tbuckley/cabot-search huggingface dataset:
The Americans With Disabilities Act and HIV/AIDS Discrimination
Authors: Jeffrey S. Crowley, Gregory R. Nevins, Melanie Thompson
Journal: JAMA (2015)

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
Bone and Soft-Tissue Neoplasms in Cats Exposed to Radiostrontium
Authors: Jerrold M. Ward, James F. Wright, Neal S. Nelson, Ezra Berman, Charles G. Liddle, Alfred Hellman
Journal: JNCI Journal of the National Cancer Institute (1972)

Journal Article Bone and Soft-Tissue Neoplasms in Cats Exposed to Radiostrontium Get access Jerrold M. Ward, Jerrold M. Ward Twinbrook Research Laboratory, Office of Research and Monitoring, Environmental Protection Agency, Rockville, Maryland 20852, and Viral Oncology, National Cancer Institute,3Bethesda, Maryland 20014 Search for other works by this author on: Oxford Academic PubMed Google Scholar James F. Wright, James F. Wright Twinbrook Research Laboratory, Office of Research and Monitoring, Environmental Protection Agency, Rockville, Maryland 20852, and Viral Oncology, National Cancer Institute,3Bethesda, Maryland 20014 Search for other works by this author on: Oxford Academic PubMed Google Scholar Neal S. Nelson, Neal S. Nelson Twinbrook Research Laboratory, Office of Research and Monitoring, Environmental Protection Agency, Rockville, Maryland 20852, and Viral Oncology, National Cancer Institute,3Bethesda, Maryland 20014 Search for other works by this author on: Oxford Academic PubMed Google Scholar Ezra Berman, Ezra Berman Twinbrook Research Laboratory, Office of Research and Monitoring, Environmental Protection Agency, Rockville, Maryland 20852, and Viral Oncology, National Cancer Institute,3Bethesda, Maryland 20014 Search for other works by this author on: Oxford Academic PubMed Google Scholar Charles G. Liddle, Charles G. Liddle Twinbrook Research Laboratory, Office of Research and Monitoring, Environmental Protection Agency, Rockville, Maryland 20852, and Viral Oncology, National Cancer Institute,3Bethesda, Maryland 20014 Search for other works by this author on: Oxford Academic PubMed Google Scholar Alfred Hellman Alfred Hellman Twinbrook Research Laboratory, Office of Research and Monitoring, Environmental Protection Agency, Rockville, Maryland 20852, and Viral Oncology, National Cancer Institute,3Bethesda, Maryland 20014 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 48, Issue 5, May 1972, Pages 1543–1546, https://doi.org/10.1093/jnci/48.5.1543 Published: 01 May 1972 Article history Received: 03 April 1972 Published: 01 May 1972
The Risks of Living Kidney Donation
Authors: Robert W Steiner
Journal: New England Journal of Medicine (2015)

Only candidates with an apparent low risk of kidney disease are accepted as living kidney donors. Postdonation studies that extend up to 12 years have shown rates of end-stage renal disease (ESRD) among donors that are similar to those observed in the general population, which suggests minimal risk from the inevitable reduction in the glomerular filtration rate (GFR) that occurs at donor nephrectomy.1 However, a recent 7.6-year study in the United States showed that the incidence of ESRD was 8 times as high among donors as among well-selected nondonor controls.2 A similar 15.2-year study in Norway showed that the risk . . .
Interleukin 4 causes isotype switching to IgE in T cell-stimulated clonal B cell cultures.
Authors: D A Lebman, R L Coffman
Journal: The Journal of Experimental Medicine (1988)

