tbuckley/cabot-search huggingface dataset:
Decontamination Strategies for Critically Ill Patients
Authors: Peter E. Spronk, Brian H. Cuthbertson
Journal: JAMA (2019)

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
Advanced-Stage Non–Small Cell Lung Cancer: Advances in Thoracic Oncology 2018
Authors: Jordi Remon, Myung-Ju Ahn, Nicolas Girard, Melissa Johnson, Dong-Wan Kim, Gilberto Lopes, Rathi N. Pillai, Benjamin Solomon, Guillermo Villacampa, Qing Zhou
Journal: Journal of Thoracic Oncology (2019)
Non-Invasive Monitoring of Urinary KRAS Circulating Tumor DNA for Treatment Response and Minimal Residual Disease in Patients with Lung Adenocarcinoma.
Authors: James Michael Randall, Mark G. Erlander, Cecile Rose T. Vibat, Saege Hancock, Vlada Melnikova, Ezra E. W. Cohen, Scott Michael Lippman, Razelle Kurzrock, Hatim Husain
Journal: Journal of Clinical Oncology (2015)

e19092 Background: Radiographic imaging in lung adenocarcinoma patients is not always reliable and a non-tissue based approach for monitoring treatment responses or minimal residual disease is desired. 15–25% of patients with lung adenocarcinoma have tumor associated KRAS mutations, and these may be detected in circulating tumor (ct) DNA. The aim of this study was to correlate the dynamics of KRAS mutational load in ctDNA with clinical responses in patients with lung adenocarcinoma receiving surgical treatment, radiation, or chemotherapy. Methods: In a blinded biomarker study of 30 patients, urine samples were obtained from 7 patients with metastatic or early stage lung adenocarcinoma harboring KRAS G12/13 mutation in the tumor tissue by CLIA laboratory testing. Following extraction of urinary ctDNA, KRAS G12/13 mutational load was quantified using a next generation sequencing-based method with standardized reporting of mutant copies per 105genome equivalents. Results: Of 7 patients enrolled, 6 patients with lung adenocarcinoma had serial urine collections with up to 3 specimens at 1-3 month intervals. Three of 7 patients had metastatic disease receiving chemotherapy, and 2 of 3 had serial detectable KRAS mutation in urinary ctDNA which tested positive 1 to 2 months prior to radiologic progression. In 3 of 4 patients with definitive stereotactic body radiation therapy (SBRT) or surgery for early stage cancer, and now with no clinical evidence of disease, mutant KRAS was not detectable in urinary ctDNA at any time points after surgery. In 1 of 4 patients with early stage disease, imaging was suspicious for progression, and this presentation correlated with an increase in urinary ctDNA KRAS mutation load after surgery. Conclusions: We demonstrate feasibility of monitoring minimal residual disease and responses to chemotherapy in patients with KRAS G12/13-positive lung adenocarcinoma using a completely non-invasive urine sample.
THU-345-Lean NAFLD patients have lower prevalence of cardiovascular, metabolic and severe liver disease compared to overweight or obese patients with NAFLD
Authors: Ethan Weinberg, Huy N. Trinh, Roberto J Firpi, Kalyan Ram Bhamidimarri, Samuel Klein, Laura Malahias, Richard Zink, Anna Lok
Journal: Journal of Hepatology (2019)
SAT-197-Quality of life measurement using wrist actigraphy in HCV genotype 1 infected, treatment naïve patients suffering from fatigue and receiving ombitasvir, paritaprevir, and ritonavir tablets and dasabuvir tablets (Viekirax/Exviera; 3D regimen)
Authors: Nasser Semmo, Beat Müllhaupt, Lisa Ruckstuhl, Lorenzo Magenta, Olivier Clerc, Ralph Torgler, David Semela
Journal: Journal of Hepatology (2019)
FRI-216-Tenofovir monotherapy versus tenofovir plus entecavir combination therapy for multi-drug resistant chronic hepatitis B: Five year follow-up data of multicenter prospective cohort study (Final results)
Authors: Hyung Joon Yim, Sang Jun Suh, Young Kul Jung, Seong Gyu Hwang, Hana Park, Yeon Seok Seo, Soon Ho Um, Sae Hwan Lee, Young Seok Kim, Jae Young Jang, In Hee Kim, Ji Hoon Kim, Young-Sun Lee, Myeong Jun Song, Jun Yong Park
Journal: Journal of Hepatology (2019)
PS-031-RNAseq of liver biopsies following DAA-based therapy reveals a greater enrichment in immune, interferon, cytokine and cell cycle pathways compared to IFN-based therapy: Implications for DAA-related sequelae
Authors: Jacinta Holmes, Ming-Lung Yu, Shu-Chi Wang, Meghan Sise, Chung-Feng Huang, Chia-Yen Dai, Wan-Long Chuang, Ching-Chin Lin, Steve Rwema, Esperance Schaefer, Batul Kaj, Dong Chen, Quijiu Sheng, Wenyu Lin, Raymond Chung
Journal: Journal of Hepatology (2019)
FRI-117-The gain of function mutation of SerpinB3 (SCCA-PD) is associated with the severity of portal hypertension and complications onset in patients with advanced liver disease
Authors: Andrea Martini, Filippo Marafatto, Cristian Turato, Erica Novo, Maurizio Parola, Alessandra Biasiolo, Santina Quarta, Mariagrazia Ruvoletto, Paolo Angeli, Patrizia Pontisso
Journal: Journal of Hepatology (2019)
Response to: ‘Could autologous adipose-derived stromal vascular fraction turn out an unwanted source of profibrotic myofibroblasts in systemic sclerosis?’ by Manetti
Authors: Melanie Velier, Jeremy Magalon, Stephanie Simoncini, Françoise Dignat-George, Brigitte Granel, Pascale Paul, Florence Sabatier
Journal: Annals of the Rheumatic Diseases (2019)

