tbuckley/cabot-search huggingface dataset:
Abstract 206: microRNA-29b Contributes to Multiple Types of Muscle Atrophy
Authors: Jin Li, Liming Cheng, Yihua Bei, Qiulian Zhou, Yan Yu, Siyi Fu, Lei Chen, Junjie Xiao
Journal: Circulation Research (2015)

Objective: Skeletal muscle atrophy has been observed in a significant proportion of heart failure patients while little is known about the mechanisms underlying muscle atrophy, especially in multiple types of muscle atrophy. MicroRNAs (miRNAs, miRs) are among key participants in gene regulatory networks and their dysregulation contribute to lots of diseases. However, miRNAs responsible for multiple types of muscle atrophy are unclear. Methods and Result: miRNAs were screened by miRNA arrays and were further verified by real-time reverse transcription polymerase chain reaction with the gastrocnemius sample from denervation -induce muscle atrophy. miR-130b, miR-212, miR-21, miR-221/222, miR-223 and miR-29b were upregulated &gt;3 fold in gastrocnemius samples from denervation mice than that of sham group. However, only miR-29b presented a common change (upregulated &gt;3) in other types of muscle atrophy models including dexamethasone-induced and fasting-induced muscle atrophy. Over-expression of miR-29b in gastrocnemius by intramuscular injection with agomiR-29b significantly promoted muscle atrophy, which is evidenced by the change in morphology (the diameter of myofiber was decrease by 60%) and increased atrophy-related genes including Atrogin-1 and MuRF-1 (upregulated for 1.5 folds and 1.4 folds, respectively). This in vivo data suggest that miR-29b is sufficient to induce muscle atrophy. In multiple types of muscle atrophy C2C12 cell models (dexamethasone, TNF-alpha and H2O2 induced), miR-29b was increased while inhibition of miR-29b could prevent that effects. Using TargetScan software, we found that IGF1 and PI3Ka were potential target genes for miR-29b, which was further validated by luciferase assays and western blotting. Moreover, over-expression of IGF1 or PI3Ka ameliorated muscle atrophy caused by miR-29b overexpression, indicating that IGF1 and PI3Ka are two target genes responsible for miR-29b’s pro-atrophy effects in muscle. Conclusions: Our data indicated that via targeting IGF1 and PI3Ka. Inhibition of miR-29b might represent a novel therapy for multiple types of muscle atrophy including in heart failure.
Six-Year Incidence of Age-Related Macular Degeneration in Asian Malays
Authors: Chui Ming Gemmy Cheung, Peng Guan Ong, Kumari Neelam, Pok Chien Tan, Yuan Shi, Paul Mitchell, Jie Jin Wang, Charumathi Sabanayagam, Ching-Yu Cheng, Tien Yin Wong
Journal: Ophthalmology (2017)
The golden hour: length of total warm ischemia time presages development of severe acute kidney injury after DCD liver transplantation
Authors: M. Kalisvaart, I. Umbro, J. de Haan, I. Scalera, A. Schlegel, J. IJzermans, T. Perera, J. Isaac, A.P. Mitterhofer, P. Muiesan, J. de Jonge
Journal: Journal of Hepatology (2017)
Circulating Tumor DNA Identifies EGFR Coamplification as a Mechanism of Resistance to Crizotinib in a Patient with Advanced MET-Amplified Lung Adenocarcinoma
Authors: Ibiayi Dagogo-Jack, David Fabrizio, Jochen Lennerz, Alexa B. Schrock, Lauren Young, Mari Mino-Kenudson, Subba R. Digumarthy, Rebecca S. Heist, Siraj M. Ali, Vincent A. Miller, Alice T. Shaw
Journal: Journal of Thoracic Oncology (2017)
Abstract PR04: Translational control of human colon tumor cell survival
Authors: Eyerusalem M. Lemma, Jamie L. McCall, Beth K. Clymer, David L. Kelly, Michael A. White, Robert E. Lewis
Journal: Cancer Research (2017)

