tbuckley/cabot-search huggingface dataset:
The Control of Labor
Authors: Errol R. Norwitz, Julian N. Robinson, John R.G. Challis
Journal: New England Journal of Medicine (1999)

Labor is the physiologic process by which a fetus is expelled from the uterus to the outside world. Labor is defined as an increase in myometrial activity or, more precisely, a switch in the pattern of myometrial contractility from irregular contractures (long-lasting, low-frequency activity) to regular contractions (high-intensity, high-frequency activity),1 resulting in effacement and dilatation of the uterine cervix. In normal labor, there appears to be a time-dependent relation between the biochemical changes in the connective tissue in the cervix that usually precede uterine contractions and cervical dilatation. All these events usually occur before the spontaneous rupture of the fetal . . .
Researchers Link Low Literacy to High Health Care Costs
Authors: S. Jenks
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article Researchers Link Low Literacy to High Health Care Costs Get access Susan Jenks Susan Jenks Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 14, 15 July 1992, Pages 1068–1069, https://doi.org/10.1093/jnci/84.14.1068 Published: 15 July 1992
THE VALUE OF ECHO DOPPLER DERIVED INDEX OF VENTRICULAR STIFFNESS AND VENTRICULO-ARTERIAL INTERACTION AS PREDICTORS OF NEW-ONSET ATRIAL FIBRILLATION IN PATIENTS WITH HEART FAILURE
Authors: Ji Hyun Yoon, Hyemoon Chung, Eui-Young Choi, Pil-Ki Min, Young Won Yoon, Byoung Kwon Lee, Bum-Kee Hong, Se-Joong Rim, Hyuck Moon Kwon, Jong-Youn Kim
Journal: Journal of the American College of Cardiology (2016)
A mathematical model for the transport and fate of organic chemicals in unsaturated/saturated soils.
Authors: F T Lindstrom, W T Piver
Journal: Environmental Health Perspectives (1985)

A mathematical model, simulating the transport and fate of nonionizable organic compounds in unsaturated/saturated porous media (soils) in a terrestrial microcosm has been developed. Using the principles of water mass, momentum, heat energy and chemical mass balance, the three fields: moisture, temperature, and liquid phase chemical concentration are solved for simultaneously by coupling the soil slab to an environmentally realistic air-soil interface (a dynamic free boundary) conditions and a prescribed height water table. The environmental conditions at the soil surface-air chamber interface are easily changed, via geometric scaling factors, to simulate either an open agricultural field or a landfill type of situation. Illustrative simulation runs examine the effects of different soil-chemical characteristics on hydrological and chemical concentration profiles.
P941 REDUCTION IN SERUM SODIUM (Na) IN PATIENTS TREATED WITH TERLIPRESSIN FOR VARICEAL BLEEDING (VB) AND HEPATORENAL SYNDROME (HRS)
Authors: A. Sugumaran, E. Lougher, C. Halpin-Evans, M.A. Czajkowski, A.D. Yeoman
Journal: Journal of Hepatology (2014)
Abstract 4269: Human monoclonal anti-angiopoietin-2 antibody, MEDI3617, inhibits angiogenesis in preclinical studies
Authors: Nikolett Molnar, Dietmar W. Siemann
Journal: Cancer Research (2011)

Abstract Angiogenesis is two-step process that is critical in tumor angiogenesis. First, endothleial-endothelial and endothelial-smooth muscle cell interactions must be broken. Then, endothelial cells must be activated to proliferate, migrate, and form tubes. Presence of Angiopoietin-2 (Ang-2) leads to vessel destabilization while pro-angiogenic factors like Vascular Endothelial Growth Factor (VEGF) are key growth factors that activate new vessel formation. Both are upregulated in the tumor microenvironment. To date most anti-angiogenic therapies have focused on inhibiting the second step in angiogenesis, or activation of the endothelium, and anti-VEGF therapies have shown some success especially in combination with conventional cancer therapies. However, resistance to such therapies has emerged due to upregulation of other pro-angiogenic factors in the absence of VEGF. The present studies examine the impact of MEDI3617, a monoclonal antibody targeting Ang-2, on tumor cell induced angiogenesis by inhibiting the first step, or endothelial-endothelial and endothelial-smooth muscle cell interactions, in angiogenesis. An intradermal assay was used to evaluate the growth of vessels induced by the tumor. Nude mice injected intradermally with colorectal cancer cells, HT29, were treated with a range of MEDI3617 doses (2, 10, 20 mg/kg) and the effect on the number of vessel formation was determined. The results showed that at 2 mg/kg dose of MEDI3617 led to a 42% reduction in the number of vessels induced and 10 and 20 mg/kg induced even greater reduction in the number of vessels (48 and 61% respectively). Current studies are evaluating the mechanistic interaction of endothelial- endothelial cell and endothelial smooth-muscle cell interactions using a co-culture spheroid model. A core of smooth muscle cells are surrounded by a layer of endothelial cells mimicking the interaction of these cells in the vasculature. The effect of Ang-2 on destabilizing this co-culture spheroid and the ability of MEDI3671 on inhibiting this destabilization are being evaluated. Preliminary studies indicate the ability of MEDI3617 to inhibit sphere destabilization in the presence of Ang-2. Human monoclonal anti-Ang-2 antibody, MEDI3617, was both developed and this study supported by MedImmune, LLC. 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 4269. doi:10.1158/1538-7445.AM2011-4269
SP0082 Ten golden rules - how to capture the patient perspective in research?
