tbuckley/cabot-search huggingface dataset:
The Thyroid Gland and Radiation for Hodgkin's Disease
Authors: I. R. MCDOUGALL
Journal: Annals of Internal Medicine (1980)

Letters1 April 1980The Thyroid Gland and Radiation for Hodgkin's DiseaseI. R. MCDOUGALL, M.B., CH.B., PH.D.I. R. MCDOUGALL, M.B., CH.B., PH.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-92-4-572_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: I should like to comment on the paper "Radiation-Related Thyroid Dysfunction: Implications for the Treatment of Hodgkin's Disease" by Schimpff and colleagues (1) in the January issue. They state that at present there are no reports of patients with Hodgkin's disease treated by radiotherapy who later had developed thyroid cancer. There are, in fact, a small number of such cases (2-5). One of these patients was subsequently found not to have Hodgkin's disease, and the radiation doses prescribed were somewhat lower than those currently used. In addition to these, we have encountered four patients who developed thyroid...References1. SCHIMPFFDIGGSWISWELLSALVATOREWIERNIK SCJPP. Radiation-related thyroid dysfunction: implications for the treatment of Hodgkin's disease. Ann Intern Med. 1980;92:91-8. LinkGoogle Scholar2. JACQUILLATBELPOMMEWEIL CDM. Les neoplasies simultanees et sussessives. Nouv Presse Med. 1973;2:3089-92. MedlineGoogle Scholar3. MEYER O. Carcinoma of the thyroid following ionizing radiation for Hodgkin's disease. Wis Med J. 1971;70:129-33. MedlineGoogle Scholar4. MORRISHARDIN JC. Thyroid cancer in adult following external irradiation. Arch Intern Med. 1964;113:97-100. CrossrefMedlineGoogle Scholar5. WESHLERKRASNOKUKIPESHINBIRAN ZDYS. Thyroid carcinoma induced by irradiation for Hodgkin's disease: report of a case. Acta Radiol Oncol. 1978;17:383-6. Google Scholar6. MCDOUGALLCOLEMANBURKESAUNDERSKAPLAN ICJWH. Thyroid carcinoma after high-dose external radiotherapy for Hodgkin's disease: report of three cases. Cancer. In press. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: I. R. MCDOUGALL, M.B., CH.B., PH.D.Affiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1980Volume 92, Issue 4Page: 572-572KeywordsHodgkin lymphomaThyroidThyroid carcinoma ePublished: 1 December 2008 Issue Published: 1 April 1980 PDF downloadLoading ...
Medicine in Art: A Cultural History
Authors: John H. Talbott
Journal: JAMA (1968)

Within the past few weeks two important books on art have appeared in this country— 20,000 Years of World Paintings , edited by Jaffe, and Medicine in Art , edited by Rousselot. The reproductions in each volume are delightful, the lithography is outstanding, and the prices are consistent with the quality.   Medicine in Art is not an encyclopedic treatise, but it fills one void among several. Each of the principal contributors is European or European-oriented. Ilza Veith, formerly of the University of Chicago and now professor of the history of medicine at the University of California and the outstanding Western scholar of Oriental medicine, prepared the section on the Far East and the Middle East. Dusseldorf and Paris claim the other contributors.  My interest in this book is directly related to the colored cover program forThe Journal, which was started more than three years ago. The weekly selection has required me
Zonal regulation of gene expression during liver regeneration of urokinase transgenic mice
Authors: Stephanie Locaputo, Terri L. Carrick, Jorge A. Bezerra
Journal: Hepatology (1999)

