tbuckley/cabot-search huggingface dataset:
AB0202 Cardiac Troponin T and Anti-Cardiac Troponin I Antibodies in Patients with Systemic Sclerosis: A Monocentric, Retrospective Pilot Study
Authors: M. Vasile, Z. Kaya, M. Frerix, U. Mueller-Ladner, A. Rolf, F. Meier
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Cardiac troponins (cTn) are widely used as biomarkers for the diagnosis and quantitation of cardiac injury (1). Autoantibodies against cTn, especially against cTnI (anti-cTnI), have been recently described in association with cardiac dysfunction (2). However, their clinical significance is still unclear. Systemic sclerosis (SSc) is a chronic autoimmune connective tissue disease that is associated with heart involvement, although often clinically occult (3,4). <h3>Objectives</h3> Hence, the value of elevated cTn levels and a possible autoimmune response against cTnI as biomarkers in patients with SSc were the aims of this study. <h3>Methods</h3> Out of our monocentric SSc cohort we retrospectively identified 113 of 190 patients in whom routine laboratory assessment including high-sensitive cTnT was performed. Stored biosamples, available for 60/113 patients (53.1%), were used to assess auto-cTnI titres as previously described (5). A 2x2 table, using chi-square test, compared the results of cTnT and anti-cTnI. If available, cardiac magnetic-resonance-imaging (cMRI) data were retrospectively evaluated to assess early myocardial gadolinium enhancement (T1 ratio, as a marker for hyperemia and capillary leakage) as well as edema (T2 ratio). <h3>Results</h3> Out of 113 patients with available results for cTNT, 41 patients (36.3%) had a positive and 72 (63.7%) a negative result. Biosamples were available for 21 cTNT positive and 39 cTNT negative patients. Anti-cTnI were detected in 17 samples (28.3%): in 8 (38.1%) cTNT positive compared to 9 (23.1%) cTNT negative patients (p=0.218). Anti-cTnI-titres were 1:40 in 7, 1:80 in 6 and 1:160 in 4 samples. cMRI data were available for three anti-cTnI positive patients (all diffuse cutaneous subtype). All of them had a distinct change in the T1 ratio (6.4-8.9), not in the T2 ratio. Late enhancement (gold standard for the detection of myocarditis) was present in one patient (6). <h3>Conclusions</h3> The preliminary results of this pilot study suggest that cTnT levels are elevated in about one third of SSc patients, and anti-cTnI are present in about a third of cTNT positive patients. Additionally, anti-cTnI can be detected in about a quarter of cTNT negative patients. Whether cTNT and/or anti-cTnI autoantibodies might serve as new biomarkers in SSc heart disease need to be evaluated in further prospective trials. <h3>References</h3> Kaya Z Clin. Immunol. 134,80–88(2010). Kaya Z Circulation Research 110,145–158(2012). Allanore Y Curr Opin Rheumatol 20,697–702(2008). Meune C Arch Cardiovasc Dis 103,46–52(2010). Leuschner F Eur. Heart J. 29, 1949–1955(2008). Desai CS Curr Opin Rheumatol 23,545–554(2011). <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3595
Abstract 4725: Interrogating region 4 of 8q24.13 for prostate cancer risk in African Americans
Authors: Wenndy Hernandez, Jada Benn-Torres, Stanley E. Hooker, Christiane Robbins, John Carpten, Rick A. Kittles
Journal: Cancer Research (2010)

