tbuckley/cabot-search huggingface dataset:
Calcium-Antagonist Receptors in the Atrial Tissue of Patients with Hypertrophic Cardiomyopathy
Authors: John A. Wagner, Frederic L. Sax, Harlan F. Weisman, James Porterfield, Charles McIntosh, Myron L. Weisfeldt, Solomon H. Snyder, Stephen E. Epstein
Journal: New England Journal of Medicine (1989)

Hypertrophic cardiomyopathy is characterized by a nondilated, hypertrophied left ventricle in the absence of any overt cause. A possible role of adrenergic innervation or of cellular calcium regulation is suggested by the presence of hyperdynamic left ventricular function and by the clinical and symptomatic improvement seen in patients treated with β-receptor antagonists or calcium antagonists. Therefore, we measured the density of calcium-antagonist receptors and β-adrenoceptors in the atrial myocardium of 16 patients with hypertrophic cardiomyopathy and 19 patients with various other cardiac disorders. For comparison, we also measured the number of voltage-sensitive sodium channels. Calcium-antagonist binding sites, measured as the amount of dihydropyridine bound to atrial tissue, were increased by 33 percent in patients with hypertrophic cardiomyopathy (mean [±SD], 397±104 fmol per milligram of protein in patients with hypertrophic cardiomyopathy, as compared with 299±108 in patients with other cardiac disorders; P<0.01). The densities of saxitoxin-binding sites on voltage-sensitive sodium channels and β-adrenoceptors were the same in the two groups, although the density of β-adrenoceptors was higher in atrial samples from patients receiving β-receptor antagonists (165±86 fmol per milligram of protein [patients receiving β-blockers] vs. 85±60 [patients not receiving β-blockers]; P<0.04). The increase in the number of calcium-antagonist receptors in hypertrophic cardiomyopathy suggests that abnormal calcium fluxes through voltage-sensitive calcium channels may play a pathophysiologic part in the disease. (N Engl J Med 1989; 320:755–61.)
Preventing Recurrent Upper Gastrointestinal Bleeding in Patients with<i>Helicobacter pylori</i>Infection Who Are Taking Low-Dose Aspirin or Naproxen
Authors: Francis K.L. Chan, S.C. Sydney Chung, Bing Yee Suen, Yuk Tong Lee, Wai Keung Leung, Vincent K.S. Leung, Justin C.Y. Wu, James Y.W. Lau, Yui Hui, Moon Sing Lai, Henry L.Y. Chan, Joseph J.Y. Sung
Journal: New England Journal of Medicine (2001)

Many patients who have had upper gastrointestinal bleeding continue to take low-dose aspirin for cardiovascular prophylaxis or other nonsteroidal antiinflammatory drugs (NSAIDs) for musculoskeletal pain. It is uncertain whether infection with Helicobacter pylori is a risk factor for bleeding in such patients.
Abstract 4961: MicroRNA profile predicts recurrence after resection in patients with hepatocellular carcinoma within the Milan criteria
Authors: Fumiaki Sato, Etsuro Hatano, Koji Kitamura, Akira Myomoto, Takeshi Fujiwara, Satoko Takizawa, Soken Tsuchiya, Shinji Uemoto, Kazuharu Shimizu
Journal: Cancer Research (2011)

Abstract Objective: Hepatocellular carcinoma (HCC) is difficult to manage due to the high frequency of post-surgical recurrence. Early detection of the HCC recurrence after liver resection is important in making further therapeutic options, such as salvage liver transplantation. In this study, we utilized microRNA expression profiling to assess the risk of HCC recurrence after liver resection. Methods: We examined microRNA expression profiling in paired tumor and non-tumor liver tissues from 73 HCC patients who satisfied the Milan Criteria. We constructed prediction models of recurrence-free survival using the Cox proportional hazard model and principal component analysis. The prediction efficiency was assessed by the leave-one-out cross-validation method, and the time-averaged area under the ROC curve (ta-AUROC). Results: The univariate Cox analysis identified 13 and 56 recurrence-related microRNAs in the tumor and non-tumor tissues, such as miR-96. The number of recurrence-related microRNAs was significantly larger in the non-tumor-derived microRNAs (N-miRs) than in the tumor-derived microRNAs (T-miRs, P&amp;lt;0.0001). The best ta-AUROC using the whole dataset, T-miRs, N-miRs, and clinicopathological dataset were 0.8281, 0.7530, 0.7152, and 0.6835, respectively. The recurrence-free survival curve of the low-risk group stratified by the best model was significantly better than that of the high-risk group (Log-rank: P=0.00029). The T-miRs tend to predict early recurrence better than late recurrence, whereas N-miRs tend to predict late recurrence better (P&amp;lt;0.0001). This finding supports the concept of early recurrence by the dissemination of primary tumor cells. and multicentric late recurrence by the ‘field effect’. Conclusion: microRNA profiling can predict HCC recurrence in Milan criteria cases. 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 4961. doi:10.1158/1538-7445.AM2011-4961
PATCH (Palliation And The Caring Hospital): a charity that is committed to improving hospital palliative care
Authors: Pamela Levack, Gordon Paterson
Journal: BMJ (2016)

