tbuckley/cabot-search huggingface dataset:
Endpiece: A man's best friend
Authors: A. t. G. Marx
Journal: BMJ (1999)

has significant anti-inflammatory properties, reducing the release of toxic mediators in response to an infective challenge. 17This contrasts with the effects of inotropes with 1 receptor activity such as adrenaline. 18 Thus dopexamine may confer an additional advantage to fluid optimisation by reducing the effect of infective complications. ConclusionThe incidence of morbidity in our control group suggests that there is a substantial population of surgical patients in the United Kingdom who are likely to benefit from the interventions described.Only 5% of all planned elective surgical admissions to intensive care are currently admitted preoperatively. 2Formal cost benefit analysis was not performed in this study, but values for usage of intensive carebeds or high dependency care beds (table 5) and length of stay in hospital suggest there may be overall savings in hospital costs when preoptimising patients for major elective surgery.An initial investment in resources may lead to economic gains for hospitals as well as a better outcome for surgical patients.We thank the patients, their surgeons, and the medical and nursing staff of the intensive care, anaesthetic, and operating theatre departments for their patience and cooperation.Andy Vale, senior medical statistician at the University of Leeds, gave advice on statistical analysis.
Gene-Specific Differential DNA Methylation and Chronic Arsenic Exposure in an Epigenome-Wide Association Study of Adults in Bangladesh
Authors: Maria Argos, Lin Chen, Farzana Jasmine, Lin Tong, Brandon L. Pierce, Shantanu Roy, Rachelle Paul-Brutus, Mary V. Gamble, Kristin N. Harper, Faruque Parvez, Mahfuzar Rahman, Muhammad Rakibuz-Zaman, Vesna Slavkovich, John A. Baron, Joseph H. Graziano, Muhammad G. Kibriya, Habibul Ahsan
Journal: Environmental Health Perspectives (2014)

Background: Inorganic arsenic is one of the most common naturally occurring contaminants found in the environment. Arsenic is associated with a number of health outcomes, with epigenetic modification suggested as a potential mechanism of toxicity.Objective: Among a sample of 400 adult participants, we evaluated the association between arsenic exposure, as measured by blood and urinary total arsenic concentrations, and epigenome-wide white blood cell DNA methylation.Methods: We used linear regression models to examine the associations between arsenic exposure and methylation at each CpG site, adjusted for sex, age, and batch. Differentially methylated loci were subsequently examined in relation to corresponding gene expression for functional evidence of gene regulation.Results: In adjusted analyses, we observed four differentially methylated CpG sites with urinary total arsenic concentration and three differentially methylated CpG sites with blood arsenic concentration, based on the Bonferroni-corrected significance threshold of p < 1 × 10–7. Methylation of PLA2G2C (probe cg04605617) was the most significantly associated locus in relation to both urinary (p = 3.40 × 10–11) and blood arsenic concentrations (p = 1.48 × 10–11). Three additional novel methylation loci—SQSTM1 (cg01225779), SLC4A4 (cg06121226), and IGH (cg13651690)—were also significantly associated with arsenic exposure. Further, there was evidence of methylation-related gene regulation based on gene expression for a subset of differentially methylated loci.Conclusions: We observed significant associations between arsenic exposure and gene-specific differential white blood cell DNA methylation, suggesting that epigenetic modifications may be an important pathway underlying arsenic toxicity. The specific differentially methylated loci identified may inform potential pathways for future interventions.Citation: Argos M, Chen L, Jasmine F, Tong L, Pierce BL, Roy S, Paul-Brutus R, Gamble MV, Harper KN, Parvez F, Rahman M, Rakibuz-Zaman M, Slavkovich V, Baron JA, Graziano JH, Kibriya MG, Ahsan H. 2015. Gene-specific differential DNA methylation and chronic arsenic exposure in an epigenome-wide association study of adults in Bangladesh. Environ Health Perspect 123:64–71; http://dx.doi.org/10.1289/ehp.1307884
Pancreatic adenocarcinoma with intratumoral anechoic components will increase the number of endoscopic ultrasound-guided fine-needle aspiration passes
Authors: JH Chen, TY Cheng, JT Lin, MS Sun, HP Wang
Journal: Endoscopy (2006)

Background For diagnosis of pancreatic cancer, endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) is currently the standard procedure because of its safety and reliability. But on considering cost, time, and risk of complications of EUS-FNA, the number of aspiration passes should be minimized. Previously, only tumor differentiation and the site of aspiration have been recognized as major determinants that influence the number of needle passes during EUS-FNA for pancreatic malignancy. The aim of this study was to prospectively evaluate factors affecting the number of passes in patients with pancreatic cancer.
