tbuckley/cabot-search huggingface dataset:
Efficacy and Toxicity of Donor Lymphocyte Infusions in the Management of Mixed Donor-Recipient Chimerism Following Allogeneic Stem Cell Transplantation for Lymphoid Malignancies:- a Study of the LWP-EBMT
Authors: Stephen Robinson, Ariane Boumendil, Irma Khvedelidze, Hervé Finel, Karl Peggs, Ram K Malladi, Victoria Potter, Anna Tsoulkani, Elisabeth Vandenberghe, Yves Chalandon, Jürgen Finke, Erik Marijt, Sabine Furst, Michel Schaap, Hannah Hunter, John A Snowden, Karan Wadehra, Sebastian Wittnebel, Dietrich W. Beelen, Nathalie Fegueux, Nicolaus Kroeger, Peter Dreger, Silvia Montoto
Journal: Blood (2018)
Abstract 14920: Long-Term Efficacy of Cardiac Contractility Modulation: Single Center Experience in 81 Patients
Authors: Juergen Kuschyk, Susanne Roeger, Raphaela Schneider, Florian Streitner, Christina Doesch, Rainer Schimpf, Boris Rudic, Martin Borggrefe
Journal: Circulation (2013)

Introduction: Cardiac contractility modulating (CCM) signals are high intensity electrical impulses applied to the septum during the absolute refractory period that are intended to enhance the stre...
Challenges of Dual-Physician Couples
Authors: Cassandra E. Henderson, Beth E. Roxland, Renee J. Webb
Journal: JAMA (2019)

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
Prevalence and Risk Factors for Opioid-Related Complications in Patients with Myeloproliferative Neoplasms: An International Survey of 502 Patients By the MPN Quality of Life Study Group
Authors: Holly L. Geyer, Robyn M. Scherber, Gina Mazza, Blake Langlais, Leslie Padrnos, Jeanne Palmer, Amylou C. Dueck, Ruben A. Mesa
Journal: Blood (2018)
Outcomes By Treatment Setting and Genomic Profile in Patients with AML on Cladribine, Idarubicin, and Cytarabine
Authors: Prajwal Boddu, Hagop M. Kantarjian, Farhad Ravandi, Elias J. Jabbour, Naval Daver, Naveen Pemmaraju, Courtney D. DiNardo, Srdan Verstovsek, Yesid Alvarado, Gautam Borthakur, Nitin Jain, Marina Konopleva, Christopher B Benton, Rebecca Slack, Keyur P. Patel, Guillermo Garcia-Manero, Jorge E. Cortes, Tapan Kadia
Journal: Blood (2017)
Abstract 183: Phosphodiesterase 9 Inhibition Improves Cardiometabolic Profile in Female Mice Independent of Estrogen Status
Authors: Sumita Mishra, Guangshuo Zhu, Susana Rodriguez, William Wong, David Kass
Journal: Circulation Research (2019)

Approximately 6.5 million Americans are living with heart failure (HF) currently and the number of persons is projected to increase 46% by 2030. One particularly notable syndrome associated with increasingly severe obesity is called - Heart failure with a preserved ejection fraction (HFpEF); which represents half of all HF patients world-wide. Epidemiologic insights have provided incremental evidence that female sex is a stronger risk factor for HFpEF, particularly post-menopausal women. Loss of estrogen after menopause reduces estrogen receptor induced-NO-cGMP-PKG activation and consequently less benefit from Phosphodiesterase 5(PDE5) inhibition which principally hydrolyze NO-derived cGMP that appears compromised in HFpEF patients. PDE9 targets cGMP generated by Natriuretic peptide (NP) signaling and is significantly increased in hearts from HFpEF patients. This supports a role of PDE9 in the heart and its value as a therapeutic target for abnormalities relevant to HFpEF. We created a murine model of postmenopausal obesity and mild cardiac stress induced HFpEF. Genetic ablation or pharmacological inhibition of PDE9 conferred higher contractile performance with increased %EF, %FS and improved diastolic relaxation and filling. Echo-MRI analysis showed an improvement in whole body metabolism with significant decrease in percent body fat associated with enhanced O 2 consumption and increased energy expenditure. The mechanisms underlying the protective effects are increased mitochondrial function and enhanced expression of transcriptional regulators pgc1α and pparα, driving mitochondrial fatty acid oxidation and increased energy dissipation. Our work identifies for the first-time reversal of changes in substrate metabolism, and mitochondrial dynamics as a direct consequence of PDE9 inhibition in heart and fat. Proteomic analysis also revealed a dynamic cross-talk of PDE9 protein with biological networks of mitochondrial membrane proteins and proteins regulating cellular metabolism. This study greatly enhances our understanding of how the cGMP/PKG activation system can be modulated in females with reduced sex hormone- paving the way for gender-selective targeting in patients with obesity and HFpEF.
Age-specific associations between HIV infection and carotid artery intima-media thickness in China: a cross-sectional evaluation of baseline data from the CHART cohort
Authors: Haijiang Lin, Yingying Ding, Chenxi Ning, Xiaotong Qiao, Xiaochen Chen, Xiaoxiao Chen, Weiwei Shen, Xing Liu, Yuling Hong, Na He
Journal: The Lancet HIV (2019)
Abstract 658: RNF20/40 Regulates Cardiomyocyte Maturation
Authors: Nathan J Vandusen, Julianna Y Lee, Wei-liang Gu, Isha Sethi, Shengbao Suo, Justin King, Yanjiang Zheng, Yuxuan Guo, William T Pu
Journal: Circulation Research (2019)

