And Function by Progesterone TLR4-Mediated Dendritic Cell
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
The National Drugs List
^ ^ ^ ^ ^[ ^ The National Drugs List Of Syrian Arab Republic Sexth Edition 2006 ! " # "$ % &'() " # * +$, -. / & 0 /+12 3 4" 5 "$ . "$ 67"5,) 0 " /! !2 4? @ % 88 9 3: " # "$ ;+<=2 – G# H H2 I) – 6( – 65 : A B C "5 : , D )* . J!* HK"3 H"$ T ) 4 B K<) +$ LMA N O 3 4P<B &Q / RS ) H< C4VH /430 / 1988 V W* < C A GQ ") 4V / 1000 / C4VH /820 / 2001 V XX K<# C ,V /500 / 1992 V "!X V /946 / 2004 V Z < C V /914 / 2003 V ) < ] +$, [2 / ,) @# @ S%Q2 J"= [ &<\ @ +$ LMA 1 O \ . S X '( ^ & M_ `AB @ &' 3 4" + @ V= 4 )\ " : N " # "$ 6 ) G" 3Q + a C G /<"B d3: C K7 e , fM 4 Q b"$ " < $\ c"7: 5) G . HHH3Q J # Hg ' V"h 6< G* H5 !" # $%" & $' ,* ( )* + 2 ا اوا ادو +% 5 j 2 i1 6 B J' 6<X " 6"[ i2 "$ "< * i3 10 6 i4 11 6! ^ i5 13 6<X "!# * i6 15 7 G!, 6 - k 24"$d dl ?K V *4V h 63[46 ' i8 19 Adl 20 "( 2 i9 20 G Q) 6 i10 20 a 6 m[, 6 i11 21 ?K V $n i12 21 "% * i13 23 b+ 6 i14 23 oe C * i15 24 !, 2 6\ i16 25 C V pq * i17 26 ( S 6) 1, ++ &"r i19 3 +% 27 G 6 ""% i19 28 ^ Ks 2 i20 31 % Ks 2 i21 32 s * i22 35 " " * i23 37 "$ * i24 38 6" i25 39 V t h Gu* v!* 2 i26 39 ( 2 i27 40 B w< Ks 2 i28 40 d C &"r i29 42 "' 6 i30 42 " * i31 42 ":< * i32 5 ./ 0" -33 4 : ANAESTHETICS $ 1 2 -1 :GENERAL ANAESTHETICS AND OXYGEN 4 $1 2 2- ATRACURIUM BESYLATE DROPERIDOL ETHER FENTANYL HALOTHANE ISOFLURANE KETAMINE HCL NITROUS OXIDE OXYGEN PROPOFOL REMIFENTANIL SEVOFLURANE SUFENTANIL THIOPENTAL :LOCAL ANAESTHETICS !67$1 2 -5 AMYLEINE HCL=AMYLOCAINE ARTICAINE BENZOCAINE BUPIVACAINE CINCHOCAINE LIDOCAINE MEPIVACAINE OXETHAZAINE PRAMOXINE PRILOCAINE PREOPERATIVE MEDICATION & SEDATION FOR 9*: ;< " 2 -8 : : SHORT -TERM PROCEDURES ATROPINE DIAZEPAM INJ. -
Prednisolone Versus Dexamethasone for Croup: a Randomized Controlled Trial Colin M
Prednisolone Versus Dexamethasone for Croup: a Randomized Controlled Trial Colin M. Parker, MBChB, DCH, MRCPCH, FACEM,a,b Matthew N. Cooper, BCA, BSc, PhDc OBJECTIVES: The use of either prednisolone or low-dose dexamethasone in the treatment of abstract childhood croup lacks a rigorous evidence base despite widespread use. In this study, we compare dexamethasone at 0.6 mg/kg with both low-dose dexamethasone at 0.15 mg/kg and prednisolone at 1 mg/kg. METHODS: Prospective, double-blind, noninferiority randomized controlled trial based in 1 tertiary pediatric emergency department and 1 urban district emergency department in Perth, Western Australia. Inclusions were age .6 months, maximum weight 20 kg, contactable by telephone, and English-speaking caregivers. Exclusion criteria were known prednisolone or dexamethasone allergy, immunosuppressive disease or treatment, steroid therapy or enrollment in the study within the previous 14 days, and a high clinical suspicion of an alternative diagnosis. A total of 1252 participants were enrolled and randomly assigned to receive dexamethasone (0.6 mg/kg; n = 410), low-dose dexamethasone (0.15 mg/kg; n = 410), or prednisolone (1 mg/kg; n = 411). Primary outcome measures included Westley Croup Score 1-hour after treatment and unscheduled medical re-attendance during the 7 days after treatment. RESULTS: Mean Westley Croup Score at baseline was 1.4 for dexamethasone, 1.5 for low-dose dexamethasone, and 1.5 for prednisolone. Adjusted difference in scores at 1 hour, compared with dexamethasone, was 0.03 (95% confidence interval 20.09 to 0.15) for low-dose dexamethasone and 0.05 (95% confidence interval 20.07 to 0.17) for prednisolone. -
Mifepristone