AB0020 The Role of Macrophage Migration Inhibitory Factor Gene Polymorphism in Susceptibility to Juvenile Arthritis
Authors: K.V. Danilko, L. Nazarova, O. Tselousova, D. Karimov, V. Malievskiy, T. Viktorova
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Background: Juvenile arthritis (JA) is an umbrella term used to describe the many autoimmune and inflammatory conditions that can develop in children ages 16 and younger. According to the ILAR criteria JA include 7 disease subtypes. It was shown that JA is as a complex trait and some genes are associated with JIA in different populations and subtypes, including macrophage migration inhibitory (MIF) gene. MIF is a lymphokine involved in cell-mediated immunity, immunoregulation, and inflammation. It plays a role in the regulation of macrophage function in host defense through the suppression of anti-inflammatory effects of glucocorticoids. <h3>Objectives</h3> The goal of the study was to examine evidence for association of the MIF*-173G&gt;C polymorphism (rs755622) with different clinical variants of JA. <h3>Methods</h3> The MIF*-173G&gt;C SNP was studied in 155 children with juvenile arthritis (JA) and 208 healthy individuals, citizens of the Bashkortostan, using real time PCR. Statistical analysis was performed in Statistica v. 6.0 and SNPStats programs. <h3>Results</h3> The genotype GG (p=0,02; OR=1,74, CI (1,12-2,72)) and allele G (p=0,03; OR=1,55, CI (1,06-2,28)) were found to be the genetic markers of increased JA risk. The earlier age debut of JA (0-6 years) was also was marked by the GG genotype (p=0,003). The GC or CC genotype were associated with the high JA activity (p=0,04). SNPStats program analysis indicated the association between the MIF*-173G&gt;C SNP and JA in additive model (p=0,022, OR=0,63, 95%CI=0,42-0,94), dominant model (p=0,014, OR=0,57 95%CI=0,37-0,90), but not in recessive model (p=0,7, OR=0,79, 95%CI=0,23-2,74). <h3>Conclusions</h3> Our data demonstrate the association of the polymorphic locus MIF*-173G&gt;C with increased JA risk and clinical variants of the disease in patients from Bashkortostan, Russia. <h3>References</h3> Angeles-Han S., Prahalad S. The genetics of juvenile idiopathic arthritis: what is new in 2010? Curr Rheumatol Rep. 2010; 12 (2): 87-93. Hinks A., Cobb J., Marion M.C. Prahalad S., Sudman M., Bowes J., et al. Dense genotyping of immune-related disease regions identifies 14 new susceptibility loci for juvenile idiopathic arthritis. Nat Genet. 2013; 45 (6): 664-669. Donn R., Alourfi Z., De Benedetti F., Meazza C., Zeggini E., Lunt M., et al. Mutation screening of the macrophage migration inhibitory factor gene: positive association of a functional polymorphism of macrophage migration inhibitory factor with juvenile idiopathic arthritis. Arthritis Rheum. 2002; 46: 2402–2409. De Dios Rosado J., Rodriguez-Sosa M. Macrophage Migration inhibitory factor (MIF): a key player in protozoan infections. Int J Biol Sci. 2011; (7) 9: 1239-1256. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3197
Abstract 3685: A strategy to identify therapeutic candidates for chronic lymphocytic leukemia from a library of FDA approved drugs
Authors: Min Shen, Yaqin Zhang, Adrian U. Wiestner, Melissa A. Ashlock, Christopher P. Austin, Douglas S. Auld
Journal: Cancer Research (2010)

Abstract Chronic lymphocytic leukemia (CLL) is an adult lymphoid malignancy with a variable clinical course. There is considerable interest in the identification of new treatments, as most current approaches are not curative. While most patients respond to initial chemotherapy, relapsed disease is often resistant to the drugs commonly used in CLL and are left without limited therapeutic options. In this study, we used a luminescent cell viability assay based on ATP levels (CellTiter-Glo, Promega) to find compounds that were potent and efficacious in killing CLL cells. We employed an in-house process of quantitative high throughput screening (qHTS) to assess 8-9 concentrations of each member of a 2,816 compound library (including FDA-approved drugs and those known to be bio-active from commercial suppliers). Using qHTS we generated potency values on each compound in lymphocytes donated from each of six individuals with CLL and five unaffected