tbuckley/cabot-search huggingface dataset:
AB0346 Investigation of alexithymia in patients affected by rheumatoid and psoriatic arthritis: cross-sectional observation
Authors: G.L. Fonti, M.S. Chimenti, P. Conigliaro, J. Hitaj, M. Galluzzo, M. Talamonti, B. Kroegler, E. Greco, R. Perricone
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Rheumatoid arthritis (RA) and Psoriatic arthritis (PsA) are chronic inflammatory diseases that lead to an overthrow of articular structure, functional limitation and disability. Alexithymia is a personality trait characterised by deficits in cognitive processing and regulation of emotions. A broad association between alexithymia and symptoms as depression, inflammation and pain has been demonstrated. <h3>Objectives</h3> to evaluate the prevalence of alexithymia in patients affected by Rheumatoid and Psoriatic arthritis. <h3>Methods</h3> We prospectively enrolled, from January to December 2017, patients affected by RA diagnosed according to the ACR revised criteria and PsA diagnosed according to the CASPAR criteria referred to the out-patients clinic of the Rheumatology Unit of Policlinico Tor Vergata, Rome. The 20-item Toronto Alexithymia Scale (TAS-20) was used to assess alexithymia. Disease activity, function and quality of life, clinimetric tests as well as ESR and CRP were assessed. Statistical comparisons were performed using Pearson's Coefficient of Skewness, the unpaired t-Test and Mann-Whitney test. <h3>Results</h3> A total of 50 RA patients and 51 PsA patients were enrolled (table 1). The TAS-20 score showed that 38.6% (39/101) of patients had alexithymia, 26.7% (27/101) patients were in the borderline of alexithymia and 34.7% (35/101) patients had not alexithymia. A statistical significant association was observed between alexithymia and inflammatory indeces (ESR: p=0.029, CRP: p=0.043, figure 1 and 2) and also between alexithymia and clinimetrics parameters (ptVAS, pVAS, GH, p&lt;0.0001 for all comparisons). No correlations were observed between alexithymia and disease duration, gender, therapies with bDMARDs. A significant trend has been demonstrated between alexithymia and corticosteroidal therapy <h3>Conclusions</h3> This study suggests that alexithymia assessment should be a part of the comprehensive care of patients with RA and PsA. We are in the process of extending this investigation on a larger sample population to improve our investigation field and to consolidate our dates. <h3>Disclosure of Interest</h3> None declared
Abrupt Deflation after Sustained Inflation Causes Lung Injury
Authors: Bhushan H. Katira, Doreen Engelberts, Gail Otulakowski, Regan E. Giesinger, Takeshi Yoshida, Martin Post, Wolfgang M. Kuebler, Kim A. Connelly, Brian P. Kavanagh
Journal: American Journal of Respiratory and Critical Care Medicine (2018)

Ventilator management in acute respiratory distress syndrome usually focuses on setting parameters, but events occurring at ventilator disconnection are not well understood.To determine if abrupt deflation after sustained inflation causes lung injury.Male Sprague-Dawley rats were ventilated (low Vt, 6 ml/kg) and randomized to control (n = 6; positive end-expiratory pressure [PEEP], 3 cm H2O; 100 min) or intervention (n = 6; PEEP, 3-11 cm H2O over 70 min; abrupt deflation to zero PEEP; ventilation for 30 min). Lung function and injury was assessed, scanning electron microscopy performed, and microvascular leak timed by Evans blue dye (n = 4/group at 0, 2, 5, 10, and 20 min after deflation). Hemodynamic assessment included systemic arterial pressure (n = 6), echocardiography (n = 4), and right (n = 6) and left ventricular pressures (n = 6).Abrupt deflation after sustained inflation (vs. control) caused acute lung dysfunction (compliance 0.48 ± 1.0 vs. 0.82 ± 0.2 m/cm H2O, oxygen saturation as measured by pulse oximetry 67 ± 23.5 vs. 91 ± 4.4%; P < 0.05) and injury (wet/dry ratio 6.1 ± 0.6 vs. 4.6 ± 0.4; P < 0.01). Vascular leak was absent before deflation and maximal 5-10 minutes thereafter; injury was predominantly endothelial. At deflation, left ventricular preload, systemic blood pressure, and left ventricular end-diastolic pressure increased precipitously in proportion to the degree of injury. Injury caused later right ventricular failure. Sodium nitroprusside prevented the increase in systemic blood pressure and left ventricular end-diastolic pressure associated with deflation, and prevented injury. Injury did not occur with gradual deflation.Abrupt deflation after sustained inflation can cause acute lung injury. It seems to be mediated by acute left ventricular decompensation (caused by increased left ventricular preload and afterload) that elevates pulmonary microvascular pressure; this directly injures the endothelium and causes edema, which is potentiated by the surge in pulmonary perfusion.
Accidental food allergy reactions: Products and undeclared ingredients
Authors: W. Marty Blom, Anouska D. Michelsen-Huisman, Harmieke van Os-Medendorp, Gert van Duijn, Mary-lène de Zeeuw-Brouwer, Astrid Versluis, Jacqueline J.M. Castenmiller, Hubert P.J.M. Noteborn, Astrid G. Kruizinga, André C. Knulst, Geert F. Houben
Journal: Journal of Allergy and Clinical Immunology (2018)
SAT0291 Creation of a european database of patients with axial spondyloarthritis treated in clinical practice– initial, preliminary findings from the eurospa research network collaboration
Authors: L.M. Ørnbjerg, M. Østergaard, F. Onen, G. Can, Z. Rotar, M. Tomsic, B. Gudbjornsson, A.J. Geirsson, M.J. Santos, A. Barcelos, D. Nordström, K. Aaltonen, M.J. Nissen, A. Ciurea, E.K. Kristianslund, T. Kvien, C. Codreanu, E.-M. Hauge, L. Jacobsson, H. Mann, G. Jones, F. Iannone, M.V. Hernandez, I. van der Horst-Bruinsma, L.H. Hyldstrup, N.S. Krogh, M.L. Hetland
Journal: Annals of the Rheumatic Diseases (2018)

