tbuckley/cabot-search huggingface dataset:
Heterogeneity of Hematopoietic Cells Immortalized by v-myc/v-raf Recombinant Retrovirus Infection of Bone Marrow or Fetal Liver
Authors: G. W. Cox, B. J. Mathieson, L. Gandino, E. Blasi, D. Radzioch, L. Varesio
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Heterogeneity of Hematopoietic Cells Immortalized by v-myc/v-raf Recombinant Retrovirus Infection of Bone Marrow or Fetal Liver Get access George W. Cox, George W. Cox Laboratory of Molecular ImmunoregulationFrederick, MD Search for other works by this author on: Oxford Academic PubMed Google Scholar Bonnie J. Mathieson, Bonnie J. Mathieson Laboratory of Experimental Immunology, Biological Response Modifiers Program, Division of Cancer Treatment, National Cancer Institute, NCI-Frederick Cancer Research FacilityFrederick, MD Search for other works by this author on: Oxford Academic PubMed Google Scholar Lucia Gandino, Lucia Gandino Institute of Histology and Embryology, University of TorinoTorino, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar Elisabetta Blasi, Elisabetta Blasi Microbiology Institute, University of Perugia, PerugiaItaly. Search for other works by this author on: Oxford Academic PubMed Google Scholar Danuta Radzioch, Danuta Radzioch Biological Carcinogenesis Development Program, Program Resources, Inc., NCI-Frederick Cancer Research FacilityFrederick, MD Search for other works by this author on: Oxford Academic PubMed Google Scholar Luigi Varesio Luigi Varesio * Laboratory of Molecular ImmunoregulationFrederick, MD *Correspondence to: Dr. Luigi Varesio, Laboratory of Molecular Immunoregulation, Biological Response Modifiers Program, Division of Cancer Treatment, National Cancer Institute, NCI-Frederick Cancer Research Facility, Frederick, MD 21701. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 19, 4 October 1989, Pages 1492–1496, https://doi.org/10.1093/jnci/81.19.1492 Published: 04 October 1989 Article history Received: 22 December 1988 Revision received: 29 June 1989 Accepted: 05 July 1989 Published: 04 October 1989
Frequency of triggering bacteria in patients with reactive arthritis and undifferentiated oligoarthritis and the relative importance of the tests used for diagnosis
Authors: C Fendler, S Laitko, H Sörensen, C Gripenberg-Lerche, A Groh, J Uksila, K Granfors, J Braun, J Sieper
Journal: Annals of the Rheumatic Diseases (2001)

Reactive arthritis (ReA) triggered by Chlamydia trachomatis or enteric bacteria such as yersinia, salmonella, Campylobacter jejuni, or shigella is an important differential diagnosis in patients presenting with the clinical picture of an undifferentiated oligoarthritis (UOA). This study was undertaken to evaluate the best diagnostic approach.52 patients with ReA, defined by arthritis and a symptomatic preceding infection of the gut or the urogenital tract, and 74 patients with possible ReA, defined by oligoarthritis without a preceding symptomatic infection and after exclusion of other diagnoses (UOA), were studied. The following diagnostic tests were applied for the identification of the triggering bacterium: for yersinia induced ReA-stool culture, enzyme immunoassay (EIA), and Widal's agglutination test for detection of antibodies to yersinia; for salmonella or campylobacter induced ReA-stool culture, EIA for the detection of antibodies to salmonella and Campylobacter jejuni; for infections with shigella-stool culture; for infections with Chlamydia trachomatis-culture of the urogenital tract, microimmunofluorescence and immunoperoxidase assay for the detection of antibodies to Chlamydia trachomatis.A causative pathogen was identified in 29/52 (56%) of all patients with ReA. In 17 (52%) of the patients with enteric ReA one of the enteric bacteria was identified: salmonella in 11/33 (33%) and yersinia in 6/33 (18%). Chlamydia trachomatis was the causative pathogen in 12/19 (63%) of the patients with urogenic ReA. In patients with the clinical picture of UOA a specific triggering bacterium was also identified in 35/74 (47%) patients: yersinia in 14/74 (19%), salmonella in 9/74 (12%), and Chlamydia trachomatis in 12/74 (16%).Chlamydia trachomatis, yersinia, and salmonella can be identified as the causative pathogen in about 50% of patients with probable or possible ReA if the appropriate tests are used.
Lipoxin Generation Is Related to Soluble Epoxide Hydrolase Activity in Severe Asthma
Authors: Emiko Ono, Stefanie Dutile, Shamsah Kazani, Michael E. Wechsler, Jun Yang, Bruce D. Hammock, David Nobuhiro Douda, Yacine Tabet, Rayan Khaddaj-Mallat, Marco Sirois, Chantal Sirois, Edmond Rizcallah, Éric Rousseau, Richard Martin, E. Rand Sutherland, Mario Castro, Nizar N. Jarjour, Elliot Israel, Bruce D. Levy
Journal: American Journal of Respiratory and Critical Care Medicine (2014)

