tbuckley/cabot-search huggingface dataset:
Pre-Treatment WT1 mRNA Expression Level In Peripheral Blood Predicts Response and Overall Survival Of Myelodysplastic Syndrome Patients In The Azacitidine Era
Authors: Tomoyasu Jo, Kazuya Sakai, Hiroyuki Muranushi, Yusuke Okamoto, Taku Tsukamoto, Hiroyuki Sugiura, Hiroyuki Matsui, Tomoaki Ueda, Kazuya Okada, Takeshi Maeda, Tatsuhito Onishi, Akane Kunitomi, Yasunori Ueda
Journal: Blood (2013)
Identification of a major epitope by anti-interferon-γ autoantibodies in patients with mycobacterial disease
Authors: Chia-Hao Lin, Chih-Yu Chi, Han-Po Shih, Jing-Ya Ding, Chia-Chi Lo, Shang-Yu Wang, Chen-Yen Kuo, Chun-Fu Yeh, Kun-Hua Tu, Shou-Hsuan Liu, Hung-Kai Chen, Chen-Hsuan Ho, Mao-Wang Ho, Chen-Hsiang Lee, Hsin-Chin Lai, Cheng-Lung Ku
Journal: Nature Medicine (2016)
Abstract A1-61: ANT2 shRNA downregulates multiple onco-miRNAs through the targets, TIMP-2, and suppresses cell death in human hepatocellular carcinoma cells
Authors: Seung Hyun Baik, Jong Kuen Lee, Chul-Woo Kim
Journal: Cancer Research (2015)

Abstract Micro RNA (miRNAs) are negative regulators of gene expression functioning either as tumor suppressors or oncogenes in cancer. As expression patterns of miRNAs and their role in the pathogenesis of hepatocellular carcinoma (HCC) are still poorly understood we investigated the roles of specific miRNAs in this study. We examined that knockdown of ANT2 by shRNA down-regulates onco-miRNA (miR-19a and miR-96) expression levels, and leads to the suppression of proliferation and tumorigenesis in HCC cell line. Microarray profiling of miRNAs showed that the expression of miR-19a and miR-96 were markedly upregulated in both Hep3B and HepG2 cells and their ectopic expression dramatically induced the proliferation and the ability of hepatoma cells to form colonies in vitro, while the inhibition of miR-19a and miR-96 reduced this effect. To investigate the in vivo function, we implanted miR-96 overexpressed-HepG2 in Balbc/nude mice and demonstrated that increase of miR-96 induces tumor growth. We also found that miR-19a and miR-96 are downregulated by ANT2 shRNA, which in turn induces the accumulation of TIMP-2 and the inactivation of p300. Taken together, our results suggest that miR-19a and miR-96 may play an important role in promoting proliferation of human HCC cells and also suggest that the knock down of ANT2 by shRNA directly down-regulates multi-onco-miRNAs, ultimately resulting in suppression of tumor growth Citation Format: Seung Hyun Baik, Jong Kuen Lee, Chul-Woo Kim. ANT2 shRNA downregulates multiple onco-miRNAs through the targets, TIMP-2, and suppresses cell death in human hepatocellular carcinoma cells. [abstract]. In: Proceedings of the AACR Special Conference on Translation of the Cancer Genome; Feb 7-9, 2015; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(22 Suppl 1):Abstract nr A1-61.
Effect of Drug Therapy on Net Cholesterol Efflux Capacity of High‐Density Lipoprotein–Enriched Serum in Rheumatoid Arthritis
Authors: Michelle J. Ormseth, Patricia G. Yancey, Joseph F. Solus, S. Louis Bridges, Jeffrey R. Curtis, MacRae F. Linton, Sergio Fazio, Sean S. Davies, L. Jackson Roberts, Kasey C. Vickers, Valentina Kon, C. Michael Stein
Journal: Arthritis & Rheumatology (2016)

