tbuckley/cabot-search huggingface dataset:
Abstract 173: Development of an Auto-Segmentation Technique Using a Convolutional Neural Network for the Segmentation of the Ventricular Cavity in Zebrafish
Authors: Tanveer Ashwini Teranikar, Xin Ma, Zachary Bailey, Jessica Lim, Bijan Gaire, Martin Hirsch, Won Hwa Kim, Juhyun Lee
Journal: Circulation Research (2019)

Light sheet fluorescence microscopy (LSFM) with a synchronization algorithm is a unique imaging technique that can be used to image the beating zebrafish heart in 4-dimensions (4-D). However, natural arrhythmic diastolic and systolic contraction and relaxation of the heart can cause aberrations in 4-D image reconstruction. These aberrations are observed as blurred lines, spikes, or holes in the myocardium of the heart, which can lead to complications when analyzing biomechanics by computational fluid dynamics (CFD). In this study, we imaged a beating zebrafish heart at 4 days post fertilization (dpf) using a 10x objective lens with our single-sided LSFM system scanning with a 2 μm step size. The obtained images were analyzed in 3-D to ensure that there were limited aberrations in the wall of the myocardium. Then, the ventricular cavity of these 3-D images was hand segmented at various time points that were spaced within two cardiac cycles. These hand segmented images were used to train a convolutional neural network (CNN) which would have the capability of performing segmentation of the ventricular chamber automatically. This auto-segmentation tool was then used to segment the ventricular cavity of ten samples contained within one cardiac cycle that had not previously been used for training purposes. The ventricular volume of these ten images calculated after auto-segmentation was found to be comparable to the images when hand segmented. Then, a Gaussian wavelet filter was used after auto-segmentation to remove aberrations and minimize errors in the CFD simulation. Both the auto-segmented images and the hand-segmented images were analyzed using a CFD solver to simulate the hemodynamic shear stress through the cardiac cycle. The results from these simulations showed no significant difference between shear stress when the images were hand-segmented or auto-segmented, and there was no leakage observed between the two sets. The results using the auto-segmentation code are promising for future applications in cardiac research where low-quality images obtained under fast acquisition times can be enhanced without the traditional costly deconvolution techniques. This can lead to faster and more accurate analysis of the ventricular cavity for related diseases.
A Novel Human CD34(+) Subset That Constitutively Expresses the High Affinity Interleukin-2 Receptor Traffics to Lymph Nodes and Differentiates into CD56Bright Natural Killer Cells.
Authors: Aharon G. Freud, Brian Becknell, Sameek Roychowdhury, Hsiaoyin C. Mao, Amy K. Ferketich, Gerard J. Nuovo, Tiffany L. Hughes, Trent B. Marburger, John Sung, Robert A. Baiocchi, Martin Guimond, Michael A. Caligiuri
Journal: Blood (2004)
Transgenic Blimp-1 Promoter Directs Hematopoietic Specific Gene Expression in Mice.
