tbuckley/cabot-search huggingface dataset:
Chronic neutrophilic leukemia 2016: Update on diagnosis, molecular genetics, prognosis, and management
Authors: Michelle A. Elliott, Ayalew Tefferi
Journal: American Journal of Hematology (2015)

Chronic neutrophilic leukemia (CNL) is a potentially aggressive myeloproliferative neoplasm, for which current WHO diagnostic criteria include leukocytosis of ≥25 × 10(9) /L (of which >80% are neutrophils) and with <10 and <1% circulating immature granulocytes and blasts, respectively without dysplasia, clinical, or molecular criteria for other myeloproliferative disorders, nor an identifiable cause for physiologic neutrophilia in the absence of markers of myeloid clonality. Such a pathogenic clonal marker has now been identified as a somatic activating mutation of CSF3R, most commonly CSF3R T618I, thus demanding revision of the current WHO diagnostic classification to include the molecular criterion of mutated CSF3R. The clinical presentation, disease course and prognosis of CSF-R mutated CNL have been recently outlined. Co-operative mutations in SETBP1 and ASXL1 appear to be of prognostic significance and correlate with disease progression. Advances in the understanding of the molecular pathogenesis of CNL, have not yet fully translated into satisfactory therapeutic strategies, but the foundations for these are strengthening. Am. J. Hematol. 91:342-349, 2016. © 2015 Wiley Periodicals, Inc.
Abstract 18817: The Role of Mst1 and Mst2 in Pressure Overload-Induced Hypertrophy and Failure
Authors: Dominic P Del Re, Takanobu Yamamoto, Peiyong Zhai, Junichi Sadoshima
Journal: Circulation (2013)

Mammalian sterile 20-like kinases 1 and 2 (Mst1/2) are highly conserved and are thought to have similar pro-apoptotic and anti-cell growth properties. Previous work has demonstrated that increased expression of Mst1 causes robust cardiomyocyte apoptosis, heart failure and premature death in mice, yet the function of endogenous Mst1/2 has not been investigated. The goal of this study was to determine the role of Mst1 and Mst2 in the development of heart failure using genetically altered Mst isoform-specific mice. Systemic deletion of both Mst isoforms is embryonic lethal; therefore we utilized mice harboring floxed Mst1 alleles on an Mst2-/- background and bred them with α-MHC Cre mice to disrupt both isoforms in cardiomyocytes (Mst DKO). Animals were subjected to transverse aortic constriction for 4 weeks or sham. Echocardiography was performed prior to intervention and immediately before sacrifice. At 8 weeks of age, no significant differences in the cardiac phenotype were observed between control, Mst1-/-, Mst2-/- or Mst DKO mice. In response to pressure overload (PO), control mice had increased heart weight/tibia length (HW/TL), left ventricle weight/tibia length (LVW/TL) and cardiomyocyte cross-sectional area as expected. Surprisingly, this hypertrophic response was significantly attenuated in Mst1-/- and Mst2-/- mice. Interestingly, Mst DKO mice hypertrophied similar to controls. Apoptosis and fibrosis were increased, and LV ejection fraction (LVEF) was decreased after PO in control mice. Mst1-/- and Mst2-/- mice had attenuated apoptosis and fibrosis; however, LVEF was decreased to levels similar to controls. Interestingly, Mst DKO mice also showed attenuated apoptosis and fibrosis but had significantly worse LVEF compared to control mice. Studies are ongoing to address the mechanism responsible for worsened cardiac function observed in Mst DKO mice despite suppression of fibrosis and apoptosis after PO.
P0876 : Safety and efficacy of simeprevir/sofosbuvir in Hepatitis C (HCV) infected patients with varying severity of cirrhosis: comparison to matched untreated and Protease Inhibitor (PI)-Triple therapy treated controls
Authors: V. Saxena, L. Nyberg, M. Pauly, J. Ready, J.-L. Szpakowski, B. Piasecki, A. Nyberg, B. Winston, J. Redd, L. Catalli, A. Dasgupta, S. Straley, K. Sommer, G. Witt, R. Rathbun, N. Terrault
Journal: Journal of Hepatology (2015)
Abstract 14819: The Red Cell Distribution Width Predicts Mortality among Patients Free from Systemic Inflammation
Authors: Benjamin D Horne, Joseph B Muhlestein, Sterling T Bennett, Jeffrey L Anderson
Journal: Circulation (2014)

