tbuckley/cabot-search huggingface dataset:
Total Antioxidant Status and Coronary Artery Calcification in Type 1 Diabetes
Authors: Jonathan Valabhji, Avril J. McColl, William Richmond, Michael Schachter, Michael B. Rubens, Robert S. Elkeles
Journal: Diabetes Care (2001)

OBJECTIVE—Type 1 diabetes is associated with a high risk of coronary heart disease (CHD), despite the absence of dyslipidemia. Oxidative modification may render LDLs more atherogenic. We aimed to assess antioxidant status in type 1 diabetes and its association with coronary artery calcification (CAC). RESEARCH DESIGN AND METHODS—Total antioxidant status (TAS) of serum was measured using the Trolox equivalent antioxidant capacity assay in 48 type 1 diabetic and 25 nondiabetic subjects. The presence of CAC was assessed in the diabetic subjects using electron beam computed tomography. RESULTS—TAS was reduced in type 1 diabetic subjects compared with nondiabetic subjects (Mann-Whitney U test, P &amp;lt; 0.0001). There were associations between TAS and HbA1c (r = −0.43; P = 0.0026) and duration of diabetes (r = −0.35; P = 0.0157). Significant CAC was considered present if the Agatston score was &amp;gt;10. The diabetic subjects with significant CAC were older (P &amp;lt; 0.0001); had longer duration of diabetes (P = 0.0002); were more likely to have high blood pressure (P = 0.040); had higher total cholesterol concentration (P = 0.039), serum creatinine concentration (P = 0.003), and urinary albumin–to–creatinine ratio (P = 0.022); and had lower serum TAS (P = 0.018) compared with those without significant calcification. In logistic regression with CAC as the dependent variable, TAS was entered as a predictor, and the effects on its predictive value of adding other explanatory variables in bivariate analyses were assessed. The power of TAS to predict CAC was independent of many of the traditional CHD risk factors. Whereas TAS as a predictor was no longer statistically significant when age or duration of diabetes were entered into the model, the odds ratio for a TAS concentration above the median value predicting significant CAC only increased from 0.19 to 0.26 and 0.32, respectively. CONCLUSIONS—TAS is reduced in type 1 diabetes and is associated with the presence of CAC.
Should steroids be first choice for asthma?
Authors: G. STRUBE;, M. RUDOLF
Journal: Thorax (1998)

Langerhans' cell histiocytosis may cause irreversible respiratory failure due to progressive destruction of lung parenchyma and widespread cystic change.Transplantation oVers a therapeutic option.A case is described of recurrence of Langerhans' cell histiocytosis which was associated with deterioration in lung function four years following bilateral lung transplantation.Patients transplanted for Langerhans' cell histiocytosis should be followed up with this complication in mind.
Genetic augmentation of nitric oxide synthase increases the vascular generation of VEGF
Authors: A Jozkowicz
Journal: Cardiovascular Research (2001)

Objective: Vascular endothelial growth factor (VEGF) induces the release of nitric oxide (NO) from endothelial cells. There is also limited data suggesting that NO may enhance VEGF generation. Methods: To further investigate this interaction, we examined the effect of exogenous and endogenous NO on the synthesis of VEGF by rat and human vascular smooth muscle cells (VSMC) by exposing cells to exogenous NO donors, or to genetic augmentation of eNOS or iNOS. Results: NO-donors potentiated by 2-fold the generation of VEGF protein by rat or human VSMC. Similarly, rat or human VSMC transiently transfected with plasmid DNA encoding eNOS or iNOS, synthesized up to 3-fold more VEGF than those transfected with control plasmid DNA, an effect which was reversed after treatment with the NOS antagonist l-NAME. Rat VSMC stably transfected with pKeNOS plasmid, constitutively produced NO and released high concentrations of VEGF. In these cells, l-NAME significantly reduced NO synthesis and decreased VEGF generation. The VEGF protein produced by NOS-transfected VSMC was biologically active, as conditioned media harvested from these cells increased endothelial cell proliferation. Conclusion: These studies reveal that NO derived from NO-donors or generated by NOS within the cells, upregulates the synthesis of VEGF in vascular smooth muscle cells. Administration of NO donors, or augmentation of endogenous NO synthesis, may be an alternative approach in therapeutic angiogenesis.
Angiopoietin-1 Induces Endothelial Cell Sprouting Through the Activation of Focal Adhesion Kinase and Plasmin Secretion
Authors: Injune Kim, Hwan Gyu Kim, Sang-Ok Moon, Soo Wan Chae, June-No So, Keum Nim Koh, Byung Cook Ahn, Gou Young Koh
Journal: Circulation Research (2000)