Authors: Ding-Yan Wang, Xiao-Yan Wen, Bo Gao, Gillian Sleep, Lihua Zhuang, Chang-Xin Shi, Zhihua Li, Yi Zhao, Hui Deng, Nadine Mbuyi, Tian-Ru Jin, Joseph Cheung, A. Keith Stewart
Journal: Blood (2004)
Comparable 2-Year-Overall and Progression Free Survival Among Unrelated Cord Blood Transplantation, Unrelated Bone Marrow Transplantation, and Related Peripheral Blood Stem Cell Transplantation In Adult Patients With Standard-Risk Hematological Diseases; A Single Center Retrospective Analysis
Authors: Aya Nishida, Daisuke Kaji, Hikari Ota, Kazuya Ishiwata, Masanori Tsuji, Hisashi Yamamoto, Shinsuke Takagi, Yuki Asano-Mori, Go Yamamoto, Naoyuki Uchida, Koji Izutsu, Atsushi Wake, Shigeyoshi Makino, Shuichi Taniguchi
Journal: Blood (2013)
Abstract 369: Epigenetic Regulation of Cardiomyocyte Proliferation and Regeneration by Swi/snf Complex Subunit Arid1a
Authors: Cornelis J Boogerd, Ilaria Perini, Phit La, Britt van der Swaan, Jari B Berkhout, Lieneke Kooijman, Danielle Versteeg, Eva van Rooij
Journal: Circulation Research (2019)

Adult mammalian hearts do not regenerate following ischemic injury, causing permanent damage to the myocardium, often leading to heart failure. In contrast, neonatal mouse hearts can fully regenerate after injury, however this ability is lost few days after birth. Loss of regenerative capacity coincides with profound changes in the epigenetic landscape. Yet, the mechanisms controlling cardiomyocyte proliferation remain poorly understood. To identify epigenetic mechanisms that underlie cardiomyocyte regeneration in response to ischemic injury, we subjected mice to sham or ischemia-reperfusion injury (IR) and performed RNA-Seq at multiple timepoints after injury. Multiple SWI/SNF chromatin remodeling complex subunits were upregulated after IR, including the AT-rich interactive domain-containing protein 1A ( Arid1a ), which has previously been implicated in tissue regeneration. Here, we show that Arid1a is abundantly expressed in cardiomyocytes during development, and is reactivated in a subset of adult cardiomyocytes after IR. Moreover, ARID1A is highly expressed in cardiomyocytes in human failing hearts, suggesting an important function in injury response. Cardiomyocyte-specific Arid1a ablation around birth ( Arid1a cKO ) in mice induced cardiomyocyte hyperplasia, and severe cardiac enlargement at 2 weeks of age. Arid1a cKO hearts displayed increased expression of key cell cycle genes, and HIPPO target genes, suggesting Arid1a is required for cell cycle withdrawal in neonatal cardiomyocytes. When Arid1a was inducibly removed from adult cardiomyocytes ( Arid1a icKO ), hearts had normal gross morphology without visible signs of cardiac pathology. Next, we performed IR injury on Arid1a icKO mice and observed increased cell cycle activity in mutant border zone cardiomyocytes. To further explore the mechanisms by which Arid1a functions in cardiomyocytes, we are currently performing ChIP-Seq and protein interaction studies. These data suggest that Arid1a regulates cardiomyocyte proliferation and function. Upregulation of Arid1a in cardiomyocytes after injury may suppress proliferation and regeneration. Suppression of Arid1a after ischemic injury may prove to be a novel target for therapeutics to enhance cardiac regeneration.
Abstract 273: The Role of Estrogen in Protection of Skeletal Muscle Function in Diastolic Dysfunction
Authors: Somik Chatterjee, Shumin Li, Aijun Zhang, Indira Vedula, Judy A AlRukby, Dale J Hamilton, Anisha A Gupte
Journal: Circulation Research (2019)

Diastolic dysfunction (DD) is prevalent in elderly post-menopausal women. In addition to impaired cardiac relaxation and output, DD is associated with loss of skeletal muscle mass, muscle strength and function, and exercise capacity. Understanding the mechanisms of estrogen (E2)-mediated regulation of skeletal muscle structure and function in DD can have broader implications in understanding the progression of heart disease in post-menopausal women. In muscle, E2 regulates autophagy and mitophagy, processes that orchestrate degradation and recycling of damaged cellular components to maintain healthy tissue and conserve energy. However, this role of E2 under a physiological stress such as DD, is largely unknown. Our study aimed to understand the relationship between E2, autophagy/mitophagy and muscle function in DD. We hypothesized that estrogen receptor (ER) signaling plays a direct role in regulation of autophagy and mitophagy-mediated maintenance of muscle mass and muscle mitochondrial function in DD. Sham or ovariectomy (OVX) surgeries were performed to induce E2-deficiency, followed by induction of DD by administering hypertension agents L-NAME and angiotensin II. NMR analysis revealed significantly reduced total lean mass in OVX mice with DD, further confirmed by direct measurement of gastrocnemius muscle mass. Expression of ERα target-genes PDK4 and STAT3 were reduced in muscle of OVX mice with DD. DD significantly reduced LC3B II/I ratio in muscle, indicative of reduced autophagy. Consistent with this, expression of transcription factor FoxO3, a master-regulator of multiple autophagy and mitophagy genes, was reduced in OVX mice with DD compared to sham control mice. Expression of SDHA gene coding for mitochondrial respiratory chain subunit II, was reduced in sham and OVX mice with DD compared to sham control mice. Mitochondrial respiratory function measured from isolated muscle mitochondria, was reduced in sham and OVX mice with DD compared to sham control mice, and in OVX mice with DD compared to OVX control mice, indicating compromised skeletal muscle mitochondrial function. Our findings indicate that OVX-induced E2-deficiency and DD leads to muscle impairments, including defects in mitochondrial function.
