tbuckley/cabot-search huggingface dataset:
Re: Raj Satkunasivam, Sheaumei Tsai, Sumeet Syan, et al. Robotic Unclamped “Minimal-margin” Partial Nephrectomy: Ongoing Refinement of the Anatomic Zero-ischemia Concept. Eur Urol 2015;68:705–12
Authors: Andrea Minervini, Riccardo Campi, Sergio Serni, Marco Carini
Journal: European Urology (2016)
Abstract 17557: Genetic Variants Primarily Associated eith Type 2 Diabetes Also Affect Coronary Artery Disease Risk
Authors: Henning Jansen, Christina Loley, Wolfgang Lieb, Michael J Pencina, Christopher P Nelson, Sekar Kathiresan, Muredach P Reilly, Themistocles L Assimes, Eric Boerwinkle, Alistair S Hall, Christian Hengstenberg, Reijo Laaksonen, Ruth McPherson, Unnur Thorsteinsdottir, Annette Peters, John R Thompson, Inke R Koenig, Ramachandran S Vasan, Jeanette Erdmann, Nilesh Samani, Heribert Schunkert
Journal: Circulation (2012)

Multiple single nucleotide polymorphisms (SNPs) have been identified to associate with type 2 diabetes (T2DM). If T2DM is a causal risk factor for coronary artery disease (CAD), SNPs increasing T2D...
Increased pretreatment serum IFN-β/α ratio predicts non-response to tumour necrosis factor α inhibition in rheumatoid arthritis
Authors: Theresa Wampler Muskardin, Priyanka Vashisht, Jessica M Dorschner, Mark A Jensen, Beverly S Chrabot, Marlena Kern, Jeffrey R Curtis, Maria I Danila, Stacey S Cofield, Nancy Shadick, Peter A Nigrovic, E William St Clair, Clifton O Bingham, Richard Furie, William Robinson, Mark Genovese, Christopher C Striebich, James R O'Dell, Geoffrey M Thiele, Larry W Moreland, Marc Levesque, S Louis Bridges, Peter K Gregersen, Timothy B Niewold
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Objective</h3> Studies suggest that circulating type I interferon (IFN) may predict response to biological agents in rheumatoid arthritis (RA). Prediction of response prior to initiating therapy would represent a major advancement. <h3>Methods</h3> We studied sera from a test set of 32 patients with RA from the Auto-immune Biomarkers Collaborative Network Consortium and a validation set of 92 patients with RA from the Treatment Efficacy and Toxicity in Rheumatoid Arthritis Database and Repository registry. The test set included those with good response or no response to tumour necrosis factor (TNF) inhibitors at 14 weeks by European League Against Rheumatism criteria. The validation set included subjects with good, moderate or no response at 12 weeks. Total serum type I IFN activity, IFN-α and IFN-β activity were measured using a functional reporter cell assay. <h3>Results</h3> In the test set, an increased ratio of IFN-β to IFN-α (IFN-β/α activity ratio) in pretreatment serum associated with lack of response to TNF inhibition (p=0.013). Anti-cyclic citrullinated peptide antibody titre and class of TNF inhibitor did not influence this relationship. A receiver–operator curve supported a ratio of 1.3 as the optimal cut-off. In the validation set, subjects with an IFN-β/α activity ratio &gt;1.3 were significantly more likely to have non-response than good response (OR=6.67, p=0.018). The test had 77% specificity and 45% sensitivity for prediction of non-response compared with moderate or good response. Meta-analysis of test and validation sets confirmed strong predictive capacity of IFN-β/α activity ratio (p=0.005). <h3>Conclusions</h3> Increased pretreatment serum IFN-β/α ratio strongly associated with non-response to TNF inhibition. This study supports further investigation of serum type I IFN in predicting outcome of TNF inhibition in RA.
Asparagine synthetase (AS) RNA and protein expression in acute lymphoblastic leukemia (ALL) cell lines and patient samples
Authors: M. Zhou, R. C. Harvey, S. P. Hunger
Journal: Journal of Clinical Oncology (2005)