Background: The causal mechanism is unknown for why the red cell distribution width (RDW) predicts mortality and morbidity outcomes. One explanation is an inflammatory process: statistically significant, weak magnitude correlations (r&lt;0.30) have been found between RDW and markers of inflammation. This study evaluated the association of RDW with mortality in patients with normal levels of inflammation, as indicated by normal high-sensitivity C-reactive protein (hsCRP) and white blood cell count (WBC). Methods: Intermountain Heart Collaborative Study patients undergoing coronary angiography (N=650) from 1994-2000 were evaluated if they never smoked, were free of acute myocardial infarction (MI), and had baseline hsCRP≤3 mg/L, WBC&gt;4 K/μL, and WBC≤10.6 K/μL. RDW and WBC were tested clinically at index hospitalization via the complete blood count; hsCRP testing used stored research samples. Subjects were followed until December, 2013, and all-cause mortality was determined from hospital records, Utah death certificates, and US Social Security data. Results: Age averaged 66.7±11.6 years, 31.1% were female, and 62.9% died during a mean follow-up of 15.2±1.6 years (range:12.6-19.6 years). Continuous RDW predicted mortality after adjustment for demographics, risk factors, comorbidities, and baseline treatments (hazard ratio [HR]=1.15 per +1%, 95% CI=1.06, 1.26; p=0.002). In quartiles, this was significant for Q4 vs. Q1 (survival 23.6% vs. 43.4%, HR=1.56, CI=1.17, 2.08; p=0.003), but not Q2 (HR=1.18, p=0.29) or Q3 (HR=1.08, p=0.60) vs.Q1. In subjects with hsCRP&lt;1 mg/L (n=259), RDW (adj. HR=1.13 per +1%, CI=0.99, 1.29, p=0.08) and RDW quartiles [Q2: adj. HR=1.70 (p=0.036), Q3: HR=1.88 (p=0.020), Q4: HR=1.97 (p=0.013) vs. Q1] predicted mortality. Among subjects free from heart failure (LVEF≥40%), diabetes, prior or current coronary disease, prior MI, stroke, renal failure, COPD, and depression (n=66), RDW had adjusted HR=1.70 per +1% (CI=1.06, 2.75; p=0.029). Conclusions: RDW predicted mortality in patients with normal hsCRP and WBC. This suggests that RDW marks the risk of a breadth of health concerns, likely including but not limited to inflammation. Further investigation is required to explain the causes of RDW elevation.
Abstract 12141: Temporal Trends in the Characteristics of Autopsy-Verified Victims of Sudden Cardiac Death Without a Known Prior Cardiac Disease
Authors: Eeva K Hookana, M Juhani Junttila, Kari S Kaikkonen, Marja-Leena Kortelainen, Robert J Myerburg, Heikki V Huikuri
Journal: Circulation (2014)

Introduction: Coronary artery disease (CAD) has been shown to be the underlying structural cardiac disease in ~80% of the victims of sudden cardiac death (SCD) in the western societies. Since the primary prevention strategies, public awareness of early symptoms of CAD, and secondary prophylaxis has changed during the past 1-2 decades, we studied the temporal trends in the etiology of unexpected SCD in the FinGesture study. Methods: FinGesture (n=3,727) is a prospective study assessing the phenotype and genotype profiles of SCD in a consecutive series of victims of SCD in a defined geographical area of Northern Finland. Because of Finnish law (Act on the Inquest into the Cause of Death, 459/1973, 7th paragraph), virtually all unexpected SCDs of subjects without a known prior cardiac disease undergo medigo-legal autopsy. In this study we analyzed the characteristics of SCD victims and autopsy findings in three 5-year periods; 1998-2002, 2003-2007 and 2008-2012, respectively. Results: Among victims of SCD as...
Interobserver Variability in the Detection of Cervical-Thoracic Hodgkin's Disease by Computed Tomography
Authors: Barry D. Fletcher, Arvin S. Glicksman, Peter Gieser
Journal: Journal of Clinical Oncology (1999)