HLA Screening for Dapsone Hypersensitivity in India—A Long Way Ahead—In Reply
Authors: Hong Liu, Zhenzhen Wang, Furen Zhang
Journal: JAMA Dermatology (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 Dermatology 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 Dermatology journal
Increasing screening for latent tuberculosis in patients with hematologic malignancy: A quality improvement project.
Authors: Nicole Veloce, Maverick Chan, Julie Seemangal, Andrea Zwolinski, Abdullah S Al Saleh, Luciana Garcia, Laura Anne Habib, Jai Jayakar, Miriam Kimpton, Jane Batt, Lisa K. Hicks
Journal: Journal of Clinical Oncology (2019)

264 Background: Latent tuberculosis infection (LBTI) affects about one quarter of the world population. Treating LTBI is the most effective way of preventing active TB. Patients with hematologic malignancy (HM) and LTBI are at heightened risk (2-40 times baseline) of progressing to active TB. Universal TB screening is recommended for this population. In 2016, a patient receiving chemotherapy for myeloma at our center developed active TB. This triggered an intensive contact tracing investigation involving local public health units, infection control, and specialists. Over 800 patients had one or more exposures to the index case. No cases of secondary TB were identified; however, the contact tracing was resource intensive and stressful for patients and staff. This project aims to prevent future incidents by developing a standardized process for completing and documenting TBSTs, ensuring LTBIs are identified and managed prior to systemic therapy for HM. We aimed to complete and document TBSTs in ≥85% of patients starting systemic therapy for HM by Feb 2018. Methods: Baseline data was determined via retrospective review of 25 patients receiving chemotherapy for HM Jul-Nov 2017. An order set, work flow process map and standard operating procedure were created over a series of plan-do-study act cycles. TBST was added to a pre-existing “ready for treatment” checklist employed by pharmacists at our site. When pharmacists could find no record of a TBST result prior to treatment, the treating physician was notified. The go-live date was Aug 15, 2018. The impact of change was evaluated via chart review of patients who started chemotherapy for HM between Aug 27, 2018-Feb 27, 2019. Results: Prior to implementation of the standardized process, 3/25 patients (12%) had documentation of prior TBST. Following implementation of the standardized process, 14/30 patients (47%) had documentation of TBST prior to starting systemic therapy for HM. All 14 patients had negative TBSTs. Conclusions: Developing a standardized process for ordering, completing, and documenting TBST for patients starting systemic therapy for HM is feasible and effective. Additional revisions of the process are required to meet our target.
The Unmet Need for Extended Thromboprophylaxis in Acutely Ill Medical Patients: The Findings of IMPROVE, ENDORSE and EXCLAIM.