8510 Background: Asparaginase (ASP) is a key component of therapy for childhood ALL that is hypothesized to be active due to low intrinsic AS expression in lymphoblasts that render them incapable of synthesizing sufficient asparagine and therefore reliant on import of extracellular asparagine for protein synthesis. Elevated AS expression can confer ASP resistance in experimental models, but there are few data on ASP sensitivity and AS expression in primary ALLs. Methods: We studied ASP sensitive Molt-4 and an ASP resistant subclone Molt-4(R), Jurkat, REH, RCH-ACV, K562, and Nalm6 cell ines and 20 primary childhood ALL samples. Cell number and viability following 72 hours of incubation with and without varying concentrations of ASP was determined for cell lines using WST-1 and the IC50 was defined as the concentration that produced 50% decrease in viable cells as compared to vehicle only controls. We developed real-time RT-PCR (qRT-PCR) assays and measured AS RNA expression in cell lines and patient samples as normalized to EEF2 expression. We also used an AS monclonal antibody to determine protein expression in cell lines via Western blot, immunofluoresence microscopy (IF) and flow cytometry. Results: The ASP IC50 of Molt-4(R) and K562 were more than 10 IU/mL while the IC50 of Molt-4(S) was 0.002 IU/mL. Other cell lines displayed intermediate ASP IC50s. qRT-PCR showed that K562 and Molt-4(R) expressed AS RNA at levels 10–20 times higher than Molt-4(S), while other cell lines expressed intermediate levels. AS RNA levels varied by approximately 10-fold among primary ALLs, with levels in high level patient samples similar to those observed in REH and RCH-ACV. AS protein levels as quantitated by Western blot, IF and flow cytometry are consistent with the AS mRNA expression for each cell line. Conclusions: AS RNA and protein levels can be readily measured by qRT-PCR, Western blot, IF and flow cytometry. Primary patient samples display variable levels of AS RNA expression. These tools will facilitate measurement of AS expression in primary ALL cells prior to and following ASP exposure to facilitate a more rational and effective use of ASP. No significant financial relationships to disclose.
Predicting the three-dimensional folding of cis-regulatory regions in mammalian genomes using bioinformatic data and polymer models
Authors: Chris A. Brackley, Jill M. Brown, Dominic Waithe, Christian Babbs, James Davies, Jim R. Hughes, Veronica J. Buckle, Davide Marenduzzo
Journal: Genome biology (2016)

The three-dimensional (3D) organization of chromosomes can be probed using methods like Capture-C. However, it is unclear how such population-level data relate to the organization within a single cell, and the mechanisms leading to the observed interactions are still largely obscure. We present a polymer modeling scheme based on the assumption that chromosome architecture is maintained by protein bridges, which form chromatin loops. To test the model, we perform FISH experiments and compare with Capture-C data. Starting merely from the locations of protein binding sites, our model accurately predicts the experimentally observed chromatin interactions, revealing a population of 3D conformations.
P-268 Impact of optimal morphologic response on survival in patients with KRAS wild-type unresectable colorectal liver metastases receiving an anti-EGFR or anti-VEGF agent
Authors: T. Masuishi, H. Taniguchi, Y. Narita, A. Komori, M. Nomura, S. Kadowaki, M. Andoh, T. Ura, T. Eto, K. Muro
Journal: Annals of Oncology (2015)
Abstract 343: Prediction of Lifesaving Interventions Using Changes in Vital Signs from Prehospital Scene to Emergency Department
Authors: Jorge H Mena Munoz, Ashley Petersen, Francis X Guyette
Journal: Circulation (2014)