Listening to patients, we know that people are afraid of dying in hospital.1 Yet we also know that more than half of us will do so. Rather than wish that this were not so, we can and should focus on improving hospital palliative care to ensure hospital patients and their families receive the appropriate care, as an outpatient, an emergency, an inpatient, or inpatient hoping …
SP0132 The Challenge of Supporting a Person with RMD to Become a Parent- A Clinical Perspective
Authors: A. Tincani
Journal: Annals of the Rheumatic Diseases (2013)

<h3></h3> The great improvement in the quality of life prompts a number of patients suffering from rheumatic diseases to desire to have a normal family. This particular period need to be skillfully guided by the physicians that have to be prepared to face a number of different situations according to the different diseases of the patients, the different drugs they are taking and according to the different gender of individuals desiring to become parents. Problems of men are mainly related to drugs uptake. In fact some drugs like salazopyrin can cause oligospermia linked to transient infertility, other one such as cyclophosphamide can irreversibly damage the gonads in unpredictable way (not dependent by the cumulative dosage) causing irreversible infertility. Sperma cryopreservation should be proposed to patients that need cyclophosphamide. Recently it was also observed an high rate of erectile dysfunctions in man suffering from systemic sclerosis, to underline that this severe disease can affect life expectances. Women that suffer from rheumatic diseases and desire to become mothers have a number of different problems related first to disease modifications in pregnancy: in this respect it is known that certain diseases, like rheumatoid arthritis, usually improve during pregnancy while others, like systemic lupus erythemetosus, seem to suffer from an increased rate of flares. A second problem is the treatment needed to keep the disease in remission: obviously it needs to be tailored respecting the safety of the fetus. In addition, some rheumatic diseases carry risk factors for the normal development of the pregnancy with a consequent increase of complications and losses. Puerperium, even after a successful pregnancy, has to be regarded as particularly challenging in patients with rheumatic disease. In fact, complications and flares are often reported and in particular the increased thromboembolic risk linked to the period can act as “second hit” for thrombosis in women with antiphospholipid syndrome with or without SLE. To be a mother and grow the child is also difficult for women with musculoskeletal problems. When mothers have a chronic disease, fatigue and pain can impair their parenting activity and can cause psychological distress if they do not feel adequate for the task. All these issues need to be discussed and clarified with patients to prevent with medical, psychological and familiar help the occurrence of problems that could spoil the satisfaction of a having a family. <h3>Disclosure of Interest</h3> None Declared
Abstract 5291: Exploring mechanisms underlying invasion in HLRCC: Assessing the contribution of HIF and ROS
Authors: Carole Sourbier, Yeong-Sang Kim, Sunmin Lee, Jane Trepel, Len Neckers, W. Marston Linehan
Journal: Cancer Research (2010)

