hideg and P. Kuppusamy
Journal: Cancer Research (2010)

Abstract Fatty acid synthase (FAS) has been found to be overexpressed in a wide range of epithelial tumors, including ovarian cancer. Expression of FAS, the key enzyme in de novo synthesis of long-chain fatty acids, is normally low but increases in cancer. The increase of FAS levels regulates cell proliferation, apoptosis and migration in tumors. In tumor cells, the inhibition of FAS elicits cell cycle arrest and apoptosis, so it is considered a potential drug target for cancer therapy. A2780 and SKOV3 ovarian cancer cells were grown in vitro and exposed to culture media containing 10 μM of HO-3867 for a period of 12 or 24 hours. FAS protein level analysis and examination of proliferation and migration genes was performed by Western blotting. RT-PCR was used to examine mRNA levels. FAS activity levels were measured by spectrophotometry. FAS, Cyclin D1 and VEGF expression levels were analyzed in vivo using both Western blotting, RT-PCR and immunohistochemistry. We found that HO-3867 significantly inhibits the FAS activity levels in A2780 and SKOV3 ovarian cancer cells. FAS mRNA levels were significantly decreased in HO-3867-treated cells. Based upon these results, we investigated how HO-3867 inhibits FAS expression and activity in ovarian cancer cells. We found that FAS-regulating genes such as SREBP1 &amp; 2 and pHER1 were clearly inhibited by HO-3867 exposure. Collectively, our results indicate that HO-3867 inhibition of FAS leads to inhibition of the cell migration genes FAK, ERK1/2, c-Myc, upregulation of the proliferation-regulating genes p21, p27 and downregulation of cyclin D1, resulting in inhibition of ovarian cancer cell proliferation, migration and tumor growth. 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 5289.
SIGNIFICANT DOWN-STREAM ACTIVATION OF THE RHO A/ RHO KINASE INTRACELLULAR SIGNALING PATHWAY IN PATIENTS WITH TYPE 2 DIABETES AND HYPERTENSION
Authors: Jorge E. Jalil, Juan Valderas, Pedro Gallardo, Paul Mac Nab, Ivan Godoy, Luigi Gabrielli, Jacqueline Moya, Luis Farias, Ivonne Padilla, Samuel Cordova, Maria Paz Ocaranza
Journal: Journal of the American College of Cardiology (2016)
Abstract 1822: An integrated approach to identify clinically relevant long non-coding RNAs (lncRNAs) in cancer.
Authors: X. Shirley Liu
Journal: Cancer Research (2013)

Abstract Despite growing appreciation of the number and importance of long non-coding RNAs (lncRNAs) in normal physiology and diseases, the knowledge on cancer-related lncRNAs is still limited. We utilized probes from array-based expression profiles that are uniquely mapped to annotated lncRNAs to investigate the expression of 10,207 lncRNAs in about 1,300 tumor samples over four different cancer types. By integrating the expression profiles of these lncRNAs with clinical outcome and somatic copy number alterations (SCNA), we identified lncRNAs that are associated with specific cancer subtypes and clinical prognosis, and predicted those that are potential drivers of cancer progression. We further validated our computational predictions by experimentally confirming the oncogenic functions of two novel lncRNAs in prostate cancer. Our results demonstrate that public genomic data contain a wealth of information on disease-relevant non-coding RNAs, and integrating orthogonal datasets and clinical information could facilitate the discovery of clinically relevant lncRNAs and help prioritize their functional studies. Citation Format: X. Shirley Liu. An integrated approach to identify clinically relevant long non-coding RNAs (lncRNAs) in cancer. [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 1822. doi:10.1158/1538-7445.AM2013-1822 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
A Trial of Artemether or Quinine in Children with Cerebral Malaria
Authors: Michaël Boele van Hensbroek, Emeka Onyiorah, Shabbar Jaffar, Gisela Schneider, Ayo Palmer, Joost Frenkel, Godwin Enwere, Sabine Forck, Anneliese Nusmeijer, Steve Bennett, Brian Greenwood, Dominic Kwiatkowski
Journal: New England Journal of Medicine (1996)