Computed tomography (CT) scans of the neck and chest are obtained at diagnosis of Hodgkin's disease to establish disease extent, plan radiotherapy, and serve as baseline studies for subsequent evaluation of response to therapy. However, differences in interpretation may occur even among experienced radiologists. This study was designed to test the extent of variation among expert radiologists' interpretations and to assess how their interpretations differed from that of the primary (institutional) radiologists.Five radiologists independently reviewed randomly selected CT scans of 59 patients enrolled onto two Pediatric Oncology Group Hodgkin's disease treatment protocols. For each patient, 31 potential disease sites were scored as positive, negative, uncertain, or unassessable. Agreement among the reviewers and between the reviewers and the primary readers was analyzed.For 58% of the sites, at least four of the five reviewers agreed in >/= 80% of the cases. Kappa analysis showed moderate agreement in approximately two thirds of the sites and poor agreement in the remainder. There was moderate agreement between a majority of the expert readers and the primary radiologist reports for approximately one third of the sites, and agreement was poor in two thirds.There are disparities among radiologists' interpretations of cervical-thoracic CT imaging of patients with Hodgkin's disease. This variability may affect patient care and the performance and results of multi-institutional clinical trials. We propose that a standardized method of reporting might improve the consistency of interpretation of CT scans in these patients.
Studies of Variation in Oncogenicity of Polyoma Virus Related to Differences in Cell Culture Media
Authors: Rabson, Alan S., Law, Lloyd W.
Journal: JNCI Journal of the National Cancer Institute (1963)

Journal Article Studies of Variation in Oncogenicity of Polyoma Virus Related to Differences in Cell Culture Media Get access Alan S. Rabson, Alan S. Rabson Pathologic Anatomy Branch and Laboratory of Biology, National Cancer Institute,3Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Lloyd W. Law Lloyd W. Law Pathologic Anatomy Branch and Laboratory of Biology, National Cancer Institute,3Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 30, Issue 2, February 1963, Pages 367–375, https://doi.org/10.1093/jnci/30.2.367 Published: 01 February 1963 Article history Received: 17 September 1962 Published: 01 February 1963
Secondary In Vitro Generation of Cytolytic T-Lymphocytes (CTL's) in the Murine Sarcoma Virus System. Virus-Specific CTL Induction Across the H-2 Barrier&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Collavo, Dino, Parenti, Anna, Biasi, Giovanni, Chieco-Bianchi, Luigi, Colombatti, Alfonso
Journal: JNCI Journal of the National Cancer Institute (1978)

Journal Article Secondary In Vitro Generation of Cytolytic T-Lymphocytes (CTL's) in the Murine Sarcoma Virus System. Virus-Specific CTL Induction Across the H-2 Barrier Get access Dino Collavo, Dino Collavo 3Laboratory of Experimental Oncology, Institute of Pathological Anatomy, University of Padova, via Gabelli 61, Padova, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar Anna Parenti, Anna Parenti 3Laboratory of Experimental Oncology, Institute of Pathological Anatomy, University of Padova, via Gabelli 61, Padova, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar Giovanni Biasi, Giovanni Biasi 3Laboratory of Experimental Oncology, Institute of Pathological Anatomy, University of Padova, via Gabelli 61, Padova, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar Luigi Chieco-Bianchi, Luigi Chieco-Bianchi 3Laboratory of Experimental Oncology, Institute of Pathological Anatomy, University of Padova, via Gabelli 61, Padova, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar Alfonso Colombatti Alfonso Colombatti 3Laboratory of Experimental Oncology, Institute of Pathological Anatomy, University of Padova, via Gabelli 61, Padova, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 61, Issue 3, September 1978, Pages 885–890, https://doi.org/10.1093/jnci/61.3.885 Published: 01 September 1978 Article history Received: 30 December 1977 Accepted: 03 April 1978 Published: 01 September 1978
Long-term results from the neoadjuvant GeparDuo trial: A randomized, multicenter, open phase III study comparing a dose-intensified 8-week schedule of doxorubicin hydrochloride and docetaxel (ADoc) with a sequential 24-week schedule of doxorubicin hydrochloride/cyclophosphamide followed by docetaxel (AC-Doc) regimen as preoperative therapy (NACT) in patients (pts) with operable breast cancer (BC).
Authors: M. Kaufmann, W. Eiermann, M. Schuette, J. Hilfrich, J. U. Blohmer, B. Gerber, S. D. Costa, S. Loibl, V. Nekljudova, G. Von Minckwitz
Journal: Journal of Clinical Oncology (2010)

