tbuckley/cabot-search huggingface dataset:
Coronary Arteriographic Findings Soon after Non-Q-Wave Myocardial Infarction
Authors: Marcus A. DeWood, William F. Stifter, Carroll S. Simpson, Julie Spores, George S. Eugster, Terrance P. Judge, Michael L. Hinnen
Journal: New England Journal of Medicine (1986)

Complete occlusion of the infarct-related coronary artery is a frequent finding soon after Q-wave (transmural) myocardial infarction. We performed coronary arteriography to study the frequency of total coronary occlusion and of angiographically visible collateral vessels in 341 patients within one week of non-Q-wave myocardial infarction. In this cross-sectional study, 192, 94, and 55 patients underwent coronary arteriography within 24 hours of peak symptoms, between 24 and 72 hours after peak symptoms, and between 72 hours and seven days after peak symptoms, respectively. In the three groups, total occlusion of the infarct-related vessel was found in 26 percent (49 of 192), 37 percent (35 of 94), and 42 percent (23 of 55) of the patients, respectively (P<0.05). The presence of visible collateral vessels increased in parallel: 27 percent (52 of 192), 34 percent (32 of 94), and 42 percent (23 of 55), respectively (P<0.05). The frequency of subtotal occlusion (i.e., ≥90 percent stenosis) decreased inversely: 34 percent (65 of 192), 25.5 percent (24 of 94), and 18 percent (10 of 55), respectively (P<0.05). Thus, in contrast to Q-wave infarction, total coronary occlusion of the infarct-related vessel is infrequently observed in the early hours of non-Q-wave infarction, but it increases moderately in frequency over the next several days. These cross-sectional data suggest that non-Q-wave infarction may be related to a preserved but marginal blood supply, which sufficiently disrupts the relation between the supply of and the demand for myocardial oxygen to cause tissue necrosis. (N Engl J Med 1986; 315:417–23.)
Impact of migration on tuberculosis epidemiology and control in the EU/EEA
Authors: Marieke J van der Werf, Jean Pierre Zellweger
Journal: Eurosurveillance (2016)

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FRI0071 Does psychological status drive patient global assessment for rheumatoid arthritis patients who do not have any clinical signs of inflammation? an exploratory analysis of near-remission using the rheumatoid arthritis impact of disease (RAID) score.
Authors: L. Gossec, J. Kirwan, S. Paternotte, A. Balanescu, D. Boumpas, M. de Wit, B. A. Dijkmans, M. Englbrecht, F. Gogus, T. Heiberg, E. Martin Mola, M. Matucci Cerinic, K. Otsa, T. Sokka-Isler, M. Dougados, T. K. Kvien
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Patients reaching remission for joint counts and CRP according to the ACR/EULAR Boolean definition fo remission (value&lt;=1/10), but not remission for patient global assessment (PGA), are termed in 'near-remission'(1). PGA may represent the wider impact of rheumatoid arthritis (RA) including psychological well-being and coping skills, rather than just the pathophysiological severity of the disease (2) and may include several concepts measured by the EULAR patient-derived RA Impact of Disease (RAID) score (3). <h3>Objectives</h3> To assess whether psychological components of the RAID score explain the elevated PGA for patients in near-remission. <h3>Methods</h3> The RAID database, based on an international multicenter cross-sectional study of consecutive RA patients from 12 European countries, was used (3). Each component of the RAID score ranges from 0 (no impact) to 10 (high impact). Patients in near-remission were compared to those in remission and not in remission for the proportion of patients with a score &lt;=1/10, in each of the RAID components. Non-parametric comparisons were performed. <h3>Results</h3> In total, 359 patients had complete data for this analysis: mean (±standard deviation) age 55.8±13.0 yrs, disease duration 12.6±10.5 yrs, 76.4% women. Mean RAID score was 4.3±2.2. With the ACR/EULAR Boolean definition, only 22 (6.1%) were in remission and 53 (14.8%) were in near-remission. In near-remission patients, the mean PGA was 3.3±1.5, and the mean RAID score was 3.6±1.8. The components of the RAID were mostly all &gt;1/10 but specifically, physical well-being, fatigue, pain and functional assessment were more frequently &gt;1/10 (94%, 89%, 87%, 83%) than sleep, coping or emotional well-being in these patients (79%, 79%, 74%, all p&lt;0.05). <h3>Conclusions</h3> The new definition of remission is extremely stringent and rarely attained for patients with long-standing RA. Near-remission is a more frequently achieved status. In this sample, psychological distress and lack of coping did not explain the raised PGA of near-remission, which was better explained by higher physical components of the RAID score. More work is needed to understand the patient perspective regarding remission. <h3>References</h3> Studenic P, et al. Ann Rheum Dis. 2012;71(10):1702-5. Sanderson T, et al. J Rheumatol 2011;38;191-194. Gossec L, et al. Ann Rheum Dis. 2011;70(6):935-42. <h3>Disclosure of Interest</h3> None Declared
P3-13-08: Survival Analysis and Recurrence Patterns in Locally Advanced Breast Cancer Following Neoadjuvant Chemotherapy and Preoperative Concurrent Chemo Radiotherapy.
Authors: RJ Shaw, F Lara, CD Robles, D Vilar
Journal: Cancer Research (2011)