Although it has been established that IL-4 enhances both IgG1 and IgE secretion in LPS-stimulated B cell cultures, these studies failed to determine whether IL-4 preferentially induces isotype switching or preferentially allows for the maturation of precommitted precursor cells. To distinguish between these possibilities, it is necessary to ascertain the effect of IL-4 on the isotypes secreted by individual precursor cells during clonal expansion. Therefore, clonal cultures of B cells stimulated with a Th2 helper cell line specific for rabbit Ig and rabbit anti-mouse IgM were established. The majority of B cells are capable of undergoing clonal expansion under these conditions. To vary the level of IL-4 present, either IL-4 or anti-IL-4 was added to cultures. In the presence of IL-4 there was an increase in the proportion of clones that secreted IgE and a decrease in the proportion of clones that secreted IgM. The addition of IL-4 to cultures also increased the amount of IgE secreted by individual clones. Thus, these experiments definitively prove that IL-4 causes specific heavy chain class switching to IgE in Th2-stimulated B cell cultures. In contrast, IL-4 does not affect the proportion of clones secreting IgG1, suggesting that other consequences of Th cell-B cell interactions play a role in the generation of an IgG1 response.
The structure of aggrecan fragments in human synovial fluid. Evidence for the involvement in osteoarthritis of a novel proteinase which cleaves the Glu 373-Ala 374 bond of the interglobular domain.
Authors: J D Sandy, C R Flannery, P J Neame, L S Lohmander
Journal: Journal of Clinical Investigation (1992)

Synovial fluid was collected from patients with recent knee injury and from patients with early or late stage osteoarthritis. Chondroitin sulfate-substituted aggrecan fragments present in these fluids, and in normal bovine synovial fluid, were purified by cesium chloride gradient centrifugation, enzymically deglycosylated and fractionated by gel filtration on Superose-12. Each sample contained two major aggrecan core protein populations with apparent molecular masses of approximately 90 kD and 150 kD. For all samples, NH2-terminal analysis of both populations gave a single major sequence beginning ARGSV. This NH2 terminus results from cleavage of the human aggrecan core protein at the Glu 373-Ala 374 bond within the interglobular domain between the G1 and G2 domains. Cleavage at this site also occurs during control and interleukin-1 stimulated aggrecan catabolism in bovine cartilage explant cultures (Sandy, J., P. Neame, R. Boynton, and C. Flannery. 1991. J. Biol. Chem. 266:8683-8685). These results indicate that the major aggrecan fragments present in both osteoarthritic human synovial fluid and in normal bovine synovial fluid are large, being composed of a short NH2-terminal stretch of the interglobular domain, the G2 domain, the keratan sulfate domain, and variable lengths of the chondroitin sulfate domain(s). We conclude that the release of aggrecan fragments from articular cartilage into the synovial fluid seen at all stages of human osteoarthritis (Lohmander, L. S. 1991. Acta Orthop. Scand. 62:623-632) is promoted by the action of a normal cartilage proteinase which cleaves the Glu 373-Ala 374 bond of the interglobular domain.
The Inflammasomes: Guardians of the Body
Authors: Fabio Martinon, Annick Mayor, Jürg Tschopp
Journal: Annual Review of Immunology (2009)

The innate immune system relies on its capacity to rapidly detect invading pathogenic microbes as foreign and to eliminate them. The discovery of Toll-like receptors (TLRs) provided a class of membrane receptors that sense extracellular microbes and trigger antipathogen signaling cascades. More recently, intracellular microbial sensors have been identified, including NOD-like receptors (NLRs). Some of the NLRs also sense nonmicrobial danger signals and form large cytoplasmic complexes called inflammasomes that link the sensing of microbial products and metabolic stress to the proteolytic activation of the proinflammatory cytokines IL-1beta and IL-18. The NALP3 inflammasome has been associated with several autoinflammatory conditions including gout. Likewise, the NALP3 inflammasome is a crucial element in the adjuvant effect of aluminum and can direct a humoral adaptive immune response. In this review, we discuss the role of NLRs, and in particular the inflammasomes, in the recognition of microbial and danger components and the role they play in health and disease.
Modeling survival in colon cancer: a methodological review.
Authors: Farid E Ahmed, Paul W Vos, Don Holbert
Journal: Molecular Cancer (2007)

The Cox proportional hazards model is the most widely used model for survival analysis because of its simplicity. The fundamental assumption in this model is the proportionality of the hazard function. When this condition is not met, other modifications or other models must be used for analysis of survival data. We illustrate in this review several methodological approaches to deal with the violation of the proportionality assumption, using survival in colon cancer as an illustrative example.
The Risk of Suicide With Selective Serotonin Reuptake Inhibitors in the Elderly
Authors: David N. Juurlink, Muhammad M. Mamdani, Alexander Kopp, Donald A. Redelmeier
Journal: American Journal of Psychiatry (2006)