We would like to thank Dr Manetti for his relevant comments1 on our recent article in the Annals of Rheumatic Disease entitled ‘Molecular profile and proangiogenic activity of the adipose-derived stromal vascular fraction used as an autologous innovative medicinal product in patients with systemic sclerosis’2. We are pleased that this study has raised such a high interest in the scientific community and allows us to provide additional comments to those recently published3 4 in order to discuss the potential profibrotic profile of adipose-derived stem cells (ADSC) derived from patients with diffuse cutaneous systemic sclerosis (SSc). We agree that SSc is a rare but potentially lethal autoimmune disease that challenges the urgent need to develop novel therapeutic approaches. In this context, autologous fat grafting has been successfully used to limit SSc-associated clinical complications such as SSc-related perioral thickening and mouth opening limitation5 facial handicap6 …
Two cases of sarcomas in the heart; one primary, one metastatic.
Authors: Gul Sema Yildiran Keskin, Arzu Oguz, Samed Rahatli, Zafer Akcali, Ozden Altundag
Journal: Journal of Clinical Oncology (2015)

e21510 Background: Cardiac sarcomas are most frequent primary cardiac malignancy with an unfavourable prognosis. Metastases to the heart from other malignancies are more common than primary cardiac tumours. Here we report two consecutively diagnosed cardiac sarcoma patients, one primary, other metastatic. Methods: Case 1: A 68 year old woman presented with progressive dyspnea and chest pain. Chest X-ray showed cardiomegali and ECG was consisted with atrial fibrillation. Radiographic imaging revealed pericardial effusion, bilateral paranchymal lung masses, a large heterogenous mass that filled right atrium, constricting vena cava superior, extending to intratrial septum and uterine mass. Since life-threatening arrhythmias were detected, she underwent palliative surgical resection for cardiac tumor infiltrating SA node and cardiac pacemaker was inserted. Histopathology was consistent with epitheloid uterine leiomyosarcoma. With a diagnosis of metastatic uterine leiomyosarcoma, she is currently undergoing chemotherapy with gemcitabine and docetaxel. Results: Case 2: A 38 year old woman presented with a three months history of fatigue and weakness. Blood tests and echocardiography performed after several syncopal episodes revealed the presence of anemia and pericardial effusion. She had been treated with ibuprofen for pericarditis but no symptomatic relief was achieved. Transesophageal echocardiogram revealed a right atrial mass compressing vena cava superior and a patent foramen ovale. Radiologic imaging confirmed the 8 cm cardiac mass, mediastinal enlarged lymph nodes and multiple nodules in the liver. The histopathological evaluation of liver nodule biopsy was consistent with a diagnosis of angiosarcoma metastases. Then, she underwent surgical resection of right atrial mass. After an uneventful recovery, the patient had gemcitabine docetaxel chemotherapy. Conclusions: Although rare, cardiac sarcomas either metastatic or primary should be kept in mind in patients with cardiac and/or lung related symptoms. Different from other metastatic tumors palliative resections for the lesions in the heart may gain priority for hemodynamic stabilisation in such patients.
TCTAP C-162 Acute Limb Occlusion of the Endurant II Stent Graft Post Endovascular Repair - The Role of Catheter Directed Thrombolysis
Authors: Shaiful Azmi Yahaya, Kumara Gurupparan Ganesan, Shawal Faizal Mohamad
Journal: Journal of the American College of Cardiology (2019)
The Medusa faces of dyspnoea in COPD
Authors: Emiel F.M. Wouters
Journal: European Respiratory Journal (2019)

