tbuckley/cabot-search huggingface dataset:
Contrasting effects of an ultraviolet B and an ultraviolet A tanning lamp on interleukin-6, tumour necrosis factor-alpha and intercellular adhesion molecule-1 expression
Authors: P.H. Clingen, M. Berneburg, C. Petit-Frere, A. Woollons, J.E. Lowe, C.F. Arlett, M.H.L. Green
Journal: British Journal of Dermatology (2001)

Background Recent studies have demonstrated that a tanning lamp emitting predominantly ultraviolet (UV) A induces significant yields of the type of potentially mutagenic DNA damage that are associated with the onset of skin cancer (i.e. cyclobutane pyrimidine dimers). UV-induced immunosuppression is also an important event leading to skin cancer.Objectives To the modulation of key immunological molecules following exposure to a broad-spectrum UVB lamp and a predominantly UVA-emitting tanning lamp using model in vitro systems.Methods We compared secretion and mRNA expression of interleukin (IL)-6 and tumour necrosis factor (TNF)-α in normal human epidermal keratinocytes, and interferon (IFN)-γ-induced intracellular adhesion molecule (ICAM)-1 in normal human fibroblasts irradiated in vitro with a broad-spectrum UVB lamp or with a Philips 'Performance' tanning lamp.Results With broad-spectrum UVB irradiation, upregulation of IL-6 and TNF-α mRNA was detected 6 h after irradiation, and a dose-dependent increase of cytokines in the supernatants of irradiated cells was found 24 h after irradiation. In contrast, there was no cytokine secretion and little evidence for mRNA upregulation following exposure to a tanning lamp. When cells were exposed first to broad-spectrum UVB, then the tanning lamp, UVB-induced cytokine secretion was inhibited, although mRNA levels were upregulated to a level close to that observed with UVB alone. By using a Schott WG 320 nm filter to attenuate the level of UVB relative to UVA emitted by the tanning lamp, the inhibition of cytokine secretion was shown to be associated with UVA exposure. Both UV sources inhibited IFN-γ-induced ICAM-1 mRNA expression in a dose-dependent fashion. By using a Schott WG 335 nm filter, inhibition of ICAM-1 mRNA expression by the tanning lamp was shown to be associated with UVB exposure.Conclusions These results suggest that UV sources emitting different levels of UVA and UVB have differential effects on the modulation of different immunoregulatory molecules, and indicate that there are potential interactions between these wavelengths.
Early B Cell Factor Promotes B Lymphopoiesis with Reduced Interleukin 7 Responsiveness in the Absence of E2A
Authors: Christopher S. Seet, Rachel L. Brumbaugh, Barbara L. Kee
Journal: The Journal of Experimental Medicine (2004)

The basic helix-loop-helix transcription factors encoded by the E2A gene function at the apex of a transcriptional hierarchy involving E2A, early B cell factor (EBF), and Pax5, which is essential for B lymphopoiesis. In committed B lineage progenitors, E2A proteins have also been shown to regulate many lineage-associated genes. Herein, we demonstrate that the block in B lymphopoiesis imposed by the absence of E2A can be overcome by expression of EBF, but not Pax5, indicating that EBF is the essential target of E2A required for development of B lineage progenitors. Our data demonstrate that EBF, in synergy with low levels of alternative E2A-related proteins (E proteins), is sufficient to promote expression of most B lineage genes. Remarkably, however, we find that E2A proteins are required for interleukin 7–dependent proliferation due, in part, to a role for E2A in optimal expression of N-myc. Therefore, high levels of E protein activity are essential for the activation of EBF and N-myc, whereas lower levels of E protein activity, in synergy with other B lineage transcription factors, are sufficient for expression of most B lineage genes.
Soil Dust Aerosols and Wind as Predictors of Seasonal Meningitis Incidence in Niger
Authors: Carlos Pérez García-Pando, Michelle C. Stanton, Peter J. Diggle, Sylwia Trzaska, Ron L. Miller, Jan P. Perlwitz, José M. Baldasano, Emilio Cuevas, Pietro Ceccato, Pascal Yaka, Madeleine C. Thomson
Journal: Environmental Health Perspectives (2014)

