tbuckley/cabot-search huggingface dataset:
Abstract 1455: A model to predict possible parameters to assess tumor progression with Optoacoustic Imaging
Authors: Andreas G. Gertsch, Nigel L. Bush, David CCJ Birtill, Jeff C. Bamber
Journal: Cancer Research (2010)

Abstract Optoacoustic (OA) imaging is a novel technique which allows optical absorption contrast to be visualized noninvasive using laser induced thermoelastically generated ultrasound. In tumors the highest optical absorption contrast is due to the blood/vascularization. Using optoacoustic biomarkers (such as gold nanoparticle-antibody conjugates) the signal of the vascularization could be enhanced or also other specific regions could be targeted. To assess tumor progression the size of the microvessels and the distance between them can be useful information. We found two different methods to quantify these two parameters using OA imaging. OA texture analysis and the analysis of the contrast-to-noise ratio in the reconstructed OA image and the acoustic frequency spectrum analysis in the raw signal. We present a model to predict the potential of using OA texture analysis combined with acoustic frequency spectrum analysis of the OA signal to assess the progression of tumors. The model is based on the simulation of OA signals using a time domain acoustic propagation method and a Fourier reconstruction algorithm, which has been tested with basic phantom studies. The properties of the receive part, the ultrasound (US) probe, such as the element size, center frequency or bandwidth can freely be adapted. This makes it possible to use this model with any OA system using an US system as the receiver. We show that it is possible to assess the size of optoacoustic absobers, such as the size of the microvasculature in tumors, and partly the distance between them using OA imaging. We also show the influence of a limited bandwidth of the US transducer on the outcome and therefore which transducers should be used for which application. The model has also been tested on different tumors in mice. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 1455.
600 NEBIVOLOL TREATMENT INCREASES SPLANCHNIC BLOOD FLOW AND PORTAL PRESSURE IN CIRRHOTIC RATS VIA MODULATION OF NO SIGNALING
Authors: T. Reiberger, B.A. Payer, P. Schwabl, H. Hayden, T. Horvatits, M. Trauner, V. Fuhrmann, B. Angermayr, M. Peck-Radosavljevic
Journal: Journal of Hepatology (2013)
Beyond response output: More logical than we think
Authors: Wim De Neys
Journal: Behavioral and Brain Sciences (2009)

Abstract Oaksford &amp; Chater (O&amp;C) rely on a data fitting approach to show that a Bayesian model captures the core reasoning data better than its logicist rivals. The problem is that O&amp;C's modeling has focused exclusively on response output data. I argue that this exclusive focus is biasing their conclusions. Recent studies that focused on the processes that resulted in the response selection are more positive for the role of logic.
The Influence of HLA Compatibility on Graft Survival after Heart Transplantation
Authors: Gerhard Opelz, Thomas Wujciak
Journal: New England Journal of Medicine (1994)

In cardiac transplantation, it is standard practice for donor hearts to be allocated to recipients without consideration of the extent of HLA matching. Because the HLA system is highly polymorphic, the likelihood that donor hearts will be well matched to their recipients by chance alone is extremely small. It has therefore not been possible in the past to analyze adequately the success rate of transplantation with HLA-matched hearts.We initiated a collaborative study in 1985 to evaluate the influence of HLA compatibility on graft survival in heart transplantation. Data were collected from 104 centers in 24 countries.Of the 8331 patients, 128 received a graft with no HLA-A, B, or DR mismatches or only one mismatch. This frequency (1.5 percent) corresponds to the rate that would be expected from a random allocation of donor organs. The three-year rate of graft survival correlated strongly with HLA compatibility, decreasing from a mean (+/- SE) of 83 +/- 4 percent for the 128 donor hearts with no mismatches or only one mismatch to 76 +/- 2 percent for the 439 hearts with two mismatches and 71 +/- 1 percent for the 7764 hearts with three to six mismatches (P < 0.001). Multifactorial Cox regression analysis showed that this effect was independent of the age and sex of the donor and recipient, the type of underlying disease, the duration of cold ischemia, and the use of prophylaxis with antilymphocyte antibodies (P = 0.005).Graft survival in heart transplantation is significantly influenced by the extent of HLA compatibility.
Abstract 324: A NUT-variant midline carcinoma showing a complex karyotype
Authors: Katherine Thompson, Alex H. Beesley, Elizabeth Baker, Tanya Grumball, Dagmara A. Kennedy, Ashleigh R. Murch, Marianne B. Philips, Adrian K. Charles, Chris A. French, Ursula R. Kees
Journal: Cancer Research (2010)

