tbuckley/cabot-search huggingface dataset:
FATTY AND FIBROID DEGENERATIONS. BRIGHT'S DISEASE, APOPLEXY, FATTY HEART, PUERPERAL CONVULSIONS, CATARACT, ETC.
Authors: EPHRAIM CUTTER
Journal: JAMA (1892)

INTRODUCTION. Space does not warrant more than a consideration here of fatty degeneration, somewhat in detail, with a short notice of fibroid degeneration; indeed, the explication of the first is none too full when the importance of the subject is noted. This medical contribution is contrary to the somewhat conventional pathology whose nomenclature ends in "itis." THE FATTY DEGENERATIONS. <i>General Principals</i>.—Fatty degeneration is where tissues that are normal parts of organs are replaced by fat in its many forms of oily, lardaceous, waxy, glassy, atheromatous, soapy and crystalline bodies. For example:<i>a</i>. When the muscular tissues of the heart are more or less changed into fat, it is fatty degeneration.<i>b</i>. When the circular muscular fibres of the arteries, the terminals of the arteries and the capillaries, are changed into cholesterine, it is fatty degeneration.<i>c</i>. When the kidneys are more or less changed into fat, it is fatty degeneration.
Strategies to help patients understand risks
Authors: J. Paling
Journal: BMJ (2003)

Explaining risks to patients in an effective way is an essential part of ensuring that consent is “informed.” A consultant in risk communication discusses the strategies that can help doctors to communicate risks clearly, and thereby also build closer relationships with their patients



Fig 2 
Paling Perspective Scale ©–for giving perspective to risks of low order of probability.16 From research report by Small P et al17





Fig 3 
Paling Palette© –for displaying most medical risks with a probability of higher than 1 in 1000.16 The doctor or genetic counsellor fills in the relevant data while sitting beside the patient. This format shows the estimates of positive and negative outcomes simultaneously and presents unambiguous visual representations of the probabilities. The patient may take a printout home for further consideration, or the form may be signed by the patient and a copy kept on file





Fig 4 
Revised Paling Perspective Scale© –for displaying risks covering widely different orders of magnitude16



Effective risk communication is the basis for informed patient consent for medical treatment, yet until recently doctors have lagged behind other professionals in learning this skill. In other industries where risks have to be conveyed to the public (such as chemical, nuclear, water, and food industries) usually only a few people carry out this task on behalf of their organisations and they are specially trained. In contrast, in health care (where the risks are usually far higher and more uncertain and complex) almost every doctor who interacts with patients has to communicate information on risk, yet few have any training.

Specific strategies can help to remedy this deficiency and improve patients' understanding of risks. Doctors can now choose from a “toolbox” of simple, practical, time efficient techniques that benefit the widest possible variety of patients.

I have taught risk communication in risk prone professions …
Homozygous silencing of T-box transcription factor EOMES leads to microcephaly with polymicrogyria and corpus callosum agenesis
Authors: Lekbir Baala, Sylvain Briault, Heather C Etchevers, Frédéric Laumonnier, Abdelhafid Natiq, Jeanne Amiel, Nathalie Boddaert, Capucine Picard, Aziza Sbiti, Abdellah Asermouh, Tania Attié-Bitach, Féréchté Encha-Razavi, Arnold Munnich, Abdelaziz Sefiani, Stanislas Lyonnet
Journal: Nature Genetics (2007)
New molecularly targeted therapies for lung cancer
Authors: Sophie Sun, Joan H. Schiller, Monica Spinola, John D. Minna
Journal: Journal of Clinical Investigation (2007)

Lung cancer is the leading cause of cancer death worldwide. The disease is particularly difficult to detect, and patients often present at an advanced stage. Current treatments have limited effectiveness, and unfortunately, the prognosis remains poor. Recent insights into the molecular pathogenesis and biologic behavior of lung cancer have led to the development of rationally designed methods of early detection, prevention, and treatment of this disease. This article will review the important clinical implications of these advances, with a focus on new molecularly targeted therapies currently in development.
Lifetime Cigarette Smoking and Colorectal Cancer Incidence in the Physicians' Health Study I
Authors: T. Sturmer
Journal: JNCI Journal of the National Cancer Institute (2000)