Background: Epidemics of meningococcal meningitis are concentrated in sub-Saharan Africa during the dry season, a period when the region is affected by the Harmattan, a dry and dusty northeasterly trade wind blowing from the Sahara into the Gulf of Guinea.Objectives: We examined the potential of climate-based statistical forecasting models to predict seasonal incidence of meningitis in Niger at both the national and district levels.Data and methods: We used time series of meningitis incidence from 1986 through 2006 for 38 districts in Niger. We tested models based on data that would be readily available in an operational framework, such as climate and dust, population, and the incidence of early cases before the onset of the meningitis season in January–May. Incidence was used as a proxy for immunological state, susceptibility, and carriage in the population. We compared a range of negative binomial generalized linear models fitted to the meningitis data.Results: At the national level, a model using early incidence in December and averaged November–December zonal wind provided the best fit (pseudo-R2 = 0.57), with zonal wind having the greatest impact. A model with surface dust concentration as a predictive variable performed indistinguishably well. At the district level, the best spatiotemporal model included zonal wind, dust concentration, early incidence in December, and population density (pseudo-R2 = 0.41).Conclusions: We showed that wind and dust information and incidence in the early dry season predict part of the year-to-year variability of the seasonal incidence of meningitis at both national and district levels in Niger. Models of this form could provide an early-season alert that wind, dust, and other conditions are potentially conducive to an epidemic.Citation: Pérez García-Pando C, Stanton MC, Diggle PJ, Trzaska S, Miller RL, Perlwitz JP, Baldasano JM, Cuevas E, Ceccato P, Yaka P, Thomson MC. 2014. Soil dust aerosols and wind as predictors of seasonal meningitis incidence in Niger. Environ Health Perspect 122:679–686; http://dx.doi.org/10.1289/ehp.1306640
Role of the p38 Mitogen-Activated Protein Kinase Pathway in the Generation of Arsenic Trioxide–Dependent Cellular Responses
Authors: Nick Giafis, Efstratios Katsoulidis, Antonella Sassano, Martin S. Tallman, Linda S. Higgins, Angel R. Nebreda, Roger J. Davis, Leonidas C. Platanias
Journal: Cancer Research (2006)

Abstract Arsenic trioxide (As2O3) induces differentiation and apoptosis of leukemic cells in vitro and in vivo, but the precise mechanisms that mediate such effects are not known. In the present study, we provide evidence that the kinases MAPK kinase 3 (Mkk3) and Mkk6 are activated during treatment of leukemic cell lines with As2O3 to regulate downstream engagement of the p38 mitogen-activated protein kinase. Using cells with targeted disruption of both the Mkk3 and Mkk6 genes, we show that As2O3-dependent activation of p38 is defective in the absence of Mkk3 and Mkk6, establishing that these kinases are essential for As2O3-dependent engagement of the p38 pathway. Pharmacologic inhibition of p38 enhances As2O3-dependent activation of the c-jun NH2-terminal kinase (JNK) and subsequent induction of apoptosis of chronic myelogenous leukemia (CML)– or acute promyelocytic leukemia (APL)–derived cell lines. In addition, in APL blasts, inhibition of p38 enhances myeloid cell differentiation in response to As2O3, as well as suppression of Bcl-2 expression and loss of mitochondrial membrane potential. Similarly, induction of As2O3-dependent apoptosis is enhanced in mouse embryonic fibroblasts (MEF) with targeted disruption of both the Mkk3 and Mkk6 genes, establishing a key role for this pathway in the regulation of As2O3-induced apoptosis. In other studies, we show that the small-molecule p38 inhibitors SD-282 and SCIO-469 potentiate As2O3-mediated suppression of myeloid leukemic progenitor growth from CML patients, indicating a critical regulatory role for p38 in the induction of antileukemic responses. Altogether, our data indicate that the Mkk3/6-p38 signaling cascade is activated in a negative regulatory feedback manner to control induction of As2O3-mediated antileukemic effects. (Cancer Res 2006; 66(13): 6763-71)
Hanford Health Information Archives Offers Unique History of Exposure to Radiation in US Northwest
Authors: M. Gaie
Journal: JAMA (1996)

