tbuckley/cabot-search huggingface dataset:
Tracheobronchial involvement in Wegener's granulomatosis.
Authors: T E Daum, U Specks, T V Colby, E S Edell, M W Brutinel, U B Prakash, R A DeRemee
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

This study was designed to characterize the clinical spectrum and course of tracheobronchial involvement in Wegener's granulomatosis (WG). Of the 51 patients with biopsy-proven WG who underwent bronchoscopy at least once at our institution between January 1982 and November 1993, 30 (59%) had endobronchial abnormalities due to WG. Initial findings included subglottic stenosis in five (17%), ulcerating tracheobronchitis with or without inflammatory pseudotumors in 18 (60%), tracheal or bronchial stenosis without inflammation in four (13%), and hemorrhage without identifiable source in two (4%) patients. Nine patients with ulcerating tracheobronchitis on initial study had subsequent bronchoscopies for continued symptoms, which in seven cases documented the progression from ulcerating tracheobronchitis to stenosis without inflammation. Bronchoscopic interventions included dilation by rigid bronchoscope in three, YAG-laser treatment in one, and placement of silastic airway stents in three patients. Only the stents provided persistent airway patency. Endobronchial biopsies were performed on 21 occasions in 17 patients. Half of the specimens were helpful in establishing the diagnosis and in all but three in assessing disease activity. While antineutrophil cytoplasmic antibody titers reflect overall disease activity, no correlation with endobronchial inflammatory activity was apparent.
Access to Care for Poor Children
Authors: R F St Peter, P W Newacheck, N Halfon
Journal: JAMA (1992)

<h3>Objective.</h3> —To determine how coverage by Medicaid affects the use of preventive care, as well as the location and continuity of care for poor children. <h3>Design.</h3> —Analysis of the 1988 National Health Interview Survey on Child Health. <h3>Setting.</h3> —Nationally representative sample of the US noninstitutionalized, civilian population. <h3>Participants.</h3> —A total of 17710 children under 18 years of age selected in a stratified cluster sampling of US households. <h3>Intervention.</h3> —None. <h3>Main Outcome Measures.</h3> —The percentage of children with a usual source of routine care; the timeliness of visits for routine care; the usual source where routine care is received; and the continuity between sources of care. <h3>Results.</h3> —Poor children with Medicaid coverage were more likely than those without Medicaid to have a usual source of routine care (91% vs 78%,<i>P</i>&lt;.001) and to receive routine care within an appropriate time interval (84% vs 69%,<i>P</i>&lt;.001). However, poor children with Medicaid were less likely than children living above the poverty line to receive routine care in physicians' offices (56% vs 82%,<i>P</i>&lt;.001) and more likely to lack continuity between usual sources of routine and sick care (18% vs 6%,<i>P</i>&lt;.001). Children receiving routine care at community clinics compared with children receiving care at physicians' offices were more likely to receive sick care at a different location than where they receive routine care (40% vs 4%,<i>P</i>&lt;.001) and also more likely to identify an emergency department as their usual source of sick care (9% vs 2%,<i>P</i>&lt;.001). <h3>Conclusions.</h3> —While Medicaid does improve access to care for poor children, it does not ensure them access to the same locations and continuity of care as that available to other children. Recent changes in the Medicaid program may address some of these inequities, but others are likely to remain. (<i>JAMA</i>. 1992;267:2760-2764)
Analysis of fumonisin B1-induced apoptosis.
Authors: C Jones, J R Ciacci-Zanella, Y Zhang, G Henderson, M Dickman
Journal: Environmental Health Perspectives (2001)

