tbuckley/cabot-search huggingface dataset:
DIMENSIONS OF SOCIOECONOMIC STATUS AND CLINICAL OUTCOME AFTER PRIMARY PERCUTANEOUS CORONARY INTERVENTION
Authors: Lars Jakobsen, Troels Niemann, Niels Thorsgaard, Leif Thuesen, Jens F. Lassen, Lisette Jensen, Per Thayssen, Jan Ravkilde, Hans&ndash;Henrik Tilsted, Frank Mehnert, S&oslash;ren P. Johnsen
Journal: Journal of the American College of Cardiology (2012)
Brain-wide pathway for waste clearance captured by contrast-enhanced MRI
Authors: Jeffrey J. Iliff, Hedok Lee, Mei Yu, Tian Feng, Jean Logan, Maiken Nedergaard, Helene Benveniste
Journal: Journal of Clinical Investigation (2013)

The glymphatic system is a recently defined brain-wide paravascular pathway for cerebrospinal fluid (CSF) and interstitial fluid (ISF) exchange that facilitates efficient clearance of solutes and waste from the brain. CSF enters the brain along para-arterial channels to exchange with ISF, which is in turn cleared from the brain along para-venous pathways. Because soluble amyloid β clearance depends on glymphatic pathway function, we proposed that failure of this clearance system contributes to amyloid plaque deposition and Alzheimer's disease progression. Here we provide proof of concept that glymphatic pathway function can be measured using a clinically relevant imaging technique. Dynamic contrast-enhanced MRI was used to visualize CSF-ISF exchange across the rat brain following intrathecal paramagnetic contrast agent administration. Key features of glymphatic pathway function were confirmed, including visualization of para-arterial CSF influx and molecular size-dependent CSF-ISF exchange. Whole-brain imaging allowed the identification of two key influx nodes at the pituitary and pineal gland recesses, while dynamic MRI permitted the definition of simple kinetic parameters to characterize glymphatic CSF-ISF exchange and solute clearance from the brain. We propose that this MRI approach may provide the basis for a wholly new strategy to evaluate Alzheimer's disease susceptibility and progression in the live human brain.
GW25-e1555 The Risk Factors of Malignant Ventricular Arrhythmia in the early stages of elderly Patients with Acute Myocardial Infarction
Authors: Yang Chengming, Lin De-Sheng, Fan Jun, Ran Xi, Zeng Chun-Yu, Cheng Qiao, Zhang Xiao-Qun
Journal: Journal of the American College of Cardiology (2014)
TCT-725 Point-of-Care Genetic Testing of Eleven CYP2C19 Single Nucleotide Polymorphisms Identifies Extensive and Reduced Metabolizers of Clopidogrel With High Accuracy in Patients With Coronary Artery Disease
Authors: David Erlinge, Stefan James, Suman Duvvuru, Joseph Jakubowski, Henrik Wanger, Christoph Varenhorst, Udaya Tantry, Patricia Brown, David Small, Brian Moser, Scott Sundseth, Joseph Walker, Kenneth Winters, Paul Gurbel
Journal: Journal of the American College of Cardiology (2012)
Response to Letter Regarding Article, “Flow-Gradient Patterns in Severe Aortic Stenosis With Preserved Ejection Fraction: Clinical Characteristics and Predictors of Survival”
Authors: Mackram F. Eleid, Paul Sorajja, Hector I. Michelena, Joseph F. Malouf, Chrisopher G. Scott, Patricia A. Pellikka
Journal: Circulation (2014)
Assessment of the epidemiological data relating lung cancer to air pollution.
Authors: F E Speizer
Journal: Environmental Health Perspectives (1983)

The epidemiological data linking air pollution and lung cancer are derived from statistical associations concerning rates of cancer among urban and rural residents, migrant studies and studies of occupational groups exposed to effluents from fossil fuel combinations. Few, if any of these studies, are adequately adjusted for both relatively simple measures of cigarette smoking or the potentially more subtle effects of the duration of smoking. Because urbanization and industrial sources of air pollution correspond chronologically with the major increases in cigarette smoking, it is not likely that the specific attributable risk to each component can be adequately assessed. Interactions between cigarette smoking and specific air pollutants, similar to those seen between cigarette smoking and asbestos and or radiation, may be occurring. Considering the various estimates made over the last 25 years, it is likely that the effect of air pollution on lung cancer is something greater than zero; however, it is unlikely that the estimate exceeds 2% of all lung cancers or 5/100,000 cases in urban males. Thus, the effect on all cancers is likely to be less than 1% of all cases.
Tubulovesicular transport of horseradish peroxidase in isolated rat hepatocyte couplets: Effects of low temperature, cytochalasin B and bile acids
Authors: Shotaro Sakisaka, Masaru Harada, Kazuhisa Gondo, Masao Yoshitake, Kyuichi Tanikawa
Journal: Hepatology (1994)