GONZAGA UNIVERSITY in Spokane, Wash, the health agencies of Washington, Oregon, and Idaho, and 9 Indian nations have collaborated to establish a unique repository of health and other personal information from the Hanford downwinders, individuals who were or may have been exposed to radiation from the Hanford Nuclear Reservation plutonium plant (known as the Hanford Site). The Hanford Health Information Archives, which opened July 24, will collect, preserve, and make available to the public unedited health records, questionnaires, and other personal information provided by the downwinders. According to the Hanford Health Information Network, the Hanford Site was established by the United States government in 1943 to produce plutonium, such as that used in the bomb dropped on Nagasaki, Japan, on August 9,1945—3 days after the first atomic bomb was dropped on Hiroshima. The events precipitated Japan's surrender on August 14, 1945. This plant was the first reactor in the world
Mutations in RDH12 encoding a photoreceptor cell retinol dehydrogenase cause childhood-onset severe retinal dystrophy
Authors: Andreas R Janecke, Debra A Thompson, Gerd Utermann, Christian Becker, Christian A Hübner, Eduard Schmid, Christina L McHenry, Anita R Nair, Franz Rüschendorf, John Heckenlively, Bernd Wissinger, Peter Nürnberg, Andreas Gal
Journal: Nature Genetics (2004)
Potential confounders in the asthma–diet association: how causal approach could help?
Authors: A. Bédard, O. Dumas, F. Kauffmann, J. Garcia‐Aymerich, V. Siroux, R. Varraso, B. I. Nwaru, U. Nurmatov, G. Devereux, A. Sheikh
Journal: Allergy (2012)
When Vaccine Injury Claims Go to Court
Authors: Alexandra M. Stewart
Journal: New England Journal of Medicine (2009)

In February 2009, the National Vaccine Injury Compensation Program (VICP) released decisions for the first three test cases heard under the program's Omnibus Autism Proceeding. In each of the cases — Cedillo v. Secretary of Health and Human Services, Hazlehurst v. Secretary of Health and Human Services, and Snyder v. Secretary of Health and Human Services — the petitioners alleged that a child's autism spectrum disorder was caused by the combination of the measles–mumps–rubella (MMR) vaccine and thimerosal-containing vaccines. The decisions will have a substantial effect on vaccine policy and practice in the United States and will influence the analysis . . .
Socioeconomic Inequalities in Health
Authors: Nancy E. Adler
Journal: JAMA (1993)

Socioeconomic status (SES) is strongly associated with risk of disease and mortality. Universal health insurance is being debated as one remedy for such health inequalities. This article considers mechanisms through which SES affects health and argues that a broader and more comprehensive approach is needed.Published articles surveyed using MEDLINE and review articles and bibliographies.Research is reviewed on the association of SES with health outcomes in different countries, including those with universal health coverage. Socioeconomic status relates to health at all levels of the SES hierarchy, and access to care accounts for little of this association. Other mechanisms are suggested and implications for policy and clinical practice are discussed.Health insurance coverage alone is not likely to reduce significantly SES differences in health. Attention should be paid both in policy decisions and in clinical practice to other SES-related factors that may influence patterns of health and disease.
A85: Effect of Childhood-Onset Systemic Lupus Erythematosus on Linear Height and Body Mass Index
Authors: Aimee O. Hersh, Mary Beth Son, Emily von Scheven
Journal: Arthritis & Rheumatology (2014)

Background/Purpose:

To explore the relationship between childhood-onset systemic lupus erythematosus (SLE) and anthropomorphic measures including linear height and body mass index (BMI).



Methods:

Cross-sectional data were obtained from the CARRAnet registry, a United States pediatric rheumatology database. Subjects included in the database were diagnosed with SLE at ≤18 years of age and were ≤ age 21 at enrollment. Subject height and BMI at registry entry were recorded and compared with the US Centers for Disease Control and Prevention standardized growth charts for age and sex in order to obtain the appropriate percentiles. A history of renal disease was defined by a prior history of a renal biopsy. Chi squared testing was used to examine associations between height and BMI percentiles and history of renal disease and daily, chronic steroid use.



Results:

Data from 834 subjects were analyzed. Median age of onset was 12.3 years (range 0.88–17.32 years), median age at baseline was 15.5 years (range 3.1–20.4 years); 84% were female. Race/ethnicities included African American (35%), Caucasian (48%), Hispanic/Latino (27%), Asian (12%) and other (5%). The mean height percentile for the entire cohort was 40% (SD ± 30.6) with a median height percentile of 35% (range 1–100). Twenty one percent of the cohort (n = 174) had a height percentile of  14 years (n = 608), 40%. In univariate analysis, height was not associated with a history of renal disease or long term daily steroid exposure. The mean BMI percentile was 69% (SD ± 38), median percentile was 78% (range 1–100). One-third of the cohort (n = 276) had a BMI percentile of ≥90%. In univariate analysis, a BMI of ≥90% was associated with renal disease (p = 0.016) but not long term daily steroid exposure.