Abstract Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) is a highly metastatic disease characterized by a disruption of the Krebs cycle due to a germline mutation of the fumarate hydratase gene (FH). We have recently shown that HLRCC kidney cancer cells are in a pseudo-hypoxic state due to normoxic stabilization of both HIF1 and HIF2 and that the expression of HIF1 can be decreased using ROS scavengers such as pyruvate or N-acetylcysteine (NAC). Our objective was to study the involvement on invasion of aberrant HIF1 and HIF2 expression in HLRCC cells. When either HIF1 or HIF2 was knocked down, invasion was dramatically inhibited in vitro. Invasion of HLRCC cells was also inhibited by decreasing the ROS level with NAC. To study further the mechanisms by which HIF1 and HIF2 mediate invasion in HLRCC, we evaluated several markers of glycolysis and ROS formation. Our results show that when HIF1, but not HIF2, is knocked down, Glut1 mRNA level, glucose uptake, and lactate secretion are decreased. Even though N-acetylcysteine treatment decreased HIF1 and HIF2 expression, it did not affect glucose uptake or lactate secretion by HLRCC cells. Moreover transient knock-down of HIF1 or HIF2 by siRNAs did not affect the ROS level in vitro. To study further the mechanism of action of both HIF1 and HIF2, microarrays and in vivo experiments with stably transfected cell lines with shRNA for HIF1, HIF2 and ARNT are in progress. These results suggest that HIF1-mediated invasion may partially involve glycolysis. The mechanisms by which HIF2 and ROS mediate invasion are still under study. Our data support the hypothesis that HIF1, HIF2 and ROS are important for invasion. If one of them is inhibited, invasiveness of the HLRCC cells is compromised. 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 5291.
P3-08-01: Effects of an Integrated Yoga Program on Mood States, Distress, Quality of Life, Diurnal Cortisol Rhythms and Natural Killer Cell Counts in Metastatic Breast Cancer Survivors.
Authors: SK Gopinath, RM Rao, VH Sanjeevarao, RB Diwakar, AS Basavalingaiah, S Patil, N Raghuram, N Ramarao, RM Usharani
Journal: Cancer Research (2011)

Abstract Background and objectives: Metastatic breast cancer patients experience tremendous psychological distress due to treatment, disease and uncertainty of their survival. In this study we evaluated the effects of an integrated yoga program versus supportive counseling in advanced breast cancer survivors. Methods: Ninety one Metastatic breast cancer survivors (group mean age 50.54 yrs ± 8.53 yrs) registered in hospital based cancer registry were recruited if they satisfied selection criteria and gave written consent for participation in the study. The study was approved by the institutional review board. Subjects were randomized to either receive yoga intervention (n=45) or supportive therapy (n=46) counseling as a standard of care for 3 months of intervention period. Subjects were assessed at baseline and after intervention for mood states using hospital anxiety and depression scale, sleep quality using Pittsburg Insomnia rating scale, quality of life using EORTC Qol C30 for breast and perceived stress using perceived stress scale. Saliva samples were collected for three consecutive days at 0600hrs, 0900hrs and 2100hrs before and after intervention for cortisol rhythms using Enzyme Immune Assay kits from Salimetrics and blood samples were collected between 0800hrs to 01000hrs for NK cell enumeration using flow cytometry. 35 subjects in yoga and 31 subjects in controls completed the post measures. Data were analyzed using both parametric (ANCOVA with respective baseline measure as a covariate) and non parametric tests (Mann whitney U test) to evaluate effects of intervention on the above outcome measures. Data for salivary cortisol data was log transformed, area under the curve and cortisol slope computed using linear mixed effects model. Results: There was a significant decrease in anxiety (p &amp;lt; 0.001), depression (p &amp;lt; 0.001), perceived stress (p = 0.01), fatigue severity (p &amp;lt; 0.001) and interference (p &amp;lt; 0.001) in yoga group compared to controls post intervention. There was a significant improvement in emotional function (p &amp;lt; 0.001), role function (p = 0.03) and cognitive function (p &amp;lt; 0.001) and global quality of life (p &amp;lt; 0.001) in yoga group compared to controls. There was significant decrease in 0600 hrs cortisol within the yoga group (p =0.03) alone. There was a significant increase in Natural killer cell percent in yoga group (p =0.03) compared to controls after intervention. Conclusion: The results suggest biobehavioral effects of yoga intervention could possibly improve quality of life, reduce psychological distress and modulate abnormal cortisol profiles and immune responses in metastatic breast cancer patients. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P3-08-01.
FENOTIPOS ENDOSCÓPICOS EN LA ESOFAGITIS EOSINOFÍLICA, UN REFLEJO DE LA HISTORIA NATURAL DE LA ENFERMEDAD
Authors: J Rodríguez Sánchez, B López Viedma, E De La Santa Belda, J Olmedo Camacho, P Reales Figueroa
Journal: Endoscopy (2013)