Authors: M. De Wit
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Many researchers use different approaches to include the patient perspective in research. Although there is a strong belief that patient experiences represent a unique and valid source of evidence, little is known about the effectiveness of different approaches. This presentation provides ten practical considerations that answer the question "how to involve patients in research?". <h3>Method</h3> Based on a responsive evaluation of patient involvement in OMERACT conferences and a review of the 8 EULAR recommendations for the inclusion of patient representatives in scientific projects the author has identified ten considerations for including the patient perspective in research. <h3>Results</h3> Many factors determine the success of collaboration between patients and researchers. The level of involvement and the intensity and duration are critical. Structural involvement guarantees a mutual learning process that enables patients and researchers to find out how the patient perspective can be utilize best. On the long term this will enhance the variety, scale and quality of patients' contributions. A main barrier is the fact that benefits of patient involvement are not immediately visible for all stakeholders. From the researchers it requires a sensitivity for the richness of patients' stories and comments that need to be learned. And it is the responsibility of the researcher to adjust approach, attitude and communication style to the individual patient. <h3>Conclusion</h3> Structural involvement of patients as equal partners is not only beneficial to capture the patient perspective in every phase of a research process, but creates partnerships with benefits that goes beyond the scope of an individual project. <h3>Disclosure of Interest</h3> None Declared
Does paraduodenal pancreatitis systematically need surgery?
Authors: René Laugier, Philippe Grandval
Journal: Endoscopy (2014)

Paraduodenal pancreatitis is a rare pathology, which is unfamiliar to most clinicians and thus usually underdiagnosed. The space between the duodenum, the head of the pancreas, and the main bile duct has been called "the groove" because of its anatomical appearance. This space is peculiar in that it allows the development of pathological situations of imprecise origin, of difficult diagnosis due to a large spectrum of clinical presentations and, above all, of difficult therapeutic approaches, which are still a matter for debate.
Abstract SY11-01: Knockout mouse models for sirtuins: Genome integrity, metabolism, and cancer
Authors: Chuxia Deng, Hyun-Seok Kim, Athanassios Vassilopoulos, Rui-Hong Wang, Tyler Lahusen, Zhen Xiao, Xiaoling Xu, Cuiling Li, Timothy D. Veenstra, Junfang Ji, Xin-Wei Wang, Seong-Hoon Park, David Gius
Journal: Cancer Research (2011)

Abstract In budding yeast, Sir2 is a NAD+-dependent histone deacetylase that plays a role in chromatin silencing, longevity and genomic stability. In mammals, sirtuins exist as a family of 7 members (SIRT1-7) that deacetylate histones and many nonhistone proteins. Currently, all sirtuins have been knocked out by gene targeting, and the mutant mice suffer various abnormalities in cell growth, apoptosis, neurological behavior, adaptation to calorie restriction, organ metabolism and function, and/or premature aging, highlighting critical roles of sirtuins in these biological processes. Of note, mice carrying mutations of SIRT1, SIRT2 or SIRT3 also developed cancers, predominantly in the mammary glands and the liver that are accompanied by genomic instability and/or abnormal energy metabolism. Our further analysis revealed distinct role of these siruins in maintaining genome integrity. SIRT1 mutant cells displayed altered histone modification, impaired DNA damage response, and reduced ability to repair DNA damage [1]; SIRT3 mutant cells had increased stress-induced superoxide levels and genomic instability [2]; and SIRT2 loss primarily affects mitotic functions. We found that SIRT2 plays a role in maintaining normal mitosis progression through modulating expression levels of several mitotic regulators, including Aurora-A and -B. Loss of SIRT2, consequently, causes centrosome amplification, aneuploidy, and mitotic catastrophe. SIRT2-deficient mice initially develop normally, however, suffer mammary tumors and hepatocellular carcinoma (HCC) when they become old. These data highlight how accurate maintenance of genomic integrity is critical for the suppression of tumorigenesis. Finally, we found that human breast cancer and HCC exhibit reduced levels of SIRT1-3. These results implicate SIRT1-3 as tumor suppressors in these organs. References: 1. Wang RH, Sengupta K, Li C. et al. Impaired DNA damage response, genome instability, and tumorigenesis in SIRT1 mutant mice. Cancer Cell. 2008; 14: 312-323. 