tbuckley/cabot-search huggingface dataset:
HIV and plasmablastic lymphoma manifesting in sinus, testicles, and bones: A further expansion of the disease spectrum
Authors: Steven A. Schichman, Rebecca McClure, Robert F. Schaefer, Paulette Mehta
Journal: American Journal of Hematology (2004)

Abstract Patients with HIV infection are at increased risk for B‐cell neoplasms and plasma cell dyscrasias. Both B cell and plasma cell tumors tend to be intermediate or high grade and are frequently associated with Epstein‐Barr virus. Patients with HIV infection are also at higher risk of acquiring plasmablastic lymphoma. Until this time, only sinus, oral gastrointestinal, and lung manifestation have been noted. In this report we describe a 41‐year‐old male with HIV infection who developed multiple pleomorphic, extramedullary plasmablastic lymphomas associated with Epstein‐Barr virus. We review the clinical and immunological features of his malignancy and thereby expand the spectrum of disease to include additional sites (bones, testicles) not previously reported. Am. J. Hematol. 77:291–295, 2004. Published 2004 Wiley‐Liss, Inc. †
Acute Angle Closure Glaucoma in a Young Negro Boy
Authors: Mark Hallett
Journal: JAMA (1971)

A Negro boy who was also suffering from infectious mononucleosis and acute streptococcal sore throat had an attack of bilateral acute angle closure glaucoma. A bromopheniramine-phenylephrine-phenylpropanolamine mixture may have been a factor in precipitating angle closure.
Outbreak of Legionnaires' disease among cruise ship passengers exposed to a contaminated whirlpool spa
Authors: D.B Jernigan, J Hofmann, M.S Cetron, J.P Nuorti, B.S Fields, R.F Benson, R.F Breiman, H.B Lipman, R.J Carter, C.A Genese, S.M Paul, P.H Edelstein, I.C Guerrero
Journal: The Lancet (1996)
Cardiac Muscle Ring Finger-1 Increases Susceptibility to Heart Failure In Vivo
Authors: Monte S. Willis, Jonathan C. Schisler, Luge Li, Jessica E. Rodríguez, Eleanor G. Hilliard, Peter C. Charles, Cam Patterson
Journal: Circulation Research (2009)

Muscle ring finger (MuRF)1 is a muscle-specific protein implicated in the regulation of cardiac myocyte size and contractility. MuRF2, a closely related family member, redundantly interacts with protein substrates and heterodimerizes with MuRF1. Mice lacking either MuRF1 or MuRF2 are phenotypically normal, whereas mice lacking both proteins develop a spontaneous cardiac and skeletal muscle hypertrophy, indicating cooperative control of muscle mass by MuRF1 and MuRF2. To identify the unique role that MuRF1 plays in regulating cardiac hypertrophy in vivo, we created transgenic mice expressing increased amounts of cardiac MuRF1. Adult MuRF1 transgenic (Tg + ) hearts exhibited a nonprogressive thinning of the left ventricular wall and a concomitant decrease in cardiac function. Experimental induction of cardiac hypertrophy by transaortic constriction (TAC) induced rapid failure of MuRF1 Tg + hearts. Microarray analysis identified that the levels of genes associated with metabolism (and in particular mitochondrial processes) were significantly altered in MuRF1 Tg + hearts, both at baseline and during the development of cardiac hypertrophy. Surprisingly, ATP levels in MuRF1 Tg + mice did not differ from wild-type mice despite the depressed contractility following TAC. In comparing the level and activity of creatine kinase (CK) between wild-type and MuRF1 Tg + hearts, we found that mCK and CK-M/B protein levels were unaffected in MuRF1 Tg + hearts; however, total CK activity was significantly inhibited. We conclude that increased expression of cardiac MuRF1 results in a broad disruption of primary metabolic functions, including alterations in CK activity that leads to increased susceptibility to heart failure following TAC. This study demonstrates for the first time a role for MuRF1 in the regulation of cardiac energetics in vivo.
Rhythm Versus Rate Control Therapy and Subsequent Stroke or Transient Ischemic Attack in Patients With Atrial Fibrillation
Authors: Meytal Avgil Tsadok, Cynthia A. Jackevicius, Vidal Essebag, Mark J. Eisenberg, Elham Rahme, Karin H. Humphries, Jack V. Tu, Hassan Behlouli, Louise Pilote
Journal: Circulation (2012)

