tbuckley/cabot-search huggingface dataset:
A PLEA FOR UNITY IN HEALTH ADMINISTRATION AT THE STATE LEVEL
Authors: JOSEPH W. MOUNTIN
Journal: JAMA (1941)

If instead of writing a paper designed for a scientific group I were giving a sermon, I could think of no better text than item 1 from the platform of the American Medical Association as published in a number of issues ofThe Journallast year: The establishment of an agency of the federal government under which shall be coordinated and administered all medical and health functions of the federal government exclusive of those of the Army and Navy. Again, if this were a sermon, in adapting the text to my purposes I should need only to substitute the word state for federal. For this resolution seems to me an excellent one to apply to the agencies conducting affairs of public health within the states even as it was to apply within the structure of the federal government. One may be inclined to qualify my use of "was" in respect
Lethal T cell immunodeficiency induced by chronic costimulation via CD27-CD70 interactions
Authors: Kiki Tesselaar, Ramon Arens, Gijs M.W. van Schijndel, Paul A. Baars, Martin A. van der Valk, Jannie Borst, Marinus H.J. van Oers, René A.W. van Lier
Journal: Nature Immunology (2002)
Abstract 4372: Radiation induces Notch-dependent de novo generation of breast cancer stem cells via expression of OCT-4/SOX2/NANOG
Authors: Chann H. Lagadec, Lorenza Della Donna, Erina Vlashi, Carmen Dekmezian, Tania Brocks, Frank Pajonk
Journal: Cancer Research (2011)

Abstract Like in normal tissues, the self-renewal of cancer stem cells (CSCs) might be also under tight control of developmental pathway like the Notch, Wnt, Sonic Hedgehog or TGFβ pathways. The Notch pathway plays an important role in normal breast development, cell fate, and normal stem cell self-renewal, and its deregulation has been shown to play a role in cancer. Aberrant Notch signaling has been implicated in the development and progression of both preinvasive ductal carcinomas in situ and invasive breast cancers. Interestingly, in breast cancer, the Notch pathway plays major role for CSCs maintenance. We previously published that BCSCs (Breast Cancer Stem Cells) are relatively resistant to radiation and we demonstrated a link between BCSCs radio-resistance and the Notch pathway. Irradiation of MCF-7 and T47D cells increased the number of CSCs and this correlated with the induction of Notch signaling protein expression in a dose- and time-dependent manner. Jagged 1 expression was quickly (1h) increased 28-fold after 2Gy, DLL1 expression was increased 15-fold, 3 to 6h after irradiation with 2 or 4 Gy, Notch 2 expression was increased 16-fold 6h after 2, 4, 6 or 8 Gy, while DLL3 was increased 10-fold after the highest doses (6 to 12 Gy). Inhibition of Notch signaling pathway by a γ-secreatase inhibitor prevented enrichment for CSCs and reduced radiation-induced Notch protein expression. Most importantly, we demonstrated that radiation-induced Notch signaling contributes to the phenotype plasticity of BCSCs and their progeny. Using 2 different cancer stem cell markers (low proteasome activity and ALDH1) to found that radiation causes de novo generation of induced BCSCs (iBCSCs) from non-tumorigenic cells and this correlated with radiation-induced the expression of OCT-4, SOX2, and NANOG, key transcription factors of used to generate induced pluripotent stem cells (iPS cells). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4372. doi:10.1158/1538-7445.AM2011-4372
1137-95 Demographics, treatment, and outcome of acute coronary syndromes: 17 years of experience in a tertiary care center
Authors: Jean-Pierre S Awaida, Jocelyn Dupuis, Pierre Théroux, Michel Joyal, Pierre De Guise, Serge Doucet, Luc Bilodeau, Jean-François Tanguay, Richard Gallo, Jean Grégoire, Philippe Lavoie-Lallier, Laurent Macle, Anil Nigam
Journal: Journal of the American College of Cardiology (2004)
Demonstration of Iodide Transport Defect but Normal Iodide Organification in Nonfunctioning Nodules of Human Thyroid Glands
Authors: James B. Field, P. Reed Larsen, Kamejiro Yamashita, Keith Mashiter, Andrew Dekker
Journal: Journal of Clinical Investigation (1973)