Abstract In the USA, African American (AA) men are at higher risk of developing and dying from prostate cancer (Pca). Strong and replicable associations between prostate cancer risk and regions 1, 2, and 3 of 8q24 among cohorts of European ancestry have been found but few for those of African ancestry. Recently, we discovered in a study of AAs, a fourth region of Pca risk at 126 Mb of 8q24.13 surrounding SNP rs7008482. Region 4 is 2 Mb upstream of the other three regions on 8q24 and contains two interesting candidate genes for Pca risk. To further interrogate region 4, we performed fine-mapping within a 500-Kb region (126.1Mb-126.6Mb). SNPs were selected for fine-mapping of the region based on the following characteristics: tagging SNPs from Yoruba HAPMAP data and non-synonymous or potential regulatory SNPs. We genotyped 250 SNPs in 263 AA Pca cases and 562 AA healthy controls. A structured-association analysis taking into account African ancestry, (local 8q24 ancestry and genomic ancestry) revealed that several SNPs within two genes KIAA0196 and NSMCE2 were significantly associated with Pca risk. The majority of the associated SNPs were common and exhibited low to moderate risk which may contribute to high population attributable risk in African Americans. Among these, rs16900305, located in an intronic region of KIAA0196, exhibited the strongest association (P=0.0003). KIAA0196 has been shown to be over-expressed in clinical prostate carcinomas and in approximately 30% of hormone-refractory tumors. Our findings strongly support region 4 in 8q24.13 as a candidate locus influencing prostate cancer risk among African Americans. Given the two interesting genes in this region and strong associations in a high risk group for Pca, further attention to this region is warranted. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4725.
Abstract 2604: PENAO: A novel tumor metabolism inhibitor for glioblastoma
Authors: Sylvia A. Chung, Pierre J. Dilda, Emma E. Ramsay, Charlie Teo, Philip J. Hogg, Kerrie L. McDonald
Journal: Cancer Research (2011)

Abstract Despite undeniable progress in the care and the treatment of primary brain tumors, for most patients diagnosed with glioblastoma (GBM) there is no realistic possibility of cure or even long term survival. Inherent resistance to conventional chemotherapy and irradiation are characteristic of GBM. Testing of new potential anti-tumorigenic drugs is needed. PENAO, (4-(N-(S-penicillaminylacetyl)amino)phenylarsonous acid) is a mitochondrial toxin that inactivates inner-membrane adenine nucleotide translocase (ANT) resulting in proliferation arrest and apoptosis of tumor and tumor-supporting cells. The cytostatic efficacy of PENAO was tested on a panel of five commercial and primary GBM cell lines that differed in tumorigenicity, drug resistance, invasion and DNA repair. PENAO demonstrated an impressive anti-proliferative activity compared to carboplatin and temozolomide, drugs commonly used to treat GBM patients. The half maximal inhibitory concentration (IC50) values for PENAO were all in the low micromolar range. The increase in anti-proliferative activity for PENAO compared to carboplatin ranged from 6 to 200-fold. PENAO is a substrate for the multidrug resistant associated proteins 1 and 2 and inhibition of this transporter enhanced PENAO anti-proliferative activity from 2 to 8-fold. In conclusion, PENAO is a potent inhibitor of GBM cell line proliferation. This activity was superior to that observed with standard chemotherapeutics and warrants further in vivo investigations. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2604. doi:10.1158/1538-7445.AM2011-2604
Abstract 258: Development of death receptor agonists - A novel therapy for breast cancer
Authors: Rakesh Srivastava, Sharmila Shankar
Journal: Cancer Research (2012)

