tbuckley/cabot-search huggingface dataset:
Abstract P034: Bone Marrow--Derived Cells Are Not an Essential Component in Cardiosphere Formation
Authors: Jianqin Ye, Andrew Boyle, Yerem Yeghiazarians
Journal: Circulation Research (2011)

Background: Cardiospheres (CS) are composed of heterogeneous population of cells but it is unknown whether bone marrow derived cells are an essential cell component in CS formation. Methods: Chimera mice were generated by transplantation of bone morrow cells from GFP transgenic mice to irradiated C57BL mice. Mice were randomized into 3 groups 5 months after transplantation: 1) myocardial infarction; 2) sham operated; 3) un-operated (n=5/group). Hearts were harvested 2-weeks post-surgery. Cardiac explants were cultured and putative cardiosphere forming cells (CFCs) (small cells migrating out from the explants) were collected 14 days later and reseeded on new culture dishes for CS formation. The number of CS from each heart was counted at 3 days. CS cell composition was analyzed by FACS. To further analyze the role of bone marrow derived CD45+ cells in forming CS, CD45+ cells was isolated from CFCs by CD45 antibody coated immunomagnetic beads. The number of CS formed from 1×10 5 putative CFCs, CFCs without CD45+ cells and CD45+ cells from CFCs (n=6-9/cell type) respectively were also counted at 3 days in culture. Results: Compared to sham (122± 23/heart) and un-operated hearts (18± 5/heart), infarcted hearts formed more CS (357± 64/heart, P&lt;0.01). In all groups, irrespective of any surgery, 18.4± 4.5% of cells in CS co-expressed GFP and CD45, indicating they originated in bone marrow. Low percentage of bone marrow stem/progenitor cells (3.9% Sca-1+GFP+CD45+ and 1% c-Kit+GFP+CD45+ cells) were detected in CS, but a high percentage of cells within CS were cardiac stem/progenitor cells (26.3± 9.4% cells were Sca-1+GFP-CD45-, 0.10± 0.04% c-Kit+GFP-CD45-). Depleting CD45+ cells from putative CFCs actually increased the formation of CS (67±10 CS/1×10 5 cells) compared to un-depleted CFCs (51± 6 CS/1×10 5 cells, P&lt;0.0001). Purified CD45+ cells from CFCs did not form CS in culture. Conclusion: Myocardial infarction increases the formation of CS in culture. Bone marrow derived CD45+ cells make up a small percentage of CS, but are not necessary for CS formation.
Long-Term Safety and Efficacy of Drug-Eluting Stents
Authors: AntonioMarzocchi, FrancescoSaia, GiancarloPiovaccari, AntonioManari, EnricoAurier, AlbertoBenassi, AlbertoCremonesi, GianfrancoPercoco, ElisabettaVarani, PaoloMagnavacchi, PaoloGuastaroba, RobertoGrilli, AleardoMaresta
Journal: Circulation (2007)

Background— The long-term safety and efficacy of drug-eluting stents (DES) have been questioned recently. Methods and Results— Between July 2002 and June 2005, 10 629 patients undergoing elective percutaneous coronary intervention with either DES (n=3064) or bare-metal stents (BMS, n=7565) were enrolled in a prospective registry comprising 13 hospitals. We assessed the cumulative incidence of major adverse cardiac events (death, acute myocardial infarction, and target-vessel revascularization) and angiographic stent thrombosis during 2-year follow-up. A propensity score analysis to adjust for different baseline clinical, angiographic, and procedural characteristics was performed. The 2-year unadjusted cumulative incidence of major adverse cardiac events was 17.8% in the DES group and 21.0% in the BMS group (P=0.003 by log-rank test). Angiographic stent thrombosis was 1.0% in the DES group and 0.6% in the BMS group (P=0.09). After adjustment, the 2-year cumulative incidence of death was 6.8% in the DES gro...
Abstract 303: Novel role of nuclear BH3-only protein BNIP3 in regulation of cellular proliferation
Authors: Amandeep Singh, Meghan Azad, Spencer Gibson
Journal: Cancer Research (2018)

