tbuckley/cabot-search huggingface dataset:
Radioimmunoassay of ACTH in plasma
Authors: Solomon A. Berson, Rosalyn S. Yalow
Journal: Journal of Clinical Investigation (1968)

Techniques are described in detail for a radioimmunoassay of plasma adrenocorticotropin (ACTH) that is capable of detecting hormone in unextracted normal human plasma at 1:5 dilution under the conditions described. The sensitivity of the assay is at the level of 1 μμg/ml (equivalent to 0.014 mU/100 ml).
Erythropoietin in Patients With ST-Segment Elevation Myocardial Infarction—Reply
Authors: Samer S. Najjar
Journal: JAMA (2011)

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
A Midpoint Assessment of the American Cancer Society Challenge Goal to Decrease Cancer Incidence by 25% Between 1992 and 2015
Authors: R. L. Sedjo, T. Byers, E. Barrera, C. Cohen, E. T. H. Fontham, L. A. Newman, C. D. Runowicz, A. G. Thorson, M. J. Thun, E. Ward, R. C. Wender, H. J. Eyre
Journal: CA A Cancer Journal for Clinicians (2007)

In 1998, the American Cancer Society (ACS) set a challenge goal for the nation to reduce cancer incidence by 25% over the period between 1992 and 2015. This report examines the trends in cancer incidence between 1992 and 2004. Trends were calculated using data on incident malignant cancer cases from the Surveillance, Epidemiology, and End Results (SEER) Registry. Delay-adjusted incidence trends for all cancer sites; all cancer sites without prostate cancer included; all cancer sites stratified by gender, age, and race; and for 20 selected cancer sites are presented. Over the first half of the ACS challenge period, overall cancer incidence rates have declined by about 0.6% per year. The greatest overall declines were observed among men and among those aged 65 years and older. The pace of incidence reduction over the first half of the ACS challenge period was only half that necessary to put us on target to achieve the 25% cancer incidence reduction goal in 2015. New understandings of preventable factors are needed, and new efforts are also needed to better act on our current knowledge about how we can prevent cancer, especially by continuing to reduce tobacco use and beginning to reverse the epidemic of obesity.
Abstract 2260: c-Myc induced senescence is dependent on transactivation of actin depolymerizing factor (ADF)/cofilin to mediate potent bystander effect
Authors: Shih-Ting Lin, Cheng-Han Tsai, Yi-Jang Lee, Chia-Chien Lo, Yen-Ting Chou
Journal: Cancer Research (2014)

Abstract Oncogene-induced senescence may prevent unlimited proliferation and lead to cell death. This phenomenon is likely to be associated with up-regulation of p53 and p16INK4 tumor suppressor. Morphological transformation is also an important feature of senescence that exhibits enlarged cell volume and flat morphology. In this study, we found that c-Myc was co-upregulated with cofilin-1, an actin-binding protein essential for actin dynamics and morphological maintenance in replicative senescence. Additionally, oxidative stress induced senescent phenotypes also accompanied by up-regulation of both c-myc and cofilin-1. Knockdown of cofilin-1 was sufficient to minimize the cell shapes and senescence associated β-galactosidase marker that was induced by over-expressed c-myc or oxidative stress. Over-expression of cofilin-1 was also sufficient to induce senescence in the absence of p53 and p16INK4, but was unable to influence c-Myc level. On the other hand, over-expression of c-Myc could induce cofilin-1 expression. We next found that c-myc was able to induce the transactivation of cofilin-1 gene according to results of quantitative polymerase chain reaction (qPCR) and luciferase reporter gene assay. Furthermore, the results of ChIP assay provided evidence that c-myc can bind to two proximal E-box elements nearby the transcriptional initiation on cofilin-1 gene promoter. Although c-myc promoted cellular senescence in vitro, the conditional medium from c-myc over-expressing A549 cells accelerated migration and proliferation in separate cultured cells without c-myc over-expression. Knockdown of cofilin-1 also alleviated this bystander effect caused by over-expression of c-myc. Therefore, c-myc oncogene may require cofilin-1 for cell senescence that influences the growth of other tumor cells. Taken together, current data provide evidence that c-myc/cofilin-1 signaling pathway is a novel mechanism on promoting oncogene-induced cellular senescence and tumor progression. Citation Format: Shih-Ting Lin, Cheng-Han Tsai, Yi-Jang Lee, Chia-Chien Lo, Yen-Ting Chou. c-Myc induced senescence is dependent on transactivation of actin depolymerizing factor (ADF)/cofilin to mediate potent bystander effect. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2260. doi:10.1158/1538-7445.AM2014-2260
Is Weight Lifting Deleterious to the Spines of Young People?
Authors: T. A. Mason
Journal: British Journal of Sports Medicine (1970)