Exercise limitation and exertional dyspnoea are common problems in patients with a variety of chronic lung diseases, as well as with heart failure. In chronic obstructive pulmonary disease (COPD) patients, the level of patient-reported dyspnoea is used as a parameter to assess COPD, currently leading to a "one size fits all" approach, largely based on pharmacological recommendations [1]. As exertional symptoms poorly correlate even with resting measurement lung function clusters [2], a more accurate estimate of functional capacity by cardiopulmonary exercise testing (CPET) can provide information about the influences of the cardiac, respiratory, musculoskeletal and haematological systems [3]. Such assessment of the integrated cardiopulmonary response to exercise remains largely underutilised in the personalised assessment and management of patients with exercise limitation and breathlessness. Cardiopulmonary exercise testing is a very useful tool in understanding dyspnoea in COPD <http://ow.ly/lHFb30oc7dY>
FRI-310-Alcohol dehydrogenase activity in liver and blood is altered in non-alcoholic fatty liver disease
Authors: Finn Jung, Ruth Ladurner, Katharina Staufer, Silvia Wagner, Anna Janina Engstler, Annette Brandt, Anika Nier, Anja Baumann, Vincent Winkler, Ina Bergheim
Journal: Journal of Hepatology (2019)
AKT3 Gene Transfer Promotes Anabolic Reprogramming and Photoreceptor Neuroprotection in a Pre-clinical Model of Retinitis Pigmentosa
Authors: Devin S. McDougald, Tyler E. Papp, Alexandra U. Zezulin, Shangzhen Zhou, Jean Bennett
Journal: Molecular Therapy (2019)

Mutations within over 250 known genes are associated with inherited retinal degeneration. Clinical success following gene-replacement therapy for congenital blindness due to RPE65 mutations establishes a platform for the development of downstream treatments targeting other forms of inherited ocular disease. Unfortunately, several challenges relevant to complex disease pathology and limitations of current gene-transfer technologies impede the development of related strategies for each specific form of inherited retinal degeneration. Here, we describe a gene-augmentation strategy that delays retinal degeneration by stimulating features of anabolic metabolism necessary for survival and structural maintenance of photoreceptors. We targeted two critical points of regulation in the canonical insulin/AKT/mammalian target of rapamycin (mTOR) pathway with AAV-mediated gene augmentation in a mouse model of retinitis pigmentosa. AAV vectors expressing the serine/threonine kinase, AKT3, promote dramatic preservation of photoreceptor numbers, structure, and partial visual function. This protective effect was associated with successful reprogramming of photoreceptor metabolism toward pathways associated with cell growth and survival. Collectively, these findings underscore the importance of AKT activity and downstream pathways associated with anabolic metabolism in photoreceptor survival and maintenance. Mutations within over 250 known genes are associated with inherited retinal degeneration. Clinical success following gene-replacement therapy for congenital blindness due to RPE65 mutations establishes a platform for the development of downstream treatments targeting other forms of inherited ocular disease. Unfortunately, several challenges relevant to complex disease pathology and limitations of current gene-transfer technologies impede the development of related strategies for each specific form of inherited retinal degeneration. Here, we describe a gene-augmentation strategy that delays retinal degeneration by stimulating features of anabolic metabolism necessary for survival and structural maintenance of photoreceptors. We targeted two critical points of regulation in the canonical insulin/AKT/mammalian target of rapamycin (mTOR) pathway with AAV-mediated gene augmentation in a mouse model of retinitis pigmentosa. AAV vectors expressing the serine/threonine kinase, AKT3, promote dramatic preservation of photoreceptor numbers, structure, and partial visual function. This protective effect was associated with successful reprogramming of photoreceptor metabolism toward pathways associated with cell growth and survival. Collectively, these findings underscore the importance of AKT activity and downstream pathways associated with anabolic metabolism in photoreceptor survival and maintenance.
Hepatitis B virus infection in children and adolescents
Authors: Giuseppe Indolfi, Philippa Easterbrook, Geoffrey Dusheiko, George Siberry, Mei-Hwei Chang, Claire Thorne, Marc Bulterys, Po-Lin Chan, Manal H El-Sayed, Carlo Giaquinto, Maureen M Jonas, Tammy Meyers, Nick Walsh, Stefan Wirth, Martina Penazzato
Journal: The Lancet. Gastroenterology & hepatology (2019)
THU-491-The role of alanine glyoxylate aminotransferase in hepatocellular carcinoma
Authors: Letizia Satriano, Monika Lewinska, Colm O Rourke, Douglas VNP Oliveira, Deepak Kumar Bhatt, Andrzej Taranta, Monika Herr, Beate Straub, Dr. Elizabeth A. Conner, Dr. Anuradha Budhu, Yotsawat Pomyen, Dr. Tao Ma, Dr. Zach Gerhart-Hines, Dr. Claus Sivertsen Stjernegaard, Matthias Matter, Dr. Christoph Crocoll, Xin W. Wang, Jens Marquardt, Jesper Andersen
Journal: Journal of Hepatology (2019)
Clinical management of advanced lung adenocarcinoma with ALK rearrangement: Real-world treatment outcomes and long-term survival
Authors: B. Zhang, S. Wang, J. Xu, Y. Zhang, X. Zhang, J. Qian, J. Lu, R. Qiao, W. Nie, L. Zhang, Y. Zhao, M. Hu, W. Zhang, B.-H. Han
Journal: Annals of Oncology (2019)