Liver gene transcription plays a fundamental role in the hepatic reparative response to injury. However, little is known about the functional relationship of gene expression between diseased and regenerative compartments following a liver injury. To address the hypothesis that the control of gene expression and the cellular proliferative response are specific to diseased and regenerative liver compartments independently, we assessed the expression of liver growth modulators, hepatocyte proliferation, and apoptosis in transgenic livers overexpressing the urokinase–type plasminogen activator (uPA). uPA livers have regenerative nodules that are visually distinct from the surrounding diseased compartments. Northern analyses using RNA from microdissected regenerative and diseased compartments showed that, among the known liver growth factors studied, there was a selective increase in the expression of hepatocyte growth factor (HGF) in diseased compartments above the levels seen in regenerative compartments and in livers of nontransgenic littermates. Despite the high level of HGF mRNA in diseased compartments, hepatocyte proliferation was low. In contrast, in regenerative compartments, where HGF mRNA was low, hepatocyte proliferation was abundant. For growth inhibitors, mRNA expression for transforming growth factor β 1 (TGF–β 1 ), p53, and activin A was increased in diseased compartments, where hepatocytes displayed apoptosis. These findings define a zone–specific regulation of gene expression in injured livers and point to an important role of the diseased microenvironment in the fate of hepatocytes during the regenerative process
Cyclic flow variations in a conscious dog model of coronary artery stenoses and endothelial injury correlate with acute ischemic heart disease syndromes in humans
Authors: Hisao Ikeda, Yoshinori Koga, Kazunori Kuwano, Hiroshi Nakayama, Takafumi Ueno, Noriko Yoshida, Kyo Adachi, In Soo Park, Hironori Toshima
Journal: Journal of the American College of Cardiology (1993)
Role of intrapulmonary release of eicosanoids and superoxide anion as mediators of pulmonary dysfunction and endothelial injury in sheep with intermittent complement activation.
Authors: S Z Perkowski, A M Havill, J T Flynn, M H Gee
Journal: Circulation Research (1983)

In 30 anesthetized sheep, we show that repeated bolus injections of autologous zymosan-activated plasma produce pulmonary hypertension, hypoxemia, intrapulmonary thromboxane release, pulmonary leukostasis, and sustained increases in lung lymph flow and protein clearance. Studies with platelet-rich plasma demonstrated that addition of zymosan-activated plasma does not induce platelet aggregation or thromboxane release. We studied the role of cyclooxygenase products as mediators of these pathophysiological responses by pretreating sheep with either meclofenamate (4 mg/kg) or ibuprofen (12.5 mg/kg). Both drugs inhibited thromboxane release and hypoxemia. Ibuprofen, but not meclofenamate, reproducibly attenuated the hypertensive responses and the increases in lymph flow and protein clearance. Neither drug prevented pulmonary leukostasis. These results demonstrate that cyclooxygenase products mediate the development of complement-induced hypoxemia but are not sole mediators of pulmonary hypertension or increases in vascular permeability. Furthermore, ibuprofen has anti-inflammatory actions, not shared by meclofenamate, which enhance the effectiveness of this drug. Since activated leukocytes release reactive oxygen metabolites, we treated sheep with superoxide dismutase (2800 U/kg per hour) to determine the role of superoxide anions in these responses. This treatment significantly attenuated the increases in lung lymph flow and protein clearance. The results suggest that multiple mediators, which may originate from activated leukocytes sequestered in the pulmonary circulation, contribute to the pathophysiological changes seen with intermittent complement activation. Cyclooxygenase products of arachidonic acid contribute to the hypertension and are solely responsible for the hypoxemia. Reactive oxygen metabolites are important mediators of the complement-induced increases in lung vascular permeability.
Effects of retinoids on glycosaminoglycan synthesis by human skin fibroblasts grown as monolayers and within contracted collagen lattices
Authors: M. EDWARD
Journal: British Journal of Dermatology (1995)