Fumonisins are mycotoxins produced by Fusarium moniliforme, a prevalent fungus that infects corn and other cereal grains. Fumonisin B1(FB1 is the most common mycotoxin produced by F. moniliforme, suggesting it has toxicologic significance. The structure of FB1 resembles sphingoid bases, and it inhibits ceramide synthase. Because sphingoid bases regulate cell growth, differentiation, transformation, and apoptosis, it is not surprising to find that FB1 can alter growth of certain mammalian cells. Previous studies concluded FB1-induced apoptosis, or cell cycle arrest, in African green monkey kidney fibroblasts (CV-1). In this study we have identified genes that inhibit FB1 induced apoptosis in CV-1 cells and two mouse embryo fibroblasts (MEF). A baculovirus gene, inhibitor of apoptosis (CpIAP), protected these cells from apoptosis. CpIAP blocks apoptosis induced by the tumor necrosis factor (TNF) pathway as well as other mechanisms. Further support for the involvement of the TNF signal transduction pathway in FB1 induced apoptosis was the cleavage of caspase 8. Inhibition of caspases by the baculovirus gene (italic)p35 also inhibited FB1-induced apoptosis. The tumor suppressor gene p53 was not required for FB1 induced apoptosis because p53-/- MEF undergo apoptosis following FB1 treatment. Furthermore, Bcl-2 was not an effective inhibitor of FB1-induced apoptosis in CV-1 cells or p53+/+ MEF. In summary, these results provide new information to help understand the mechanism by which FB1 induces apoptosis.
Compound heterozygosity for ARS component B mutations in a Dutch patient with mal de Meleda
Authors: R.G.L. Nellen, M. van Geel, P.M. Steijlen, M.A.M. van Steensel
Journal: British Journal of Dermatology (2008)

Journal Article Compound heterozygosity for ARS component B mutations in a Dutch patient with mal de Meleda Get access R.G.L. Nellen, R.G.L. Nellen Department of Dermatology, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, the Netherlands and GROW Research School, University of Maastricht, Maastricht, the Netherlands E‐mail: rnel@sder.azm.nl Search for other works by this author on: Oxford Academic Google Scholar M. Van Geel, M. Van Geel Department of Dermatology, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, the Netherlands and GROW Research School, University of Maastricht, Maastricht, the Netherlands E‐mail: rnel@sder.azm.nl Search for other works by this author on: Oxford Academic Google Scholar P.M. Steijlen, P.M. Steijlen Department of Dermatology, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, the Netherlands and GROW Research School, University of Maastricht, Maastricht, the Netherlands E‐mail: rnel@sder.azm.nl Search for other works by this author on: Oxford Academic Google Scholar M.A.M. Van Steensel M.A.M. Van Steensel Department of Dermatology, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, the Netherlands and GROW Research School, University of Maastricht, Maastricht, the Netherlands E‐mail: rnel@sder.azm.nl Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 160, Issue 4, 1 April 2009, Pages 878–880, https://doi.org/10.1111/j.1365-2133.2008.08980.x Published: 01 April 2009
Uric acid and anti-TNF antibody improve mitochondrial dysfunction in ob/ob mice
Authors: Inmaculada García-Ruiz, Cristina Rodríguez-Juan, Teresa Díaz-Sanjuan, Pilar del Hoyo, Francisco Colina, Teresa Muñoz-Yagüe, José A. Solís-Herruzo
Journal: Hepatology (2006)

The mechanisms responsible for low mitochondrial respiratory chain (MRC) activity in the liver of patients with nonalcoholic steatohepatitis are unknown. In this study, we examined the cause of this dysfunction in ob/ob mice. Forty-six mice were distributed in six groups: group I: C57BL/6J mice; group II: C57BL/6J Lep(−/−) mice (ob/ob); group III, ob/ob mice treated with manganese [III] tetrakis (5,10,15,20 benzoic acid) porphyrin (MnTBAP); group IV, ob/ob mice treated with IgG1 immunoglobulin; group V, ob/ob mice treated with anti-TNF antibody; group VI: ob/ob mice treated with uric acid. In liver tissue, we measured MRC activity, fatty acid β-oxidation, tumor necrosis factor (TNF), inducible nitric oxide synthase (iNOS), 3-tyrosine-nitrated proteins, 3-tyrosine-nitrated mitochondrial proteins, including cytochrome c and ND4 subunit of complex I. MRC activity was decreased in ob/ob mice. TNF levels, iNOS protein expression, and tyrosine nitrated proteins were markedly increased in the liver of ob/ob mice. In these animals, mitochondrial proteins were markedly tyrosine nitrated, particularly the ND4 subunit of complex I and cytochrome c . Treatment of these animals with uric acid, a peroxynitrite scavenger, anti-TNF antibody, or MnTBAP decreased tyrosine nitrated proteins, improved the activity of MRC complexes, and led to a marked regression of hepatic steatosis and inflammation. In conclusion , MRC dysfunction and liver lesions found in ob/ob mice are likely to reflect the tyrosine nitration of mitochondrial proteins by peroxynitrite or a peroxynitrite-derivate radical. Increased hepatic TNF and iNOS expression might enhance peroxynitrite formation and inhibition of MRC complexes. Supplementary material for this article can be found on the HEPATOLOGY website (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html).
Initial chemotherapy with mitoxantrone, chlorambucil, prednisone impairs the collection of stem cells in patients with indolent lymphomas—results of a randomized comparison by the German Low-Grade Lymphoma Study Group
Authors: C. Nickenig, M. Dreyling, E. Hoster, W.-D. Ludwig, B. Dörken, M. Freund, C. Huber, A. Ganser, L. Trümper, R. Forstpointner, M. Unterhalt, W. Hiddemann
Journal: Annals of Oncology (2006)
Liquid diets for Crohn's disease
Authors: M O'Sullivan, C O'Morain
Journal: Gut (2001)