The transcytotic vesicular pathway in isolated rat hepatocyte couplets was investigated using horseradish peroxidase. Ten to 20 min after horseradish peroxidase labeling, vesicles and tubules containing horseradish peroxidase were observed to be predominantly around the bile canaliculi. In hepatocytes incubated in a 4 degrees C medium for 10 min after horseradish peroxidase labeling, few horseradish peroxidase-containing structures were observed around the bile canaliculi, and the fine reticular immunofluorescence of microtubules was reduced. Cells treated with cytochalasin B (a microfilament inhibitor) showed a fair number of horseradish peroxidase-containing structures around the markedly dilated bile canaliculi and the distribution of microtubules was preserved. Cells labeled by horseradish peroxidase and then incubated for 10 min in a horseradish peroxidase-free medium containing 50 mumol/L of taurocholic acid, ursodeoxycholic acid or tauroursodeoxycholic acid had more tubular structures containing horseradish peroxidase around the bile canaliculi than control cells, whereas 50 mumol/L of taurochenodeoxycholic acid, taurodeoxycholic acid, dehydrocholic acid and taurodehydrocholic acid each failed to increase the number of tubular structures. These findings show that horseradish peroxidase was transported in hepatocyte couplets from the cell periphery to the bile canalicular front through the tubulovesicular pathway, depending on cytoplasmic microtubules. Cytoplasmic microfilaments appeared to play a minor role in this transport. Several specific bile acids such as taurocholic acid, ursodeoxycholic acid and tauroursodeoxycholic acid each promoted the tubular transformation.
Heart Valve Tissue Engineering
Authors: Ivan Vesely
Journal: Circulation Research (2005)

Tissue-engineered heart valves have been proposed by physicians and scientists alike to be the ultimate solution for treating valvular heart disease. Rather than replacing a diseased or defective native valve with a mechanical or animal tissue–derived artificial valve, a tissue-engineered valve would be a living organ, able to respond to growth and physiological forces in the same way that the native aortic valve does. Two main approaches have been attempted over the past 10 to 15 years: regeneration and repopulation. Regeneration involves the implantation of a resorbable matrix that is expected to remodel in vivo and yield a functional valve composed of the cells and connective tissue proteins of the patient. Repopulation involves implanting a whole porcine aortic valve that has been previously cleaned of all pig cells, leaving an intact, mechanically sound connective tissue matrix. The cells of the patients are expected to repopulate and revitalize the acellular matrix, creating living tissue that already has the complex microstructure necessary for proper function and durability. Regrettably, neither of the 2 approaches has fared well in animal experiments, and the only clinical experience with tissue-engineered valves resulted in a number of early failures and patient death. This article reviews the technological details of the 2 main approaches, their rationale, their strengths and weaknesses, and the likely mechanisms for their failure. Alternative approaches to valvular tissue engineering, as well as the role of industry in shaping this field in the future, are also reviewed.
Lactate dehydrogenase (LDH) gene duplication during chordate evolution: the cDNA sequence of the LDH of the tunicate Styela plicata
Authors: D. W. Stock, J. M. Quattro, G. S. Whitt, D. A. Powers
Journal: Molecular Biology and Evolution (1997)

L-Lactate dehydrogenase (L-LDH, E.C. 1.1.1.27) is encoded by two or three loci in all vertebrates examined, with the exception of lampreys, which have a single LDH locus. Biochemical characterizations of LDH proteins have suggested that a gene duplication early in vertebrate evolution gave rise to Ldh-A and Ldh-B and that an additional locus, Ldh-C arose in a number of lineages more recently. Although some phylogenetic studies of LDH protein sequences have supported this pattern of gene duplication, others have contradicted it. In particular, a number of studies have suggested that Ldh-C represents the earliest divergence among vertebrate LDHs and that it may have diverged from the other loci well before the origin of vertebrates. Such hypotheses make explicit statements about the relationship of vertebrate and invertebrate LDHs, but to date, no closely related invertebrate LDH sequences have been available for comparison. We have attempted to provide further data on the timing of gene duplications leading to multiple vertebrate LDHs by determining the cDNA sequence of the LDH of the tunicate Styela plicata. Phylogenetic analyses of this and other LDH sequences provide strong support for the duplications giving rise to multiple vertebrate LDHs having occurred after vertebrates diverged from tunicates. The timing of these LDH duplications is consistent with data from a number of other gene families suggesting widespread gene duplication near the origin of vertebrates. With respect to the relationships among vertebrate LDHs, our data are not consistent with previous claims that Ldh-C represented the earliest divergence. However, the precise relationships among some of the main lineages of vertebrate LDHs were not resolved in our analyses.
LYMPHOID TISSUE—CENTRAL AND PERIPHERAL
Authors: PAUL J. EDELSON
Journal: Annals of Internal Medicine (1968)