Benign and malignant nodules in human thyroid glands, which did not concentrate iodide in vivo, were also unable to accumulate iodide in vitro. The mean thyroid-to-medium ratio (T/M) in seven benign nodules was 0.8±0.2 compared with 7±2 in adjacent normal thyroid tissue. In four malignant thyroid nodules, the mean T/M was 0.5±0.1 compared with 11±4 in adjacent normal thyroid. Despite the inability of such nodules to concentrate iodide, iodide organification was present but was only one-half to one-third as active as in surrounding normal thyroid. Thyroid-stimulating hormone (TSH) increased iodide organification equally in both benign nodules and normal thyroid although it had no effect in three of the four malignant lesions. The reduction in organification is probably related to the absence of iodide transport, since incubation of normal thyroid slices with perchlorate caused similar diminution in iodide incorporation but no change in the response to TSH. Monoiodotyrosine (MIT) and di-iodotyrosine (DIT) accounted for most of the organic iodide in both the nodules and normal tissue. The MIT/DIT ratio was similar in normal and nodule tissue. The normal tissue contained much more inorganic iodide than the nodules, consistent with the absence of the iodide trap in the latter tissue. The thyroxine content of normal thyroid was 149±17 μg/g wet wt and 18±4 μg/g wet wt in the nodules. The transport defect in the nodules was not associated with any reduction in total, Na+-K+- or Mg++-activated ATPase activities or the concentration of ATP. Basal adenylate cyclase was higher in nodules than normal tissue. Although there was no difference between benign and malignant nodules, the response of adenylate cyclase to TSH was greater in the benign lesions.
Incidence of Distal Symmetric (Sensory) Neuropathy in NIDDM: The San Luis Valley Diabetes Study
Authors: M L Sands, S M Shetterly, G M Franklin, R F Hamman
Journal: Diabetes Care (1997)

OBJECTIVE To determine the incidence and risk factors for distal symmetric sensory neuropathy (DSN) in people with NIDDM. RESEARCH DESIGN AND METHODS Prospective follow-up was conducted from 1988 to 1992 on 231 people free of DSN during the baseline period 1984–1988 (mean follow-up, 4.7 years). Subjects with incident DSN (n = 66) were defined by any two of three criteria: 1) bilateral paresthesia in legs or feet; 2) bilateral decreased or absent ankle reflexes; and/or 3) bilateral decreased or absent cold temperature discrimination in feet. Of all 66 cases, 42 had one positive follow-up visit; 14 cases had 2 positive follow-up visits. RESULTS The overall incidence rate of DSN was 6.1 per 100 person-years (95% CI, 4.7–7.8). The rate for Hispanics (n = 164) and non-Hispanic whites (n = 67), adjusted for age, sex, and NIDDM duration, was 5.3 per 100 person-years (95% CI, 3.9–7.0) and 5.0 per 100 person-years (95% CI, 2.8–8.1), respectively. Adjusting for age and sex, higher glycohemoglobin level and lower C-peptide secretion were associated with increased DSN but were no longer predictive after accounting for duration of diabetes. Logistic regression models found significantly increased risk of DSN for insulin treatment, current smoking, and history of myocardial infarction. Duration was related to DSN incidence until insulin treatment was included. Other risk factors, including height, weight, family history of diabetes, peripheral vascular disease, hypertension, urinary albumin, protein:creatinine ratio, retinopathy, and alcohol use, were not significantly related to incident DSN. CONCLUSIONS Hispanic and non-Hispanic whites with NIDDM have similar risks of DSN. Current cigarette smoking and a history of myocardial infarction may represent independent risk factors for DSN in addition to glycemic control.
A Criticism of Psychiatry's Board Examinations
Authors: ALAN L. MORGENSTERN
Journal: American Journal of Psychiatry (1970)