Objective: The authors explored the relationship between the initiation of therapy with selective serotonin reuptake inhibitor (SSRI) antidepressants and completed suicide in older patients. Method: The authors linked population-based coroner's records with patient-level prescription data, physician billing claims, and hospitalization data for more than 1.2 million Ontario residents 66 years of age and older from 1992 to 2000. For each suicide case, four closely matched comparison subjects were selected using propensity score methods. The authors determined the odds ratio for suicide with SSRIs versus other antidepressant treatment, calculated at discrete monthly intervals from the start of treatment. Results: Of 1,329 suicide cases, 1,138 (86%) were each fully matched to four comparison subjects using propensity scores. During the first month of therapy, SSRI antidepressants were associated with a nearly fivefold higher risk of completed suicide than other antidepressants (adjusted odds ratio: 4.8, 95% confidence interval=1.9–12.2). The risk was independent of a recent diagnosis of depression or the receipt of psychiatric care, and suicides of a violent nature were distinctly more common during SSRI therapy. Numerous sensitivity analyses revealed consistent results. No disproportionate suicide risk was seen during the second and subsequent months of treatment with SSRI antidepressants, and the absolute risk of suicide with all antidepressants was low. Conclusions: Initiation of SSRI therapy is associated with an increased risk of suicide during the first month of therapy compared with other antidepressants. The absolute risk is low, suggesting that an idiosyncratic response to these agents may provoke suicide in a vulnerable subgroup of patients.
PRIME: A Programme to Reduce the Treatment Gap for Mental Disorders in Five Low- and Middle-Income Countries
Authors: Crick Lund, Mark Tomlinson, Mary De Silva, Abebaw Fekadu, Rahul Shidhaye, Mark Jordans, Inge Petersen, Arvin Bhana, Fred Kigozi, Martin Prince, Graham Thornicroft, Charlotte Hanlon, Ritsuko Kakuma, David McDaid, Shekhar Saxena, Dan Chisholm, Shoba Raja, Sarah Kippen-Wood, Simone Honikman, Lara Fairall, Vikram Patel
Journal: PLoS Medicine (2012)

Crick Lund and colleagues describe their plans for the PRogramme for Improving Mental health carE (PRIME), which aims to generate evidence on implementing and scaling up integrated packages of care for priority mental disorders in primary and maternal health care contexts in Ethiopia, India, Nepal, South Africa, and Uganda.
Increased transforming growth factor-beta1circulating levels and production in human monocytes after 3-hydroxy-3-methyl-glutaryl-coenzyme a reductase inhibition with pravastatin
Authors: Ettore Porreca, Concetta Di Febbo, Giovanna Baccante, Marcello Di Nisio, Franco Cuccurullo
Journal: Journal of the American College of Cardiology (2002)
Biomechanically Induced Gene <i>iex-1</i> Inhibits Vascular Smooth Muscle Cell Proliferation and Neointima Formation
Authors: P. Christian Schulze, Gilles W. de Keulenaer, Kimberly A. Kassik, Tomosaburo Takahashi, Zhiping Chen, Daniel I. Simon, Richard T. Lee
Journal: Circulation Research (2003)

