tbuckley/cabot-search huggingface dataset:
Circulatory Bypass of the Right Side of the Heart
Authors: William W. L. Glenn
Journal: New England Journal of Medicine (1958)

IN the first publication of this series of papers attention was called to the need of a method for the direct delivery of venous blood into the pulmonary arterial circulation.1 The congenital anomalies of the heart that might be remedied from this operation are characterized by malfunction of the right atrium or right ventricle or both. More specifically, the cardiac conditions that would benefit from circulatory bypass of the right side of the heart include stenosis or atresia of the tricuspid and pulmonary outflow tracts, Ebstein's anomaly, single ventricle, bilocular heart and transposition of the great vessels with an associated . . .
Mast Cells Are Crucial for Induction of Group 2 Innate Lymphoid Cells and Clearance of Helminth Infections
Authors: Chikako Shimokawa, Takashi Kanaya, Masami Hachisuka, Kenji Ishiwata, Hajime Hisaeda, Yosuke Kurashima, Hiroshi Kiyono, Tomohiro Yoshimoto, Tsuneyasu Kaisho, Hiroshi Ohno
Journal: Immunity (2017)
Cardiac safety analysis for a phase III trial of sunitinib (SU) or sorafenib (SO) or placebo (PLC) in patients (pts) with resected renal cell carcinoma (RCC).
Authors: Naomi B. Haas, Judith Manola, Bonnie Ky, Keith T. Flaherty, Robert G. Uzzo, Christopher G. Wood, Christopher J Kane, Michael A. S. Jewett, Michael B. Atkins, Janice P. Dutcher, Robert S. DiPaola
Journal: Journal of Clinical Oncology (2012)

4500 Background: We performed a cardiac analysis of E2805, a well population of pts with resected high risk RCC. The objectives were to determine if pts treated with SU or SO had clinically significant decreases in left ventricular (LV) ejection fraction (EF) and to describe the frequency of clinically significant heart failure (HF). We also report the frequency of other events including (un)stable angina or myocardial infarction. Methods: EF was measured by multiple gated acquisition scan (MUGA) at baseline, 3, 6, and 12 months (mo), and end of treatment, if symptoms developed, and 3 mo after the last abnormal assessment. The primary cardiac endpoint was defined as an EF decline &lt; the institutional lower limit of normal (ILN) that was a ≥ 16% decline from baseline, and that occurred ≤ 6 mo into therapy. Clinically significant HF was ≥ Grade 3 LV systolic or diastolic dysfunction (severe symptoms with any activity or from drop in EF responsive (Grade 3) or refractory (Grade 4) to therapy. Late LVEF events were a drop in LVEF of ≥ 16% occurring after 6 mo of therapy. Event rates on each treatment arm were calculated, with 90% exact binomial confidence intervals (CI). Results: Post-baseline MUGAs are available for 1589 of 1943 total pts accrued. 1293 pts had MUGA assessment ≥ 6 mo. 21 pts had primary events (Table). 71 pts had worst LVEF declines of ≥16% from baseline, including 52 of which occurred ≤ 6 mo from baseline, with the majority not meeting full primary event criteria. There were 11 reported grade 3 LV systolic events (5 SU, 4 SO and 2 PLC). 8 pts had cardiac ischemia possibly or probably from agent. Only one grade 4 event followed a primary LVEF event. 4 of 7 pts who began treatment with LVEF &lt;ILN had primary LVEF events. Conclusions: In detailed followup of SU and SO use, cardiac function in pts starting with normal EF, was not impaired significantly over placebo. Ischemic events were uncommon and not clearly associated with treatment. The data demonstrate that SU or SO for adjuvant therapy will likely not cause significant cardiac toxicity. [Table: see text]
The Genomic Landscape of Childhood and Adult Acute Erythroid Leukemia
Authors: Ilaria Iacobucci, Ji Wen, Manja Meggendorfer, Catherine Carmichael, John K Choi, Katherine Masih, Yongjin Li, Debbie Payne, Daisuke Tomizawa, Nobutaka Kiyokawa, Laura J. Janke, Thomas B. Alexander, Stanley Pounds, Lei Shi, Marcus Valentine, Giuseppe Basso, Franco Locatelli, Shirley Kham Kow Yin, Allen Yeoh Eng Juh, Ries E Rhonda, Elliot Stieglitz, Andrew Wei, Ian D Lewis, Richard D'Andrea, Benjamin T. Kile, Jinghui Zhang, Mignon L. Loh, Soheil Meshinchi, Torsten Haferlach, Charles Mullighan
Journal: Blood (2016)
Fludarabine-Based Reduced Intensity Hematopoietic Stem Cell Transplantation (RIST) for Patients Aged 50–70 Years with Acute Lymphoblastic Leukemia (ALL) in Remission: A Study From the ALL Working Group of the Japan Society for Hematopoietic Cell Transplantation (JSHCT)
Authors: Heiwa Kanamori, Shinichi Kako, Harumi Kato, Satoshi Nishiwaki, Tatsuo Furukawa, Mari Saito, Shuichi Taniguchi, Hirohisa Nakamae, Toshiaki Yujiri, Tokiko Naganuma-Inoue, Yasuo Morishima, Ritsuro Suzuki, Hisashi Sakamaki, Junji Tanaka
Journal: Blood (2011)
Outcomes of patients with relapsed/refractory Hodgkin lymphoma progressing after autologous stem cell transplant in the current era of novel therapeutics: A retrospective analysis
Authors: Steven M. Bair, Lauren Strelec, Sarah J. Nagle, Sunita D. Nasta, Daniel J. Landsburg, Anthony R. Mato, Alison W. Loren, Stephen J. Schuster, Edward A. Stadtmauer, Jakub Svoboda
Journal: American Journal of Hematology (2017)