Abstract Kinase Suppressor of Ras 1 (KSR1), a molecular scaffold for the Raf/MEK/ERK kinase cascade, is required for transformation and survival of cells bearing oncogenic Ras, but is not required for normal cell survival. KSR1 knockout mice are phenotypically normal, and depletion of KSR1 by RNAi does not kill immortalized, non-transformed human colon epithelial cells (HCECs), suggesting that KSR1 or KSR1-dependent effectors may serve as highly selective therapeutic targets. Our previous work showed that KSR1 regulates expression of the transcription factor peroxisome proliferator-activated receptor gamma coactivator 1 (PGC1β), whose expression is critical to colon cancer cell survival. Using RNAi and pharmacological inhibition, we observed that KSR1 and ERK drive both cap-dependent and cap-independent translation of Myc in human colon tumor cell lines, which increases PGC1β mRNA expression (McCall et al. MCB, 2016). This effect is mediated through the KSR1 and ERK-dependent phosphorylation of 4E-PB1 and phosphorylation-dependent loss of PDCD4 that reverses their inhibitory effect on eIF4E and eIF4A, respectively. Treatment with ERK inhibitor SCH772984 showed that ERK regulates PDCD4 protein expression and 4EBP1 phosphorylation to promote Myc expression in four of the seven colon cancer cell lines. These observations suggest that KSR1-dependent regulation of translation may be a common mechanism used to support tumor cell survival. Using KSR1 as a reference standard, Functional Signature Ontology (FUSION, Potts et al. Sci. Signaling 2013) was used to identify genetic vulnerabilities in human colon tumor cells that are absent in HCECs. Comparison of results from this screen to genome-wide polysome profiling data from cells transformed with Ras and Myc (Truitt et al. Cell 2015) identified 25 candidate mRNAs with altered translational efficiency that are predicted to support the survival of human colon tumor cells. These data suggest that KSR1 and ERK-dependent alteration of the translational landscape is a common strategy used to support colon tumor cell survival. Identification of mRNAs preferentially translated in colon tumor cells may yield novel targets for therapeutic manipulation and may provide unique markers with which to classify colon tumors, predict patient outcome, and select effective treatment. This abstract is also being presented as Poster B36. Citation Format: Eyerusalem M. Lemma, Jamie L. McCall, Beth K. Clymer, David L. Kelly, Michael A. White, Robert E. Lewis. Translational control of human colon tumor cell survival. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr PR04.
Autoimmune Hepatitis with normal IgG levels at diagnosis: subtype with a higher rate of successful treatment withdrawal?
Authors: J. Hartl, A. Asghar, G.W. Wong, S. Pape, A.W. Lohse, J.P. Drenth, Y.H. Oo, H.A. Michael, C. Schramm
Journal: Journal of Hepatology (2017)
Survival predictors in cirrhotic patients with refractory ascites treated with transjugular intrahepatic portosystemic shunt
Authors: M. Aicart-Ramos, L. Ibáñez-Samaniego, H. Martínez-Lozano, M.-V. Catalina, E. Rodríguez-de Santiago, R. Bañares, A. Albillos
Journal: Journal of Hepatology (2017)
Local environment in cirrhotic liver induces Th2 polarization of CD4+ cells which amplify fibrogenesis by activating hepatic stellate cells
Authors: J.A. Reissing, D. Kroy, A. Wree, M.E. Inzaugarat, M.L. Berres, C. Trautwein, H.W. Zimmermann
Journal: Journal of Hepatology (2017)
Comparison of patient performance between PEG/no PEG placement in head and neck cancer patients during chemoradiotherapy treatment.
