tbuckley/cabot-search huggingface dataset:
Successful Treatment of Cerebral Cryptococcoma and Meningitis with Miconazole
Authors: LOUIS WEINSTEIN
Journal: Annals of Internal Medicine (1980)

Cryptococcal meningitis and a cerebral cryptococcoma developed in a patient with pulmonary cryptococcosis ("coin lesion") shortly after infected area of lung was removed. Treatment with amphotericin B and flucytosine failed to clear the organisms and antigen from the spinal fluid or alter the neurologic manifestations related to the cerebral lesion. Therapy with miconazole cured the meningitis and led to disappearance of the lesion in the brain (serial computed tomographic scan). Study of the patient over the next 5 years disclosed no evidence of relapse of infection and completely normal findings on neurologic examination.
Progression of Myocardial Necrosis During Reperfusion of Ischemic Myocardium
Authors: Kaname Matsumura, Richmond W. Jeremy, Jutta Schaper, Lewis C. Becker
Journal: Circulation (1998)

Background —The occurrence of myocyte necrosis during reperfusion of ischemic myocardium is controversial. This study measured myocardial 2-deoxyglucose uptake, correlated with histology, to determine whether loss of viability occurred during reperfusion of ischemic myocardium. Methods and Results —In 12 anesthetized dogs, the left anterior descending coronary artery was occluded for 90 minutes before 4 hours reperfusion. Myocardial blood flow was measured by microspheres and the tracers 14 C-2-deoxyglucose and 18 F-2-deoxyglucose were injected intravenously after 5 and 180 minutes of reperfusion, respectively. After 240 minutes, the heart was stained with thioflavin-S (size of no-reflow zone) and triphenyl-tetrazolium chloride (TTC, extent of necrosis). Samples from normal, salvaged, and necrotic myocardium were counted for 14 C- and 18 F-deoxyglucose and microspheres. With the use of a three-compartment model of 2-deoxyglucose uptake, the rate constant k 3 for phosphorylation of 14 C- and 18 F-2-deoxyglucose was calculated for each sample. Viability was defined as k 3 ≥ 0.125 min -1 (predictive accuracy 88% versus electron microscopy and 97% versus TTC). Among 58 samples from no-reflow regions, 97% were nonviable after 5 minutes of reperfusion ( k 3 =0.096±0.027 min -1 ). Among 164 samples from salvaged myocardium, 95% were viable after both 5 and 180 minutes of reperfusion ( k 3 =0.170±0.056 min -1 P &lt;.01 versus no-reflow). Among 179 samples from infarcted myocardium, mean k 3 after 5 minutes of reperfusion was 0.184±0.070 min -1 and 65% of samples were viable, but after 180 minutes of reperfusion mean k 3 had decreased to 0.077±0.032 min -1 ( P &lt;.0001) and 98% of samples were nonviable. Conclusions —A large proportion of samples from infarcted myocardium are viable at the end of the ischemic period but lose viability during the first hours of reperfusion.
The Babinski Sign
Authors: F A Neelon, E N Harvey
Journal: New England Journal of Medicine (1999)

Figure 1. As a 5-month-old infant and his 30-month-old brother sat together for an informal portrait, the pressure of the infant's right great toe against his left sole induced reflex dorsiflexion of the left great toe. This reflex phenomenon constitutes one of the most famous signs in medicine: the Babinski reflex. The Babinski reflex is present in normal newborn infants and disappears as the central nervous system matures. Persistence of the reflex after the age of three years or its reappearance in later life indicates dysfunction of the pyramidal tract. The stimulus needed to elicit the reflex sign need not . . .
712-3 Predictive Value of Intraoperative Transesophageal Color Doppler Flow Imaging During Mitral Valve Repair
Authors: Irene M. Hellemans, Els G. Pieper, Johannes P.M. Hamer, Wybren Jaarsma, Renee B.A. van den Brink, Kees B. Prenger, Patricia F.A. Bakker, Eric Berreklouw, Jan G.P. Tijssen, Cees A. Visser
Journal: Journal of the American College of Cardiology (1995)
Heterogeneity of human serum amyloid A proteins.
Authors: L L Bausserman, P N Herbert, K P McAdam
Journal: The Journal of Experimental Medicine (1980)