Enteral diets: primary therapeutic role In the early 1970s, disease modifying eVects of an elemental diet in Crohn's disease (CD) were observed.The first controlled study in 1984 confirmed that an elemental diet was as eVective as steroids in inducing remission in acute CD. 1 Several subsequent studies supported this primary therapeutic eVect for both elemental and polymeric enteral diets (see review 2 ).Pooling the data however has shown a less favourable outcome with three meta-analyses similarly concluding that corticosteroids were more eVective than enteral diet therapy.A heterogeneous study mix may not be representative of the clinical situation.Data, from a single centre spanning 10 years of enteral diet therapy supported remission rates equal to that of drug therapy. 3In addition to therapeutic eVect, liquid diets for acute CD oVer an unrivalled safety profile and significant nutritional benefits.We consider these diets as ideal therapy in paediatric CD, especially in the presence of malnutrition or growth impairment, and in patients with severe drug induced side eVects.Patients with CD typically relapse in the longer term, irrespective of the therapeutic approach, and therefore maintenance and retreatment strategies for diet induced remission should be more fully investigated.
Arterial lysosomes and connective tissue in primate atherosclerosis and hypertension.
Authors: H Wolinsky, S Goldfischer, M M Daly, L E Kasak, B Coltoff-Schiller
Journal: Circulation Research (1975)

The cellular events that occur in the vessel wall consequent to changes in endothelial permeability result in the progression of vascular disease, particularly atherosclerosis. Female rhesus monkeys were fed an atherogenic diet or were made hypertensive for 6-8 months; and their vessels were then compared with vessels from control monkeys. Length-defined segments of coronary vessels, the thoracic aorta, and the abdominal aorta showed significant increases in total connective tissue in the atherosclerotic and hypertensive groups; pulmonary vessels did not. The diseased aortic segments had increased levels of two lysosomal enzymes, acid phosphatase and beta-N-acetylglucosaminidase; pulmonary vessels were not diseased and did not show these changes. Coronary vessels from the atherosclerotic and hypertensive groups did not show an increase in enzyme levels on biochemical measurements, but focal accumulations of lysosomes were identified by cytochemical techniques. In atherosclerotic lesions, a doubling of cholesterol and more than a tenfold increase in cholesterol ester were found. These connective tissue and lysosomal changes are early features of primate vascular disease and may result from the accumulation of excessive substrate (cholesterol ester) in the lysosomes of vascular smooth muscle cells.
Dual Targeting of the Type 1 Insulin-like Growth Factor Receptor and Its Ligands as an Effective Antiangiogenic Strategy
Authors: Hemant K. Bid, Cheryl A. London, Jin Gao, Haihong Zhong, Robert E. Hollingsworth, Soledad Fernandez, Xiaokui Mo, Peter J. Houghton
Journal: Clinical Cancer Research (2013)