Patients with relapsed/refractory Hodgkin lymphoma (RR-HL) who progress or relapse following autologous stem cell transplantation (ASCT) have historically had a poor prognosis. Several novel agents, particularly brentuximab vedotin, have shown efficacy in this setting. However, there remains a paucity of data characterizing outcomes outside of clinical trials and how these novel agents have impacted prognosis in general population of patients with RR-HL. Here, we conducted a retrospective analysis to evaluate outcomes in 87 patients with RR-HL with relapse post-ASCT. Treatment with novel agents (including brentuximab vedotin) was associated with significant improvement in median overall survival (OS) compared to patients who did not receive novel agents (85.6 vs 17.1 months; P < .001). Additional factors associated with improved OS in univariate analysis include treatment with radiation therapy post-ASCT (34.1 vs 17.0 months; P = .015), chemosensitivity (i.e., relapsed compared to primary refractory disease; 51.8 vs 25.6 months; p = 0.013), initial response to ASCT (i.e., CR/PR compared to SD/PD; 46.1 vs 20.4 months; P = .011), and transplantation in 2010 and later compared to prior to 2010 (not reached vs 24.5 months; P = .025). The current study demonstrates markedly improved OS in RR-HL patients treated with novel therapeutics and lends "real world" credence to the role of these agents in improving outcomes in the current era.
Considering the Role of the Laparoscopic Adjustable Gastric Band
Authors: Jon C. Gould
Journal: JAMA Surgery (2017)

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 Surgery 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 Surgery journal
Phase II study of gemcitabine (2′,2′-difluorodeoxycytidine) given as a twice weekly schedule to previously untreated patients with non-small cell lung c
Authors: B. Lund, M. Ryberg, P. Meidahl Petersen, H. Anderson, N. Thatcher, P. Dombernowsky
Journal: Annals of Oncology (1994)
Abstract P194: CCAAT/Enhancer-Binding Protein Beta Negatively Regulates Hemodynamic Stress-Induced Cardiac Hypertrophy
Authors: Jota Oyabu, Osamu Yamaguchi, Takafumi Oka, Shungo Hikoso, Kazuhiko Nishida, Issei Komuro, Kinya Otsu
Journal: Circulation Research (2011)