Serum amyloid A proteins (SAA), presumed precursors of the tissue amyloid A proteins (AA) characteristic of secondary amyloidosis, have been isolated from the plasma high-density lipoproteins (HDL) of normals after etiocholanolone-induced inflammation and from patients with Wegener's granulomatosis, systemic lupus erythematosis, juvenile rheumatoid arthritis, Waldenström's macroglobulinemia, and Goodpasture's syndrome. At least six polymorphic forms of SAA wer identified among the low molecular weight proteins of HDL, and these comprosed up to 27% of the total HDL protein. Gel and ion-exchange chromatography permitted isolation of the SAA polymorphs in homogeneous form. Their amino acid compositions were very similar, they were indistinguishable in cationic and sodium dodecyl sulfate-polyacrylamide gel electrophoresis systems, and each had the terminal sequency COOH-Tyr-Lys-Phe-. Charge heterogeneity in anionic-urea polyacrylamide gel electropherograms was unaffected by neuaminidase treatment, and none of the SAA protein bands stained with the periodate-Schiff reagent. The two major SAA polymorphs, designated SAA4 and SAA5 according to their order of elution from DEAE-cellulose, had different NH2-terminal sequences. Manual Edman degradation demonstrated NH2-arg-ser-phe-phe- for SAA4 and NH2-ser-phe-phe- for SAA5. This NH2-terminal heterogeneity corresponds to that most frequently reported for AA and suggests that microheterogeneity in SAA may underlie that already documented in AA. Sufficient quantitites of the other SAA polymorphs were not available for similar analyses, but the amino acid compositions do not indicate that NH2-terminal heterogeneity accounts for all of the observed polymorphism. Artifactual polymorphism also appears unlikely, and the heterogeneiy of SAA may reflect origin from more than one cell type with or without posttranslational modificaton. We calculate from quantitative COOH-terminal analyses that SAA is of 11,000-11,900 mol wt. Primary structure studies have shown AA t be a single chain protein of 76 residues, and SAA, therefore, appears to contain a peptide of 33 amino acids that is missing from AA.
In pursuit of "humanitarian science"
Authors: G. Watts
Journal: BMJ (2003)

In the late 1960s a research institute in Bangladesh pioneered a treatment that has saved 40 million lives worldwide. What happened next? David Sack explains 

“We ought to pass a UN resolution that no country should be allowed to make a nuclear weapon until its infant mortality rate has dropped below 30 [per thousand].” Dry humour from Professor David Sack, as he points out how different countries—Pakistan and Bangladesh, in this case—have different priorities. Pakistan possesses the bomb, but Bangladesh, though poorer, and without nuclear weapons, has fewer deaths in infancy.

As director of the International Centre for Diarrhoeal Disease Research in Dhaka, Sack rejoices in the positive things he can say about Bangladesh, a country often dismissed as one of the world's basket cases. Sack views it in a more sympathetic light. “I often say it's one of the most successful nations. Nowhere else is there a piece of land that supports so many people with such little adverse impact on its ecology.”

The centre itself is descended from the Cholera Research Laboratory set up in 1960 by the South East Asian Treaty Organisation. It runs hospitals and clinics in Dhaka and elsewhere, does research, and was the first—and remains the only—international health research organisation based in a …
Vascular endothelial growth factor promotes proliferation and function of hepatocyte-like cells in embryoid bodies formed from mouse embryonic stem cells
Authors: Hiroaki Fujimori, Kinji Asahina, Keiko Shimizu-Saito, Reiko Ikeda, Yujiro Tanaka, Kenichi Teramoto, Ikuo Morita, Hirobumi Teraoka
Journal: Journal of Hepatology (2008)
Electrophysiologic Effects of Quinidine
Authors: ANDREW G. WALLACE, ROBERT E. CLINE, WILL C. SEALY, W. GLENN YOUNG, WILLIAM G. TROYER
Journal: Circulation Research (1966)

Experiments were performed on awake dogs with chronic recording electrodes implanted on the SA node, His bundle, and right bundle branch. Quinidine at serum concentrations of 5 to 10 mg/liter had little effect on AV conduction, but slowed conduction in Purkinje tissue, prolonged ventricular activation, decreased the excitability of atrium and ventricle, and prolonged the atrial refractory period without a consistent effect on the ventricular refractory period. In awake dogs that had previously undergone cardiac denervation, quinidine decreased the excitability and prolonged the refractory period of atrium and ventricle. The effects of quinidine on excitability were dependent on the duration of the stimulus used to test excitability. The actions of quinidine on intraventricular conduction and excitability were enhanced at rapid rates of stimulation. These data indicate that slowing of intraventricular conduction is observed consistently at serum quinidine concentrations that are generally considered to be within the therapeutic range, but changes of the refractory period of the ventricle are not observed consistently. Although the vagolytic properties of quinidine may contribute to changes of heart rate, they do not appear to influence significantly the effects of quinidine on atrial refractoriness and AV conduction.
Abstract 3877: An inhibitor-2 complex regulates cell cycle checkpoints in response to DNA damage
Authors: Mianen Sun, Chenghe Lin, Xi Tang, Bo Xu
Journal: Cancer Research (2010)