Rationale: Severe asthma is characterized by airway inflammatory responses associated with aberrant metabolism of arachidonic acid. Lipoxins (LX) are arachidonate-derived pro-resolving mediators that are decreased in severe asthma, yet mechanisms for defective LX biosynthesis and a means to increase LXs in severe asthma remain to be established.Objectives: To determine if oxidative stress and soluble epoxide hydrolase (sEH) activity are linked to decreased LX biosynthesis in severe asthma.Methods: Aliquots of blood, sputum, and bronchoalveolar lavage fluid were obtained from asthma subjects for mediator determination. Select samples were exposed to t-butyl-hydroperoxide or sEH inhibitor (sEHI) before activation. Peripheral blood leukocyte–platelet aggregates were monitored by flow cytometry, and bronchial contraction was determined with cytokine-treated human lung sections.Measurements and Main Results: 8-Isoprostane levels in sputum supernatants were inversely related to LXA4 in severe asthma (r = −0.55; P = 0.03) and t-butyl-hydroperoxide decreased LXA4 and 15-epi-LXA4 biosynthesis by peripheral blood leukocytes. LXA4 and 15-epi-LXA4 levels were inversely related to sEH activity in sputum supernatants and sEHIs significantly increased 14,15-epoxy-eicosatrienoic acid and 15-epi-LXA4 generation by severe asthma whole blood and bronchoalveolar lavage fluid cells. The abundance of peripheral blood leukocyte–platelet aggregates was related to asthma severity. In a concentration-dependent manner, LXs significantly inhibited platelet-activating factor–induced increases in leukocyte–platelet aggregates (70.8% inhibition [LXA4 100 nM], 78.3% inhibition [15-epi-LXA4 100 nM]) and 15-epi-LXA4 markedly inhibited tumor necrosis factor-α–induced increases in bronchial contraction.Conclusions: LX levels were decreased by oxidative stress and sEH activity. Inhibitors of sEH increased LXs that mediated antiphlogistic actions, suggesting a new therapeutic approach for severe asthma.Clinical trial registered with www.clinicaltrials.gov (NCT 00595114).
Impaired Postprandial Blood Flow in Adipose Tissue May Be an Early Marker of Insulin Resistance in Type 2 Diabetes
Authors: George Dimitriadis, Vaia Lambadiari, Panayota Mitrou, Eirini Maratou, Eleni Boutati, Demosthenes B. Panagiotakos, Theofanis Economopoulos, Sotirios A. Raptis
Journal: Diabetes Care (2007)

