tbuckley/cabot-search huggingface dataset:
P203Triglicerid level, atherosklerosis of the carotid arteries and inflammation in patient with coronary heart disease in combination with nonalcoholic fatty liver disease
Authors: M Grechanyk, OV Kuryata
Journal: Cardiovascular Research (2014)

Objective: To compare the relationship of triglyceride levels with atherosclerosis of the carotid arteries and inflammation. Methods: We studied 25 patients with stable coronary artery disease in combination with nonalcoholic fatty liver disease (NAFLD) (group A) and 21 patients without a NAFLD (group B), mean age 59±6. Patients with diabetes were excluded. We studied biochemical parameters: triglycerides (TG), C-reactive protein (CRP). All patients underwent ultrasound imaging of carotid arteries. Results: The mean value of TG were 2,95±0,21mmol/l in a group A and 1,54±0,34mmol/l in a group B (p<0,001); of CRP: 1,55±0,21mmol/l and 0,86±0,12mmol/l (p<0,001). Frequency of exposure of atherosclerotic carotid plaques in a group A – 80%, was higher than in a group B – 65%. (p<0,05); There was correlation between the level of TG and degree of stenosis of vessels (r=0,64, p<0,05) and level of CRP (r=0,63, p<0,05) in a group A however in a group B such connection was not observed. Conclusion: In group A the value of TG were more expressed (r=0,50, p<0,05) than in group B. There was an association between the increase of TG, CRP and degree of stenosis of carotid vessels of head in patients with coronary heart disease in combination with NAFLD.
BENCHMARKING IN THE MYOCARDIAL INFARCTION REGISTRY RHEINLAND-PFALZ (MIR-RLP) RESULTED IN INCREASE IN PRE-HOSPITAL ECG-RECORDING AND REDUCTION IN ISCHEMIC TIME TO REPERFUSION IN STEMI
Authors: Anselm K. Gitt, Jan Karcher, Steffen Schneider, Ralf Zahn
Journal: Journal of the American College of Cardiology (2016)
Pediatric Inflammatory Bowel Disease Imaged with Tc-99m White Blood Cells
Authors: MARTIN CHARRON
Journal: Clinical Nuclear Medicine (2000)

Studies have suggested that Tc-99m white blood cell (WBC) imaging is superior to contrast radiology for assessing the extent and activity of inflammatory bowel disease (IBD). The Tc-99m WBC scan seems ideally suited to obtain, in only one examination, a precise temporal snapshot of the distribution and intensity of inflammation, whereas radiographic methods of investigation tend to represent changes that are more chronic. The test is useful in children with inconspicuous signs suggesting IBD in whom laboratory test results are either normal or slightly abnormal. In those cases, a negative Tc-99m WBC study will obviate endoscopic investigations. The author's current experience, in more than 500 patients, indicates that the Tc-99m WBC scan is a virtual gold standard to establish, or exclude, the diagnosis of IBD. The minimal invasiveness of the Tc-99m WBC scan makes it an especially attractive method for evaluating children with IBD. It is economical compared with endoscopy, and its diagnostic sensitivity is excellent. The ability to evaluate the small and large bowel simultaneously is an important advantage for the patient. In conclusion, the Tc-99m WBC scan is a useful tool to evaluate IBD and should be added to the clinician's investigative armamentarium.
Visualization of Papillary Thyroid Carcinoma and Its Metastatic Lymph Nodes
Authors: ERAY ALPER, TAYYAR AKBUNAR, FEYZI TAMGAC
Journal: Clinical Nuclear Medicine (1996)

A 19-year-old woman with pathologically documented papillary thyroid carcinoma and lymph node metastases underwent anterior neck scans using Tc-99m pertechnetate, Tl-201, and Tc-99m sestamibi. Results from Tc-99m sestamibi scans provided the clearest image of the carcinoma and its metastases. It also showed an upper-left thoracic lymph node not detected with Tl-201.
Combined EUS and Pancreatic Juice IL-8 Concentration Are Highly Predictive to Diagnose Chronic Pancreatitis
Authors: S Pungpapong, K Noh, M Al-Haddad, M Wallace, T Woodward, M Raimondo
Journal: Endoscopy (2006)

Background: The diagnosis of chronic pancreatitis (CP) remains challenging. EUS seems to be highly sensitive, but not specific enough. Pancreatic juice (PJ) IL-8 concentration has been proposed as a marker for pancreatic diseases. In this study, we aim to compare the accuracy of PJ IL-8 concentration and EUS to diagnose CP.
Abstract 1604: HFE is a new target molecule for cancer treatment
Authors: Sang Y. Lee, Becky Slagle-Webb, Jonas M. Sheehan, James R. Connor
Journal: Cancer Research (2010)