Abstract Binding of TRAIL to death receptors (TRAIL-R1/DR4 and TRAIL-R2/DR5) induces apoptosis in cancer cells without affecting normal cells. The purpose of this study was to identify and characterize TRAIL-death receptor agonist (DRA) that induces apoptosis in breast cancer cells. DRA is a small organic molecule. The pharmacokinetics of the DRA with a single oral dose was also characterized in nude mice. Blood was collected over 72-hour period after DRA administration, and analyzed by HPLC-MS/MS for plasma drug concentration. The Cmax, tmax, and AUC of DRA were measured. DRA inhibited cell viability and colony formation, and induced apoptosis in estrogen-dependent (MCF-7) and independent (MDA-MB-231 and MDA-MB-468) human breast cancer cell lines, but had no effect on human normal mammary epithelial cells and hepatocytes. The combination of DRA with paclitaxel or doxorubicin had synergistic effects on apoptosis in breast cancer cell lines. DRA formed active TRAIL-DISC (death-inducing signaling complex) similar to that of TRAIL. DRA inhibited the growth of orthotopically implanted MDA-MB-231 and MDA-MB-468 tumors in nude mice. Histological examination of tumor tissues derived from DRA-treated nude mice revealed massive caspase-3 activation and apoptosis. Pharmacokinetic data demonstrate that DRA possesses a long terminal half-life, which is acceptable for further clinical development. In conclusion, we have identified DRA that can be used either alone or in combination with chemotherapeutic drugs for the treatment of human breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 258. doi:1538-7445.AM2012-258
PHARMACOKINETIC AND PHARMACODYNAMIC RESPONSE TO ORAL AND SUBCUTANEOUS FUROSEMIDE ADMINISTRATION: FIRST EXPERIENCES WITH A NOVEL BUFFERED FUROSEMIDE FORMULATION IN PATIENTS WITH CHRONIC HEART FAILURE
Authors: Rudolf A. De Boer, Jozine ter Maaten, Kevin Damman, Pieter Muntendam, Domenic A. Sica, Dirk van Veldhuisen, Bertram Pitt
Journal: Journal of the American College of Cardiology (2016)
Abstract P4-14-04: Total skin-sparing mastectomy in BRCA mutation carriers
Authors: Peled A Warren, ES Hwang, CA Ewing, M Alvarado, LJ Esserman
Journal: Cancer Research (2012)

Abstract BACKGROUND: Total skin-sparing mastectomy (TSSM) with preservation of the nipple-areolar complex skin has become increasingly accepted as an oncologically safe procedure for both prophylactic and therapeutic indications. The goal of this study was to evaluate the oncologic outcomes after TSSM in BRCA mutation carriers. METHODS: We identified 53 BRCA-positive patients who underwent bilateral TSSM for prophylactic (27 patients) or therapeutic (26 patients) indications from 2001 to 2011. Cases were age-matched (for prophylactic cases) or age- and stage-matched (for therapeutic cases) with non-BRCA-positive patients who underwent bilateral TSSM during this time period. Outcomes included tumor involvement of the resected nipple tissue, the development of new breast cancers in patients who underwent bilateral risk-reducing TSSM, and the development of any local-regional recurrence in patients who underwent therapeutic TSSM. RESULTS: Outcomes from 212 TSSM procedures in 53 cases and 53 controls were analyzed. In patients undergoing TSSM for prophylactic indications, in situ cancer was found in 1 (1.9%) of the nipple specimens in the BRCA-positive patients vs. 2 specimens (3.7%) in the non-BRCA-positive cohort (p = 1). At a mean follow-up of 56 months, no new cancers developed in the BRCA-positive or the non-BRCA-positive cohorts. In patients undergoing TSSM for therapeutic indications, in situ or invasive cancer was found in 0 of the nipple specimens in the BRCA-positive patients vs. 2 specimens (3.9%) in the non-BRCA-positive cohort (p = 0.49). At a mean follow-up of 33 months, there were no local-regional recurrences in the BRCA-positive cohort. CONCLUSIONS: TSSM is an oncologically safe procedure in BRCA-positive patients, as is evidenced by the low rates of tumor involvement of the nipple tissue and local-regional recurrence after therapeutic mastectomy. In BRCA-positive patients undergoing TSSM as a risk-reducing strategy, five-year follow-up demonstrates no increased risk for the development of new breast cancers; longer-term follow-up is anticipated to further confirm its safety. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P4-14-04.
1137 EFFECTIVENESS OF HCV TRIPLE THERAPY WITH TELAPREVIR IN NEW YORK CITY
Authors: V. Martel-Laferriere, K. Bichoupan, A. Pappas, E. Schonfeld, M. Ng, R. Sefcik, M.-L. Vachon, M. Standen, P. Perumalswami, T.D. Schiano, J.A. Odin, L. Liu, D.T. Dieterich, A.D. Branch
Journal: Journal of Hepatology (2012)
NECROSECTOMÍA ENDOSCÓPIA TRANSGÁSTRICA. EXPERIENCIA EN NUESTRO CENTRO
Authors: B Merino Rodríguez, O Nogales Rincón, A Huerta Madrigal, A Cruz Moratinos, E Cos Arregui, P Menchén Fernández Pacheco, C González Asanza
Journal: Endoscopy (2010)