Authors: Frederick A Anderson, Russell D Hull, Sebastian M Schellong, Bruno Deslandes, Victor F Tapson, Meyer Michel Samama, Alexander GG Turpie, Roger D Yusen, Herve Decousus, Alexander T Cohen, Manuel Monreal
Journal: Blood (2008)
Management of Acute Leukemia Relapse After Allogeneic Hematopoietic Stem Cell Transplantation: Comparison of Different Salvage Strategies
Authors: Michela Tassara, Elisa Sala, Massimo Bernardi, Consuelo Corti, Jacopo Peccatori, Maria Teresa Lupo Stanghellini, Andrea Assanelli, Matteo Carrabba, Elena Guggiari, Sarah Marktel, Francesca Lunghi, Magda Marcatti, Daniela Clerici, Fabio Ciceri, Chiara Bonini
Journal: Blood (2011)
Abstract 338: Motivating Myosin: 2 deoxy-ATP Induced Structural Alterations That Increase Myosin Activity
Authors: Michael Regnier
Journal: Circulation Research (2019)

When 2-deoxy-ATP (dATP) replaces ATP as the contractile substrate, cardiac myosin binding to actin and the rate of cross-bridge cycling is increased. To understand the structural basis of this we employed low-angle x-ray diffraction and computational modeling. Molecular Dynamics (MD) simulations of pre-powerstroke myosin suggest dADP.Pi (vs. ADP.Pi) induces changes in contact pairs for nucleotide binding that translate to structural changes on the actin binding surface, exposing positive charge in regions that make electrostatic interactions with actin. Brownian Dynamics simulations suggest M.dADP.Pi binds more rapidly to actin at distances (angstrom) associated with weak binding. X-ray diffraction analysis of resting demembranated cardiac muscle indicated a large increase in the I 1,1 /I 1,0 intensity ratio for M.dADP.Pi, suggesting myosin moves towards thin filaments. This difference was eliminated at low ionic strength (100 vs. 170mM), where more protein surface charge is exposed, thus decreasing the electrostatic interaction advantage of M.dADP.Pi. The S M3 meridional reflection indicated spacing between myosin crowns was increased for M.dADP.Pi at rest, making it similar was to the activated position of M.ADP.Pi during contraction, with no change in axial ordering ( I M3 ).In intact soleus muscle of transgenic mice with 1% dATP (99% ATP), time-resolved x-ray structure indicates myosin dissociation from actin following tetanic contraction is slightly slower (vs WT) bu the first-order myosin layer line ( MLL1 ) intensity recovers faster, suggesting dATP increases the rate myosin heads return to an ordered resting state. At rest the radii to the center of mass of myosin heads (R m ) and I 1,1 /I 1,0 were larger, indicating myosin heads were closer to actin. MD simulations of post-powerstroke myosin showed greater dADP mobility in the binding pocket via altered interactions with key amino acids, resulting in altered conformation of residues on the actin binding surface in regions interacting with actin. Combined our results suggest that with dATP myosin moves closer to actin and S1 heads are more activated in resting muscle, staying primed for reactivation following relaxation, all via increased myosin-actin electrostatic interactions.
Evaluation of Clinical Usefulness of Monocyte Gating Using CD14 and CD64 for Detecting PNH Clone By Flow Cytometry
Authors: Woo Jae Kwoun, Jeong-Yeal Ahn, Ja Young Seo, Jae Hoon Lee, Hawk Kim, Jinny Park, Kwai Han Yoo, Sung-Ran Cho, Hye Ryoun Kim
Journal: Blood (2018)
Is gender inequity in ventilator management a “women's issue”?