Abstract —Angiopoietin-1 (Ang1) is a strong inducer of endothelial cell sprouting, which is a first step in both angiogenesis and neovascularization. We examined the mechanisms underlying Ang1-induced cell sprouting using porcine pulmonary artery endothelial cells. Ang1 induced the nondirectional and directional migration of endothelial cells mediated through the Tie2 but not the Tie1 receptor. Ang1 induced tyrosine phosphorylation of p125 FAK , and this phosphorylation was dependent on phosphatidylinositol (PI) 3′-kinase activity. Ang1 induced the secretion of plasmin and matrix metalloproteinase-2 (MMP-2), which is inhibited by PI 3′-kinase inhibitors. Ang1 also induced the secretion of small amounts of proMMP-3 and proMMP-9 but not proMMP-1. Ang1 suppressed the secretion of tissue inhibitor of metalloproteinase-2 (TIMP-2), but not of TIMP-1. Addition of α 2 -antiplasmin, a combination of TIMP-1 and TIMP-2, or PI 3′-kinase inhibitors inhibited Ang1-induced sprouting activity. Therefore, Ang1-induced sprouting activity in endothelial cells may be accomplished by cytoskeletal changes and secretion of proteinases and may be largely mediated through intracellular PI 3′-kinase activation.
American Society of Clinical Oncology Endorsement of the Cancer Care Ontario Practice Guideline on Adjuvant Ovarian Ablation in the Treatment of Premenopausal Women With Early-Stage Invasive Breast Cancer
Authors: Jennifer J. Griggs, Mark R. Somerfield, Holly Anderson, N. Lynn Henry, Clifford A. Hudis, James L. Khatcheressian, Ann H. Partridge, Ann Alexis Prestrud, Nancy E. Davidson
Journal: Journal of Clinical Oncology (2011)

The American Society of Clinical Oncology (ASCO) has policies and procedures for endorsing practice guidelines that have been developed by other professional organizations.The Cancer Care Ontario (CCO) Guideline on Adjuvant Ovarian Ablation (OA) in the Treatment of Premenopausal Women With Early-Stage Invasive Breast Cancer was reviewed for developmental rigor by methodologists. An ad hoc review panel of experts reviewed the content.The ASCO ad hoc OA guideline review panel concurred that the recommendations are clear, thorough, based on the most relevant scientific evidence in this content area, and present options that will be acceptable to patients. According to the CCO guideline: one, OA should not be routinely added to systemic therapy with chemotherapy, tamoxifen, or the combination of tamoxifen and chemotherapy; two, OA alone is not recommended as an alternative to any other form of systemic therapy, except in the specific case of patients who are candidates for other forms of systemic therapy but who, for some reason, will not receive any other systemic therapy (eg, patients who cannot tolerate other forms of systemic therapy or patients who choose no other form of systemic therapy); and three, when chemical suppression using luteinizing hormone-releasing hormone agonists is the chosen method of OA, in the opinion of the Breast Cancer Disease Site Group, monthly injection is the recommended mode of administration. The mode of administration in nearly all of the available trials has been monthly administration.The ASCO review panel agrees with the recommendations as stated in the CCO guideline, with the qualification that ongoing research studies may alter the recommendations of the panel.
Efficacy of pazopanib in progressive, radioiodine-refractory, metastatic differentiated thyroid cancers: results of a phase 2 consortium study
Authors: Keith C Bible, Vera J Suman, Julian R Molina, Robert C Smallridge, William J Maples, Michael E Menefee, Joseph Rubin, Kostandinos Sideras, John C Morris, Bryan McIver, Jill K Burton, Kevin P Webster, Carolyn Bieber, Anne M Traynor, Patrick J Flynn, Boon Cher Goh, Hui Tang, Susan Percy Ivy, Charles Erlichman
Journal: The Lancet Oncology (2010)
Possible Loss of the Chloroplast Genome in the Parasitic Flowering Plant Rafflesia lagascae (Rafflesiaceae)
Authors: Jeanmaire Molina, Khaled M. Hazzouri, Daniel Nickrent, Matthew Geisler, Rachel S. Meyer, Melissa M. Pentony, Jonathan M. Flowers, Pieter Pelser, Julie Barcelona, Samuel Alan Inovejas, Iris Uy, Wei Yuan, Olivia Wilkins, Claire Iphanise Michel, Selina Locklear, Gisela P. Concepcion, Michael D. Purugganan
Journal: Molecular Biology and Evolution (2014)

