tbuckley/cabot-search huggingface dataset:
What Is a Clinician and What Does He Do?
Authors: Philip A. Tumulty
Journal: New England Journal of Medicine (1970)

Abstract A clinician is one whose prime function is to manage a sick person with the purpose of alleviating the total effect of his illness. The multifocal character of the impact of illness upon the patient and his family is stressed. Clinical evidence is the material with which the physician works, and a meticulous history and physical examination are paramount. The availability of more specific forms of therapy requires a clinician to be more of a scientist and, at the same time, more expert in clinical methods. Ability to listen and to talk, so that valid clinical evidence is gathered, anxieties are dissipated, and understanding and motivation are instilled, are the clinicians' greatest assets.
PTH-035 Salvage Endoscopic Subucosal Dissection for Refractory Post Polypectomy Fibrosis and Recurrent Intraepithelial Neoplasia: Expandning the Technological Envelope in the Uk
Authors: P Hurlstone, E Said
Journal: Gut (2013)

<h3>Introduction</h3> Submucosal desmoplasis post EMR confers the natural history of regenerative luminal healing. Index R1 or Rx dissections of colorectal neoplasia using either EMR, EPMR or simple snare polypepctomy complicated by remnant or recurrent intraepithelial is clinically challenging. Formal open surgical resection or ablation is usually inevitable in this cohort. We describe, using video presentation data, the technique of primary endoscopic fibrosis divissional dissection with curative intent for recurrent or remant intraepithelial neoplasia of the right-hemi colon post index EMR. <h3>Methods</h3> Recurrent disease or refractory intraepithelial neoplasia was defined according to Higaki criteria. Patients were consented for progression to salvage dissection prior to endoscopy. Pre-resection peripheral margin APC ‘mark out’ was performed following index indigo carmine chromoscopy to deliniate the lesion’s horizontal axis with thermal mucosal tattoos placed 2–4 mm away from the lesion margin and within a type I crypt mucosal zone. Peripheral smi with 1/10,000 adrenaline solution was performed with 6 mm marginal circumfrential 6 mm incisions made to the level of the deep submucosal layer using the straight flex knife. Dissection of the exposed submucosal desmoplastic fibrosis layer was then performed using a fixed en face IT knife distance coupled with a blunt tractional endoscopic ‘tunnelling’ technique. Prophylactically, sm vessels were ablated or clipped prior to tissue recovery. <h3>Results</h3> n = 12 patients. Paris class LST-NG/G (6)/0-IIa (6). Median operating time 64 mins (range 34–82). Median lesion size 22mm (range 12–46 mm). Asymetrical, partial or complete NL = 12 (100%). Perforation rate 0/12. Median hospital stay 24 hours (range 6–120). 30 day mortality 0%. R0 resection achieved in 11/12 (92%). Endoscopic recurrence rate 0% (median follow-up 18/12 (range 2–43 months). Post dissection late bleed occured in 3/12 (25%) of the cohort all treated conservatively. There were no cases of immediate or early dissection bleeding. <h3>Conclusion</h3> Salvage endoscopic dissection of remnant or recurrent intraepithelial neoplasia post index EMR, EPMR or conventional polypectomy is technically possible in the UK in this pilot clinical experience. Dissection is however technically demanding, is complicated by a high delayed bleeding risk and is time consuming. In an appropriately selected patient cohort however this novel therapy may negate the need for formal surgical excision which in the elderly and those with significant comorbidity becomes an attractive therapeutic modality changing the paradigm away from palliative ablative methods in those unfit for formal surgical resection. <h3>Disclosure of Interest</h3> None Declared.
Comments on "Concentration and Size of Asbestos in Water Supplies"
Authors: William E. Smith
Journal: Environmental Health Perspectives (1980)