Conclusion:

In this large cohort of subjects with childhood-onset SLE, average height was reduced and BMI was increased as compared to the general population. Longitudinal studies of this population are needed to assess change in height and BMI over time, and to determine the impact of age of disease onset, disease activity and treatment on these important anthropomorphic measures.
Oxfam warns of future global hunger crisis unless rules on food markets are changed
Authors: N. Stafford
Journal: BMJ (2011)

The non-profit organisation Oxfam International has launched a global campaign to inform the public of the potential food shortage crisis facing the world, and to encourage policy makers to take decisive action to increase food production and ensure distribution to the world’s poor.

In a report released on 31 May as part of its GROW (Growing a Better Future) campaign, Oxfam says that decades of steady progress in fighting global hunger is now being reversed as demand increases faster than production, which is being negatively influenced by depleting natural resources, a scramble for fertile land and water, and the gathering pace of climate change. …
Development of novel sustained-release system, disintegration-controlled matrix tablet (DCMT) with solid dispersion granules of nilvadipine
Authors: Nobuyuki Tanaka, Keiji Imai, Kazuto Okimoto, Satoshi Ueda, Yuji Tokunaga, Atsuo Ohike, Rinta Ibuki, Kazutaka Higaki, Toshikiro Kimura
Journal: Journal of Controlled Release (2005)
Ventriculoperitoneal Shunting for Hydrocephalus
Authors: J. S. Robertson, M. I. Maraqa, B. Jennett
Journal: BMJ (1973)

<h3>Abstract</h3> Cell senescence may promote epidermal inflammation and degeneration, termed as inflammaging, which is accompanied by keratinocyte loss, resulting in fine lines of wrinkles. Recent findings showed that healthy elderly skin expresses age- and neuron-related amyloidogenic proteins, such as tau, β-Amyloid34, and α-synuclein (α-Syn), typically found in patients with neurodegenerative diseases. These proteins form toxic aggregates that trigger inflammatory signals. Herein, we investigated the impact of oligomeric α-Syn (Oα-Syn) on the neurosphere (NP) and the reconstructed human epidermis (RHE) 3D models. First, we found the expression of α-Syn, β-Amyloid, and amyloid precursor protein (APP) in the RHE. Second, we challenged the RHE and NP with Oα-Syn, which decreased RHE regeneration, measured by the percentage of cell proliferation and thickness of the stratum basale, but did not affect NP neurite outgrowth. Oα-Syn did not decrease the number of human neonatal epidermal keratinocytes (HEKn) but, as seen for the RHE, it also decreased the proliferation of HEKn. We confirmed that the oligomeric, and not the monomeric α-Syn species, accounted for the proliferation-decreasing effect. Oα-Syn also increased the NF-kB nuclear translocation in HEKn analyzed by nucleus/cytoplasm NF-κB fluorescence intensity. In addition, Oα-Syn triggered inflammation in the RHE, by increasing the mRNA levels of IL-1β and tumor necrosis factor-alpha (TNF-α), and the release of TNF-α in a time-dependent manner. These findings show that Oα-Syn does not affect neurite outgrowth but induces a decrease in keratinocyte proliferation along with epidermal inflammation. With our tridimensional models, we demonstrated that the neurodegenerative protein Oα-Syn also degenerates the epidermis, drawing attention to the need of target-based screening to prevent and treat the effects of skin aging.
II. Histochemical Observations on Enzyme Distribution in Surgically Resected Human Myocardium
Authors: Arthur A. Stein
Journal: JAMA (1962)

The distribution of a group of enzymes was determined histochemically in the surgically resected auricular myocardium of 5 cases of rheumatic and 6 cases of congenital heart disease. The enzymes studied included succinic dehydrogenase, diphosphopyridine nucleotide diaphorase, adenosine triphosphatase (ATPase), glucose-6-phosphatase, alkaline and acid phosphatase, and nonspecific esterase. The only abnormality noted was the apparent marked reduction in ATPase activity in the myocardium.
Plasma Renin Levels and Vascular Complications in Hypertension
Authors: A. E. Doyle, G. Jerums, C. I. Johnston, W. J. Louis
Journal: BMJ (1973)