Background— Stroke is a debilitating condition with an increased risk in patients with atrial fibrillation. Although data from clinical trials suggest that both rate and rhythm control are acceptable approaches with comparable rates of mortality in the short term, it is unclear whether stroke rates differ between patients who filled prescriptions for rhythm or rate control therapy. Methods and Results— We conducted a population-based observational study of Quebec patients ≥65 years with a diagnosis of atrial fibrillation during the period 1999 to 2007 with the use of linked administrative data from hospital discharge and prescription drug claims databases. We compared rates of stroke or transient ischemic attack (TIA) among patients using rhythm (class Ia, Ic, and III antiarrhythmics), versus rate control (β-blockers, calcium channel blockers, and digoxin) treatment strategies (either current or new users). The cohort consisted of 16 325 patients who filled a prescription for rhythm control therapy (with or without rate control therapy) and 41 193 patients who filled a prescription for rate control therapy, with a mean follow-up of 2.8 years (maximum 8.2 years). A lower proportion of patients on rhythm control therapy than on rate control therapy had a CHADS 2 (congestive heart failure, hypertension, age ≥75 years, diabetes mellitus, and previous stroke or TIA) score of ≥2 (58.1% versus 67.0%, P &lt;0.001). Treatment with any antithrombotic drug was comparable in the 2 groups (76.8% in rhythm control versus 77.8% in rate control group). Crude stroke/TIA incidence rate was lower in patients treated with rhythm control in comparison with rate control therapy (1.74 versus 2.49, per 100 person-years, P &lt;0.001). This association was more marked in patients in the moderate- and high-risk groups for stroke according to the CHADS 2 risk score. In multivariable Cox regression analysis, rhythm control therapy was associated with a lower risk of stroke/TIA in comparison with rate control therapy (adjusted hazard ratio, 0.80; 95% confidence interval, 0.74, 0.87). The lower stroke/TIA rate was confirmed in a propensity score–matched cohort. Conclusions— In comparison with rate control therapy, the use of rhythm control therapy was associated with lower rates of stroke/TIA among patients with atrial fibrillation, in particular, among those with moderate and high risk of stroke.
Structure and Functions of the Heidelberg University Organisation for After-Care of Cancer Patients
Authors: A. Sellschopp, H. Lüdeke, G. Haertel
Journal: Psychotherapy and Psychosomatics (1981)

The functions of the psycho-social after-care centre are: care of patients, co-operation with self-help groups, and training of therapists in psycho-social work. We describe the psycho-social therapist's work with out-patients and in-patients (e.g., in surgical wards; children's hospital), including the various focuses of attention in conversations with patients. Frequently the family has to be involved in helping to cope with the illness. Some account is given of our work with self-help groups, and of the training courses developed for therapists working with cancer patients. Finally, we discuss the question of individual suitability for work with cancer patients and for related research projects.
KSHV-Initiated Notch Activation Leads to Membrane-Type-1 Matrix Metalloproteinase-Dependent Lymphatic Endothelial-to-Mesenchymal Transition
Authors: Fang Cheng, Pirita Pekkonen, Simonas Laurinavicius, Nami Sugiyama, Stephen Henderson, Thomas Günther, Ville Rantanen, Elisa Kaivanto, Mervi Aavikko, Grzegorz Sarek, Sampsa Hautaniemi, Peter Biberfeld, Lauri Aaltonen, Adam Grundhoff, Chris Boshoff, Kari Alitalo, Kaisa Lehti, Päivi M. Ojala
Journal: Cell Host & Microbe (2011)