Patients with rheumatoid arthritis (RA) have an increased risk of coronary heart disease (CHD). Some RA therapies may modify this risk, but the underlying mechanisms are unclear. The cholesterol efflux capacity of high-density lipoprotein (HDL) is associated with a reduced CHD risk in non-RA populations; however, inflammation may impair the function of HDL. The aim of this study was to evaluate whether reduced inflammation resulting from treatment with methotrexate (MTX), adalimumab (ADA), or tocilizumab (TCZ) would increase the net cholesterol efflux capacity of HDL in patients with RA.A longitudinal multicenter study repository (Treatment Efficacy and Toxicity in Rheumatoid Arthritis Database and Repository) provided clinical information for and serum samples from 70 patients with RA before and 6 months after starting treatment with a new drug (MTX [n = 23], ADA [n = 22], or TCZ [n = 25]). Disease activity was measured using the Disease Activity Score in 28 joints using the erythrocyte sedimentation rate (DAS28-ESR). The net cholesterol efflux capacity was measured in paired serum samples using THP-1 macrophages, and total cellular cholesterol was measured by fluorometric assay.The DAS28-ESR decreased with all treatments (P < 0.001). Net cholesterol efflux capacity was not significantly changed after 6 months of new RA therapy (mean ± SD 36.9 ± 17.3% units at baseline versus 38.0% ± 16.9% units at 6 months [P = 0.58]). However, change in net cholesterol efflux capacity was associated with change in the DAS28-ESR (ρ = -0.25, P = 0.04). In a post hoc analysis of patients with impaired net cholesterol efflux capacity at baseline, treatment with TCZ resulted in significant improvement in net cholesterol efflux capacity (21.9 ± 14.7% units at baseline versus 31.3% ± 12.8% units at 6 months [P < 0.02]), but this was not observed with MTX or ADA.Net cholesterol efflux capacity of HDL cholesterol did not change significantly after 6 months of new RA therapy, except in patients with impaired baseline cholesterol efflux capacity who were receiving TCZ. Change in disease activity was associated with change in the net cholesterol efflux capacity.
Vital Signs: Epidemiology of Sepsis: Prevalence of Health Care Factors and Opportunities for Prevention
Authors: Shannon A. Novosad, Mathew R.P. Sapiano, Cheri Grigg, Jason Lake, Misha Robyn, Ghinwa Dumyati, Christina Felsen, Debra Blog, Elizabeth Dufort, Shelley Zansky, Kathryn Wiedeman, Lacey Avery, Raymund B. Dantes, John A. Jernigan, Shelley S. Magill, Anthony Fiore, Lauren Epstein
Journal: MMWR Morbidity and Mortality Weekly Report (2016)

Sepsis is a serious and often fatal clinical syndrome, resulting from infection. Information on patient demographics, risk factors, and infections leading to sepsis is needed to integrate comprehensive sepsis prevention, early recognition, and treatment strategies.To describe characteristics of patients with sepsis, CDC and partners conducted a retrospective chart review in four New York hospitals. Random samples of medical records from adult and pediatric patients with administrative codes for severe sepsis or septic shock were reviewed.Medical records of 246 adults and 79 children (aged birth to 17 years) were reviewed. Overall, 72% of patients had a health care factor during the 30 days before sepsis admission or a selected chronic condition likely to require frequent medical care. Pneumonia was the most common infection leading to sepsis. The most common pathogens isolated from blood cultures were Escherichia coli in adults aged ≥18 years, Klebsiella spp. in children aged ≥1 year, and Enterococcus spp. in infants aged <1 year; for 106 (33%) patients, no pathogen was isolated. Eighty-two (25%) patients with sepsis died, including 65 (26%) adults and 17 (22%) infants and children.Infection prevention strategies (e.g., vaccination, reducing transmission of pathogens in health care environments, and appropriate management of chronic diseases) are likely to have a substantial impact on reducing sepsis. CDC, in partnership with organizations representing clinicians, patients, and other stakeholders, is launching a comprehensive campaign to demonstrate that prevention of infections that cause sepsis, and early recognition of sepsis, are integral to overall patient safety.
Tie1: an orphan receptor provides context for angiopoietin-2/Tie2 signaling
Authors: Sarah B. Mueller, Christopher D. Kontos
Journal: Journal of Clinical Investigation (2016)