Abstract Optimal DNA damage responses such as cell cycle checkpoints are essential for cell survival and prevention of genetic instability. Comprehensive knowledge on the regulation of cell cycle checkpoints will provide molecular insights into tumorigenesis as well as tumor responses to radiation and chemotherapy. The signal transduction network orchestrated by the ATM protein kinase through phosphorylation of downstream targets is critical to activate cell cycle checkpoints in response to ionizing radiation (IR). Among them, Inhibitor 2 (I-2), a regulatory subunit of Protein Phosphatase 1 (PP1), is phosphorylated by ATM on Serine 43 after IR and required for PP1 activation. However, the detailed mechanism of the signaling network involving ATM, PP1 and I-2 has not been elucidated. In the present study, we show that I-2 phosphorylation is required for activation of the S-phase and G2/M checkpoints. We also identified a complex associated with the phosphorylated form of I-2. Several DNA damage responsive proteins such as ATM, Brca1, Cdc7 and Chk2 are presented in the complex. Further, we demonstrate that Brca1 is required for ATM-mediated I-2 phosphorylation and PP1 activation after DNA damage. We find Brca1 is essential for recruiting I-2 to DNA damage sites, and Brca1 interaction with I-2 increases after DNA damage. This DNA damage-induced Brca1/I-2 interaction further lead to I-2/PP1 dissociation, the process required for PP1 activation after DNA damage. Taken together, our results highlighted that a comprehensive pathway mediated by I-2 phosphorylation in response to DNA damage. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3877.
Large Reverse Mismatch Associated With Pulmonary Embolism
Authors: RENATO ARMAS
Journal: Clinical Nuclear Medicine (1994)

Because alveolar hypoxia causes reflex vasoconstriction, areas of absent ventilation on lung scans usually are accompanied by matching perfusion defects. Perfusion of nonventilated lung, or reverse mismatch, has been described in a variety of conditions, including bronchial obstruction, atelectasis, and pneumonia (1–3), but not in pulmonary embolism. In this patient, a reverse mismatch involving almost the entire left lung was associated with extensive emboli to the opposite lung. It is likely that the increased vascular resistance produced by the emboli forced blood flow into the left lung, overcoming hypoxic vasoconstriction.
Physician Characteristics and Distribution in the U.S. 1997/98
Authors: Eugene C. Rich
Journal: Annals of Internal Medicine (1998)

Medical Writings15 February 1998Physician Characteristics and Distribution in the U.S. 1997/98Eugene C. Rich, MDEugene C. Rich, MDCenter for Practice Improvement and Outcomes, Omaha, NebraskaSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-128-4-199802150-00053 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail 356 pages. Chicago: American Med Assoc; 1997. $125.95. ISBN 0899708935. Order phone 312-464-5602.Field of medicine: Health services administration and health policy.Format: Softcover book.Audience: Physicians, health care administrators, and health policy professionals.Purpose: To present historical and current data on the U.S. physician population for health services research, program planning, and policy development.Content: This edition of Physician Characteristics and Distribution in the U.S. is the latest in a series begun in 1963. The Division of Survey and Data Resources of the American Medical Association (AMA) develops these reports from the AMA physician master files, and this report ... Author, Article, and Disclosure InformationAffiliations: Center for Practice Improvement and Outcomes, Omaha, Nebraska PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 February 1998Volume 128, Issue 4Page: 331KeywordsHealth care policyHealth care providersHealth services administration and managementHealth services researchInformation storage and retrievalMedical servicesPublic policyQuestionnairesResidencySub-specialty care ePublished: 15 August 2000 Issue Published: 15 February 1998 Copyright & PermissionsCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Albright's Syndrome in an Adult Male
Authors: P. Hall
Journal: BMJ (1962)