SummaryKaposi sarcoma (KS), an angioproliferative disease associated with Kaposi sarcoma herpesvirus (KSHV) infection, harbors a diversity of cell types ranging from endothelial to mesenchymal cells of unclear origin. We developed a three-dimensional cell model for KSHV infection and used it to demonstrate that KSHV induces transcriptional reprogramming of lymphatic endothelial cells to mesenchymal cells via endothelial-to-mesenchymal transition (EndMT). KSHV-induced EndMT was initiated by the viral proteins vFLIP and vGPCR through Notch pathway activation, leading to gain of membrane-type-1 matrix metalloproteinase (MT1-MMP)-dependent invasive properties and concomitant changes in viral gene expression. Mesenchymal markers and MT1-MMP were found codistributed with a KSHV marker in the same cells from primary KS biopsies. Our data explain the heterogeneity of cell types within KS lesions and suggest that KSHV-induced EndMT may contribute to KS development by giving rise to infected, invasive cells while providing the virus a permissive cellular microenvironment for efficient spread.Graphical abstractGraphical AbstractHighlights► KSHV induces mesenchymal reprogramming of lymphatic endothelial cells (LECs) in 3D ► KSHV-activated Notch-MT1-MMP axis regulates LEC reprogramming ► KSHV-reprogrammed LECs are invasive ► 3D microenvironment of infected LECs leads to viral gene expression changes
NHLBI Task Force summary. Task Force on Research in Cardiopulmonary Dysfunction in Critical Care Medicine.
Authors: C Lenfant
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Research accomplishments during the past decade have led to a much greater understanding of molecular, cellular, and pathophysiological derangements occurring in the lung and other organ systems during critical illness. Despite this progress, care of critically ill patients with cardiopulmonary dysfunction remains a major health challenge. Expansion of research efforts is imperative and particularly opportune at this time because of exciting developments in understanding various mediators involved in inflammation and repair. Future advances in treating critical illness depend on basic understanding of the pathogenesis and pathophysiology of acute injury and repair. Key observations gained through clinical and epidemiological studies must be tested in the basic science laboratory. Increased and coordinated efforts in epidemiology, clinical, and basic research are essential for future progress.
Molecular Evolution and Phylogeny of the buzzatii Complex (Drosophila repleta Group): A Maximum-Likelihood Approach
Authors: Francisco Rodríguez-Trelles, Lourdes Alarcón, Antonio Fontdevila
Journal: Molecular Biology and Evolution (2000)

The buzzatii complex of the mulleri subgroup (Drosophila repleta group) consists of three clusters of species whose evolutionary relationships are poorly known. We analyzed 2,085 coding nucleotides from the xanthine dehydrogenase (Xdh) gene in the 10 available species of the complex and Drosophila mulleri and Drosophila hydei. We adopted a statistical model-fitting approach within the maximum-likelihood (ML) framework of phylogenetic inference. We first modeled the process of nucleotide substitution using a tree topology which was reasonably accurate. Then we used the most satisfactory description so attained to reconstruct the evolutionary relationships in the buzzatii complex. We found that a minimally realistic description of the substitution process of Xdh should allow six substitution types and different substitution rates for codon positions. Using this description we obtained a strongly supported, fully resolved tree which is congruent with the already-known (yet few) relationships. We also analyzed published data from three mitochondrial cytochrome oxidases (CO I, II, and III). In our analyses, these relatively short DNA sequences failed to discriminate statistically among alternative phylogenies. When the data of these three gene regions are combined with the Xdh sequences, the phylogenetic signal emerging from Xdh becomes reinforced. All four of the gene regions evolve faster in the buzzatii and martensis clusters than in the stalkeri cluster, paralleling the amount of chromosomal evolution.
Reviews and Notes: Infectious Diseases: Tuberculosis
Authors: Harvey S. Kantor
Journal: Annals of Internal Medicine (1996)

Literature of Medicine15 November 1996Reviews and Notes: Infectious Diseases: TuberculosisHarvey S. Kantor, MDHarvey S. Kantor, MDTexas Tech University Health Sciences Center, Odessa, TX 79763.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-10-199611150-00026 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail WN Rom and SM Garay; eds. 1002 pages. Boston: Little, Brown; 1996. $179.95. ISBN 0-316-75574-5. Order phone 800-759-0190.Worldwide, tuberculosis is the leading cause of death associated with infectious diseases. The incidence of tuberculosis is expected to increase substantially during the next 10 years because of the interaction between tuberculosis and human immunodeficiency virus (HIV) epidemics. An estimated 1.7 billion persons, one third of the world's population, are currently infected with Mycobacterium tuberculosis.Is there a need for another textbook on tuberculosis? Five publications on this topic are listed in Medical and Health Care Books in Print (1995). Rom and ... Author, Article, and Disclosure InformationAffiliations: Texas Tech University Health Sciences Center, Odessa, TX 79763. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 November 1996Volume 125, Issue 10Page: 862-863KeywordsHIVImmune responseInfectious diseasesPathogenesisPrimary care physiciansPulmonary medicineSalivaSputumThoraxTuberculosis Issue Published: 15 November 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
IRE1 Signaling Is Essential for Ischemia-Induced Vascular Endothelial Growth Factor-A Expression and Contributes to Angiogenesis and Tumor Growth <i>In vivo</i>
Authors: Benjamin Drogat, Patrick Auguste, Duc Thang Nguyen, Marion Bouchecareilh, Raphael Pineau, Josephine Nalbantoglu, Randal J. Kaufman, Eric Chevet, Andréas Bikfalvi, Michel Moenner
Journal: Cancer Research (2007)