Abstract Iron can enhance cell growth and metabolism. However insufficiently regulated iron can lead iron accumulation, enhancing oxidative stress and subsequent damage to DNA, and finally promote cancer. The HFE protein plays a key role in the regulation of body iron and is part of the innate immune system. HFE is the most commonly occurring polymorphism in Caucasians. The two most common HFE polymorphic alleles are C282Y and H63D. The variant forms of HFE have increased iron accumulation. To see the impact of HFE on the brain tumor development, at first, we determined the HFE expression. HFE strongly express in the brain tumors such as meningioma, glioblastoma, and astrocytoma at immunohistochemistry. Then, to assess the association between HFE variants and growth, we measured cell growth and tumor development. We found that human neuroblastoma cell lines that were stably transfected with the C282Y allelic HFE variant proliferated at a much higher rate than the same cell lines expressing the wild type or H63D gene variant at the cell proliferation assay and counting cell number. Furthermore, nude mice injected with glioma cells with the C282Y allele developed much faster and bigger tumor than the other type of HFE cell lines. Next, we transfected HFE siRNA into the cells to determine if the increased rate of proliferation was directly related to the protein associated with the C282Y allelic variant. HFE siRNA treatment significantly inhibited cell proliferation of C282Y transfected neuroblastoma cells. The effect was dose dependent. The cell growth was over 60 % decreased for cells cultured for 4 days after exposure to 15 nM of HFE siRNA. Meanwhile, cells transfected with non-specific siRNA (negative control) or the transfection reagent (mock) control siRNA showed no evidence of inhibited cell proliferation. HFE siRNA also inhibited cell proliferation of wild type and H63D allele cells. We also observed that HFE siRNA inhibited tumor development in the glioma cells injected nude mice. We are currently studying specific delivery system of HFE siRNA to the tumor cells. In summary, we found that HFE inhibition is enough to prevent cancer cell proliferation and tumor development. 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 1604.
PLAQUE ANALYSIS WITH CARDIAC MAGNETIC RESONANCE IMAGING FOR CHRONIC TOTAL OCCLUSION AND STRATEGY OF INTERVENTION
Authors: Koichiro Asawa, Kojiro Yoshimura, Hiroshi Ueda, Seiji Matsuhisa, Naohiro Yoshida, Hidetoshi Yoshitani, Yukiko Kuga, Kazuya Ueda, Yasunori Nishida
Journal: Journal of the American College of Cardiology (2015)
Modification of Post-Transfusion Hepatitis by Gamma Globulin
Authors: George S. Mirick, Robert Ward, Robert W. McCollum
Journal: New England Journal of Medicine (1965)

THE following report presents the results of studies carried out to evaluate the effectiveness of gamma globulin in the prophylaxis of post-transfusion hepatitis. Some preliminary results have already been published in abstract form.1 , 2 The detected incidence of post-transfusion hepatitis varies with the method and the intensity and duration of follow-up observations. Icteric hepatitis has been reported to occur at the rate of 1 to 15 cases per thousand units of blood,3 4 5 6 7 8 but in most series it has ranged from 1 to 3 cases. Recent reports9 , 10 suggest that nonicteric hepatitis after transfusion may be ten or more times as common as . . .
Event coding, executive control, and task-switching
Authors: Nachshon Meiran
Journal: Behavioral and Brain Sciences (2001)

Like the Theory of Event Coding (TEC), theories of executive functions depict cognition as a flexible and goal-directed system rather than a reflex-like one. Research on task-switching, a dominant paradigm in executive control, has revealed complex and some apparently counterintuitive results. Many of these are readily explained by assuming, like TEC, that cognitive control is based on selecting information from commensurate representations of stimuli and actions.
Abstract 4141: Tumor cell enrichment is critical for assessing cell signaling pathways in glioblastoma multiforme.
Authors: Claudius Mueller, Ana C. deCarvalho, Tom Mikkelsen, Valerie Calvert, Virginia Espina, Lance A. Liotta, Emanuel F. Petricoin
Journal: Cancer Research (2013)