Between birth and adulthood, cardiomyocytes (CMs) undergo profound changes in size, ultrastructure, metabolism, and gene expression, a process collectively referred to as CM maturation. Although highly coordinated, the transcriptional network that governs this process is not understood. This lack of understanding is a barrier to cardiac regenerative medicine, where our current inability to mature CMs differentiated from non-myocytes limits their use for disease modeling or replacement therapy. In addition, disruption of maturation by abnormal hemodynamic loads in neonates who have undergone surgery to correct congenital heart defects likely contributes to their high incidence of heart failure in adulthood. A sound understanding of the regulatory network governing CM maturation will inspire hypothesis driven attempts to surmount these challenges. In mice, a key hallmark of CM maturation is sarcomere isoform switching, including the well documented neonatal switch from Myosin Heavy Chain 7 (Myh7) to Myosin Heavy Chain 6 (Myh6). We have conducted and validated an in vivo high throughput CRISPR screen for transcriptional regulators of CM maturation, using the Myh7/6 isoform switch as the readout. Two top candidates from this screen, Rnf20 and Rnf40, form a complex which deposits the epigenetic mark H2bub1 (histone-2B mono-ubiquitinated on lysine 120). Defects in RNF20/40 and H2Bub1 regulation have been associated with human congenital heart disease, but their mechanistic function in the heart has not been studied. We performed ChIP and RNA-sequencing experiments in control and RNF loss-of-function models to characterize the role of H2Bub1 in transcriptional control of CM maturation. The resulting mechanistic insights into how gene expression is coordinately controlled during maturation will inform efforts to improve CM production protocols and develop targeted therapies.
Integrated Analysis of Global DNA Methylation and Transcription Reveals a Leukemia Subtype with Extreme Hypermethylation Associated with Silencing of Regulators of Differentiation
Authors: Claudia Gebhard, Roger Mulet-Lazaro, Lucia Schwarzfischer, Dagmar Glatz, Margit Nuetzel, Daniel Heudobler, Sandra Pohl, Wolfgang Herr, Gerhard Ehninger, Claudia Erpelinck-Verschueren, Stanley van Herk, B.J. Wouters, Christian Thiede, Ruud Delwel, Michael Rehli
Journal: Blood (2018)
In-Depth miRNA Profiling Of Germinal Center Derived B-Cell Lymphomas By Next Generation Sequencing: A Report From The German Icgc-Mmml-Seq Project
Authors: Jessica I Hoell, Kebria Hezaveh, Stephan Bernhart, Steve Hoffmann, David Langenberger, Matthias Schlesner, Peter Stadler, Vera Binder, Dido Lenze, Reiner Siebert, Michael Hummel, Arndt Borkhardt
Journal: Blood (2013)
Living with advanced colorectal cancer: How prepared are informal caregivers to care for their loved ones?
Authors: Marc Kerba, Shireen Kassam, Crystal Beaumont, Patricia Biondo, Madalene Earp, Patricia A. Tang, Jessica Simon, Sharon Watanabe, Aynharan Sinnarajah
Journal: Journal of Clinical Oncology (2019)