Letters and Comments1 November 1968LYMPHOID TISSUE—CENTRAL AND PERIPHERALPAUL J. EDELSON, M.D.PAUL J. EDELSON, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-69-5-1076 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor: In a recent NIH Clinical Staff Conference (Ann. Intern. Med. 69: 333, 1968), Dr. Lawrence Chessin provided a quick survey of current concepts of the organization of the immune system that seems to have dislocated some of its focusing ideas. He states, "In man, the central lymphoid organ is the thymus. Thymus-dependent functions have been shown to include those associated with cellbound immunity, while the peripheral lymphoid tissues are associated with the production of circulating antibody." Dr. Chessin has conflated two different organizing principles, both crucial to current immunologic thought. First, a distinction has been made, as...References1. PETERSON RD, COOPER MD, and GOOD RA: The pathogenesis of immunologic deficiency diseases. Amer. J. Med. 38: 579, 1965. CrossrefMedlineGoogle Scholar2. HOYER JR, COOPER MD, GABRIELSON AE, and GOOD RA: Lymphopenic forms of congenital immunologic deficiency diseases. Medicine (Bait.) 47: 201, 1968. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: PAUL J. EDELSON, M.D. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 November 1968Volume 69, Issue 5Page: 1076-1077KeywordsImmune systemImmunityLymphoid tissueThymus ePublished: 1 December 2008 Issue Published: 1 November 1968 PDF downloadLoading ...
893. Using QPCR and Automation to Assign Infectious Potencies to Adenovirus Based Vaccines and Vectors for Gene Therapy
Authors: Alan C. Puddy, Jenny Xu, Amy M. Bowman, Yuhua Zhang, Charles Y. Tan, Timothy L. Schofield, Peter A. DePhillips, John A. Lewis, Jayanthi J. Wolf
Journal: Molecular Therapy (2005)

The potencies of test articles generated during bioprocess development supporting the manufacture of Ad5 based HIV vaccine have been assigned since 1999 using a QPCR-based Potency Assay (QPA). We report here the simplification of the Ad5 QPA through (1) the introduction of a facile method for the harvest of DNA for QPCR quantitation and (2) the integration of automated liquid handling systems for performing semi-automated or completely automated QPA assays. We demonstrate semi-automated QPA operation using the Beckman Coulter Multimek for the addition of reagents, preparation of dilutions, and set-up of PCR reactions in 384 well formats, which greatly reduce reagent cost and analyst time involved with QPA assays. We show preliminary results indicating that a fully automated assay is possible using a more versatile liquid handling system such as the Tecan Freedom Evo. We also present the results of a PreValidation Exercise (PreVEx) for the semi-automated QPA assay we designate Triton Lysis with the Multimek (TLM) Ad5 QPA, which exhibits a remarkable precision. The PreVEx demonstrated that the TLM Ad5 QPA has a root variability of approximately 16.8% and a format dependent variability (1|[times]|3 assay format, with 4 infection replicates per assay) of approximately 5.8%, allowing samples differing in potency by 17.4% to be discriminated with 95% confidence. This precision equals or exceeds the precision associated with the previous Ad5 QPA.
INPP4B overexpression is associated with poor clinical outcome and therapy resistance in acute myeloid leukemia
Authors: I Dzneladze, R He, J F Woolley, M H Son, M H Sharobim, S A Greenberg, M Gabra, C Langlois, A Rashid, A Hakem, N Ibrahimova, A Arruda, B Löwenberg, P J M Valk, M D Minden, L Salmena
Journal: Leukemia (2015)
Epigenetic therapy is associated with similar survival compared with intensive chemotherapy in older patients with newly diagnosed acute myeloid leukemia
Authors: Alfonso Quintás-Cardama, Farhad Ravandi, Theresa Liu-Dumlao, Mark Brandt, Stefan Faderl, Sherry Pierce, Gautam Borthakur, Guillermo Garcia-Manero, Jorge Cortes, Hagop Kantarjian
Journal: Blood (2012)
Activation of peroxisome proliferator‐activated receptor gamma suppresses mast cell maturation involved in allergic diseases
Authors: M. Tachibana, K. Wada, K. Katayama, Y. Kamisaki, K. Maeyama, T. Kadowaki, R. S. Blumberg, A. Nakajima
Journal: Allergy (2008)

