tbuckley/cabot-search huggingface dataset:
Risk of Thyroxine-Treated Autoimmune Thyroid Disease Associated With Disease Onset in Patients With Rheumatoid Arthritis
Authors: Kristin Waldenlind, Saedis Saevarsdottir, Camilla Bengtsson, Johan Askling
Journal: JAMA Network Open (2018)

<h3>Importance</h3> Autoimmune thyroid disease ([AITD] including hypothyroidism and hyperthyroidism) is the most common organ-specific autoimmune disorder and is more prevalent among patients with rheumatoid arthritis (RA). Real-world studies on when and how this increased risk of AITD develops, in association with the time before or after the onset of RA, are lacking. <h3>Objective</h3> To estimate the risk of thyroxine-treated AITD among patients with RA at different time points before and after the diagnosis of RA. <h3>Design, Setting, and Participants</h3> A nationwide register-based case-control and cohort study was conducted between January 1, 2006, and June 30, 2013, with a maximum follow-up time of 7 years before and 8 years after diagnosis of RA. The study used the Swedish Rheumatology Quality Register and linkage to other nationwide registers to identify 8090 adults with new-onset RA and a random population-based sample of 80 782 referents matched by age, sex, and residential area. Statistical analysis was performed from July 1, 2015, to June 30, 2017. <h3>Exposures</h3> Presence of AITD in the participants in the case-control design and RA in the participants in the cohort design. <h3>Main Outcomes and Measures</h3> Prevalence and relative risk of incident AITD before (odds ratios) and after (hazard ratios) diagnosis of RA compared with the population as reference. <h3>Results</h3> There were 8090 patients with RA (5529 women and 2561 men; mean [SD] age, 58.3 [15.2] years) and 80 782 population-based participants as reference who were identified. By the time of diagnosis of RA, the prevalence of AITD was 10.3% among the patients with RA (n = 832) vs 7.1% among the controls (5725 of 80 350) (odds ratio, 1.5; 95% CI, 1.4-1.7). This increased risk of AITD developed during the 5 years (range, 2-5 years) before diagnosis of RA (odds ratio, 1.5; 95% CI, 1.2-1.8) and peaked by the time of diagnosis of RA (range, 0-3 months before diagnosis of RA) (odds ratio, 5.3; 95% CI, 3.7-7.6). From diagnosis of RA and onward, the risk of developing AITD decreased (range, 2-5 years after diagnosis of RA) (hazard ratio, 0.7; 95% CI, 0.5-1.0). <h3>Conclusions and Relevance</h3> Compared with the general population, Swedish patients with RA appear to have a higher prevalence of thyroxine-treated AITD at diagnosis of RA and an increased incidence of AITD during the 5-year period before diagnosis of RA. After diagnosis of RA, the risk of developing AITD is suggested to decrease below the expected rate. Besides temporal changes in diagnostic intensity, this pattern of risk raises the question whether AITD may influence the pathogenesis of RA (or vice versa) and, conversely, the question whether antirheumatic therapies may prevent AITD.
Abstract 15785: Long-term Cardiac Prognosis and Risk Stratification in 260 Adults Presenting With Mitochondrial Diseases
Authors: Karim Wahbi, Wulfran Bougouin, Henri Marc Bécane, Denis Duboc
Journal: Circulation (2015)