Angiopoietin-1/Tie2 (ANG1/Tie2) signaling is well documented as regulating angiogenesis and vessel maturation. This pathway is complicated by involvement of the orphan receptor Tie1, which has been implicated as both a positive and negative regulator of ANG1/Tie2 signaling, and ANG2, which can serve as both a Tie2 agonist and antagonist, depending on the context. Two papers in this issue of the JCI provide new insight into this complicated pathway. Korhonen et al. reveal that Tie1 acts to modulate the effects of ANG1 and ANG2 on Tie2 in vitro and in vivo. Kim et al. demonstrate that ANG2 acts as a Tie2 agonist in non-pathological conditions, whereas in the setting of inflammation, ANG2 functions as a Tie2 antagonist and promotes vascular dysfunction. Both studies indicate that inflammation promotes cleavage of the ectodomain of Tie1 and that this cleavage event corresponds with the switch of ANG2 from a Tie2 agonist to an antagonist. The results of these studies lay the groundwork for future strategies to therapeutically exploit this pathway in diseases characterized by adverse vascular remodeling and increased permeability.
Bone Mineral Density At Diagnosis Determines Fracture Rate in Children Treated According to the DCOG-ALL9 Protocol
Authors: Mariel L te Winkel, Rob Pieters, Wim C.J. Hop, Jan C. Roos, Inge M. van der Sluis, Jos P.M. Bökkerink, Jan A. Leeuw, Marrie C. A. Bruin, Wouter J.W. Kollen, Anjo J.P. Veerman, Hester A. de Groot-Kruseman, Marry M. van den Heuvel-Eibrink
Journal: Blood (2012)
Review: In acute depression, interpersonal psychotherapy is more effective than control but not other therapies
Authors: Patrick G. O’Malley
Journal: Annals of Internal Medicine (2016)

Source Citation Cuijpers P, Donker T, Weissman MM, Ravitz P, Cristea IA. Interpersonal psychotherapy for mental health problems: A comprehensive meta-analysis. Am J Psychiatry. 2016;173:680-7. 27032627
Identification of Optimal Mouse Models of Systemic Sclerosis by Interspecies Comparative Genomics
Authors: Jennifer L. Sargent, Zhenghui Li, Antonios O. Aliprantis, Matthew Greenblatt, Raphael Lemaire, Ming‐hua Wu, Jun Wei, Jaclyn Taroni, Adam Harris, Kristen B. Long, Chelsea Burgwin, Carol M. Artlett, Elizabeth P. Blankenhorn, Robert Lafyatis, John Varga, Stephen H. Clark, Michael L. Whitfield
Journal: Arthritis & Rheumatology (2016)