We investigated the changes in subcutaneous adipose tissue blood flow (ATBF) after a meal in the various stages of type 2 diabetes.Five groups were examined: healthy control subjects, first-degree relatives of subjects with type 2 diabetes, subjects with impaired glucose tolerance (IGT), subjects with type 2 diabetes and postprandial hyperglycemia but normal fasting plasma glucose levels (diabetes group A [DMA]), and subjects with type 2 diabetes with both postprandial and fasting hyperglycemia (diabetes group B [DMB]). ATBF was measured with (133)Xe.ATBF was higher in control subjects (1,507 +/- 103 ml/100 cm(3) tissue x min) versus relatives and IGT, DMA, and DMB subjects (845 +/- 123, 679 +/- 69, 765 +/- 60, and 757 +/- 69 ml/100 cm(3) tissue x min, respectively; P < 0.001). Insulin sensitivity index (ISI) in control subjects (82 +/- 3 mg x l(2)/mmol x mU x min) was higher versus that for relatives and IGT, DMA, and DMB subjects (60 +/- 3, 45 +/- 1, 40 +/- 6, and 29 +/- 4 mg x l(2)/mmol x mU x min, respectively; P < 0.0001). ISI was positively associated with peak-baseline ATBF (beta coefficient 0.029 +/- 0.013, P = 0.03).After meal ingestion, insulin-stimulated ATBF was decreased in relatives and and IGT, DMA, and DMB subjects. This defect could be an early marker of insulin resistance that precedes the development of type 2 diabetes.
One Risk Assessment Tool for Cardiovascular Disease, Type 2 Diabetes, and Chronic Kidney Disease
Authors: Marjan Alssema, Rachel S. Newson, Stephan J.L. Bakker, Coen D.A. Stehouwer, Martijn W. Heymans, Giel Nijpels, Hans L. Hillege, Albert Hofman, Jacqueline C.M. Witteman, Ron T. Gansevoort, Jacqueline M. Dekker
Journal: Diabetes Care (2012)

Individuals at high risk for chronic cardiometabolic disease (cardiovascular disease [CVD], type 2 diabetes, and chronic kidney disease [CKD]) share many risk factors and would benefit from early intervention. We developed a nonlaboratory-based risk-assessment tool for identification of people at high cardiometabolic disease risk.
Is IgA antineutrophil cytoplasmic antibody a marker for patients with erythema elevatum diutinum? A further three cases demonstrating this association
Authors: S.M. Crichlow, A.B. Alexandroff, R.C. Simpson, G. Saldanha, S. Walker, K.E. Harman
Journal: British Journal of Dermatology (2010)

Journal Article Is IgA antineutrophil cytoplasmic antibody a marker for patients with erythema elevatum diutinum? A further three cases demonstrating this association Get access S.M. Crichlow, S.M. Crichlow Departments of Dermatology and Immunology, University Hospitals of Leicester NHS Trust, and Search for other works by this author on: Oxford Academic Google Scholar A.B. Alexandroff, A.B. Alexandroff Departments of Dermatology and Immunology, University Hospitals of Leicester NHS Trust, and Search for other works by this author on: Oxford Academic Google Scholar R.C. Simpson, R.C. Simpson Departments of Dermatology and Immunology, University Hospitals of Leicester NHS Trust, and Search for other works by this author on: Oxford Academic Google Scholar G. Saldanha, G. Saldanha Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester Royal Infirmary, Leicester LE1 5WW, U.K. Search for other works by this author on: Oxford Academic Google Scholar S. Walker, S. Walker Departments of Dermatology and Immunology, University Hospitals of Leicester NHS Trust, and Search for other works by this author on: Oxford Academic Google Scholar K.E. Harman K.E. Harman Departments of Dermatology and Immunology, University Hospitals of Leicester NHS Trust, and Karen E. Harman. E‐mail: karenharman@doctors.org.uk Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 164, Issue 3, 1 March 2011, Pages 675–677, https://doi.org/10.1111/j.1365-2133.2010.10172.x Published: 01 March 2011
Are Human Immunodeficiency Virus Test Reports Clear to Clinicians?
Authors: D. Peter Drotman
Journal: JAMA (1989)