Abstract NUT-midline carcinomas (NMC) are rare, almost uniformly lethal malignant tumours arising in the midline organs. Originally diagnosed predominantly in the young, they have since been identified in people ranging in age from 3 to 78 years. The tumours are typically very aggressive in behaviour, with an average survival of only nine months. NMCs are typified by a single, conserved underlying genetic translocation t(15;19)(q14;p13.1), that results in a fusion of the BRD4 and NUT genes. There are a few cases described in which NUT is fused to a different gene (primarily BRD3) and these are known as NUT-variants. It is very rare however, for translocations other than the primary one, to be present. We present an NMC case with a far more complex karyotype, with the translocations t(6;19)(q14;p13.1) and t(1;18;7)(q42;q11.2;q21) present in all cells, as well as approximately 10% of cells demonstrating t(12;15)(q13;q22). Initial FISH experiments, using break-apart probes, established a translocation of the 19p13.1 (BRD4) region, and demonstrated no translocation of the 15q14 (NUT) region. Subsequent experiments, using BRD4 specific probes in a cell line derived from the patient specimen, have shown that BRD4 was inserted into chromosome 15, in a region proximal to the NUT gene. We are currently determining whether BRD4 was fused directly to NUT through a cryptic translocation in this case. Illumina Human-Cyto-SNP-12 BeadChip array analysis has also shown that a 3.3MB region of 6q14 (adjacent to the region translocated onto chromosome 19) was deleted in the tumour cells. The array indicated no deletions or duplications at the sites of any of the other translocations. Given the aggressive nature of these tumours, a better understanding of the underlying genetic causes and precipitating factors of the disease processes remains imperative to improving the outcome for such patients. 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 324.
A Woman with Fever and Dyspnea
Authors: Damaris D. Nou, Anand Vaidya, Laura Dichtel, Joel T. Katz, Katherine McGowan
Journal: New England Journal of Medicine (2014)

A 65-year-old woman presented to an urgent care clinic with a 1-week history of fatigue, dyspnea on exertion, and daily fevers of up to 38.9°C. She reported no chills but did have night sweats. She had difficulty breathing, especially when climbing stairs and when attempting to sleep while lying supine. She had no cough, sore throat, chest pain, edema of the legs, rash, or . . .
Abstract 5452: High-fat diet induces inflammation by increasing estrogen levels through Stat3, estrogen receptor alpha and aromatase in the mouse prostate.
Authors: Natarajan Bhaskaran, Sanjeev Shukla, Vijay S. Thakur, Melissa A. Babcook, Gregory T. MacLennan, Guiming Liu, Firouz Daneshgari, Sanjay Gupta
Journal: Cancer Research (2013)

Abstract High-fat diet (HFD), an unfortunate lifestyle choice common in the Western world, is associated with inflammation and thereby is regarded as a risk factor for various diseases including obesity, diabetes, and cancer. The molecular mechanism(s) responsible for HFD-induced inflammation in the prostate gland are not well understood. Estrogen receptor alpha (ER-α), signal transducer and activator of transcription (Stat)-3 and aromatase are important signaling molecules constitutively activated during inflammation and have been shown to be upregulated in prostate cancer. We have previously reported that HFD activates a pro-inflammatory response in the prostate through elevated expression of Stat-3 (Prostate 72:233-43, 2012). In the current study, we sought to investigate a possible link between intraprostatic inflammation, HFD feeding, signaling molecules involved in inflammation viz. ER-α, Stat-3, p-Stat3 (Ser727) and aromatase. C57BL/6 mice were fed either a regular diet (RD) or a HFD for 4, 8 and 12 weeks. Serum, visceral fat and prostate tissues were obtained for analysis. HFD intake caused an increase in fat and serum testosterone levels. No significant changes were observed in the testosterone levels in the prostate. A marked increase in estrogen levels was noted in the prostate and visceral fat at 8 weeks of HFD intake. HFD feeding resulted in a significant increase in the expression of aromatase, ER-α, Stat-3 and p-Stat3 (Ser727) at the message and protein levels. Immunoprecipitation and ChIP analysis demonstrated an increased association between aromatase, p-Stat-3 and ER-α in the HFD group. IHC analysis revealed higher expression of Stat-3, ER-α and aromatase in the prostate, accompanied by the morphologic evidence of increased intraprostatic inflammation in the HFD group. Taken together, our findings suggest that HFD increases estrogen levels by increased binding of ER-α and p-Stat-3 to the promoter of aromatase and their interaction is associated with increased intraprostatic inflammation which might contribute to the initiation and development of prostate cancer. Citation Format: Natarajan Bhaskaran, Sanjeev Shukla, Vijay S. Thakur, Melissa A. Babcook, Gregory T. MacLennan, Guiming Liu, Firouz Daneshgari, Sanjay Gupta. High-fat diet induces inflammation by increasing estrogen levels through Stat3, estrogen receptor alpha and aromatase in the mouse prostate. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5452. doi:10.1158/1538-7445.AM2013-5452
DECLINING EXERCISE CAPACITY AND INCREASING OBESITY IN PATIENTS UNDERGOING STRESS TESTING: INSIGHTS FROM A 25 YEAR PROSPECTIVE REGISTRY
Authors: Serge C. Harb, Venu Menon, Yuping Wu, Carol Rouphael, Paul Cremer, Theresa Guy, Leslie Cho, Wael Jaber
Journal: Journal of the American College of Cardiology (2016)
Persistent Stapedial Artery Visualized through a Perforated Tympanic Membrane
Authors: Kevin W Lollar, Alexander G Bien
Journal: New England Journal of Medicine (2011)