Objective Understanding the pathogenesis of systemic sclerosis (SSc) is confounded by considerable disease heterogeneity. Animal models of SSc that recapitulate distinct subsets of disease at the molecular level have not been delineated. We applied interspecies comparative analysis of genomic data from multiple mouse models of SSc and patients with SSc to determine which animal models best reflect the SSc intrinsic molecular subsets. Methods Gene expression measured in skin from mice with sclerodermatous graft‐versus‐host disease (GVHD), bleomycin‐induced fibrosis, Tsk1/+ or Tsk2/+ mice was mapped to human orthologs and compared to SSc skin biopsy–derived gene expression. Transforming growth factor β (TGFβ) activation was assessed using a responsive signature in mice, and tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression was measured in SSc patient and mouse skin. Results Gene expression in skin from mice with sclerodermatous GVHD and bleomycin‐induced fibrosis corresponded to that in SSc patients in the inflammatory molecular subset. In contrast, Tsk2/+ mice showed gene expression corresponding to the fibroproliferative SSc subset. Enrichment of a TGFβ‐responsive signature was observed in both Tsk2/+ mice and mice with bleomycin‐induced skin fibrosis. Expression of TNFRSF12A (the TWEAK receptor/fibroblast growth factor–inducible 14) was elevated in skin from patients with fibroproliferative SSc and the skin of Tsk2/+ mice. Conclusion This study reveals similarities in cutaneous gene expression between distinct mouse models of SSc and specific molecular subsets of the disease. Different pathways underlie the intrinsic subsets including TGFβ, interleukin‐13 (IL‐13), and IL‐4. We identify a novel target, Tnfrsf12a , with elevated expression in skin from patients with fibroproliferative SSc and Tsk2/+ mice. These findings will inform mechanistic and translational preclinical studies in SSc.
Transdisciplinary Approach to Managing Hepatitis C Virus Infection in Patients at a Tertiary Care Cancer Center
Authors: Harrys A. Torres, Lillian R. Roach, Parag Mahale, Minas P. Economides, Boris Blechacz, Ethan Miller, Roy Borchardt, Anis Rashid, Thein H. Oo, Bhavarth Shukla, Malik Farida, Charles D. Ericsson, Bruno P. Granwehr, Issam I. Raad
Journal: Journal of the National Comprehensive Cancer Network (2016)
Nasal and sinus symptoms and chronic rhinosinusitis in a population-based sample
Authors: A. G. Hirsch, W. F. Stewart, A. S. Sundaresan, A. J. Young, T. L. Kennedy, J. Scott Greene, W. Feng, B. K. Tan, R. P. Schleimer, R. C. Kern, A. Lidder, B. S. Schwartz
Journal: Allergy (2016)

The objective of this study was to describe the first US-based study to use the European Position Paper on Rhinosinusitis (EPOS) criteria to study the prevalence of chronic rhinosinusitis (CRS) in a general-population sample.A CRS symptom questionnaire was mailed to 23 700 primary care patients from Geisinger Clinic, a health system serving 45 counties in Pennsylvania. CRS cases were categorized into four unique subgroups based on EPOS symptoms: obstruction and discharge with no smell loss or pain/pressure; smell loss without pain/pressure; facial pain and/or pressure without smell loss; and both smell loss and pain/pressure. All cases were required to have nasal obstruction or discharge. Logistic regression was used to evaluate potential factors associated with CRS subgroups.We found that 11.9% of patients met criteria for CRS. Prevalence peaked at 15.9% between ages 50 and 59 years and then dropped to 6.8% after age 69. The odds of CRS was higher among patients who were white, younger, smokers, had a history of Medical Assistance, and had other diseases. When CRS subgroups were modeled separately, these associations were no longer significant for some CRS subgroups. Comorbid diseases were most strongly associated with CRS cases who reported smell loss and facial pain and/or pressure and had the weakest associations with CRS cases who did not report these symptoms.CRS is a highly prevalent and heterogeneous condition. Differences in risk factors and health outcomes across symptom subgroups may be indicative of differences in etiology that have implications for disease management.
Association of different <i>EGFR</i> mutations with different outcomes in <i>EGFR</i>-mutated NSCLC patients treated with tyrosine kinase inhibitors.
Authors: Paola Ulivi, Elisabetta Petracci, Claudio Dazzi, Alberto Verlicchi, Matteo Canale, Elisa Chiadini, Laura Capelli, Alessandro Gamboni, Maximilian Papi, Marco Angelo Burgio, Marita Mariotti, Nicoletta De Luigi, Vienna Ludovini, Chiara Bennati, Rita Chiari, Lucio Crino, Dino Amadori, Angelo Delmonte
Journal: Journal of Clinical Oncology (2016)