Kelly (1961) has shown that the intravenous administration of oestrogen does not affect spontaneous uterine motility.It is likely that it is the concentration of active oestrogen in the uterine muscle which matters.In this event the only effective route of administration may be into the utero-placental space or into the amniotic cavity.The possibility of intra-amniotic injection is foreshadowed by the work of Diczfalusy et al. (1961) on the metabolism of intra-amniotic oestrogens, and we propose to extend our trials using this route.Summary A controlled trial was done on the effect of oral oestriol or stilboestrol in women who were to be subjected to artificial rupture of the membranes for surgical induction of labour.It was found that these oestrogens had no demonstrable effect on the induction- delivery interval or on the length of labour.We are grateful to our statistical colleagues Mr. W. Z Billewicz and Miss R. Holliday for their help in the design of the trial and in dispensing tablets.Our thanks are due to the nursing staff at the Maternity Hospital for their co-operation, and to Dr. C. L. Hewett, of the Organon Laboratories, for the gift of oestrogen and dummy tablets.
Acute Delayed Gastric Emptying after Ablation of Atrial Fibrillation: Treatment with Botulinum Toxin Injection
Authors: J. Dumonceau, E. Giostra, C. Bech, L. Spahr, A. Schroft, D. Shah
Journal: Endoscopy (2006)

Percutaneous transcatheter radiofrequency (RF) ablation of pulmonary veins is increasingly used for the treatment of refractory atrial fibrillation. With this technique, lesions are created around the ostia of each pulmonary vein to electrically isolate them from the left atrium [1]. We report a case of acute pyloric spasm after RF ablation, which improved after intrapyloric botulinum toxin injection.
510. Neonatal Gene Transfer with Non-Human Primate AAV Vector Serotypes Results in Widespread Transduction and Gene Activity in the Mouse Brain
Authors: Brian A. Karolewski, Hennessy Howell, John H. Wolfe
Journal: Molecular Therapy (2005)

Mucopolysaccharidosis (MPS) VII is a heritable lysosomal storage disease caused by the deficiency of Beta-glucuronidase (GUSB). MPS VII is a chronic and progressive multiorgan disorder with signs of pathology presenting early in life. Most therapeutic approaches for MPS VII have focused on adult treatments. Although these approaches can reverse storage lesions, the central nervous system (CNS) is more difficult to treat. Our lab has previously shown complementary patterns of transduction between AAV1 and after neonatal injection into the lateral cerebral ventricles (Passini et al., 2003; Journal of Virology). Using an AAV2 ITR backbone, we investigated neonatal gene transfer to the CNS of normal and MPS VII mice with capsid proteins from AAV7, AAV8, and AAV9. We injected 1.8 |[times]| 10^10 genomes of vector into the lateral cerebral ventricles (2 |[mu]|l each) of normal and MPS VII mice at birth (P O.5). At one month postinjection, each of the AAV serotypes demonstrated extensive and widespread GUSB activity and mRNA expression in the brain, but variations in transduction patterns related to substructures of the brain were observed. AAV 2/7 and AAV 2/8 transduced more cells and expressed more GUSB compared to AAV 2/9. Significant amounts of GUSB were present in the ganglion cells of the retina and spinal cord for each of the tested AAV serotypes. Evaluations of AAV gene transduction patterns and lysosomal storage correction for the eye, brain and spinal cord are ongoing. These results suggest that AAV7, AAV8, and AAV9 are suitable vectors for targeting the CNS, and may be useful for CNS gene therapy.
Transient Renal Failure Due to Simultaneous Ibuprofen and Aminoglycoside Therapy in Children with Cystic Fibrosis
Authors: Thomas A. Kovesi, Ronald Swartz, Noni MacDonald
Journal: New England Journal of Medicine (1998)

To the Editor: Ibuprofen can retard the decline in pulmonary function in children with cystic fibrosis.1 Aminoglycosides are often given to treat pulmonary infections in children with cystic fibros...
Anthony Reynold Lucius Weekes
Authors: C. Otigbah
Journal: BMJ (2008)

Anthony Reynold Lucius Weekes (“Tony”) was born in St Philip in Barbados. He was the son of a prominent parliamentarian in the Bajan government, the only boy of a family of eight sisters. His pioneering instincts were first evident when he applied for and obtained a scholarship to study medicine in Calcutta. Afterwards he came to England and worked at Oldchurch, Hackney, and Tottenham …
Emergence of Drug Tolerance in Cancer Cell Populations: An Evolutionary Outcome of Selection, Nongenetic Instability, and Stress-Induced Adaptation
Authors: Rebecca H. Chisholm, Tommaso Lorenzi, Alexander Lorz, Annette K. Larsen, Luís Neves de Almeida, Alexandre Escargueil, Jean Clairambault
Journal: Cancer Research (2015)

