tbuckley/cabot-search huggingface dataset:
Abstract 17287: Increase in Utilization of High-intensity Statin Among New Users After the Release of the 2013 ACC/AHA Cholesterol Management Guideline
Authors: Tope Olufade, Deborah Anzalone, David M Kern, Ozgur Tunceli, Siting Zhou, Vince Willey, Mark J Cziraky
Journal: Circulation (2015)

Introduction: To characterize changes in statin utilization patterns after the release of the 2013 ACC/AHA cholesterol management guideline. Methods: Using administrative claims and laboratory results data from the HealthCore Integrated Research Database, statin use was captured during the 4 quarters before and after release of the 2013 ACC/AHA guideline. Individuals were classified into 4 statin benefit groups (SBG), as described in the ACC/AHA guideline. Patients new to statins were identified independently during each quarter. Results: An average of 205,358 patients were identified across the 4 SBG groups during each quarter, of whom an average of 3,658 were new statin users. New users were 41% women and 61 years old on average. Results are shown in Figure 1. In SBG 1, high-intensity statin use in patients &lt;75 years increased from an average of 19.6% per quarter before the guideline to 24% in the quarters afterward. In SBG 2, there was a gradual increase in high-intensity statin use following introduction of the guideline. In SBG 3, high-intensity statin use for patients with 10-year atherosclerotic cardiovascular disease (ASCVD) risk ≥7.5% increased during the post-guideline period, but little change was seen for moderate-intensity statin use for patients with ASCVD risk &lt;7.5%. In SBG 4, a small increase in moderate- to high-intensity statin use was observed. Conclusions: The 2013 ACC/AHA guideline appeared to have a modest effect in the utilization of high-intensity statins among new users in the period immediately following its release. The increase was most marked in the use of high-intensity statins in ASCVD patients and in patients treated by specialists. Follow-up in future years to assess the impact of the ACC/AHA guideline is warranted.
Abstract LB-412: TargetRich™ cancer gene panels: targeted next generation sequencing in cancer samples
Authors: Katherine J. Spayd, Irina Vasenkova, Tatiana Shvetsova, Randall C. Bachmeyer, Richard M. Myers, D. Troy Moore, Katherine E. Varley
Journal: Cancer Research (2012)

Abstract Crucial to the adoption of next-generation sequencing within clinical cancer research is the ability to deeply sequence hundreds to thousands of targeted genomic regions across a large number of patient samples. Several targeting (PCR) and capture (hybridization) methods have been developed for next-generation sequencing, however these methods have limited utility with cancer patient specimens due to drawbacks such as large input DNA quantity requirements, wasted off-target sequencing, high cost of reagents, low sample throughput, specialized equipment, and inflexible content design. We developed TargetRich cancer gene panels employing Nested PatchPCR, which enables the targeted sequencing of hundreds of genomic regions in large numbers of patient samples to fully and efficiently utilize next-generation sequencers. Nested PatchPCR required only 250 ng genomic DNA, and was compatible with the fragmented DNA obtained from formalin fixed paraffin embedded samples (FFPE). No special equipment was needed, only a standard PCR machine. Patient samples were processed in parallel in a single 96-well plate. For each patient sample, we simultaneously amplified hundreds of exons from genes that are frequently mutated in cancer. We utilized standard library construction and barcoding methods to sequence targeted genes from 96 patient samples on a single Illumina GAIIx flowcell. The TargetRich cancer gene panels were highly specific; 95% of sequencing reads aligned to the targeted regions. The high percentage of on-target sequence data and focused content, allowed us to achieve high coverage across the loci (average of 400X read depth) for the sensitive detection of cancer mutations. We have created two cancer panels: CR (157 regions covering exons from 10 genes) and CS (760 regions covering exons from 62 genes) for use on the Illumina MiSeq, GAIIx &amp; HiSeq platforms. Additionally, a CR panel for the Ion Torrent PGM has been developed with platform-specific primers added during the Nested PatchPCR reaction, allowing direct sequencing of products without time-consuming library construction. 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 LB-412. doi:1538-7445.AM2012-LB-412
A CASE SERIES OF LISTERIA MONOCYTOGENES INFECTION IN INFLAMMATORY BOWEL DISEASE PATIENTS TREATED WITH ANTI-TNFα THERAPY