Authors: Robin Metcalfe-Klaw, Hasan Husaini, Cathy L Lazarus, Louis Benjamin Harrison, Bruce Culliney, Zujun Li, Mark L Urken, Adam Jacobson, Daniel Buchbinder, Mark Persky, Theresa Tran, Michael Pitman, Catherine Concert, Daisy Maria Palacios, Bridget Bennett, Mahesh Kumar, Kenneth Hu
Journal: Journal of Clinical Oncology (2013)

6091 Background: Many head and neck cancer patients suffer from side effects of chemoradiotherapy that can result in reduced oral intake, and weight loss. To prevent this malnutrition they often undergo preventative percutaneous endoscopic gastrostomy (PEG) placement. We aim to determine whether PEG placement is necessary for successful patient performace during treatment. Methods: We compared 2 groups: patients that underwent PEG (Gp-1=P) (n=20), and those that did not undergo PEG (GP-2=NP) (n=47). All patients were treated with chemoradiotherapy. All were assessed at baseline (BL), and wk 5 of tx. WHO variables including weight loss, mucositis, dysphagia, and odynophagia ratings, along with patient-rated modified “distress thermometers”, were analyzed. Results: Patients with no PEGs had higher weights at BL (NP=193 vs P= 171, p=0.073) and at wk 5 (NP=179 vs P= 160, p=0.056). Weight loss in these groups were 8.09 % - P (p=0.000), 8.25% - NP (p=0.000) respectively from BL - wk 5. The median distress level of each group was 0-P and 1-NP at BL (p=0.302) and 6-P and 3-NP at wk 5 (p=0.086). 27 patients had a distress level of &gt; = 4 at wk 5. Of these 27, 12 were PEG’d and 15 were not (p=0.008). 86 % of patients in the PEG group had distress &gt;=4 and 44 % in the NP group had distress levels &gt;=4. Patients that underwent PEG had slightly higher odds (NS) of associating their distress to nausea, fatigue and/or eating than patients that were not PEG’d. The wk 5 WHO toxicity scale assessment showed 15 PEG’d patients had Grade 1 (n=5), Grade 2 (n=9) &amp; Grade 3 (n=1) dysphagia and 28 NP patients had Grade 1 (n=23) &amp; Grade 2 (n=5) dysphagia (CHI square =11.66, p=0.009). Conclusions: Patients that underwent PEG placement before or during treatment performed worse in every assessment (weight loss, distress thermometer &amp; toxicity scale) as compared to the no PEG group. Patients who have a normal or above average BMI are candidates to be monitored for PEG placement. However, both groups examined were able to complete treatment without significant treatment breaks. Close multidisciplinary monitoring and more intensive supportive care are needed when determining need for PEG placement during treatment.
Estimation of serum “true collagen type III formation” (Pro-C3) levels as a marker of non-alcoholic steatohepatitis in a prospective cohort
Authors: D.J. Leeming, J.I. Grove, P. Kaye, C. Hoad, S. Francis, M.J. Nielsen, M.A. Karsdal, I.N. Guha, G.P. Aithal
Journal: Journal of Hepatology (2017)
B. pseudocatenulatum CECT7765 effect on intestinal microbiota of rats with bile duct ligation
Authors: O.J. Juárez, I. Gómez-Hurtado, K.J. Portune, P. Zapater, P. Piñero, P. Giménez, J. Such, J.M. González-Navajas, Y. Sanz, R. Francés
Journal: Journal of Hepatology (2017)
MicroRNA-146a reduces MHC-II expression via targeting JAK/STAT signaling in dendritic cells after stem cell transplantation
Authors: N Stickel, K Hanke, D Marschner, G Prinz, M Köhler, W Melchinger, D Pfeifer, A Schmitt-Graeff, T Brummer, A Heine, P Brossart, D Wolf, N von Bubnoff, J Finke, J Duyster, J Ferrara, U Salzer, R Zeiser
Journal: Leukemia (2017)
Comprehensive NAFLD diagnosis based on a noninvasive metabolomic approach in a liquid biopsy
Authors: P. Puri, I. Martinez-Arranz, I. Mincholé, M.O. Idowu, R. Mayo, J.-F. Dufour, M. Romero-Gómez, R. Bruha, J. Crespo, J.M. Banales, C. García-Monzón, A. Martín-Duce, C. Alonso, P. Ortiz, M. Noureddin, S.C. Lu, P. Bedossa, A.J. Sanyal, J.M. Mato
Journal: Journal of Hepatology (2017)
NASH Therapy: omega 3 supplementation, vitamin E, insulin sensitizers and statin drugs
Authors: Stephen Caldwell
Journal: Clinical and Molecular Hepatology (2017)