This matter arises for me as a weight lifter since 1924, with a long record of youth work, because the Governing Body for Weight Lifting recently held a "schoolboys ' Championship" on the three Olympic Lifts for lads of 14 to 16 years of age.
TWO UNCOMMON CASES OF NASAL TUMORS.
Authors: RICHMOND McKINNEY
Journal: JAMA (1902)

<h3>CYST OF INFERIOR BONY TURBINAL.</h3> Alice S., of Grenada, Miss., colored, aged approximately between 30 and 35 years, a stout, apparently healthy woman, consulted me on Nov. 16, 1901, with the following history: She had had a fulness in the right nostril for some time, the exact date of its beginning being indefinite, but perhaps could be traced back several months. The condition occasioned no pain, only inconvenience. The growth in her nose had been incised on two different occasions, but according to her statement nothing other than a little blood followed each of these incisions. Examination revealed an enlargement of the anterior end of the inferior turbinated body. This growth was sessile and practically completely occluded the naris. On pressure with a probe, the swelling proved to be edematous. Under cocain anesthesia the tumor was incised, and a thin, sero-purulent discharge, about a teaspoonful in quantity, followed the incision.
The Diagnosis of Neonatal Diabetes in a Mother at 25 Years of Age
Authors: Divya Khurana, Maria Contreras, Neha Malhotra, Renee Bargman
Journal: Diabetes Care (2012)

Neonatal diabetes (ND) is defined as persistent hyperglycemia in the first 3 months of life (1). Heterozygous—usually autosomal-dominant—activating mutations in KCNJ11 , which encode the Kir6.2 subunit of the ATP-potassium (KATP) channel, cause the majority of cases (2). Sulfonylureas close the KATP channel by an ATP independent route (2).

A 25-year-old Bangladeshi woman with type 1 diabetes gave birth to a baby girl. The mother had been on insulin for more than 20 years with inadequate glycemic control but never ketoacidosis. The baby was small for gestational age (2.4 kg, <3%). On day 2 of her life, the baby was noted to be increasingly hyperglycemic, reaching 312 mg/dL by day 7. Given the clinical suspicion for ND, a trial of glyburide was initiated at 0.45 mg/kg/day, and the baby responded well. The …
The Future of Health Care: Military Model? Canadian Cost Cutting?-Reply
Authors: Ronald Bronow
Journal: JAMA (1990)

In Reply.—  Captain Miller has capably presented his views about military medicine. However, I won't work for the government. If it runs the health care system, the budget rather than my patients' needs will get primary consideration. The newspapers announce that the budget deficit will be $200 billion this year, largely because of the savings and loan fiasco ( Los Angeles Times . June 22, 1990:A18). Who will pay? It certainly won't be the crooks who created the mess. President Bush has decided he wants to cut $17 billion out of Medicare and Medicaid instead. Entitlement programs are the fairest game for the cost cutters. After that, our taxes will be raised. The military experience, with 9 million patients, won't work for 250 million. The government can't and won't fund it.  Captain Miller is certainly correct, however, about the regulation, litigation, and vilification of the American physician. This has led many of
Myelotoxicity induced in female B6C3F1 mice by inhalation of methyl isocyanate.
Authors: H L Hong, J R Bucher, J Canipe, G A Boorman
Journal: Environmental Health Perspectives (1987)