A 29-year-old woman presented with a perforation of the right tympanic membrane secondary to previously placed tympanostomy tubes. The perforation was 25% of the size of the tympanic membrane. She also reported mild intermittent pulsatile tinnitus and hearing loss.
OP0049 The lenght of remission and rate of relapse after tocilizumab withdrawal in rheumatoid arthritis patients
Authors: L. Aguilar-Lozano, J. Padilla-Ibarra, C. Sandoval-Castro, J.D. Castillo-Ortiz, J. Morales-Torres, C. Hernandez, R. Burgos-Vargas, C. Pacheco-Tena, C. Ramos-Remus
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Although there is much discussion regarding when to initiate a biological agent in rheumatoid arthritis (RA) patients, data on when to stop these agents is scant. Disease activity outcomes after the ending of an industry sponsored clinical trials may provide useful information regarding the duration of drug-free remission for a given biological agent. <h3>Objectives</h3> To assess the length of remission and rate of relapse of disease activity after ending the open label, long-term extension study (5 yrs) using tocilizumab in RA patients enrolled in the OPTION trial. <h3>Methods</h3> Patients who no longer received tocilizumab because of the ending of the extension study (5 yrs) of the OPTION trial were analyzed. All patients were: a) in remission (DAS28 &lt;2.6, 0 swollen joints) at the time of the last tocilizumab administration (week 260), b) followed thereafter every 8 weeks until relapse (1 or more swollen joints), c) on a stable methotrexate dose during the follow-up. <h3>Results</h3> Forty patients were analyzed, 85% females with a mean age of 53.5 yrs. During the first 12 months of follow-up, 21 (52.5%) patients continued in remission. Relapses occurred in 19 (47.5%) patients, 11 (58%) of them during the first three months after the last tocilizumab administration. No variables were identified to predict length of remission. <h3>Conclusions</h3> Long-term remission is possible in a substantial number of RA patients after suspension of tocilizumab. Additional data are required to support recommendations for discontinuing a biological agent after achieving remission. These recommendations would impact in patients' safety and the economic burden imposed by these treatments. <h3>References</h3> Smolen JS, Beaulieu A, Rubbert-Roth A, Ramos-Remus C, Rovensky J, et al. Effect of interleukin-6 receptor inhibition with tocilizumab in patients with rheumatoid arthritis (OPTION study): a double-blind, placebo-controlled, randomised trial. Lancet 2008;371:989–97. <h3>Disclosure of Interest</h3> None Declared
Effect of Theophylline on Sleep-Disordered Breathing in Heart Failure
Authors: S. Javaheri, T.J. Parker, L. Wexler, J.D. Liming, P. Lindower, G.A. Roselle
Journal: New England Journal of Medicine (1996)