PCS (24.9 vs. 24.7, p=0.210) and p=0.532) scores at 12 months.During follow-up, 7.4% of ADA patients initiated another biologic and 23.7% of patients in the nbDMARD group initiated biologic treatment (p<0.001).Conclusions: AS patients initiating ADA in Canadian routine clinical care have significantly greater disease severity and impaired quality of life at baseline compared with those initiating non-biologic treatment.Treatment with ADA for 12 months resulted in greater reduction in the prevalence of EAMs and a greater reduction in disease severity scores compared to treatment with non-biologic agents.
Abstract 18620: Who Performs Endovascular Aortic Aneurysm Repair?
Authors: Adam Tanious, Nirmani Karunathilake, Joel Toro, Afif Abu-Hanna, Timothy J Fawcett, Brian Graves, Peter R Nelson
Journal: Circulation (2016)

Introduction: Endovascular aortic aneurysm repair (EVAR) technology has realized significant advances, making it more readily available to a wider array of practitioners. We analyzed a statewide ad...
PTH-044 Improving safety and reducing error in endoscopy (ISREE) – a jag initiative
Authors: Siwan Thomas-Gibson, Manmeet Matharoo, Keith Siau, Nick Sevdalis, Neil Hawkes, Debbie Johnston, Adam Haycock, John Green
Journal: Endoscopy (2018)