The author questions the efficacy of the Board examinations in identifying "safe professional competency." The lack of helpful feedback from the examinations, the uncertainty about the behaviors that contribute to competence in clinical practice, the artificial stresses related to a day of testing—these and other issues raise doubts about the current relevance of certifying examinations. In the contemporary atmosphere of reevaluation of American educational premises and practices, the author suggests, it may be wise to reexamine the goals and functions of the Board.
Increased expression of bronchial epithelial transient receptor potential vanilloid 1 channels in patients with severe asthma
Authors: Lorcan P. McGarvey, Claire A. Butler, Susan Stokesberry, Liam Polley, Stephen McQuaid, Hani’ah Abdullah, Sadaf Ashraf, Mary K. McGahon, Tim M. Curtis, Joe Arron, David Choy, Tim J. Warke, Peter Bradding, Madeleine Ennis, Alexander Zholos, Richard W. Costello, Liam G. Heaney
Journal: Journal of Allergy and Clinical Immunology (2013)
Abstract 1157: Ubiquitin-proteolytic control of HOX homeodomain proteins in normal and malignant hematopoiesis
Authors: Pengbo Zhou, Jennifer Lee, Jianxuan Zhang, Liren Liu, Jae-Hung Shieh, Malcolm A. S. Moore
Journal: Cancer Research (2010)

Abstract The HOX homeodomain proteins are key regulators of hematopoiesis. HOX genes are expressed in primitive hematopoietic cells, and their prompt downregulation is associated with hematopoietic differentiation and maturation. Although transcriptional inactivation of HOX genes during hematopoietic differentiation has been established, little is known about the biochemical mechanisms underlying the subsequent removal of HOX proteins. We have previously shown that the CUL4A ubiquitin ligase controls the stability of HOXA9 by promoting its ubiquitination and proteasome-dependent degradation. Interfering with CUL4A biosynthesis resulted in alterations of the abundance of HOXA9, mirrored by impairment of the myeloid progenitor cells to undergo proper terminal differentiation into granulocytes. Here we show that other HOX family members are also subjected to CUL4A-mediated ubiquitination and destruction, and defined the degradation signal (degron) for these HOX proteins. A degradation-resistant recombinant HOX protein was engineered and affinity-purified, and when directly transduced into G-CSF-mobilized CD34+ adult hematopoietic cells, demonstrated significant enhancement of promoting ex vivo expansion of these primitive hematopoietic progenitors. These results revealed a novel regulatory mechanism of hematopoiesis by ubiquitin-dependent proteolysis, and opened up new avenues for ex vivo expansion of hematopoietic stem cells for therapeutic use. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1157.
Randomized double-blind study of cyclosporin in chronic ‘idiopathic’ urticaria
Authors: C.E.H. Grattan, B.F. O’Donnell, D.M. Francis, N. Niimi, R.J. Barlow, P.T. Seed, A. Kobza Black, M.W. Greaves
Journal: British Journal of Dermatology (2000)

Background Histamine-releasing activity (HRA) is detectable in up to 50% of patients with chronic ordinary urticaria. Objectives To determine the effect of cyclosporin on clinical features and HRA in patients with chronic urticaria. Methods Thirty patients with severe unremitting disease, responding poorly to antihistamines and showing a positive autologous serum skin test (ASST) as a marker of HRA, were randomized to 4 mg kg−1 daily of cyclosporin (Sandimmun®, n = 20) or placebo (n = 10) for 4 weeks. Non-responders were offered open-label cyclosporin for 4 weeks. All were followed for up to 20 weeks or until clinical relapse; all took cetirizine 20 mg daily throughout the study. The primary measure of efficacy was a daily urticaria activity score (UAS) of weal numbers and itch (maximum score 42 per week). A positive response was defined as a reduction to < 25% of baseline weekly UAS and relapse as a return to > 75%. The effect of cyclosporin on serum HRA was assessed by in vitro basophil histamine release assays and ASSTs before and after treatment. Results Twenty-nine patients (19 active, 10 controls) completed the randomized trial medication. Eight of 19 on active treatment but none on placebo had responded at 4 weeks (P < 0·05). Three others on active drug met the criterion for response at 2 weeks but not at 4 weeks. Mean reduction in UAS between weeks 0 and 4 was 12·7 (95% confidence interval, CI 6·6–18·8) for active and 2·3 (95% CI − 3·3–7·9) for placebo (P = 0·005). Seventeen non-responders (seven randomized to active and 10 to placebo) chose open-label cyclosporin and 11 responded after 4 weeks. Six of the eight randomized active drug responders relapsed within 6 weeks. Of the 19 responders to randomized and open-label cyclosporin, five (26%) had not relapsed by the study end-point. Mean in vitro serum HRA fell from 36% (95% CI 22–49%) to 5% (95% CI 1–8%) after cyclosporin treatment (n = 11, P < 0·0001). The ASST response to post-treatment serum was also reduced (P < 0·05). Conclusions This study shows that cyclosporin is effective for chronic urticaria and provides further evidence for a role of histamine-releasing autoantibodies in the pathogenesis of this chronic ‘idiopathic’ disease.
Rifabutin-induced Ageusia
Authors: Joseph T. Morris
Journal: Annals of Internal Medicine (1993)