1. NAME OF THE MEDICINAL PRODUCT Mifegyne 200 mg tablets 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Each tablet contains 200-mg mifepristone. For the full list of excipients, see section 6.1 3. PHARMACEUTICAL FORM Tablet. Light yellow, cylindrical, bi-convex tablets, with a diameter of 11 mm with “167 B” engraved on one side. 4. CLINICAL PARTICULARS For termination of pregnancy, the anti-progesterone mifepristone and the prostaglandin analogue can only be prescribed and administered in accordance with New Zealand’s abortion laws and regulations. 4.1 Therapeutic indications 1- Medical termination of developing intra-uterine pregnancy. In sequential use with a prostaglandin analogue, up to 63 days of amenorrhea (see section 4.2). 2- Softening and dilatation of the cervix uteri prior to surgical termination of pregnancy during the first trimester. 3- Preparation for the action of prostaglandin analogues in the termination of pregnancy for medical reasons (beyond the first trimester). 4- Labour induction in fetal death in utero. In patients where prostaglandin or oxytocin cannot be used. 4.2 Dose and Method of Administration Dose 1- Medical termination of developing intra-uterine pregnancy The method of administration will be as follows: • Up to 49 days of amenorrhea: 1 Mifepristone is taken as a single 600 mg (i.e. 3 tablets of 200 mg each) oral dose, followed 36 to 48 hours later, by the administration of the prostaglandin analogue: misoprostol 400 µg orally or per vaginum. • Between 50-63 days of amenorrhea Mifepristone is taken as a single 600 mg (i.e. 3 tablets of 200 mg each) oral dose, followed 36 to 48 hours later, by the administration of misoprostol. -
Opposing Effects of Dehydroepiandrosterone And
European Journal of Endocrinology (2000) 143 687±695 ISSN 0804-4643 EXPERIMENTAL STUDY Opposing effects of dehydroepiandrosterone and dexamethasone on the generation of monocyte-derived dendritic cells M O Canning, K Grotenhuis, H J de Wit and H A Drexhage Department of Immunology, Erasmus University Rotterdam, The Netherlands (Correspondence should be addressed to H A Drexhage, Lab Ee 838, Department of Immunology, Erasmus University, PO Box 1738, 3000 DR Rotterdam, The Netherlands; Email: [email protected]) Abstract Background: Dehydroepiandrosterone (DHEA) has been suggested as an immunostimulating steroid hormone, of which the effects on the development of dendritic cells (DC) are unknown. The effects of DHEA often oppose those of the other adrenal glucocorticoid, cortisol. Glucocorticoids (GC) are known to suppress the immune response at different levels and have recently been shown to modulate the development of DC, thereby influencing the initiation of the immune response. Variations in the duration of exposure to, and doses of, GC (particularly dexamethasone (DEX)) however, have resulted in conflicting effects on DC development. Aim: In this study, we describe the effects of a continuous high level of exposure to the adrenal steroid DHEA (1026 M) on the generation of immature DC from monocytes, as well as the effects of the opposing steroid DEX on this development. Results: The continuous presence of DHEA (1026 M) in GM-CSF/IL-4-induced monocyte-derived DC cultures resulted in immature DC with a morphology and functional capabilities similar to those of typical immature DC (T cell stimulation, IL-12/IL-10 production), but with a slightly altered phenotype of increased CD80 and decreased CD43 expression (markers of maturity). -
Canine Vascular Tissues Are Targets for Androgens, Estrogens, Progestins, and Glucocorticoids
Canine vascular tissues are targets for androgens, estrogens, progestins, and glucocorticoids. K B Horwitz, L D Horwitz J Clin Invest. 1982;69(4):750-758. https://doi.org/10.1172/JCI110513. Research Article Sex differences and steroid hormones are known to influence the vascular system as shown by the different incidence of atherosclerosis in men and premenopausal women, or by the increased risk of cardiovascular diseases in women taking birth control pills or men taking estrogens. However, the mechanisms for these effects in vascular tissues are not known. Since steroid actions in target tissues are mediated by receptors, we have looked for cytoplasmic steroid receptor proteins in vascular tissues of dogs. We find specific saturable receptors, sedimenting at 8S on sucrose density gradients for estrogens (measured with [3H]estradiol +/- unlabeled diethylstilbestrol), androgens (measured with [3H]R1881 +/- unlabeled R1881 and