Abstract Introduction: Although not widely used, preoperative concurrent chemo radiotherapy (CCRth) following poor response to neo adjuvant chemotherapy (CT) has been recently associated with an improved prognosis in patients with locally advanced breast cancer (LABC) and high recurrence risk, showing acceptable toxicity profiles, acceptable post surgical complication rates and increases in both clinical and pathologic response rates and local control rates. The objective of this study was to assess disease free survival (DFS), overall survival (OS) and patterns of recurrence in a cohort of patients with LABC treated with pre operative CCRth following poor response to neo adjuvant CT. Methods: This longitudinal study included a total of 287 patients with LABC treated with pre operative CCRth following poor response to neo adjuvant CT between February 2000 and December 2002. Demographic, clinical/pathologic, therapeutic and follow up data were collected from patient charts to determine DFS, OS and recurrence patterns. Results: Stages IIB, IIIA and IIIB accounted for 22.3, 37.6 and 40% of the population, respectively. Clinical response rates compared to pathologic response rates following anthracyline based CT and CCRth were minimal or stable in 16% vs 62.4%, partial in 53 vs 76.3% and complete in 30 vs 23.3%. No significant treatment related toxicities were identified. Post surgical complications included flap ischemia in 16%, partial flap necrosis in 18%, both ischemia and partial flap necrosis in 13.2% and partial wound dehiscence in 7.7%. With an average follow up of 64.1 ± 37.2 months, (0-126.3 months), 36.9% of the population relapsed and 55.1% remained disease free. With regard to recurrence patterns, 22.6% presented loco regional relapse, 67.7% recurred at a distant site and 9.8% showed presented both. Median OS was 64.2 months (0-126 months). Five and ten year survival probability was shown to be 75% and 60%, respectively. Conclusions Despite improvements in local control rates and overall outcomes with current therapeutic regimens combining chemotherapy, surgery, and radiotherapy, 30 to 40% of patients with locally advanced breast cancer develop post treatment loco regional recurrence and 5 year overall survival remains low (50%). Multimodal treatment integrating pre operative CCRth is therefore a valid alternative in the LABC setting, showing promising results in regard to OS, DFS and recurrence rates. Prospective clinical studies to evaluate its use are warranted. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P3-13-08.
GLIOBLASTOMA STEM CELL-DERIVED PERICYTES AND TUMOR ANGIOGENESIS
Authors: S. Bao, L. Cheng, Z. Huang, W. Zhou, Q. Wu, J. N. Rich
Journal: Neuro-Oncology (2014)

BACKGROUND: Glioblastoma (GBM) is the most lethal type of primary brain tumor with florid angiogenesis. GBMs display striking cellular hierarchies containing self-renewing glioma stem cells (GSCs) that are highly tumorigenic. GSCs not only produce elevated levels of VEGF to promote tumor angiogenesis but also contribute to cellular compartments of tumor vessels. METHODS: 1. In vivo cell lineage tracing with constitutive and Desmin promoter-driven GFP or RFP fluorescent reporters. 2. Selective elimination of GSC-derived pericytes with Desmin promoter-driven HsvTK. 3. GSC-derived GBM xenograft models. RESULTS: Cell lineage tracing with constitutive and lineage specific fluorescent reporters demonstrated that GSCs generate the majority of vascular pericytes in vivo. Selective elimination of GSC-derived pericytes disrupted tumor vessels and potently suppressed GSC tumor growth. Thus, GSCs can function as pericyte progenitors and contribute to vasculature formation and maintenance in GBMs. CONCLUSIONS: The ability of GSCs to generate the majority of pericytes allows active tumor angiogenesis to promote rapid tumor growth in GBMs. GSC-derived pericytes also play a critical role in the resistance to the anti-angiogenic therapy targeting endothelial cells only, suggesting that selective targeting of GSC-derived pericytes may significantly improve the efficacy and specificity of the anti-angiogenic treatment. SECONDARY CATEGORY: n/a.
Abstract 1902: A multilevel map of the immunological terrain in an orthotopic mouse model of lung cancer with emphasis on PGD2/DP1-dependent immunomodulation
Authors: Lotte Pyfferoen, Sofie De Prijck, Manon Vanheerswynghels, Kim Deswarte, Karl Vergote, Hamida Hammad, Bart N. Lambrecht, Karim Y. Vermaelen
Journal: Cancer Research (2010)