Abstract Introduction &amp; Methods: Glioblastoma tumor cells are generally assumed to be mixed with few distinct non-tumorigenic cell types and few cells of the microenvironment in general, owing to their location in the brain and the high tumor cell density compared to normal brain parenchyma. However, even small cell populations can have a significant impact on the abundance of phosphorylated proteins. We have analyzed the level and/or phosphorylation of 133 proteins in laser capture microdissected glioblastoma primary tumors (n=39) and compared the results to non-tumor cell enriched, whole tissue lysates. Results: A large portion (44 percent) of endpoints were significantly different between matched tumor cell enriched and non-enriched samples - even when limiting the investigation to tumor samples with at least 90 percent tumor content. EGFR protein levels, which is highly expressed in tumor cells compared to normal brain parenchyma, increased in enriched and non-enriched samples following EGFR mutation, while EGFR phosphorylation was only significantly increased in tumor cell enriched samples. In contrast, PTEN, which has a higher expression in normal brain compared to tumor cells, was only found to be reduced in tumor cell enriched samples from patients with either PTEN mutation or loss in PTEN copy number, with no difference seen in non-enriched samples. Patient stratification by either phosphorylated EGFR, Akt, mTOR, Stat1, VEGFR2 or Bcl-2 based on non-tumor cell enriched samples was dramatically different from tumor cell enriched samples, showing significant misclassification for up to 40 percent of patients even in high tumor content samples. Conclusions: This study demonstrates the critical necessity for selected tumor cell population procurement when investigating protein levels and phosphorylation in glioblastoma. Only tumor cell enriched samples correctly reflected expected tumor biology in the face of EGFR and PTEN mutations. Moreover, tumor cell enrichment had a dramatic effect on the stratification of clinical patient samples that would form the basis for targeted therapy selection. Citation Format: Claudius Mueller, Ana C. deCarvalho, Tom Mikkelsen, Valerie Calvert, Virginia Espina, Lance A. Liotta, Emanuel F. Petricoin III. Tumor cell enrichment is critical for assessing cell signaling pathways in glioblastoma multiforme. [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 4141. doi:10.1158/1538-7445.AM2013-4141
THU0129 Selective elimination of pathogenic TH17 cells from peripheral blood of rheumatoid arthritis patients by a purified fungal polysaccharide
Authors: A. Alunno, E. Pericolini, E. Gabrielli, O. Bistoni, S. Caterbi, E. Bartoloni, S.-K. Chow, A. Casadevall, A. Vecchiarelli, R. Gerli
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> It has been shown that the microbial polysaccharide Galactoxylomannan (GalXM) from the opportunistic fungus <i>Cryptococcus neoformans</i> is able to impair T-cell proliferation and to induce apoptosis in T lymphocytes following the interaction with CD45. GalXM administration in experimental arthritis is able to ameliorate synovitis, reduced the concentration of pro-inflammatory cytokines in affected joints and to prevent articular damage. <h3>Objectives</h3> Aim of the present study was to investigate the effects of GalXM on circulating T-cell subsets in rheumatoid arthritis (RA) to pursue potential therapeutic application. <h3>Methods</h3> Sixty RA patients and 40 HD were included in the study. RA and HD magnetic sorted-CD3<sup>+</sup> T cells were cultured in presence or absence of GalXM (10 mg/ml) and activation stimuli (either anti-CD3 antibody of IL-6+TGFβ). Both apoptosis and proliferation assays were performed at different time-points. IL-17 expression and cleaved-caspase 3 were evaluated by flow cytometry, STAT-3 phosphorilation was assessed by western blot. <h3>Results</h3> GalXM selectively targeted RA Th17 cells. Indeed, GalXM was able to increase caspase-3 activation and eventually apoptosis rate of this cell subset. Moreover, it was able to reduce STAT3 phosphorilation culminating in reduced IL-17 production. Finally, Th17 cell proliferation was also reduced. In addition, we confirmed that CD45 expression on target T cells is required to mediate GAlXM immune-modulatory effects. <h3>Conclusions</h3> This study confirms immune-modulatory effects mediated by GalXM (increase of caspase-3 activation and apoptosis rate, reduction of proliferation, reduction of IL-17 synthesis) in RA Th17 cells. Since Th17 cells represent a pathogenic cell subset deeply involved in the development of rheumatoid synovitis, these findings may suggest possible therapeutic applications of GalXM in RA. <h3>References</h3> Pericolini E. et al. J Immunol 2009;182:6003 Pericolini E. et al PloS One 2010;5:e12720 <h3>Disclosure of Interest</h3> None Declared
Endoscopic sphincterotomy using a stabilizer-attached sphincterotome in Billroth II anatomy
Authors: K. Fujita, Y. Kawase
Journal: Endoscopy (2011)