Introduction: The long-term cardiac prognosis of adults with mitochondrial diseases is unknown. Methods and Results: Between January 2000 and May 2014, we retrospectively included in this study 260 consecutive patients (60% women) ≥18 years of age, (interquartile range [IQR]; 31 to 54), with genetically proven mitochondrial diseases, including 109 with mitochondrial DNA (mtDNA) single large-scale deletions, 64 with the m.3243A&gt;G mutation in MT-TL1 , 51 with other mtDNA point mutations, and 36 patients with nuclear genes mutations. Cardiac involvement was present at baseline in 81 patients (30%). Single and multiple variable analyses were performed in search of predictors of major adverse cardiac event (MACE), and hazard ratios (HR) and 95% confidence intervals (CI) were calculated. Over a median follow-up of 7 years [3.6 to 11.7], 27 patients (10%) suffered a MACE, defined as sudden death, death due to heart failure (HF), resuscitated cardiac arrest, 3 rd degree atrioventricular block, sinus node dysfunction, cardiac transplantation, or hospitalization for management of HF. Patients with single large-scale mtDNA deletions or m.3243A&gt;G mutations had the highest incidence of MACE. By multiple variable analysis, intraventricular conduction block (HR = 16.9; 95% CI: 7.2 to 39.4), diabetes (HR = 7.0; 95% CI: 2.9 to 16.7), premature ventricular complexes (HR = 3.6; 95% CI: 1.4 to 9.2) and left ventricular (LV) hypertrophy (HR = 2.5; 95% CI: 1.1 to 5.8) were independent predictors of MACE. In patients with 0, 1, and ≥2 risk factors, the incidence of MACE was 1.7, 15 and 42% respectively. Conclusions: Patients with mitochondrial diseases are at high risk of MACE, independently predicted by intraventricular conduction block, diabetes, ventricular prematurity and LV hypertrophy.
Impact of deleterious germline BRCA mutations, addition of taxanes and use of adjuvant endocrine therapy (ET) on anti-müllerian hormone (AMH) levels in early breast cancer (EBC) patients treated by adjuvant chemotherapy (CT)
Authors: N. Olympios, M. Lambertini, C. Calbrix, M. Saint-Ghislain, M. Fontanilles, A. Loeb, M. Leheurteur, I. Demeestere, F. Di Fiore, A. Perdrix, F. Clatot
Journal: Annals of Oncology (2018)
A Case of a College Student Presenting With Mild Mental Health Problems
Authors: Paolo Fusar-Poli, Cathy Davies, Ilaria Bonoldi
Journal: JAMA Psychiatry (2018)

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Abstract 10344: Transcriptional Patterning of the Cardiac Conduction System Prevents Arrhythmias
Authors: Ozanna Burnicka-Turek, Michael T Broman, Jeffrey D Steimle, Bastiaan J Boukens, Kohta Ikegami, Yun Qiao, David E Arnolds, Rangarajan D Nadadaru, Xinan H Yang, Vickas V Patel, Marcelo A Nobrega, Michael J Rust, Igor R Efimov, Ivan P Moskowitz
Journal: Circulation (2018)
Pathologic Oxidation of PTPN12 Underlies ABL1 Phosphorylation in Hereditary Leiomyomatosis and Renal Cell Carcinoma
Authors: Yang Xu, Paul Taylor, Joshua Andrade, Beatrix Ueberheide, Brian Shuch, Peter M. Glazer, Ranjit S. Bindra, Michael F. Moran, W. Marston Linehan, Benjamin G. Neel
Journal: Cancer Research (2018)

Abstract Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) is an inherited cancer syndrome associated with a highly aggressive form of type 2 papillary renal cell carcinoma (PRCC). Germline inactivating alterations in fumarate hydratase (FH) cause HLRCC and result in elevated levels of reactive oxygen species (ROS). Recent work indicates that FH−/− PRCC cells have increased activation of ABL1, which promotes tumor growth, but how ABL1 is activated remains unclear. Given that oxidation can regulate protein-tyrosine phosphatase (PTP) catalytic activity, inactivation of an ABL-directed PTP by ROS might account for ABL1 activation in this malignancy. Our group previously developed “q-oxPTPome,” a method that globally monitors the oxidation of classical PTPs. In this study, we present a refined q-oxPTPome, increasing its sensitivity by &amp;gt;10×. Applying q-oxPTPome to FH-deficient cell models showed that multiple PTPs were either highly oxidized (including PTPN12) or overexpressed. Highly oxidized PTPs were those with relatively high sensitivity to exogenous H2O2. Most PTP oxidation in FH-deficient cells was reversible, although nearly 40% of PTPN13 was irreversibly oxidized to the sulfonic acid state. Using substrate-trapping mutants, we mapped PTPs to their putative substrates and found that only PTPN12 could target ABL1. Furthermore, knockdown experiments identified PTPN12 as the major ABL1 phosphatase, and overexpression of PTPN12 inhibited ABL1 phosphorylation and HLRCC cell growth. These results show that ROS-induced oxidation of PTPN12 accounts for ABL1 phosphorylation in HLRCC-associated PRCC, revealing a novel mechanism for inactivating a tumor suppressor gene product and establishing a direct link between pathologic PTP oxidation and neoplastic disease. Significance: This work identifies a novel mechanism of activation of the oncogenic kinase ABL1 via ROS-induced, oxidation-mediated inactivation of cognate protein tyrosine phosphatases.
Benefit of Early versus Deferred Antiretroviral Therapy on Progression of Liver Fibrosis among People with HIV in the START Randomized Trial
Authors: Nila J. Dharan, Jacqueline Neuhaus, Juergen K. Rockstroh, Lars Peters, Fred Gordin, Alejandro Arenas‐Pinto, Carol Emerson, Kristen Marks, Jose Hidalgo, Rui Sarmento‐Castro, Christoph Stephan, Nagalingeswaran Kumarasamy, Sean Emery, Gail V. Matthews
Journal: Hepatology (2018)