Objective: We investigate whether changes in vital signs between the prehospital scene and emergency department (ED) can be used to develop triage tools to predict the need for life-saving interventions (LSI) and survival in trauma patients. Methods: We analyzed a prospective cohort with any prehospital systolic blood pressure (SBP) ≤ 90 mmHg or Glasgow Coma Scale ≤ 8 who were admitted to an ED at 11 sites of the Resuscitation Outcomes Consortium. The primary outcome was the need for in-hospital LSI (e.g. invasive airway management, invasive bleeding control, blood transfusion, craniotomy, cardiopulmonary resuscitation). Secondary outcome was survival to hospital discharge. Changes in heart rate (HR), SBP, shock index (SI), and respiratory rate (RR) from first prehospital assessment to first ED assessment were considered as predictors in addition to sex, age, mechanism of injury, trauma center level, duration of transport, type of transport, and prehospital fluid volume. Decision trees for each outcome were developed using binary recursive partitioning with predictive performance measured using sensitivity, specificity, and classification error. Results: 5625 subjects were included in our analysis with 49% in need of LSI and 21% dying prior to discharge. Patients needing an LSI tended to either: (1) have an increasing SI (delta ≥ 0.22), (2) have a decreasing SI (delta &lt; 0.22) and &gt;500 mL prehospital fluids, or (3) have a decreasing SI (delta &lt; 0.22), ≤500 mL prehospital fluids, and large change in RR (delta ≥ 9.5 or delta &lt; -7.5). Those surviving to discharge tended to either: (1) have a decreasing SI (delta &lt; 0.57) and a HR that did not decrease greatly (delta &gt; -47) or (2) have an increase in SI (0.57 ≤ delta &lt; 1) and a declining RR (delta &lt; 5). LSI tree had a sensitivity of 58.7% and specificity of 63.3%. Survival tree had sensitivity of 96.2% and specificity of 21.3%. Conclusion: Though the decision trees were constructed with the best data in terms of initial triage and early secondary triage, the classification performance was limited. This highlights the difficulties of developing vital sign based triage tools to predict the need for LSI and survival.
Capecitabine (X) plus irinotecan (XELIRI) as first-line treatment for metastatic colorectal cancer (MCRC): Final safety findings from a phase II trial
Authors: Y. Z. Patt, J. Liebmann, D. Diamandidis, S. G. Eckhardt, M. Javle, G. R. Justice, W. Keiser, F. C. Lee, W. Miller, E. Lin
Journal: Journal of Clinical Oncology (2004)

3602
WITHDRAWN: Contribution of system A subtypes to neutral amino acid transport in human and rat placental barrier
Authors: Yu Takahashi, Tomohiro Nishimura, Tetsuo Maruyama, Masatoshi Tomi, Emi Nakashima
Journal: Asian Journal of Pharmaceutical Sciences (2015)

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy.
Prognostic variables in patients with diffuse large-cell lymphoma treated with MACOP-B.
Authors: P J Hoskins, V Ng, J J Spinelli, P Klimo, J M Connors
Journal: Journal of Clinical Oncology (1991)

One hundred twenty-six patients with diffuse large-cell lymphoma were treated with methotrexate with leucovorin, doxorubicin, cyclophosphamide, vincristine, prednisone, and bleomycin (MACOP-B) between April 1981 and June 1986. Univariate and multivariate analyses were performed using overall survival as of September 1989 as the end point. Four independent negative predictors of survival were identified: presence of B symptoms; more than two involved lymph node sites; more than one extranodal site (variables related to tumor burden), and age older than 60, a variable related to the patient's ability to tolerate treatment. Each variable contributed the same relative risk of dying and, accordingly, this simple predictive formula was developed empirically: (4-N) x 30 = the approximate percentage of chance of survival at 5 years. "N" is the number of predictive variables present. The same four predictors were also found to be significant by multivariate analysis when only those patients achieving a complete response were analyzed.
Only time can tell: a commentary: AUTHORS' RETROSPECTIVE
Authors: I. E. Hoefer, W. Schaper
Journal: Cardiovascular Research (2012)

This editorial refers to an article by I.E. Hoefer et al .[3][1] published in Cardiovascular Research in 2001 (see [Box 1][2]). It is accompanied by an editorial by M. Post (doi:10.1093/cvr/cvs176) as part of this Spotlight on Landmark Papers in Cardiovascular Research . 

