tbuckley/cabot-search huggingface dataset:
Prospective Evaluation of Magnetic Resonance Imaging and [<sup>18</sup>F]Fluorodeoxyglucose Positron Emission Tomography-Computed Tomography at Diagnosis and Before Maintenance Therapy in Symptomatic Patients With Multiple Myeloma Included in the IFM/DFCI 2009 Trial: Results of the IMAJEM Study
Authors: Philippe Moreau, Michel Attal, Denis Caillot, Margaret Macro, Lionel Karlin, Laurent Garderet, Thierry Facon, Lotfi Benboubker, Martine Escoffre-Barbe, Anne-Marie Stoppa, Kamel Laribi, Cyrille Hulin, Aurore Perrot, Gerald Marit, Jean-Richard Eveillard, Florence Caillon, Caroline Bodet-Milin, Brigitte Pegourie, Veronique Dorvaux, Carine Chaleteix, Kenneth Anderson, Paul Richardson, Nikhil C. Munshi, Herve Avet-Loiseau, Aurelie Gaultier, Jean-Michel Nguyen, Benoit Dupas, Eric Frampas, Françoise Kraeber-Bodere
Journal: Journal of Clinical Oncology (2017)

Purpose Magnetic resonance imaging (MRI) and positron emission tomography–computed tomography (PET-CT) are important imaging techniques in multiple myeloma (MM). We conducted a prospective trial in patients with MM aimed at comparing MRI and PET-CT with respect to the detection of bone lesions at diagnosis and the prognostic value of the techniques. Patients and Methods One hundred thirty-four patients received a combination of lenalidomide, bortezomib, and dexamethasone (RVD) with or without autologous stem-cell transplantation, followed by lenalidomide maintenance. PET-CT and MRI were performed at diagnosis, after three cycles of RVD, and before maintenance therapy. The primary end point was the detection of bone lesions at diagnosis by MRI versus PET-CT. Secondary end points included the prognostic impact of MRI and PET-CT regarding progression-free (PFS) and overall survival (OS). Results At diagnosis, MRI results were positive in 127 of 134 patients (95%), and PET-CT results were positive in 122 of 134 patients (91%; P = .33). Normalization of MRI after three cycles of RVD and before maintenance was not predictive of PFS or OS. PET-CT became normal after three cycles of RVD in 32% of the patients with a positive evaluation at baseline, and PFS was improved in this group (30-month PFS, 78.7% v 56.8%, respectively). PET-CT normalization before maintenance was described in 62% of the patients who were positive at baseline. This was associated with better PFS and OS. Extramedullary disease at diagnosis was an independent prognostic factor for PFS and OS, whereas PET-CT normalization before maintenance was an independent prognostic factor for PFS. Conclusion There is no difference in the detection of bone lesions at diagnosis when comparing PET-CT and MRI. PET-CT is a powerful tool to evaluate the prognosis of de novo myeloma.
The Limited &amp; Extensive Staging System Is More Suitable for Extranodal Natural Killer/T-Cell Lymphoma, Nasal Type: Comparison with Other Staging Systems
Authors: Jie Liu, Chong Jiang, Yao-Tiao Deng, Li Zhang, Na Li, Rong Tian, Yu Wu, Ming Jiang, Yu Jiang, Li-Qun Zou
Journal: Blood (2016)
NMDA receptor type 2A at 16p13 is epigenetically inactivated in human colorectal carcinoma
Authors: Myoung Sook Kim, Junwei Liu, Keishi Yamashita, Xiaofei Chang, Jin Hyen Baek, Hannah L. Park, Jang Hee Woo, Motonobu Osada, Sunil Upadhyay, Chulso Moon, David Sidransky
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