Abstract In recent experiments on isogenetic cancer cell lines, it was observed that exposure to high doses of anticancer drugs can induce the emergence of a subpopulation of weakly proliferative and drug-tolerant cells, which display markers associated with stem cell–like cancer cells. After a period of time, some of the surviving cells were observed to change their phenotype to resume normal proliferation and eventually repopulate the sample. Furthermore, the drug-tolerant cells could be drug resensitized following drug washout. Here, we propose a theoretical mechanism for the transient emergence of such drug tolerance. In this framework, we formulate an individual-based model and an integro-differential equation model of reversible phenotypic evolution in a cell population exposed to cytotoxic drugs. The outcomes of both models suggest that nongenetic instability, stress-induced adaptation, selection, and the interplay between these mechanisms can push an actively proliferating cell population to transition into a weakly proliferative and drug-tolerant state. Hence, the cell population experiences much less stress in the presence of the drugs and, in the long run, reacquires a proliferative phenotype, due to phenotypic fluctuations and selection pressure. These mechanisms can also reverse epigenetic drug tolerance following drug washout. Our study highlights how the transient appearance of the weakly proliferative and drug-tolerant cells is related to the use of high-dose therapy. Furthermore, we show how stem-like characteristics can act to stabilize the transient, weakly proliferative, and drug-tolerant subpopulation for a longer time window. Finally, using our models as in silico laboratories, we propose new testable hypotheses that could help uncover general principles underlying the emergence of cancer drug tolerance. Cancer Res; 75(6); 930–9. ©2015 AACR.
Antibodies to Human T-Cell Leukemia Virus Types I and III in Blood Donors from Calabar, Nigeria
Authors: Robert A. Okpara, Eka Williams, Josef Schneider, Irene Wendler, Gerhard Hunsmann
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 January 1986Antibodies to Human T-Cell Leukemia Virus Types I and III in Blood Donors from Calabar, NigeriaROBERT A. OKPARA, M.D., EKA WILLIAMS, Ph.D., JOSEF SCHNEIDER, Ph.D., IRENE WENDLER, Ph.D., GERHARD HUNSMANN, M.D.ROBERT A. OKPARA, M.D.Search for more papers by this author, EKA WILLIAMS, Ph.D.Search for more papers by this author, JOSEF SCHNEIDER, Ph.D.Search for more papers by this author, IRENE WENDLER, Ph.D.Search for more papers by this author, GERHARD HUNSMANN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-104-1-132_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Antibodies to the human T-cell leukemia virus (HTLV) have been detected in sera of African green monkeys (Cercopithecus aethiops) which are in captivity in West Germany but which naturally inhabit the savanna regions of Africa (1). This virus, or one closely related, has also been cultured from mononuclear cells of these monkeys (2). Furthermore, antibodies have been detected in blood donors and some patients with leukemia or lymphoma living in the Sahel and savanna zones of northern Nigeria (3). Recently, HTLV antibodies were detected in the blood of two patients with T-cell lymphoma as well as in...References1. HUNSMANNSCHNEIDERSCHMITTYAMATOTO GJJN. Detection of serum antibodies to adult T-cell leukemia virus in non-human primates and in people from Africa. Int J Cancer. 1983;32:329-32. CrossrefMedlineGoogle Scholar2. YAMATOTOHINUMAZUR HANSENSCHNEIDERHUNSMANN NYHJG. African green monkeys are infected with adult T-cell leukemia virus or a closely related agent. Lancet. 1983;1:240-1. CrossrefGoogle Scholar3. FLEMINGYAMATOTOBHUSNURMATHMAHARAJANSCHNEIDERHUNSMANN ANSRJG. Antibodies to ATLV (HTLV) in Nigerian blood donors and patients with chronic lymphatic leukemia or lymphoma. Lancet. 1983;2:334-5. CrossrefMedlineGoogle Scholar4. WILLIAMSALABIJUNAID CGT. Human T-cell leukemia virus-associated lymphoproliferative disease: report of two cases in Nigeria. Br Med J. 1984;288:1495-6. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByHuman retrovirusesTransmission of human immunodeficiency virus (HIV/HTLV-III/LAV): A review 1 January 1986Volume 104, Issue 1Page: 132-132KeywordsAntibodiesBloodBlood donorsCellsHIVHuman t lymphotropic virusLymphocytic leukemiaLymphoma Issue Published: 1 January 1986 PDF DownloadLoading ...
CAN STRAIN BY SPECKLE TRACKING IMAGING PREDICT MORTALITY IN PRIMARY AMYLOID PATIENTS WITH NORMAL LEFT VENTRICLE EJECTION FRACTION?
Authors: Haydar K. Saleh, Hector R. Villarraga, Diego Bellavia, Yang Yu, Yuki Koshino, Su-Feng Hsiao, Garvan C. Kane, Patricia A. Pellikka, Fletcher A. Miller
Journal: Journal of the American College of Cardiology (2010)