Abstract Background: In pediatric tumor xenograft models, tumor-derived insulin growth factor (IGF-2) results in intrinsic resistance to IGF-IR–targeted antibodies, maintaining continued tumor angiogenesis. We evaluated the antiangiogenic activity of a ligand-binding antibody (MEDI-573) alone or in combination with IGF-I receptor binding antibodies (MAB391, CP01-B02). Methods: IGF-stimulated signaling was monitored by increased Akt phosphorylation in sarcoma and human umbilical cord vascular endothelial cells (HUVEC). Angiogenesis was determined in vitro using capillary tube formation in HUVECs and in vivo using a VEGF-stimulated Matrigel assay. Tumor growth delay was examined in 4 sarcoma xenograft models. Results: The IGF ligand-binding antibody MEDI-573 suppressed Akt phosphorylation induced by exogenous IGF-I and IGF-2 in sarcoma cells. Receptor-binding antibodies suppressed IGF-I stimulation of Akt phosphorylation, but IGF-2 circumvented this effect and maintained HUVEC tube formation. MEDI-573 inhibited HUVEC proliferation and tube formation in vitro, but did not inhibit angiogenesis in vivo, probably because MEDI-573 binds murine IGF-I with low affinity. However, in vitro antiangiogenic activity of MEDI-573 was also circumvented by human recombinant IGF-I. The combination of receptor- and ligand-binding antibodies completely suppressed VEGF-stimulated proliferation of HUVECs in the presence of IGF-I and IGF-2, prevented ligand-induced phosphorylation of IGF-IR/IR receptors, and suppressed VEGF/IGF-2–driven angiogenesis in vivo. The combination of CP1-BO2 plus MEDI-573 was significantly superior to therapy with either antibody alone against IGF-I and IGF-2 secreting pediatric sarcoma xenograft models. Conclusions: These results suggest that combination of antibodies targeting IGF receptor and ligands may be an effective therapeutic strategy to block angiogenesis for IGF-driven tumors. Clin Cancer Res; 19(11); 2984–94. ©2013 AACR.
Responsible and Irresponsible Use of Very-Low-Calorie Diets in the Treatment of Obesity
Authors: T A Wadden, T B Van Itallie, G L Blackburn
Journal: JAMA (1990)

AMERICA'S most celebrated weight loss was announced on November 15,1988, when Oprah Winfrey disclosed to her 18 million television viewers that she had lost 30.5 kg (67 lb) in 4 months by consuming a medically supervised very-low-calorie diet (<i>New York Times</i>. November 24,1988:B17). Ms Winfrey's announcement sparked a frenzy of interest among the nation's dieters, reminiscent of that which greeted the appearance of the liquid protein diets in 1976 and 1977<sup>1</sup>and the Cambridge Diet in the early 1980s.<sup>2</sup>Sadly, consumption of these diets was inadequately supervised; at least 58 deaths were reported among users of liquid protein products<sup>1,3</sup>and 6 deaths in persons who consumed the Cambridge Diet.<sup>2</sup> Current very-low-calorie diets that provide essential nutrients and high-quality proteins are unquestionably safer than their liquid protein predecessors, as noted in a timely report prepared by the American Medical Association's Council on Scientific Affairs.<sup>4</sup>But the
CONCERNING THE EFFECTS OF MAGNESIUM SULFATE ON RENAL FUNCTION, ELECTROLYTE EXCRETION, AND CLEARANCE OF MAGNESIUM 1
Authors: B. I. Heller, J. F. Hammarsten, F. L. Stutzman
Journal: Journal of Clinical Investigation (1953)

indicated that concentrations of magnesium exceeding those found in the urine in these experiments had no effect on the flame photometric determination of sodium or potassium. Chloride was determined by the method of Schales and Schales (6). Serum magnesium was determined by the molybdivanadate method of Simonsen, Westover, and Wertnan (7). Urinary magnesium was determined by a similar method as modified by Stutzman
Some costs of over-assimilating data to the implicit/explicit distinction
Authors: Mark A. Sabbagh, Benjamin A. Clegg
Journal: Behavioral and Brain Sciences (1999)

We applaud Dienes &amp; Perner's efforts while raising some concerns regarding their assimilation of diverse data into a unifying framework. Some of the findings need not fit the framework they suggest. It is also not always clear what, above logico-semantic consistency, assimilation adds to the data that do fit their framework. These concerns are highlighted with reference to their arguments regarding the developmental data and the neuropsychological data, respectively.
Sex steroids and bone mass. A study of changes about the time of menopause.
Authors: C Slemenda, S L Hui, C Longcope, C C Johnston
Journal: Journal of Clinical Investigation (1987)

To examine the relationships between bone loss and sex steroids, 84 peri- and postmenopausal women were studied at 4-mo intervals for 3 yr. At each visit, measurements were made of bone mass at the midshaft and distal radius, of steroids, of gonadotropins, and of bone gla protein (BGP). Bone loss was approximately 1% per yr among late perimenopausal and postmenopausal groups, whereas the early perimenopausal group lost no bone. Mean serum estrogen and BGP concentrations predicted rates of bone loss. BGP was negatively correlated with the rate of bone loss (r = -0.45) and with mean estrogen concentrations (r = -0.40). Multivariate regressions showed estrogen concentrations to be strong independent predictors of the slope of bone mass over time. When BGP concentrations were added to the models, the significance of estrogen was reduced, suggesting that a portion of the estrogen effect was mediated through effects on rates of bone remodelling.
Predicting Cardiac Arrhythmias and Sudden Death in Diabetic Users of Proarrhythmic Drugs
Authors: Marie L. De Bruin, Tjeerd P. van Staa, Svetlana V. Belitser, Hubert G.M. Leufkens, Arno W. Hoes
Journal: Diabetes Care (2005)