William E. Smith (Fairleigh-Dickinson Univ., Madison, N.J. 07940): Findings of fibers in water supplies bring up the question of whether they present any hazard to people drinking the water. To develop experimental information on this question, we maintained 600 hamsters from the age of about two months throughout their lives on drinking water with and without addition of some mineral fibers. We found some tumors that may be related to treatment in hamsters that drank water containing fibers of naturally crystallized amosite asbestos from South Africa. No tumors attributed to treatment occurred in hamsters that drank water containing tailings from milling of taconite ore rich in cummingtonite/grunerite mineralogically related to amosite. Since carcinogenicity of mineral fibers has been related to their dimensions by results of intrapleural injections in experimental animals, it is of interest to look at dimensions of fibers in our drinking water exposures. In considering dimensions of fibers, I was glad to see that Dr. Millette's data did not show merely mean dimensions. Mean dimensions were not impressively different in our sample of amosite as compared to our samples of tailings as measured by electron microscopy at 2500x. However, differences in fiber length distributions were obvious, as better seen in measurements at 600x, which show that the percent of fibers longer than 10 gum was 14% in the amosite as compared to 4% in the tailings. Among fibers measured as longer than 10 ,m, 25% were longer than 20 Atm in the amosite; none were longer than 20 ,um in the tailings. Following Dr. Millette's paper, a question was asked as to how mineral fibers were suspended in water to assure ingestion by animals. I responded as follows: To maintain suspension of insoluble mineral fibers in water, and thus assure their ingestion by animals drinking the water, we designed drinking fountains in which the water was put in funnels and agitated with a stream of air. We described this method in a paper last year [Am. Ind. Hyg. Assoc. J. 39: 583 (1978)].
Abstract LB-134: Analysis of restored FFPE samples on high-density SNP arrays
Authors: Dmitry K. Pokholok, Jennie M. Le, Frank J. Steemers, Mostafa Ronaghi, Kevin L. Gunderson
Journal: Cancer Research (2010)

Abstract Millions of Formalin Fixed Paraffin Embedded (FFPE) cancer tissue samples currently present in the US and worldwide provide an enormous, invaluable repository to the discovery of biomarkers in cancer research, drug development, diagnosis and treatment of diseases. However, the processes of fixation and storage of FFPE samples lead to degradation and base modification with chemical residues. This degraded FFPE DNA is inefficiently amplified in the Infinium® whole genome amplification (WGA) step leading to poor performance in the Infinium® assay. In this study, FFPE DNA (100 ng input) was restored through a treatment with DNA polymerase, DNA repair enzyme, ligase, and modified Infinium® WGA reaction conditions. Canonical genotype cluster files were generated by creating artificially degraded Coriell DNAs and processing the samples through the restoration process and Infinium® assay. Results of genotyping on high density HumanCytoSNP-12 BeadChip®, featuring approximately 300k SNPs indicated that even highly degraded samples which show initial call rates of 40-70% can be successfully restored to a state that achieved call rates of greater than 90%, at a concordance greater than 99.0%, and associated standard deviation of log intensity less than 0.4. In general, over 80% of FFPE samples, which passed a QC assay metric were successfully restored and genotyped. Infinium® genotyping of restored DNA from a collection of tumor FFPE samples confirmed the presence of genomic aberrations around known cancer genes. Finally, we further demonstrated that paired sample analysis using canonical genotype clusters provide improved precision in CNV and LOH analysis compared to single sample analysis. 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 LB-134.
Abstract 4225: Annexin A4 induces chemoresistance for multiple drugs in ovarian clear cell carcinoma
Authors: Akiko Morimoto, Takayuki Enomoto, Satoshi Serada, Shinya Matsuzaki, Takuhei Yokoyama, Toshihiro Kimura, Yutaka Ueda, Kiyoshi Yoshino, Masami Fujita, Minoru Fujimoto, Tadashi Kimura, Tetsuji Naka
Journal: Cancer Research (2012)