Authors: Marcus J. Schultz, Christian Karagiannidis
Journal: European Respiratory Journal (2019)

<b>Caregivers involved in artificial ventilation need to pay more and special attention to females: due to their shorter height they are at higher risk of receiving non-protective ventilation, which may affect their outcomes</b>http://bit.ly/2HbkG4n
Haemopoietic Improvement Following Iron Chelation for Transfusional Haemosiderosis in Patients with Haematopoietic Neoplasia and Aplastic Anaemia: An Observational Study
Authors: Stephen Opat, Robert Bird, Cecily J Forsyth, Jeffrey Szer, Constantine S. Tam, Penelope Motum, Mark A. Bentley
Journal: Blood (2011)
Abstract 590: EphrinA1-Fc Attenuates Dysfunction and Fibrosis in Nonreperfused Myocardium at 4 weeks Post-MI in WT B6 but Not EphA2-R Mutant Mice
Authors: K'Shylah S Whitehurst, Heather K Estes, Robert C Chase, Uma M Sharma, Jitka A Virag
Journal: Circulation Research (2019)

Each year, an estimated 805,000 US citizens have a new or recurrent myocardial infarction (MI), causing over 360,000 deaths. We have previously reported that a single intramyocardial administration of recombinant ephrinA1-Fc, a member of the ephrinA/EphA family of membrane-anchored receptor tyrosine kinases, significantly reduced ischemic injury and remodeling 4 days in nonreperfused WT B6 mice via reduced apoptosis and inflammation and increased autophagic flux. After acute ischemia/reperfusion (30 min I/24hr or 4 days R) in WT B6 mice, ephrinA1-Fc demonstrated anti-inflammatory effects coupled with complete functional preservation due to modulation of cardiomyocyte ultrastructure and metabolism. The goal of this study is to assess the capacity of a single intramyocardial administration of ephrinA1-Fc at the time of permanent coronary artery ligation to maintain the structural and functional salvage effects through the wound healing process to stable scar formation in both B6 and EphA2-R-M (EphA2 receptor null mutant) mice. At 4 weeks post-MI in WT B6 mice, ephrinA1-Fc improved ejection fraction by 11%, attenuated cardiomyocyte hypertrophy by 38%, and decreased interstitial fibrosis by 35%. In contrast, these parameters were not different or worsened in EphA2-R-M mice treated with ephrinA1-Fc, suggesting that this receptor plays an important role in ephrinA1-Fc-mediated mitigation of the deleterious ventricular remodeling caused by permanent coronary artery occlusion. To further investigate the effects of ephrinA1-Fc directly on fibroblast function, isolated primary mouse cardiac fibroblasts were cultured with ephrinA1-Fc both with and without pro-fibrotic TGF-β stimulation to determine the direct effects of ephrinA1-Fc on col I and III production, remodeling mediators MMP-2, MMP-9, and TIMP-1, as well as signaling molecules DDR2 and SMADs2/3 as potential mechanistic pathways involved. The results of these assays are forthcoming. This study demonstrates the potential of a single administration of ephrinA1-Fc to not only attenuate acute ischemic injury but also mitigate pathological accumulation of interstitial fibrosis and remodeling, thereby reducing ventricular stiffening and the resultant progression to heart failure.
