tbuckley/cabot-search huggingface dataset:
Abstract 4511: Wireless Technology Improves Outcomes and Eliminates Gender Bias in Acute Myocardial Infarction
Authors: Monica G Sanchez-Ross, Gerard Oghlakian, James M Maher, David Sedaghat, Brijesh Patel, Vivek N Dhruva, David Langley, William Dougan, Edo Kaluski, Marc Klapholz
Journal: Circulation (2009)

Background Recent studies demonstrate women who present with ST elevation myocardial infarctions (STEMI) are more likely to experience delays in treatment and worse outcomes. We previously reported...
Smoking in public places
Authors: K. Padki
Journal: BMJ (1996)

Van der Sijs-Bos and colleagues claim that our evidence is insufficient to challenge the specifi- city of prenatal diagnosis of Turner's syndrome karyotypes made by amniocentesis, but at the same time they present data that point in the same direction as our data.We must re-emphasise the conclusion of our paper: the only study that will resolve this ques- tion is one looking at every fetus with a prenatal diagnosis of a Turner's syndrome karyotype, with special reference to the distribution of cells in cases of mosaic karyotypes, results from karyotyping of aborted fetuses, and karyotyping of infants with the syndrome who have not yet been examined postnatally.
Canadian Thalidomide Experience
Authors: J F WEBB
Journal: JAMA (1963)

Data are presented on 115 children, including three sets of twins, born in Canada in 1961 and 1962 with congenital malformations associated with the use of thalidomide by their mothers in early pregnancy. The epidemiological method is described. Of the 115 children, 74 were alive at the time of reporting, 41 of these being severely handicapped; 8 had been stillborn; 33 had died. Limb involvement was usually bilateral, affecting the upper limbs alone in 42 cases, and the upper and lower limbs in 41. Of 112 mothers, only 60 had had the drug prescribed by the physician providing maternity care; 87 were estimated to have first taken the drug before their last menstrual period or within 56 days thereafter. A plea is made for the development of better methods of collecting information on the occurrence of congenital malformations, with the aid of practising physicians.
Abstract 4274: Anticancer mechanisms of a small amphipathic molecule, LTX-401, against B16 melanoma cancer cells
Authors: Liv-Marie Eike, Brynjar Mauseth, Ketil Camilio, Oystein Rekdal, Baldur Sveinbjornsson
Journal: Cancer Research (2015)

Abstract In the present study we investigated the mechanism behind the killing of B16F1 murine melanoma cells by the small amphipathic β(2,2)-amino acid derivative, LTX-401 (Mw&amp;lt;500Da). In vitro, LTX-401 induced lytic cell death and the release of Danger-Associated-Molecular-Pattern Molecules(DAMPs) such as ATP and HMGB-1. In addition, the cells released pro-Cathepsin-B and cytochrome-c following LTX-401 treatment. Flow cytometry and confocal microscopy studies revealed reduced signal from the lysomal dye Lysotracker-DND-26, indicating loss of lysomal integrity. Furthermore, flow cytometry analysis showed that the mitochondrial membrane potential was unaffected in the LTX-401 treated cells. Transmission electron microscopy of LTX-401 treated cells showed little or no ultra structural changes in the mitochondria. The in vivo antitumor effect of LTX-401 against intradermally established B16F1 melanoma was assessed in syngeneic mice. Intratumoral administration of the molecule caused rapid tumor necrosis and complete tumor regression in the majority of the animals treated. In conclusion, these findings demonstrate that LTX-401 has the ability to cause immunogenic cell death in cancer cells and induce complete tumor regression in solid tumors and thus might have a potential as an immunotherapeutic agent. Citation Format: Liv-Marie Eike, Brynjar Mauseth, Ketil Camilio, Oystein Rekdal, Baldur Sveinbjornsson. Anticancer mechanisms of a small amphipathic molecule, LTX-401, against B16 melanoma cancer cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4274. doi:10.1158/1538-7445.AM2015-4274
Abstract A54: Ly6Chi inflammatory monocytes mediate tumor regression in a mouse model of spontaneously arising pancreatic ductal adenocarcinoma
Authors: Whitney L. Gladney, Graham M. Tooker, Gregory L. Beatty
Journal: Cancer Research (2015)