Abstract BACKGROUND: Platinum drugs play the key role for postoperative adjuvant therapy and treatment in progress and recurrent ovarian cancer. We have previously reported that ovarian clear cell carcinoma (CCC) has increased expression of Annexin A4 (Anx A4) in comparison with other subtypes of ovarian cancer. Enhanced expression of Anx A4 has been shown to induce chemoresistance via extracellular efflux of carboplatin. However, it remains unclear whether targeting Anx A4 is effective for improving the sensitization against chemotherapy, like platinum drugs. The aim of this study was to evaluate the role of Anx A4 in chemoresistance in ovarian CCC. MATERIAL AND METHODS: RMG-I cell lines were used to establish the stable knockdown of Anx A4. Plasmids encoding short hairpin RNAs (shRNAs) targeting Anx A4 were transfected. Chemoresistance was assessed by IC50 value in various drugs. RESULTS: Compared with control cells, knockdown of Anx A4 gene expression in RMG-I cells induced chemosentisitzation around 2-fold to cisplatin (IC50: 11.2 μM to 5.8 μM, P&amp;lt;0.01) and Carboplatin (IC50: 130.4 μM to 63.3 μM, P&amp;lt;0.01). Unexpectedly, knockdown of Anx A4 also improved the chemosentisitzation of epirubicin (IC50: 256.7 nM to 180.3 nM, P&amp;lt;0.01) and Paclitaxel (IC50: 5.5 nM to 2.9 nM, P&amp;lt;0.01). In consistent with the improved chemosensitivity, drugs induced p53 was markedly increased by knockdown of Anx A4 in RMG-I cells. In xenograft models, significant chemosensitization toward cisplatin was demonstrated by knockdown of Anx A4 in RMG-I cells. CONCLUSIONS: Inhibition of Anx A4 induced chemosensitization in ovarian CCC cells. Anx A4 blockade might be a novel therapeutic target of chemoresistance in patients with ovarian CCC. 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 4225. doi:1538-7445.AM2012-4225
FIRST IN MAN OBSERVATIONS WITH SIMULTANEOUS 18F-FDG PET AND MR IMAGING IN PERIPHERAL ARTERY DISEASE USING A WHOLE-BODY INTEGRATED SCANNER
Authors: Tobias Koppara, Isabel Dregely, Kristin Kuhs, Stephan Nekolla, Karl-Ludwig Laugwitz, Markus Schwaiger, Renu Virmani, Tareq Ibrahim
Journal: Journal of the American College of Cardiology (2015)
Gastric glomus tumor: a rare case of dyspepsia
Authors: Andrea Casarotto, Fabio Zarantonello, Gianluca Piccirillo, Paolo Criscenti, Massimiliano Verza, Maurizio Zirillo, Matteo Rebonato
Journal: Endoscopy (2015)

Gastric glomus tumors (GGTs) are rare mesenchymal tumors of the gastrointestinal tract originating in the neuromyoarterial glomus [1] and accounting for 1 % of gastrointestinal stromal tumors (GISTs). GGTs are generally considered to be clinically benign [2], but malignant behavior cannot be excluded [3] [4]. They present as submucosal masses that project into the lumen or out onto the serosa [5] and are distinct lesions that should be considered in the differential diagnosis of a gastric submucosal mass.
THU0334 Clinical Composite Measures of Disease Activity and Damage to Evaluate Patients with Systemic Lupus Erythematosus: A Systematic Literature Review
Authors: I. Castrejon, I. Rúa-Figueroa, M. P. Rosario, L. Carmona
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Systemic lupus erythematosus (SLE) is a highly heterogeneous autoimmune rheumatic disease characterized by inflammation across multiple organ systems. The assessment of lupus patients is difficult and requires a complex approach. Multiple instruments to evaluate disease activity and damage have been developed in SLE but there is no agreement on a single activity index to be used universally. <h3>Objectives</h3> To critically appraise the validity of activity and damage indices used in the assessment of patients with SLE. <h3>Methods</h3> A systematic literature search was performed in MEDLINE, EMBASE, and the Cochrane Library (up to March 2012). Validation studies, cohort studies, reviews and meta-analyses were included. Selection criteria were: a) age ≥ 18 years, b) diagnosis of SLE defined by the ACR criteria, and c) the assessment of instruments to evaluate disease activity or damage, and assessment of validity of the instruments. A reviewer screened title/abstracts and collected data concerning validation using ad hoc forms. <h3>Results</h3> From 704 initial studies captured, 37 articles and 1 review meeting the predefined criteria were identified. Studies addressed validation of 6 composite indices to evaluate disease activity: the British Isles Lupus Assessment Group (BILAG), the European Consensus Lupus Activity Measurement (ECLAM), the Systemic Lupus Activity Index (SLAM), the Systemic Lupus Erythematosus Disease Activity Measure (SLEDAI), the UCSF/JHU Lupus Activity Index (LAI) and the Systemic Lupus Activity Questionnaire (SLAQ); and 2 indices to evaluate damage: the Systemic Lupus International Collaborating clinics/American College of Rheumatology-Damage Index (SLICC/ACE-DI; SDI) and its patient self-administered version the Lupus Damage Index Questionnaire (LDIQ). Only the SLAQ and the LDIQ were self-administered, the others were completed by the physician. Internal consistency was only studied in the BILAG, the SLAQ and the SDI; Cronbach's α ranged from 0.35 to 0.87. The reliability intra-observer or test-retest examined by intraclass correlation coefficient (ICC) ranged from 0.48 to 0.81. Construct validity, examined by means of convergence with other instruments, was generally similar between indices. Responsiveness was tested in all indices except LAI, SDI and LDIQ, with a standardized response mean (SRM) ranging from 0.12 to 0.75. <h3>Conclusions</h3> Multiple instruments of disease activity have been fully validated for use in SLE. We found no direct evidence of what is the most useful index to follow up patients with SLE, although the two indices with a most completed validation and more used in RCT and cohorts are the BILAG and the SLEDAI. <h3>Disclosure of Interest</h3> None Declared
S52 MiR-181 increases in the quadriceps muscle of COPD patients after an acute bout of exercise: Abstract S52 Table 1.
Authors: AVJ Donaldson, RJ Tanner, CA Davey, N Hopkinson, W D-C Man, PR Kemp, MI Polkey
Journal: Thorax (2013)