The CCAAT/enhancer-binding proteins (C/EBP) beta is a member of family of leucine-zipper transcription factors that regulate gene expression to control cellular proliferation, differentiation, inflammation and metabolism. Previous reports showed that the protein and mRNA levels of C/EBP beta were increased in rat ischemia-reperfused or human failing hearts. Recent study indicates an important role of C/EBP beta in physiological cardiac hypertrophic responses. In the present study, we generated cardiac-specific C/EBP beta-deficient mice (CKO) to elucidate its in vivo function in pathological cardiac hypertrophy. We crossed floxed C/EBP beta mice with mice expressing Cre recombinase in cardiac-specific manner. Echocardiographic and physiological analyses revealed that CKO showed no cardiac phenotypes under basal conditions at 10 weeks old, indicating that the C/EBP beta is not essential for mouse heart development. Then, we subjected CKO and control mice (CTL) to pressure overload by means of transverse aortic constriction (TAC). In wild-type mouse hearts, the expression level of C/EBP beta was increased after TAC. One week after TAC, CKO showed left ventricle (LV) hypertrophy (LV/body weight, CKO 4.64 ± 0.08 mg/g versus CTL 4.14 ± 0.06 mg/g, p&lt;0.01, LV mass index, CKO 106.1 ± 1.7 versus CTL 98.5 ± 1.8, p&lt;0.05), without showing contractile dysfunction. Cross-sectional area of cardiomyocytes was increased in CKO after TAC (CKO 373.6 ± 2.1 μm 2 versus CTL 300.5 ± 3.6 μm 2 , p&lt;0.01). The increase in the atrial natriuretic factor (ANF) or alpha skeletal actin mRNA expression, molecular markers for cardiac remodeling, was observed in CKO hearts. Furthermore, overexpression of C/EBP beta in isolated neonatal rat cardiomyocytes inhibited an increase in 3 H-leucine uptake induced by phenylephrine stimulation. C/EBP beta is expressed as three distinct protein isoforms, namely FL, LAP, and LIP, which are encoded by a single gene, but transcribed from different initiation sites. Luciferase reporter gene assay showed that overexpression of LAP isoform attenuated the transcriptional activity of ANF induced by phenylephrine, but not LIP. Thus, we conclude that C/EBP beta attenuates the pathological cardiac hypertrophy induced by hemodynamic stresses.
Effect of Lenalidomide (LEN) Exposure on Response and Outcomes in Patients (Pts) with Lower-Risk Non-Del(5q) Myelodysplastic Syndromes (MDS)
Authors: Guillermo Garcia-Manero, Valeria Santini, Antonio Almeida, Pierre Fenaux, Norbert Gatterman, Keiya Ozawa, Stuart L. Goldberg, Jerry Weaver, Mary M. Sugrue
Journal: Blood (2016)
PTU-016 Albumin restores renal blood flow (RBF) autoregulation in patients with refractory ascites and acute-on-chronic liver failure (ACLF) through stabilisation of endothelial function: Abstract PTU-016 Figure 1
Authors: R Garcia Martinez, J O'Brien, L Noiret, N Davies, R Mookerjee, R Jalan
Journal: Gut (2012)