The effects of a 4-day inhalation exposure (6 hr/day) to 0, 1, and 3 ppm methyl isocyanate (MIC) on bone marrow parameters in female mice were examined at 5, 8, and 21 days following exposure. The MIC exposure was associated with myelotoxicity as evidenced by hypocellularity, suppression of pluripotent stem cells (CFU-S), granulocyte-macrophage progenitors (CFU-GM) and erythroid precursors (CFU-E) in both dose groups. Hematopoietic parameters returned to normal by 21 days in the 1 ppm dose group, but not in the 3 ppm dose group. This indicates that the alterations in the bone marrow parameters persist for a relatively long period at dose levels where there are little or no changes in body weight, clinical pathology, or immunological parameters, suggesting that the bone marrow may be a sensitive endpoint for MIC exposure in mice. MIC is a highly reactive chemical that appears to exert its effect directly on the lining epithelium of the nasal cavity and major airways; there was no histological evidence of a systemic effect. The pathogenesis of the bone marrow depression is unknown; however, there were chronic bronchitis and bronchial fibrosis in the 3 ppm dose group. One possible explanation is that the cell injury induced in the lung is associated with the release of inhibitory factors for hematopoiesis, as the rodent lung is a potent source of both stimulatory and inhibitory growth factors for bone marrow progenitor cells. A second possibility is that the thymic atrophy found in MIC-exposed mice might be related to myelotoxicity. The pathogenesis of myelotoxicity in MIC exposure and its relationship with pulmonary injury require further study.
A phase 1/2 study of lenalidomide with low-dose oral cyclophosphamide and low-dose dexamethasone (RdC) in AL amyloidosis
Authors: Efstathios Kastritis, Evangelos Terpos, Maria Roussou, Maria Gavriatopoulou, Constantinos Pamboukas, Ioannis Boletis, Smaragda Marinaki, Theofanis Apostolou, Nikitas Nikitas, Georgios Gkortzolidis, Eurydiki Michalis, Sossana Delimpasi, Meletios A. Dimopoulos
Journal: Blood (2012)
Abstract 5349: Cancer stem cells isolation and characterization from breast tumor of a germline carrier of TP53 p.R337H (Brazilian founder) mutation
Authors: Lisley I. Mambelli, Irina Kerkis, Pierre Hainaut, Maria Isabel W. Achatz
Journal: Cancer Research (2012)

Abstract Li-Fraumeni syndrome (LFS), an inherited cancer predisposition syndrome, is associated with germ line mutations in TP53. It is characterized by high risk of multiple, early cancers. In Brazil, a variant form of LFS is exceedingly frequent due to a widespread founder TP53 mutation, p.R337H, detected in about 0.3% of the general population in Southern Brazil. This mutation occurs in p53 oligomerization domain and its effect on p53 oligomerization is supposed to be dependent upon pH conditions. We have isolated and characterized Cancer Stem Cells from tumors of p.R337H mutation carriers. After informed consent and surgical resection fragments were dissociated and brought in culture. Adherent cells and spheroids were derived from different tumor types. Spheroids derived from a breast cancer (BC) were further analyzed to demonstrate positive immunolabeling for CD44, CD24, Oct4 and Sox2 antibodies. Time-lapse videomicroscopy showed rapid growth, frequent asymmetric division and absence of senescent phenotypes for least 17 passages. At confluence, some cells spontaneously differentiated into adipogenic and muscle-like cells. Floating and adherent spheroids contained self-renewing cells capable of long-term proliferation without losing their primary characteristics. These properties are similar to those of stem cells with inactivated p53 protein. However, treatment of adherent cells with the DNA damaging agent doxorubicin elicited p53 accumulation, p21 induction, cell cycle arrest at low doses of Dox and cell death/apoptosis at higher doses. These results are consistent with the notion that p.R337H may retain a quasi-normal p53 function in response to stress while expressing properties similar to mutant p53 in long-term CSC culture. These p.R337H CSC may provide a very useful model for studying the defects underlying inherited cancer in p.R337H carriers. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5349. doi:1538-7445.AM2012-5349
Population Versus Clinical View of Case Fatality From Acute Coronary Heart Disease
Authors: Lloyd Chambless, Ulrich Keil, Annette Dobson, Markku Mähönen, Kari Kuulasmaa, Anna-Maija Rajakangas, Hannelore Löwel, Hugh Tunstall-Pedoe
Journal: Circulation (1997)