Introducción: La necrosis pancreática es una complicación grave de la pancreatitis aguda. La cirugía se asocia con una elevada morbimortalidad. El tratamiento endoscópico tiene el potencial para ofrecer una alternativa más segura y eficaz.
PET IMAGING IN PATIENTS WITH BIOCHEMICAL FAILURE FOLLOWING TREATMENT FOR LOCALIZED PROSTATE CANCER
Authors: M. A. Seltzer, Z. Barbaric, J. Naitoh, D. H.S. Silverman, J. B. deKernion, A. Belldegrun, P. Rosen, M. E. Phelps, C. K. Hoh
Journal: Clinical Nuclear Medicine (1998)

Seltzer, M. A.; Barbaric, Z.; Naitoh, J.; Silverman, D. H.S.; deKernion, J. B.; Belldegrun, A.; Rosen, P.; Phelps, M. E.; Hoh, C. K. Author Information
Abstract LB-67: COX-2/PGE2: molecular ambassadors of Kaposi's sarcoma associated herpes virus (KSHV) oncoprotein-v-FLIP
Authors: Neelam Sharma-Walia, Kinjan Patel, Karthic Chandran, Alexandru Marginean, Virginie Bottero, Nagaraj Kerur, Arun George-Paul
Journal: Cancer Research (2012)

Abstract Kaposi's sarcoma herpesvirus latent oncoprotein viral FLICE-like inhibitory protein (v-FLIP) or K13, a potent activator of NF-κB has well established roles in KSHV latency and oncogenesis. KSHV induced COX-2 represents a novel strategy employed by KSHV to promote latency and inflammation/angiogenesis/invasion. Here, we demonstrate that v-FLIP/K13 promotes tumorigenic effects via induction of host protein COX-2 and its inflammatory metabolite PGE2 in an NF-κB dependent manner. In addition to our previous studies demonstrating COX-2/PGE2's role in transcriptional regulation of KSHV latency promoter and latent gene expression, current study adds to the complexity that though LANA-1 (latency associated nuclear antigen) is utilizing COX-2/PGE2 as critical factors for its transcriptional regulation, it is the v-FLIP/K13 gene in the KSHV latency cluster that maintains continuous COX-2/PGE2 levels in infected cells. We demonstrate that COX-2 inhibition, via its chemical inhibitors (NS-398 or celecoxib), reduced v-FLIP/K13 mediated NF-κB induction, and extracellular matrix (ECM) interaction mediated FAK/Src/AKT, Rac-1 activation, mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) levels, and subsequently down-regulated detachment-induced apoptosis (anoikis) resistance. COX-2 inhibition in v-FLIP/K13-Human microvascular endothelial cells (HMVECs) reduced inflammation and invasion/metastasis related genes along with reduced anchorage independent colony formation via modulating ‘extrinsic’ as well as ‘intrinsic’ cell death pathways. COX-2 blockade in v-FLIP/K13-HMVECs drastically augmented cell death induced by removal of essential growth/survival factors secreted in the microenvironment. Transformed cells obtained from anchorage independent colonies of COX-2 inhibitor treated v-FLIP/K13-HMVEC cells expressed lowered levels of endothelial mesenchymal transition (EndMT) genes such as slug, snail and twist, and higher expression of the tumor suppressor gene E-cadherin. Taken together, our study provides strong evidences that FDA approved COX-2 inhibitors have great implications in blocking tumorigenic events linked to KSHV's oncogenic protein v-FLIP/K13. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-67. doi:1538-7445.AM2012-LB-67
Abstract 331: C-MYC gene amplification in endometrial cancer is associated with aggressive tumors
Authors: Even Birkeland, Antje Krohn, Jone Trovik, Frederik Holst, Henrica M.J. Werner, Camilla K. Krakstad, Elisabeth Wik, Lars Akslen, Ronald Simon, Helga B. Salvesen
Journal: Cancer Research (2011)