56 

N-methyl-D-aspartate receptors (NMDARs) are glutamate receptors and the predominant excitatory neurotransmitter receptors in the mammalian brain. However, little is known about the role of NMDARs in human cancers. We have previously demonstrated that NMDA receptor 2B is epigenetically inactivated and exhibits tumor suppressor activity in human esophageal cancer. In this current study, we further investigated the role of NMDA receptor 2A in human primary colorectal cancers. We found that NMDA receptor 2A was epigenetically silenced in human colorectal carcinoma. Demethylating agent, 5-aza-2′-deoxycytidine could highly reactivate NMDA receptor 2A expression, despite that the normal expression of NMDA receptor 2A is undetectable in all seven colorectal carcinoma (CRC) cell lines we tested. Direct sequencing of bisulfate treated DNA from 7 CRC cell lines confirmed the promoter hypermethylation of NMDA receptor 2A in CRC cell lines. Furthermore, we analyzed NMDA receptor 2A methylation status on 100 paired normal colon and primary CRC using methylation specific quantittive PCR, and detected promoter hypermethylation in 82% of CRC and 20% of paired normal tissue, suggesting that hypermethylation of NMDA receptor 2A promoter in CRC is tumor specific. We also demonstrated that overexpression of NMDA receptor 2A in CRC cells almost abolished the ability of the cells to form colonies in culture, suggesting its tumor suppressive activity. Taken together, we conclude that NMDA receptor 2A hypermethylation is a common event and could be a potential tumor suppressor gene in CRC.
Surgical margins a niche for cancer stem like cells in colorectal cancer and its role in tumorogenicity and drug resistance.
Authors: Chandramohan Krishnan Nair, Asha Nair, Radhakrishna Pillai
Journal: Journal of Clinical Oncology (2015)

e14549 Background: Our postulate was that the cells which are actually responsible for cancer progression are only a fractions of tumor cells with high potential for cell division and resistance to chemotherapy, called Cancer Stem Cells (CSC) .Surgical margins after resection of colorectal cancers could be a heterogeneous potential niche for CSC and these have a very crucial role in metastasis, disease relapse and escaping chemo-radio therapy. Objectives of our study were to identify CSC in Colorectal Cancer (CRC) and surgical margins and employ this knowledge to study tumor heterogeneity and its relevance in local recurrence, distant metastasis and drug resistance property of CRC. Methods: CSC from biopsy tumor tissue, proximal, distal and circumferential margins and draining lymph nodes would be isolated and enriched by specific surface markers using flow cytometry and magnetic beads assisted cell sorting and molecular profiling would be done. Immunohistochemical studies would be also be done. Finally In-vivo study would be done by developing xenograftrectal model in nude mice. Results: Side population analysis for CSC showed that distal margin is enriched with CSC comparative to tumor. Out of 33 patients studied, CSC were present in distal margins of resection in 9(81.8%) cases when length of resected distal margins was less than 2 cm, 12(63.2%) cases when it was 2-5cms and none when margin was more than 5cms (p-value = 0.0001) .To further confirm these findings we analyzed CD133 (surface marker for CRC CSCs) positive population in tumor and surgical margins, which was the same. Immunohistochemistry and western blot analysis also proved that distal margins highly express drug resistance proteins. With these observation we are moving ahead with culture them in non-adherent conditions to obtain colonspheres (which have enriched CSC population) which will be inoculated in orthotopicSCID mice model to understand the tumorogenicity and drug resistant property of CSCs in an in vivo scenario. Conclusions: Cancer stem cell like cells exists at margin of resected Colorectal Cancer specimen. The implications of this finding need to be studied further.
Use of a Single Baseline Versus Multiyear 24-Hour Urine Collection for Estimation of Long-Term Sodium Intake and Associated Cardiovascular and Renal Risk
Authors: Rik H.G. Olde Engberink, Thomas C. van den Hoek, Nicky D. van Noordenne, Bert-Jan H. van den Born, Hessel Peters-Sengers, Liffert Vogt
Journal: Circulation (2017)