Introducción: Recientemente se han descrito tres fenotipos de EoE en base a los hallazgos endoscópicos: fenotipo inflamatorio (FI) (surcos longitudinales, edema, exudados blanquecinos), fenotipo fibroestenosante (FE) (pseudoanillos, estenosis) y fenotipo mixto (FM) (FI+FE). Sin embargo son pocos los estudios que analizan qué factores (influyen) están implicados en la génesis de estos signos endoscópicos y como condicionan la clínica de los pacientes. Objetivo: Comparar las características clínicas, epidemiológicas e histológicas de los fenotipos endoscópicos en una (muestra) serie de pacientes diagnosticados de EoE. Material y Método: Estudio prospectivo, observacional y descriptivo sobre una cohorte de pacientes adultos con EoE. La muestra se clasificó en 3 fenotipos (FI, FM, FE). Se estudiaron características epidemiológicas, tiempo de evolución de los síntomas (meses), afectación clínica y mejoría tras tratamiento con VAS-EoE Score (0 – 70 puntos), respuesta a tratamiento, eo/cga en las biopsias, eosinófilos/mm3 de suero. Resultados: 32 pacientes (edad media 33,22 años; 62,5% varones). FI 31,3%, FM 43,8%, FE 21,9%. No (hubo) se encontraron diferencias en cuanto a edad, sexo y antecedentes de atopia. La afectación clínica pretratamiento fue significativamente mayor en FM (FM 32,50 vs. FI 21,90; p = 0,01 vs. FE 22,14; p = 0,03) y similar posttratamiento (FI 3,43 vs. FM 5,93 vs. FE 2;p = ns). No hubo diferencias en el número de eo/cga ni en los eo/mm3. Sin embargo, sí se evidenció diferencia en el tiempo de evolución de los síntomas (FI 25,30 vs. FM 66,50; p = 0,03 vs. FE 101,71; p = 0,06). Conclusiones: Los fenotipos endoscópicos de la EoE traducen el tiempo de evolución de la enfermedad, siendo el fenotipo inflamatorio el estadio inicial y el fenotipo estenosante el estadio más avanzado. Existe una clara disociación endoscópico-clínico-histológica, que hace difícil predecir la respuesta a los tratamientos (< 15eo/cga) tan sólo con criterios clínicos.
Abstract 4276: PGE2 induces LEF-1 expression in breast cancer cells, but is not required for the nuclear localization of beta-catenin
Authors: Ioannis Stasinopoulos, Tiffany Greenwood, Kristine Glunde, Zaver M. Bhujwalla
Journal: Cancer Research (2012)

Abstract We have previously demonstrated that poorly differentiated MDA-MB-231 cells displayed delayed tumor onset, reduced frequency of occurrence and loss of their capacity for extrapulmonary colonization when transfected stably with a potent and specific cyclooxygenase (COX) −2 shRNA sequence. We attributed the reduction in tumor growth and extrapulmonary colonization to reduced invasive capabilities, reduced angiogenesis, altered metabolism and differences in the stabilization of hypoxia-inducible factor-1α. We also observed loss of expression of oncogenes, receptors and degradative enzymes associated with tumor growth and metastasis including matrix metalloproteinase-1, CXC Receptor-4, roundabout-1, hyaluronan synthase-2, and monocarboxylate transporter 2. In addition to these previously reported transcriptome changes, we observed that the most highly downregulated transcription factor was Lymphoid-Enhancer Factor-1 (LEF-1) a result validated by qPCR showing an 8-fold loss of LEF-1 in COX-2-silenced cells. Here, we present evidence demonstrating that LEF-1 accumulation in the nucleus of COX-2-silenced cells is reduced compared to COX-2 containing parental cells. Induction of COX-2 by phorbol esters resulted in nuclear accumulation of LEF-1 in COX-2 containing, but not in COX-2-silenced, cells. Addition of physiological concentrations of PGE2 to COX-2-silenced cells partially restored LEF-1 expression in the nucleus of these cells. LEF-1 is a member of the T-cell specific factor (TCF) family of transcription factors that direct transcription of downstream target genes upon nuclear translocation of β-catenin from the cytoplasm. β-catenin translocation to the nucleus occurs in response to canonical signaling of the ligand Wnt to its receptor Frizzled. An earlier study showed that the COX-2 product prostaglandin E2 promoted the translocation of β-catenin to the nucleus of colon cancer cells via G-protein coupled receptor signaling. As expected, immunofluorescence of COX-2 containing MDA-MB-231 breast cancer cells showed nuclear expression of β-catenin. However, the nuclear localization of β-catenin persisted even in the absence of PGE2, as observed in COX-2-silenced cells, suggesting that PGE2 expression is not necessary for the nuclear localization of β-catenin in MDA-MB-231 cells. Taken together, our results demonstrate that while PGE2 is not necessary for the nuclear localization of β-catenin in MDA-MB-231 cells, it can promote the nuclear accumulation of the TCF family member LEF-1, thereby further promoting the non-canonical activation of the Wnt pathway in breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4276. doi:1538-7445.AM2012-4276
COMPARISON OF RADIATION DOSE BETWEEN DIFFERENT X-RAY SYSTEM IN THE CARDIAC CATHETERIZATION LABORATORY: RESULTS FROM BENCH TESTING USING AN ANTHROPOMORPHIC PHANTOM
Authors: Georgios Christopoulos, Georgios Christakopoulos, Bavana Rangan, Ronald Layne, Rebecca Grabarkewitz, Donald Haagen, Mazen Abu-Fadel, Subhash Banerjee, Emmanouil Brilakis
Journal: Journal of the American College of Cardiology (2015)
Hypertension and cardiac dysfunction in male mice deficient in the alpha 1 subunit of soluble guanylate cyclase
Authors: Emmanuel Buys, Mj Raher, Jj Passeri, F Ichinose, Mh Picard, Patrick Sips, Peter Brouckaert, M Scherrer-Crosbie, Kd Bloch
Journal: Circulation (2006)
Seafood Fatty Acids May Lower Cancer Risk
Authors: J. Corliss
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Seafood Fatty Acids May Lower Cancer Risk Get access Julie Corliss Julie Corliss Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 20, 18 October 1989, Pages 1530–1531, https://doi.org/10.1093/jnci/81.20.1530 Published: 18 October 1989
Abstract 611: AID/APOBEC cytidine deaminases can mimic the phenomenon of localized hypermutation in cancer or <i>kataegis</i>.
Authors: Serena Nik-Zainal, Ben Taylor, Yee Ling Wu, David Wedge, Cristina Rada, Mike Stratton, Michael Neuberger
Journal: Cancer Research (2013)