1.5 (0.9) 1.5 (0.9) 1.4 (0.9) Mean fruit servings (SD), No. per day 0.9 (0.7) 0.8 (0.7) 0.8 (0.7) Smoking history, pack-years‡
Shepard’s Prayer
Authors: Jeremy M. Blumberg
Journal: JAMA (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Increased risk for CNS relapse in pre-B cell leukemia with the t(1;19)/TCF3-PBX1
Authors: S Jeha, D Pei, S C Raimondi, M Onciu, D Campana, C Cheng, J T Sandlund, R C Ribeiro, J E Rubnitz, S C Howard, J R Downing, W E Evans, M V Relling, C-H Pui
Journal: Leukemia (2009)
Tips for a Physician in Getting the Right Job, Part XXII
Authors: Jay A. Harolds
Journal: Clinical Nuclear Medicine (2015)

This article discusses contract negotiations on multiple issues including bonuses, restrictive covenants, and fringe benefits. However, the job seeker should be very careful about attempting to negotiate what is already a very good contract if he/she does not have alternative employment opportunities or is not a very strong candidate. In addition, often more important than the contract is the character of the people the job seeker would be working for. If the employers do not seem to be honorable, it is usually best to look elsewhere.
Noxythiolin-resistant organisms.
Authors: K G Edwards
Journal: BMJ (1977)

some studies.As an example of a possible relationship between malignant lymphoma and PMR on this ground they refer to a case described by usI in which malignant lymphoma occurred four years after the diagnosis of PMR was made.Among our 54 patients with PMR we have recently reported another case', in which chronic lymphatic leukaemia developed five years after the onset of typical PMR.In this patient lymphocytic infiltration was detected in renal, liver, and muscle biopsy specimens at the time of diagnosis of PMR, when the number of lymphocytes in the peripheral blood and bone marrow was normal.The significance of the combination of the two diseases in this patient is unclear.It may simply be the coincidental coexistence of two diseases, both relatively common in elderly people.However, the clinical course does point to a more direct relationship.Histocompatibility antigens have been studied in patients with chronic lymphatic leukaemia, but, so far as I know, no increase in any specific HLA haplotype has been shown.
Elevated IgE level in relationship to nutritional status and immune parameters in early human immunodeficiency virus–1 disease
Authors: Gail Shor-Posner, Maria Jose Miguez-Burbano, Ying Lu, Daniel Feaster, MaryAnn Fletcher, Howerde Sauberlich, Marianna K. Baum
Journal: Journal of Allergy and Clinical Immunology (1995)
Communication and consciousness: A neural network conjecture
Authors: N. A. Schmajuk, E. Axelrad
Journal: Behavioral and Brain Sciences (1995)

Abstract The communicative aspects of the contents of consciousness are analyzed in the framework of a neural network model of animal communication. We discuss some issues raised by Gray, such as the control of the contents of consciousness, the adaptive value of consciousness, conscious and unconscious behaviors, and the nature of a model's consciousness.
Abstract A30: NF1 is a tumor suppressor in neuroblastoma that determines retinoic acid response and disease outcome
Authors: Michael Hölzel, Sidong Huang, Jan Koster, Ingrid Ora, Arjan Lakeman, H. N. Caron, Tom Callens, Jing Xie, Wouter Nijkamp, Shahab Asgharzadeh, Robert C. Seeger, Ludwine Messiaen, Rogier Versteeg, Rene Bernards
Journal: Clinical Cancer Research (2010)