Abstract Macrophage infiltration into solid malignancies most often portends a poor prognosis. In pancreatic ductal adenocarcinoma (PDAC), macrophages dominate the leukocyte infiltrate with effector T lymphocytes remaining scarce. Strategies to restore productive immunosurveillance in PDAC have largely focused on inducing anti-tumor T cell immunity. However, we have previously shown in patients and a mouse model of PDAC that immune modulation with a CD40 agonist can induce macrophages to facilitate tumor regression. Thus, strategies that restore innate immunosurveillance may hold promise in the treatment of PDAC. To further investigate the role of macrophages as targets for anti-tumor immunotherapy, we utilized the KrasG12D; Trp53R172H; Pdx-1 Cre (KPC) genetically engineered mouse model of PDAC. We previously reported a role for liposomal targeted macrophages in facilitating tumor regression induced with CD40 therapy. However, unexpectedly we found by immunohistochemistry that macrophages targeted by liposomes do not infiltrate PDAC tumors in response to CD40 therapy. This finding suggested a role for additional leukocyte subsets in mediating the anti-tumor effect. Using immunohistochemistry, we found that systemic CD40 activation induced the infiltration of Ly6C+ myeloid cells into KPC tumors. Based on this finding, we hypothesized that macrophages may regulate the infiltration of Ly6Chi inflammatory monocytes, which are the critical effector myeloid cells mobilized in the peripheral blood by CD40 agonist therapy. In support of this hypothesis, we found that tumor regression induced with a CD40 agonist was abrogated by treatment with the anti-Ly6C/Ly6G RB6-8C5 depleting antibody. Flow cytometric analysis of peripheral blood revealed that RB6-8C5 and liposomes target distinct myeloid subsets. Whereas RB6-8C5 was found to deplete Ly6ChiCCR2+ inflammatory monocytes, CEL depleted Ly6Cneg myeloid cells. Our findings suggest that CD40-induced tumor regression in PDAC is mediated by inflammatory monocytes which infiltrate tumor lesions under the regulation of extra-tumoral macrophages. Citation Format: Whitney L. Gladney, Graham M. Tooker, Gregory L. Beatty. Ly6Chi inflammatory monocytes mediate tumor regression in a mouse model of spontaneously arising pancreatic ductal adenocarcinoma. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr A54.
Abstract 85: CCAAT/enhancer binding protein beta facilitates castrate-resistant prostate cancer cell growth and sensitivity to mTOR inhibitors
Authors: David J. Barakat, Jing Zhang, Alan D. Friedman, Samuel R. Denmeade, Ido Paz-Priel
Journal: Cancer Research (2015)

Abstract Adaptive changes that frequently occur in castrate-resistant prostate cancer (CRPC) cells are genomic mutations which enhance the activity of the PI3K-mTOR signaling pathway. Although there have been several promising clinical trials for the treatment of CRPC utilizing inhibitors of mTOR, these efforts failed to show significant improvement of patient outcomes. Thus, identifying potential mechanisms of resistance to these agents could improve their therapeutic efficacy. CCAAT/enhancer binding protein beta (C/EBPβ) is a broadly expressed transcription factor, with three isoforms that are differentially translated by mTOR activity. T reatment of cells with mTOR inhibitors increases the translation of the larger C/EBPβ LAP isoforms and decreases the truncated LIP isoform. The function of C/EBPβ LAP has been previously associated with survival and cellular senescence, while the LIP isoform facilitates cell cycle progression. Our central hypothesis was that the differential translation of LAP and LIP C/EBPβ isoforms was essential for the survival of CRPC cells treated with mTOR inhibitors. We found that treatment of PC3 cells with mTOR inhibitors unexpectedly increased the protein levels of all three C/EBPβ isoforms, while androgen-sensitive LNCaP cells largely showed decreased C/EBPβ protein levels. However, the PI3K inhibitor LY294002, decreased the LIP isoform of C/EBPβ without affecting LAP expression in LNCaP and PC3 cells. C/EBPβ gene expression decreased in both LNCaP and PC3 cells in response to treatment with mTOR inhibitors. We next evaluated whether C/EBPβ facilitated cell survival during mTOR inhibition. We found that PC3 cells deficient in C/EBPβ, via shRNA knockdown or TALEN gene editing, were less sensitive to the mTORC1/2 inhibitor, INK128, as assessed by a significant increase in IC50 value determined by the WST-1 assay. Further, suppression of C/EBPβ through shRNA KD or TALEN targeting dramatically decreased the rate of PC3 cell growth, clonogenic potential and induced a senescent phenotype. Intriguingly, loss of C/EBPβ in LNCaP cells increased clonogenic potential. Collectively, these data suggest that C/EBPβ has a differential role for cell growth in androgen-sensitive versus castrate-resistant prostate cancer and that C/EBPβ levels inversely correlate with mTOR inhibitor resistance. Citation Format: David J. Barakat, Jing Zhang, Alan D. Friedman, Samuel R. Denmeade, Ido Paz-Priel. CCAAT/enhancer binding protein beta facilitates castrate-resistant prostate cancer cell growth and sensitivity to mTOR inhibitors. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 85. doi:10.1158/1538-7445.AM2015-85
Abstract 11803: Extracellular Mitochondrial DNA is a Putative Toll-Like Receptor 9 Agonist on Cardiac Fibroblasts During Myocardial Infarction
Authors: Ingrid Kristine Ohm, Oystein Sandanger, Stale Haugset Nymo, Alexandra Vanessa Finsen, Marte Bliksoen, Lars Henrik Mariero, Guro Valen, Ingebjorg Seljeflot, Svein Solheim, Pal Aukrust, Arne Yndestad, Leif Erik Vinge
Journal: Circulation (2011)
Reversal of multidrug resistance by Pluronic block copolymers correlates with inhibition of drug efflux transporters and depletion of intracellular ATP and GSH levels.
Authors: Qingnan Yu, Elena Batrakova, Lori Jerome, Kris Banerjee, Shu Li, Yuli Li, Viviane Page, Alexander Kabanov, Brian Leyland-Jones
Journal: Cancer Research (2004)