<h3>Introduction</h3> JAG is committed to providing universal high quality and safe endoscopy as embedded in the Global Rating Scale. This requires acknowledgement that error is common, may not result in harm or complications, but that addressing latent risk can prevent patient safety incidents. Many errors relate to failures in human factors, ENTS and teamwork, which require training and assessment. Medical error is more prevalent in situations of complexity. Though generally safe, endoscopy is a complex task, performed in teams. As population demographics evolve, straight-to-test pathways become embedded and complex therapeutic options extended; endoscopists need to develop a proactive culture towards safety and learning from error. <h3>Aims</h3> JAG aims to develop a work stream to Improve Safety and Reduce Error in Endoscopy (ISREE). A 1 day workshop was designed to develop an implementation plan to achieve this goal. <h3>Methods</h3> 35 multi-disciplinary clinicians and a patient with specific expertise in this area were invited to ISREE workshop. Participants were asked to recall as many endoscopy adverse events or errors as possible. Key presentations highlighted the background to medical error, how to investigate it, development of non-technical skills frameworks (anaesthetics and endoscopy), safe sedation, human factors training and implementation science. A patient recounted her experiences of endoscopy. Facilitated group sessions focused on 5 key areas – improving training in ENTS and human factors, error prevention, reporting error, learning from error and managing underperformance (endoscopists, teams or units). Wider discussion synthesised a list of feasible actions that JAG could prioritise for staged implementation. <h3>Results</h3> Multiple errors were reported by all delegates and recurrent themes were common. Examples related to wrong patient for procedure (n=4), histology mislabelling (n=5), drug errors (n=3) and failure to follow MDT advice (n=1). 23 key priorities were agreed and formulate an implementation strategy for JAG (table 1): <h3>Summary</h3> JAG plans to develop a 5 y ISREE Implementation Strategy reflecting the identified priorities to 1) improve endoscopists training in effective error reporting and learning and 2) implement system level approaches to safety and performance improvement. JAG also aims to improve its communication to disseminate learning and support endoscopy services in the UK.
FRI0362 Prevalence, risk factors, and impact on mortality of neuropsychiatric lupus: a large prospective single-centre study
Authors: G.Y. Ahn, D. Kim, S. Won, S.T. Song, H.-J. Jeong, I.W. Sohn, S. Lee, Y.B. Joo, S.-C. Bae
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Neuropsychiatric involvement is one of the most serious involvement of SLE and generally associated with a worse prognosis. However, previous reports about the prevalence and risk factors of neuropsychiatric systemic lupuc erythematosus (NPSLE) have yielded inconsistent findings. Also, there are only few studies of the prognosis of NPSLE, especially in a large prospective cohort. <h3>Objectives</h3> To identify the prevalence, risk profiles, and impact on mortality of NPSLE. <h3>Methods</h3> Patients from the Hanyang BAE lupus cohort were registered and followed from 1998 to 2015. Demographics, autoantibodies, SLEDAI-2K and SLICC/ACR damage index were collected at baseline and then annually. Patients registered within 12 months of SLE development were grouped as the inception cohort and analysed separately to elucidate the clinical features at disease onset. NP manifestations were defined using the ACR 19 case definitions and Ainiala NPSLE that did not include minor NP events<sup>1</sup>. Mortality data were derived by linking data from the Korean National Statistics Office. <h3>Results</h3> The prevalence of NPSLE by ACR 19 case definition was 38.3%, and 19.3% by Ainiala criteria. Higher SLEDAI, APLA positivity, absence of anti-dsDNA antibody at SLE diagnosis and fewer years of education incresed NPSLE risk. Patients with any NPSLE manifestation had a three-fold increased risk of mortality (HR 3.09, p=0.04), and patients with focal CNS NPSLE showed nearly an eight-fold increased risk of mortality in SLE patients (HR=7.83, p&lt;0.01). Among the 216 patients with Ainiala NPSLE, sixty-four (29.6%) had multiple events. The two most common symptom combinations were seizure with CVA (18 patients) and seizure with psychosis (8 patients). <h3>Conclusions</h3> Higher SLEDAI, APLA positivity, absence of anti-dsDNA antibody at SLE diagnosis and fewer years of education are risk factors for development of NPSLE. Presence of NPSLE, especially focal CNS NPSLE, increased the risk of mortality in SLE patients. <h3>Reference</h3> [1] Ainiala H, Hietaharju A, Loukkola J, et al. Validity of the new American College of Rheumatology criteria for neuropsychiatric lupus syndromes: a population-based evaluation. Arthritis Rheum. 2001;45:419–423. <h3>Disclosure of Interest</h3> None declared
Cross Talk Between Autophagy and Apoptosis Contributes to ZnO Nanoparticle‐Induced Human Osteosarcoma Cell Death
Authors: Guanping He, Yunlong Ma, Ye Zhu, Lei Yong, Xiao Liu, Peng Wang, Chen Liang, Chenlong Yang, Zhigang Zhao, Bao Hai, Xiaoyu Pan, Zhongjun Liu, Xiaoguang Liu, Chuanbin Mao
Journal: Advanced Healthcare Materials (2018)

Killing osteosarcoma cells by zinc oxide nanoparticles (NPs) and its underlying subcellular mechanism are never studied. Here, it is found that the NPs induce cross talk between apoptosis and autophagy, which leads to osteosarcoma cell death. Specifically, the NP uptake promotes autophagy by inducing accumulation of autophagosomes along with impairment of lysosomal functions. The autophagy further causes the uptaken NPs to release zinc ions by promoting their dissolution. These intracellular zinc ions, together with those that are originally released from the extracellular NPs and flowed into the cells, collectively target and damage mitochondria to produce reactive oxygen species (ROS). Then the ROS inhibit cell proliferation by arresting S phase and trigger apoptosis by extrinsic and intrinsic pathways, ultimately leading to cell death. More importantly, suppression of the early stage autophagy restores cell viability by abolishing apoptosis whereas blockade of the late stage autophagy inversely enhances apoptosis. In contrast, inhibition of apoptosis shows a limited ability to restore cell viability but obviously enhance autophagy. Notably, cell viability is strongly ameliorated by the combination of inhibitors for both the late stage autophagy and the apoptosis. These findings provide a mechanistic understanding of the NP-directed autophagy and apoptosis in osteosarcoma cells.
Stem Cell Implants for Age-Related Macular Degeneration
Authors: Jennifer Abbasi
Journal: JAMA (2018)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
血浆中25-羟基维生素D水平偏高,且罹患非黑色素瘤皮肤癌的风险较高:97,849名受试者参加的一项孟德尔随机化研究
Authors: U.C. Winsløw, B.G. Nordestgaard, S. Afzal
Journal: British Journal of Dermatology (2018)