The clinical view of case fatality (CF) from acute myocardial infarction (AMI) in those reaching the hospital alive is different from the population view. Registration of both hospitalized AMI cases and out-of-hospital coronary heart disease (CHD) deaths in the WHO MONICA Project allows both views to be reconciled. The WHO MONICA Project provides the largest data set worldwide to explore the relationship between CHD CF and age, sex, coronary event rate, and first versus recurrent event.All 79,669 events of definite AMI or possible coronary death, occurring from 1985 to 90 among 5,725,762 people, 35 to 64 years of age, in 29 MONICA populations are the basis for CF calculations. Age-adjusted CF (percentage of CHD events that were fatal) was calculated across populations, stratified for different time periods, and related to age, sex, and CHD event rate. Median 28-day population CF was 49% (range, 35% to 60%) in men and 51% (range, 34% to 70%) in women and was particularly higher in women than men in populations in which CHD event rates were low. Median 28-day CF for hospitalized events was much lower: in men 22% (range, 15% to 36%) and in women 27% (range, 19% to 46%). Among hospitalized events CF was twice as high for recurrent as for first events.Overall 28-day CF is halved for hospitalized events compared with all events and again nearly halved for hospitalized 24-hour survivors. Because approximately two thirds of 28-day CHD deaths in men and women occurred before reaching the hospital, opportunities for reducing CF through improved care in the acute event are limited. Major emphasis should be on primary and secondary prevention.
981 EPITHELIAL-TO-MESENCHYMAL TRANSITION (EMT) IN CHOLANGIOCYTES DOES NOT CONTRIBUTE TO THE POPULATION OF α-SMA+ MYOFIBROBLASTS IN EXPERIMENTAL MODELS OF LIVER FIBROSIS
Authors: D. Scholten, A. Scholten, C. Östereicher, D.A. Brenner, T. Kisseleva
Journal: Journal of Hepatology (2010)
Tuberculosis and Parasitism as Causes of Abdominal Pain in Korean Patients
Authors: Melvin I. Shoul
Journal: New England Journal of Medicine (1955)

DURING recent military campaigns in the Far East, American physicians treated large numbers of native Korean patients. Abdominal pain in the Korean as compared to the Occidental required a different interpretation. Intestinal parasites caused complications hitherto little thought of in the preoperative, operative and postoperative course of the surgical patient. At a large American military hospital in South Korea there was an excellent opportunity to study these problems. The majority of patients admitted were South Korean men of military age. An analysis of this group points out significant distinctive features in the diagnosis and treatment of abdominal pain in a . . .
SIRT7 Controls Hepatic Lipid Metabolism by Regulating the Ubiquitin-Proteasome Pathway
Authors: Tatsuya Yoshizawa, Md. Fazlul Karim, Yoshifumi Sato, Takafumi Senokuchi, Keishi Miyata, Takaichi Fukuda, Chisa Go, Masayoshi Tasaki, Kohei Uchimura, Tsuyoshi Kadomatsu, Zhe Tian, Christian Smolka, Tomohiro Sawa, Motohiro Takeya, Kazuhito Tomizawa, Yukio Ando, Eiichi Araki, Takaaki Akaike, Thomas Braun, Yuichi Oike, Eva Bober, Kazuya Yamagata
Journal: Cell Metabolism (2014)
Mechanism of Release of Ferritin Iron In Vivo by Xanthine Oxidase1
Authors: A. Mazur, S. Green, A. Saha, A. Carleton
Journal: Journal of Clinical Investigation (1958)

Studies of the biochemical mechanism for the release of iron from hepatic ferritin stores have revealed the participation of the enzyme xanthine oxidase (1). During this reaction between the enzyme and ferritin iron some of the iron in the ferric state is reduced to the ferrous form and can be removed from the protein in the presence of iron-binding agents such as cr,a'-dipyridyl or the plasma iron-binding globulin, siderophilin. Evidence for the participation of this enzyme in the release of ferritin iron is based for the most part on in vitro studies using rat liver slices subjected to lowered oxygen tension. Such tissue slices accumulate ferrous-ferritin and high levels of hypoxanthine and xanthine, substrates for xanthine oxidase, as well as uric acid, their oxidation product. In addition, indirect evidence implicates this mechanism in the release of ferritin iron to the plasma in the intact animal; as a result of liver hypoxia following extensive blood loss, the plasma iron and uric acid of dogs is found to increase to a considerable extent. (2). The results of the present study serve to confirm the participation of xanthine oxidase in the in tivo liberation of tissue iron to the circulation.
The Doctor Buys on Credit
Authors: Bernard D. Hirsh
Journal: JAMA (1963)