<h3>Introduction</h3> MicroRNAs (miRs) are small non-coding RNAs that regulate gene expression and have been implicated in the control of skeletal muscle phenotype. Our group has previously shown that muscle-specific miRs are altered, and correlate with physiological parameters in the quadriceps<sup>1</sup> and plasma<sup>2</sup> of COPD patients. MiRs may therefore have a mechanistic role in the development of skeletal muscle dysfunction in COPD. We hypothesised that muscle-specific miRs are involved in skeletal muscle adaptation to exercise and that changes in quadriceps miR expression after acute exercise would differ between patients and controls. <h3>Methods</h3> 20 COPD patients and 11 controls were studied. Fasted quadriceps biopsies were taken before and one hour after an incremental, symptom limited, cycle exercise test. Muscle-specific miR-1,-499,-133, and -206 as well as miR-181, a more widely expressed miR associated with inflammatory responses, were quantified using qPCR. Paired analyses were performed using paired T-test or paired Wilcoxon. <h3>Results</h3> See table of characteristics (Table 1) <i>Muscle miR results: </i> MiR-1, -499, -133 did not change with exercise. MiR-181 increased x1.5 in the COPD patients only one hour after exercise (p = 0.017, controls p = 0.83). There was also a trend for miR-206 to increase in the COPD group only (p = 0.07). <h3>Conclusions</h3> Muscle-specific miRs do not change one hour after an acute bout of exercise in COPD patients or controls. However, miR-181 increased in the quadriceps of COPD patients. MiR-181 is not restricted to, but functions in muscle, and in addition has been shown to be linked to inflammatory signalling. The difference in the response of miR-181 expression to exercise is consistent with COPD patients having a greater inflammatory response to exercise stimulus than controls. <h3>References</h3> Lewis A, <i>et al</i><i>Thorax</i> 2012;67:26–34 Donaldson AVJ <i>et al</i><i>Thorax</i> 2013: EPUB 28/06/2013
IOM Works With U.S. Army To Disperse Breast Cancer Research Funds
Authors: N. S. Larsen
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article IOM Works With U.S. Army To Disperse Breast Cancer Research Funds Get access Natalie S. Larsen Natalie S. Larsen Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 3, 3 February 1993, Pages 187–188, https://doi.org/10.1093/jnci/85.3.187-a Published: 03 February 1993
Abstract 1248: 14-3-3 interacts with TC1(C8orf4) to protect the protein from rapid degradation and regulates cancer cell invasiveness
Authors: Inchul Lee
Journal: Cancer Research (2010)