Cerebral malaria has a mortality rate of 10 to 30 percent despite treatment with parenteral quinine, a situation that may worsen with the spread of quinine resistance. Artemether is a new antimalarial agent that clears parasites from the circulation more rapidly than quinine, but its effect on mortality is unclear.
Abstract 4618: Effect of restoration of estrogen receptor-α (ER α) expression on drug sensitivities of gastric cancer cell lines
Authors: In Sook Woo, Kyung Ae Kim, Kyu Sang Lee, Jae Ho Byun, Chi Wha Han
Journal: Cancer Research (2010)

Abstract Introduction: The significance of expression of estrogen receptor-α (ER α) and hormone manipulation is not established in gastric cancer. Positivity of ER α expression in gastric cancer ranges from 0-67%. We previously reported that promoter methylation of ER α is associated with loss of ER α in gastric cancer cell lines. The aim of this study was to examine the changes in sensitivity to tamoxifen and 5-fluorouracil (5-FU) after induction of ER α by the DNA methyltransferase-1(DNMT1) inhibitor 5′-aza-deoxycytidine (AZA) and the histone deacetylase (HDAC) inhibitor trichostatin A (TSA), following gene transfection of ER α into gastric cancer cell lines. Methods: ER α-negative gastric cancer cell lines including SNU-484, −638, and −71 were treated with AZA (10 μmol/L) and TSA (500 nmol/L). An ER α-encoding plasmid was transfected into an ER α-negative breast cancer cell line, MDA-MB-231, and gastric cancer cell lines. Cell proliferation was assayed in ER α-negative and -restored cell lines treated with tamoxifen (0, 1, 2.5, 5, 10, 15, 20, and 25 μM) or 5-FU (0, 0.02, 0.2, 2, 20, 200, and 1,000 μM). Results: Restoration of ER α expression in ER α-negative gastric cancer cell lines after treatment with AZA and TSA was confirmed by RT-PCR. Growth inhibition was more prominent in gastric cancer cell lines transfected with the ER α gene (with tamoxifen at a concentration of more than 15 μM) or treated with trichostatin (with tamoxifen at a concentration of more than 20 μM) than in ER α-negative gastric cancer cell lines. No differences in sensitivity to 5-FU were observed regardless of whether ER α was present or absent. Conclusion: The DNMT inhibitor AZA and the HDAC inhibitor TSA, together with tamoxifen, deserve further investigation as new targeted therapies in ER α-negative gastric cancers. 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 4618.
OP0018 Epigenetic Study of Advanced Ankylosis in Patients with Ankylosing Spondylitis
Authors: D.D. O'Rielly, Y. Zhang, N. Al-Ghanim, R. Ardern, A. Munn, S. Hamilton, R. Bricknell, G. Zhai, P. Rahman
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Ankylosing spondylitis (AS) is an inflammatory spinal disease characterized by ankylosis of the spine. A subset of patients develops significant ankylosis resulting in mobility issues. <h3>Objectives</h3> To determine if epigenetic modifications may account for differences in the degree of ankylosis of the axial spine in ankylosing spondylitis. <h3>Methods</h3> AS patients satisfying the New York criteria with advanced ankylosing (characterized clinically with spinal flexion) and radiographically with at least 4 continuous ankylosed vertebrae were categorized as advanced ankylosis. Control AS patients had normal posture on clinical evaluation and had absence of syndesmophytes on plain radiographs. All patients were Caucasians of Northern European Ancestry. Genome-wide DNA methylation profiling was performed on the blood DNA samples from 23 AS patients with advanced ankylosis and 25 patients with no syndesmophytes. The profiling was performed using Illumina HumanMethylation450k Beadchip, which measures up ∼480,000 different CpG sites per sample and covers 96% of RefSeq genes. The methylation level at each CpG site was measured by β values varying from 0 (no methylation) to 1 (100% methylation). <h3>Results</h3> Advanced ankylosis patients were predominantly males (22/23), with mean of disease onset at age 21.9 years and age at time of assessment was 43.72. Meanwhile, AS patients with no syndesmophytes were also predominantly males (24/25), with mean of disease onset at age 24.6 years and age at time of assessment was 44.1 years. Methylation data were normalized using BMIQ method and no batch effects were detected by PCA analysis. Methylation analysis was performed on 382,232 autosomal CpG sites after quality controls. One outlier was identified and excluded in the subsequent analysis. Analysis revealed 100 locations where there was a difference between patients with and without spinal ankylosis. The three locations that differentiated the most included CPG sites in <i>KIAA0319</i> (hypomethylated) (p=1.7×10<sup>-5</sup>); <i>JAKMIP3</i> (p=6.4×10<sup>-5</sup>) and <i>LYG2</i> (p=9.6×10<sup>-4</sup>). Based on functional relevance to AS pathogenesis, particularly antigen presentation, cytokine signalling, and bone remodeling, 5 candidate genes (4 hypomethylated; 1 hypermethylated) emerged: <i>IL18RAP</i> (beta diff=-0.1473; p=0.01), <i>SMAD3</i> (beta diff=-0.16664; p=0.047), <i>MCF2L</i> (beta diff=-0.10894; p=0.009), <i>DDAH2</i> (beta diff=0.11494; p=0.007), and <i>NLRC5</i> (beta diff=-0.11542; p=0.052). <h3>Conclusions</h3> These preliminary results demonstrate that the global DNA methylation pattern in advanced ankylosis differs from AS patients with no spinal damage. High priority candidate genes identified in this study warrants further validation. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3270
Metabolic Phenotype of Stage IV Lung Adenocarcinoma
Authors: Elaine Yuen Phin Lee, Pek-Lan Khong, Victor Ho Fun Lee, Wenshu Qian, Xue Yu, Maria Pik Wong
Journal: Clinical Nuclear Medicine (2015)