Abstract Neuroblastoma is a malignancy of early childhood that derives from the developing neural crest and accounts for 15% of all paediatric oncology deaths. The vitamin A derivative retinoic acid (RA) controls neural development and promotes differentiation, cell cycle arrest and apoptosis of neuronal and neuroblastoma cells. These diverse effects of RA are exerted primarily through the ability to differentially regulate gene expression mediated by the retinoic acid receptors (RARs). RA is used in the clinic to treat high-risk neuroblastoma patients, however with variable success. This variability in clinical response to RA is enigmatic as no mutations in components of the RA signaling cascade have been found. By using large-scale RNAi-based genetic screens, we aimed to identify predictive biomarkers for RA sensitivity in neuroblastoma. We found an unexpected crosstalk between the tumor suppressor neurofibromin (NF1) and RA signaling. NF1 is a negative regulator of RAS signaling that promotes conversion of the active GTP bound form into the inactive GDP bound form of RAS. Activation of RAS-MEK signaling by loss of NF1 repressed ZNF423, a critical transcriptional co-activator of the retinoic acid receptors, and blocked RA induced differentiation and target gene activation. Restoration of ZNF423 levels resensitized NF1 knockdown cells to the inhibitory effect of RA. Moreover, ZNF423 and NF1 expression predicted sensitivity to RA in a large panel of neuroblastoma cell lines. Neuroblastomas with low levels of both NF1 and ZNF423 have extremely poor outcome. We found NF1 mutations in neuroblastoma cell lines and also in primary tumors. Inhibition of MEK signaling downstream of NF1 restored responsiveness to RA, suggesting a therapeutic strategy to overcome RA resistance in NF1 deficient neuroblastomas. Citation Information: Clin Cancer Res 2010;16(7 Suppl):A30
TISSUE DISTRIBUTION OF I131 LABELED HUMAN SERUM ALBUMIN FOLLOWING INTRAVENOUS ADMINISTRATION
Authors: Marcus A. Rothschild, Arthur Bauman, Rosalyn S. Yalow, Solomon A. Berson
Journal: Journal of Clinical Investigation (1955)

Previous studies utilizing I'sl' labeled human serum albumin have revealed that approximately 60 per cent of the total exchangeable albumin of nonedematous subjects is in extravascular loca- tions (1, 2).Following intravenous administra- tion, approximately 4 to 7 days are required for essentially complete equilibration of the labeled albumin between plasma and extravascular tissues (2, 3).In almost all cases the plasma disappearance curves, appropriately corrected for metabolic degradation, manifest two major components with half times of approximately 3 to 5 hours and 24 to 30 hours, respectively, suggesting that there are at least two groups of albumin containing extravascu- lar compartments which equilibrate with plasma at different rates (2, 3).However, the distribu- tion of extravascular albumin and the anatomical sites of the rapidly and slowly equilibrating ex- travascular compartments have not yet been quan- titatively defined although previous studies utiliz- ing massive doses of heterologous serum proteins in rabbits established the presence of these pro- teins in the extravascular phase of muscle 48 hours after intravenous administration (4).During the course of recent investigations on the fate of Ils' labeled human serum albumin in heart failure (3), the deaths of two subjects, 1 and 22 days, respectively, following the intravenous administration of the labeled albumin, offered the opportunity for post mortem analysis of radio- activity in the various tissues.The times of death were such that comparison between the two cases yielded suggestive information regarding the dis- tribution of iodoalbumin and the sites of the slowly and rapidly equilibrating extravascular compartments.Further observations were then made on skin and muscle tissue removed during surgical operations.
Couple select healthy embryo to provide stem cells for sister
Authors: D. Josefson
Journal: BMJ (2000)

A couple in Colorado, United States, has used in vitro fertilisation and preimplantation genetics to produce embryos and have them screened for a child who could be a stem cell and bone marrow donor for their daughter.

The case, which has provoked widespread discussion about the ethical issues involved, is believed to be the first known instance where preimplantation genetics was used both to screen for a disease and to ensure a tissue donor match in a sibling.

The couple's daughter, 6 year old Molly Nash, was born with Fanconi's anaemia. Fanconi's anaemia is a rare, autosomal recessive disease …
708 IL-5 secretion by allergen-specific CD4+ cells in short-term culture: dissociation from allergen-induced proliferation and dependence on B7-2 co-stimulation
Authors: J BUNGRE, S TILL, M LARCHE, M HUMBERT, D ROBINSON, D HUSTON, R DICKASON, A KAY, C CORRIGAN
Journal: Journal of Allergy and Clinical Immunology (1996)
The origin of the chemiluminescence of phagocytosing granulocytes.
Authors: B D Cheson, R L Christensen, R Sperling, B E Kohler, B M Babior
Journal: Journal of Clinical Investigation (1976)

