tbuckley/cabot-search huggingface dataset:
The dexamethasone suppression test in normal control subjects: comparison of two assays and effect of age
Authors: A H Rosenbaum, A F Schatzberg, R A MacLaughlin, K Snyder, N S Jiang, D Ilstrup, A J Rothschild, B Kliman
Journal: American Journal of Psychiatry (1984)

he authors used competitive protein binding assay and radioimmunoassay to measure cortisol levels in 38 normal control subjects three times before and three times after administration of 1 mg of dexamethasone. They found significant interassay differences at 11:00 p.m. before dexamethasone and at all three postdexamethasone times. Analysis of variance revealed significant overall positive relationships between age and cortisol levels measured by both techniques. Age correlated significantly with postdexamethasone cortisol levels measured by radioimmunoassay but not when measured by competitive protein binding assay. Clinicians should obtain data from their laboratories as to appropriate cutoffs for cortisol suppression on the specific assay used.
Mutations in a gene encoding a novel protein tyrosine phosphatase cause progressive myoclonus epilepsy
Authors: Berge A. Minassian, Jeffrey R. Lee, Jo-Anne Herbrick, Jack Huizenga, Sylvia Soder, Andrew J. Mungall, Ian Dunham, Rebecca Gardner, Chung-yan G. Fong, Stirling Carpenter, Laura Jardim, P. Satishchandra, Eva Andermann, O. Carter Snead, Iscia Lopes-Cendes, Lap-Chee Tsui, Antonio V. Delgado-Escueta, Guy A. Rouleau, Stephen W. Scherer
Journal: Nature Genetics (1998)
Acquired Resistance of<i>EGFR-</i>Mutant Lung Cancer to a T790M-Specific EGFR Inhibitor
Authors: Helena A. Yu, Shaozhou K. Tian, Alexander E. Drilon, Laetitia Borsu, Gregory J. Riely, Maria E. Arcila, Marc Ladanyi
Journal: JAMA Oncology (2015)

EGFR-mutant lung cancers represent a paradigm for the use of tyrosine kinase inhibitors (TKIs) to treat molecular subsets of cancer, with randomized trials demonstrating the efficacy of first-generation, reversible epidermal growth factor receptor (EGFR) TKIs. However, acquired resistance invariably develops, and rebiopsy of patients with clinical progression has elucidated EGFR T790M mutation as the major resistance mechanism.1

To address this clinical challenge, third-generation pyrimidine-based EGFR TKIs have been designed to have selectivity for EGFR T790M over wild-type EGFR.2 They form a covalent bond with cysteine 797 in the adenosine triphosphate–binding cleft. Early-phase clinical trials have demonstrated their efficacy in patients with double-mutant tumors (EGFR L858R/T790M and ex19del/T790M) and acquired resistance to first-generation EGFR inhibitors.3 Specificity for EGFR T790M may be the result of hydrophobic interactions between the bulky methionine moiety of EGFR T790M and these pyrimidine-based drugs.

Mechanisms of resistance to these third-generation EGFR TKIs have been identified in preclinical in vitro models, but none have so far been identified in patients. Mutations at the EGFR C797 codon, located within the kinase-binding site, are a predicted resistance mechanism to irreversible EGFR inhibitors also confirmed in vitro.4 Loss of the potential for covalent bond formation at position 797 by the missense mutation C797S results in a markedly reduced cellular potency of this class of TKIs.5 Interestingly, an analogous cysteine-to-serine mutation is a mechanism of resistance to the irreversible Bruton tyrosine kinase inhibitor ibrutinib in patients with chronic lymphocytic leukemia.6
Multiple minute digitate hyperkeratoses
Authors: S. Takagawa, T. Satoh, H. Yokozeki, K. Nishioka
Journal: British Journal of Dermatology (2000)

A familial case of multiple minute digitate hyperkeratoses is reported. Hundreds of tiny, spiked, keratotic papules were scattered on the trunk and limbs. Microscopically, the lesions showed digitiform orthohyperkeratosis with tenting of the epidermis. Neither atypical epidermal cells nor a dermal infiltrate were observed. This disease has three types: familial, sporadic and postinflammatory. We have analysed the histopathological features of all the cases reported to date. While the familial and sporadic types are similar, the lesions in the postinflammatory type are composed of parakeratotic columns with an invaginated epidermis. Although morphological analysis may not provide any clues to pathogenetic differences, it seems reasonable to assume that the postinflammatory type is an entity different from the other two forms.
LSC 2012 abstract - LRIG1 regulates cadherin-dependent contact inhibition directing epithelial homeostasis and preinvasive squamous cell carcinoma development
Authors: Vitor Teixeira, L. Lu, A. Nicholson, T. Graham, M. Falzon, B. Carrol, F. Watt, J. George, A. Giangreco, K. Jensen, S. Janes
Journal: European Respiratory Journal (2012)