<h3>Introduction</h3> Haemodynamic alterations in liver failure are associated with endothelial dysfunction, a pro-inflammatory state and sympathetic activation which lead to disturbed RBF autoregulation and renal failure. Albumin is a multifunctional protein that has been shown in several studies to prevent and treat renal dysfunction in patients with advanced cirrhosis and liver failure. We hypothesised that the beneficial effects of albumin in cirrhosis is likely to be through mechanisms in addition to volume expansion. The aims of the study were to investigate the effects of albumin on systemic and renal haemodynamics, inflammation and endothelial dysfunction in refractory ascites and patients with acute kidney injury (AKI) in the setting of ACLF. <h3>Methods</h3> Twenty-two patients were recruited [Group 1, n=12, refractory ascites; Group 2, n=10 patients with AKI admitted with an acute deterioration of their liver function due to either alcoholic hepatitis or infection]. Both groups were treated with Albumin 60 g/d over 3–4 days. Cardiac output (CO) and renal blood flow (RBF) haemodynamics were measured. Endothelial dysfunction was assessed through measurement of von Willebrand factor (vWF) and serum nitrite (NO) levels. F2α Isoprostanes (F2α), resting neutrophil burst and Interleukin (IL)-6 were quantified as markers of oxidative stress, endotoxemia and inflammation respectively. <h3>Results</h3> Albumin therapy was associated with significant improvements in haemodynamic parameters (increased RBF, MAP, decreased CO, HR; p&lt;0.05) which resulted in a shift in the RBF autoregulation curve towards normalisation (Abstract PTU-016 figure 1). In parallel, improvement of renal dysfunction (creatinine, creatinine clearance and Na+ excretion; p&lt;0.05 each), sympathetic activation (noradrenaline levels; p&lt;0.01), inflammation/oxidative stress (F2α and neutrophil burst; p&lt;0.05), endothelial dysfunction (vWF and NO metabolism p&lt;0.05) and the functional capacity of albumin (IMAR p&lt;0.005) was observed. Restoration of RBF correlated inversely with change in vWF (r<sup>2</sup>=0.55, p&lt;0.001). <h3>Conclusion</h3> This study suggests that albumin infusion improves albumin function which has pleiotropic effects and results in a reduction in inflammation and improvement in endothelial function leading to improved systemic haemodynamics and renal blood flow autoregulation. <h3>Competing interests</h3> None declared.
Evaluation of Medical-Technology Strategies
Authors: John P. Bunker, Jinnet Fowles, Ralph Schaffarzick
Journal: New England Journal of Medicine (1982)

RationaleThe current federal policy is to reduce the government's responsibility for health care and its evaluation, substituting market mechanisms whenever possible, and to vest residual control in regional and local authorities. Toward this end, the administration has recommended to Congress sharp reductions in expenditures for medical-technology assessment. This point of view is reflected in the sharply reduced budgets of the National Centers of Health Services Research and Health Statistics and of the research-and-development component of the Health Care Financing Administration, as well as termination of all funding for the National Center for Health Care Technology. The budget of the . . .
Differences in the mechanisms of uptake and endocytosis of small and large chylomicron remnants by rat liver
Authors: E Windler, J Greeve, H Robenek, F Rinninger, H Greten, S Jäckle
Journal: Hepatology (1996)