2. Kim HS, Patel K, Muldoon-Jacobs K. et al. SIRT3 is a mitochondria-localized tumor suppressor required for maintenance of mitochondrial integrity and metabolism during stress. Cancer Cell. 2010; 17: 41-52. 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 SY11-01. doi:10.1158/1538-7445.AM2011-SY11-01
THU0056 Acute Aerobic Exercise Induces Increases on Plasma Levels of α-Melanocyte Stimulating Hormone in Patients with Active Systemic Lupus Erythematosus
Authors: L. Perandini, B. Gualano, A.L.D.S. Pinto, F. Lima, E. Bonfá, E.F. Borba, H. Roschel, S.B. Mello
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Systemic lupus erythematosus (SLE) is an autoimmune disease associated with chronic inflammation. Pro-opiomelanocortin (POMC) axis activation leads to the production of several bioactive hormones, such as adrenocorticotropic hormone (ACTH) and the neuropeptide α-melanocyte stimulating hormone (α-MSH). Both hormones are closely related to the inflammatory process with pro- or anti-inflammatory effects. Although physical exercise has been described as a promoter of alterations in the neuroendocrine profile, no studies have addressed the participation of melanocortins in SLE patients in response to acute aerobic exercise. <h3>Objectives</h3> To evaluate α-MSH production in SLE patients under acute aerobic exercise. <h3>Methods</h3> Ten active SLE patients [age: 29.9±4.2yrs; body mass index (BMI): 26.0±4.8 kg/m<sup>2</sup>; SLEDAI: 5.9±2.1; glucocorticoid: 16.0±6.0 mg] and 10 age- and BMI-matched healthy controls performed 30 minutes of aerobic exercise (∼70% of VO<sub>2</sub> peak) in a treadmill. The a-MSH and ACTH serum levels were assessed at baseline and immediately after exercise session by a multiplex system (HNP-35K kit, Millipore, Billerica, MA, USA). <h3>Results</h3> Similar levels of a-MSH were observed at baseline between active SLE patients and healthy controls (<i>P=</i>0.69). However, after exercise, a distinct pattern of response was noted (Fig. 1). The serum levels of a-MSH was not altered in healthy controls, but a significant increase in mean levels was observed in active SLE patients after exercise (92.39±16.12 vs. 146.23±25.01 pg/mL, <i>P</i>=0.04). ACTH levels did not differ between groups at baseline and after exercise (<i>P</i>&gt;0.05). <h3>Conclusions</h3> The present study provides novel evidence that acute aerobic exercise induces a hypothalamic-pituitary-adrenal axis response with an increase in the levels of neuropeptide α-MSH in active SLE patients. We speculate that this is an exacerbated adaptive response to exercise stress to avoid further stimulation of proinflammatory cytokines in these patients. <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5206
Abstract 4108: BH3 only Bcl-2 family member BNIP3 repressed expression of death receptor 5 (DR5) in glioblastoma cells: Implications for regulation of the tumor necrosis factor related apoptosis inducing ligand (TRAIL) cell death pathway
Authors: Elizabeth S. Henson, Teralee R. Burton, Meghan B. Azad, David D. Eisenstat, Spencer B. Gibson
Journal: Cancer Research (2011)