Abstract Recently, using whole-genome sequencing data of breast cancer genomes we revealed localized regions of dense somatic hypermutation, called kataegis, in which substitutions at C:G base pairs occurring within a distinctive sequence context were found associated with clusters of genomic rearrangements. The mechanism of kataegis is unknown. On the basis of similarities in mutation class and sequence context in experimental systems, members of the AID/APOBEC family of cytidine deaminases were implicated. Here we expressed members of this gene family in yeast and demonstrate that mutation clusters mimicking many of the features of kataegis in cancer, can be generated. Because the genomic location of each stretch of kataegis is different between individual human cancer genomes, it was reasoned that kataegis is triggered by a local stochastic event, such as a DNA double strand break. Here, we have introduced double strand breaks into the yeast genome and shown that kataegis is elicited in its vicinity. Furthermore, kataegis is substantially diminished in the absence of uracil-DNA glycosylase, indicating that base excision DNA repair is implicated in its genesis. Additionally, the mutation sequence context preferences revealed by these yeast experiments suggest that APOBEC3B and APOBEC3A are the deaminases most likely responsible for the kataegis observed in human cancer. The results therefore provide insights into the mechanism of kataegis and indicate a contribution of APOBEC3B/A-catalyzed DNA deamination to genome mutation in cancer. Finally, we show using an algorithm developed to allow efficient detection of kataegis in other publicly available whole-genome sequenced datasests that this phenomenon is not restricted to breast cancer. Citation Format: Serena Nik-Zainal, Ben Taylor, Yee Ling Wu, David Wedge, Cristina Rada, Mike Stratton, Michael Neuberger. AID/APOBEC cytidine deaminases can mimic the phenomenon of localized hypermutation in cancer or kataegis. [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 611. doi:10.1158/1538-7445.AM2013-611
Images of a Case of Carney Triad by Combined F-18 FDG PET/CT
Authors: Katsuhiko Kato, Wataru Koike, Shingo Iwano, Norihiro Usami, Kohei Yokoi, Yuichi Ueda, Shinji Naganawa
Journal: Clinical Nuclear Medicine (2011)

Carney triad is a very rare condition with gastrointestinal stromal tumor, pulmonary chondroma, and extra-adrenal paragangliomas. We present the images of a patient with the complete triad, including total gastrectomy for gastrointestinal stromal tumor at the age of 13, and a left pneumonectomy for pulmonary chondroma at the age of 15. Results of F-18 FDG PET/CT that was performed at age of 22 for recurrent pulmonary chondroma also demonstrated new lesions in the neck, mediastinum, and abdomen representing extra-adrenal paragangliomas.