Plasma renin levels, measured in 39 untreated patients in 1967, under conditions of sodium loading and sodium depletion have been related to the incidence of stroke and myocardial infarction. Renin levels were not significantly different in patients with or without vascular complications. Out of 13 patients with persistently low renin levels 6 had suffered either a stroke or a myocardial infarction and 7 had not. Plasma renin levels were also measured in 116 treated hypertensive patients. There was no relation between plasma renin level and vascular complications. It is concluded that levels of plasma renin are not a reliable index of the probability of hypertensive patients suffering a stroke or myocardial infarction.
Comparative genomic hybridization in extramammary Paget's disease
Authors: M-W. Lee, K-J. Jee, G-Y. Gong, J-H. Choi, K-C. Moon, J-K. Koh
Journal: British Journal of Dermatology (2005)

Background Extramammary Paget's disease (EMPD) is a distinct skin cancer of unknown histogenesis. Data from genome‐wide surveys for chromosomal aberrations in EMPD are limited.
Landmark article Nov 3, 1962: New method for terminating cardiac arrhythmias. Use of synchronized capacitor discharge. By Bernard Lown, Raghavan Amarasingham, and Jose Neuman
Authors: B. Lown
Journal: JAMA (1986)

THE ECTOPIC TACHYCARDIAS are currently treated by either vagal stimulation or drugs. The 3 most effective drugs are quinidine, procainamide hydrochloride, and the digitalis glycosides. When the ectopic mechanism drives the ventricles at rates above 160 per minute, cardiac output falls and coronary blood flow is compromised. This is most likely to occur with ventricular tachycardia which constitutes a serious cardiac emergency requiring immediate treatment. Frequently, however, the arrhythmia cannot be terminated promptly. Reversion with drugs generally involves a time-consuming biologic titration. Since it is impossible in any one patient to predict either the effective or the toxic dose, small increments of antiarrhythmic drugs are given at frequent intervals until a therapeutic end point is reached. The interval between doses is determined by the gravity of the patient's illness as well as by the rapidity of action of the particular agent. It may thus take minutes, days, or even weeks
Book Review How Healthy Are We? A National Study of Well-Being at Midlife (Studies on Successful Midlife Development.) Edited by Orville Gilbert Brim, Carol D. Ryff, and Ronald C. Kessler. 687 pp. Chicago, University of Chicago Press, 2004. $42. 0-226-07475-7
Authors: Sarita Bhalotra
Journal: New England Journal of Medicine (2004)
Inhaled Corticosteroids Increase Interleukin-10 but Reduce Macrophage Inflammatory Protein-1 α , Granulocyte-Macrophage Colony-stimulating Factor, and Interferon- γ Release from Alveolar Macrophages in Asthma
Authors: MATTHIAS JOHN, SAM LIM, JOACHIM SEYBOLD, PETER JOSE, ANNETTE ROBICHAUD, BRIAN O'CONNOR, PETER J. BARNES, K. FAN CHUNG
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

We determined the effect of inhaled corticosteroid, budesonide, on the release of the anti-inflammatory cytokine, interleukin-10 (IL-10), and of pro-inflammatory cytokines, macrophage inflammatory protein-1 α (MIP-1 α ), interferon- γ (IFN- γ ), and granulocyte-macrophage colony-stimulating factor (GM-CSF), from blood monocytes and alveolar macrophages of mild asthmatic subjects in a double-blind, cross-over, placebo-controlled study. Budesonide reduced bronchial hyperresponsiveness and improved baseline FEV1. Alveolar macrophages were obtained by bronchoalveolar lavage performed at the end of each treatment phase. IL-10 from blood monocytes was not altered, but both IL-10 mRNA and protein expression from alveolar macrophages stimulated by lipopolysaccharide and IL-1 β were increased after corticosteroid therapy. By contrast, alveolar macrophages released significantly less MIP-1 α , IFN- γ , and GM-CSF after steroid treatment. In comparison to alveolar macrophages from normal nonasthmatic volunteers, those from asthmatic patients released more MIP-1 α , IFN- γ , and GM-CSF but lower amounts of IL-10 particularly at baseline and after IL-1 β stimulation. The ability of steroids to inhibit pro-inflammatory cytokines but to enhance the anti-inflammatory cytokine such as IL-10 may contribute to their beneficial actions in asthma. Asthma is characterized by alveolar macrophages exhibiting both an enhanced capacity to release pro-inflammatory cytokines and a reduced capacity to produce IL-10.