The role of antiretroviral therapy (ART) in reducing or contributing to liver fibrosis in persons with human immunodeficiency virus (HIV) is unclear. We evaluated participants in the Strategic Timing of AntiRetroviral Treatment (START) trial for liver fibrosis using the AST to Platelet Ratio Index (APRI) and Fibrosis‐4 Index (FIB‐4), and assessed for a benefit of early versus delayed ART on liver fibrosis progression. ART‐naïve persons with high CD4 counts (&gt;500 cells/µL) from 222 clinical sites in 35 countries were randomized to receive ART either at study enrollment (immediate treatment arm) or when their CD4 count fell below 350 cells/µL (deferred treatment arm). The following outcomes were evaluated: fibrosis (APRI &gt; 0.5 or FIB‐4 &gt; 1.45), significant fibrosis (APRI &gt; 1.5 or FIB‐4 &gt; 3.25), hepatic flare, and resolution of elevated APRI and FIB‐4 scores. Of the 4,684 enrolled into the START study, 104 did not have APRI or FIB‐4 results and were excluded. Among 4,580 participants (2,273 immediate treatment; 2,307 deferred treatment), the median age was 36 years, 26.9% were female, and 30.4% were black. Three percent had an alcoholism or substance abuse history, 6.4% had hepatitis B and/or C, and 1.1% had significant fibrosis at baseline. The median CD4 count was 651, and 5.3% had HIV RNA ≤ 200. Immediate arm participants were at lower risk of developing increased fibrosis scores than deferred arm participants (hazard ratio [HR] = 0.66; 95% confidence interval [CI] = 0.57‐0.78; P &lt; 0.001) and more likely to have resolution of elevated baseline scores (HR 1.6; 95% CI 1.3‐1.9; P &lt; 0.001). Conclusions: Significant liver fibrosis was rare among ART‐naïve HIV‐positive persons with high CD4 counts. Our findings suggest a benefit of early ART in preventing the development of liver fibrosis.
A randomized controlled trial of alanyl-glutamine supplementation in peritoneal dialysis fluid to assess impact on biomarkers of peritoneal health
Authors: Andreas Vychytil, Rebecca Herzog, Paul Probst, Werner Ribitsch, Karl Lhotta, Veronika Machold-Fabrizii, Martin Wiesholzer, Michaela Kaufmann, Hermann Salmhofer, Martin Windpessl, Alexander R. Rosenkranz, Rainer Oberbauer, Franz König, Klaus Kratochwill, Christoph Aufricht
Journal: Kidney International (2018)