Authors: J A Gray, P B Allen, K Diong, M Kane, A Varghese
Journal: Gut (2013)

<h3>Introduction</h3> Anti-TNFα therapy has had a huge impact on the treatment of inflammatory bowel disease. The inhibition of TNFα not only reduces inflammation but also increases the risk of opportunistic infections. Intracellular organisms such as Myobacterium tuberculosis and Listeria monocytogenes are particularly high risk. Much has been written on TB with infliximab therapy whereas Listeria has not received similar attention. Case Series We report 2 cases of Listeria bacteraemia observed with infliximab for IBD. Case 1: A 65 year old male with known Crohns colitis presents with worsening diarrhoea &amp; discharge. EUA and MRI confirm intersphincteric horsehoe fistula with moderate distal colitis. After failing steroid therapy he was commenced on infliximab. Ten days after his first dose he began to spike temperatures. Blood cultures confirmed Listeria monocytogenes bacteraemia. Case 2: A 50 year old male with known ulcerative colitis maintained on 5-ASA therapy presents with a severe exacerbation. He was commenced on infliximab after failing steroid therapy. After initially responding well to treatment he re-presented with flu-like symptoms and temperatures. Blood cultures confirmed Listeria monocytogenes. Both cases responded well to intra-venous amoxicillin. Of significance both patients presented within the loading dose period and were also receiving azathioprine and corticosteroids. Currently only 17 cases of invasive Listeriosis secondary to anti-TNFα therapy have been observed in IBD patients. <h3>Conclusion</h3> We conclude that patients requiring anti-TNF? therapy should be informed of the risk of food borne infections and advised to avoid high risk foods. These cases highlight the need for strict guidelines and prescribing physicians to be aware of such complications.
TCTAP A-159 Optical Coherence Tomography Assessment of Calcium Fracture by Percutaneous Coronary Intervention in Heavily Calcified Lesions
Authors: Yosuke Katayama, Kunihiro Shimamura, Makoto Orii, Yasutsugu Shiono, Yoshiki Matsuo, Takashi Yamano, Yasushi Ino, Tomoyuki Yamaguchi, Takashi Kubo, Takashi Akasaka
Journal: Journal of the American College of Cardiology (2015)
Myocardial Infarction during Nifedipine Therapy for Preterm Labor
Authors: S. Guid Oei, S. Koen Oei, Hans A.M. Brölmann
Journal: New England Journal of Medicine (1999)

To the Editor: Recent studies have suggested that nifedipine is a safer, more effective treatment for preterm labor than the sympathomimetic agents routinely in use.1,2 On the basis of these promising results, calcium-channel antagonists are increasingly prescribed for tocolysis. On the other hand, a case–control study of hypertensive patients found that patients who were taking calcium-channel antagonists had an increased risk of myocardial infarction,3 and a meta-analysis found a dose-dependent association between the use of nifedipine and the risk of death.4 These data, however, are not necessarily applicable to pregnant women who are being treated for preterm labor. We . . .
Hazards of Handling Chemotherapeutic Agents Known But Not Heeded
Authors: A. Stone
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Hazards of Handling Chemotherapeutic Agents Known But Not Heeded Get access Amy Stone Amy Stone Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 6, 20 March 1991, Pages 392–393, https://doi.org/10.1093/jnci/83.6.392 Published: 20 March 1991
Factors related to the development of cat scratch colon during colonoscopy
Authors: J. Baudet, A. Aguirre-Jaime
Journal: Endoscopy (2013)

Cat scratch colon (CSC) is an entity characterized by bright red linear tears which appear in the colonic mucosa during colonoscopy. Although they do not generally have clinical implications, cases of secondary pneumoperitoneum have been reported. To date, the prevalence, associated diseases, and factors that determine the appearance of CSC have not been adequately determined. We report a series of 20 cases of CSC found in 10715 consecutive colonoscopies. Demographic data, indication for the colonoscopy, endoscopy findings, and complications related to the procedure were recorded. Older age and male sex were significantly associated with CSC. In 15 of the 20 cases the CSC was related to diversion colitis, and 5 cases appeared in patients with collagenous colitis. In patients with diversion colitis, the longer the time elapsed since surgery, the greater the risk of these lesions occurring. None of the patients with CSC had complications related to the colonoscopy.