Intracranial Hemorrhage and Mortality In 1461 Patients After Allogeneic Hematopoietic Stem Cell Transplantation For 6-Year Follow-Up: Study Of 44 Cases
Authors: Xiaohui Zhang, Wei Han, Yuhong Chen, Huan Chen, Daihong Liu, Lanping Xu, Kaiyan Liu, Xiaojun Huang
Journal: Blood (2013)
Paraneoplastic Leukemoid Reaction Associated with Increased Levels of and Tumor Overexpression of Receptors for G-CSF, GM-CSF, and IL-6: A Clinico-Pathological-Molecular Study
Authors: Alejandro Recio Boiles, Eric M. Lander, George S. Watts, Steffan T. Nawrocki, Andrew M. Yeager
Journal: Blood (2018)
Abstract 351: Suppression of Store Operated Ca <sup>2+</sup> Entry Components, dStim and dOrai, Results in Dilated Cardiomyopathy
Authors: Courtney Petersen, Jeremy T Smyth, Matthew J Wolf
Journal: Circulation Research (2019)

Cardiac disease is a leading cause of morbidity and mortality throughout the western world with current treatment options limited to palliative pharmacological or invasive therapy. The discovery of curative treatments will rely on thorough understanding of the molecular mechanisms that govern cardiac patho-physiology. Significantly, irregularities in calcium (Ca 2+ ) homeostasis are a major contributing factor to the pathogenesis of cardiac diseases, and targeting Ca 2+ signaling mechanisms may therefore be an important approach to novel therapeutic development. Our lab has recently identified a requirement for the store operated Ca 2+ entry (SOCE) pathway, whereby Ca 2+ enters the cell in response to endo/sarcoplasmic reticulum (ER/SR) store depletion, in Drosophila cardiac physiology. Heart-specific suppression of key SOCE pathway components, Stim and Orai, induced dilated cardiomyopathy characterized by enlarged end-diastolic and end-systolic diameters and decreased fractional shortening. Animals with SOCE suppression had a significant delay in development and ultimately died considerably earlier than controls, suggesting pathological impairment of cardiac function. Additionally, Stim and Orai suppressed hearts exhibited highly disorganized or disrupted myofibrils, suggesting either defective heart development, tissue remodeling, or degeneration resulting from disrupted Ca 2+ homeostasis. We are currently testing these possibilities by restricting Stim and Orai suppression to specific lifecycle stages, and we are analyzing Ca 2+ transients in intact hearts to determine whether SOCE is required for contractile Ca 2+ cycling or may have a contraction-independent signaling role. Collectively, our results demonstrate an essential role for SOCE in normal cardiac physiology, and present how powerful genetic tools and in vivo analyses in Drosophila will allow us to define the mechanistic basis for this requirement.
Abstract 506: Trpm4 Contributes to Ca <sup>2+</sup> -dependent Triggered Arrhythmias in Pathological Conditions
Authors: Frone Vandewiele, Griet Jacobs, Andy Pironet, Wouter Oosterlinck, Rudi Vennekens
Journal: Circulation Research (2019)

Rationale: TRPM4 is a Ca 2+ -activated non-selective cation channel that is abundantly expressed in the heart. Mutations in the Trpm4 gene are associated with human cardiac conduction disorders, including Progressive Familial Heart Block type I (PFHBI) and Brugada Syndrome. However, the mechanistic role and in vivo significance of TRPM4 in the triggering of cardiac arrhythmias is still completely unclear. Objective: To investigate the role of TRPM4 during pathological Ca 2+ handling in the heart. Methods and results: Using three in vivo pro-arrhythmic assays, we found that Trpm4 -/- mice show a reduced arrhythmic burden compared to control mice. First, aconitine intoxication resulted in severe cardiac arrhythmias, both in WT and Trpm4 -/- animals, but Trpm4 -/- mice developed significantly less ventricular ectopic beats (VEBs) and showed a lower arrhythmic score. Second, during ischemia-reperfusion, induced by 30 min of LAD ligation, significantly more WT animals developed arrhythmias compared to Trpm4 -/- mice. Third, catecholaminergic polymorphic ventricular tachycardia (CPVT) mice, carrying mutations in RyR2, were subjected to a stress test. Significantly more RyR +/R2474S -Trpm4 +/+ animals developed arrhythmias compared to RyR +/R2474S -Trpm4 -/- mice. Conclusion: Our data establish that TRPM4 represents a novel target in the prevention and treatment of cardiac arrhythmias.
Patient Characteristics Associated With Receiving Hematopoietic Stem Cell Transplantation In An Older, Transplant-Appropriate MDS Cohort: The MDS-TAO Study
Authors: Gregory A. Abel, Haesook T. Kim, David P. Steensma, Angel M Cronin, Kristofer D. Earles, Corey S. Cutler, Yi-Bin Chen, Richard M. Stone, Robert J. Soiffer
Journal: Blood (2013)