A decrease in sodium intake has been shown to lower blood pressure, but data from cohort studies on the association with cardiovascular and renal outcomes are inconsistent. In these studies, sodium intake was often estimated with a single baseline measurement, which may be inaccurate considering day-to-day changes in sodium intake and sodium excretion. We compared the effects of single versus repetitive follow-up 24-hour urine samples on the relation between sodium intake and long-term cardiorenal outcomes.We selected adult subjects with an estimated glomerular filtration rate >60 mL/min/1.73m2, an outpatient 24-hour urine sample between 1998 and 1999, and at least 1 collection during a 17-year follow-up. Sodium intake was estimated with a single baseline collection and the average of samples collected during a 1-, 5-, and 15-year follow-up. We used Cox regression analysis and the landmark approach to investigate the relation between sodium intake and cardiovascular (cardiovascular events or mortality) and renal (end-stage renal disease: dialysis, transplantation, and/or >60% estimated glomerular filtration rate decline, or mortality) outcomes.We included 574 subjects with 9776 twenty-four-hour urine samples. Average age was 47 years, and 46% were male. Median follow-up was 16.2 years. Average 24-hour sodium excretion, ranging from 3.8 to 3.9 g (165-170 mmol), was equal among all methods (P=0.88). However, relative to a single baseline measurement, 50% of the subjects had a >0.8-g (>34-mmol) difference in sodium intake with long-term estimations. As a result, 45%, 49%, and 50% of all subjects switched between tertiles of sodium intake when the 1-, 5-, or 15-year average was used, respectively. Consequently, hazard ratios for cardiorenal outcome changed up to 85% with the use of sodium intake estimations from short-term (1-year) and long-term (5-year) follow-up instead of baseline estimations.Relative to a single baseline 24-hour sodium measurement, the use of subsequent 24-hour urine samples resulted in different estimations of an individual's sodium intake, whereas population averages remained similar. This finding had significant consequences for the association between sodium intake and long-term cardiovascular and renal outcomes.
Health and Function of Patients With Untreated Idiopathic Scoliosis
Authors: Martha C Hawes
Journal: JAMA (2003)

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
Human monocytes bind to two cytokine-induced adhesive ligands on cultured human endothelial cells: endothelial-leukocyte adhesion molecule-1 and vascular cell adhesion molecule-1
Authors: T Carlos, N Kovach, B Schwartz, M Rosa, B Newman, E Wayner, C Benjamin, L Osborn, R Lobb, J Harlan
Journal: Blood (1991)
Abstract P213: Epidermal Growth Factor Receptor and c-Src Are Involved in Stretch-Induced Activation of JNK1/2 and P38 in Cardiac Myocytes and Cardiac Fibroblasts
Authors: Hao Feng, Fnu Gerilechaogetu, Honey B Golden, Ricardo Cristalis, Kumar Dasuri, Damir Nizamutdinov, Donald M Foster, Carl Tong, David E Dostal
Journal: Circulation Research (2011)

Mechanical stretch is a major determinant that leads to heart failure. Heart failure is associated with a steady increase in myocardial angiotensinogen (Ao) expression and the biological peptide angiotensin II (Ang II) formation. We have previously identified key downstream effectors that couple to mechanical stretch-induced Ao gene expression. JNK1/2 and p38α were found to have opposing roles on stretch-induced Ao gene expression in neonatal rat cardiac myocytes (NRVM) and cardiac fibroblasts (NRFB). JNK negatively regulated Ao expression in NRVM and NRFB following acute stretch, whereas with prolonged stretch, p38α was responsible for upregulation of Ao expression. However, the mechanisms leading to activation of these kinases and cross-talk between these signal molecules remain to be determined. Epidermal growth factor receptor (EGFR) is expressed in both NRVM and NRFB, but its precise role in mechanosensing is poorly understood. In NRVM, stretch caused JNK1/2 activation (phosphorylation) within 2 min, with a peak response at 15 min (3.96 ± 0.71 fold, p&lt;0.01). Stretch induced p38 activation within 5 min, which remained elevated (2.93 ± 0.49 fold, p&lt;0.05) at 60 min (final time point). Pretreatment with EGFR blockers AG1478 (100 nM) and BIBX 1382 (200 nM) inhibited stretch-induced activation of JNK at early time points (5 and 15 min), whereas BIBX 1382 and the Ang II receptor type I inhibitor losartan (10 µM) inhibited p38 activation at 60 min. Stretch induced activation of c-Src (phosphorylation of tyrosine 416) at 60 min (1.56 ± 0.21 fold, p&lt;0.01), which was attenuated by losartan. In NRFB, stretch-induce-JNK-phosphorylation can be inhibited by both AG1478 and Src inhibitor PP2 (100 nM) at 15 min. Stretch also increased phosphorylation levels of c-Src at tyrosine 416 and EGFR at tyrosine 1068 at 15 and 60 min, which were blocked in the presence of losartan. In a summary, these studies give strong evidence that both EGFR and c-Src are involved in stretch-induced signal cascade in NRVM and NRFB.
Central evaluation for surgical treatment options in FIRE-3- updated results and impact on overall Survival
Authors: Dominik P. Modest, Johann Pratschke, Hauke Lang, Marc Bemelmans, Thomas Becker, Markus Rentsch, Daniel Seehofer, Christiane J. Bruns, Bernhard Gebauer, Sebastian Stintzing, Heike I. Modest, Swantje Held, Gunnar Folprecht, Volker Heinemann, Ulf P. Neumann, Timm Denecke
Journal: Annals of Oncology (2017)
Usefulness of 18F-FDG PET/CT, LDH and tumor markers in the prognosis and evaluation of tumor response after RMB therapy in advanced, metastatic colorectal cancer (mCRC)
Authors: Angelica Nazarian, Zoe Andrada, Joanne Thomas, Sudipta Sureshbabu, Nathaniel Berman, David Wolf, Lawrence Gazda, Thomas Fahey, Allyson Ocean, Barry Smith
Journal: Annals of Oncology (2017)
Bone marrow hematons: An access point to the human hematopoietic niche
Authors: Alexandre Janel, Juliette Berger, Céline Bourgne, Richard Lemal, Nathalie Boiret‐Dupré, Frédérique Dubois‐Galopin, Pierre Déchelotte, Charlotte Bothorel, Eric Hermet, Sara Chabi, Jacques‐Olivier Bay, Céline Lambert, Bruno Pereira, Françoise Pflumio, Rima Haddad, Marc G. Berger
Journal: American Journal of Hematology (2017)