Abstract The influence of the organ-specific micro-environment on the host immune response to tumors has been insufficiently adressed. We examined tumor-induced immunomodulation in an orthotopic mouse model of lung cancer. We focused on the PGD2-DP1 signalling axis given its contrasting roles in dendritic cell (DC)-dependent immunomodulation on one hand, and tumor angiogenesis on the other. We found an enrichment of CD11b+ (inflammatory type) DCs within lung tumors. In sharp contrast to DCs in immediately adjacent peritumoral lung tissue, intratumoral DCs displayed a strong upregulation of the T-cell co-inhibitory molecules PD-L1 and ICOS-L on the cell surface. Remarkably, tumor-infiltrating CD4 and CD8 T-cells showed a robust upregulation of the activation marker CD69, while increased numbers of double-negative T-cells were seen within lung tumors as well. Regulatory T-cells were also clearly elevated within tumors as well as in draining lymph nodes (LN) of tumor-bearing hosts. Interestingly, DCs in lung-draining LNs appeared more immature in end-stage tumor bearing mice. Finally, systemic tumor-induced effects were manifest as a strong expansion of myeloid derived suppressor cells in the spleen. DP1-deficiency did not significantly affect any of these immunological parameters. Moreover, in contrast to previous observations using heterotopically implanted lung tumor cells, DP1-deficiency had no impact on survival in our orthotopic lung cancer model. In summary, we provide a multi-level detailed map of tumor-immune system interactions in an orthotopic mouse model of lung cancer. Our findings in DP1-deficient mice stress the importance of the local, organ-specific milieu in driving tumor development and shaping host immune responses. 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 1902.
Co-option of Liver Vessels and Not Sprouting Angiogenesis Drives Acquired Sorafenib Resistance in Hepatocellular Carcinoma
Authors: Elizabeth A. Kuczynski, Melissa Yin, Avinoam Bar-Zion, Christina R. Lee, Henriett Butz, Shan Man, Frances Daley, Peter B. Vermeulen, George M. Yousef, F. Stuart Foster, Andrew R. Reynolds, Robert S. Kerbel
Journal: JNCI Journal of the National Cancer Institute (2016)

Background: The anti-angiogenic Sorafenib is the only approved systemic therapy for advanced hepatocellular carcinoma (HCC). However, acquired resistance limits its efficacy. An emerging theory to explain intrinsic resistance to other anti-angiogenic drugs is 'vessel co-option,' ie, the ability of tumors to hijack the existing vasculature in organs such as the lungs or liver, thus limiting the need for sprouting angiogenesis. Vessel co-option has not been evaluated as a potential mechanism for acquired resistance to anti-angiogenic agents. Methods: To study sorafenib resistance mechanisms, we used an orthotopic human HCC model (n = 4-11 per group), where tumor cells are tagged with a secreted protein biomarker to monitor disease burden and response to therapy. Histopathology, vessel perfusion assessed by contrast-enhanced ultrasound, and miRNA sequencing and quantitative real-time polymerase chain reaction were used to monitor changes in tumor biology. Results: While sorafenib initially inhibited angiogenesis and stabilized tumor growth, no angiogenic 'rebound' effect was observed during development of resistance unless therapy was stopped. Instead, resistant tumors became more locally infiltrative, which facilitated extensive incorporation of liver parenchyma and the co-option of liver-associated vessels. Up to 75% (±10.9%) of total vessels were provided by vessel co-option in resistant tumors relative to 23.3% (±10.3%) in untreated controls. miRNA sequencing implicated pro-invasive signaling and epithelial-to-mesenchymal-like transition during resistance development while functional imaging further supported a shift from angiogenesis to vessel co-option. Conclusions: This is the first documentation of vessel co-option as a mechanism of acquired resistance to anti-angiogenic therapy and could have important implications including the potential therapeutic benefits of targeting vessel co-option in conjunction with vascular endothelial growth factor receptor signaling.
Matrix Elastin
Authors: Gerard M. Turino, Shuren Ma, Yong Y. Lin, Jerome O. Cantor, Maurizio Luisetti
Journal: American Journal of Respiratory and Critical Care Medicine (2011)