Despite the persistent use of the term ‘angiogenesis’ to cover several forms of post-natal vessel growth, the molecular, cellular, and—most important—functional differences between de novo vascularization, capillary sprouting, and collateral vessel enlargement became evident in the late 1990s. This finally caused us to introduce ‘arteriogenesis’ as a distinct mechanism into the Cardiovascular Research field, describing the maturation of pre-existent arteriolar connections into functional collateral arteries rather than an extended network of small-calibre vessels.1,2 The growing perception of these discrepancies and the recognition that any effects of exogenous manipulation have to be evaluated in the light of the natural response triggered our study on the natural time course of arteriogenesis in the rabbit hindlimb model.3 Until then, the field was dominated by the hypothesis that adaptations to arterial occlusions were driven by the resulting tissue ischaemia, and stimulators hence had to be among hypoxia-induced factors. Then and now, vascular endothelial growth factor (VEGF) probably is the most prominent representative of these factors with innumerable studies on its angiogenic properties. Various encouraging reports on the use of VEGF and basic fibroblast growth factor (FGF-2) to improve tissue perfusion preceded the publication of our study in the context of a dedicated Cardiovascular Research special focus issue on therapeutic angiogenesis.4–9 The resulting enthusiasm from these case reports and uncontrolled Phase I/II trials was dampened by the negative results of a placebo-controlled Phase II study and the awareness of potential major safety concerns.10 Enthusiasm was followed by caution and we recognized the need for a deeper …

 [1]: #ref-3
 [2]: #F1
Disparities in the clinical trial participation of adult cancer patients
Authors: T. R. Wassenaar, M. C. Walsh, J. F. Cleary, P. L. Remington, A. Trentham Dietz
Journal: Journal of Clinical Oncology (2008)

9524 Background: Only 2–4% of newly diagnosed adult cancer patients participate in clinical trials, and the reasons for low participation are unclear. Methods: We conducted a cross-sectional study of clinical trial participation including 1,839 cancer patients (breast, colorectal, lung, and prostate) in Wisconsin. Covariates of interest included demographic (age, gender, race, marital status), economic (employment status, income level, education) and clinical (type of malignancy, modality of treatment, use of alternative therapies, influence of cancer support groups) factors as well as satisfaction with care. Chi-square tests were calculated for participation in clinical trials and whether patients were told about clinical trial options. Results: Patient participation in clinical trials varied by cancer site: breast cancer (9.8%), colorectal cancer (11.0%), lung cancer (11.6%) and prostate cancer (2.5%). Of the patients that did not participate in a clinical trial, 60% reported they were not told about trials as a treatment option. Overall, clinical trial participation did not vary according to age, income, education, or employment status. Sample size limitations prevented adequate analysis of the association between race/ethnicity and trial participation. Factors that were associated with an increase in participation were increased time traveled for care (breast p=0.02, lung p=0.04), living in a more rural setting (lung p=0.009), treatment with chemotherapy (breast p=0.007, colorectal p=0.001, lung p=0.03), openness to alternative therapies (breast p=0.05, colorectal p=0.004), and having treatment decisions influenced by support groups (breast p=0.05, lung p=0.02). Additionally, patients were less likely to be told about participation in a clinical trial if they were not satisfied with the care they received (colorectal p=0.009, lung p=0.001, prostate p=0.03). Conclusions: While participation in clinical trials among cancer patients remains low, it is alarming that 60% of the subjects in our study who did not participate in a trial stated they were not told that clinical trials were a treatment option. Patient satisfaction with care and cancer specific support groups, among other factors, appears to be related with participation in clinical trials. No significant financial relationships to disclose.
Epidemiologic risk factors associated with breast cancer subtypes.
Authors: A. Bambhroliya, M. Bondy, P. Thompson, A. Sahin, J. L. Murray, R. Zhou, K. Sexton, A. M. Brewster
Journal: Journal of Clinical Oncology (2010)