Abstract To understand the complex interactions between hematopoietic stem cells and the bone marrow niche, a human experimental model is needed. Our hypothesis is that hematons are an appropriate ex vivo model of human bone marrow. We analyzed the hierarchical hematopoietic cell content and the tissue organization of single hematons from healthy donors. Most (&gt;90%) hematons contained precursors of all cell lineages, myeloid progenitors, and LTC‐ICs without preferential commitment. Approximately, half of the hematons could generate significant levels of lympho‐myeloid hematopoiesis after transplantation in an NSG mouse model, despite the low absolute numbers of transplanted CD34 + cells. Mesenchymal STRO‐1 + and/or CD271 + cells formed a critical network that preserved hematon cohesion, and STRO‐1 + cells colocalized with most hematopoietic CD34 + cells (68%). We observed an influence of age and gender. These structures represent a particularly attractive model for studying the homeostasis of the bone marrow niche and pathological changes that occur during diseases.
Testing for Respiratory Viruses in Children
Authors: Peter J. Gill, Susan E. Richardson, Olivia Ostrow, Jeremy N. Friedman
Journal: JAMA Pediatrics (2017)

While most viral respiratory tract infections can be diagnosed clinically, clinicians frequently order tests to identify the specific offending virus. While there has been tremendous growth in the variety, availability, and sophistication of the types of respiratory viral tests, there may have been less critical thought and discussion among frontline clinicians about the clinical utility and specific indications for testing. We summarize the rationale historically used to support respiratory virus testing in children, with a review of the supporting evidence. We outline potential considerations and limitations of the various types of respiratory viral tests and suggest some clinical indications where viral testing may play an important role in clinical management.The main value of testing for viruses in children who present with a respiratory tract infection is to differentiate between viral and bacterial infections, hopefully facilitating clinical decision making regarding further investigations and the need for antibiotics. We have highlighted commonly cited rationale used to support testing and the generally poor evidence on which to base this rationale. In addition, difficulties with interpretation of respiratory viral testing results include somewhat poor diagnostic test characteristics for some tests, uncertainty regarding true positives and causation of illness, delay in receiving the test result, and the incidence of concurrent bacterial infections or the presence of multiple viruses. We have given some examples of clinical scenarios where respiratory viral testing results could be expected to contribute to more appropriate clinical management decisions.It is not good enough to "do" just because we "can." We suggest that for many healthy immune-competent children presenting with typical viral respiratory tract symptoms, the diagnosis can be made clinically, and frontline clinicians should think critically before automatically requesting a somewhat uncomfortable, expensive respiratory viral test, the result of which may not contribute to the child's treatment.
Early clinical efficacy of TAS-120, a covalently bound FGFR inhibitor, in patients with cholangiocarcinoma
Authors: Lipika Goyal, Hendrik-Tobias Arkenau, Ben Tran, Jean-Charles Soria, Rastilav Bahleda, Gabriel Mak, Andrew Zhu, Milind Javle, Hirai Hiroshi, Fabio Benedetti, Jerry Huang, Robert Winkler, Funda Meric-Bernstam
Journal: Annals of Oncology (2017)
Signet-ring cell carcinoma of the colon and rectum: About 24 cases
Authors: Raihana Boujarnija, Ibtihal Ahalli, Kawthar Messoudi, Lamiae Amaadour, Zineb Benbrahim, Fatima Lmrabet, Samia Arifi, Nawfal Mellas
Journal: Annals of Oncology (2017)
Consequences of Arterial Narrowing
Authors: Bonaccorsi A, Garattini S, Jori A
Journal: BMJ (1964)