Mast cells play a central role in allergic and inflammatory diseases. Several reports indicated role of peroxisome proliferator-activated receptor gamma (PPARgamma) on mast cell function. However, there is no report about the role of PPARgamma on differentiation of mast cells from the progenitors. In this study, we investigated the role of PPARgamma in regulating bone marrow-derived mast cell maturation and the therapeutic implications for mast cell-related diseases such as atopic or contact dermatitis.We used in vitro cell culture system for mast cell differentiation from bone marrow-progenitors using specific ligands and lentiviral-mediated short hairpin RNA of PPARgamma, and in vivo murine dermatitis models.Activation of PPARgamma inhibited the maturation of bone marrow progenitors into connective tissue-type mast cells (CTMCs) through up-regulation of GATA-4 and GATA-6 resulting in a decrease in expression of histidine decarboxylase and mast cell histamine content. In comparison, the differentiation of bone marrow progenitors into CTMCs was significantly accelerated by the knockdown of PPARgamma expression by lentiviral-mediated short hairpin RNA. Peroxisome proliferator-activated receptor gamma ligand administration to mice inhibited the maturation of mast cells resulting in attenuation of atopic and contact dermatitis via diminishment of the number of mature mast cells.Our results indicate that PPARgamma is one of master regulators on mast cell maturation and potentially useful for the therapy in various disorders involving mast cell activation.
Involvement of Transcriptional and Posttranscriptional Mechanisms in Cardiac Overload–Induced Increase of B-Type Natriuretic Peptide Gene Expression
Authors: Jarkko Magga, Olli Vuolteenaho, Heikki Tokola, Minna Marttila, Heikki Ruskoaho
Journal: Circulation Research (1997)

Abstract The induction of atrial and ventricular B-type natriuretic peptide (BNP) gene expression is one of the earliest events occurring during hemodynamic overload. To examine the molecular mechanisms for increased BNP gene expression during cardiac overload, we studied the induction of the BNP gene expression compared with that of atrial natriuretic peptide (ANP) in a modified perfused rat heart preparation. An increase in right atrial pressure of 5 mm Hg resulted in a 1.4-fold ( P &lt;.05) and 2.2-fold ( P &lt;.01) increase in BNP mRNA levels after 1 and 2 hours, respectively, whereas ANP mRNA levels remained unchanged. Stretching for up to 2 hours also significantly increased right atrial immunoreactive BNP (ir-BNP) levels (from 15.8±2.2 to 20.1±1.2 ng/mg, P &lt;.05). Actinomycin D (10 μg/mL), a transcriptional inhibitor, completely inhibited the stretch-induced increase in atrial BNP mRNA levels at 1 hour ( P &lt;.05) and 2 hours ( P &lt;.001), whereas a protein synthesis inhibitor, cycloheximide (90 μg/mL), had no effect on basal or direct mechanical stretch-induced increase in right atrial BNP mRNA levels. Furthermore, we examined the role of tyrosine kinase and protein kinase C activities in acute mechanical stretch–induced increase in BNP synthesis. Tyrosine kinase inhibitors lavendustin A (1 μmol/L) and tyrphostin A25 (3 μmol/L) and protein kinase C inhibitors staurosporine (30 nmol/L) and chelerythrine (1 μmol/L) prevented the stretch-induced increase in right atrial ir-BNP concentrations at 2 hours. In addition, chelerythrine inhibited the increase of right atrial BNP mRNA levels stimulated by cardiac overload. These results demonstrate that the early increase of BNP mRNA levels by mechanical stretch results from increased transcriptional activation and is independent of protein synthesis. Our results also suggest that protein kinase C and tyrosine kinases activities may be involved in coupling cardiac overload to alterations in atrial BNP synthesis.
Stimulated mitotic counts in the non-lesional skin of patients with psoriasis and controls
Authors: M.J. RICO, K.M. HALPRIN, L. BAKER, M. CAYER, J.R. TAYLOR
Journal: British Journal of Dermatology (1985)

Mitotic counts have been determined in the symptomless skin of nine psoriatic patients and nine healthy controls 48 h after pressure-tape stripping. A significantly increased response was seen in the symptomless psoriatic epidermis compared with the controls.
Superiority of "Camoquin" Over Other Antimalarials
Authors: I. Singh, T. S. Kalyanum
Journal: BMJ (1952)