Epidermal growth factor receptor (EGFR) mutation status is important in treatment stratification of stage IV lung adenocarcinoma. We evaluated the relationship between the SUV max measured on PET/CT and EGFR mutations and the value of SUV max in predicting EGFR mutations.Seventy-one stage IV lung adenocarcinoma patients with verified EGFR mutations (48 EGFR mutant, 23 EGFR wild-type) having pretreatment PET/CT were retrospectively reviewed. SUV max values of the primary tumors (n = 71), nodal (n = 246), and distant metastases (n = 618) were compared between EGFR-mutant and EGFR wild-type adenocarcinoma by Mann-Whitney U test. The receiver operating characteristics curve and logistic regression were performed for factors, SUV max, age, sex, and smoking status. The significant predictors were assessed individually and in combination in discriminating EGFR mutation status. Statistical significance was assumed at P < 0.05 RESULTS: The metastases in EGFR-mutant adenocarcinoma had lower SUV max than EGFR wild-type adenocarcinoma (nodal SUV max 3.4 vs 5.5, distant metastasis SUV max 3.4 vs 4.7, respectively; both P < 0.001). No statistical significant difference was observed in the primary tumors SUV max between the 2 groups (SUV max 7.4 vs 8.1, P = 0.311). A receiver operating characteristics-derived SUV max less than or equal to 7.2 in metastasis could separate EGFR-mutant from EGFR wild-type adenocarcinoma (area under the curve, 0.71-0.74; P < 0.05). SUV max was a significant independent predictor, and when combined with age, sex, and smoking status, it is highly predictive of EGFR mutation status (area under the curve, 0.90).Low SUV max in the metastasis favors the presence of EGFR mutations in stage IV lung adenocarcinoma, and SUV max is an independent predictor of EGFR mutations.
TREATMENT OF SLEEP DISORDERED BREATHING IN PATIENTS ADMITTED FOR DECOMPENSATED HEART FAILURE REDUCES 6 MONTHS HOSPITAL VISITS
Authors: Sunil Sharma, Ankit Gupta, Sharon Rubin, Gordon Reeves, Raphael Bonita, Robert Tavella, Leslee Willes, Paul Mather
Journal: Journal of the American College of Cardiology (2015)
Apport du scanner multi-détecteurs dans la prise en charge des hémorragies digestives basses aiguës
Authors: L Milot, O Monneuse, JA Chayvialle, PJ Valette, F Pilleul
Journal: Endoscopy (2007)