All physicians, regardless of their specialty, will be ordering and interpreting larger numbers of tests for human immunodeficiency virus (HIV) in the near future. Estimates provided by nearly 1000 US laboratories enrolled in the Centers for Disease Control's Model Performance Evaluation Program for HIV-1 antibody testing<sup>1</sup>indicate that these laboratories performed between 23 and 32 million tests for HIV-1 antibody in 1988. The reasons for increased HIV testing are manifold. Not only are millions of HIV antibody tests being performed in mandated screening programs (such as those for blood donors and military recruit applicants), but clinical uses of the test are also on the rise. The availability of effective medical intervention at earlier stages of HIV infection, such as the administration of zidovudine to patients who are asymptomatically infected to prevent onset of acquired immunodeficiency syndrome and the recommendation to use sulfamethoxazole and trimethoprim or aerosolized pentamidine for<i>Pneumocystis carinii</i>
Effects of the spatial dispersion of acetylcholine release on the chronotropic responses to vagal stimulation in dogs.
Authors: T E Yang, J Cheng, M N Levy
Journal: Circulation Research (1990)

We determined the effects of changing the spatial dispersion of acetylcholine release on the phase-dependent chronotropic responses to vagal stimulation in anesthetized dogs. We stimulated the vagus nerves with one brief burst of electrical pulses each cardiac cycle, and we changed the timing of the stimulus by a small, constant amount each cardiac cycle to scan the entire cycle. To vary the heterogeneity of acetylcholine release, we changed the voltage of the stimulus pulses over a range of submaximal values. To achieve the maximum homogeneity of acetylcholine release, we used supramaximal voltages, and we varied the level of acetylcholine release from each excited fiber by changing the number of pulses per burst. We used the average cardiac cycle length of the phase-response curve to assess the overall vagal effect, independent of its timing within the cardiac cycle. We found that the amplitude of the phase-response curve varied directly and the minimum-to-maximum phase difference varied inversely with the overall efficacy of vagal activity. However, for any given alteration in the overall efficacy, the specific changes in the characteristics of the phase-response curve did not depend on whether the alteration was achieved by varying the number of pulses per burst or by varying the stimulus voltage. Therefore, we conclude that although the cardiac chronotropic response is very sensitive to changes in the timing of vagal stimulation, it is not influenced appreciably by the spatial dispersion of acetylcholine release from the vagal nerve endings over a wide range of stimulation strengths.
Expression of functional CD40 by vascular endothelial cells.
Authors: D Hollenbaugh, N Mischel-Petty, C P Edwards, J C Simon, R W Denfeld, P A Kiener, A Aruffo
Journal: The Journal of Experimental Medicine (1995)

The interaction between activated vascular endothelium and T cells has been shown to play an important role in the recruitment and activation of T cells at sites of inflammation. Here we report the expression of CD40 by vascular endothelial cells and its regulation by inflammatory agents. Using the soluble recombinant CD40 ligand, sgp39, we show that the interaction of CD40 with its ligand can lead to endothelial cell activation, which in turn leads to leukocyte adhesion. This adhesion is partly mediated by the expression of E-selectin. In addition to E-selectin expression, sgp39 induces the expression of intercellular adhesion molecule 1 and augments the tumor necrosis factor alpha-induced expression of vascular cell adhesion molecule 1. The effects of sgp39 on endothelial cells can be blocked with anti-gp39 monoclonal antibody (mAb), anti-CD40 mAb, or soluble CD40. Staining of tissues from healthy human skin using anti-CD40 mAb showed very weak expression of CD40 by the endothelium, while skin involved in inflammatory disease showed marked upregulation of CD40 expression. These studies suggest that interactions between cell surface proteins expressed by activated T cells with their receptors on vascular endothelium can stimulate the vasculature at sites of inflammation and may be involved in normal inflammatory responses and in inflammatory disease.
Screening strategies for chronic kidney disease in the general population: follow-up of cross sectional health survey
Authors: Stein I Hallan, Ketil Dahl, Cecilia M Oien, Diana C Grootendorst, Arne Aasberg, Jostein Holmen, Friedo W Dekker
Journal: BMJ (2006)