Endoscopic sphincterotomy (EST) is challenging in patients with Billroth II (BII) gastrectomy [1] [2] [3] [4]. Recently, we have described the advantages of the stabilizer-attached sphincterotome for performing EST in BII anatomy when using a forward-viewing endoscope [5]. Here we evaluate the same device with a side-viewing duodenoscope for EST in BII gastrectomy patients.
Abstract 357: CYP3A4 Activates Stat3 in ER + breast cancer
Authors: David A. Potter, Zhijun Guo, Ranjana Mitra, Monica Milani, Mariangellys Rodriguez, Li Ding, Robin Bliss, Julia Nguyen, Xianghua Luo, Kalpna Gupta, Jorge Capdevila, Ian Blair, Dafydd Thomas, Young K. Bae
Journal: Cancer Research (2011)

Abstract CYP3A4 expression in breast cancer has been reported to correlate with nodal metastases and decreased overall survival, but its mechanisms in cancer progression are unknown. ERalpha has been reported to promote CYP3A4 expression. We have previously demonstrated that CYP3A4 is an arachidonic acid (AA) epoxygenase that activates breast cancer cell proliferation through biosynthesis of 14,15-epoxyeicosatrienoic acid (EET). Methods: Effects of 14,15-EET on Stat3 regulation were studied in MCF7 lines expressing CYP3A4 shRNA. Quantitative immunofluorescence (AQUA) interrogation of a tissue microarray was performed to evaluate CYP3A4 in cytoplasm, ERalpha and pY705Stat3 (pYStat3) in nuclei, and HER2 in cytoplasm/membrane. Values were transformed using the natural logarithm. These values were then averaged across the two spot sets. Pearson's correlation was calculated between the markers of interest. Results: Stat3 (Tyr 705) phosphorylation is inhibited by CYP3A4 silencing. CYP3A4 synthesizes 14,15-EET in breast cancer cells and silencing of Stat3 blocks breast cancer cell growth and abrogates 14,15-EET-induced proliferation, indicating that CYP3A4 requires 14,15-EET biosynthesis and Stat3 to induce cell growth. Silencing of CYP3A4 reduces nuclear pY705-Stat3, while 14,15-EET restores this signaling process. By preliminary immunofluorescence study of consecutive breast cancers (n=48) nuclear ERalpha was associated with cytoplasmic CYP3A4 with a correlation of r=0.7575 (p-value &amp;lt; 0.0001). Cytoplasmic CYP3A4 correlated with nuclear pYStat3, with a correlation of r=0.2708, approaching statistical significance (p = 0.0656). Cytoplasmic/membrane HER2, known to be induced by Stat3, was associated with nuclear pYStat3, exhibiting a correlation of r=0.4460 (p-value = 0.0015). Conclusions: ER+ breast cancer cell growth is therefore mediated, in part, by CYP3A4 biosynthesis of 14,15-EET that induces nuclear pY705-Stat3. These studies indicate that CYP3A4 is an AA epoxygenase that is expressed in ER+ breast cancer and promotes Stat3-mediated breast cancer cell growth, in part, through 14,15-EET biosynthesis. Activated Stat3 may mediate cytoplasmic/membrane HER2 expression. 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 357. doi:10.1158/1538-7445.AM2011-357
Abstract 4307: Paradoxical activation of the MEK/ERK pathway promotes melanoma invasion and metastasis.
Authors: Berta Sanchez-Laorden, Amaya Viros, Maria Romina Girotti, Matthew Martin, Malin Pedersen, Alfonso Zambon, Dan Niculescu-Duvaz, Caroline Springer, Richard Marais
Journal: Cancer Research (2013)