Rafflesia is a genus of holoparasitic plants endemic to Southeast Asia that has lost the ability to undertake photosynthesis. With short-read sequencing technology, we assembled a draft sequence of the mitochondrial genome of Rafflesia lagascae Blanco, a species endemic to the Philippine island of Luzon, with ∼350× sequencing depth coverage. Using multiple approaches, however, we were only able to identify small fragments of plastid sequences at low coverage depth (<2×) and could not recover any substantial portion of a chloroplast genome. The gene fragments we identified included photosynthesis and energy production genes (atp, ndh, pet, psa, psb, rbcL), ribosomal RNA genes (rrn16, rrn23), ribosomal protein genes (rps7, rps11, rps16), transfer RNA genes, as well as matK, accD, ycf2, and multiple nongenic regions from the inverted repeats. None of the identified plastid gene sequences had intact reading frames. Phylogenetic analysis suggests that ∼33% of these remnant plastid genes may have been horizontally transferred from the host plant genus Tetrastigma with the rest having ambiguous phylogenetic positions (<50% bootstrap support), except for psaB that was strongly allied with the plastid homolog in Nicotiana. Our inability to identify substantial plastid genome sequences from R. lagascae using multiple approaches—despite success in identifying and developing a draft assembly of the much larger mitochondrial genome—suggests that the parasitic plant genus Rafflesia may be the first plant group for which there is no recognizable plastid genome, or if present is found in cryptic form at very low levels.
Hypersensitivity pneumonitis: current concepts
Authors: S.J. Bourke, J.C. Dalphin, G. Boyd, C. McSharry, C.I. Baldwin, J.E. Calvert
Journal: European Respiratory Journal (2001)

Hypersensitivity pneumonitis (HP), or extrinsic allergic alveolitis, is due to a hypersensitivity reaction after repeated inhalation of finely dispersed antigens, mainly organic particles or low molecular weight chemicals. The essence of this disease is an interaction between the host's immune system and external antigen, influenced by both genetic and environmental factors. In susceptible subjects, it leads to a combined type III allergic reaction of Gell and Coombs (with formation of precipitines) and a type IV lymphocytic reaction (with a granulomatous inflammation in the distal bronchioles and alveoli). This review gives an update on epidemiology, antigens, pathogenesis, host susceptibility, environmental factors, clinical features, diagnosis and treatment in HP. The list of aetiological agents is long and new sources of antigens are constantly being identified. Host risk factors are poorly characterized, with the exception of those linked to exposure factors. Environmental factors and cofactors may be critical for the pathogenesis of the disease. HP is not a uniform disease entity, but a complex dynamic clinical syndrome such that different patterns of disease emerge over time. The diagnosis is made from a combination of clinical features, radiographic abnormalities, lung function tests and immunological tests. The use of inhalation challenge tests for the diagnosis has been hampered by the lack of standardization. Antigen avoidance is the key element in the treatment. There is often an apparent beneficial response to corticosteroids, but it may be difficult to distinguish between the effects of treatment, the natural course of the disease and the effect of antigen avoidance.
Correction of Signal Transduction and Activator of Transcription 3 (STAT3) Function in an Adolescent with Autosomal Dominant Hyper-IgE Syndrome (AD-HIES) Following Hematopoietic Stem Cell Transplantation (HSCT)
Authors: Joel L. Gallagher, Andrew Gilman, Troy R. Torgerson, Niraj C. Patel
Journal: Journal of Allergy and Clinical Immunology (2013)
NFBD1/Mdc1 Mediates ATR-Dependent DNA Damage Response
Authors: Aimin Peng, Phang-Lang Chen
Journal: Cancer Research (2005)