<b>Objective</b> To find an effective screening strategy for detecting patients with chronic kidney disease and to describe the natural course of the disease. <b>Design</b> Eight year follow-up of a cross sectional health survey (the HUNT II study). <b>Setting</b> Nord-Trøndelag County, Norway <b>Participants</b> 65&nbsp;604 people (70.6 % of all adults aged ≥20 in the county). <b>Main outcome measures</b> Incident end stage renal disease (ESRD) and cardiovascular mortality monitored by individual linkage to central registries. <b>Results</b> 3069/65 604 (4.7%) people had chronic kidney disease (estimated glomerular filtration rate &lt;60 ml/min/1.73 m<sup>2</sup>), so we would need to screen 20.6 people (95% confidence interval 20.0 to 21.2) to identify one case. Restriction of screening to those with hypertension, diabetes, or age &gt;55 would identify 93.2% (92.4% to 94.0%) of patients with chronic kidney disease, with a number needed to screen of 8.7 (8.5 to 9.0). Restriction of screening according to guidelines of the United States kidney disease outcomes quality initiative (US KDOQI) gave similar results, but restriction according to the United Kingdom9s chronic kidney disease guidelines detected only 60.9% (59.1% to 62.8%) of cases. Screening only people with previously known diabetes or hypertension detected 44.2% (42.7% to 45.7%) of all cases, with a number needed to screen of six. During the eight year follow-up only 38 of the 3069 people with chronic kidney disease progressed to end stage renal disease, and the risk was especially low in people without diabetes or hypertension, women, and those aged ≥70 or with a glomerular filtration rate 45-59 ml/min/1.73 m<sup>2</sup> at screening. In contrast, there was a high cardiovascular mortality: 3.5, 7.4, and 10.1 deaths per 100 person years among people with a glomerular filtration rate 45-59, 30-44, and &lt;30 ml/min/1.73 m<sup>2</sup>, respectively. <b>Conclusion</b> Screening people with hypertension, diabetes mellitus, or age &gt;55 was the most effective strategy to detect patients with chronic kidney disease, but the risk of end stage renal disease among those detected was low.
Development and Validation of the Type 1 Diabetes Nutrition Knowledge Survey
Authors: Alisha J. Rovner, Tonja R. Nansel, Sanjeev N. Mehta, Laurie A. Higgins, Denise L. Haynie, Lori M. Laffel
Journal: Diabetes Care (2012)

OBJECTIVE The purpose of this study was to develop a survey of general and diabetes-specific nutrition knowledge for youth with type 1 diabetes and their parents and to assess the survey’s psychometric properties. RESEARCH DESIGN AND METHODS A multidisciplinary pediatric team developed the Nutrition Knowledge Survey (NKS) and administered it to youth with type 1 diabetes (n = 282, 49% females, 13.3 ± 2.9 years) and their parents (82% mothers). The NKS content domains included healthful eating, carbohydrate counting, blood glucose response to foods, and nutrition label reading. Higher NKS scores reflect greater nutrition knowledge (score range is 0–100%). In youths, glycemic control was assessed by A1C, and dietary quality was determined by the Healthy Eating Index-2005 (HEI-2005) derived from 3-day diet records. Validity was based on associations of NKS scores with A1C and dietary quality. Reliability was assessed using the Kuder-Richardson Formula 20 (KR-20) and correlations of domain scores to total score. RESULTS Mean NKS scores (23 items) were 56.9 ± 16.4% for youth and 73.4 ± 12.5% for parents. The KR-20 was 0.70 for youth and 0.59 for parents, representing acceptable internal consistency of the measure. In multivariate analysis, controlling for youth age, family income, parent education, diabetes duration, and insulin regimen, parent NKS scores were associated with corresponding youth A1C (β = −0.13, P = 0.03). Both parent (β = 0.20, P = 0.002) and youth (β = 0.25, P &amp;lt; 0.001) NKS scores were positively associated with youth HEI-2005 scores. CONCLUSIONS The NKS appears to be a useful measure of general and diabetes-specific nutrition knowledge for youth with type 1 diabetes and their parents.
Relationship between Ankle-Brachial Index and Chronic Kidney Disease in Hypertensive Patients with No Known Cardiovascular Disease
Authors: Jose M. Mostaza, Carmen Suarez, Luis Manzano, Marc Cairols, Francisca García-Iglesias, Julio Sanchez-Alvarez, Javier Ampuero, Diego Godoy, Andrés Rodriguez-Samaniego, Miguel A. Sanchez-Zamorano
Journal: Journal of the American Society of Nephrology (2006)