Fibroblasts grown within contracted collagen lattices synthesize substantially less glycosaminoglycans than fibroblasts grown as monolayers on a plastic substrate. [3H]glucosamine incorporation into hyaluronate was reduced by 70%, and incorporation into sulphated glycosaminoglycans was reduced by 40%. However, incorporation into heparan sulphate and chondroitin sulphates was reduced by 14 and 49%, respectively, resulting in a substantial change in the proportions of the individual glycosaminoglycans. On the basis of [3H]glucosamine incorporation, hyaluronate constituted 80% of the total glycosaminoglycans synthesized in monolayer cultures, but only 67% in collagen lattice cultures. Incorporation of 35SO4 into chondroitin sulphates was reduced by 22%, whereas no change was observed in heparan sulphates following culture within collagen lattices. Exposure of the fibroblast cultures to retinotc acid (10−6mol/l) and retinyl propionate (2 × 10−6mol/l) resulted in a decrease in the incorporation of [3H]glucosamine into hyaluronate by up to 41 % in monolayer cultures, and 25% in collagen lattice cultures. The retinoids stimulated the incorporation of [3H]glucosamine into heparan sulphate by up to 72%, and chondroitin sulphates by up to 30%, whereas 35SO4 incorporation remained essentially unaltered. Only modest changes in the incorporation of both isotopes into tibroblasl sulphated glycosaminoglycans were observed following exposure to the retinoids in lattice cultures. Q-Sepharose ion-exchange chromatography at pH 2–0 revealed that there was no change in the degree of polymer sulphation of either chondroitin sulphate or heparan sulphate isolated from collagen lattice cultures compared with monolayer cultures. Retinoic acid (10−6mol/l) treatment did, however, reduce the degree of polymer sulphation of heparan sulphates and chondroitin sulphates in both monolayer and lattice cultures. The molecular mass of the sulphated glycosaminoglycans was unaffected by culture conditions, but hyaluronate isolated from collagen lattice cultures had a higher molecular mass than that from monolayer cultures. Retinoic acid treatment had no effect on the molecular mass of the glycosaminoglycans isolated from either culture system.
Predicting complete cytogenetic response and subsequent progression-free survival in 2060 patients with CML on imatinib treatment: the EUTOS score
Authors: Joerg Hasford, Michele Baccarani, Verena Hoffmann, Joelle Guilhot, Susanne Saussele, Gianantonio Rosti, François Guilhot, Kimmo Porkka, Gert Ossenkoppele, Doris Lindoerfer, Bengt Simonsson, Markus Pfirrmann, Rudiger Hehlmann
Journal: Blood (2011)
The Lilly Lecture: Macromolecular Organization of Chemical Synapses in the Central Nervous System.
Authors: E. De Robertis
Journal: Annals of Internal Medicine (1971)

Meeting Abstracts1 May 1971The Lilly Lecture: Macromolecular Organization of Chemical Synapses in the Central Nervous System.E. De Robertis, F.A.C.P., (Hon.)E. De Robertis, F.A.C.P., (Hon.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-74-5-843_4 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptElectron microscopy, in conjunction with cell fractionation and neurochemical studies, has greatly advanced our knowledge of chemical synapses in the central nervous system.The isolation of nerve endings and the recognition that synaptic vesicles are the sites of storage of the transmitters in quantal units have led to a better understanding of the mechanisms by which these active substances are synthesized, stored, released, reuptaken, or degraded, opening the possibility of a direct investigation of the action of neuro- and psycho-active drugs.Special emphasis will be placed on the separation of the nerve-ending membranes and junctional complexes with their important membrane-bound... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Buenos Aires Argentina PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1971Volume 74, Issue 5Page: 843-843KeywordsCentral nervous systemDrug synthesisDrugsElectron microscopyNerve endingsVesicles Issue Published: 1 May 1971 PDF downloadLoading ...
Adaptive differentiation of murine lymphocytes. I. Both T and B lymphocytes differentiating in F1 transplanted to parental chimeras manifest preferential cooperative activity for partner lymphocytes derived from the same parental type corresponding to the chimeric host.
Authors: D H Katz, B J Skidmore, L R Katz, C A Bogowitz
Journal: The Journal of Experimental Medicine (1978)

The concept of adaptive (selective) differentiation preducts that early differentiation of lymphocytes is conditioned by the environment in which such differentiation takes place. These processes appear to involve selection of lymphocytes according to their self-recognition between interacting lymphocytes is, at least in part, controlled by major histocompatibility complex-linked genes, then adaptive differentiation is also controlled by these genes. In these studies, we have tested the capacities of helper T lymphocytes and hapten-specific B lymphocytes primed in the environments of various combinations of bone marrow chimeras prepared between two parental strains (i.e. A/J and BALB/c) and their corresponding F1 hybrid (CAF1) to interact with primed B and T lymphocytes derived from conventional parent and F1 donors as well as all of the corresponding bone marrow chimera combinations. The results demonstrate clearly that (a) F1 transplanted to F1 chimeric lymphocytes display no restriction in terms of cooperative activity with all of the various partner cell combinations; (b) parent transplanted to F1 chimeric lymphocytes manifest effective cooperative activity only for partner cells from F) or parental donors corresponding to the haplotype of the original bone marrow donor, thereby behaving phenotypically just like conventional parental lymphocytes; and (c) F1 transplanted to parent chimeric lymphocytes display restricted haplotype preference in cooperating best with partner lymphocytes sharing the H-2 haplotype, either entirely or codomimantly, of the parental chimeric host. The implications of these findings for understanding certain controlling mechanisms for lymphocyte differentiation are discussed.
Fatal Pancarditis in a Patient with Coexistent Lyme Disease and Babesiosis
Authors: LEONARD C. MARCUS
Journal: Annals of Internal Medicine (1985)