<h3>SUMMARY</h3> NG2 glia or oligodendrocyte precursor cells (OPCs) are distributed throughout the gray and white matter and generate myelinating cells. OPCs in white matter proliferate more than those in gray matter in response to platelet-derived growth factor AA (PDGF AA), despite similar levels of its alpha receptor (PDGFRα) on their surface. Here we show that the type 1 integral membrane protein Neuropilin-1 (Nrp1) is expressed not on OPCs but on amoeboid and activated microglia in white but not gray matter in an age- and activity-dependent manner. Microglia-specific deletion of Nrp1 compromised developmental OPC proliferation in white matter as well as OPC expansion and subsequent myelin repair after acute demyelination. Exogenous Nrp1 increased PDGF AA-induced OPC proliferation and PDGFRα phosphorylation on dissociated OPCs, most prominently in the presence of suboptimum concentrations of PDGF AA. These findings uncover a novel mechanism of regulating oligodendrocyte lineage cell density that involves trans-activation of PDGFRα on OPCs via Nrp1 expressed by adjacent microglia.
Incident acute coronary syndromes in chronic dialysis patients in the United States11The opinions are solely those of the authors and do not represent an endorsement by the Department of Defense or the National Institutes of Health. This is a U.S. Government work. There are no restrictions on its use.
Authors: Fernando C. Trespalacios, Allen J. Taylor, Lawrence Y. Agodoa, Kevin C. Abbott
Journal: Kidney International (2002)
New Avenues of Exploration for Erythropoietin
Authors: Kenneth Maiese
Journal: JAMA (2005)

Discovery that the hormone erythropoietin (EPO) and its receptor play a significant biological role in tissues outside of the hematopoietic system has fueled significant interest in EPO as a novel cytoprotective agent in both neuronal and vascular systems. Erythropoietin is now considered to have applicability in a variety of disorders that include cerebral ischemia, myocardial infarction, and chronic congestive heart failure. Erythropoietin modulates a broad array of cellular processes that include progenitor stem cell development, cellular integrity, and angiogenesis. As a result, cellular protection by EPO is robust and EPO inhibits the apoptotic mechanisms of injury, including the preservation of cellular membrane asymmetry to prevent inflammation. As the investigation into clinical applications for EPO that maximize efficacy and minimize toxicity progresses, a deeper appreciation for the novel roles that EPO plays in the brain and heart and throughout the entire body should be acquired.
Tibial shaft fractures
Authors: M F Porter
Journal: BMJ (1975)

<h3>Background</h3> Recent work in comparative social epidemiology uses an expenditures approach to examine the link between welfare states and population health. More work is needed that examines the impact of disaggregated expenditures within nations. This study takes advantage of provincial differences within Canada to examine the effects of subnational expenditures and a provincial welfare generosity index on population health. <h3>Methods</h3> Time-series cross-sectional data are retrieved from the Canadian Socio-Economic Information Management System II Tables for 1989–2009 (10 provinces and 21 years=210 cases). Expenditures are measured using 20 disaggregated indicators, total expenditures and a provincial welfare generosity index, a ombined measure of significant predictors. Health is measured as total, male and female age-standardised mortality rates per 1000 deaths. Estimation techniques include the Prais-Winsten regressions with panel-corrected SEs, a first-order autocorrelation correction model, and fixed-unit effects, adjusted for alternative factors. <h3>Results</h3> Analyses reveal that four expenditures effectively reduce mortality rates: medical care, preventive care, other social services and postsecondary education. The provincial welfare generosity index has even larger effects. For an SD increase in the provincial welfare generosity index, total mortality rates are expected to decline by 0.44 SDs. Standardised effects are larger for women (β=−0.57, z(19)=−5.70, p&lt;0.01) than for men (β=−0.38, z(19)=−5.59, p&lt;0.01). <h3>Conclusions</h3> Findings show that the expenditures approach can be effectively applied within the context of Canadian provinces, and that targeted spending on health, social services and education has salutary effects.
Duplicate VegfA genes and orthologues of the KDR receptor tyrosine kinase family mediate vascular development in the zebrafish
Authors: Nathan Bahary, Katsutoshi Goishi, Carsten Stuckenholz, Gerhard Weber, Jocelyn LeBlanc, Christopher A. Schafer, Sarah S. Berman, Michael Klagsbrun, Leonard I. Zon
Journal: Blood (2007)