individuals. We found 102 compounds efficacious against cells from all six individuals with CLL (“consensus” drugs) with seven of these showing no efficacy on lymphocytes from a majority of unaffected donors, suggesting some degree of specificity for the leukemic cells. Furthermore, to determine if we could save time and cost we screened the same library using CLL cells pooled from these individuals. We found that over 90% of the 102 drugs identified as efficacious on cells from individuals were also efficacious in the pooled experiment. Importantly, a near perfect correlation was observed in potency values between the single and pooled studies. The results of this “pooling” approach suggests it is rationale to apply pooling and qHTS when screening CLL cells against much larger collections (&amp;gt;300,000 unapproved compounds) where novel compounds could be identified as starting points for drug discovery and development. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3685.
REGIONAL RIGHT VENTRICULAR EJECTION FRACTION AND CARDIAC OUTPUT IN REPAIRED TETRALOGY OF FALLOT
Authors: Waseem J. Cossor, Francesco Maffessanti, Karima Addetia, Victor Mor-Avi, Keigo Kawaji, David Roberson, Karin Dill, Roberto Lang, Amit Patel
Journal: Journal of the American College of Cardiology (2015)
More Patients to Receive Taxol
Authors: E. Blune
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article More Patients to Receive Taxol Get access Elaine Blune Elaine Blune Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 19, 7 October 1992, Page 1464, https://doi.org/10.1093/jnci/84.19.1464 Published: 07 October 1992
FRI0395 Digital ulcers as a “sentinel” sign for early internal organ involvement in very early systemic sclerosis: evidence from a single vedoss/eustar centre.
Authors: C. Bruni, S. Guiducci, S. Bellando-Randone, G. Lepri, F. Braschi, G. Fiori, F. Bartoli, M. Matucci-Cerinic
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Objectives</h3> Evaluation of the presence of digital lesions [1] in patients with diagnosis of very early systemic sclerosis (VEDOSS) [2] and of their correlation with clinical, laboratory and imaging parameters. <h3>Methods</h3> 110 VEDOSS patients were investigated for presence of digital pitting scar, calcinosis, digital ulcers (DUs), necrosis or gangrene, nailfold videocapillaroscopic abnormalities, disease specific autoantibodies (anti-centromere and anti-topoisomerase I) and internal organ involvement (chest HRCT, pulmonary function tests with DLCO evaluation, oesophagealmanometry, Holter ECG, cardiac Doppler US, renal arteries Doppler US) [3]. <h3>Results</h3> 4 patients reported a history of digital pitting scars, 16 patients presented active DU and 14/16 also reported a history of previous DUs. Other 9 patients reported a history of DUs only. Both the history and the presence of DUs showed statistically significant correlation with esophageal manometry only (analyzed through IBM SPSS Statistics version 19, using Spearman's Rho test:ρ=0,681 &amp;ρ=0,633 respectively, p &lt; 0,05). Clustering patients according to the presence of internal organ involvement, DUs were observed in VEDOSS patients with internal organ involvementbut not in those without organ involvement. <h3>Image/graph</h3> <h3>Conclusions</h3> DUs are already present in VEDOSS patients and correlate with esophageal involvement [4]. DU may be considered as a sentinel sign for the presence of early organ involvement, meaning the evolution from thevery early to the early phase of systemic sclerosis [5]. <h3>References</h3> Amanzi L et al. Digital ulcers in scleroderma:staging, characteristics and sub-setting through observation of 1614 digital lesions. Rheumatology (Oxford).2010 ;49:1374-82. Avouac J et al, "Preliminary criteria for the very early diagnosis of systemic sclerosis: results of a Delphi Consensus Study from EULAR Scleroderma Trials and Research Group", Ann Rheum Dis. 2011 Mar;70:476-81. Czirjak L, Matucci Cerinic M: Beyond Raynaud's phenomenon hides a very early systemic sclerosis: the assessment of organ involvement is always mandatory. Rheumatology 2011;50:250-1 Lepri G et al: Evidence for Esophageal and anorectal involvement in patients with very early diagnosis of systemic sclerosis (VEDOSS):report from a single EUSTAR centre. (Submitted) Matucci Cerinic M et al: Very early versus early disease: the evolving definition of the many faces of Systemic Sclerosis Ann Rheum Dis; 2012 Nov 23 <b>Disclosure of Interest</b>: None Declared