A 66-year-old man developed fever, chills, myalgias, three erythematous skin lesions, and transient left eyelid lag. Because of persistent fever, he was hospitalized 4 weeks after the onset of disease; a peripheral blood smear showed Babesia microti in 3% of his erythrocytes. Eighteen hours later, he died unexpectedly. Autopsy showed pancarditis with a diffuse lymphoplasmacytic infiltrate, and spirochetes were found in the myocardium. Antibody titers to both the Lyme disease spirochete Borrelia burgdorferi and Babesia microti were elevated. The finding of spirochetes in the myocardium and the elevated antibody titers to Borrelia burgdorferi suggest that the patient died from cardiac involvement of Lyme disease.
THE BREATHING AND THE PULSE UNDER THE INFLUENCE OF CHLOROFORM
Authors: J. Snow
Journal: BMJ (1855)

APRIL 6, esusctated from a state of suspended animation.*The acidents were, no doubt, chiefly due to the circumstance tat it had been the custom to use the diluted preparation more freely than pure chlorororm would have been used; still they illustrate equally well the compartive safety of diluted and undiluted chloroform, when used on a sponge or handkerchief.Dr. J. Mason Warren has informed me that, since these accidents, the governors of the hospital have prohibited the inhalation of any other agent than sulphuric ether, for pre- venting pain in surgical operations.
Evolution of Beta Satellite DNA Sequences: Evidence for Duplication-Mediated Repeat Amplification and Spreading
Authors: M. F. Cardone, L. Ballarati, M. Ventura, M. Rocchi, A. Marozzi, E. Ginelli, R. Meneveri
Journal: Molecular Biology and Evolution (2004)

In this article, we report studies on the evolutionary history of beta satellite repeats (BSR) in primates. In the orangutan genome, the bulk of BSR sequences was found organized as very short stretches of approximately 100 to 170 bp, embedded in a 60-kb to 80-kb duplicated DNA segment. The estimated copy number of the duplicon that carries BSR sequences ranges from 70 to 100 per orangutan haploid genome. In both macaque and gibbon, the duplicon mapped to a single chromosomal region at the boundary of the rDNA on the marker chromosome (chromosome 13 and 12, respectively). However, only in the gibbon, the duplicon comprised 100 bp of beta satellite. Thus, the ancestral copy of the duplicon appeared in Old World monkeys (∼25 to ∼35 MYA), whereas the prototype of beta satellite repeats took place in a gibbon ancestor, after apes/Old World monkeys divergence (∼25 MYA). Subsequently, a burst in spreading of the duplicon that carries the beta satellite was observed in the orangutan, after lesser apes divergence from the great apes–humans lineage (∼18 MYA). The analysis of the orangutan genome also indicated the existence of two variants of the duplication that differ for the length (100 or 170 bp) of beta satellite repeats. The latter organization was probably generated by nonhomologous recombination between two 100-bp repeated regions, and it likely led to the duplication of the single Sau3A site present in the 100-bp variant, which generated the prototype of Sau3A 68-bp beta satellite tandem organization. The two variants of the duplication, although with a different ratios, characterize the hominoid genomes from the orangutan to humans, preferentially involving acrocentric chromosomes. At variance to alpha satellite, which appeared before the divergence of New World and Old World monkeys, the beta satellite evolutionary history began in apes ancestor, where we have first documented a low-copy, nonduplicated BSR sequence. The first step of BSR amplification and spreading occurred, most likely, because the BSR was part of a large duplicon, which underwent a burst dispersal in great apes' ancestor after the lesser apes' branching. Then, after orangutan divergence, BSR acquired the clustered structural organization typical of satellite DNA.
Nanotechnology: small science, big deal
Authors: Tony Delamothe
Journal: BMJ (2005)