CROSS SECTIONAL STUDY OF PATIENTS WITH ACUTE CORONARY SYNDROME REQUIRING LONG TERM ORAL ANTICOAGULATION THERAPY: RESULTS FROM NATIONAL INPATIENT SAMPLE
Authors: Parasuram Krishnamoorthy, Saurav Chatterjee, Jalaj Garg, Partha Sardar, Chirag Bavishi, Nainesh Patel, Jay Giri, Debabrata Mukherjee
Journal: Journal of the American College of Cardiology (2016)
FRI0137 Effects of tofacitinib on lipid biomarkers in patients with active rheumatoid arthritis
Authors: I. B. McInnes, I. Kaplan, M. Boy, R. Riese, A. Zuckerman, D. Gruben, M. J. Brosnan, S. Zwillich, J. Bradley
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Tofacitinib is a novel, oral Janus kinase (JAK) inhibitor for the treatment of rheumatoid arthritis (RA). Administration of tofacitinib to RA patients (pts) is associated with increases in lipid moieties. However, active RA is in turn associated with altered lipid parameters. <h3>Objectives</h3> To explore changes in biomarkers relevant to lipid biochemistry and cardiovascular (CV) risk in pts treated with tofacitinib or placebo. <h3>Methods</h3> CV biomarkers were evaluated in blood samples reserved during two Phase 2 studies (NCT00413660; NCT00550446) and one Phase 3 study (NCT00853385) of tofacitinib in pts with an inadequate response to methotrexate (MTX) or traditional disease-modifying antirheumatic drugs (DMARDs). Analyses were conducted at baseline and Month 3 in pts receiving tofacitinib 5 and 10 mg twice daily (BID) as monotherapy or with background MTX, or placebo. Mean changes at Month 3 were analysed using ANOVA. To investigate the impact of outliers, trimmed analyses were also performed whereby extreme values (lower and upper percentiles) were removed in 1% increments, and ANOVA repeated for each. <h3>Results</h3> Tofacitinib increased the activity of lecithin-cholesterol acyltransferase (LCAT) and paraoxonase, and reduced serum amyloid A (SAA) and high-density lipoprotein (HDL)-associated SAA levels. No significant changes were observed in lipoprotein (a) (Lp[a]), cholesteryl ester transfer protein (CETP), or lipoprotein-associated phospholipase A<sub>2</sub> (Lp PLA2) levels in both full (Table 1) and trimmed analyses. <h3>Conclusions</h3> Tofacitinib induced increases in LCAT and paraoxonase and decreases in SAA and HDL-associated SAA, implicating JAK-dependent pathways in structural and functional modifications of lipoprotein particles, thereby suggesting a potential for reduction in CV risk in pts treated with tofacitinib. Consequences on vascular co-morbidity require further investigation. <h3>Disclosure of Interest</h3> I. McInnes Grant/research support from: Pfizer Inc, Speakers bureau: Pfizer Inc, I. Kaplan Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, M. Boy Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, R. Riese Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, A. Zuckerman Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, D. Gruben Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, M. Brosnan Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, S. Zwillich Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, J. Bradley Shareholder of: Pfizer Inc, Employee of: Pfizer Inc
The Animal Research Issue
Authors: R. ALLISON
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article The Animal Research Issue Get access RON ALLISON RON ALLISON 3107 Bedford Ave. Brooklyn, NY 11210 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 17, 6 September 1989, Page 1332, https://doi.org/10.1093/jnci/81.17.1332 Published: 06 September 1989
THU0170 The effect of the antiphospholipid syndrome (APS) on survival in 679 patients with sle: A prospective study
Authors: C.C. Mok, L.Y. Ho, K.L. Yu, C.H. To
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Objectives</h3> To study the effect of the antiphospholipid syndrome (APS) on survival in Chinese patients with SLE <h3>Methods</h3> A cohort of 679 southern Chinese patients who fulfill at least 4 of the ACR criteria for SLE from 1995 to 2011 was studied. The status of the patients at last clinical visits (alive or death) was evaluated. The cumulative survival rate over time was studied by Kaplan-Miere's plot. For those who died during the course of their disease, data were censored at the time of their deaths whereas data of other patients were censored at the time of last clinic visits. APS was defined by the modified Sydney criteria in 2006, ie. presence of arterial or venous thrombosis, or miscarrages (recurrent abortion or intra-uterine death) plus any one of the following positive twice at least 12 weeks part: (1) lupus anticoagulant; (2) moderate to high titers of anticardiolipin antibodies (IgG or IgM); or (3) beta-2-glycoprotein-I. Comparison of the survival of patients with and without APS was made. <h3>Results</h3> 679 SLE patients were prospectively followed (623 women, 92%). The mean age of onset of SLE was 32.5±13.6 years and the mean follow-up time of the entire cohort of patients was 117±89 months. 