Abstract Glioblastoma multiforme (GBM) is the most aggressive form of brain cancer. The median survival for patients with GBM is less than 15 months, even with treatment such as surgery, radiation and chemotherapy with temozolomide. Resistance to the standard treatment regimes represents a serious clinical challenge. GBM tumors contain extensive regions of necrosis, indicative of hypoxia. BNIP-3 (Bcl-2 nineteen kilodalton interacting protein) is a BH-3 only, pro-cell death member of the Bcl-2 family. BNIP-3 is up-regulated in hypoxia and leads to a non-classical programmed cell death through the mitochondria. In the majority of glioblastoma multiforme tumors, BNIP3 is localized to the nucleus and does not induce cell death. Our group has shown that when located in the nucleus, BNIP3 binds to DNA including the promoters of cell death genes such as AIF (apoptosis inducing factor). Herein, we found that BNIP3 bound to the promoter region of death receptor 5 (DR5). DR5 binds to the tumor necrosis factor related apoptosis inducing ligand (TRAIL) leading to induction of apoptosis. TRAIL is currently in phase 2 clinical trials for a wide variety of tumor types but glioblastoma tumors are resistant to TRAIL induced apoptosis. Our data showed that binding of BNIP3 to the promoter of DR5 prevented its expression and led to resistance to TRAIL induced cell death in glioma cells. Furthermore, when a BNIP3 construct was transiently over-expressed in the nucleus, DR5 mRNA and protein levels were reduced; also when BNip3 was knocked down using shRNA, DR5 message and protein levels increased. In BNIP3 knockout mice, we demonstrated that increased DR5 levels were increased in primary astrocytes compared to wild type controls as detected by western blot and immunofluorescence. We also showed similar results in brain sections from BNIP3 knockout mice. In paraffin embedded GBM tumors, we found that tumors that had BNIP3 in the nucleus had decreased levels of DR5, whereas tumors without BNIP3 in the nucleus had higher levels of DR5. Taken together, this represents a novel mechanism for regulation of DR5 expression, contributing to TRAIL resistance in GBM tumors. 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 4108. doi:10.1158/1538-7445.AM2011-4108
OP0219 TLR2 differentially mediates A-SAA induced pro-inflammatory pathways in rheumatoid arthritis
Authors: P. Rooney, W. Gao, J. McCormick, L. Harty, D.J. Veale, U. Fearon, M. Connolly
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Acute Serum Amyloid A (A-SAA) is strongly expressed in rheumatoid arthritis (RA) synovial tissue (ST) and is critically involved in regulating cell migration and invasion. In this study we examine the effect of A-SAA on Notch and chemokine signalling pathways and examine if these effects are mediated through TLR2 activation. <h3>Methods</h3> Expression of Notch 1 IC, downstream target genes HRT1, HRT2 and ligands JAGGED 1 and DLL-4 were assessed in synovial tissue and cells by Real-Time PCR and Western blot. Human microvascular endothelial cells (HMVEC) and primary Rheumatoid Arthritis Synovial Fibroblasts (RASFC) were cultured in the presence of anti-TLR2 or IgG control antibody. IL-6, IL-8, GROα and MCP-1 were assessed by ELISA, EC activation was assessed by matrigel tube formation and invasion assays. MMP expression in HMVEC and RASFC was assessed by real-time PCR, ELISA and gelatin zymography. <h3>Results</h3> NOTCH-1, target genes HRT 1, HRT 2 and ligands JAGGED 1 and DLL-4 mRNA was demonstrated in RA and PsA synovial biopsies. A-SAA significantly induced Notch-1 IC protein expression (p&lt;0.05), and HRT 1 and JAGGED 1 mRNA expression (p&lt;0.05). In contrast DLL-4 mRNA was significantly inhibited in response to A-SAA (p&lt;0.05). A-SAA significantly induced IL-6, IL-8, GROa and MCP-1 in HMVEC and RASFC, effects which were significantly inhibited by the presence of anti-TLR2 (all p&lt;0.05). Furthermore, A-SAA induced EC activation and invasion were inhibited by anti-TLR2 (p&lt;0.05). Conversly the presence of TLR2 had a nominal effect on MMP mRNA and protein expression. However we observed differential effects on Notch pathway signalling components. <h3>Conclusions</h3> TLR2 differentially mediates A-SAA induced pro-inflammatory mechanisms involved in the pathogenesis of Rheumatoid Arthritis. <h3>Disclosure of Interest</h3> P. Rooney: None Declared, W. Gao: None Declared, J. McCormick: None Declared, L. Harty: None Declared, D. Veale Grant/Research support from: Wyeth, GSK, Abbott, Opsona, Consultant for: Wyeth, GSK, Abbott, Pfizer, Schering Plough, Centocor, Speakers Bureau: Wyeth, GSK, Abbott, Pfizer, Schering Plough, Centocor, Mundipharma, U. Fearon: None Declared, M. Connolly: None Declared
Endoscopic Ultrasound (EUS) Guided Opacification Of Mediastinal Lymph Nodes
Authors: P Magno, CW Ko, S Giday, SB Jagannath, MI Canto, AN Kalloo, SV Kantsevoy