Background: Anaplastic lymphoma kinase-tyrosine kinase inhibitors (ALK-TKIs) have been demonstrated to be effective in ALK-rearranged, advanced lung adenocarcinoma patients. However, data from a real-world setting is very limited. The aim of the study was to: a) determine long-term survival in these patients and investigate factors associated with their prognosis; and b) analyze the clinical outcomes of patients who were sequentially treated with next-generation ALK-TKIs. Methods: ALK-rearranged, advanced lung adenocarcinoma patients who were treated with crizotinib were included between January 2013 and December 2016. Progression-free survival (PFS) and overall survival (OS) were calculated by the Kaplan-Meier method. The hazard ratio (HR) for the risk of progression or death was calculated using multivariate Cox regression model. Results: A total of 5286 patients were screened and 176 eligible patients were included. Median PFS and OS were 12.4 months (95% CI, 10.3-14.6 months) and 45.6 months (95% CI, 37.6-53.7 months), respectively. 36.3% of patients were 5-year survivors. Extrathoracic metastasis before crizotinib treatment was independently associated with worse PFS (HR, 1.77, 95% CI, 1.24-2.53, P < 0.01) and OS (HR, 1.61, 95% CI, 1.02-2.54, p = 0.04). 45 patients were sequentially treated with newer-generation ALK-TKIs, obtaining a statistically longer OS (54.8 months, 95% CI, not calculable) than patients who were solely treated with crizotinib during clinical management (36.6 months, 95% CI, 29.2-43.9 months, P < 0.01). Conclusions: Our study provides useful information about ALK-rearranged, advanced lung adenocarcinoma patients treated with ALK-TKIs in a real-world setting. Legal entity responsible for the study: The authors. Funding: Has not received any funding. Disclosure: All authors have declared no conflicts of interest.
FRI-342-Combining probiotics and an angiotensin-2 type 1 receptor blocker has beneficial effects on hepatic fibrogenesis in a rat model of non-alcoholic steatohepatitis
Authors: Yasuhiko Sawada, Hideto Kawaratani, Takuya Kubo, Yukihisa Fujinaga, Masanori Furukawa, Soichiro Saikawa, Shinya Sato, Kenichiro Seki, Hiroaki Takaya, Yasushi Okura, Kosuke Kaji, Naotaka Shimozato, Mitsuteru Kitade, Kei Moriya, Tadashi Namisaki, Takemi Akahane, Hitoshi Yoshiji
Journal: Journal of Hepatology (2019)
The Natural History of Advanced Fibrosis Due to Nonalcoholic Steatohepatitis: Data From the Simtuzumab Trials
Authors: Arun J. Sanyal, Stephen A. Harrison, Vlad Ratziu, Manal F. Abdelmalek, Anna Mae Diehl, Stephen Caldwell, Mitchell L. Shiffman, Raul Aguilar Schall, Catherine Jia, Bryan McColgan, C. Stephen Djedjos, John G. McHutchison, G. Mani Subramanian, Robert P. Myers, Zobair Younossi, Andrew J. Muir, Nezam H. Afdhal, Jaime Bosch, Zachary Goodman
Journal: Hepatology (2019)