e20513 Background: Epidermal growth factor receptor (EGFR) mutations are associated with response to tyrosine kinase inhibitors (TKIs). However, different EGFR mutations appear to have different predictive role. We analyzed the impact of different EGFR mutations in EGFR-mutated non-small cell lung cancer (NSCLC) patients receiving first-line TKI treatment. Methods: 136 EGFR-mutated NSCLC patients receiving first-line TKI treatment were considered. The different EGFR mutations were analyzed in relation to overall response rate (ORR), disease control rate (DCR: complete response [CR] + partial response [PR] + stable disease [SD]), progression-free survival (PFS) and overall survival (OS). Results: 6 (4%) patients had an exon 18 mutation, 74 (54%) an exon 19 deletion, and 56 (41%) an exon 21 mutation (49 L858R and 7 L861Q). Global ORR and DCR were 56% and 84%, respectively. Patients with exon 19 deletion showed an ORR of 69% and a DCR of 92% compared to 39% and 71% in patients with other EGFR mutations (p = 0.001 and p = 0.004, respectively). Patients with exon 19 deletion starting from codon 746 had the highest ORR and DCR (74% p < 0.001 and 97% p < 0.001, respectively) and the lowest risk of recurrence (RR 0.10 [95% CI 0.02-0.38], p = 0.003). Overall median PFS and OS were 11.6 (7.9-14.6) and 32.3 (22.9-not reached [nr]) months, respectively. In patients with exon 19 deletion, PFS was 14.6 (95% CI 11.6-19.8) months and OS was not reached with respect to patients with other mutations (7.3 [5.0-12.2], p = 0.026, and 22.8 [12.0-nr], p = 0.003, respectively). Exon 19 deletion was associated with a lower risk of recurrence (HR = 0.64 [95% CI 0.43-0.95], p = 0.027) or death (HR = 0.47 [95% CI 0.27-0.79], p = 0.005). Moreover, exon 19 deletions starting from codon 746 were associated with a longer PFS and OS (16.8 [11.8 – 22.7] and nr [35.0-nr], respectively) with respect to the other patients (10.8 [5.68-nr] and nr [5.8-nr], respectively) (HR 0.63 [95% CI 0.42-0.94], p = 0.02 and HR 0.39 [95% CI 0.22-0.69], p = 0.001, respectively). Conclusions: EGFR exon 19 deletion and, in particular, deletions starting from codon 746, confer a higher responsiveness to TKI and a better prognosis with respect to the other EGFR mutations.
Bam Regimen Followed By High-Dose Therapy and Autologous Stem Cell Transplantation As First-Line Treatment Of Primary Central Nervous System Lymphoma: A Multicenter Study From Spanish Group GEL-TAMO
Authors: M López-Parra, A Martín, C Grande, S Bobillo, S M Rojas, JM Sancho, N Alonso, E González-Barca, L Escoda, P Fernández-Abellán, A Álvarez-Carmona, C Montalbán, JM Moraleda, E Pardal, MJ Peñarrubia, E Pérez-Ceballos, P González-Sierra, J Pérez-Oteyza, MJ Ramírez, A Salar, P Sánchez-Godoy, F Graus, M.D. Caballero, A López-Guillermo
Journal: Blood (2013)
Comparison of four validated psoriatic arthritis screening tools in diagnosing psoriatic arthritis in patients with psoriasis (COMPAQ Study)
Authors: S. Mishra, H. Kancharla, S. Dogra, A. Sharma
Journal: British Journal of Dermatology (2016)