Abstract Melanoma is the most deadly form of skin cancer. An important feature of melanoma is its ability to metastasize and this contributes to its poor prognosis. RAS is mutated in ∼20% of melanomas and its downstream kinase BRAF is mutated in a further 50% of cases, these oncogenes regulate proliferation and survival through the MEK-ERK cascade. Selective inhibitors of BRAF such as vemurafenib have a remarkable clinical activity in patients with BRAF mutant melanomas with response rates of approximately 60-80%. In cells expressing activating BRAF mutations, vemurafenib blocks activation of the MAPK pathway. However, in cells expressing wild type BRAF and constitutively active upstream components that activate the MAPK pathway, BRAF inhibitors drive the paradoxical activation of this pathway. Here we show that kinase-dead BRAF promotes melanoma cell invasion and metastasis in the presence of oncogenic RAS. Notably, drugs that target BRAF mimic these effects and also induce RAS mutant melanoma cell invasion. The underlying mechanism is driven by paradoxical activation of the MEK-ERK pathway, resulting in increased secretion of the chemokine IL8 and subsequent secretion of extracellular matrix proteases, which induce invasion. We also show that BRAF inhibitors promote melanoma metastasis in an allograft model and that BRAF inhibitors induce invasion of drug-resistant BRAF mutant melanoma cells. We conclude that paradoxical activation of the MAPK pathway by BRAF inhibitors can drive melanoma invasion and metastasis in RAS mutant melanoma and in drug-resistant BRAF mutant melanoma cells. Citation Format: Berta Sanchez-Laorden, Amaya Viros, Maria Romina Girotti, Matthew Martin, Malin Pedersen, Alfonso Zambon, Dan Niculescu-Duvaz, Caroline Springer, Richard Marais. Paradoxical activation of the MEK/ERK pathway promotes melanoma invasion and metastasis. [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 4307. doi:10.1158/1538-7445.AM2013-4307
P154 VASCULAR ADHESION PROTEIN-1 ATTENUATES MYELOID DENDRITIC CELL FUNCTION AND MATURATION IN THE PRESENCE OF EXOGENOUS LPS
Authors: C.J. Weston, S.M. Curbishley, M. Blahova, H.W. Zimmermann, D.J. Smith, D.H. Adams
Journal: Journal of Hepatology (2014)
FRI0187 The effectiveness of abatacept in a large RA real world database including durability and changes in haq over time: Post DMARDs and post TNF:
Authors: J.E. Pope, E. Rampakakis, J. Sampalis, O. Desjardins
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Assessment of the real-world effectiveness of newer biologics such as abatacept is essential in determining true benefits in routine practice. Patient registries represent a valuable supplement to randomized controlled trials including real world durability, and improvement of function over time. <h3>Objectives</h3> A large Canadian database was used to determine effectiveness of abatacept in real world RA patients including how many people need to be treated to improve 1 RA patient by a minimally important difference (MID) of the HAQ. <h3>Methods</h3> RA patients administered abatacept via clinic or home infusions from the Orencia Response Program network, between 2006 and Feb. 2011 with follow-up evaluation(s) were included. The number needed to treat (NNT) to improve HAQ by at least the MID (≥0.22) and abatacept survival until last follow up were calculated overall; and for abatacept as first or subsequent biologic. <h3>Results</h3> Among the 2,929 patients enrolled, 1,771 (60.5%) were eligible for the study (79.2% had past TNFi) with a mean (SD) follow up of 13.8 (12.3) months. Mean (SE) durability of treatment was 26.8 (0.53) months; where 66% were still on abatacept at 12 and 53% at 24 months. The survival was longer where abatacept was the first biologic vs. post TNFi (P=0.0001). In abatacept as 1stbiologic, 70% achieved MID in HAQ vs. 71% if post TNFi (P=0.65) with NNT=1.4 in each group and there were also no differences in % achieving MID comparing no past biologic to 2, 3 or 4 pervious biologics. Increased baseline HAQ (OR 2.13 (1.89, 2.39)) and less years of RA (OR 0.98 (0.97, 0.99)) were significant predictors of achieving the MID for HAQ. For those staying on abatacept, the mean improvement in HAQ increased over time; changing at 6, 12, 18 and 24 months by -0.29, -0.41, -0.45 and – 0.51 respectively with no difference between abatacept as first biologic vs. post TNFi (unadjusted) and if adjusting for baseline differences, change in HAQ was better as first biologic (p&lt;0.001). <h3>Conclusions</h3> Abatacept is effective in improving HAQ in RA despite long disease duration. For those still on abatacept, HAQ continued to improve over the first 2 years. The durability of abatacept is better as first biologic but NNT to improve HAQ is the same post DMARDs and TNFi. This can help to inform treatment decisions. <h3>Disclosure of Interest</h3> J. Pope Grant/Research support from: This study was supported by a grant from BMS. The protocol was developed by the authors for data analysis., E. Rampakakis: None Declared, J. Sampalis: None Declared, O. Desjardins: None Declared
Genetic vs. Quantitative Analysis of Serum Alpha<sub>1</sub>-Antitrypsin
Authors: Richard C. Talamo, Carol E. Langley, Barry W. Levine, Homayoun Kazemi
Journal: New England Journal of Medicine (1972)

Abstract In a study of the potential usefulness of quantitative methods for identifying heterozygous serum alpha1-antitrypsin genetic types that may be associated with chronic pulmonary disease, wide ranges of serum alph1-antitrypsin function and concentration were found in series of samples of protease inhibitor (Pi) types MM, MS and MZ samples. Ranges were wider in a group of 99 patients with obstructive pulmonary disease than in 106 normal adults, and demonstrated a greater overlap of types MS and MZ with type MM. Measurement of alpha1-antitrypsin function or concentration cannot be expected to detect Pi types MZ or MS reliably; quantitative screening methods must be accompanied by Pi typing analysis.