Leading Articles19s. in the previous year.The cost of treating a patient, which is calculated by dividing the total in-patient expenditure by the number of discharges and deaths (ignoring long-stay units and departments), went up, on the other hand, by less than 3 %, a smaller increase than in the previous year.This indicates that the hospitals are using their beds more efficiently; that is, they are increasing their turnover of patients by discharging them earlier and maintaining a high rate of occupancy.The effect of this on a hospital's costs can be seen in the Oxford region.Oxford has the highest cost per in-patient week of all the regional boards (£38 4s.lid.).But its cost per case is remarkably low (£49 1is.2d., compared with the regional average of £58 1 is.), and this is presumably
Abstract P053: Impaired Autophagosome Removal in Cardiomyocytes Triggers Programmed Necrosis in Mouse Hearts
Authors: Huabo Su, Zongwen Tian, Changhua Wang, Suleman Said, Jie Li, Mark J Ranek, Xuejun (XJ) Wang
Journal: Circulation Research (2011)

Programmed cell death includes apoptosis and programmed necrosis. The latter is also known as necroptosis. A well-recognized feature of necrosis is the loss of membrane integrity of the dying cell, resulting in inflammatory responses at the surrounding tissue. Cells undergoing apoptosis, however, maintain their membrane integrity very well and hence do not trigger inflammation. These features are effectively captivated to detect necrotic cells. By assessing Evans Blue Dye (EBD) uptake and CD45+ leukocytes, we previously detected massive cardiomyocyte (CM) necrosis, before increased apoptosis was evident, in mouse hearts deficient of COP9 signalosome (CSN) subunit 8 (Csn8) ( Circ Res 2011; 108:40–50 ). We show here that the detection of necrosis is confirmed by immuno-detection of endogenous IgG inside the CM. We found that virtually all EBD positive cells were also mouse IgG positive whereas some of the IgG positive CMs, as expected, did not show increased EBD uptake, suggesting that probing intracellular IgG offers a simpler and even more sensitive method for detecting necrotic CMs in vivo. Notably, we were able to demonstrate that both the EBD uptake assay and the immuno-detection of intracellular IgG clearly have a resolution at the single cell level. We then explored the mechanism by which Csn8/CSN deficiency causes necrosis. Autophagosomes are accumulated due to a defect in their fusion with lysosomes in mouse hearts with perinatal CM-restricted Csn8 knockout (CR-Csn8KO) but the accumulation is heterogeneous among CMs likely due to a temporal heterogeneity of Csn8 gene ablation and/or a spatial difference in the microenvironment and functionality of different CMs. A remarkably higher percentage of CMs with greater autophagosome accumulation were undergoing necrosis than those with less or without autophagosome accumulation. Importantly, chronic lysosomal inhibition caused CM necrosis in wild type mice. Moreover, the protein levels of RIP1, RIP3 kinases and the RIP1-bound RIP3 were all significantly increased in the CR-Csn8KO heart. Taken together, these novel findings strongly suggest that impaired autophagosome removal causes CM necrosis in Csn8/CSN deficient hearts through likely activating the RIP1-RIP3 mediated necroptotic pathway.
Impact of TNF-inhibitor treatment on radiographic joint destruction in theumatoid arthritis patients treated in clinical practice
Authors: L. Ørnbjerg, M Østergaard, A. Thormann, P. Bøyesen, U. Tarp, W. Böhme, D. Dencker, Hanne Merete Lindegaard, Uta Engling Poulsen, A. Hansen, V. Ringsdal, A. Schlemmer, N. Graudal, A. Andersen, J Espesen, G. Kollerup, T. Christensen, R. Pelck, B. Glintborg, O. Madsen, D. Jensen, O. Majgaard, M.L. Hetland
Journal: Annals of the Rheumatic Diseases (2010)