Initial binding and subsequent endocytosis of small and large chylomicron remnants by rat liver were compared. Small and large chylomicrons were obtained from mesenteric lymph of glucose– or fat–fed rats, respectively. The low–density lipoprotein (LDL) receptor was up– and down–regulated as shown by LDL receptor messenger RNA (mRNA). The rate of removal of small chylomicron remnants by isolated perfused rat livers followed closely the activity of the LDL receptor. When mRNA was undetectable, the uptake was as low as that of lymphatic small chylomicrons. In contrast, the uptake of large chylomicron remnants into perfused rat livers was unaffected by changes of the LDL–receptor activity, but significantly reduced after livers were flushed with heparin or heparinase. Large chylomicron remnants were cleared from plasma much faster than small chylomicron remnants, but were more slowly internalized into hepatocytes. Both, small and large chylomicron remnants entered the pathway of receptor–mediated endocytosis as shown by electron microscopy and analysis of isolated endosomes. Yet, large chylomicron remnants were taken up into the compartment of uncoupling of receptors and ligands and multivesicular bodies at a much slower rate. This was independent of the activity of the LDL receptor and the heparin–releasable binding site. From these findings it is concluded that large chylomicron remnants initially bind rapidly to surface components other than the LDL receptor, one of which may be hepatic lipase. Yet, the consecutive internalization is slow. In contrast, small chylomicron remnants are removed at a slower rate from plasma, binding predominantly to the LDL receptor, but are more readily taken up into endosomes.
Association of Graft-Versus-Host Disease and Immunosuppressive Treatment with Risks of Recurrent Malignancy and Mortality After Allogeneic Hematopoietic Cell Transplantation
Authors: Yoshihiro Inamoto, Mary E.D. Flowers, Stephanie J. Lee, Paul A. Carpenter, Edus H. Warren, H. Joachim Deeg, Rainer F. Storb, Frederick R. Appelbaum, Barry E. Storer, Paul J. Martin
Journal: Blood (2010)
Milk-induced eczema is associated with the expansion of T cells expressing cutaneous lymphocyte antigen.
Authors: K J Abernathy-Carver, H A Sampson, L J Picker, D Y Leung
Journal: Journal of Clinical Investigation (1995)

The extravasation of T cells at sites of inflammation is critically dependent on the activity of homing receptors (HR) involved in endothelial cell recognition and binding. Two such HR (the cutaneous lymphocyte antigen [CLA] and L-selectin) have been shown to be selectively involved in T cell migration to skin and peripheral lymph nodes, respectively. This study was designed to assess the relationship between the organ specificity of an allergic reaction to food and the expression of HR on T cells activated in vitro by the relevant food allergen. Peripheral blood mononuclear cells were isolated from seven milk allergic children with a history of eczema when exposed to milk. All patients had a positive prick skin test and double-blind placebo-controlled food challenge to milk. 10 children with either allergic eosinophilic gastroenteritis or milk-induced enterocolitis and 8 nonatopic adults served as controls. Five-parameter flow cytometry using monoclonal antibodies was used for detection of the specific HR on freshly isolated T cells versus T cell blasts induced by a 6-d incubation with casein, as compared with Candida albicans. After in vitro stimulation with casein, but not C. albicans, patients with milk allergy and atopic dermatitis had a significantly greater percentage of CLA+ T cells (P < 0.01) than controls with milk-induced enterocolitis, allergic eosinophilic gastroenteritis, or nonatopic healthy controls. In contrast, the percentage of L-selectin-expressing T cells did not differ significantly between these groups. These data suggest that after casein stimulation allergic patients with milk-induced skin disease have an expanded population of CLA+ T cells, as compared with nonatopics or allergic patients without skin involvement. We postulate that heterogeneity in the regulation of HR expression on antigen-specific T cells may play a role in determining sites of involvement in tissue-directed allergic responses.
Multigene Testing for Hereditary Cancer: When, Why, and How
Authors: Kenneth Offit
Journal: Journal of the National Comprehensive Cancer Network (2017)

Multigene testing is a complicated area, with advantages and disadvantages of testing for hereditary cancer syndromes. Currently, NCCN does not endorse routing multiplex testing outside of a research setting, and/or intensive genetic counseling regarding risks and benefits. The 2017 NCCN Clinical Practice Guidelines in Oncology for Genetic/Familial High-Risk Assessment: Breast and Ovarian and Colorectal provide suggestions for mutation carriers identified by panel tests.
Breast Cancer Genetic Testing Among African Patients With Breast Cancer
Authors: Emmanuel Amankwaa-Frempong, Francis Agyemang Yeboah, Samuel Blay Nguah, Lisa A. Newman
Journal: JAMA Surgery (2017)