Granulocytes engaged in the phagocytosis of opsonized zymosan emit light by a process that is inhibited by superoxide dismutase and catalase. In the present report is is shown that light emission is the result of reactions between certain unspecified constituents of the ingested particles and some or all of the oxidizing agents (H2O2, O2),and possibly the hydroxyl radical and singlet oxygen) produced by the activated cells. This conclusion is based on a study of light emission by both activated cells ans artificial O2 generating system containing xanthine oxidase and purine. With these two systems light production required the presence of both zymosan and oxidizing agent, suggesting that the oxidation of particle components is necessary for luminescence to occur. The characteristics of the emission spectrum as well as the finding that granulocytes activated by a nonparticulate agent (F-) fail to liminesce show that light emission by the relaxation of singlet oxygen to the ground state does not contribute in a major way to the chemiluminescence of phagocytosing granulocytes; whether singlet oxygen contributes to chemiluminescence in other ways cannot be decided from the data available. Inasmuch as the oxidation of constituents of ingested particles is an important bacterial killing mechanism in the granulocyte, chemiluminescence may be viewed as a manifestation of the microbicidal activity of the cell.
Randomised double blind trial of somatostatin in the treatment of massive upper gastrointestinal haemorrhage.
Authors: I Magnusson, T Ihre, C Johansson, U Seligson, S Torngren, K Uvnas-Moberg
Journal: Gut (1985)

In order to evaluate the effect of somatostatin in the treatment of massive upper gastrointestinal bleeding a randomised double blind trial of 95 patients has been undertaken during a 28 months period. Patients with oesophageal varices have been excluded as well as patients with diabetes. All patients were endoscoped within eight hours of admission to the hospital, whereupon the source of bleeding and types of stigmata were assessed. Forty six patients, chosen at random, were given a 72 hour infusion of somatostatin, while the remaining 49 patients received infusion of placebo. The two groups were well matched for sex, age, and source of bleeding. On the day after admission, an additional endoscopy was performed at which eight patients in the somatostatin group and 16 in the placebo group were found to have a persistent bleeding. A total of five patients in the somatostatin group and 14 in the placebo group underwent surgery (Fisher9s exact test, 2-tail, p = 0.04). Rebleeding occurred in six patients in the somatostatin group, of whom five experienced rebleeding after completion of the somatostatin treatment. In the placebo group, rebleeding occurred in five patients, of whom four rebled on the day after admission. The need for blood transfusions and the mortality rate did not differ significantly between the two groups. No toxic side effects were found as a result of the infusion of somatostatin. In this study, somatostatin reduced the number of patients needing surgery with massive upper gastrointestinal bleeding.
Adjuvant Chemotherapy of Breast Cancer
Authors: Stephen K. Carter
Journal: New England Journal of Medicine (1981)

Adjuvant chemotherapy of breast cancer involves the use of cytotoxic drugs after local and regional therapy has been given. It received extensive notice throughout the last half of the 1970s and is now established as a therapeutic concept. Its purpose is to eradicate micrometastases and to permit long-term, disease-free survival (cure) in patients who would otherwise relapse with surgery alone.Adequate analysis of adjuvant trials will take many years of follow-up.1 Early analysis will compare relapse-free survival or time to recurrence against acute toxicity and economic and psychosocial costs. Late analysis will involve comparison of overall survival and pattern of . . .
Pregnancy-Associated Plasma Protein A as a Marker of Acute Coronary Syndromes
Authors: Antoni Bayes-Genis, Cheryl A. Conover, Michael T. Overgaard, Kent R. Bailey, Michael Christiansen, David R. Holmes, Renu Virmani, Claus Oxvig, Robert S. Schwartz
Journal: New England Journal of Medicine (2001)

Circulating markers indicating the instability of atherosclerotic plaques could have diagnostic value in unstable angina or acute myocardial infarction. We evaluated pregnancy-associated plasma protein A (PAPP-A), a potentially proatherosclerotic metalloproteinase, as a marker of acute coronary syndromes.
The Suitability of HIV-Positive Individuals for Marriage and Pregnancy
Authors: Ronald O. Gilcher
Journal: JAMA (1989)