Epidermal Growth Factor Receptor (EGFR) pathway activation is a frequent event in human lung cancer with over-expression one of the earliest abnormalities in the bronchial epithelium of smokers and present in all stages of preinvasive cancer. Mutations in EGFR itself are rare and the mechanisms regulating EGFR pathway activation remained elusive. Leucine-rich immunoglobulin repeats-1 (LRIG1), an inhibitor of EGFR activity, is one of 4 genes identified that predict patient survival across solid tumor types.  We hypothesize that tissue homeostasis is maintained via strong endogenous regulation of EGFR signaling by the inhibitor LRIG1 and its loss is the key step in the initiation of preinvasive lung disease.  Our experiments show that deletion of LRIG1 is sufficient to promote murine airway hyperplasia. In vitro, LRIG1 deficient cells display loss of contact inhibition, whereas re-expression of LRIG1 in human lung cancer cell lines impairs growth. We find that LRIG1 forms a ternary complex with EGFR and E-Cadherin at the cell surface. This complex modulates the activity of the EGFR and downstream pathways. We also show that loss of heterozygosity at the LRIG1 locus as well as down-regulation of LRIG1 gene expression are early events in the development of preinvasive human squamous lung cancer.  Our findings imply that lung cancer development is driven by a change in the amplitude of EGFR signaling governed by the loss of contact inhibition.
Localization of paternal H-2K antigens on murine trophoblast cells in vivo.
Authors: S Chatterjee-Hasrouni, P K Lala
Journal: The Journal of Experimental Medicine (1982)

We have previously shown the presence of H-2K and D antigens of both parental haplotypes on dispersed murine trophoblast cells. The question still remained whether such antigens are sequestered away from the sinusoidal face of these cells making them inert as allografts. The in vivo expression of H-2 antigens on these cells was therefore examined radioautographically after perfusion of 125I-labeled monoclonal and anti-H-2Kk (anti-paternal) antibody directly into individual placental branches of the uterine artery suppling 15-d-old (C57BL/6J female) X CBA/J male) placentae. Syngeneic C57BL/6J placentae served as negative controls. A radioautographic examination of 0.5-micrometer-thick sections revealed specific labeling of labyrinthine trophoblasts lining the sinusoids of allogeneic placentae. Most of this labeling was localized to the sinusoidal face of the cells as opposed to a weak labeling of the intracellular aspect. Spongiotrophoblasts and trophoblast giant cells did not label, but specific labeling of fetal capillary endothelium and some macrophages was also noted.
Interphase and metaphase detection of the breakpoint of 14q32 translocations in B-cell malignancies by double-color fluorescence in situ hybridization
Authors: M Taniwaki, K Nishida, Y Ueda, S Misawa, M Nagai, S Tagawa, T Yamagami, H Sugiyama, M Abe, S Fukuhara
Journal: Blood (1995)
A Telomerase-dependent Conditionally Replicating Adenovirus for Selective Treatment of Cancer
Authors: Thomas Wirth, Lars Zender, Bernd Schulte, Bettina Mundt, Ruben Plentz, Karl Lenhard Rudolph, Michael Manns, Stefan Kubicka, Florian Kühnel
Journal: Cancer Research (2003)

The catalytic component of human telomerase reverse transcriptase (hTERT) is not expressed in most primary somatic human cells, whereas the majority of cancer cells reactivate telomerase by transcriptional up-regulation of hTERT. Several studies demonstrated that the hTERT promoter can be used to restrict gene expression of E1-deleted replication defective adenoviral vectors to telomerase-positive cancer cells. In this study, a conditionally replicating adenovirus (hTERT-Ad) expressing E1A genes under control of a 255-bp hTERT-promoter was constructed. Additionally, an internal ribosomal entry site-enhanced green fluorescent protein cassette was inserted downstream of the E1B locus to monitor viral replication in vivo. Adenoviral replication of hTERT-Ad and enhancement of enhanced green fluorescent protein expression could be observed in all investigated telomerase-positive tumor cell lines. In contrast, hTERT-Ad infection of telomerase-negative primary human hepatocytes did not result in significant replication. The capability of hTERT-Ad to induce cytopathic effects in tumor cells was comparable with that of adenovirus wild type and significantly higher compared with ONYX-015, regardless of the p53 status of the tumor cells. Single application of low-dose hTERT-Ad to tumor xenografts led to significant inhibition of tumor growth, confirming the potential therapeutic value of conditionally replicative adenoviral vectors. These in vivo experiments also revealed that hTERT-Ad-mediated oncolysis was more efficient than ONYX-015 treatment. These results demonstrate that expression of E1A under transcriptional control of the hTERT promoter is sufficient for effective telomerase-dependent adenovirus replication as a promising perspective for the treatment of the majority of epithelial tumors.
Abstract 18929: Pacing in the Adult Fontan Patient: Risky Business?
Authors: Matthew J Lewis, Nalini Colaco, Jonathan Ginns, Marlon Rosenbaum
Journal: Circulation (2014)