In diabetic patients, the corrected QT (QTc) interval is relatively long (1). In accordance with the concept of “reduced repolarization reserve” (2), a subsequent increase in QTc interval by proarrhythmic drugs may lead to cardiac arrhythmias and sudden death. Recently, it was shown that patients with diabetes are at increased risk of drug-induced arrhythmias (3). We developed a decision tool to predict the risk of serious ventricular arrhythmias and sudden death among diabetic users of nonantiarrhythmic proarrhythmic drugs.

A cohort study among 61,280 diabetic patients using nonantiarrhythmic proarrhythmic medication (amitriptyline, astemizole, chloroquine, chlorpromazine, cisapride, clarithromycin, clomipramine, cotrimoxazole, diphenhydramine/dimenhydrinate, domperidone, doxepine, droperidol, erythromycin, grepafloxacin, halofantrine, haloperidol, indapamide, ketanserin, lidoflazine, mianserine, pentamidine, pimozide, probucol, promethazine, protriptyline, sulfamethoxazole, sultopride, tacrolimus, terfenadine, terodiline, thioridazine, trimethoprim, and zimeldine) (4) in the General Practice Research Database (1987–2001) was performed. This database contains computerized medical records of ∼650 general practices, including ∼6.5% of the population of England and Wales. Diabetic patients were followed from the 1st day of prescription of any nonantiarrhythmic proarrhythmic drug. Follow-up was censored when the duration of (one of) the prescription(s) had elapsed, when the study outcome occurred, in case of death, upon exit from the study population, or at the end of the study period, whichever of these events came first. The combined study outcome included ventricular tachycardia, ventricular fibrillation and flutter, cardiac arrest, and sudden death. …
The Farnesoid X Receptor Is Expressed in Breast Cancer and Regulates Apoptosis and Aromatase Expression
Authors: Karen E. Swales, Márta Korbonits, Robert Carpenter, Desmond T. Walsh, Timothy D. Warner, David Bishop-Bailey
Journal: Cancer Research (2006)

Abstract Bile acids are present at high concentrations in breast cysts and in the plasma of postmenopausal women with breast cancer. The farnesoid X receptor (FXR) is a member of the nuclear receptor superfamily that regulates bile acid homeostasis. FXR was detected in normal and tumor breast tissue, with a high level of expression in ductal epithelial cells of normal breast and infiltrating ductal carcinoma cells. FXR was also present in the human breast carcinoma cells, MCF-7 and MDA-MB-468. Activation of FXR by high concentrations of ligands induced MCF-7 and MDA-MB-468 apoptosis. At lower concentrations that had no direct effect on viability, the FXR agonist GW4064 induced expression of mRNA for the FXR target genes, small heterodimer partner (SHP), intestinal bile acid binding protein, and multidrug resistance–associated protein 2 (MRP-2), and repressed the expression of the SHP target gene aromatase. In contrast to MRP-2, mRNA for the breast cancer target genes MDR-3, MRP-1, and solute carrier transporter 7A5 were decreased. Although multidrug resistance transporters were regulated and are known FXR target genes, GW4064 had no effect on the cell death induced by the anticancer drug paclitaxel. Our findings show for the first time that FXR is expressed in breast cancer tissue and has multiple properties that could be used for the treatment of breast cancer. (Cancer Res 2006; 66(20): 10120-6)
Agreement of Mexican rheumatologists with the ASsessment in Ankylosing Spondylitis International Working Group and the EUropean League Against Rheumatism recommendations for the management of ankylosing spondylitis
Authors: J A Simon, R Burgos-Vargas
Journal: Annals of the Rheumatic Diseases (2006)

blockers is likely, given the temporal relationship between the onset of signs with treatment, resolution after withdrawal of the drug and flare after reintroduction.These results suggest that TNF blockers could trigger systemic necrotising vasculitis.