In early clinical testing, acute addition of alanyl-glutamine (AlaGln) to glucose-based peritoneal dialysis (PD) fluids restored peritoneal cellular stress responses and leukocyte function. This study was designed to test the effect of extended treatment with AlaGln-supplemented PD fluid on biomarkers of peritoneal health. In a double-blinded, randomized crossover design, stable PD patients were treated with AlaGln (8 mM) or placebo added to PD fluid for eight weeks. As primary outcome measures, dialysate cancer-antigen 125 (CA-125) appearance rate and ex vivo stimulated interleukin-6 (IL-6) release were assessed in peritoneal equilibration tests. In 8 Austrian centers, 54 patients were screened, 50 randomized, and 41 included in the full analysis set. AlaGln supplementation significantly increased CA-125 appearance rate and ex vivo stimulated IL-6 release. AlaGln supplementation also reduced peritoneal protein loss, increased ex vivo stimulated tumor necrosis factor (TNF)-α release, and reduced systemic IL-8 levels. No adverse safety signals were observed. All 4 peritonitis episodes occurred during standard PD fluid treatment. A novel AlaGln-supplemented PD fluid improves biomarkers of peritoneal membrane integrity, immune competence, and systemic inflammation compared to unsupplemented PD fluid with neutral pH and low-glucose degradation. A phase 3 trial is needed to determine the impact of AlaGln supplementation on hard clinical outcomes.
Efficacy and safety of intravenous immunoglobulin plus prednisolone therapy in patients with Kawasaki disease (Post RAISE): a multicentre, prospective cohort study
Authors: Koichi Miyata, Tetsuji Kaneko, Yoshihiko Morikawa, Hiroshi Sakakibara, Takahiro Matsushima, Masahiro Misawa, Tsutomu Takahashi, Maki Nakazawa, Takuya Tamame, Takatoshi Tsuchihashi, Yukio Yamashita, Toshimasa Obonai, Michiko Chiga, Naoaki Hori, Osamu Komiyama, Hiroyuki Yamagishi, Masaru Miura
Journal: The Lancet Child & Adolescent Health (2018)
MicroRNA-668 represses MTP18 to preserve mitochondrial dynamics in ischemic acute kidney injury
Authors: Qingqing Wei, Haipeng Sun, Shuwei Song, Yong Liu, Pengyuan Liu, Man Jiang Livingston, Jianwen Wang, Mingyu Liang, Qing-Sheng Mi, Yuqing Huo, Norris Stanley Nahman, Changlin Mei, Zheng Dong
Journal: Journal of Clinical Investigation (2018)

The pathogenesis of ischemic diseases remains unclear. Here we demonstrate the induction of microRNA-668 (miR-668) in ischemic acute kidney injury (AKI) in human patients, mice, and renal tubular cells. The induction was HIF-1 dependent, as HIF-1 deficiency in cells and kidney proximal tubules attenuated miR-668 expression. We further identified a functional HIF-1 binding site in the miR-668 gene promoter. Anti–miR-668 increased apoptosis in renal tubular cells and enhanced ischemic AKI in mice, whereas miR-668 mimic was protective. Mechanistically, anti–miR-668 induced mitochondrial fragmentation, whereas miR-668 blocked mitochondrial fragmentation during hypoxia. We analyzed miR-668 target genes through immunoprecipitation of microRNA-induced silencing complexes followed by RNA deep sequencing and identified 124 protein-coding genes as likely targets of miR-668. Among these genes, only mitochondrial protein 18 kDa (MTP18) has been implicated in mitochondrial dynamics. In renal cells and mouse kidneys, miR-668 mimic suppressed MTP18, whereas anti–miR-668 increased MTP18 expression. Luciferase microRNA target reporter assay further verified MTP18 as a direct target of miR-668. In renal tubular cells, knockdown of MTP18 suppressed mitochondrial fragmentation and apoptosis. Together, the results suggest that miR-668 is induced via HIF-1 in ischemic AKI and that, upon induction, miR-668 represses MTP18 to preserve mitochondrial dynamics for renal tubular cell survival and kidney protection.
Association of Intraventricular Hemorrhage and Death With Tocolytic Exposure in Preterm Infants
Authors: Gaëlle Pinto Cardoso, Estelle Houivet, Laetitia Marchand-Martin, Gilles Kayem, Loïc Sentilhes, Pierre-Yves Ancel, Elsa Lorthe, Stéphane Marret
Journal: JAMA Network Open (2018)