Section:ChooseTop of pageAbstract <<Matrix ElastinProteases and Antiproteas...Detection of Elastolysis ...Elastin Peptides and the ...The Usefulness of Di as a...ReferencesCITING ARTICLES
Typological variation of kinship terminologies is a function of strict ranking of constraints on nested binary classification trees
Authors: Paul Miers
Journal: Behavioral and Brain Sciences (2010)

Abstract Jones argues that extending Seneca kin terms to second cousins requires a revised version of Optimality Theoretic grammar. I extend Seneca terms using three constraints on expression of markers in nested binary classification trees. Multiple constraint rankings on a nested set coupled with local parity checking determines how a given kin classification grammar marks structural endogamy.
Abstract 995: The role of intracellular ATP in regulating glycolysis, HIF1α and drug resistance of cancer cells
Authors: Jinyu Chen, Zhang Weihua
Journal: Cancer Research (2011)

Abstract Cancer is also considered to be a metabolic disease due to a shift of glucose metabolism from oxidative phosphorylation to anaerobic glycolysis. This study is to understand the effect of intracellular ATP of cancer cells on various metastatsis related phenotypes, including glycolysis, hypoxia stability and drug resistance. In this study, we delivered ATP directly into cancer cells by embedding ATP into liposomes. Normal cells and its corresponding tumor cells were measured for their whole cell ATP content. Glycolysis was evaluated by measurement of glucose consumption and lactate accumulation of cell culture media. Cell cycle was analyzed using flow cytometry after drug treatment and delivery of ATP. HIF-1α expression level was measured by western blot after delivery of ATP. In summary, normal cells have overall higher ATP content than tumor cells. After delivery of ATP, cells consumed less glucose and produced less lactate acid, which indicated a decrease in glycolysis. ATP liposomes prevented MDA-MB-231 cells from G2 arrest by adriamycin. HIF1a was down regulated after delivery of ATP. Taken together, ATP content is lower in cancer cells than normal cells, and intracellular ATP plays a role in regulating glycolysis, HIF-1α stability and drug resistance of cancer cells. 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 995. doi:10.1158/1538-7445.AM2011-995
Abstract 619: O6-Benzylguanine inhibits tamoxifen-resistant breast cancer cell growth and resensitizes breast cancer cells to anti-estrogen therapy
Authors: Smith S. Joshua, George C. Bobustuc, Beth Isley, Arati Limaye, Jonathan Ticku, Rafael Madero-Visbal, Jimmie Colon, Cheryl H. Baker, Srivenugopal S. Kalkunte, Santhi D. Konduri
Journal: Cancer Research (2011)

Abstract Endocrine therapies using anti-estrogens are less toxic and very effective for breast cancers however tumor resistance to tamoxifen remains a stumbling block for successful therapy. Based on our recent study on the involvement of the DNA repair protein MGMT in pancreatic cancer (Clin Cancer Res. 15, 6087, 2009), we investigated whether MGMT overexpression mediates tamoxifen resistance. Specifically, we determined whether administration of MGMT inhibitor [O6-benzylguanine (BG)] at a non-toxic dose alone or in combination with the anti-estrogens (tamoxifen/fulvestrant) curtails human tamoxifen resistant breast cancer cell growth. Furthermore, we also determined whether BG sensitizes breast cancer cells to tamoxifen using tamoxifen resistant cells. MGMT expression was found to be increased in breast cancer cells relative to normal breast epithelial cells. Also, MGMT levels were significantly higher in tamoxifen resistant MCF-7 compared to the parent cells. Silencing of the ER-α expression using a specific siRNA resulted in augmentation of MGMT mRNA and protein levels by two fold. We also observed an inverse correlation between MGMT and p53 levels in breast cancer cell lines; moreover, p53 downregulation was accompanied by increased MGMT expression. Other experiments showed that BG alone or BG in combination with tamoxifen or fulvestrant decreased ER-α expression, whereas tamoxifen alone and fulvestrant alone increased and decreased the same respectively. All these treatments increased the p21cip1 mRNA and protein expression significantly. BG inhibited tamoxifen resistant breast cancer growth in a dose-dependent manner and it also resensitized resistant breast cancer cells to anti-estrogen therapy (TAM/ICI). These combinations also enhanced the cytochrome C release and PARP cleavage, indicative of apoptosis. In breast cancer xenografts, BG alone or a combination of BG with tamoxifen or fulvestrant caused a significant tumor growth delay and immunohistochemistry revealed that BG inhibited the expression of MGMT, ER- α, ki-67 and increased p21cip1 staining. These findings suggest that MGMT inhibition may provide a novel and effective approach for overcoming tamoxifen resistance (supported by a Florida Biomedical grant to SK). 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 619. doi:10.1158/1538-7445.AM2011-619
Increased 131I Accumulation in the Polyacrylamide Hydrophilic Gel Used for Breast Augmentation
Authors: Jing Lv, Yumin Qu, Min Zhang, Yu Pan, Yifan Zhang
Journal: Clinical Nuclear Medicine (2014)