Abstract In solid tumors, cancer cells subjected to ischemic conditions trigger distinct signaling pathways contributing to angiogenic stimulation and tumor development. Characteristic features of tumor ischemia include hypoxia and glucose deprivation, leading to the activation of hypoxia-inducible factor-1–dependent signaling pathways and to complex signaling events known as the unfolded protein response. Here, we show that the activation of the endoplasmic reticulum stress sensor IRE1 is a common determinant linking hypoxia- and hypoglycemia-dependent responses to the up-regulation of vascular endothelial growth factor-A (VEGF-A). Tumor cells expressing a dominant-negative IRE1 transgene as well as Ire1α-null mouse embryonic fibroblasts were unable to trigger VEGF-A up-regulation upon either oxygen or glucose deprivation. These data correlated with a reduction of tumor angiogenesis and growth in vivo. Our results therefore suggest an essential role for IRE1-dependent signaling pathways in response to ischemia and identify this protein as a potential therapeutic target to control both the angiogenic switch and tumor development. [Cancer Res 2007;67(14):6700–7]
MODIFICATION OF PRESENT METHODS OF GASTRODUODENOSTOMY
Authors: WALTER HUGHSON
Journal: JAMA (1926)

The increasing interest in pyloric resection and its growing importance as a method of treating ulcerations of the stomach and duodenum are matters of common knowledge. Furthermore, there is the mounting conviction that in suitable cases some form of pyloroplasty or gastroduodenostomy is the operation of choice. Unfortunately, until quite recently the choice of operations of this type was comparatively small. The Billroth I operation, the Finney pyloroplasty and the physiologic pyloroplasty of Horsley for many years offered the only satisfactory surgical means of restoring the normal physiologic relations of the stomach after resection of an ulcer at the pylorus or in the duodenum. The Billroth I operation fell into a rather undeserved disrepute, and in the latter two operations ordinarily half the pyloric ring remained intact, which may possibly be a disadvantage, for certain it is that there is a marked delay in emptying in many cases following pyloroplasty.
Ala54Thr polymorphism of the fatty acid binding protein 2 gene and saturated fat intake in relation to lipid levels and insulin resistance: the Coronary Artery Risk Development in Young Adults (CARDIA) study
Authors: Alanna M. Chamberlain, Pamela J. Schreiner, Myriam Fornage, Catherine M. Loria, David Siscovick, Eric Boerwinkle
Journal: Metabolism (2009)
In vivo neutralization of P-selectin protects feline heart and endothelium in myocardial ischemia and reperfusion injury.
Authors: A S Weyrich, X Y Ma, D J Lefer, K H Albertine, A M Lefer
Journal: Journal of Clinical Investigation (1993)

The cardioprotective effects of an mAb to P-selectin designated mAb PB1.3 was examined in a feline model of myocardial isch- emia (MI) and reperfusion.PB1.3 (1 mg/kg), administered after 80 min of ischemia (i.e., 10 min before reperfusion), significantly attenuated myocardial necrosis compared to a non- blocking mAb (NBP1.6)for P-selectin (15±3 vs 35±3% of area at risk, P < 0.01).Moreover, endothelial release of endo- thelium derived relaxing factor, as assessed by relaxation to acetylcholine, was also significantly preserved in ischemic-re- perfused coronary arteries isolated from cats treated with mAb PB1.3 compared to mAb NBP1.6 (67±6 vs 11±3, P < 0.01).This endothelial preservation was directly related to reduced endothelial adherence of PMNs in ischemic-reperfused coro- nary arteries.Immunohistochemical localization of P-selectin was significantly upregulated in the cytoplasm of endothelial cells that lined coronary arteries and veins after 90 min of isch- emia and 20 min of reperfusion.The principal site of intracytoplasmic expression was in venous vessels.mAb PB1.3 significantly decreased (P < 0.01 ) adherence of unstimulated PMNs to thrombin and histamine stimulated endothelial cells in a con- centration-dependent manner in vitro.These results demon- strate that PMN adherence to endothelium by P-selectin is an important early consequence of reperfusion injury, and a specific monoclonal antibody to P-selectin exerts significant endo- thelial preservation and cardioprotection in myocardial isch- emia and reperfusion.(
OVERDOSAGE OF SPINAL ANESTHETIC
Authors: Alexander Zabin
Journal: JAMA (1934)