<h3>Importance</h3> No trials to date have demonstrated the benefits of tocolysis on death and/or neonatal morbidity in preterm infants; tocolytics may affect the fetal blood-brain barrier. <h3>Objectives</h3> To assess the risks associated with tocolysis in women delivering prematurely as measured by death and/or intraventricular hemorrhage (IVH) in preterm infants and to compare the association of calcium channel blockers (CCBs) nifedipine and nicardipine hydrochloride vs atosiban used for tocolysis with death and/or IVH. <h3>Design, Settings, and Participants</h3> The French 2011 EPIPAGE-2 (Enquête Épidémiologique sur les Petits Âges Gestationnels) cohort was limited to mothers admitted for preterm labor without fever, who delivered from 24 to 31 weeks of gestation from April 1 through December 31, 2011. Groups of preterm infants with vs without tocolytic exposure and groups with atosiban vs CCB exposure were compared. Data analysis was performed from June 7, 2014, through September 3, 2017. <h3>Exposures</h3> Tocolytics. <h3>Main Outcomes and Measures</h3> The primary outcome was a composite of death and/or IVH in preterm infants. Secondary outcomes included death, IVH, and a composite of death and/or grades III to IV IVH. <h3>Results</h3> A total of 1127 mothers (mean [SD] age, 25.5 [6.0] years) experienced preterm labor and gave birth to 1343 preterm infants with a male to female ratio of 1.23 and mean (SD) gestational age of 27 (2.5) weeks. Of these, 789 mothers (70.0%) received tocolytics; 314 (39.8%) received only atosiban, and 118 (15.0%) received only a CCB. In the first analysis, the primary outcome (death and/or IVH) was not significantly different in preterm infants with vs without tocolytic exposure (183 of 363 [50.4%] vs 207 of 363 [57.0%]; relative risk [RR], 0.88; 95% CI, 0.77-1.01;<i>P</i> = .07). The secondary outcome (death and/or grades III-IV IVH) was significantly lower in preterm infants with vs without tocolytic exposure (92 of 363 [25.3%] vs 118 of 363 [32.5%]; RR, 0.78; 95% CI, 0.62-0.98;<i>P</i> = .03). Other outcomes did not differ significantly. In the secondary analysis, death and/or IVH was not significantly different in preterm infants with atosiban vs CCB exposure (96 of 214 [44.9%] vs 62 of 121 [51.2%]; RR, 0.88; 95% CI, 0.70-1.10;<i>P</i> = .26), nor was IVH (77 of 197 [39.1%] vs 48 of 106 [45.3%]; RR, 0.86; 95% CI, 0.66-1.13;<i>P</i> = .29). <h3>Conclusions and Relevance</h3> In this population-based study, findings suggest that tocolytics were associated with a reduction of death and severe IVH. Other studies are necessary to compare perinatal outcomes after use of atosiban vs CCBs.
Antitumor efficacy and pharmacokinetics of a novel gemcitabine oral formulation (INNO-D07001) in xenograft animal models.
Authors: CS Hsu, W-H Hao, J-J Wang, T-H Lin, R-Y Kuo
Journal: Journal of Clinical Oncology (2012)