A 37-year-old woman with papillary thyroid cancer received repeat 131I therapy. The first posttherapy scan revealed only activity in the neck. However, both the second and third posttherapy scans showed intense activity in the anterior lower chest bilaterally, suggestive of breast uptake. However, the SPECT/CT images demonstrated that the iodine activity was not located in the breast tissue. Instead, the activity was inside the polyacrylamide hydrophilic gels she received 10 years ago for breast augmentation.
Gastrointestinal Manifestations of Chronic Granulomatous Disease
Authors: Marvin E. Ament, Hans D. Ochs
Journal: New England Journal of Medicine (1973)

Four of nine patients with chronic granulomatous disease had gastrointestinal symptoms; in three of these perianal fistulas developed, and two had friable rectal mucosa. All four had vitamin B12 malabsorption, and two had steatorrhea. In addition two asymptomatic patients had malabsorption of vitamin B12. In eight of the nine cases characteristic histiocytes were found in rectal biopsies; the appearance of these histiocytes is suggestive of chronic granulomatous disease but not invariably diagnostic. Histiocytes with the same appearance were noted in seven of the eight patients undergoing small-bowel biopsy. Histiocytes are rarely seen by light microscopy in the jejunal mucosa of normal persons. Thus, their presence in jejunal biopsies strongly suggests the disease. Our findings indicate that gastrointestinal involvement in chronic granulomatous disease may be frequent.
A Ticking Time Bomb
Authors: Sharon George, Shaifali Sandal
Journal: New England Journal of Medicine (2013)

An 80-year-old man presented with a 3-week history of malaise, hyperglycemia, and low-grade fevers. Diabetic ketoacidosis was diagnosed. A workup revealed leukopenia, anemia, thrombocytopenia, and elevated aminotransferase levels.
Abstract B60: From plasma peptide to phenotype: An emerging role of quiescin-sulfhydryl oxidase 1 in tumor cell invasion
Authors: Benjamin A. Katchman, Kwasi Antwi, Galen Hostetter, Michael Demeure, Aprill Wantanabe, G. Anton Decker, Lawrence J. Miller, Daniel D. Von Hoff, Douglas F. Lake
Journal: Cancer Research (2011)

Abstract Quiescin-sulfhydryl oxidase (QSOX1) oxidizes sulfhydryl groups to form disulfide bonds in proteins. We previously mapped a peptide in plasma from pancreatic ductal adenocarcinoma patients back to an overexpressed QSOX1 parent protein in tumor cells. It is not known why, or in what capacity, pancreatic tumors overexpress QSOX1. To begin to address this question, we first showed through immunohistochemistry that QSOX1 is overexpressed in patients diagnosed with pancreatic cancer, while it is not expressed in adjacent normal tissue or infiltrating lymphocytes. To determine the potential advantages QSOX1 might provide to tumor cells we knocked down QSOX1 using shRNA that suppressed both short and long isoforms of the protein. Loss of QSOX1 expression suppressed cell growth over time, while changes in cell cycle and apoptotic markers were minimal. However, QSOX1 shRNA dramatically inhibited the abilities of BxPC3 and Panc-1 pancreatic tumor cells to invade through Matrigel in a modified Boyden chamber assay. Mechanistically, gelatin zymography indicated that QSOX1 may play an important role in intracellular processing and extracellular activation of MMP-2 and MMP-9. Taken together, our results suggest that pancreatic tumors that express QSOX1 demonstrate an invasive phenotype through MMP activation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the Second AACR International Conference on Frontiers in Basic Cancer Research; 2011 Sep 14-18; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2011;71(18 Suppl):Abstract nr B60.