This population-based study of Ghanian women with a family history of breast cancer analyzes breast cancer gene mutations to determine whether the triple-negative breast cancer phenotype is a risk factor for mutation carrier status.
MYC-dependent oxidative metabolism regulates osteoclastogenesis via nuclear receptor ERRα
Authors: Seyeon Bae, Min Joon Lee, Se Hwan Mun, Eugenia G. Giannopoulou, Vladimir Yong-Gonzalez, Justin R. Cross, Koichi Murata, Vincent Giguère, Marjolein van der Meulen, Kyung-Hyun Park-Min
Journal: Journal of Clinical Investigation (2017)

Osteoporosis is a metabolic bone disorder associated with compromised bone strength and an increased risk of fracture. Inhibition of the differentiation of bone-resorbing osteoclasts is an effective strategy for the treatment of osteoporosis. Prior work by our laboratory and others has shown that MYC promotes osteoclastogenesis in vitro, but the underlying mechanisms are not well understood. In addition, the in vivo importance of osteoclast-expressed MYC in physiological and pathological bone loss is not known. Here, we have demonstrated that deletion of Myc in osteoclasts increases bone mass and protects mice from ovariectomy-induced (OVX-induced) osteoporosis. Transcriptomic analysis revealed that MYC drives metabolic reprogramming during osteoclast differentiation and functions as a metabolic switch to an oxidative state. We identified a role for MYC action in the transcriptional induction of estrogen receptor-related receptor α (ERRα), a nuclear receptor that cooperates with the transcription factor nuclear factor of activated T cells, c1 (NFATc1) to drive osteoclastogenesis. Accordingly, pharmacological inhibition of ERRα attenuated OVX-induced bone loss in mice. Our findings highlight a MYC/ERRα pathway that contributes to physiological and pathological bone loss by integrating the MYC/ERRα axis to drive metabolic reprogramming during osteoclast differentiation.
Abstract 145: Apelin Reduces Myocardial Infarction Size and Promotes Angiogenesis by Increasing SDF-1/CXCR4 and AKT/eNOS/VEGF Pathways
Authors: Lanfang Li, Heng Zeng, Jian-xiong Chen
Journal: Circulation Research (2012)

Background: Apelin is an endogenous ligand for the angiotensin-like 1 receptor (APJ) and is emerging as a key player in the regulation of angiogenesis as well as ischemia/reperfusion injury. So far, little is known about the functional role of apelin in myocardial ischemia. We investigated the potential intracellular molecular mechanisms and protective role of apelin during myocardial ischemic injury. Methods and Results: Myocardial ischemia was achieved by ligation of the left anterior descending coronary artery (LAD) for 24 hours and 14 days. Myocardial apoptosis was detected by TUNEL staining. Akt, endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), SDF-1 and CXCR4 expression were measured by western blot. The CD133+/cKit+/Sca1+, CD133/SDF-1+ and cKit/CXCR4+ cells were determined by immunostaining. Myocardial capillary and arteriole densities were analyzed in the border zone of infarcted myocardium at 14 d of ischemia. Treatment of C57BL/6J mice with apelin-13 (1 mg/Kg.d) by i.p. injection for 3 days before surgery results in significant decreases in TUNEL positive cells and myocardial infarct size at 24 hours of ischemia. Treatment with apelin increases the phosphorylation of AKT and eNOS and upregulates VEGF expression in the ischemic heart. Furthermore, treatment with apelin leads to the expression of SDF-1 and CXCR4 and increases in the number of CD133+/cKit+/Sca1+, CD133/SDF-1+ and cKit/CXCR4+ cells in ischemic hearts. Treatment with apelin also significantly increases myocardial capillary densities and arteriole formation together with a significant decrease in the ratio of heart weight to body weight at 14 days of ischemia. This is accompanied by a significant improvement of cardiac function after 14 days of ischemia. Conclusions: Our data demonstrate that apelin contributes to the protection of myocardial infarction and angiogenesis by the mechanisms involving in upregulation of SDF-1/CXCR4 and AKT/eNOS/VEGF pathways.