e14699 Background: INNO-D07001 is a novel oral gemcitabine formulation which was developed to enhance the oral bioavailability of gemcitabine and it has been successfully demonstrated in both beagle dogs as well as nude mice. The objectives of this study were to examine the antitumor activity of this novel gemcitabine oral formulation in human xenograft models of pancreatic tumors with different daily doses as well as various dosing schedules. Methods: The INNO-D07001 dosing solutions (gemcitabine oral formulation) were formulated freshly before treatment and water for injection (USP) was used as the diluent. There were seven groups in the study and it was ten female NCr-nu/nu mice (with human CFPAC-1 pancreatic tumor) per group. Two doses (5 mg/kg and 10 mg/kg) and three dosing schedules (Q1D, Q2D, and Q3D) were examined. Water for injection (by oral administration) was used as the blank control and Gemzar (180 mg/kg by I.V.) was used as the active control. All INNO-D07001 dosing solutions were administered to mice by P.O. and, on the other hand, Gemzar was administered to mice by I.V. All animals were designed to receive doses for 12 days based on different doses and dosing schedules. Total body weights and tumor sizes were recorded continuously for evaluating the toxicity and antitumor activity, respectively, of INNO-D07001. Results: Oral administration of INNO-D07001 once daily at doses of 10 and 5 mg/kg/dose was not tolerated. In contrast, oral administration of INNO-D07001 on a Q2Dx6 schedule at a dose of 10 mg/kg/dose and on a Q3Dx4 schedule at doses of 10 and 5 mg/kg/dose was well tolerated. Moreover, the INNO-D07001 treatment at a dose of 10 mg/kg/dose on a Q2Dx6 schedule produced statistically significant inhibition of tumor growth (i.e. more than 60% inhibition rate comparing to the blank control) on the last treatment day. Conclusions: The novel gemcitabine oral formulation (INNO-D07001) is well tolerated and effective at a dose of 10 mg/kg/dose on a Q2Dx6 schedule to show the significant inhibition of pancreatic tumor growth. Future preclinical study in toxicity evaluation with repeating doses is ongoing in order to provide adequate safety information before entering phase I clinical study.
47 A case of primary gastric melanoma: no light at the end of the tunnel
Authors: GM Callaghan, FC Kelleher, PF Ridgway, BM Ryan
Journal: Gut (2017)

Background  Malignant melanoma of the gastrointestinal tract is usually a metastasis from a cutaneous source. Primary gastric melanoma is an extremely rare clinical entity, with only 14 reported cases worldwide. It is often advanced at time of diagnosis and is associated with a poor outcome.  Aim  To describe a case of primary gastric melanoma.  Method  A 76 year old gentleman, presented with a one month history of fatigue and exertional dyspnoea. Laboratory investigations indicated an anaemia, with a haemoglobin level of 11.0 g/dL. Subsequent gastroscopy visualised a large, atypical, crater-like ulcerated lesion distal to the cardia in the proximal stomach.  Results  Provisional histology was suggestive of a poorly differentiated adenocarcinoma but subsequent cyto-morphology and immunophenotyping were consistent with melanoma, with positive S100 protein, HMB45 and Melan A. Further molecular genetic testing revealed a V600R mutation in the BRAF gene, which is the first primary gastric melanoma with this mutation to be reported in the literature. Given the rarity of the findings, an extensive secondary work-up was undertaken, which concluded the diagnosis primary gastric melanoma.  Conclusions  Primary gastric melanoma is a rare disease that can present similarly to other upper gastrointesinal lesions, with weight loss, abdominal pain, malena, and anaemia. Given its rarity, the pathogenesis is poorly understood. Lesions are often endoscopically atypical. Important points to note would include the absence of a primary lesion, as supported by a full skin examination and PET-CT findings, which can help to delineate the limitation to the stomach, thus helping to inform subsequent management.
Phase I dose escalation of pembrolizumab given concurrently with palliative thoracic radiotherapy (RT) for NSCLC
Authors: R. Kumar, D.P. Walder, A. Pejanaute, R. Gunapala, J. Bhosle, N. Yousef, S. Popat, F. McDonald, I. Locke, K. Harrington, A. Tree, S. Lalondrelle, R. Huddart, M.E.R. O’Brien, M. Ahmed
Journal: Annals of Oncology (2018)
Abstract 9947: Predictors of Left Ventricular Dysfunction After Aortic Valve Replacement in Patients With Mixed Aortic Valve Disease
Authors: Alexander Egbe, Joeseph Poterucha, Carole Warnes
Journal: Circulation (2015)

Objectives: Predictors of left ventricular dysfunction (LVD) after aortic valve replacement (AVR) in mixed aortic valve disease (MAVD) have not been studied. Objective was to determine prevalence a...
A phase III, randomized, open-label, multicenter study of SHR-1210 (anti-PD-1 antibody) in combination with pemetrexed and carboplatin as first line therapy in subjects with advanced/metastatic non-squamous non-small cell lung cancer
Authors: F. Wu, G. Gao, C. Zhou, X. Kang, Y. Zhou
Journal: Annals of Oncology (2018)