Non-alcoholic steatohepatitis (NASH) is the more aggressive form of non-alcoholic fatty liver disease (NAFLD). NASH can progress to hepatic fibrosis, cirrhosis, portal hypertension and primary liver cancer. Therapy is evolving with a substantial number of trials of promising new agents now in progress. In this article however, we will examine data for several older forms of therapy which have been fairly extensively studied over the years: Polyunsaturated Fatty Acid (PUFA) supplements, vitamin E, insulin sensitizing agents with a focus on pioglitazone and statin agents. Early interest in PUFA derived from their potential benefit in cardio-metabolic disease and the close association of NAFLD/NASH with Metabolic Syndrome. Results have been variable although most studies show reduction of liver fat without other major effects and their effects are influenced by concomitant weight loss and underlying genetic factors. Vitamin E has had some efficacy in pediatric NASH but questionable efficacy in even mild NASH among adults. Pioglitazone has shown significant histological benefit in a number of trials but concern over side-effects (especially weight gain) have dampened enthusiasm. A newer insulin sensitizer, liraglutide, has also shown promise in a small randomized, controlled trial. Very limited data exists regarding the histological effects of the statins in NASH and these agents appear to be fairly neutral with neither clear cut benefit nor detriment. Their use is best guided by cardiovascular risks rather than liver histology. Keywords: Fatty liver; Steatohepatitis; Non-alcoholic steatohepatitis (NASH); Non-alcoholic fatty liver disease (NAFLD); Polyunsaturated Fatty Acid (PUFA)
Dilated cardiomyopathy in homozygous myosin-binding protein-C mutant mice
Authors: Bradley K. McConnell, Karen A. Jones, Diane Fatkin, Luis H. Arroyo, Richard T. Lee, Orlando Aristizabal, Daniel H. Turnbull, Dimitrios Georgakopoulos, David Kass, Meredith Bond, Hideshi Niimura, Frederick J. Schoen, David Conner, Donald A. Fischman, Christine E. Seidman, J.G. Seidman
Journal: Journal of Clinical Investigation (1999)
Community Approach Targeting Cirrhosis and Hepatocellular carcinoma (CATCH): community prevalence of advanced fibrosis in viral hepatitis
Authors: S. Bloom, W. Kemp, A. Dev, P. Gow, A. Nicoll, S. Roberts, S. Bell, I. Kronborg, V. Knight, S. Sood, D. Lewis, J. Lubel
Journal: Journal of Hepatology (2017)
An outbreak of acute hepatitis C GT1b in onco-hematological patients. Treatment with Sofosbuvir + Ledipasvir and concomitant chemotherapy
Authors: G. Brancaccio, M.C. Sorbo, F. Frigeri, V. Rizzo, M. Cantone, F. Genderini, L. Fabeni, A. Pinto, C.F. Perno, F. Ceccherini-Silberstein, G.B. Gaeta
Journal: Journal of Hepatology (2017)
Advances in ultrasound-targeted microbubble-mediated gene therapy for liver fibrosis
Authors: Cuiyuan Huang, Hong Zhang, Ruidan Bai
Journal: Acta Pharmaceutica Sinica B (2017)

Hepatic fibrosis develops as a wound-healing scar in response to acute and chronic liver inflammation and can lead to cirrhosis in patients with chronic hepatitis B and C. The condition arises due to increased synthesis and reduced degradation of extracellular matrix (ECM) and is a common pathological sequela of chronic liver disease. Excessive deposition of ECM in the liver causes liver dysfunction, ascites, and eventually upper gastrointestinal bleeding as well as a series of complications. However, fibrosis can be reversed before developing into cirrhosis and has thus been the subject of extensive researches particularly at the gene level. Currently, therapeutic genes are imported into the damaged liver to delay or prevent the development of liver fibrosis by regulating the expression of exogenous genes. One technique of gene delivery uses ultrasound targeting of microbubbles combined with therapeutic genes where the time and intensity of the ultrasound can control the release process. Ultrasound irradiation of microbubbles in the vicinity of cells changes the permeability of the cell membrane by its cavitation effect and enhances gene transfection. In this paper, recent progress in the field is reviewed with emphasis on the following aspects: the types of ultrasound microbubbles, the construction of an ultrasound-mediated gene delivery system, the mechanism of ultrasound microbubble–mediated gene transfer and the application of ultrasound microbubbles in the treatment of liver fibrosis.