Four validated psoriatic arthritis (PsA) screening tools are used for diagnosing PsA in patients with psoriasis. To evaluate the sensitivity and specificity of the Toronto Psoriatic Arthritis Screen II (ToPAS II), the Psoriatic Arthritis Screening and Evaluation (PASE), the Psoriasis Epidemiology Screening Tool (PEST) and the Early Arthritis for Psoriatic Patients (EARP) questionnaires in diagnosing PsA in patients with psoriasis. This was a noninterventional, cross‐sectional study. In total, 302 patients with psoriasis completed all the questionnaires prior to rheumatological evaluation. Patients diagnosed as having a rheumatological disease were excluded. Characteristics of joint involvement in PsA were noted, but details of non‐PsA rheumatological diseases were not captured. Of 302 patients with psoriasis, 45 (14·9%) had PsA, according to the Classification of Psoriatic Arthritis criteria; 27 (8·9%) had a ToPAS II score ≥ 8, suggestive of PsA; 36 (11·9%) had a PEST questionnaire score ≥ 3, suggestive of PsA; 50 (16·5%) had a PASE questionnaire score ≥ 44 (PASE 44), suggestive of PsA; 47 (15·5%) had a PASE score of 47 (PASE 47; used in development of the PASE questionnaire); and 72 (23·8%) patients had an EARP questionnaire score ≥ 3, suggestive of PsA. The sensitivities and specificities of EARP, PASE 44, PASE 47, PEST and ToPAS II were 91%, 80%, 76%, 53% and 44%, and 88%, 95%, 95%, 95% and 97%, respectively. EARP was found to have the best sensitivity; ToPAS II had the highest specificity. A major limitation of the study design was the exclusion of pre‐existing rheumatological diseases.
Atypical Antipsychotic-Induced Weight Gain in Children and Adolescents
Authors: Christopher J. McDougle
Journal: JAMA Psychiatry (2016)

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Immunochemotherapy with rituximab in combination with fludarabine and epirubicine as first-line treatment in patients with chronic lymphocytic leukemia.
Authors: K. U. Chow, S. Kim-Wanner, S. Hermann, L. Wunderle, H. J. Cordes, L. Bergmann
Journal: Journal of Clinical Oncology (2010)

8075 Background: Clinical trials of monoclonal antibodies in combination with chemotherapy have shown previously high response rates in patients with B-cell chronic lymphocytic leukemia (B-CLL). We conducted a phase-II study combining the CD20-antibody rituximab with the effective cytotoxic regimen fludarabine and epirubicine. Methods: 6 cycles of rituximab at a dose of 375 mg/m2 day 1 in the first cycle and at a dose of 500 mg/m2 all consecutive cycles combined with fludarabine 25 mg/m2 on days 1 to 5 and epirubicine 25 mg/m2 on days 4 and 5 following a maintenance therapy of 12 cycles of rituximab 375 mg/m2 every second month have been given as a first- or second-line treatment to patients with B-CLL, prolymphocytic leukemia (PLL) and leukemic immunocytoma (IC). Results: 45 patients have been enrolled with a median age of 65 years (range 43-84 years). 44 patients are evaluable according to the NCIWG criteria. 38 patients had B-CLL, 4 PLL and 2 IC. 19 patients had stage Binet C, 15 patients Binet B and 8 patients progressive stage Binet A. Cytogenetic features showed 10 patients with normal karyotype, 13 with single del 13q, 8 with trisomy 12 and 2 with del 11 and 6 with del 17p. 51% revealed mutated IgVH genes, 21% were CD38 positive and 12% were ZAP-70 positive.The overall response rate was 98%, including 64% complete remissions (CR) and 34% partial remissions. All patients with PLL and IC achieved CR and 50% of patients with del 17p achieved CR. Hematological toxicity was high with leukopenia grade 3/4 in 44% of all evaluable courses. The performance free survival rate (PFS) and the overall survival was 80% and 90% after a median follow-up period of 32 months (0-69 months). There was a significantly longer PFS for patients having achieved CR. Conclusions: The combination of rituximab with fludarabine and epirubicine is effective in the first-line treatment of CLL. Especially, comparatively high CR rates could be achieved in patients with del 17p. Nevertheless, hematological toxicity is high and therapy has to be discontinued in some cases. No significant financial relationships to disclose.