在本项在丹麦开展的研究中,我们就维生素D状态(通常通过血液样本中的25‐羟基维生素D来测量)与罹患非黑色素瘤皮肤癌(NMSC)是否相关开展了调查。先前的研究证明,要回答这一具体问题颇为困难。如果将所有人简单地分成两组,即25‐羟基维生素D测量值较高的人群,以及25‐羟基维生素D测量值较低的人群,我们会发现前者的NMSC发病率更高。但是,这项简单的观察很容易造成误解,例如阳光中的紫外线辐射会造成皮肤损伤,进而诱发皮肤癌,并且会诱导皮肤中维生素D的合成(即帮助人体生成维生素D)。平均而言,体内25‐羟基维生素D水平较高的人群接受的阳光和紫外线辐射可能也更多,罹患皮肤癌的风险更高。鉴于这个原因,如果我们仅依据根据原始数据得出的结论去探究25‐羟基维生素D和癌症之间的关联性,有可能会得出错误的结果。在本研究中,我们使用了一项名为孟德尔随机化研究的方法,该方法不易受到上述潜在错误的影响。我们发现,影响维生素D的基因变异体既不会增加也不会降低罹患皮肤癌的风险。本研究的意义在于,不应从表面看待25‐羟基维生素D和皮肤癌之间的关联性,需要开展针对其他类型癌症的类似研究.
Thoracic and cutaneous sarcoid-like reaction associated with anti-PD-1 therapy: longitudinal monitoring of PD-1 and PD-L1 expression after stopping treatment
Authors: Léa Paolini, Caroline Poli, Simon Blanchard, Thierry Urban, Anne Croué, Marie-Christine Rousselet, Sarah Le Roux, Nathalie Labarrière, Pascale Jeannin, José Hureaux
Journal: Journal for ImmunoTherapy of Cancer (2018)

<h3>Background</h3> Immune checkpoint inhibitors (ICI) target T cell inhibitory pathways that are responsible for cancer tolerance by down-modulating immune functions. ICI have revolutionized patients care with lung cancer. Nevertheless, restoring endogenous antitumor T-cell responses can induce immune related adverse events, such as sarcoidosis. <h3>Case presentation</h3> We report here the first case of a thoracic and cutaneous sarcoid-like reaction in a patient with a relapsing unresectable non-small cell lung cancer (NSCLC) treated with nivolumab, an anti-PD-1 mAb. The expression of PD-1 and its ligands, PD-L1 and PD-L2, was assessed by flow cytometry on peripheral blood mononuclear cells (PBMC) and compared to patients who had discontinued nivolumab therapy without having developed any immune related adverse events. PD-L1 expression was transiently increased on B cells, T cells and monocytes, whereas PD-L2 expression was not modulated. PD-1 was transiently undetectable when PD-L1 was maximal, before returning to basal level. Sarcoidosis spontaneously resolved, without corticotherapy. <h3>Conclusion</h3> This case sheds the light on a complex regulation of PD-L1 expression in vivo on PBMC after nivolumab arrest and triggers the question of monitoring the expression of immune checkpoint on immune cells during and after treatment with ICI.
Role of chemotherapy in improving survival in stage IV colon cancer patients without surgery: An NCDB analysis.
Authors: Lakshmi Manogna Chintalacheruvu, Avanija Buddam, Osama Diab, Peter T. Silberstein, Ryan W Walters
Journal: Journal of Clinical Oncology (2017)