2138  Drug resistance (intrinsic or acquired) is a common problem for all chemotherapeutic agents which limits their efficacy in the treatment of numerous cancer types. Multiple drug resistance mechanisms exist which may act simultaneously and/or in concert. Recently, Pluronic block copolymers (PBC) were evaluated for use in drug formulations to treat resistant cancer. It was found that PBC dramatically increased the cytotoxicity of antineoplastic agents in resistant P-glycoprotein (Pgp)-overexpressing cancer cells. Mechanistic studies indicated that exposure of resistant cancer cells to PBC induced significant decreases in intracellular ATP levels along with membrane fluidization, which decreases the affinity of Pgp for the drug and ATP molecules, resulting in powerful sensitization of Pgp-overexpressing cells. To further elucidate the tumor spectrum effectively sensitized by PBC, the present study explored the effects of PBC in a panel of cancer cell lines representing different cell types and drug resistance mechanisms: Pgp-, MRP- (multidrug resistance protein), BCRP- (breast cancer resistance protein) and cisplatin-related resistance. Cytotoxicity studies (measured by MTT assay) were conducted with various antineoplastic agents formulated with PBC in parental/drug-resistant cancer cell line pairs. The results indicated that the trend for sensitization by PBC was Pgp- >> MRP- ≥ BCRP- >> cisplatin-resistance. PBC sensitized Pgp-resistant cells by 100- to 500-fold, MRP- or BCRP-resistant cells by 10- to 130-fold, and had almost no affect on cisplatin-resistant cells. Drug accumulation studies indicated that the extent of inhibition of the drug efflux transporter by PBC decreases in the same order: Pgp (complete) > MRP (partial) > BCRP (low). Thus, the ability of PBC to inhibit drug efflux in resistant cancer cells correlated with the potency of sensitization. A relationship was also found within each drug resistance group: the stronger the decline in intracellular ATP levels following PBC treatment, the higher the sensitization effect in these cells. A similar trend was found for intracellular glutathione levels, which were also depleted following treatment with PBC. Finally, we established that, with some exceptions, epithelial, leukemia, breast and lung cancer cells were the most responsive to PBC treatment and that pancreatic carcinoma cells were among the worst. Hence, reversal of multidrug resistance by PBC correlates with the extent of ATP and glutathione depletion, and inhibition of drug efflux. Overall, these results indicate that careful examination of the cancer type and drug resistance mechanism should be conducted to maximize clinical benefits of PBC formulations for chemotherapy. This study was supported by the National Institutes of Health grant CA89225.
Abstract 10696: Enhancing Endothelial Insulin Sensitivity Reduces NO Bioavailability: a role for NADPH Oxidase-Derived Reactive Oxygen Species
Authors: Hema Viswambharan, Piruthivi Sukumar, Helen Imrie, Matthew Gage, Nadira Yuldasheva, Stacey Galloway, Richard Cubbon, Stephen Wheatcroft, Mark Kearney
Journal: Circulation (2011)