Mechanotransduction plays a prominent role in vascular pathophysiology but is incompletely understood. In this study, we report the biomechanical induction of the immediate early response gene iex-1 in vascular smooth muscle cells (SMCs). Mechanical induction of iex-1 was confirmed by Northern (30-fold induction after 2 hours) and Western (6-fold induction after 24 hours) analyses. Expression of iex-1 was regulated by mechanical activation of nuclear factor (NF)-κB and abolished by overexpression of IκB in SMCs. The function of iex-1 in SMCs was explored by gene transfer using adenoviral vectors overexpressing iex-1 . After 48 hours of 4% cyclic mechanical strain, adenoviral vectors overexpressing iex-1 –infected cells had lower 3 [H]-thymidine incorporation compared with AdGFP-infected controls (71.3±8.5% versus 180.2±19.4% in controls; P &lt;0.001). Overexpression of iex-1 suppressed mitogenesis induced by platelet-derived growth factor (208.1±108.3% versus 290.0±120.5% in controls; P &lt;0.05). This was accompanied by reduced degradation of p27 kip1 , inhibition of Rb hyperphosphorylation, and reduced cell cycle progression. To investigate functional effects of iex-1 in vivo, we performed carotid artery mechanical injury and endothelial denudation in low-density lipoprotein receptor–deficient mice followed by intraluminal injection of adenoviral vectors (3×10 9 pfu in 50 μL) for overexpression of iex-1 or gfp (control). Vascular overexpression of iex-1 reduced neointima formation 2 weeks after injury (intima/media ratio, 0.23±0.04 versus 0.5±0.24 in controls; P &lt;0.05). Our findings demonstrate that biomechanical strain induces iex-1 with subsequent antiproliferative effects in SMCs and that selective gene transfer of iex-1 inhibits the local vascular response after injury. These findings suggest that the induction of iex-1 represents a novel negative biomechanical feedback mechanism limiting the vascular response to injury.
Neutrophilic Inflammation in Severe Persistent Asthma
Authors: ANON JATAKANON, CARINA UASUF, WAZIM MAZIAK, SAM LIM, KIAN FAN CHUNG, PETER J. BARNES
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Airway inflammation in severe asthma is not well characterized but may involve neutrophils. We have compared induced sputum profiles in patients with asthma of varying severity and normal control subjects. We have also measured exhaled nitric oxide (NO) as a noninvasive marker of inflammation. Asthma severity was based on clinical features before treatment and the minimum medication required to maintain asthma control at the time of sputum induction, and classified as (1) mild: treated with inhaled beta(2)-agonist occasionally (n = 23; FEV(1), 91%; peak expiratory flow (PEF) variability, 10.5%), (2) moderate: requiring medium dose inhaled steroids to maintain control (n = 16; FEV(1), 88%; PEF variability, 9.1%), and (3) severe: despite using inhaled and oral steroids (n = 16; FEV(1), 61%; PEF variability, 36.2%). The asthmatic patients were nonsmokers with evidence of airway hyperresponsiveness or reversible airway obstruction, and free of respiratory tract infection for at least 6 wk. Sputum revealed significantly increased neutrophil numbers in severe asthma (53.0 [38.4- 73.5]%, p < 0.05) compared with mild asthma (35.4 [29.8-46.1]%) and normal control subjects (27.7 [20.6-42.2]%). Interleukin-8 (IL-8) and neutrophil myeloperoxidase (MPO) levels were increased in asthmatic patients, with the highest levels in severe asthma. Eosinophil numbers were increased in both mild and severe asthma, but interleukin-5 (IL-5) levels were highest in mild asthma, whereas eosinophil cationic protein (ECP) levels were highest in severe asthma. Exhaled NO levels were highest in asthmatic untreated with corticosteroids, but there was no significant difference between asthmatics using corticosteroids (Groups 2 and 3), regardless of clinical asthma severity. This confirms the role of eosinophils in asthma but suggests a potential role of neutrophils in more severe asthma.
Effect of 3-Month Yoga on Oxidative Stress in Type 2 Diabetes With or Without Complications
Authors: Shreelaxmi V. Hegde, Prabha Adhikari, Shashidhar Kotian, Veena J. Pinto, Sydney D’Souza, Vivian D’Souza
Journal: Diabetes Care (2011)

To assess the effect of yoga on anthropometry, blood pressure, glycemic control, and oxidative stress in type 2 diabetic patients on standard care in comparison with standard care alone.The study involved 123 patients stratified according to groups with microvascular complications, macrovascular complications, and peripheral neuropathy and without complications and assigned to receive either standard care or standard care along with additional yoga for 3 months.In comparison with standard care alone, yoga resulted in significant reduction in BMI, glycemic control, and malondialdehyde and increase in glutathione and vitamin C. There were no differences in waist circumference, waist-to-hip ratio, blood pressure, vitamin E, or superoxide dismutase in the yoga group at follow-up.Yoga can be used as an effective therapy in reducing oxidative stress in type 2 diabetes. Yoga in addition to standard care helps reduce BMI and improve glycemic control in type 2 diabetic patients.
Expression of the atrial natriuretic peptide gene in the cardiac muscle of rat extrapulmonary and intrapulmonary veins.
Authors: D R Springall, M Bhatnagar, J Wharton, Q Hamid, S Gulbenkian, M Hedges, L Meleagros, S R Bloom, J M Polak
Journal: Thorax (1988)