1066 LIVER STIFFNESS IN A SERIES OF CELIAC PATIENTS
Authors: R.E. Rossi, S. Massironi, M. Fraquelli, M.T. Bardella, L. Elli, M. Maggioni, M.P. Spampatti, F. Cavalcoli, M. Colombo, D. Conte
Journal: Journal of Hepatology (2012)
Abstract 4085: The roles of HDACs in chromatin remodelling and response to chemotherapy in cancer
Authors: Rui Huang, Simon P. Langdon, David J. Harrison, Dana Faratian
Journal: Cancer Research (2012)

Abstract Background: Chromatin is dynamic in higher-order structure in response to extracellular and environmental signals. We observed nuclear morphological changes in clinical cancer tissues after chemotherapy. Since chromatin structure dictates gene expression, and therefore function, further investigation of this phenomenon may help us to better understand therapeutic responses. We hypothesise that nuclear morphological changes in cancer in response to DNA-damage by chemotherapy are mediated by histone deacetylases (HDACs). Methods: Ovarian cancer cell lines PEO1/PEO4 (platinum sensitive/resistant) were selected as in vitro models, and primary ovarian cancer xenografts OV1002 and HOX424 as in vivo models. Expression levels of HDACs and heterochromatin protein 1 (HP1) were screened by reverse phase protein array (RPPA) and western blot after treatment with cisplatin. Immunofluorescence imaging was undertaken using confocal microscopy and nuclear texture was measured in Image J using GLCM texture analysis plugin. 38 ovarian cancer patient and 175 xenograft samples were assessed for HDAC and HP1 expression in response to chemotherapy by quantitative immunofluorescence. HDAC2 expression was modulated by interfering RNAs (siRNA). Results: We demonstrate nuclear morphological changes in clinical tumours, xenografts, and cell lines in response to platinum chemotherapy. HDACs and HP1 isoforms showed differential expression in a panel of 25 ovarian cancer cell lines associated with response to chemotherapy with increased expression in treated or resistant lines. Expression of HDACs increased in PEO1 cells treated with cisplatin in a time-dependent fashion. This was accompanied by quantifiable changes in nuclear texture (increased heterogeneity), and high expression of HP1s at early time point (4-24h). The proliferation of PEO1 cells was inhibited and HP1 protein expression decreased after HDAC2 knockdown. In clinical specimens, HDAC8 and HP1 gamma expression significantly increased after chemotherapy, and class I HDAC (1, 2, and 8) and HP1 expression were increased after carboplatin treatment in carboplatin-sensitive xenografts. Chromatin conformation, DNA damage response, and cell cycle progression showed sequential changes over time with carboplatin treatment. Conclusion: These results demonstrate alterations in chromatin structure after chemotherapy, and implicate the role of class I HDACs in higher order chromatin changes and the DNA damage response in ovarian cancer in vitro and in vivo. 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 4085. doi:1538-7445.AM2012-4085
Abstract 3883: Multiplexed formats for detection of SNPs for cell line authentication and cancer related mutations
Authors: Rixun Fang, Manohar R. Furtado
Journal: Cancer Research (2011)

Abstract Rapid and accurate identification of SNPs and mutations are useful in ensuring that the correctly identified cell lines are being used in cancer research studies and for accurate identification of SNPs and indels in cancer cells. In this study we report on a method that uses nucleic acid isolation methods, multiplexed PCR to amplify up to 48 regions within the human genome followed by an oligonucleotide ligation assay that can detect SNPs, mutations and indels. The protocol takes about 4 hrs to complete and uses panels optimized for human cell identification and detection of mutations in EGFR and KRAS genes. We typed the NCI-60 panel and several cell lines from the ATCC using two panels. One is a panel of SNPs that has been tested with samples from over 46 human populations to identify a set