179 Background: The ‘Living with Colorectal Cancer’ prospective cohort study seeks to characterize the experiences of patients diagnosed with advanced colorectal cancer and their caregivers, in order to inform care improvements. Here we describe informal caregivers’ perceived preparedness for caregiving. Methods: Eligible patients were identified by oncologists in Alberta, Canada’s two tertiary cancer centers. Consenting patients were given the option to invite a caregiver to participate. Caregivers’ preparedness for caregiving was assessed at enrollment and every 3 months thereafter using the Preparedness for Caregiving survey. This survey assesses levels of preparedness using 5-point Likert scales for 8 caregiving domains (e.g. caring for the patient’s physical and emotional needs, finding and setting up services, stress of caregiving, responding to emergencies), and one open-ended question. Results: In one year of recruitment, 55 caregivers in Calgary and Edmonton were enrolled, of which 65% were female, and 80% lived with the patient. Caregiver preparedness decreased over time from months 1 to 7 of follow-up, across all categories. Caregivers were least prepared for the stress of caregiving and caring for the patient’s emotional needs. They were most prepared for taking care of the patient’s physical needs at enrollment. Open-ended comments on specific preparedness needs were numerous and extensive. A range of topics were reported, the top three being: caregiver health (physical, mental, self-care), emotional aspects (preparing children and family, feeling alone) and end of life (hospice, palliative care, transitioning). Conclusions: Our data suggest that in the advanced cancer setting, caregiver perceived preparedness declines, with increasing stress and emotional distress over time. This may be related to patient illness progression. The open-ended qualitative comments on the Preparedness for Caregiving survey were particularly useful in understanding specific caregiver concerns. Caregiver experience, including sense of preparedness, is often under evaluated and this study suggests more attention is needed. Clinical trial information: NCT03572101.
Intrabone Delivery of CD34+ Cells Using an Optimized Delivery System Does Not Enhance Engraftment in a Rhesus Macaque Model of Hematopoietic Stem Cell Transplantation
Authors: Kate Stringaris, Robert F Hoyt, Jan Davidson, Jeremy Pantin, John F. Tisdale, Naoya Uchida, Lydia Raines, Robert Reger, Noriko Sato, Cynthia E. Dunbar, Tim Hunt, Randy Clevenger, Allen Krouse, Mark Metzger, Aylin Bonifacino, Theresa Engels, Sandra Price, Peter Choyke, Robert E. Donahue, Richard W. Childs
Journal: Blood (2018)
Abstract 887: Activation of Autophagic Flux Rescues Mitochondrial Homeostasis During Cardiac Ischemia/Reperfusion Injury
Authors: Jing Yang, Geoffrey W Cho, Jin He, Xiachang Zeng, Kaeli Ebner, Scott Ballinger, Martin Young, Sumanth Prabhu, Jianyi Zhang, Joseph A Hill, Min Xie
Journal: Circulation Research (2019)

Objective: Reperfusion injury accounts for ~50% of myocardial infarct size, and meaningful clinical therapies targeting this do not exist. We have shown that HDAC inhibition-enhanced cardiomyocyte autophagy blunts ischemia/reperfusion (I/R) injury given at the time of reperfusion. However, as HDAC inhibition may have off-target effects, we set out to test whether augmentation of autophagy protects myocardium through maintenance of mitochondrial homeostasis and reduction of oxidative stress during reperfusion injury. Methods: 10-week-old, wild-type, C57BL6 mice were randomized into 3 groups: vehicle control, or exposed to a Tat-Scrambled (TS) peptide, or a Tat-Beclin (TB, autophagy-inducing molecule) peptide. Each group was subjected to I/R surgery (45min coronary ligation, 24h reperfusion). Infarct size, systolic function, and mitochondrial dynamics were assayed. Cultured neonatal rat ventricular myocytes (NRVMs) were exposed to TB during simulated ischemia/reperfusion injury. ATG7 knockout (ATG7 KO) mice and ATG7 knockdown by siRNA in NRVMs was used to evaluate the role of autophagy. Results: TB treatment at reperfusion reduced infarct size by 20.1% (n=23, p&lt;0.05) and improved systolic function (n=11, p&lt;0.05). Improvement correlated with increased autophagic flux in the border zone with less oxidative stress. ATG7 KO mice did not manifest TB-promoted cardioprotection during I/R. TB increased mtDNA content in the border zone (n=10, p&lt;0.05). In NRVMs subjected to I/R, TB reduced cell death by 41% (n=12, p&lt;0.001), reduced I/R-induced mtDNA damage, and increased mtDNA content by &gt;60% (n=3, p&lt;0.05). Moreover, TB promoted expression of the gene coding for PGC-1α, which controls mitochondrial biogenesis, in the border zone (n=10, p&lt;0.05) and in NRVMs subjected to I/R (n=3, p&lt;0.05), along with expression of the mitochondrial dynamics genes Drp1, Fis1 and MFN1 / 2 (n=9, p&lt;0.05). Conversely, ATG7 knockdown in NRVMs abolished these beneficent effects of TB on mitochondria. Conclusions: Autophagy is a sufficient and essential process to mitigate reperfusion injury through maintenance of mitochondrial homeostasis. Augmentation of autophagic flux may emerge as a viable clinical therapy to reduce reperfusion injury in myocardial infarction
5-Azacytidine Is Effective for Targeting Leukemia-Initiating Cells in Juvenile Myelomonocytic Leukemia
Authors: Christopher Felix Krombholz, Lorena Gallego Villar, Pritam Kumar Panda, Sushree Sangita Sahoo, Marcin W. Wlodarski, Daniel B. Lipka, Christoph Plass, Charlotte Niemeyer, Miriam Erlacher, Christian Flotho
Journal: Blood (2018)
Lenalidomide Upregulates Erythropoietin Receptor Expression Through Inhibition of the E3-Ubiquitin Ligase Ring Finger Protein 41 (RNF41)
Authors: Ashley A. Basiorka, Kathy L. McGraw, Lori N. Griner, Ling Zhang, Leentje De Ceuninck, Gisela Caceres, Lubomir Sokol, Rami S. Komrokji, Sheng Wei, Jan Tavernier, Alan F. List
Journal: Blood (2012)
Achieving best possible cancer treatment outcomes in care pathways through benchmarking: ABC benchmarking.
Authors: Anke Wind, Maud Bessems, Ramon RJP van Eekeren, Carl J Wijburg, Rob P.W.F. Wijn, Johanna Mattson, Marina Borges, Joaquim Abreu de Sousa, Jorge Oliveira, Jana Halamkova, Marek Svoboda, Wim H van Harten
Journal: Journal of Clinical Oncology (2019)