Introduction: Chronic ventricular pacing can induce a cardiomyopathy in patients with a biventricular heart; however, the effect of chronic pacing in adult patients with a Fontan has not been well characterized. We hypothesized that paced adult Fontan patients would be at higher risk for death or heart transplant. Methods: We performed a retrospective, cohort of study of all adult Fontan patients at the Schneeweiss Adult Congenital Heart Center seen between 1/1997 and 5/2014. Two Cohorts were defined based on whether a patient did or did not have a permanent pacemaker. Demographic and clinical characteristics were collected via chart review. The primary endpoint was a composite of death or heart transplant. Results: Of the 98 adult Fontan patients followed (mean age at last follow-up 32± 8 years), 30 (31%) had a pacemaker. Pacemaker specific data was available on 25 of the 30 (83%) paced patients. Of those, 88% were paced &gt;50% of the time. Patient diagnoses included double inlet left ventricle in 33 (34%), tricuspid atresia in 26 (27%), hypoplastic left heart in 9 (9%), heterotaxy in 8 (8%), and 22 (22%) with other diagnoses. Fifty-two patients (53%) had a classic RA-PA Fontan and 46 (47%) had a lateral tunnel or extracardiac Fontan. Over the study period, 16 patients met the primary endpoint and 12 (75%) were paced. Paced patients were significantly more likely to have worse functional status (p&lt;0.001), be on diuretics (p&lt;0.001), and have a higher mean creatinine (P=0.025), mean total bilirubin (p=0.025), and mean Fontan pressure (p&lt;0.001). Pacing was associated with &gt;4-fold increase in the rate of death or heart transplant (p=0.009) in a multivariate cox-proportional hazard model that included Fontan type, age at Fontan completion, age at follow-up, and pacing status. Discussion: In our cohort of 98 adult Fontan patients, paced patients were more likely to have worse functional status, require diuretics and had a &gt;4-fold increased risk of death or heart transplant. These results suggest that chronic pacing may be detrimental in this population.
Lecithin and Allied Substances. The Lipins.
Authors: Hugh Maclean
Journal: JAMA (1918)

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
Mechanical Reperfusion More Than 12 Hours After Acute Myocardial Infarction—Reply
Authors: Albert Schömig, Gjin Ndrepepa, Adnan Kastrati
Journal: JAMA (2005)

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
Abstract 19524: Time Series Feature Extraction and Machine Learning for Prediction of In-Hospital Cardiac Arrest
Authors: Sharad Shandilya, Pouya Sabouriazad, Mina Attin, Kayvan Najarian
Journal: Circulation (2014)

Introduction: Electrocardiogram (ECG) predictors prior to in-hospital cardiac arrest (I-HCA) have not been fully investigated. ECG from telemetry may provide information about diagnostic clues prior to I-HCA. Machine learning algorithms can be used for integration of information from several ECG features in order to build predictive models for clinical decision-support. Hypothesis: Machine learning (ML) can be used to develop a model to predict I-HCA. Methods: In a multi-center study, full-disclosure ECG papers (25 mm/s paper speed) from telemetry were obtained for two minutes prior to I-HCA and three other same-duration segments within one hour of I-HCA. Signal segments were also obtained for two minutes within each of the seven hours prior to I-HCA. The full-disclosure ECG was digitized using the connected-component method for lead II and R detection was performed by HAT algorithm. Multiple computational features were extracted including heart rate, QRS duration and morphology, and ST-segment changes. A...
Lifetime cost effectiveness of simvastatin in a range of risk groups and age groups derived from a randomised trial of 20 536 people
Journal: BMJ (2006)