Progression of nonalcoholic steatohepatitis (NASH) is incompletely characterized. We analyzed data on longitudinal changes in liver histology, hepatic venous pressure gradient (HVPG), and serum markers of fibrosis in 475 patients with NASH with bridging fibrosis (F3) or compensated cirrhosis (F4) enrolled in two phase 2b, placebo‐controlled trials of simtuzumab. The trials were terminated after 96 weeks because of lack of efficacy, so data from treatment groups were combined. Liver biopsies and HVPG measurements (only for patients with F4 fibrosis) were collected at screening and at weeks 48 and 96. Patients were assessed for Ishak fibrosis stage, hepatic collagen content and alpha‐smooth muscle actin (by morphometry), NAFLD Activity Score (NAS), and serum markers of fibrosis. Associations with progression to cirrhosis (in patients with F3 fibrosis) and liver‐related clinical events (in patients with F4 fibrosis) were determined. Progression to cirrhosis occurred in 22% (48/217) of F3 patients, and liver‐related clinical events occurred in 19% (50/258) of patients with cirrhosis. Factors significantly associated with progression to cirrhosis included higher baseline values of and greater increases in hepatic collagen content, level of alpha‐smooth muscle actin, and Enhanced Liver Fibrosis score. Similar factors, plus lack of fibrosis stage improvement (hazard ratio, 9.30; 95% confidence interval, 1.28‐67.37), higher HVPG at baseline, and greater increase in HVPG over time, were associated with an increased risk of liver‐related clinical events in patients with cirrhosis. Disease progression was not associated with the NAS at baseline or changes in NAS during treatment after adjustment for fibrosis stage. Conclusion : In patients with advanced fibrosis due to NASH, the primary determinant of clinical disease progression is fibrosis and its change over time.
Abstract 051: Genome-wide Association Study Identifies 12 Loci for Habitual Consumption of Bitter and Sweet Beverages
Authors: Victor W Zhong, Sandra Sanchez-Roige, Peter Kraft, Rob M Van Dam, Daniel I Chasman, Marilyn C Cornelis
Journal: Circulation (2018)

Introduction: Widely consumed beverages (e.g., soft drinks, coffee, tea) are critical sources of energy, added sugar and phytochemicals and are associated with obesity and chronic disease. Taste perception and preferences are highly heritable and strong determinants of food and beverage choice. We aimed to identify novel loci underlying habitual bitter and sweet beverage intake. Methods: We performed a genome-wide association study (GWAS) of self-reported bitter and sweet beverage intake in participants of European ancestry in the UK Biobank. Diet was assessed via multiple 24-h diet recalls (n=84703, subset) or questionnaire (n=335909, all). Bitter beverage intake was the sum of coffee, tea and grapefruit juice. Sweet beverage intake was the sum of artificially and sugar sweetened beverages and other fruit juice. Multivariable linear regression under an additive genetic model was applied. GW-significant (P &lt; 5х10 -8 ) SNPs were followed-up for replication in independent studies of European ancestry. Results: Multiple SNPs spanning 11 loci were associated with bitter beverage intake (P &lt;5х10 -8 , Table 1), and at least 5 of them reflected the caffeine content of coffee and tea. Multiple SNPs in the obesity candidate gene FTO were associated with sweet beverage intake (P &lt;5х10 -8 ). The effect size per allele ranged from 0.02 to 0.2 cup per day. Loci in/near AHR, CYP1A2, and FTO were associated with both bitter and sweet beverage intake but in opposite directions. Replication efforts are ongoing. So far, associations at all loci, except 1q25.2 and 2q36.2, were replicated (P range: 0.04 to 1.8x10 -8 ) in independent studies (n=17322) which provided 80% power for replicating 8 of these 12 loci at P=0.05. Conclusions: Loci linked to caffeine metabolism and obesity predisposition rather than taste are major determinants of beverage intake. These and other identified loci have been linked to chronic disease and risk factors, suggesting causal or pleiotropic effects. Our findings have potential public health and methodological implications.