1585 Background: Four biomarkers (estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and Ki67) can be used to classify tumors into subtypes (luminal A, luminal B, HER2 and basal-like) that exhibit different clinical behaviors. We investigated the epidemiological risk factors associated with these subtypes with additional stratification of HER2 tumors for which no specific risk factors have been identified. Methods: This study utilized 709 Caucasian patients from a retrospective cohort study of approximately 2,400 women diagnosed with stage I-II breast cancer at the MD Anderson Cancer Center between 1985 and 2000 with information available on epidemiological factors. Tumors were classified into 5 breast cancer subtypes: luminal A (ER positive and/or PR positive, HER2 negative, low KI67), luminal B (ER positive and/or PR positive, HER negative, high KI67), ER negative/HER2-positive (ER negative and PR negative, HER2 positive), luminal- HER2 (ER positive and/or PR positive and HER2 positive) and basal-like (ER negative, PR negative and HER2 negative). Logistic regression with backward selection was used to estimate the odds ratio (OR) and 95% confidence interval (CI) for the associations between epidemiological factors and subtypes. Results: Luminal B and basal-like cases were less likely to be postmenopausal (OR = 0.35, 95% CI = 0.18 - 0.68) and (OR = 0.33, 95% CI = 0.16 - 0.66), respectively compared to luminal A cases. ER negative/HER2 positive cases were more likely to consume 1- < 20 drinks of alcohol per month versus never (OR = 2.88, 95% CI = 1.83 - 24.18), have a positive family history of breast cancer (OR = 6.50, 95% CI = 1.97 - 21.40) and have menarche at < 12 versus ≥13 years (OR = 6.41, 95% CI = 1.67 - 24.59) compared to luminal A cases. No epidemiological risk factors were found to be significantly associated with the luminal-HER2 subtype compared to luminal A subtype. Conclusions: Clinically, HER2 tumors are considered a distinct subtype based on their aggressiveness and response to targeted therapies. We identified different epidemiological risk factors associated with HER2 breast cancers based on ER and PR status suggesting different etiological pathways along luminal and basal lineages. No significant financial relationships to disclose.
Deliberate Self-harm Following Bariatric Surgery
Authors: David J. R. Morgan, Kwok M. Ho
Journal: JAMA Surgery (2016)

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Abstract 11609: Aberrant Expression of Smooth Muscle Markers and Regulators, Myocardin and MRTFA/B in Calcific Aortic Valve Disease
Authors: Najma Latif, Padmini Sarathchandra, Adrian Chester, Magdi H Yacoub
Journal: Circulation (2012)

Similar mediators and pathogenetic pathways are invloved in calcific aortic stenosis (CAS) and atherosclerosis. Smooth muscle (SM) cells play a major role in atherosclerosis and undergo phenotypic modulation. Normal valves harbour a low percentage of smooth muscle cells however their role in CAS is not defined. We hypothesized that the SM cell phenotype plays a role in the pathophysiology of CAS. We analysed 12 normal and 22 calcified valves for early and late, differentiated SM markers by immunocytochemistry. The expression of co-activators and key regulators of SM gene expression, myocardin and myocardin-related transcription factors, (MRTFA/B), was also evaluated. Key cytokines were used to activate MRTFs and transmission electron microscopy (TEM) used to detect the presence of SM cells in atypical regions of the valve leaflets. In normal valves SM markers are localised to the base of the ventricularis. The expression of calponin, SM1, SM2 and SM22 was dysregulated (increased and in fibrosa) in all 22 calcified valves with caldesmon, SM myosin, SM α-actin and desmin dysregulated in 40-91% of calcified valves. SM markers were abundantly expressed in surface and microvessel endothelial cells and vasculature in 40% of the calcified valves. Normal valves showed expression of myocardin, MRTF-A and -B in the base of the ventricularis, similar to the pattern of SM in normal valves. An aberrant expression of myocardin, MRTF-A and MRTF-B, was found in 71%, 53% and 67% respectively of calcified valves, in a similar pattern to the aberrant expression of SM markers. The expression of MRTFs was nuclear in both valve interstitial cells (VICs) and endothelial cells in calcified valves suggestive of activation. TGFβ1 (10ng/ml) was able to upregulate the nuclear expression of MRTF-A by 11-fold in VICs (p<0.05). TEM of the fibrosa layer of calcified valves demonstrated the presence of bundles of SM cells and SM-derived foam cells. In conclusion, SM cells were abundant and SM-derived foam cells were observed in atypical regions of calcified valves. SM markers and co-activators were increased and aberrantly expressed in calcified valves. These findings strongly suggest that the SM phenotype plays an important role in the pathophysiology of CAS which has, as yet, been neglected.