<b>Objectives</b> To evaluate the cost effectiveness of 40 mg simvastatin daily continued for life in people of different ages with differing risks of vascular disease. <b>Design</b> A model developed from a randomised trial was used to estimate lifetime risks of vascular events and costs of treatment and hospital admissions in the United Kingdom. <b>Setting</b> 69 hospitals in the UK. <b>Participants</b> 20 536 men and women (aged 40-80) with coronary disease, other occlusive arterial disease, or diabetes. <b>Interventions</b> 40 mg simvastatin daily versus placebo for an average of 5 years. <b>Main outcome measures</b> Cost effectiveness of 40 mg simvastatin daily expressed as additional cost per life year gained. Major vascular event defined as non-fatal myocardial infarction or death from coronary disease, any stroke, or revascularisation procedure. Results were extrapolated to younger and older age groups at lower risk of vascular disease than were studied directly, as well as to lifetime treatment. <b>Results</b> At the April 2005 UK price of £4.87 (€7; $9) per 28 day pack of generic 40 mg simvastatin, lifetime treatment was cost saving in most age groups and vascular disease risk groups studied directly. Gains in life expectancy and cost savings decreased with increasing age and with decreasing risk of vascular disease. People aged 40-49 with 5 year risks of major vascular events of 42% and 12% at start of treatment gained 2.49 and 1.67 life years, respectively. Treatment with statins remained cost saving or cost less than £2500 per life year gained in people as young as 35 years or as old as 85 with 5 year risks of a major vascular event as low as 5% at the start of treatment. <b>Conclusions</b> Treatment with statins is cost effective in a wider population than is routinely treated at present.
Two Sisters With Puppy and Flowers
Authors: M. Therese Southgate
Journal: JAMA (2002)

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
THE IMPORTANCE OF BRONCHOSCOPY IN BRONCHIECTASIS
Authors: Horace P. Marvin
Journal: Annals of Internal Medicine (1934)

Article1 January 1934THE IMPORTANCE OF BRONCHOSCOPY IN BRONCHIECTASISHORACE P. MARVIN, M.D.HORACE P. MARVIN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-7-7-903 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptBronchoscopy plays a very important part in both the diagnosis and treatment of cases of bronchiectasis. Practically all of the limited literature on this subject has been contributed by the bronchoscopist or the surgeon, with an occasional brief note by an internist. Jackson states that "in most cases of bronchiectasis there are strong indications for a bronchoscopic diagnosis." Ballon, Singer and Graham report that "the bronchoscope is a great aid in the diagnosis of bronchiectasis," and also state that "the value of the bronchoscope in the treatment of foreign body bronchiectasis and in certain cases which are due to partial...Bibliography GRAHAM EA: Bronchoscopic and surgical treatments of pulmonary suppuration, Am. Rev. Tuberculosis, 1928, xvii, 33-41. Google Scholar BALLONSINGERGRAHAM HJJEA: Bronchiectasis, Jr. Thorac. Surg., 1931, 1, 154; 1932, i, 296, 397, 502-561. CrossrefGoogle Scholar MARVIN HP: Chronic bronchiectasis, Mil. Surg., 1932, lxxi, 1-15. Google Scholar CLERF LH: Peroral endoscopy, Arch. Otolaryng., 1930, xi, 343-360. CrossrefGoogle Scholar BALLON DH: Some observations upon value of bronchoscopy in treatment of bronchiectasis, Jr. Thorac. Surg., 1933, ii, 267-269. CrossrefGoogle Scholar JACKSON C: Bronchoscopy and esophagoscopy; a manual of peroral endoscopy and laryngeal surgery, 1927, Saunders, Philadelphia and London. Google Scholar JACKSON C: Teaching bronchoscopy and esophagoscopy, Arch. Otolaryng., 1928, vii, 1-12. CrossrefGoogle Scholar MARVIN HP: Bronchiectasis, its prevalence and importance. (To be published in an early issue of The Medical Bulletin of the Veterans' Administration.) Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Honolulu, Hawaii*Received for publication March 31, 1933.From the Bronchiectasis Branch of the Medical Service, Fitzsimons General Hospital. Published by permission of The Surgeon General, U. S. Army.†Captain, Medical Corps, U. S. Army. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1934Volume 7, Issue 7Page: 903-912KeywordsBronchiectasisBronchoscopyMedical servicesSurgeons Issue Published: 1 January 1934 PDF downloadLoading ...
Mucosal dendritic cells in allergy and immunotherapy
Authors: N. Novak, J.‐P. Allam
Journal: Allergy (2011)

The oral epithelium contains oral mucosal Langerhans cells (oLCs) that constitutively express the high-affinity IgE-receptor FcεRI, the lipopolysaccharide receptor CD14 and toll-like receptor (TLR)4. The distribution of oLCs profoundly differs at distinct oral mucosal sites, with higher numbers of oLCs detectable in the vestibulum compared with the sublingual region. The oLC response to activation of TLR4 and FcεRI and to binding of allergen suggests that these cells are involved in the maintenance of tolerance towards bacterial components and allergens. Thus, oLCs are important targets for allergens and adjuvants during sublingual immunotherapy, and characterizing them is crucial for improving allergen-specific immunotherapy.