Abstract The objective of this study is to investigate the role of Bcl-2 nineteen kilodalton interacting protein 3 (BNIP3) in regulating cellular proliferation and identifying the proliferation pathways mediated by BNIP3. BNIP3 is a BH3-only proapoptotic member of Bcl-2 family of cell death regulating proteins. The function of BNIP3 is dependent on its localization and expression levels. Under normal conditions, low levels of BNIP3 are present in the nucleus of cells. Low oxygen or hypoxic conditions lead to increased expression of BNIP3, and high levels of BNIP3 are found in the cytoplasm. Cytoplasmic BNIP3 is associated with caspase-independent apoptotic cell death through mitochondria. If, however, BNIP3 levels are increased in the nucleus, it promotes survival of cells by transcriptionally inhibiting several apoptosis-inducing factors. High levels of BNIP3 in nucleus are seen in majority of glioblastoma tumors, where hypoxic environment of tumor core causes an increase in expression of BNIP3 but high amounts of BNIP3 localize to the nucleus, possibly aiding in the survival of the tumor cells. In this study, we found that BNIP3 knockout mice brains have increased cellularity compared to wild-type brains. We also found that both mouse primary astrocytes and embryonic fibroblasts (MEFs) lacking BNIP3 expression have an increased capacity for proliferation compared to wild-type MEFs. Overexpressing BNIP3 in the nucleus of HEK 293 cells also resulted in reduced proliferation. In contrast, both astrocytes and MEFs lacking BNIP3 failed to show differences in cell death compared to wild-type cells. This reveals a novel function for BNIP3 in regulating cellular proliferation that may lead to new targets for cancer therapy. In future studies, we will identity genes regulated by nuclear BNIP3 that may lead to suppression of cellular proliferation in cancer cells. Citation Format: Amandeep Singh, Meghan Azad, Spencer Gibson. Novel role of nuclear BH3-only protein BNIP3 in regulation of cellular proliferation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 303.
Cellular Basis for the Electrocardiographic J Wave
Authors: Gan-XinYan, CharlesAntzelevitch
Journal: Circulation (1996)

Background The J wave is a deflection that appears in the ECG as a late delta wave following the QRS or as a small secondary R wave (R′). Also referred to as an Osborn wave, the J wave has been observed in the ECG of animals and humans for more than four decades, yet the mechanism underlying its manifestation is poorly understood. The present study investigates the cellular basis for the J wave using an isolated arterially perfused preparation consisting of a wedge of canine right or left ventricle. Methods and Results A 12-lead ECG was initially recorded in vivo. After isolation and arterial perfusion of the right or left ventricular wedge, transmembrane action potentials were simultaneously recorded from epicardial, M region, and endocardial transmural sites with three floating microelectrodes. A transmural ECG was recorded concurrently. A J wave was observed at the R-ST junction of the ECG in 17 of 20 adult dogs, usually in leads II, III, aVR, and aVF and the mid to lateral precordial leads. The J wave...
Bendamustine followed by obinutuzumab and venetoclax in chronic lymphocytic leukaemia (CLL2-BAG): primary endpoint analysis of a multicentre, open-label, phase 2 trial
Authors: Paula Cramer, Julia von Tresckow, Jasmin Bahlo, Sandra Robrecht, Petra Langerbeins, Othman Al-Sawaf, Anja Engelke, Anna-Maria Fink, Kirsten Fischer, Eugen Tausch, Till Seiler, Ludwig Fischer von Weikersthal, Holger Hebart, Karl-Anton Kreuzer, Sebastian Böttcher, Matthias Ritgen, Michael Kneba, Clemens-Martin Wendtner, Stephan Stilgenbauer, Barbara Eichhorst, Michael Hallek
Journal: The Lancet Oncology (2018)
Cellular Basis for the Brugada Syndrome and Other Mechanisms of Arrhythmogenesis Associated With ST-Segment Elevation
Authors: Gan-XinYan, CharlesAntzelevitch
Journal: Circulation (1999)