Abstract Budding yeast Rad9 (scRad9) plays a central role in mediating Mec1-dependent phosphorylation by recruiting its downstream substrates. The human scRad9 orthologues 53BP1 and NFBD1 associate with ionizing radiation-induced foci (IRIF) at sites of DNA repair. RNAi-based gene silencing of 53BP1 or NFBD1 has shown impaired phosphorylation of SQ/TQ [ataxia-telangiectasia mutated/ATM and Rad3-related (ATM/ATR) substrates] at IRIF, intra-S, and G2-M checkpoints and has thereby revealed essential roles for 53BP1 and NFBD1 in the DNA damage signaling pathway. Whether 53BP1 and NFBD1 are required for activation of kinases and/or for recruitment of substrates at IRIF, however, is not clear. Here we show that both 53BP1 and NFBD1 are required for recruitment of ATR to DNA damage sites, as well as for ATR-dependent phosphorylation in response to DNA damage. NFBD1 is not required for ssDNA generation at DNA damage sites and is not recruited by replication protein A (RPA)–coated ssDNA. We therefore show that recruitment of NFBD1 and/or 53BP1, the factors downstream of H2AX, is independent of ssDNA generation and RPA coating, whereas both ssDNA and RPA coating play key roles in regulation of the ATR-dependent pathway. These novel findings help clarify where NFBD1 functions in DNA damage early responses.
Glucose turnover and gluconeogenesis in human pregnancy.
Authors: S Kalhan, K Rossi, L Gruca, E Burkett, A O'Brien
Journal: Journal of Clinical Investigation (1997)

The rate of appearance (Ra) of glucose in plasma and the contribution of gluconeogenesis were quantified in normal pregnant women early ( approximately 10 wk) and late ( approximately 34 wk) in gestation. Their data were compared with those of normal nonpregnant women. Glucose Ra was measured using the [U-13C]glucose tracer dilution method. Gluconeogenesis was quantified by the appearance of 2H on carbon 5 and 6 of glucose after deuterium labeling of body water pool. Weight-specific glucose Ra was unchanged during pregnancy (nonpregnant, 1.89+/-0.24; first trimester, 2.05+/-0.21; and third trimester 2.17+/-0.28 mg/kg.min, mean+/-SD), while total glucose Ra was significantly increased (early, 133.5+/-7.2; late, 162.6+/-16.4 mg/min; P = 0.005). The fractional contribution of gluconeogenesis via pyruvate measured by 2H enrichment on C-6 of glucose (45-61%), and of total gluconeogenesis quantified from 2H enrichment on C-5 of glucose (i.e. , including glycerol [68-85%]) was not significantly different between pregnant and nonpregnant women. Inasmuch as total glucose Ra was significantly increased, total gluconeogenesis was also increased in pregnancy (early pregnancy, 94.7+/-15.9 mg/min; late pregnancy, 122.7+/-9.3 mg/min; P = 0.003). These data demonstrate the ability of the mother to adapt to the increasing fetal demands for glucose with advancing gestation. The mechanism for this unique quantitative adjustment to the fetal demands remains undefined.
POISONING DUE TO THE PAPAW (ASIMINA TRILOBA).
Authors: M. A. BARBER
Journal: JAMA (1905)

Some seven or eight years ago, in late summer, I found in this vicinity several fruits of the common papaw which had fallen to the ground and ripened prematurely. The fruit was ripe enough to be palatable, and I ate a small portion, perhaps equivalent to one fruit. About six hours later I experienced an urticaria, beginning with itching and burning in the hair at the back of the head and soon extending over a considerable part of the body. Accompanying symptoms were nausea, throbbing at the head and disturbance of the bowels. The urticaria would at times diminish suddenly; then the nausea would increase, to be relieved a few moments later with the reappearance of the "hives." The symptoms lasted several hours, but they had almost wholly disappeared by the next morning and the skin had resumed its normal condition. A friend ate some of the fruit at the
CD28-dependent Activation of Protein Kinase B/Akt Blocks Fas-mediated Apoptosis by Preventing Death-inducing Signaling Complex Assembly
Authors: Russell G. Jones, Alisha R. Elford, Michael J. Parsons, Linda Wu, Connie M. Krawczyk, Wen-Chen Yeh, Razqallah Hakem, Robert Rottapel, James R. Woodgett, Pamela S. Ohashi
Journal: The Journal of Experimental Medicine (2002)