67 (9.9%) patients died during the course of illness and 33 (4.9%) patients were lost to follow-up. The main contributing causes of death were: infection (51%), cardiovascular events (12%), cerebrovascular events (16%), and cancer (9%). 44 (6.5%) patients qualified the criteria for secondary APS. The clinical manifestations of APS in these patients were, in decreasing order of frequency, cerebrovascular accident (N=24, 55%), deep venous thrombosis (N=13, 30%), recurrent abortion/intrauterine fetal death (N=5, 11%), cardiovascular events (N=4, 9%) and peripheral vascular disease (N=4, 9%). Eight of 44 (18%) patients with APS died, which was more frequent in non-APS patients (59 deaths/635 patients, 9%; p=0.056). The cumulative mortality of patients with APS was 4.7% at 5 years, 7.8% at 10 years and 22.2% at 15 years, whereas the cumulative mortality of patients without APS was 5.2% at 5 years, 8.8% at 10 years and 10.9% at 15 years. Although the survival of APS patients was poorer than those without APS, the difference did not reach statistical significance (log rank test; p=0.23). However, if patients with APS involving only arterial thrombosis were considered, the presence of APS was significantly associated with mortality (HR 2.11 [1.004-4.45]; p=0.049). <h3>Conclusions</h3> The presence of APS increases the mortality risk of patients with SLE, which is mainly contributed by arterial thrombotic events that occur late in the disease course. <h3>Disclosure of Interest</h3> None Declared
Abstract 2238: A novel prognostic marker in patients with squamous cell carcinoma of the tongue: high endothelial venules
Authors: Ser Yee Lee, Aik Seng Ooi, Chao-Nan Qian, Siok Gek Hwang, Bin Tean Teh, Khee-Chee Soo
Journal: Cancer Research (2010)

Abstract AIMS: To evaluate tumor-induced vascularization in regional lymph nodes (LN) of patients with tongue carcinoma by studying the morphological and functional alterations of high endothelial venules (HEV) and its correlation to clinico-pathological features. BACKGROUND: Squamous cell carcinoma (SCC) of the tongue is one of the most prevalent tumors of the head and neck region. The extent of LN metastasis is a major determinant for the staging and the most reliable adverse prognostic factor. Primary tumors can induce lymphatics and vasculature reorganizations within sentinel LN before the arrival of cancer cells and these key blood vessels are identified as HEV. The morphological altera[[Unsupported Character - Codename &amp;shy;]]tion of HEV in the presence of a cancer, coupled with the increased proliferation rate of the endothelial cells, results in a functional shift of HEV from immune response mediator to blood-flow carrier. METHODS: This study is based on 65 consecutive patients with tongue SCC who underwent primary surgical treatment at Singapore General Hospital from January 2001 to December 2005. The patients were categorized into 2 groups (Cases and Controls) based on the presence of malignancy in their cervical lymph nodes. A review of the patients’ pathological and clinical data was performed from a prospective database. Immunohistochemical staining of the tissue blocks for HEV and high-power-field image analysis were performed and analyzed with correlation to the patients’ clinico-pathological features. RESULTS: The total number of HEVs is significantly associated to disease-free interval when controlling for the group (p=0.022) as well as combining both groups as one cohort (p=0.023). There also a similar association comparing the HEV parameters to overall survival. CONCLUSION: Our results suggest that the HEV possibly plays a key role in the pathogenesis of lymphatic and subsequent distant metastases. Confirmation of this hypothesis would offer a novel therapeutic approach to preventing metastasis by blocking the remodeling processes of HEV in LN. 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 2238.