Atrial natriuretic peptide is a peptide regulating salt and water balance, originally isolated from the cardiac atrium, where it is synthesised as part of a precursor molecule in specialised myocardial cells. The myocardium extends into the extrapulmonary part of the pulmonary veins in many species, including man. In some small mammals, however, such as the rat, mouse, and bat, it extends further to veins in the peripheral parts of the lung. Since this myocardial layer is continuous with that in the atrium, we have looked for the possible expression of the atrial natriuretic peptide gene in this tissue in rats. Strong immunoreactivity was seen for both the peptide and the N terminal sequence (cardiodilatin) of its precursor in extrapulmonary veins and in intrapulmonary veins extending into the lung as far as the second branching point, where it was localised in the dense cored granules by electron microscopy; in situ hybridisation showed atrial natriuretic peptide messenger RNA at identical sites. Chromatography and radioimmunoassay of extracts of extrapulmonary and intrapulmonary veins showed most of the atrial natriuretic peptide immunoreactivity to be in the uncleaved (precursor molecule) form. Thus the peptide is synthesised in veins both outside and inside the lung, and these extra-atrial sites may be an important additional source of circulating atrial natriuretic peptide.
Coronary Dilatation and Constriction Visualized by Selective Arteriography
Authors: JAMES W. WEST, SANTIAGO V. GUZMAN
Journal: Circulation Research (1959)

Selective coronary angiograms were made in dogs with intact chests prior to and following various groups of drugs. They demonstrated visible constriction and dilatation of the coronary vessels and the appearance of previously invisible channels following coronary vasodilators and embolization with lycopodium spores.
Phenotypic plasticity of fibrocytes upon culture with airway smooth muscle
Authors: Ruth Saunders, Davinder Kaur, Camille Doe, Fay Hollins, Christopher Brightling
Journal: European Respiratory Journal (2012)

Asthma is a major cause of morbidity and mortality worldwide and its prevalence is increasing. Increased airway smooth muscle (ASM) mass is a hallmark of asthma, which increases with disease severity and is associated with decline in lung function. Fibrocytes (FCs) are elevated in the peripheral blood and ASM in asthma and ASM has the potential to mediate FC recruitment (Saunders  et al , J Allergy Clin Immunol, 2009;123:376-84). We hypothesised that once recruited to the ASM FCs differentiate into a more ASM like phenotype under the influence of local factors.  FCs were isolated from peripheral blood, ASM from bronchial biopsies and lung resection material. FCs were labelled with CFSE prior to culture with ASM cells for 7d, allowing identification by gating following flow cytometry.  24h after isolation from the peripheral blood cells are predominantly CD14 high /α-smooth muscle actin (αSMA) low . Subsequent monoculture yields CD14 low /αSMA high  cells, consistent with differentiation to fibrocytes. Coculture with ASM from both non-asthmatic (NA) and asthmatic (A) donors yields CD14 high  FCs, whereas ASM from NA donors yields αSMA low  FCs and ASM from A donors yields αSMA high  FCs (Table 1).  Our results show that FCs have the capability to undergo phenotypic plasticity, depending on culture conditions. Further work is required to understand the factors affecting FC differentiation upon localisation to the ASM in asthma and the resultant contribution of FCs to ASM dysfunction.
Regulation of Hepcidin and Iron-Overload Disease
Authors: Pauline L. Lee, Ernest Beutler
Journal: Annual Review of Pathology Mechanisms of Disease (2009)

Hepcidin, a 25-amino-acid antimicrobial peptide, is the central regulator of iron homeostasis. Hepcidin transcription is upregulated by inflammatory cytokines, iron, and bone morphogenetic proteins and is downregulated by iron deficiency, ineffective erythropoiesis, and hypoxia. The iron transporter ferroportin is the cognate receptor of hepcidin and is destroyed as a result of interaction with the peptide. Except for inherited defects of ferroportin and hepcidin itself, all forms of iron-storage disease appear to arise from hepcidin dysregulation. Studies using multiple approaches have begun to delineate the molecular mechanisms that regulate hepcidin expression, particularly at the transcriptional level. Knowledge of the regulation of hepcidin by inflammation, iron, erythropoiesis, and hypoxia will lead to an understanding of the pathogenesis of primary hemochromatosis, secondary iron overload, and anemia of inflammatory disease.