268 Background: Care pathways are used to manage quality in healthcare and concern the organization and standardization of care processes. By benchmarking care pathways, new knowledge is generated that can be utilized to optimize care pathways. A recent development in healthcare is the transformation from volume-based healthcare to value-based healthcare, which amongst others emphasizes the need for IPU (Integrated Practice Unit) development. The ABC-Benchmarking project is an international benchmarking project aiming to further develop the BENCH-CAN pathway benchmark, establish comparative scores on IPU development, and link outcome data to benchmark results. Methods: The 13 step benchmarking process as developed by Van Lent et al. was used. Indicators were primarily derived from the BENCH-CAN pathway benchmark format and secondary from expert opinion. An adapted Delphi method, in which clinical experts on breast and prostate cancer provided feedback in three rounds, was used to select the final set of indicators. The indicator sets containing structure, process and outcome indicators were piloted in 5 centers. Clinical outcome indicators were collected primarily through cancer registries. Site visits were performed to clarify additional questions based on the provided data and to grasp the context of the care pathway. Results: The final set contained 79 indicators for breast and 69 indicators for prostate cancer. Due to differences in registration and data availability of cancer registries not all data could be collected for all centers. Differences between cancer centers were found for example in the measurement of patient reported outcomes and status of the IPU. Aggregated and comparative data can be shown during the symposium. Conclusions: Further validating the pathway benchmark tool and adding more focus to IPU development and outcome indicators led to new knowledge on adding value for cancer patients. Examples given were optimizing care organized in care pathways for breast and prostate cancer patients. The results provided improvement opportunities for all centers. A study into patient involvement in pathway development, evaluation and improvement is also part of this project.
Recombinant human TNF Related Apoptosis Inducing Ligand (rhTRAIL) in combination with irradiation and or aspirin induces apoptosis in cervical cancer cell lines
Authors: John H. Maduro, Brigitte M. Hougardy, Ate G. Van der Zee, Elisabeth G. De Vries, Steven De Jong
Journal: Cancer Research (2005)