Insulin resistance in the whole body and endothelium is a hallmark of type 2 diabetes. Insulin resistance at the level of the endothelium reduces bioavailability of the anti-atherosclerotic signall...
Abstract 12414: Are Functional Literacy Scores Time Dependent in Rural Heart Failure Patients?
Authors: Susan Robinson, Debra Moser, Michele Pelter, Thomas Nesbitt, Steven Paul, Kathleen Dracup
Journal: Circulation (2010)

Purpose: Levels of literacy, determined from the Shortened-Test of Functional Health Literacy in Adults (S-TOFHLA) scores, have important implications for health interventions and outcomes. Despite...
Survival Outcome and Long-Term Follow-up of Autologous and Allogeneic Stem Cell Transplantation (SCT) in Acute Myeloid Leukemia (AML): A 30 Years Single-Center Experience
Authors: Carmen Montes-Gaisán, German Perez, Arancha Bermudez, Amalia Cuesta, Carlos Richard, Eulogio Conde
Journal: Blood (2014)
Bilharziasis. Ciba Foundation Symposium.
Authors: Quentin M. Geiman
Journal: Annals of Internal Medicine (1963)

Some of the entities discussed are common but many are rare.Aside from the hereditary aspects this book gives a concise description and summary of all that is known of them.I find it most interesting and worth while and believe that not only dermatologists but all physicians and students and others in medical and related fields will also find it so.
Abstract 15936: Missed Opportunities to Save Lives? The Geography of Non-Transported Cardiac Decedents in a Large Metropolitan Area
Authors: Steven Reader, Michele L Casper, Jean Paul Tanner, Elizabeth B Pathak
Journal: Circulation (2011)

Background: People who die from heart disease at home before any attempt at transport may represent missed opportunities for life-saving medical intervention. We undertook a GIS-based, statistical ...
Impact of Delay to Angioplasty in Patients With Acute Coronary Syndromes Undergoing Invasive Management
Authors: Paul Sorajja, Bernard J. Gersh, David A. Cox, Michael G. McLaughlin, Peter Zimetbaum, Costantino Costantini, Thomas Stuckey, James E. Tcheng, Roxana Mehran, Alexandra J. Lansky, Cindy L. Grines, Gregg W. Stone
Journal: Journal of the American College of Cardiology (2010)
The relationship between EGFR expression and intrinsic radiosensitivity in carcinoma of the cervix
Authors: Catharine M. West, Claire Miller, Helen Valentine, Susan E. Davidson, Pat M. Price, Robin D. Hunter
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

1292 

Epidermal growth factor receptor (EGFR) expression is a common feature of solid tumours and in many cancer types is associated with a poor prognosis. There is evidence suggesting a link between EGFR expression and the radiation response of a tumour. A link between the intrinsic radiosensitivity of primary human tumours and EGFR expression has not been established. A retrospective study was carried out in 125 patients with locally advanced carcinoma of cervix. The patients had all received radiotherapy alone with curative intent. Pretreatment tumour EGFR expression was examined immunohistochemically and analysed using a scoring system of 0, 1, 2 and 3 for increasing intensity of staining. Tumour radiosensitivity was measured using a clonogenic assay as surviving fraction at 2 Gy (SF2). Tumours with high EGFR expression (n=8; median SF2=0.38) were significantly more radioresistant than tumours with low EGFR expression (n=59; median SF2=0.61) with p=0.048 (Mann-Whitney U-test). In 125 patients tumour EGFR expression was a significant prognostic factor for disease-free survival (p=0.0085), local recurrence-free survival (0.0082), but not metastasis-free survival (p=0.078). This study has shown that high levels of EGFR expression are associated with the intrinsic radioresistance of human tumours. High EGFR expression may act as a marker of radioresistance and might aid the identification of patients with a high risk of local failure following radiotherapy.
A verocytotoxin-producing E. coli outbreak with a surprisingly high risk of haemolytic uraemic syndrome, Denmark, September-October 2012
Authors: B Soborg, S G Lassen, L Muller, T Jensen, S Ethelberg, K Mølbak, F Scheutz
Journal: Eurosurveillance (2013)