e15058 Background: Approximately 20% of patients with colorectal cancer have metastases at the time of presentation. Use of systemic chemotherapy for stage IV colon cancer has greatly increased over past several years with newer advancements. With advancements in chemotherapy annual rate of Primary tumor resection dropped from 74.5 percent in 1988 to 57.4 percent in 2010 with improved survival rates. Methods: A total of 39,428 patients with stage IV colon cancer were analyzed from the national cancer data base (NCDB). Differences in demographic and clinical co-variates were compared using Fisher’s exact test, where as survival differences were estimated by the Kaplan-Meier method and associated log-rank test; p &lt; 0.05 indicated statistical significance. Results: The log-rank tests indicated statistically significant difference in survival (p &lt; 0.001), such that patients receiving chemotherapy survived significantly longer (median survival = 12.0 months, 95% CI = 11.8 to 12.2 months) compared to patients not receiving chemotherapy (median survival = 1.5 months, 95% CI = 1.5 to 1.5 months). Patients receiving chemotherapy were younger (63.2 +/- 13.2 vs 73.8 +/- 13.0 ) with lesser co morbidity when compared to people who did not receive chemotherapy. Conclusions: Patients receiving chemotherapy are considerably younger, with less co-morbidity, and they survive significantly longer. This study signifies the survival advantage with chemotherapy in Stage IV colon cancer patients who did not get any type of surgery. Further studies need to be establish to define the role of chemotherapy comparing to surgery in stage 4 colon cancer patients.
Anticoagulation and Antiplatelet Strategies After On-X Mechanical Aortic Valve Replacement
Authors: John D. Puskas, Marc Gerdisch, Dennis Nichols, Lilibeth Fermin, Birger Rhenman, Divya Kapoor, Jack Copeland, Reed Quinn, G. Chad Hughes, Hormoz Azar, Michael McGrath, Michael Wait, Bobby Kong, Tomas Martin, E. Charles Douville, Steven Meyer, Jian Ye, W.R. Eric Jamieson, Lance Landvater, Robert Hagberg, Timothy Trotter, John Armitage, Jeffrey Askew, Kevin Accola, Paul Levy, David Duncan, Bobby Yanagawa, John Ely, Allen Graeve, John Puskas, Marc Gerdisch, Dennis Nichols, Allen Graeve, Lilibeth Fermin, Birger Rhenman, Divya Kapoor, Jack Copeland, Reed Quinn, G. Chad Hughes, Hormoz Azar, Michael McGrath, Michael Wait, Bobby Kong, Tomas Martin, E. Charles Douville, Steven Meyer, W.R. Eric Jamieson, Jian Ye, Lance Landvater, Timothy Trotter, John Armitage, Jeffrey Askew, Kevin Accola, Paul Levy, David Duncan, Gulshan Sethi, Alfredo Razi, Robert Hagberg, Barron Hamman, Daniel Swistel, M. Fawaz Shoukfeh, Peter Tutuska, C.B. Sai-Sudhakar, Ralph Damiano, Gosta Pettersson, Matthew Campbell, Igor Gregoric, Duke Cameron, Ray Blackwell, Keith Allen
Journal: Journal of the American College of Cardiology (2018)
Mortality in interstitial lung disease: do race and skin colour matter?
Authors: Julie Morisset, Yolanda Mageto, Ganesh Raghu
Journal: European Respiratory Journal (2018)

In recent years, research surrounding health disparities has begun to focus more on the complex relationship between race, genetics and disease. Race has come to be recognised as an important factor, not only when discussing disparities and determining policy, but also in the diagnosis, approach and response to treatment. African-Americans with interstitial lung disease exhibit a unique clinical phenotype <http://ow.ly/NId830k4c0c>
Transcription factor AP-4 promotes tumorigenic capability and activates the Wnt/β-catenin pathway in hepatocellular carcinoma
Authors: Junwei Song, Chan Xie, Lili Jiang, Geyan Wu, Jinrong Zhu, Shuxia Zhang, Miaoling Tang, Libing Song, Jun Li
Journal: Theranostics (2018)

It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers. However, the precise mechanisms underlying the oncogenic role of TFAP4 remain largely unknown. Methods: TFAP4 expression levels in hepatocellular carcinoma (HCC) cells and tissues were detected by quantitative real-time PCR (qPCR) and immunohistochemistry (IHC). In vitro and in vivo assays were performed to investigate the oncogenic function of TFAP4 in the tumor-initiating cell (TIC)-like phenotype and the tumorigenic capability of HCC cells. Luciferase reporter and chromatin immunoprecipitation (ChIP)-qPCR assays were performed to determine the underlying mechanism of TFAP4-mediated HCC aggressiveness. Results: TFAP4 was markedly upregulated in human HCC, and was associated with significantly poorer overall and relapse-free survival in patients with HCC. Furthermore, we found that overexpression of TFAP4 significantly enhanced, whereas silencing TFAP4 inhibited, the tumor sphere formation ability and proportion of side-population cells in HCC cells in vitro, and ectopic TFAP4 enhanced the tumorigenicity of HCC cells in vivo. Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). Conclusions: Our results provide new insight into the mechanisms underlying hyperactivation of the Wnt/β-catenin pathway in HCC, as well the oncogenic ability of TFAP4 to enhance the tumor-forming ability of HCC cells.