<h3>To the Editor. —</h3> In the Oct 7 issue of<i>JAMA</i>, Drs Haverkos and Edelman<sup>1</sup>reviewed the current epidemiology of acquired immunodeficiency syndrome among heterosexuals. In reviewing the prevalence of human immunodeficiency virus (HIV) seropositivity among selected segments of the general population, they cited the<i>Morbidity and Mortality Weekly Report</i><sup>2</sup>article in which HIV seroprevalence among blood donors was presented. The prevalence for HIV seropositivity was 0.035% in mid1985 (35 individuals per 100 000 blood donor population) and had declined to 0.012% (12 per 100 000) by mid-1987, not 35 per 1000 donors and 12 per 1000 donors, respectively, as quoted by the authors. With the current climate concerning the safety of the blood supply, one must be careful to quote accurate statistical data.
Glycogen Synthase Kinase 3β Inhibits Myocardin-Dependent Transcription and Hypertrophy Induction Through Site-Specific Phosphorylation
Authors: Cornel Badorff, Florian H. Seeger, Andreas M. Zeiher, Stefanie Dimmeler
Journal: Circulation Research (2005)

Cardiomyocyte hypertrophy is transcriptionally controlled and inhibited by glycogen synthase kinase 3beta (GSK3beta). Myocardin is a muscle-specific transcription factor with yet unknown relation to hypertrophy. Therefore, we investigated whether myocardin is sufficient to induce cardiomyocyte hypertrophy and whether myocardin is regulated by GSK3beta through site-specific phosphorylation. Adenoviral myocardin overexpression induced cardiomyocyte hypertrophy in neonatal rat cardiomyocytes, with increased cell size, total protein amount, and transcription of atrial natriuretic factor (ANF). In vitro and in vivo (HEK 293 cells) kinase assays with synthetic peptides and full-length myocardin demonstrated that myocardin was a "primed" GSK3beta substrate, with serines 455 to 467 and 624 to 636 being the major GSK3beta phosphorylation sites. Myocardin-induced ANF transcription and increase in total protein amount were enhanced by GSK3beta blockade (10 mmol/L LiCl), indicating that GSK3beta inhibits myocardin. A GSK3beta phosphorylation-resistant myocardin mutant (8xA) activated ANF transcription twice as potently as wildtype myocardin under basal conditions with GSK3beta being active. Conversely, a GSK3beta phospho-mimetic myocardin mutant (8xD) was transcriptionally repressed after GSK3beta blockade, indicating that GSK3beta phosphorylation at the sites identified inhibits myocardin transcriptional activity. GAL4-myocardin fusion constructs demonstrated that GSK3beta phosphorylation reduced the intrinsic myocardin transcriptional activity. A cell-permeable (Antennapedia protein transduction tag) peptide containing the mapped myocardin GSK3beta motifs 624 to 636 induced hypertrophy of cultured cardiomyocytes, suggesting that the peptide acted as substrate-based GSK3beta inhibitor in cardiomyocytes. Therefore, we conclude that the GSK3beta-myocardin interaction constitutes a novel molecular control of cardiomyocyte hypertrophy. Phosphorylation by GSK3beta comprises a novel post-transcriptional regulatory mechanism of myocardin.
Interaction of glucagon and pentagastrin on pepsin secretion in healthy subjects.
Authors: J Christiansen, J J Holst, J Molin
Journal: Gut (1982)

The effect of pentagastrin in step-wise increasing doses of 0 . 02, 2 . 0 and 20 nmol/kg/h (0 . 01, 1 . 0, and 10 . 0 micrograms/kg/h) on pepsin and acid secretion was studied in seven healthy subjects. The study was repeated on another day during infusion of glucagon in a dose of 103 pmol/kg/h (0 . 36 micrograms/kg/h) which results in plasma-glucagon concentrations comparable with those seen after a protein-rich meal. Pepsin output was maximal after 0 . 2 nmol/kg/h (0 . 1 microgram/kg/h) of pentagastrin and 20 nmol/kg/h (10 micrograms/kg/h) resulted in a marked decrease. The dose of pentagastrin required for half-maximal pepsin output was less than 0 . 1 nmol/kg/h (0 . 05 micrograms/kg/h). When the study was repeated during infusion of glucagon, the dose-response curve was shifted to the right. The highest pepsin output was obtained with 20 nmol/kg/h (10 micrograms/kg/h) of pentagastrin and D50 increased to well over 1 microgram/kg/h. The dose of pentagastrin required for half-maximal acid secretion was about 0 . 3 nmol/kg/h (0 . 15 micrograms/kg/h) indicating that the sensitivity of the chief cells to pentagastrin is more than three times that of the parietal cells.