An exhibition at the Science Museum, London, until 31 August 2005, after which it will tour the United Kingdom www.sciencemuseum.org.uk/antenna/nano/index.asp Rating: ![Graphic][1]</img>![Graphic][2]</img>![Graphic][3]</img> T he Science Museum's latest exhibition defines its subject as the active making, manipulation, and measurement of extremely tiny things. These things are measured in nanometres, with a nanometre being a millionth of a millimetre, or about as far as a fingernail grows in a second. At the nanoscale, materials behave differently, and it's their weird and wonderful properties that nanotechnology sets out to exploit. Increased reactivity is one such property—a function of the increased ratio of an object's surface area to its volume as … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif [3]: /embed/inline-graphic-3.gif
Association Between Body Iron Stores and the Risk of Acute Myocardial Infarction in Men
Authors: Tomi-Pekka Tuomainen, Kari Punnonen, Kristiina Nyyssönen, Jukka T. Salonen
Journal: Circulation (1998)

Background —Epidemiological evidence concerning the role of iron, a lipid peroxidation catalyst, in coronary heart disease (CHD) is inconsistent. We investigated the association of the concentration ratio of serum transferrin receptor to serum ferritin (TfR/ferritin), a state-of-the-art measurement of body iron stores, with the risk of acute myocardial infarction (AMI) in a prospective nested case-control study in men from eastern Finland. Methods and Results —Transferrin receptor assays were carried out for 99 men who had an AMI during an average 6.4 years of follow-up and 98 control men. Both the cases and the controls were nested from the Kuopio Ischemic Heart Disease Risk Factor Study (KIHD) cohort of 1931 men who had no clinical CHD at the baseline study. The controls were matched for age, examination year, and residence. AMIs were registered prospectively. Soluble transferrin receptors were measured by immunoenzymometric assay and ferritin concentration by radioimmunoassay from frozen baseline serum samples. The mean TfR/ferritin ratio was 15.1 (SE, 2.0) among cases and 21.3 (SE, 2.2) among controls ( P =.035 for difference). In logistic regression models adjusting for other strongest risk factors for AMI and indicators of inflammation and alcohol intake, men in the lowest and second lowest thirds of the TfR/ferritin ratio had a 2.9-fold (95% CI, 1.3 to 6.6, P =.011) and 2.0-fold (0.9 to 4.2, P =.081) risk of AMI compared with men in the highest third ( P =.010 for trend). Conclusions —These data show an association between increased body iron stores and excess risk of AMI, confirming previous epidemiological findings.
Sideroblastic Anemia with Splenic Abscess and Fatal Thromboemboli after Splenectomy
Authors: SYED H. ALEALI
Journal: Annals of Internal Medicine (1975)

A man with sideroblastic anemia had a splenectomy because of a salmonella abscess of the spleen that had ruptured into the colon. Two months later he developed recurrent thrombophlebitis and fatal thromboembolism associated with thrombocytosis. A review of the literature showed multiple additional cases of sideroblastic anemia with thrombocytosis and thromboembolism after splenectomy. In many of these cases the patient died. Splenectomy for treatment of a sideroblastic anemia probably is contraindicated. If splenectomy is done, long-term therapy to avoid thromboembolic complications probably should be maintained for many months or even years.
Withdrawal From Benzodiazepine Therapy
Authors: Leo E. Hollister
Journal: JAMA (1977)

<h3>To the Editor.—</h3> The report of three cases of "withdrawal psychosis" following abrupt discontinuation of benzodiazepine therapy (237:36, 1977) could be misleading because of the use of this unfortunate term. What the authors observed was the same spectrum of psychic symptoms repeatedly reported from withdrawal reactions to alcohol or other sedativehypnotic drugs. "Acute brain syndrome due to drug withdrawal" is a much more precise phrase. Psychotic symptoms have not been prominent in the relatively few withdrawal reactions to benzodiazepines reported in the medical literature since our first experimental study (<i>Psychopharmacologia</i>2:63-68, 1961). These reactions are modified in severity and attenuated over time because of the long persistence of the drug and its active metabolites in the body. Withdrawal reactions are dependent on high dosage of drug sustained rather constantly over time, with rapid rate of disappearance of the drug when it is discontinued. Drugs such as the benzodiazepines (or phenobarbital)