537 Background: This study demonstrated that AC-DOoc is superior to dose dense ADOC in inducing pathologic complete response (pCR) for pts with primary operable BC in NACT. Whether this advantage translates into improved survival rates remains unanswered. Methods: This phase III study investigated 913 women with primary BC (T2-3, N0-2, M0) randomly assigned to receive either neoadjuvant 4xADoc (A 50 mg/m2 plus D 75 mg/m2) q2w or 4xAC-4xDoc (A 60 mg/m2, C 600 mg/m2 - Doc 100 mg/m2) q3w. The primary end point was the incidence of pathologic complete (invasive and noninvasive) response (pCR) in the breast and axillary nodes (von Minckwitz et al. JCO 2005). Main secondary aims were the disease-free (DFS) and overall survival (OS).The sample size calculation was based on pCR as primary endpoint. Results: In the GeparDuo study, 913 pts were recruited between 6/1999 and 9/2001 in 77 German centers, 904 of them received study treatment and were included into analysis. Both groups were well balanced regarding the baseline characteristics: the median age was 51 years; 7 (0.8%) had a T1 tumor (by palpation), 758 (83.8%) a T2, 139 (15.4%) a T3 tumor. 361 (39.9%) were nodal positive, and 345 (38.2%) had a G3 tumor. A pCR was reached in 7% with ADoc and 14.3% with AC-Doc (OR 2.22; 95% [1.41-3.49]; p < 0.001). The median follow up is 64.3 months. 225 pts have recurred and 148 died, overall 251 events for DFS occurred. In the group achieving a pCR 22.3% recurred and 11.8% died whereas in the group without pCR 28.5% recurred and 17.1% died, respectively (p = 0.37 and p = 0.32). Conclusions: There is a trend for an improved DFS and OS for pts achieving a pCR. The final long-term efficacy analysis will be presented at the meeting. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration AstraZeneca, Merck, Novartis, Roche, sanofi-aventis AstraZeneca, Merck, Novartis, Roche, sanofi-aventis
25-Hydroxyvitamin D in Patients With Cognitive Decline
Authors: Marijn M. Speeckaert, Joris R. Delanghe
Journal: JAMA Neurology (2016)

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 Neurology HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Neurology journal
The market in healthcare data
Authors: Ruth Gilbert, Harvey Goldstein, Harry Hemingway
Journal: BMJ (2015)

Seriously inhibiting research

Healthcare generates a vast rainforest of data that could be used more widely for research if barriers to access could be overcome. One barrier is cost. Government and commercial traders in the precious hardwoods of healthcare data charge five or six figure sums per year for data access.1 2 Other barriers include the slow, tortuous application processes that are driven by rigid rules, often arbitrarily applied. These barriers obstruct access to more affordable data from the Health and Social Care Information Centre (HSCIC), the Office for National Statistics, the Healthcare Quality Improvement Partnership, and Public Health England. 

A fundamental problem with all these data suppliers is the lack of incentives to provide data for research. Although the research might save lives through improving services or developing new tests or treatments, denying access carries no penalties. HSCIC has a growing backlog of more than 200 applications,3 but queues for data from the other suppliers are rarely recorded. We see little attempt to quantify the research not done, the …
Ion channels in the cardiovascular system: Function and dysfunction: Edited by P.M. Spooner, A.M. Brown, W.A. Catterall, G.J. Kaczorowski and H.C. Strauss. 580 pp., $85.00 US (hardback), Armonk, NY, USA: Futura Inc., 1994. ISBN 0-87993-591-X
Authors: J.F. Faivre
Journal: Cardiovascular Research (1995)