Letters15 July 1993Rifabutin-induced AgeusiaJoseph T. Morris, MD and J. William Kelly, MDJoseph T. Morris, MDSearch for more papers by this author and J. William Kelly, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-119-2-199307150-00026 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Ageusia, the loss of the sense of taste, is an infrequently reported adverse effect of antimicrobial use. We describe a patient who developed ageusia while receiving rifabutin therapy for Mycobacterium simiae pulmonary infection.A 71-year-old white woman with cavitary lung disease had a transbronchial biopsy specimen that yielded Nocardia asteroides and M. simiae. She received sulfisoxazole for the former infection and clarithromycin and rifabutin for the latter. Six weeks after starting therapy with clarithromycin and rifabutin, she reported ageusia, arthralgias, and myalgias. Physical examination showed cachexia and mild skin hyperpigmentation. The patient had no edema, tenderness, or ...References1. Torseth J, Bhatia G, Harkonen S, Child C, Skinner M, Robinson W, et al. Evaluation of the antiviral effect of rifabutin in AIDS-related complex. J Infect Dis. 1989; 159:1115-8. Google Scholar2. O'Brien RJ, Geiter LJ, Lyle MA. Rifabutin (Ansamycin LM427) for the treatment of pulmonary Mycobacterium avium complex. Am Rev Respir Dis. 1990; 141:821-6. Google Scholar3. Rifabutin receives treatment IND status for AIDS related use. In: FDA Talk Paper On Mycobutin. T92-12. March 1992. Google Scholar4. Jenkins AC, Knill JR, Dreslinski GR. Captopril in the treatment of the elderly hypertensive patient. Arch Intern Med. 1985; 145:2029-31. Google Scholar5. Rollin H. Drug-related gustatory disorders. Ann Otol Rhinol Laryngol. 1978; 87:37-42. Google Scholar Author, Article, and Disclosure InformationAuthors: Joseph T. Morris, MD; J. William Kelly, MD PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTherapy of Multidrug‐Resistant and Extensively Drug‐Resistant TuberculosisTherapy of Multidrug-Resistant and Extensively Drug-Resistant TuberculosisTherapy of Multidrug-Resistant and Extensively Drug-Resistant TuberculosisThe failure to detect drug-induced sensory loss in standard preclinical studiesRifabutinLes troubles du goûtMultidrug-resistant tuberculosisMedication‐Induced Taste DisturbancesDisturbances of Taste and Smell Induced by DrugsRRifabutin 15 July 1993Volume 119, Issue 2Page: 171-172KeywordsAIDSAntimicrobialsArthralgiaLungsMagnesiumMyalgiaNocardiaPulmonary diseasesTasteUrine ePublished: 15 August 2000 Issue Published: 15 July 1993 Copyright & PermissionsCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Can altruism be understood in terms of socially-discounted extrinsic reinforcement?
Authors: Randolph C. Grace, Anthony McLean, Orn Bragason
Journal: Behavioral and Brain Sciences (2002)

Altruism can be understood in terms of traditional principles of reinforcement if an outcome that is beneficial to another person reinforces the behavior of the actor who produces it. This account depends on a generalization of reinforcement across persons and might be more amenable to experimental investigation than the one proposed by Rachlin.
Prolonged circulatory support with the intra-aortic balloon pump after myocardial infarction.
Authors: P B Disler, R N Scott Millar, I W Obel
Journal: Thorax (1978)