Denmark faced an outbreak of verocytotoxin-producing E. coli (VTEC) O157:H7 infections in autumn 2012. Thirteen cases were diagnosed of which eight had haemolytic uraemic syndrome (HUS). Epidemiological investigations suggested ground beef as the vehicle of the outbreak. The outbreak strain had a rare toxin gene subtype profile: eae, vtx1a and vtx2a, and a high proportion of HUS (62%) among cases, a finding previously linked with the outbreak subtype profile. Toxin subtyping can be useful to identify high risk VTEC strains.
Corrigendum to “Superparamagnetic PLGA-iron oxide microcapsules for dual-modality US/MR imaging and high intensity focused US breast cancer ablation” [Biomaterials 33 (2012) 5854–5864]
Authors: Yang Sun, Yuanyi Zheng, Haitao Ran, Yang Zhou, Hongxia Shen, Yu Chen, Hangrong Chen, Tianyi M. Krupka, Ao Li, Pan Li, Zhibiao Wang, Zhigang Wang
Journal: Biomaterials (2015)
Upregulation of miR-125b by estrogen protects against non-alcoholic fatty liver in female mice
Authors: Zhi-Chun Zhang, Yan Liu, Liu-Ling Xiao, Shu-Fen Li, Jing-Hui Jiang, Yue Zhao, Shu-Wen Qian, Qi-Qun Tang, Xi Li
Journal: Journal of Hepatology (2015)
Diagnostic Accuracy of Coronary In-Stent Restenosis Using 64-Slice Computed Tomography
Authors: Mariko Ehara, Masato Kawai, Jean-François Surmely, Tetsuo Matsubara, Mitsuyasu Terashima, Etsuo Tsuchikane, Yoshihisa Kinoshita, Tatsuya Ito, Yoshihiro Takeda, Kenya Nasu, Nobuyoshi Tanaka, Akira Murata, Hiroshi Fujita, Koyo Sato, Atsuko Kodama, Osamu Katoh, Takahiko Suzuki
Journal: Journal of the American College of Cardiology (2007)
A phase 1 study of oral CC5013, an immunomodulatory thalidomide (Thal) derivative, in patients with relapsed and refractory multiple myeloma (MM).
Authors: PG Richardson, RL Schlossman, T Hideshima, F Davies, R LeBlanc, L Catley, D Doss, KA Kelly, M McKenney, J Mechlowicz, A Freeman, R Deocampo, R Rich, J Ryoo, D Chauhan, N Munshi, E Weller, S Thomas, J Zeldis, KC Anderson
Journal: Blood (2001)
Abstract #4607: The indolocarbazole Gö6976 abrogates cisplatin-induced cell cycle arrest in SCLC cell lines and enhances the cytotoxic effect of the drug.
Authors: Ruth Thompson, Sarah Danson, Penella Woll, Mark Meuth
Journal: Cancer Research (2009)

AACR Annual Meeting-- Apr 18-22, 2009; Denver, CO

SCLC accounts for approximately 25% of lung cancers and chemoresistance is a considerable problem in this disease. Unfortunately, little in vitro work has been carried out due to the difficulties involved in working with the SCLC suspension cell lines. The six SCLC cell lines that were studied were classified into two groups. The first group showed decreased viability based on the MTT assay and a rapid activation of caspase 3 at low cisplatin concentrations. The second, more resistant, group showed relatively low loss of viability and delayed caspase 3 activation following incubation with the same drug concentrations. The two groups could also be distinguished on the basis of cell cycle profile following incubation with IC50 doses of cisplatin. The more sensitive cells showed a marked accumulation at the G2 phase of the cell cycle following 48 hours incubation whereas the more resistant cells arrested earlier, around the G1/S border. In an attempt to increase the efficacy of cisplatin in the resistant cells, the indolocarbazole Go6976 was used which is known to abrogate G2 and S phase arrest. This abrogation is thought to arise from the inhibition of the cell cycle checkpoint kinase Chk1. When cells were treated with Go6976 concurrently with cisplatin, the previously observed cell cycle arrests were diminished in the resistant cells and caspase 3 was activated at much lower cisplatin concentrations. For example, in the resistant H345 cell line, 6\#956;M cisplatin alone resulted in 25.66% (+/- 14.21) cell death and 6\#956;M cisplatin plus 1\#956;M Go6976 results in 40.09% (+/- 14.17) cell death. These results suggest a possible role for Go6976 in combination therapy with cisplatin for treatment of SCLC and further laboratory work will seek to clarify this further and study the cell cycle proteins involved.

Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 4607.