Comparative effects of liraglutide, elafibranor and obeticholic acid on NAFLD activity score and fibrosis stage in a diet-induced obese mouse model of biopsy-confirmed NASH
Authors: M. Feigh, K.S. Tølbøl, M.B. Kristiansen, S.S. Veidal, L.D. Fensholdt, N. Vrang
Journal: Journal of Hepatology (2017)
The optimal cutoff value of serum alpha-fetoprotein in the diagnosis of hepatocellular carcinoma
Authors: J.-F. Tsai, S.-C. Chen, Z.-Y. Lin, C.-Y. Dai, M.L. Yi, W.-L. Chuang, J.-F. Huang, S.-C. Chen, Z.-Y. Lin, M.-L. Yu, C.-Y. Dai, W.-L. Chuang, J.-F. Huang
Journal: Journal of Hepatology (2017)
ATOH1 Promotes Leptomeningeal Dissemination and Metastasis of Sonic Hedgehog Subgroup Medulloblastomas
Authors: Katie B. Grausam, Samuel D.R. Dooyema, Laure Bihannic, Hasitha Premathilake, A. Sorana Morrissy, Antoine Forget, Amanda M. Schaefer, Justin H. Gundelach, Slobodan Macura, Diane M. Maher, Xin Wang, Alex H. Heglin, Xijin Ge, Erliang Zeng, Stephanie Puget, Indra Chandrasekar, Kameswaran Surendran, Richard J. Bram, Ulrich Schüller, Michael D. Talyor, Olivier Ayrault, Haotian Zhao
Journal: Cancer Research (2017)

Abstract Medulloblastoma arising from the cerebellum is the most common pediatric brain malignancy, with leptomeningeal metastases often present at diagnosis and recurrence associated with poor clinical outcome. In this study, we used mouse medulloblastoma models to explore the relationship of tumor pathophysiology and dysregulated expression of the NOTCH pathway transcription factor ATOH1, which is present in aggressive medulloblastoma subtypes driven by aberrant Sonic Hedgehog/Patched (SHH/PTCH) signaling. In experiments with conditional ATOH1 mouse mutants crossed to Ptch1+/− mice, which develop SHH-driven medulloblastoma, animals with Atoh1 transgene expression developed highly penetrant medulloblastoma at a young age with extensive leptomeningeal disease and metastasis to the spinal cord and brain, resembling xenografts of human SHH medulloblastoma. Metastatic tumors retained abnormal SHH signaling like tumor xenografts. Conversely, ATOH1 expression was detected consistently in recurrent and metastatic SHH medulloblastoma. Chromatin immunoprecipitation sequencing and gene expression profiling identified candidate ATOH1 targets in tumor cells involved in development and tumorigenesis. Among these targets specific to metastatic tumors, there was an enrichment in those implicated in extracellular matrix remodeling activity, cytoskeletal network and interaction with microenvironment, indicating a shift in transcriptomic and epigenomic landscapes during metastasis. Treatment with bone morphogenetic protein or SHH pathway inhibitors decreased tumor cell proliferation and suppressed metastatic tumor growth, respectively. Our work reveals a dynamic ATOH1-driven molecular cascade underlying medulloblastoma metastasis that offers possible therapeutic opportunities. Cancer Res; 77(14); 3766–77. ©2017 AACR.