Ion channels in the cardiovascular system: Function and dysfunction: Edited by P.M. Spooner, A.M. Brown, W.A. Catterall, G.J. Kaczorowski and H.C. Strauss. 580 pp., $85.00 US (hardback), Armonk, NY, USA: Futura Inc., 1994. ISBN 0-87993-591-X Get access J.F. Faivre J.F. Faivre Saint Grégoire, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 30, Issue 1, July 1995, Page 158, https://doi.org/10.1016/S0008-6363(95)90142-6 Published: 01 July 1995
Analysis of serum free light chains by crossed immunoelectrophoresis: comparison with urinary light chains in light chain disease.
Authors: B C McLeod, A Viernes, R A Kyle, R J Sassetti
Journal: Journal of Clinical Oncology (1984)

We investigated the relationship between serum free light chain levels measured by crossed immunoelectrophoresis in ten patients with light chain disease and traditional 24-hour urinary light chains in the same patients. The crossed immunoelectrophoresis test requires only a venipuncture for specimen acquisition, can be completed within 24 hours, and has a reproducibility (+/- 14%) comparable with that of other immunoprecipitin techniques. Twenty-eight serum-urine pairs, representing 18 discrete intervals, were analyzed. There was a close relationship between changes in serum and urine light chain levels, with a correlation coefficient of .77 or .93, depending on the method of calculation. This suggests that serum light chain levels measured by crossed immunoelectrophoresis would be equivalent to urinary light chain levels as indicators of tumor burden. Monitoring serum levels would have the advantage of greatly simplified specimen acquisition. In patients with renal failure, serum light chain levels should be a superior indicator of light chain synthesis.
Local Excision for Rectal Cancer
Authors: John M. Skibber
Journal: Journal of the National Comprehensive Cancer Network (2005)

Local excision can be a definitive surgical procedure for some early cancers of the rectum, and it is an appealing technique in many ways. It reduces overall surgical trauma and can assure sphincter preservation. It is also associated with low morbidity. However, this technique has a number of limitations also. This article discusses the results of local excision for rectal carcinoma, including histologic features that impact survival and local recurrence-free rates, the importance of careful patient selection, and the potential role of adjuvant and salvage therapies. Technical considerations and alternative therapies are also discussed.
Abstract 19715: Silencing of Mineralocorticoid Receptors in the Heart Blunts the Anrep Effect
Authors: Néstor G Pérez, Romina G DÍaz, Patricio E Morgan, Horacio E Cingolani
Journal: Circulation (2012)

The stretch-induced increase of cardiac force is biphasic. A first abrupt increase (Farnk-Starling mechanism) is followed by a slower response that takes minutes to develop, which is believed to be the in vitro manifestation of the Anrep effect. This slow force response (SFR) is due to an increase in the intracellular Ca 2+ transient. Although the cause of the increase in Ca 2+ is controversial, an increased NHE1 activity as result of a stretch-triggered autocrine/paracrine mechanism was proposed to be crucial. Furthermore, based on pharmacological approaches we have recently suggested a role for mineralocorticoid receptors (MR) activation in the signaling pathway to the SFR. However, a recent report in smooth muscle cells called attention to the fact that MR inhibitors spironolactone or eplerenone can also affect signaling pathways that do not depend on MR activation. Therefore definitive evidence about the participation of MR in the SFR development needs of MR silencing by molecular techniques. In this study, an interference RNA sequence (small hairpin) able to mediate specific MR knockdown was incorporated into a lentiviral vector (l-shMR) and injected into the left ventricular wall of rat myocardium. Injection of a vector expressing a non-silencing sequence (scramble) served as control. Rats were sacrificed one month after injection. Myocardial MR protein expression was determined and the SFR as well as the stretch-triggered NHE1-mediated increase in pH i in the absence of bicarbonate was evaluated in isolated papillary muscles. Hearts with l-shMR showed reduced MR protein expression (100 ± 5.7 %, n=8, scramble vs. 57 ± 5.6 %, n=9, l-shMR, P&lt;0.05) as well as inhibition of the SFR (in % of initial rapid phase: 125.9 ± 1.8, n=8, scramble, vs. 103.9 ± 1.3, n=8, l-shMR, P&lt;0.05) and of the stretch-induced increase in pH i in bicarbonate free medium (ΔpH units: 0.156 ± 0.025, n=7, scramble, vs. 0.009 ± 0.015, n=10, l-shMR, P&lt;0.05). These data provide unequivocal support to our proposal that MR activation is crucial in the stretch-triggered myocardial mechanism leading to NHE1 activation that determines the Anrep effect.