of SNPs that would discriminate globally. This SNP set has 48 markers with high heterozygosity (&amp;gt;0.4) and low Fst values (&amp;lt;0.06) across multiple human populations. The panel has a high power of discrimination. (Hum Genet; 127 (3) 315-324; 2010) comparable to that obtained with STR kits. A panel of 31 samples from closely related individuals within families was typed to test the power of discrimination. In another study, we applied this system to a cancer mutation study, in which an assay for detecting 29 EGFR and 5 KRAS gene mutations was developed. These mutations are frequently found in human cancers. DNA preparations from 48 ATCC and 60 NCI tumor cell lines were genotyped by this assay. These SNPs and mutations were further confirmed by the Sanger sequencing chemistry, showing 100% concordance between two technologies. The information generated from this study will be definitely useful when these cell lines are used as models for cancer study and cancer drug screening. In conclusion, we have developed a sensitive, highly accurate, high throughput genotyping system. Studies have demonstrated its effectiveness for successful SNP/InDel detection and mutation screening. This system has been successfully used for oncogen mutation studies in cancer cell lines. Overall, the system can become a valuable tool for molecular and clinical diagnostics. 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 3883. doi:10.1158/1538-7445.AM2011-3883
Health-Care of the Baby. A Hand-book for Mothers and Nurses.
Journal: JAMA (1906)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
NATIONWIDE TRENDS IN PULMONARY ARTERY ENDARTERECTOMY FOR CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION
Authors: Arun Kanmanthareddy, Saurabh Aggarwal, Alok Saurav, Hemantha Koduri, Jitendra Pandya, Abhilash Akinapelli, Muhammad Soubhi Azzouz, Michael White, Manu Kaushik, Dennis Esterbrooks, Michael Del Core, Claire Hunter, Aryan Mooss, Venkata Alla
Journal: Journal of the American College of Cardiology (2016)
Abstract 1981: Tumor suppressor functions of the Src-like adaptor protein (SLAP) in colorectal cancer cells
Authors: Cécile Naudin, Cédric Leroy, Audrey Sirvent, Valérie Simon, Jean-François Bourgaux, Bruno Robert, Julie Pannequin, Frédéric Hollande, Serge Roche
Journal: Cancer Research (2011)

Abstract Background : The cytoplasmic tyrosine kinase Src is frequently deregulated in colorectal cancer (CRC) and this deregulation is implicated in tumour growth and in the induction of metastasis. How Src is activated in this cancer has not been clearly established. In contrast to Ras, Src activating mutations are rare events, suggesting the existence of alternative mechanisms for the induction of Src oncogenic activity. Here, we addressed whether Src deregulation involves inhibition of its negative regulators, including the Src-Like Adaptor Protein (SLAP). Experimental procedures : SLAP expression was analyzed in colon cancer cells and in microdissected tissue samples of patients with CRC. The effect of SLAP was analyzed on the capacity of CRC cells to grow in soft agar and to induce tumours once engrafted in nude mice. The effect of SLAP on the invasive properties of CRC cells was investigated in vitro using Matrigel Boyden chamber assays, as well as in vivo following injection in the spleen of Balb-c mice. Results : We found that SLAP is expressed in the healthy colon and that its expression is reduced in 60% of CRC biopsies tested. Moreover, we showed that SLAP overexpression dramatically reduced the capacity of CRC cells to induce primary tumours and liver metastases in vivo. Conversely, SLAP knock-down in early-stage CRC cells led to a remarkable induction of liver metastasis in mice. This novel function of SLAP required its myristoylation site as well as intact SH3 and SH2 domains. A proteomic approach is under way to identify SLAP partners involved in this tumor suppressor activity. Conclusions: Our results suggest that, in addition to lymphocytes, SLAP also regulates transforming properties of CRC cells. We hypothesize that SLAP negatively regulates oncogenic signalling initiated by tyrosine kinases including Src. 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 1981. doi:10.1158/1538-7445.AM2011-1981