Abstract Endometrial cancer is among the most common gynaecological malignancies in industrialized countries. Although 75% of cancers are treated at an early stage, 15% to 20% recur. Due to these recurrences the demand for systemic therapies and better prognostic markers are vital. Our recent study of global genetic characterisation has identified that C-MYC amplifications associate with aggressive phenotype in uterine cancers (Salvesen et al., PNAS 2009). The present study was conducted to validate the phenotype associated with C-MYC amplification in a large population based prospectively collected sample series from primary tumours and corresponding metastatic lesions from patients with endometrial cancer. Primary tumours from 399 patients and 80 corresponding metastatic lesions were analysed for amplification of the C-MYC gene using fluorescence in situ hybridization (FISH). We found that 5% of primary endometrial cancer tumors have C-MYC amplifications or gains. C-MYC amplification is correlated with high FIGO stage (P = 0.003), non-endometroid subtype (P = 0.002), and high grade (P &amp;lt;0.001). Patients with C-MYC amplifications had a significantly poorer recurrence free- (P = 0.002) and disease specific survival (P = &amp;lt;0.001). These data suggest that C-MYC amplification might be one important mechanism involved in endometrial cancer tumourigenesis. Further characterization of C-MYC amplifications in corresponding metastatic lesions are in progress. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 331. doi:10.1158/1538-7445.AM2011-331
THU0093 Deiminated Histone 4 from Neutrophil Extracellular Traps is a Novel Autontigen in Rheumatoid Arthritis
Authors: P. Migliorini, F. Pratesi, I. Dioni, M. C. Alcaro, I. Paolini, F. Panza, P. Rovero
Journal: Annals of the Rheumatic Diseases (2013)

Liver cancer, primarily hepatocellular carcinoma (HCC), is a major cause of cancer-related death worldwide. HCC is a suitable model of inflammation-induced cancer because more than 90% of HCC cases are caused by liver damage and chronic inflammation. Several inflammatory response pathways, such as NF-κB and JAK/STAT3 signaling pathways, play roles in the crosstalk between inflammation and HCC. MicroRNAs (miRNAs) are evolutionarily conserved, short endogenous, non-coding single-stranded RNAs that are involved in various biological and pathological processes by regulating gene expression and protein translation. Evidence showed that miRNAs play a pivotal role in hepatitis virus infection and serve as promoters or inhibitors of inflammatory response. Aberrant miRNA was observed during liver inflammation and HCC. Many dysregulated miRNAs modulate the initiation and progression of inflammation-induced HCC. This review summarizes the role and functions of miRNAs in inflammation-associated HCC, as well as the designed therapeutics targeting miRNAs to treat liver inflammation and HCC.
Hugh Henry Bentall
Authors: A. Gulland
Journal: BMJ (2012)

Pioneer in heart-lung surgery

In April 1959, at the height of the cold war, a team of specialists from Hammersmith Hospital boarded a container ship and set sail for Moscow. On board the ship was the “heart-lung machine” developed by Denis Melrose and used in 1953 to perform the first successful open heart operation in the UK.

That operation was carried out by a team that included Hugh Bentall, who went on to become the first professor of cardiac surgery at Imperial College. The team’s fame had spread and at a conference a Russian heart specialist, Alexander Bakulev, challenged them to prove that the heart-lung machine worked.