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
cGMP and Nitric Oxide Modulate Thrombin-Induced Endothelial Permeability
Authors: Richard Draijer, Douwe E. Atsma, Arnoud van der Laarse, Victor W.M. van Hinsbergh
Journal: Circulation Research (1995)

Abstract Previous studies have demonstrated that cGMP and cAMP reduce the endothelial permeability for fluids and macromolecules when the endothelial permeability is increased by thrombin. In this study, we have investigated the mechanism by which cGMP improves the endothelial barrier function and examined whether nitric oxide (NO) can serve as an endogenous modulator of endothelial barrier function. Thrombin increased the passage of macromolecules through human umbilical vein and human aortic endothelial cell monolayers and concomitantly increased [Ca] 2+ in vitro. Inhibition of these increases by the intracellular Ca 2+ chelator BAPTA indicated that cytoplasmic Ca 2+ elevation contributes to the thrombin-induced increase in endothelial permeability. The cGMP-dependent protein kinase activators 8-bromo-cGMP (8-Br-cGMP) and 8-(4-chlorophenylthio)cGMP (8-PCPT-cGMP) decreased the thrombin-induced passage of macromolecules. Two pathways accounted for this observation. Activation of cGMP-dependent protein kinase by 8-PCPT-cGMP decreased the accumulation of cytoplasmic Ca 2+ in aortic endothelial cells and hence reduced the thrombin-induced increase in permeability. On the other hand, in umbilical vein endothelial cells, cGMP-inhibited phosphodiesterase (PDE III) activity was mainly responsible for the cGMP-dependent reduction of endothelial permeability. The PDE III inhibitors Indolidan (LY195115) and SKF94120 decreased the thrombin-induced increase in permeability by 50% in these cells. Thrombin treatment increased cGMP formation in the majority of, but not all, cell cultures. Inhibition of NO production by N G -nitro- l- arginine methyl ester (L-NAME) enhanced the thrombin-induced increase in permeability, which was restricted to those cell cultures that displayed an increased cGMP formation after addition of thrombin. Simultaneous elevation of the endothelial cGMP concentration by atrial natriuretic factor, sodium nitroprusside, or 8-Br-cGMP prevented the additional increase in permeability induced by L-NAME. These data indicate that cGMP reduces thrombin-induced endothelial permeability by inhibition of the thrombin-induced Ca 2+ accumulation and/or by inhibition of cAMP degradation by PDE III. The relative contribution of these mechanisms differs in aortic and umbilical vein endothelial cells. NO can act in vitro as an endogenous permeability-counteracting agent by raising cGMP in endothelial cells of large vessels.
Honeycomb Lung (Interstitial Fibrosis)
Authors: James C. Reed
Journal: JAMA (1975)

<h3>Common</h3> [Cystic bronchiectasis] Histiocytosis X (especially eosinophilic granuloma) Idiopathic interstitial fibrosis (Hamman-Rich ) Pneumoconiosis Sarcoidosis <h3>Uncommon</h3> Amyloidosis Chemical inhalation (late stage) Desquamative interstitial pneumonitis (DIP) Drug sensitivity, chronic or recurrent (eg, nitrofurantoin, hexamethonium, busulfan) Gaucher disease Lipoid pneumonia (eg, mineral oil aspiration) [Lymphangiomyomatosis] Oxygen toxicity [Mucoviscidosis] Neurofibromatosis Rheumatoid lung Scleroderma; dermatomyositis Sensitivity pneumonitis, recurrent (eg, farmer's lung, bagassosis) Tuberous sclerosis (Entities in brackets can be confused roentgenographically with true honeycomb lung. ) <h3>Diagnosis</h3> Eosinophilic granuloma. <h3>COMMENTS</h3> In analyzing this Gamut, a number of the possibilities offered, such as chemical inhalation, rheumatoid lung, and scleroderma are excluded by the lack of specific clinical information. Of the common causes, cystic bronchiectasis tends to show fluid in the cysts and to expand on inspiration; pneumoconiotics have a history of dust exposure. Therefore, idiopathic interstitial fibrosis (the