To the Editor:—  The following case is of interest to the profession because of the large dose of spinal anesthetic administered with a subsequent almost fatal outcome: A white woman, aged 40, weighing 160 pounds (72.6 Kg.), with a systolic blood pressure of 140 and a diastolic blood pressure of 80, was given a spinal anesthetic for a cholecystectomy for hydrops of the gallbladder. Novocain crystals (a brand of procaine hydrochloride) dissolved in the patient's spinal fluid were injected into the third lumbar space. While the gallbladder contents were being emptied the patient became pulseless and stopped breathing. Cardiac and respiratory action was restored by means of subdiaphragmatic cardiac massage, epinephrine by vein and artificial respiration. The operation was terminated at this point by a cholecystostomy. The postoperative course was uneventful. As I had given and seen given many similar spinal anesthesias with the same drug with no untoward reactions,
A Phase II Study of Concurrent Carboplatin and Paclitaxel and Thoracic Radiotherapy for Completely Resected Stage II and IIIA Non-small Cell Lung Cancer
Authors: Steven J. Feigenberg, Alexandra L. Hanlon, Corey Langer, Melvyn Goldberg, Nicos Nicolaou, Michael Millenson, Lawrence R. Coia, Rachelle Lanciano, Benjamin Movsas
Journal: Journal of Thoracic Oncology (2007)
The genetic landscape of mutations in Burkitt lymphoma
Authors: Cassandra Love, Zhen Sun, Dereje Jima, Guojie Li, Jenny Zhang, Rodney Miles, Kristy L Richards, Cherie H Dunphy, William W L Choi, Gopesh Srivastava, Patricia L Lugar, David A Rizzieri, Anand S Lagoo, Leon Bernal-Mizrachi, Karen P Mann, Christopher R Flowers, Kikkeri N Naresh, Andrew M Evens, Amy Chadburn, Leo I Gordon, Magdalena B Czader, Javed I Gill, Eric D Hsi, Adrienne Greenough, Andrea B Moffitt, Matthew McKinney, Anjishnu Banerjee, Vladimir Grubor, Shawn Levy, David B Dunson, Sandeep S Dave
Journal: Nature Genetics (2012)
CD10 enhances metastasis of colorectal cancer by abrogating the anti-tumoural effect of methionine-enkephalin in the liver
Authors: H. Kuniyasu, Y. Luo, K. Fujii, T. Sasahira, Y. Moriwaka, N. Tatsumoto, T. Sasaki, Y. Yamashita, H. Ohmori
Journal: Gut (2009)

<h3>Objective</h3> To examine the role of CD10, a characteristic marker of liver metastasis of colorectal cancers (CRCs). <h3>Design</h3> The effect of CD10 and Met-enkephalin (MENK) in CD10-positive and -negative human CRC cells was investigated under in vitro and in vivo conditions. Human CRC samples were examined. <h3>Main outcome measure</h3> CD10-positive and CD10-knockdown HT29 cells and CD10-negative and CD10-transfected Colo320 cells in nude mice were treated with MENK and/or the CD10 inhibitor (thiorphan). Intracellular signalling of MENK and δ-opioid receptor (DOR) was examined by immunoblotting. <h3>Results</h3> MENK inhibited the growth, invasion and survival of CRC cells following thiorphan-induced CD10 inactivation. Thiorphan suppressed liver metastasis of CD10-positive CRC cells. Inoculation of mice with CRC cells induced MENK expression in the liver. Inhibition of hepatic MENK expression by cholesterol-conjugated antisense S-oligodeoxynucleotide increased liver metastasis of CRC cells even when the cells did not express CD10. DOR activation by MENK decreased the phosphorylation of epidermal growth factor receptor and extracellular signal-regulated kinase and increased p38-dependent apoptosis. Nitric oxide was found to induce DOR expression in CRC cells. Co-treatment with thiorphan and a nitric oxide donor had a marked anti-tumour effect on liver metastasis of HT29 cells. Of 68 CRC patients, 19 (28%) showed CD10 expression, which was dependent on the extent of liver metastasis. MENK concentration in metastasis-positive human liver was higher than that in the normal liver. <h3>Conclusion</h3> CD10 expression in CRC cells abrogates the anti-tumour effect of hepatic MENK by degrading it, which enhances liver metastasis of CD10-positive CRC cells.