Abstract 14-3-3 interacts with TC1(C8orf4) to protect the protein from rapid degradation and regulates cancer cell invasiveness. Jungtae Kim, Yusun Jung, Dong Wook Kim, Hyunju Lee, Kyuyoung Song, Inchul Lee. Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, Republic of Korea TC1(C8orf4) is a multifunctional regulator associated with aggressive biological behavior of cancer and poor survival of patients (Clin Cancer Res 2006;12:3541-8). It regulates the Wnt/β-catenin pathway (Cancer Res 2006;66:723-8).and induces endothelial inflammation (J Immunol 2009;183:3996-4002). TC1 is up-regulated by NF-kB (FEBS letters 2006;580:3519-24), and heat shock and other cellular stress (Biochem Biophys Res Commun 2007;360:447-52). TC1 is a small protein present in vertebrates, which is degraded rapidly. TC1 interacted with 14-3-3β upon yeast two hybrid screening. The interaction of TC1 with 14-3-3β and 14-3-3ε was confirmed in HEK293T cells upon cotransfection. The deletion mutant analysis showed that the N-terminus of TC1 and C-terminus of 14-3-3 interacted with each other. The binding site of TC1 appeared to involve the Ser15 residue. The interaction was inhibited by serum starvation, staurosporine, and GSK3β inhibitor, indicating the requirement of TC1 phosphorylation, probably of Ser15, for the interaction. The half-life of transfected HA-TC1 was 2.49 hours in HEK293T cells, while it was elongated to 5.07 hours upon co-transfection with 14-3-3β. 14-3-3 knock down reduced TC1 expression. Our data together suggested that 14-3-3 protected TC1 in vivo. 14-3-3 proteins have been implicated in the regulation of various biological functions. However, the role in cancer is not clear. TC1 was shown to enhance the Matrigel invasiveness of cancer cells (Clin Cancer Res 2006;12:3541-8). 14-3-3 knock down using si14-3-3β reduced the Matrigel invasiveness of HeLa cells significantly (p&amp;lt;0.0001). Cancer cell proliferation was not affected by 14-3-3 transfection or knock down. Our data suggest the requirement of 14-3-3 in cancer cell invasiveness potentially by regulating TC1. 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 1248.
BLEEDING COMPLICATIONS AND PROCEDURAL TIMING IN PATIENTS UNDERGOING PERCUTANEOUS CORONARY AND PERIPHERAL VASCULAR INTERVENTIONS
Authors: Cameron W. Donaldson, Stephen Waldo, Darrick K. Li, Eugene Pomerantsev, Joseph Garasic, Kenneth Rosenfield, Robert Yeh, Douglas Drachman
Journal: Journal of the American College of Cardiology (2015)
Case 5-1997
Authors: Roger L. Snow, Judith A. Ferry
Journal: New England Journal of Medicine (1997)

Presentation of CaseA 24-year-old Asian woman was admitted to the hospital because of left cervical lymphadenopathy and fever.The patient had been well until two weeks earlier (one week after returning from a visit to her native Hong Kong), when she experienced pain and tenderness in the left side of her neck and felt a small lymph node in the cervical region. At about the same time, she began to have a low-grade fever, for which she took ibuprofen. Eight days before admission, hematologic tests were performed at another hospital (Table 1). A test for heterophil agglutinins was negative. . . .
Abstract 5396: LPS mimotopes: A novel class of TLR4 agonist
Authors: Arulkumaran Shanmugam, Shilpi Rajoria, Andrea George, Abraham Mittelman, Raj K. Tiwari, Robert Suriano
Journal: Cancer Research (2011)

Abstract Adjuvant driven inflammation is crucial to mounting an antigen specific immune response and is initiated by the activation of toll like receptor (TLR) proteins. Currently, aluminum based adjuvants remain the only FDA approved adjuvants for vaccines. In an effort to develop a new class of adjuvants, TLR agonists, would be natural candidates. LPS, a major structural component of gram negative bacteria cell walls, has been well studied for its property to induce the systemic inflammation observed in septic shock. The objective of the present study was to identify peptide mimics of LPS that could activate TLR-4 and induce an inflammatory condition congenial to an adaptive immune response and in contrast to LPS not induce septic shock. To this end we used phage display peptide library to identify and isolate LPS peptide mimics. The activity of LPS-TLR-4 interaction was assessed by NF-κB translocation analyses in HEK-BLUE™-4 cells, a cell culture model that expresses only TLR-4. NF-κB nuclear translocation and inflammatory cytokine production was assayed by using the murine macrophage cell line RAW264.7. Increasing the NF-κB nuclear translocation is reflected by IκB-degradation within the cytoplasm. As expected, the concentration of cytoplasmic NF-κB was also decreased, which further attests to the shuttling of NF-κB within the nucleus. Similar results pertaining to increased nuclear localization of NF-κB with simultaneous decrease of cytoplasmic IκB-α and NF-κB were observed with HEK-BLUE™-4 cells. Thus, the results observed in this study suggest that the LPS peptide mimics identified act as adjuvants by virtue of their interaction with TLR-4 and thus serve as novel candidates to be considered as a new class of TLR-4 agonist adjuvants. 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 5396. doi:10.1158/1538-7445.AM2011-5396