Swallowing disorders after thyroidectomy: What we know and where we are. A systematic review
Authors: Gregorio Scerrino, Chiara Tudisca, Sebastiano Bonventre, Cristina Raspanti, Dario Picone, Calogero Porrello, Nunzia Cinzia Paladino, Federica Vernuccio, Francesco Cupido, Gianfranco Cocorullo, Giuseppe Lo Re, Gaspare Gulotta
Journal: International Journal of Surgery (2017)
Predictors of access and response to DAA in a cohort of human immunodeficiency virus/hepatitis C virus co-infected patients in Italy
Authors: A. d 'Arminio Monforte, A. Antinori, A. Cozzi-Lepri, F. Ceccherini-Silberstein, A. Castagna, S.L. Caputo, C. Mussini, A. De Luca, G. Madeddu, A. Cingolani, A. Tavelli, G. Taliani, A. Gori, E. Girardi, M. Puoti
Journal: Journal of Hepatology (2017)
Chemotherapeutic drug-photothermal agent co-self-assembling nanoparticles for near-infrared fluorescence and photoacoustic dual-modal imaging-guided chemo-photothermal synergistic therapy
Authors: Yang Li, Guihua Liu, Jinyuan Ma, Jinyan Lin, Huirong Lin, Guanghao Su, Dengyue Chen, Shefang Ye, Xiaoyuan Chen, Xuan Zhu, Zhenqing Hou
Journal: Journal of Controlled Release (2017)
World Hepatitis Day — July 28, 2018
Journal: MMWR Morbidity and Mortality Weekly Report (2018)

World Hepatitis Day is commemorated each year on July 28 with the goal of promoting awareness and inspiring action to prevent and treat viral hepatitis. The World Health Organization's (WHO's) theme of this year's World Hepatitis Day is "Test. Treat. Hepatitis" to underscore the urgent need to scale up testing and treatment activities.
Retrospective review of the impact of a dedicated Cancer of Unknown Primary (CUP) clinic.
Authors: Lavinia Tsia Yi Tan, Jeremy Howard Lewin, Damien Urban, Hao-Wen Sim, Rodney J Hicks, Keith Byron, Lisa Guccione, Ellen Schaef, Stephen James Luen, Richard Tothill, Penelope Schofield, David Bowtell, Linda R. Mileshkin
Journal: Journal of Clinical Oncology (2015)

e17680 Background: Patients (pts) with CUP may not be well managed in a tumour-stream based cancer centre. Hence we set up a dedicated CUP clinic in 2012. Referrals are accepted for pts with a minimum of a CT (+/- biopsy) reported to suggest extracervical CUP. Methods: A retrospective review of the initial clinic experience, with a primary aim to determine the number of pts in whom a primary site was found or named. Secondary aims were to describe the number and utility of additional investigations ordered with a specific focus on PET/CT and the CUPGuide tissue of origin assay. Results: 121 pts were referred to CUP clinic from Feb 2012 - July 2014: 52% female with a median age of 65. The table below lists additional investigations ordered. A primary site was identified or named in 57%, 12% were found to have benign lesions and 31% remained unknown primary. Amongst those whose primary site was named, 36 were named on biopsy, 20 on further pathology review, 23 based on more imaging and 18 based on CUPGuide. 42 pts (58%) in whom a biopsy was obtained prior to attending CUP clinic had their primary tumour identified compared with 25 pts (51%) without a prior biopsy. A total of 93 PET/CT scans were performed with 53% of scans helping to identify a primary (n = 31) or the best site to biopsy (n = 19). PET/CT changed management in 46% of pts. In 28 a high impact was seen: change in treatment intent from palliative to curative or vice vera (n = 6), change in treatment recommended (n = 12), confirmation of benign disease (n = 10). In a further 15 pts, PET/CT guided a site for biopsy, which led to a diagnosis, but did not change the treatment plan. 58 CUPGuide tests were ordered with 13 tests not performed due to insufficient tissue. 17/45 (38%) of pts had a change of diagnosis or treatment after receipt of the result. Conclusions: More than half the pts attending CUP clinic had their primary site identified with PET/CT and CUPGuide commonly impacting on patient care. Biopsy Prior No Biopsy Prior No. % No. % No. of patients 72 60 49 40 Additional investigations CT chest, abdomen and pelvis 9 13 12 25 PET/CT 30 42 30 61 MRI 3 4 5 10 Mammogram 4 5 0 0 Biopsy 11 15 41 84 Tumour Markers 41 57 41 84 CUPGuide 47 67 10 20 Gastroscopy & Colonoscopy 5 7 4 8 Bronchoscopy 1 1 1 2