5350  Increased expression of the DR4 (TRAIL-R1) or DR5 (TRAIL-R2) TRAIL receptors and loss of TRAIL expression is frequently found in malignant tumors (including cervical cancer) as compared to their normal counter parts. In tumor cell lines and animal models ionizing radiation in combination with rhTRAIL can render tumor cells more sensitive to apoptosis. It was previously demonstrated that sulindac sulfide a non-selective Cox-inhibitor, similar to aspirin, induced apoptosis by engaging the mitochondrial pathway and the DR5-dependent pathway. This makes it potentially interesting to combine rhTRAIL with ionizing radiation and aspirin in cervical cancer. We investigated whether irradiation and or aspirin enhances rhTRAIL induced apoptosis and cell survival. In the present study we used three HPV positive cervical cancer cell lines,a highly sensitive (Caski), an intermediate sensitive (HeLa S3) and a rhTRAIL resistant (SiHa) cell line. Cells were irradiated with five Gray and treated with different concentrations aspirin (1mM - 10mM) and or rhTRAIL (0.001 μg/ml - 1.0 μg/ml). As read out for apoptosis we used caspase 8 activation, PARP cleavage and acridine orange staining of nuclear chromatin. The MTT assay was used to determine cell survival. The combination of irradiation and rhTRAIL enhanced apoptosis and overall cell kill in HeLaS3 and SiHa with a factor of 1.1 to 2.5. The combination of aspirin and rhTRAIL resulted in a more than additive effect in all three cell lines enhancing the treatment result with a factor of 2.5 to 8. In this experimental setting combining all three the treatment modalities was not superior over the combination of rhTRAIL and aspirin. At the molecular level there was activation of caspase 8 and cleavage of FLIP in all three the cell lines. Because Caski lacks Cox-2 protein expression it seems that this combined effect of TRAIL and aspirin is Cox-2 independent, yet further studies must be undertaken to prove this. In conclusion both aspirin and irradiation enhance rhTRAIL-induced apoptosis in cervical cancer cell lines. Supported by a fellowship and a grant (RUG 2000-2289) from the Dutch Cancer Society
Cardiac resynchronization therapy reduces expression of inflammation-promoting genes related to interleukin-1β in heart failure
Authors: Kenneth Bilchick, Hema Kothari, Aditya Narayan, James Garmey, Abdullah Omar, Brian Capaldo, Coleen McNamara
Journal: Cardiovascular Research (2019)

Abstract Aims In light of recent data regarding inflammatory signalling pathways in cardiovascular disease and the recently demonstrated impact of pharmacologic inhibition of interleukin-1β (IL-1β) in heart failure, the primary aim was to assess the physiologic effects of cardiac resynchronization therapy (CRT) on the expression of systemic inflammatory, immune-modulatory, metabolic, and apoptotic genes in peripheral blood mononuclear cells (PBMCs) of patients with heart failure. Methods and results We used RNA sequencing (RNA-Seq) and reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) to identify gene expression changes in PBMCs in response to CRT. In total, 27 patients were analysed: 12 with heart failure undergoing CRT, 6 with heart failure undergoing standard implanted cardioverter defibrillators, and 9 with coronary artery disease but not heart failure. In CRT patients (median age 65.5 years, interquartile range 63.0–66.8 years, 33% female), RNA-Seq analysis identified 40 genes, including multiple genes associated with the IL-1β pathway, with significant correlations (false discovery rate &amp;lt; 0.05) with four key CRT response measures. CRT was associated with suppression of PBMC expression of IL-1β (1.80-fold decrease, P = 0.047), FOS proto-oncogene (FOS) (3.25-fold decrease, P = 0.01), dual specificity phosphatase 1 (DUSP1) (2.05-fold decrease, P = 0.001), and early growth response 1 (EGR1) (7.38-fold decrease, P = 0.03), and suppression was greater in responders vs. non-responders (P = 0.03 for IL-1β, P = 0.02 for FOS, P = 0.02 for DUSP1, and P = 0.11 for EGR1). Baseline FOS and DUSP-1 levels were greater in responders vs. non-responders (6.15-fold higher, FOS, P = 0.002; 2.60-fold higher, DUSP1, P = 0.0001). CRT responders but not non-responders showed higher baseline gene expression of FOS (P = 0.04) and DUSP1 (P = 0.06) compared with control patients without heart failure. Baseline serum high-sensitivity C-reactive protein levels were 3.47-fold higher in CRT responders vs. non-responders (P = 0.008). Conclusion Treatment of heart failure with CRT resulted in decreased PBMC expression of genes linked to inflammation. Moreover, CRT responders had higher expression of these inflammatory genes prior to CRT and greater suppression of these genes after CRT compared with non-responders.
Fungal and Bacterial Infections in Acute Myeloid Leukemia Patients Treated with Induction Regimens Including Fludarabine: A Retrospective Analysis of 224 Cases.
Authors: Michele Malagola, Annalisa Peli, Daniela Damiani, Anna Candoni, Mario Tiribelli, Giovanni Martinelli, Pier Paolo Piccaluga, Stefania Paolini, Francesco Lauria, Monica Bocchia, Marco Gobbi, Ivana Pierri, Alfonso Zaccaria, Eliana Zuffa, Patrizio Mazza, Giancarla Priccolo, Luigi Gugliotta, Alessandro Bonini, Giuseppe Visani, Skert Cristina, Bergonzi Cesare, Roccaro Aldo, Fili Carla, Renato Fanin, Michele Baccarani, Domenico Russo
Journal: Blood (2007)