The T cell costimulatory molecule CD28 is important for T cell survival, yet both the signaling pathways downstream of CD28 and the apoptotic pathways they antagonize remain poorly understood. Here we demonstrate that CD4+ T cells from CD28-deficient mice show increased susceptibility to Fas-mediated apoptosis via a phosphatidylinositol 3-kinase (PI3K)-dependent pathway. Protein kinase B (PKBα/Akt1) is an important serine/threonine kinase that promotes survival downstream of PI3K signals. To understand how PI3K-mediated signals downstream of CD28 contribute to T cell survival, we examined Fas-mediated apoptosis in T cells expressing an active form of PKBα. Our data demonstrate that T cells expressing active PKB are resistant to Fas-mediated apoptosis in vivo and in vitro. PKB transgenic T cells show reduced activation of caspase-8, BID, and caspase-3 due to impaired recruitment of procaspase-8 to the death-inducing signaling complex (DISC). Similar alterations are seen in T cells from mice which are haploinsufficient for PTEN, a lipid phosphatase that regulates phosphatidylinositol-3,4,5-trisphosphate (PIP3) and influences PKBα activity. These findings provide a novel link between CD28 and an important apoptosis pathway in vivo, and demonstrate that PI3K/PKB signaling prevents apoptosis by inhibiting DISC assembly.
Is chest CT useful in newborn screened infants with cystic fibrosis at 1 year of age?
Authors: Lena P Thia, Alistair Calder, Janet Stocks, Andrew Bush, Catherine M Owens, Colin Wallis, Carolyn Young, Yvonne Sullivan, Angie Wade, Angus McEwan, Alan S Brody
Journal: Thorax (2013)

<h3>Rationale</h3> Sensitive outcome measures applicable in different centres to quantify and track early pulmonary abnormalities in infants with cystic fibrosis (CF) are needed both for clinical care and interventional trials. Chest CT has been advocated as such a measure yet there is no validated scoring system in infants. <h3>Objectives</h3> The objectives of this study were to standardise CT data collection across multiple sites; ascertain the incidence of bronchial dilatation and air trapping in newborn screened (NBS) infants with CF at 1 year; and assess the reproducibility of Brody-II, the most widely used scoring system in children with CF, during infancy. <h3>Methods</h3> A multicentre observational study of early pulmonary lung disease in NBS infants with CF at age 1 year using volume-controlled chest CT performed under general anaesthetic. <h3>Main results</h3> 65 infants with NBS-diagnosed CF had chest CT in three centres. Small insignificant variations in lung recruitment manoeuvres but significant centre differences in radiation exposures were found. Despite experienced scorers and prior training, with the exception of air trapping, inter- and intraobserver agreement on Brody-II score was poor to fair (eg, interobserver total score mean (95% CI) κ coefficient: 0.34 (0.20 to 0.49)). Only 7 (11%) infants had a total CT score ≥12 (ie, ≥5% maximum possible) by either scorer. <h3>Conclusions</h3> In NBS infants with CF, CT changes were very mild at 1 year, and assessment of air trapping was the only reproducible outcome. CT is thus of questionable value in infants of this age, unless an improved scoring system for use in mild CF disease can be developed.
Use of tolonium chloride in localization of parathyroid tissue
Authors: W. Di Giulio
Journal: JAMA (1970)

Tolonium chloride (toluidine blue 0) is a phenothiazine dye which selectively concentrates in parathyroid tissue, abnormal thyroid tissue, heart, and pancreas. Utilization of tolonium chloride infusions at the time of neck exploration for hyperparathyroidism has shortened and simplified the operative procedure, and has more often allowed identification of the remaining normal parathyroid glands. Tissue distribution ratios and preliminary work with analogues of tolonium chloride labeled with<i>131</i>I suggest that tolonium chloride may be successfully adapted as a vehicle for parathyroid scintiscanning.
Bergey's Manual of Determinative Bacteriology.
Authors: S. T. Cowan
Journal: JAMA (1924)

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