Journal: Endoscopy (2006)

Background: EUS has become the preferred modality for local staging of esophageal cancer and gaining popularity for lung cancer staging as well. Reliable and long-lasting non-invasive opacification of malignant lymph nodes may help to determine the treatment field to guide radiation and surgical therapy. Tantalum, a physiologically inert metal, has been used as radio-opaque material in various areas of medicine. AIM: To assess the feasibility of EUS-guided opacification of the mediastinal lymph nodes in a porcine model. Methods: The study was approved by the Animal Institutional Review Board. All procedures were performed on 50-kg pigs under general anesthesia. A linear EUS (Olympus® GF-UCT140) was introduced into the esophagus. Mediastinal lymph nodes were identified and injections with 1ml of a tantalum suspension (5 gm of tantalum powder with 10 cc of normal saline) were attempted via 19 and 23 gauge fine needle aspiration (FNA) needles (Wilson-Cook®) under the fluoroscopic observation. The EUS and fluoroscopy were repeated 1 week later followed by euthanasia and necropsy. Results: The injection through the 23-gauge FNA needle was impossible due to a rapid precipitation of tantalum leading to complete occlusion of the needle. EUS-guided intranodal injection was performed through the 19-guage FNA needle resulting in a good fluoroscopic opacification of the mediastinal lymph node. Repeated fluoroscopy 1 week later demonstrated stable deposition of the tantalum in the place of injection. There were no complications during the procedure and in the post-procedure period. Conclusions: EUS-guided marking of mediastinal lymph nodes is technically simple and safe and can facilitate radiation therapy and surgical resection.
Abstract 4543: Targeting the NADPH binding site of dihydrofolate reductase for cancer therapy
Authors: Yi-Ching Hsieh, Rialnat AdeBisi Lawal, Kathleen Scotto, Debabrata Banerjee, Emine Ercikan Abali, Joseph R. Bertino
Journal: Cancer Research (2010)

Abstract Dihydrofolate reductase (DHFR) catalyzes the reduction of dihydrofolate into tetrahydrofolate using NADPH as the cofactor. Folate-dependent one carbon metabolism is essential for the de novo synthesis of purines, pyrimidines and certain amino acids. Thus, DHFR plays an essential role in production and maintaining reduced folates for cellular proliferation, and consequently it has been a critical target for chemotherapy. Methotrexate (MTX), an antifolate that targets DHFR, has been used for decades in the clinic. However, both intrinsic and acquired resistance occurs due to decreased uptake, gene amplification and protein mutation. We have initiated studies to find an inhibitor that targets the cofactor NADPH binding site that would bypass these resistance mechanisms to MTX in contrast to analogs that target the dihydrofolate binding site. Fourteen NAD/NADP analogues were screened by the MTT assay in Chinese hamster ovary (CHO) cells which lack endogenous DHFR expression but were stably transfected with a DHFR-EGFP fusion construct driven by a CMV promoter (DG44 DHFR-EGFP). Two compounds, thionicotinamide adenine dinucleotide (NAD-S) and thionicotinamide adenine dinucleotide phosphate (NADP-S), had IC50 values of 1 μM. NAD-S and NADP-S were also found to be potent inhibitors of two other cancer cell lines, C85 (metastatic human colon cancer cell line) and CCRF-CEM (human T-cell lymphoblastic leukemia cell line). Surprisingly, both NAD-S and NADP-S decreased the levels of DHFR in CEM-CCRF cells. Pulse-chase experiments showed that the half life of DHFR is significantly reduced upon treatment of cells with 10 μM NADP-S. Furthermore, this NADP analog caused an increase in cells at the G1 phase (11% at 10 μM and 44% at 40 μM NADP-S treatment) that was reversible by removing NADP-S from the cell culture. Because NADP-S decreased DHFR levels, the combination of NADP-S with MTX was tested and found to significantly reduce colony formation, and was synergetic in vitro (Chou-Talalay analysis). We conclude that NADPS has a novel mechanism of action, i.e., it causes degradation of DHFR, likely by competing with NADPH binding, known to stabilize DHFR. 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 4543.