Background—The Brugada syndrome is characterized by marked ST-segment elevation in the right precordial ECG leads and is associated with a high incidence of sudden and unexpected arrhythmic death. Our study examines the cellular basis for this syndrome. Methods and Results—Using arterially perfused wedges of canine right ventricle (RV), we simultaneously recorded transmembrane action potentials from 2 epicardial and 1 endocardial sites, together with unipolar electrograms and a transmural ECG. Loss of the action potential dome in epicardium but not endocardium after exposure to pinacidil (2 to 5 μmol/L), a K+ channel opener, or the combination of a Na+ channel blocker (flecainide, 7 μmol/L) and acetylcholine (ACh, 2 to 3 μmol/L) resulted in an abbreviation of epicardial response and a transmural dispersion of repolarization, which caused an ST-segment elevation in the ECG. ACh facilitated loss of the action potential dome, whereas isoproterenol (0.1 to 1 μmol/L) restored the epicardial dome, thus reducing...
Exaggerated Endothelin Release in High-Altitude Pulmonary Edema
Authors: ClaudioSartori, LaurentVollenweider, Bernd-MichaelLöffler, AlainDelabays, PascalNicod, PeterBärtsch, UrsScherrer
Journal: Circulation (1999)

Background—Exaggerated pulmonary hypertension is thought to play an important part in the pathogenesis of high-altitude pulmonary edema (HAPE). Endothelin-1 is a potent pulmonary vasoconstrictor peptide that also augments microvascular permeability. Methods and Results—We measured endothelin-1 plasma levels and pulmonary artery pressure in 16 mountaineers prone to HAPE and in 16 mountaineers resistant to this condition at low (580 m) and high (4559 m) altitudes. At high altitude, in mountaineers prone to HAPE, mean (±SE) endothelin-1 plasma levels were ≈33% higher than in HAPE-resistant mountaineers (22.2±1.1 versus 16.8±1.1 pg/mL, P<0.01). There was a direct relationship between the changes from low to high altitude in endothelin-1 plasma levels and systolic pulmonary artery pressure (r=0.82, P<0.01) and between endothelin-1 plasma levels and pulmonary artery pressure measured at high altitude (r=0.35, P=0.05). Conclusions—These findings suggest that in HAPE-susceptible mountaineers, an augmented release...
Abstract 652: Mutational profile of papillary thyroid microcarcinoma with extensive lymph node metastasis: Comparison of primary thyroid cancer and metastatic lymph nodes
Authors: Min Ji Jeon, Won Gu Kim, Sung Min Chun, Dong Eun Song, Tae Yong Kim, Young Kee Shong, Won Bae Kim
Journal: Cancer Research (2018)

Abstract Introduction: Papillary thyroid microcarcinoma (PTMC) has excellent clinical outcomes, but distant metastasis of PTMC can be fatal. We previously reported that change to an aggressive pathologic subtype of metastatic lymph nodes (LNs) were associated with distant metastasis of PTMC. This study aimed to evaluate and compare the mutational profile of primary tumor and metastatic LNs of PTMC. Method: We included 16 PTMC patients with lateral cervical LN metastases. One of them has distant metastases. DNAs from formalin-fixed, paraffin-embedded archival samples of 16 sets of the normal thyroid tissue, primary PTMC, and the largest metastatic LN were used for targeted next-generation sequencing by Oncopanel AMC version 2.0. Results: A total of 7 somatic variants were confirmed in primary PTMC compared to normal thyroid tissue. BRAF V600E mutation was the most common and seen in 12 primary PTMCs (75%) and 11 metastatic LNs (69%). Missense mutation of KMT2A, RAF1, and ROS1 was detected only in one primary PTMC (6.3%), respectively. Frame-shift mutation of JAK2, inframe deletion of ACVR2A and nonsense mutation of AR was detected one primary PTMC (6.3%) with its metastatic LN, respectively. When we compare the mutational profile of primary tumor and metastatic LNs, there were no newly developed somatic mutations in metastatic LNs. We also found ALK/STRN rearrangement in one PTMC with its metastatic LN (6.3%). CCDC6/RET rearrangement and RET intergenic rearrangement was detected only in 2 metastatic LNs (12.5%) and one metastatic LN (6.3%), respectively. BARD1 deletion was detected in one primary PTMC with its metastatic LNS (6.3%) and FLT4 deletion was detected only in one primary PTMC (6.3%). We also found JAK1, AURKC, and TP53 deletions, which were detected only in one metastatic LN, respectively (6.3%). Conclusion: The mutation frequency of PTMC was really low even in patients with extensive LN metastasis. The mutational status of primary tumor and their regional metastatic LNs were not significantly different and this suggests the minor role of genetic mutations in the process of LN metastases. Citation Format: Min Ji Jeon, Won Gu Kim, Sung Min Chun, Dong Eun Song, Tae Yong Kim, Young Kee Shong, Won Bae Kim. Mutational profile of papillary thyroid microcarcinoma with extensive lymph node metastasis: Comparison of primary thyroid cancer and metastatic lymph nodes [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 652.
Abstract 1476: Landscape of fusion RNAs generated by cis-spliced adjacent genes in cancer and normal physiology
Authors: Fujun Qin
Journal: Cancer Research (2018)