Theophylline has been used to treat central apnea associated with Cheyne-Stokes respiration (periodic breathing). We studied the effect of short-term oral theophylline therapy on periodic breathing associated with stable heart failure due to systolic dysfunction.Fifteen men with compensated heart failure (left ventricular ejection fraction, 45 percent or less) participated in the study. Their base-line polysomnograms showed periodic breathing, with more than 10 episodes of apnea and hypopnea per hour. In a double-blind crossover study, the patients received theophylline or placebo orally twice daily for five days, with one week of washout between the two periods.After five days of treatment, the mean (+/-SD) plasma theophylline concentration was 11 +/- 2 microgram per milliliter. Theophylline therapy resulted in significant decreases in the number of episodes of apnea and hypopnea per hour (18 +/- 17, vs. 37 +/- 23 with placebo and 47 +/- 21 at base line; P<0.001), the number of episodes of central apnea per hour (6 +/- 14, vs. 26 +/- 21 and 26 +/- 20, respectively; P<0.001), and the percentage of total sleep time during which the arterial oxyhemoglobin saturation was less than 90 percent (6 +/- 11 percent, vs., 23 +/- 37 and 14 +/- 14 percent, respectively; P<0.04). There were no significant differences in the characteristics of sleep, the frequency of ventricular arrhythmias, daytime arterial-blood gas values, or the left ventricular ejection fraction during the base-line, placebo, and theophylline phases of the study.In patients with stable heart failure, oral theophylline therapy reduced the number of episodes of apnea and hypopnea and the duration of arterial oxyhemoglobin desaturation during sleep.
Abstract 4455: Influence of convective fluid flow on the penetration of anti-cancer drugs through multicell layers
Authors: Roger M. Phillips, Hafiz Makeen, Raj Periasamy, Paul M. Loadman, Pamela F. Jones, Brian D. Sleeman, Stephen W. Smye, Chris Twelves
Journal: Cancer Research (2011)

Abstract One consequence of elevated interstitial fluid pressures (IFP) within solid tumours is disruption to the normal process of convective fluid flow (CFF) from the vasculature into the interstitium. Loss of convective fluid flow in tumours has a significant effect on reducing drug delivery and is recognised as a major factor that contributes to the drug resistant phenotype of many solid tumours. Experimental models of IFP and CFF have traditionally relied upon in vivo tumour models but here, we describe an in vitro assay which could be used to evaluate strategies designed to manipulate convective fluid flow. The model is based upon a conventional transwell model for assessing drug penetration across multicell layers which has been modified to allow the fluid level in top chamber to be raised above that in the bottom chamber. The difference in hydrostatic pressure across the multicell layer drives convective fluid flow, the rate of which can be varied by increasing or decreasing the height of fluid in the top chamber and/or by using multicell layers of different thicknesses. When CFF was 0.19 ml/min, the penetration of gefitinib, imatinib and doxorubicin across DLD-1 human colon carcinoma multicell layers was significantly enhanced compared to similar experiments where CFF was zero. The enhancement of penetration rates was 75 fold for doxorubicin, 53 fold for gefitinib and 62 fold for imatinib. The magnitude of these effects has potential therapeutic significance and support the proposal that strategies aimed at reducing tumour IFP and increasing CFF may enhance the efficacy of chemotherapy. 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 4455. doi:10.1158/1538-7445.AM2011-4455
The Cutting Edge for Cancer Information Is Interactive
Authors: K. Nagy
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article The Cutting Edge for Cancer Information Is Interactive Get access Kate Nagy Kate Nagy Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 13, 7 July 1993, Pages 1030–1031, https://doi.org/10.1093/jnci/85.13.1030 Published: 07 July 1993
Autoantibody-Mediated Acquired Deficiency of C1 Inhibitor
Authors: Jochem Alsenz, Konrad Bork, Michael Loos
Journal: New England Journal of Medicine (1987)

During the past 25 years, three forms of deficiency of the inhibitor of the first component of complement (C1 inhibitor) with angioedema have been recognized; two forms are hereditary and one is acquired. As compared with hereditary angioedema, the syndrome of acquired C1-inhibitor deficiency is rare, and it is usually associated with lymphoproliferative diseases. We report another type of acquired C1-inhibitor deficiency with angioedema. Two patients with recurrent angioedema but no associated diseases were found to have IgG1 autoantibodies against C1 inhibitor. The anti-C1-inhibitor antibodies prevented binding of C1 inhibitor to activated C1s. Both patients had 60 to 70 percent of normal levels of C1 inhibitor, but it was functionally inactive, with a molecular weight of 96,000 (normal C1 inhibitor, 105,000). In vitro studies of the patients' serum revealed degradation of 125I-labeled 105,000-dalton C1 inhibitor into the inactive 96,000-dalton molecule, caused by activated C1s and not found in normal human serum. We conclude that these cases of acquired C1-inhibitor deficiency resulted from a blockade of C1-inhibitor function by the anti-C1-inhibitor antibodies and from subsequent inactivation of C1 inhibitor by the now uncontrolled enzyme, activated C1s. As in other forms of C1-inhibitor deficiency, the unopposed activation of the complement system led to angioedema. (N Engl J Med 1987; 316: 1360–6.)
P17.50 * PHASE II STUDY OF ARSENIC TRIOXIDE AND TEMOZOLOMIDE IN COMBINATION WITH RADIATION THERAPY IN PATIENTS WITH MALIGNANT GLIOMAS
Authors: P. Kumthekar, S. A. Grimm, M. Marymont, M. Mehta, J. Chandler, K. Muro, B. Jovanovic, I. Helenowski, K. McCarthy, J. Raizer
Journal: Neuro-Oncology (2014)