Both decreased GFR and albuminuria are associated with an elevated prevalence of peripheral artery disease. However, the combined effects of these alterations previously were not evaluated. Patients with hypertension and with no known vascular disease (n = 955; mean age 66 yr; 56% male) were selected from internal medicine outpatient clinics throughout Spain. Cardiovascular risk factors, urinary albumin excretion, and the ankle-brachial index (ABI) were assessed in all participants. GFR was estimated according to the Cockroft-Gault equation. Of the study population, 62% had diabetes, 23.8% had a GFR <60 ml/min per 1.73 m2, and 43.8% had albuminuria. The prevalence of ABI <0.9 was greater in patients with a GFR <60 ml/min per 1.73 m2 (37.4 versus 24.3%; P < 0.0001) and in those who had albuminuria (32.2 versus 23.3%; P = 0.001). In patients with both alterations, the prevalence of ABI <0.9 was 45.7%. Multivariate analysis indicated that the factors that were associated independently with low ABI were age (odds ratio [OR] 1.06; 95% confidence interval [CI] 1.03 to 1.08; P < 0.0001), triglyceride concentration (OR 1.003; 95% CI 1.001 to 1.005; P = 0.001), presence of albuminuria (OR 1.61; 95% CI 1.18 to 2.20; P = 0.003), smoking habit (OR 1.72; 95% CI 1.13 to 2.63; P = 0.012), and a GFR <60 ml/min per 1.73 m2 (OR 1.47; 95% CI 1.01 to 2.17; P = 0.049). In patients with hypertension and without known vascular disease, reduced GFR and albuminuria are associated independently with an ABI <0.9. Their combined presence characterizes a subgroup of the population who have an elevated prevalence of peripheral artery disease and could benefit from early diagnosis and treatment.
Osteopontin Expression Is Required for Myofibroblast Differentiation
Authors: Yair Lenga, Adeline Koh, Aruni Shamalee Perera, Christopher A. McCulloch, Jaro Sodek, Ron Zohar
Journal: Circulation Research (2007)

Osteopontin (OPN) is a multifunctional cytokine that is strongly expressed in healing wounds and fibrotic lesions, both of which are characterized by the formation of myofibroblasts. We examined the role of OPN in myofibroblast differentiation induced by the profibrotic cytokine transforming growth factor-beta1. In cultured cardiac or dermal fibroblasts treated with transforming growth factor-beta1, there was a 2- to 5-fold increase in the expression of the myofibroblast markers alpha-smooth muscle actin and extradomain A fibronectin but no significant increase of these proteins in OPN-null fibroblasts. Phalloidin staining for actin filaments and immunostaining for alpha-smooth muscle actin and focal adhesion proteins showed reduced stress fibers, focal adhesions, and lamellipodia in OPN-null fibroblasts compared with wild-type cells. OPN-null fibroblasts exhibited 40% to 60% less spreading, 50% less resistance to detachment by shear force, and a approximately 3-fold reduction in collagen gel contraction. These defects were partially rescued by ectopic expression of OPN. Mass spectrometric analysis of proteins in focal adhesions formed on collagen type I beads revealed an enrichment of HMGB1 protein in wild-type cells, whereas HMGB1 was not detected in OPN-null cells. Treatment of wild-type cells with small interfering RNA to knock down OPN reduced transforming growth factor-beta1-induced alpha-smooth muscle actin and HMGB1 to levels observed in OPN-null cells. These studies demonstrate that OPN is required for the differentiation and activity of myofibroblasts formed in response to the profibrotic cytokine transforming growth factor-beta1.