Evaluer le scanner multi-détecteurs comparativement à la chirurgie, et à l'endoscopie dans le diagnostic et la prise en charge des hémorragies digestives basses aiguës.
CIANOACRILATO EN SPRAY COMO ALTERNATIVA DE TRATAMIENTO EN LAS HEMORRAGIAS DIGESTIVAS DE DIFÍCIL CONTROL
Authors: A Rincón, JM Alcívar, R León, T López, S Sobrino, JA Caballero, TI Arambula
Journal: Endoscopy (2014)

Introducción: La terapia endoscópica convencional es altamente efectiva para el control de la hemorragia gastrointestinal, sin embargo en ocasiones el sangrado es persistente a pesar de un tratamiento óptimo, requiriendo intervencionismo radiológico o quirúrgico. El instilación endoscópica de cianoacrilato de forma directa como alternativa de tratamiento tiene una experiencia limitada.
Abstract 910: High dietary fat promotes inflammation and intestinal neoplasia, independently of diet-induced obesity, in B6.ApcMin/+ congenic-consomic mouse strains
Authors: Stephanie K. Doerner, Elaine S. Leung, Nathan A. Berger, Joseph H. Nadeau
Journal: Cancer Research (2011)

Abstract Obesity and high fat (HF) diet are associated with increased risk of colon cancer. However, assessing their independent contributions to intestinal carcinogenesis is difficult due to their close association in humans. We utilized Chromosome Substitution Strains (CSSs) in combination with the B6.ApcMin/+ mouse model of intestinal cancer to generate Congenic-Consomic Strains (C-CSs). Using C-CSs, we tested whether a HF diet promotes the development of intestinal cancer, independent of obesity, and found that dietary fats are strong and independent determinants of polyp formation. CSSs, which have contrasting responses to a HF diet, were used to construct C-CSs that were susceptible to intestinal cancer, but were either resistant or susceptible to diet-induced obesity, depending on the substituted A/J chromosome. A2.ApcMin/+ (obese), A7.ApcMin/+ (lean), and A17.ApcMin/+ (lean) mouse strains were maintained on diets high or low in coconut oil (HFCoco and LFCoco, respectively). If obesity is crucial in polyp formation, all obese strains should develop more polyps than the lean strains. In contrast, if diet is important, we expected to find an increase in polyp number in all strains fed the HFCoco diet, independent of their susceptibility to diet-induced obesity. Polyp numbers were significantly increased in all strains after 60 days exposure to the HFCoco diet, regardless of obese or lean status, suggesting that a HF diet promotes polyp development. Polyp numbers were also significantly higher in B6.ApcMin/+ after similar exposure to a high fat corn oil (HFCorn) diet. We measured levels of circulating inflammatory factors and showed that adiponectin is decreased and leptin, interleukin (IL)-1beta and IL-6 are increased in B6.ApcMin/+ fed either of the HF diets compared to mice fed the corresponding LF control diets, implicating a role of inflammation in diet-induced intestinal neoplasia. With the novel C-CS systems, we were able to elucidate complex diet-gene interactions involved in intestinal carcinogenesis and provide evidence for a crucial role of a HF diet in the development of intestinal polyps. These dietary studies have implications for both prevention and non-invasive treatment of intestinal cancer. 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 910. doi:10.1158/1538-7445.AM2011-910
IMPACT OF HCV INFECTION ON DEVELOPMENT OF CARDIO-METABOLIC DISORDERS AND MAJOR ADVERSE CARDIAC EVENTS IN A POPULATION-BASED COHORT OF HIV-INFECTED AND NON-HIV-INFECTED ADULTS
Authors: Avnish Tripathi, Jeanette M. Jerrell, Arti Saraswat, Abdur Khan, Glenn Hirsch, Jawahar Mehta
Journal: Journal of the American College of Cardiology (2016)