BACKGROUND: Current standard treatment for GBM is surgery followed by radiation (RT) and temozolomide (TMZ). We published phase I data of the addition of arsenic trioxide (ATO) to RT and TMZ. We now present the phase II data. METHODS: Patients with newly diagnosed malignant gliomas were eligible for treatment in this single arm phase II. Patients were treated with RT (60GY), TMZ (75 mg/m2 daily x 42 days) and ATO 0.20 mg/kg daily in week 1 then twice a week x 5 weeks. RESULTS: Twenty-five patients (14 M and 11 W) were enrolled with a median age of 56 (28-73). Histology was GBM 18, AA 6 and AO 1. All patients completed RT/TMZ/ATO. Median number of post RT cycles of TMZ was 3 (0-12); 9 patients completed 6 or more cycles. Median PFS was 6 m for GBM and 15 m for AG and median OS was 15 m for GBM and NR for AA. Response was SD in 20, PR in 1 and PD in 4. CONCLUSIONS: Adding ATO to RT and TMZ is feasible and tolerable but does not appear to improve outcome compared to RTOG 0525 data where OS is 16.6 months in newly diagnosed GBM. Tissue MGMT status is being analyzed for PFS and OS correlation.
A2.03 The PD-1/PD-L1 axis is modulated by pro-inflammatory cytokines
Authors: D Bommarito, C Hall, LS Taams, VM Corrigall
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> The Programmed Cell Death 1 (PD-1) receptor plays a major role in maintaining self-tolerance. Engagement of PD-1 with its ligand PD-L1 on CD4<sup>+</sup> T cells is reported to downregulate inflammatory responses through inhibition of cell proliferation and cytokine production. In inflammatory arthritis (IA), PD-1 is described as overexpressed on synovial fluid (SF) CD4<sup>+</sup> T cells compared to peripheral blood (PB) CD4<sup>+</sup> T cells while conflicting evidence exists regarding the expression and functionality of PD-L1 during chronic inflammation. The aim of this study was to determine (i) PD-1 and PD-L1 expression on IA SF CD4<sup>+</sup> T cells and (ii) the effects of the pro-inflammatory cytokines TNFα and IL-6 on PD-1 ligation in healthy control (HC) CD4<sup>+</sup>T cells. <h3>Materials and methods</h3> CD4<sup>+</sup> T cells were isolated from PB of HC or patients with IA and cultured in anti-CD3 or anti-CD3/PD-L1fc chimaera coated plates. IL-6 (10&nbsp;ng/ml) +/- anti-IL-6R (tocilizumab; 1&nbsp;ug/ml), or TNFα (10&nbsp;ng/ml) or acellular SF (0.5%) +/- anti-TNFα (adalimumab; 1ug/ml) were added to the cultures. Proliferation was assessed at day 5 by <sup>3</sup>H-thymidine uptake. Day 5 supernatants were analysed by ELISA for soluble PD-1 (sPD-1). <h3>Results</h3> IA SF samples were enriched for PD-1+CD4<sup>+</sup> T cells compared to PB (n = 6, p = 0.03) while no significant difference was observed in the percentage of PD-L1+ T cells. CD4<sup>+</sup> T cells from HC showed a significant decrease in proliferation upon PD-1 ligation (n = 8; p &lt; 0.05) while CD4<sup>+</sup> T cells from IA patients appeared more resistant (n = 8; p &gt; 0.05). In HC CD4<sup>+</sup> T cell cultures, addition of TNFα or IL-6 completely abrogated PD-L1fc activity (n = 10; p &gt; 0.05). In these cultures, the TNFα and IL-6 effect was neutralised by adalimumab (n = 9) and tocilizumab (n = 6) (p &lt; 0.05). Addition of a-cellular SF (0.5%) to HC CD4<sup>+</sup> cell cultures (n = 3) also reduced the effects of PD-1 crosslinking. ELISA analysis showed that both TNFα or IL-6 induced sPD-1 production (n = 7; p &lt; 0.05) and that adalimumab and tocilizumab successfully blocked this effect. <h3>Conclusion</h3> We hypothesise that the pro-inflammatory cytokines TNFα and IL-6 modulate CD4<sup>+</sup> T cells reactivity to PD-L1 by inducing the release of a soluble form of PD-1 which might interfere with PD-1/PD-L1 signalling.