<h3>Abstract</h3> The coronavirus disease 2019 (COVID-19) pandemic is caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is spread primary via respiratory droplets and infects the lungs. Currently widely used cell lines and animals are unable to accurately mimic human physiological conditions because of the abnormal status of cell lines (transformed or cancer cells) and species differences between animals and humans. Organoids are stem cell-derived self-organized three-dimensional culture <i>in vitro</i> and model the physiological conditions of natural organs. Here we demonstrated that SARS-CoV-2 infected and extensively replicated in human embryonic stem cells (hESCs)-derived lung organoids, including airway and alveolar organoids. Ciliated cells, alveolar type 2 (AT2) cells and rare club cells were virus target cells. Electron microscopy captured typical replication, assembly and release ultrastructures and revealed the presence of viruses within lamellar bodies in AT2 cells. Virus infection induced more severe cell death in alveolar organoids than in airway organoids. Additionally, RNA-seq revealed early cell response to SARS-CoV-2 infection and an unexpected downregulation of ACE2 mRNA. Further, compared to the transmembrane protease, serine 2 (TMPRSS2) inhibitor camostat, the nucleotide analog prodrug Remdesivir potently inhibited SARS-CoV-2 replication in lung organoids. Therefore, human lung organoids can serve as a pathophysiological model for SARS-CoV-2 infection and drug discovery.
Making It Easier
Authors: Hunter Heath
Journal: Annals of Internal Medicine (1992)

Letters15 October 1992Making It EasierHunter Heath III, MDHunter Heath III, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-117-8-701 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors: Hurrah for "Making it Easier"! Your policy of clarifying generic drug names, abbreviations, and SI unit conversions at the beginnings of articles represents a long overdue acknowledgment that readers need help dealing with these issues.This new feature will improve both communication and education.... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByPredictors of empathy in dementia care staff 15 October 1992Volume 117, Issue 8Page: 701-701KeywordsDrug policyDrugs Issue Published: 15 October 1992 PDF DownloadLoading ...
Hypoglycemia in Adults With Cystic Fibrosis During Oral Glucose Tolerance Testing
Authors: Irl B. Hirsch, Mary M. Janci, Christopher H. Goss, Moira L. Aitken
Journal: Diabetes Care (2013)

Cystic fibrosis–related diabetes (CFRD) is the most common comorbidity in patients with cystic fibrosis (CF) (1). Consensus guidelines state that all patients above the age of 10 years should be screened annually for CFRD with a 2-h 75-g oral glucose tolerance test (OGTT) (2). There are four categories of glucose tolerance based on OGTT fasting and 75-g 2-h glucose levels: normal glucose tolerance, impaired glucose tolerance (IGT) with 2 h level 7.8–11.1 mmol/L, CFRD without fasting hyperglycemia (CFRD FH−) with 2-h level > 11.1 mmol/L, and CFRD with fasting hyperglycemia (CFRD FH+) (2).

At our institution in 2011, there were 167 pre–lung transplant adult CF patients, of whom 46 had preexisting CFRD. Of the remaining, 28 agreed to the test; 3 were found to have CFRD FH−, 1 was …
Abstract 2454: High susceptibility to azoxymethane-induced ear duct and intestinal carcinogenesis in diabetic OLETF rats
Authors: Keisuke Izumi, Ezar Hafez, Tetsuyuki Takahashi, Hirohisa Ogawa
Journal: Cancer Research (2010)

Abstract Diabetes and obesity are thought to be risk factors for colorectal cancer in humans. In our recent study, whole body X-irradiated Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model animal of type 2 diabetes, developed low incidence of small intestine adenocarcinoma, but not in nondiabetic Long-Evans Tokushima Otsuka (LETO) rats. In the present study, six-week-old male OLETF and LETO rats (n=24) were given weekly s.c. injections of 15 mg/kg azoxymethane (AOM) for three weeks and killed after 30 weeks from the initial treatment. The incidences of ear duct tumors in LETO and OLETF rats were 0% and 67% (P&amp;lt;0.001), respectively. Those of small intestine tumors in these strains were 0% and 43% (P&amp;lt;0.001), respectively, and those of colon tumors were 46% and 79% (P&amp;lt;0.05), respectively. Serum triglyceride and free fatty acid levels in OLETF rats were significantly higher than those in LETO rats at sacrifice, but average serum insulin was lower than that in LETO rats. Fatty change of hepatocytes was common in OLETF rats, but not in LETO rats. Hepatic IGF-1, leptin and PAI-1 mRNA levels were not different in two strains. These data suggest that hyperlipidemia plays an important role in high susceptibility to AOM-induced carcinogenesis in OLETF rats. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2454.