As well as acting as first surgical assistant, Bentall’s job was to arrange the complex logistics for the trip and to pack everything that could “conceivably be needed to perform six operations in Moscow.”1 Once arrived in the USSR, he tested the equipment and the on-site blood transfusion facilities by performing a mitral valvotomy, a routine heart …
ASSOCIATIONS OF BODY MASS INDEX, WASTING SYNDROME AND PROGNOSIS IN PATIENTS WITH CHRONIC HEART FAILURE
Authors: Tetsuji Morishita, Hiroyasu Uzui, Naoki Amaya, Kenichi Kaseno, Kentaro Ishida, Yoshitomo Fukuoka, Hiroyuki Ikeda, Naoto Tama, Kanae Hasegawa, Yuichiro Shiomi, Takayoshi Aiki, Akira Matsui, Moe Mukai, Jong-Dae Lee, Hiroshi Tada
Journal: Journal of the American College of Cardiology (2016)
VALUE OF NEUTROPHIL TO LYMPHOCYTE RATIO AS A PREDICTOR OF MORTALITY IN PATIENTS WITH HEART FAILURE WITH PRESERVED EJECTION FRACTION
Authors: Habib Habib, Mohammad Thawabi, Amer Hawatmeh, Ashesha Mechineni, Anas J. Alkhateeb, Yamini Sundermurthy, Youssef Botros, Kelvin Luu, Amore Giuseppe, Mirette Habib, Ashraf Jmeian, Walid Elkhalili, Zaid Altheeb, Fayez Shamoon, Medhat Zaher
Journal: Journal of the American College of Cardiology (2016)
AB0500 B-Cell Depleting Therapy for SLE Related Refractory Thrombocytopenia
Authors: Y.J. Kim, E.-J. Lee, S. Hong, B.S. Koo, W.J. Seo, J. Oh, Y.-G. Kim, C.-K. Lee, B. Yoo
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Autoimmune thrombocytopenia is a common manifestation of systemic lupus erythematosus (SLE) which may accompany bleeding risk and complications. B cell depleting therapy has been tried experimentally in SLE related thrombocytopenia refractory to standard treatment including corticosteroids, intravenous immunoglobulin, cyclophosphamide, and mycophenolate mofetil. <h3>Objectives</h3> Here, we evaluated the efficacy of rituximab in SLE patients with severe thrombocytopenia refractory to conventional treatment. <h3>Methods</h3> In our retrospective study, rituximab was administered in 5 patients with severe thrombocytopenia (platelet count &lt;50 x10<sup>9</sup>/l) refractory to traditional treatments. Patients received i.v. rituximab at a dose of 500mg every week for 4 doses or 1000mg every 2 weeks for two doses. Peripheral CD 19<sup>+</sup> B cell counts were evaluated before and after rituximab infusion. <h3>Results</h3> Among five patients with refractory thrombocytopenia, 2/5 (40%) patients achieved complete responses (CR, platelet count &gt;100 x10<sup>9</sup>/l) at week 4 after rituximab infusion. The CR rate increased to 3/5 patients at week 12, and 5/5 at week 24. Overall response (OR, platelet count &gt;50 x10<sup>9</sup>/l) was achieved in 4/5 and 5/5 at week 4 and 12 respectively. Baseline B cell count was 158±133 x10<sup>6</sup>/l (range 3-348 x10<sup>6</sup>/l) and complete depletion (&lt;5 x10<sup>6</sup>/l) was achieved in all 5 patients at week 4. Although 4 patients maintained normal platelet counts through 28 (range 11-48) months follow up period, one patient had relapsed 2 years after the last rituximab infusion with increasing B cell counts. However, good response was observed after reinfusion with rituximab. <h3>Conclusions</h3> Our study showed that rituximab therapy induces a rapid and sustained remission in severe and refractory autoimmune thrombocytopenia in SLE patients. <h3>References</h3> Pinto LF, Velasquez CJ, Prieto C et al. Rituximab induces a rapid and sustained remission in Colombian patients with severe and refractory systemic lupus erythematosus. Lupus 2011;20:1219-26. Lee JW, Kim HA, Sung JM et al. Successful treatment of refractory immune thrombocytopenia with anti-CD20 antibody in a patient with systemic lupus erythematosus. Lupus 2010;19:227-8. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3221
202 USE OF TELAPREVIR PLUS PEG INTERFERON/RIBAVIRIN FOR NULL RESPONDERS POST OLT WITH ADVANCED FIBROSIS/CHOLESTATIC HEPATITIS C
Authors: P. Kwo, M. Ghabril, M. Lacerda, R. Vinayek, A.J. Tector, J. Fridell, R. Vianna
Journal: Journal of Hepatology (2012)