Abstract The fusion RNA, SLC45A3-ELK4, was found to be a product of cis-splicing between the two adjacent genes (cis-SAGe). Previously, we used LNCaP, a prostate cancer cell line as a model, and identified 16 additional cis-SAGe events by silencing transcription factor CTCF and paired-end RNA sequencing. One out of the 16 fusion RNAs, D2HGDH-GAL3ST2, is more frequently seen in cancer samples, and seems to be enriched in the African American group. It is more frequently detected in late stage cancer, suggesting a role in cancer progression. By studying the features associated with the 16 fusions, we developed a set of rules: 1) the parental genes are same-strand-neighboring genes, 2) the distance of between the genes is within 30kb; 3) the 5' genes are actively transcribing; and 4) the fusion RNAs tend to have the second-to-last exon in the 5' genes joined to the second exon in the 3' genes. To investigate the cis-SAGe fusion RNAs at global, we first randomly selected 20 neighboring genes in the genome, and detected four fusion events using these rules in prostate cancer and non-cancerous cells. To further understand the cis-SAGe fusions in human tissues and cells, we then performed, curated and analyzed nearly 300 RNA-seq libraries covering 30 different non-neoplastic human tissues and cells. More than 10,000 fusion transcripts were found. We focused on the neighboring fusions and performed analysis. Appling our cis-SAGe rules, we identified around 1486 cis-SAGe fusion candidates. A few sequence motifs were found enriched close to the fusion junction sites. We performed functional experiments on a few widely expressed fusions, such as ADCK4-NUMBL, CLN6-CAML4, DUS4L-BCAP29, and found that silencing them resulted in dramatic reduction in moral cell growth and /or motility. Citation Format: Fujun Qin. Landscape of fusion RNAs generated by cis-spliced adjacent genes in cancer and normal physiology [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1476.
Abstract 1416: Pan-cancer mutual vulnerability and viability
Authors: Huwate Yeerna, William Kim, William C. Hahn, Jill Mesirov, Pablo Tamayo
Journal: Cancer Research (2018)

Abstract We used a skew-distribution-based statistical methodology to fit parametric models of cell-viability profiles from genome-wide RNAi-gene knockdowns. We identify the subset of genes with the highest degree of skewness that represent most oncogenes and tumor suppressors. We decomposed those genes using matrix decomposition in order to define mutual vulnerabilities. The resulting matrix decomposition components represent coordinated patterns of gene dependency shared by many genes in many cell lines across cancer types. We identify the most salient mutual vulnerabilities, generate a comprehensive catalog of them, and annotate them based on their association with a variety of genomic features including: gene, protein, and pathway expression, mutational landscape, copy number alterations, promoter methylations, metabolites, miRNAs, and drug sensitivities. We also generate an Onco-GPS (Oncogenic Positioning System) Map that provides a summary and visual representation of the mutual vulnerabilities and their components, and allow us to compare them with their counterparts in Pan-Cancer transcriptional and drug sensitivity spaces. Citation Format: Huwate Yeerna, William Kim, William C. Hahn, Jill Mesirov, Pablo Tamayo. Pan-cancer mutual vulnerability and viability [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1416.
Biosynthesis of Epinephrine and Norepinephrine by Sympathetic Nerves and Ganglia
Authors: Normankirshner
Journal: Circulation (1958)

It is generally believed by the neurophysiologists that the sympathetic neurohormone is norepinephrine and not epinephrine as originally supposed. This concept of norepinephrine as the sympathetic neurohormone has evolved from much impressive circumstantial evidence; however, it has not been demonstrated that the biosynthesis of norepinephrine takes place in the sympathetic nerves and ganglia. This paper shows, through the use of labeled precursors, that the sympathetic nerves and ganglia synthesize norepinephrine in a systematic sequence from tyrosine and that this synthesis apparently terminates with norepinephrine rather than progressing to the formation of epinephrine.
Abstract 13955: NEDD9 is Upregulated by Hypoxia and Modulates Platelet Adhesion to Human Pulmonary Artery Endothelial Cells
Authors: George A Alba, Andriy O Samokhin, Bradley M Wertheim, Elena Arons, Julia R Ceglowski, Elisabeth M Battinelli, Bradley A Maron
Journal: Circulation (2017)

Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by local hypoxemia, vascular fibrosis, and in situ thrombosis of pulmonary arterioles. The CAS-L protein NEDD9 regulates colla...
Drawing Lessons From Canada’s Experience With Single-Payer Health Insurance
Authors: Joseph White
Journal: JAMA Internal Medicine (2018)

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 Internal Medicine 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 Internal Medicine journal
Optogenetic Control of Synaptic AMPA Receptor Endocytosis Reveals Roles of LTD in Motor Learning
Authors: Wataru Kakegawa, Akira Katoh, Sakae Narumi, Eriko Miura, Junko Motohashi, Akiyo Takahashi, Kazuhisa Kohda, Yugo Fukazawa, Michisuke Yuzaki, Shinji Matsuda
Journal: Neuron (2018)
Art: Arctic art
Authors: Sally Carter
Journal: BMJ (2006)

Put artists, scientists, and educators together on a ship, send them to the Arctic, and see how the artists translate their reactions to the rising sea levels, melting ice, and changes in biodiversity into art. This was the idea that prompted David Buckland, an artist, to set up the Cape Farewell organisation that took three expeditions to the Svalbard archipelago between 2003 and 2005.​2005.




Figure 1



Contextascope by Michele Noach

Credit: CAPE FAREWELL




On these journeys, the artists drew, wrote, photographed, and filmed, and the exhibition at Natural History Museum in London brings together their works. The wide range of media and artists makes this exhibition a fascinating mix and certainly made me think. It also shows that art can be a powerful communicator of the science behind climate change.

From the sparkling skeleton of a whale (Stranded) and Gary Hume's comical painting (Hermaphrodite Polar Bear) to the bleak photographs by David Buckland and Gautier Deblonde, and the eerie soundtrack of cracking, melting ice—all manage to give an insight into the experiences of the artists. During one expedition, an artist discovered an island that had appeared as a glacier retreated. The discovery, claiming, naming, and registration of Nymark (Norwegian for new ground) are recorded in a series of framed documents and photographs.

Photographs show how artist Antony Gormley and architect Peter Clegg collaborated on Three Made Places, ice works made in the Arctic that show the spaces humans occupy individually and collectively. Choreographer Siobhan Davies also concentrates on humans—Endangered Species is a museum display case showing a film projection of a woman dancing in a costume of flexible rods that eventually extinguish her. Trying to combine science with emotion, Michele Noach made a series of images from hundreds of tiny lenses called The Arctic Feel-o-Graphs—fantasy scientific charts and graphs that structure her response to the Arctic environment.​environment.




Figure 2



Ice Burning Ice by David Buckland

Credit: CAPE FAREWELL




If you're feeling inspired by the artworks to do your own bit towards helping the environment, then visit the interactive “ideas tank” where a touch-screen video helps you explore a collection of green ideas, including ecodesign courses, “gooshing” (an online guide to ethical shopping), and home brewed fuel; you can then email the links to yourself.
Abstract 17974: Sulphonylation of SERCA Cysteine-674 Contributes to Cardiac Dysfunction in Endotoxemic Mice
Authors: Ion Hobai, Emmanuel S Buys, Justin C Morse, Jessica Edgecomb, Xiuyun Hou, Alok Khandelwal, Deborah Siwik, Richard A Cohen, Peter Brouckaert, Wilson Colucci
Journal: Circulation (2013)

Background: Functional inhibition of the sarcoplasmic reticulum (SR) calcium (Ca2+) pump (SERCA) contributes to cardiac dysfunction and cardiac Ca2+ dysregulation in sepsis and endotoxemia. Here we...
John Duncan Holden
Authors: Steve Cox
Journal: BMJ (2018)

John Duncan Holden had strong links to the Royal College of General Practitioners, having been a fellow, council member, provost of Mersey Faculty, and recipient of the president’s medal. He had led work on college fellowship by assessment, worked on the membership by assessment of performance (MAP) scheme, and was an “evangelist” for both locally. He achieved his MD when he was 50 and worked on numerous research projects. He was a trainer …