ACTIVATED PLATELET TECHTIDE TM Tc-99m P280: SAFETY AND EFFICACY FOR THE DETECTION AND LOCALIZATION OF ACUTE DEEP VENOUS THROMBOSIS (DVT).
Authors: G. Obranovich, F. L. Weiland, P. Vande Streek, R. F. Carretta, R. W. Dann, K. S. Madsen, E. M. Aten
Journal: Clinical Nuclear Medicine (1998)

s Presented At The 22Nd Annual Western Regional Meeting Of The Society Of Nuclear Medicine October 1997
Abstract 3050: MicroRNA expression profiling of human Barrett's carcinogenesis
Authors: Matteo Fassan, Stefano Volinia, Jeff Palatini, Marco Pizzi, Raffaele Baffa, Roberto Clemente, Christian Rizzetto, Carlo M. Croce, Giovanni Zaninotto, Ermanno Ancona, Massimo Rugge
Journal: Cancer Research (2010)

Abstract Barrett's Mucosa (BM) is a metaplastic replacement of the native esophageal (squamous) epithelium (ESq) by columnar-intestinalized mucosa. BM is the main risk factor for Barrett's adenocarcinoma (BAc). MicroRNAs (miRNAs) are a class of small non-coding RNAs that control gene expression by targeting mRNAs; miRNAs deregulation has been associated with Barrett's oncogenesis. To explore the hypothesis that a specific miRNAs signature is associated with BM (and its associated cancer risk) a miRNA microarray analysis (OSU-CCC version 4.0; Ohio State University) compared ESq versus all the spectrum of the phenotypic lesions of the Barrett's carcinogenesis. Specimens were collected at Department of Pathology of Padova University from 14 patients undergone esophagectomy for BAc or High-grade non-invasive neoplasia (HG-NiN). Tissues samples for the microarray study included: ESq= 14 samples; BM= 14; Low-grade non-invasive neoplasia (LG-NiN)= 7; HG-NiN= 5; BAc= 11. The miRNA-profiling study consistently disclosed increased expression of 6 miRNAs (hsa-miR-215, hsa-miR-560, hsa-miR-615-3p, hsa-miR-192, hsa-miR-326, hsa-miR-147), and decreased expression of 7 others (hsa-miR-100, hsa-miR-23a, hsa-miR-605, hsa-miR-99a, hsa-miR-205, hsa-let-7c, hsa-miR-203). Microarray results were further validated by qRT-PCR, using a different series of 10 consecutive BAc cases (Esq= 10 samples; BM= 6 samples; BAc= 10 samples). Interestingly, some of the miRNAs found deregulated in this series are already known as suitable markers of cancer progression in other models of epithelial oncogenesis (i.e.: hsa-let-7c, hsa-miR-192, hsa-miR-203, hsa-miR-205, hsa-miR-215). The results achieved by the miRNA profiling study were further validated by the immunohistochemical (IHC) analysis on a well-defined miRNA gene target (HMGA2 [hsa-let-7c]). The IHC expression of the protein product was consistent with the corresponding miRNA's deregulation. In fact, HMGA2 IHC expression was up-regulated in HG-NiN and BAc. The achieved results confirm that specific miRNAs are involved in BM carcinogenesis and that they may represent a novel diagnostic/prognostic tool in the characterization of BAc gene targets. 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 3050.