triamcinolone acetonide), and glucocorticoids (measured with [3H]dexamethasone +/- unlabeled dexamethasone); they are absent for progesterone (measured with [3H]R5020 +/- unlabeled R5020 and dihydrotestosterone). Progesterone receptors can, however, be induced by 1-wk treatment of dogs with physiological estradiol concentrations (100 pg/ml serum estrogen), indicating a functional estrogen receptor. Receptor levels range from 20 to 2,000 fmol/mg DNA. They are specific for each hormone; unrelated steroids fail to complete for binding. Low dissociation constants, measured by Scatchard analyses, show that binding is of high affinity. Steroid binding sites are in the media and/or adventitia since they persist when the intima is removed. Compared with the arteries, receptor levels are reduced 80% in inferior venae cavae of […] Find the latest version: https://jci.me/110513/pdf Canine Vascular Tissues Are Targets for Androgens, Estrogens, Progestins, and Glucocorticoids KATHRYN B. -
Dexamethasone Inhibits the Induction of NAD+-Dependent 15
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Biochimica et Biophysica Acta 1497 (2000) 61^68 www.elsevier.com/locate/bba Dexamethasone inhibits the induction of NAD-dependent 15-hydroxyprostaglandin dehydrogenase by phorbol ester in human promonocytic U937 cells Min Tong 1, Hsin-Hsiung Tai * Division of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY 40536-0082, USA Received 29 December 1999; received in revised form 2 March 2000; accepted 9 March 2000 Abstract Pro-inflammatory prostaglandins are known to be first catabolized by NAD-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) to inactive metabolites. This enzyme is under regulatory control by various inflammation-related agents. Regulation of this enzyme was investigated in human promonocytic U937 cells. 15-PGDH activity was found to be optimally induced by phorbol 12-myristate 13-acetate (PMA) at 10 nM after 24 h of treatment. The induction was blocked by staurosporine or GF 109203X indicating that the induction was mediated by protein kinase C. The induction by PMA was inhibited by the concurrent addition of dexamethasone. Nearly complete inhibition was observed at 50 nM. Other glucocorticoids, such as hydrocortisone and corticosterone, but not sex hormones, were also inhibitory. Inhibition by dexamethasone could be reversed by the concurrent addition of antagonist mifepristone (RU-486) indicating that the inhibition was a receptor-mediated event. Either induction by PMA or inhibition by dexamethasone the 15-PGDH activity correlated well with the enzyme protein expression as shown by the Western blot analysis. These results provide the first evidence that prostaglandin catabolism is regulated by glucocorticoids at the therapeutic level. -
Dexamethasone in Patients with Acute Lung Injury from Acute Monocytic Leukaemia
Eur Respir J 2012; 39: 648–653 DOI: 10.1183/09031936.00057711 CopyrightßERS 2012 Dexamethasone in patients with acute lung injury from acute monocytic leukaemia E´. Azoulay*, E. Canet*, E. Raffoux#, E. Lengline´#, V. Lemiale*, F. Vincent*, A. de Labarthe#, A. Seguin*, N. Boissel#, H. Dombret# and B. Schlemmer* ABSTRACT: The use of steroids is not required in myeloid malignancies and remains AFFILIATIONS controversial in patients with acute lung injury (ALI) or acute respiratory distress syndrome *Medical ICU and #Hematology Dept, Saint-Louis (ARDS). We sought to evaluate dexamethasone in patients with ALI/ARDS caused by acute Hospital, Paris, France. monocytic leukaemia (AML FAB-M5) via either leukostasis or leukaemic infiltration. Dexamethasone (10 mg every 6 h until neutropenia) was added to chemotherapy and intensive CORRESPONDENCE ´ care unit (ICU) management in 20 consecutive patients between 2005 and 2008, whose data were E. Azoulay AP-HP compared with those from 20 historical controls (1994–2002). ICU mortality was the primary Hoˆpital Saint-Louis criterion. We also compared respiratory deterioration rates, need for ventilation and nosocomial Medical ICU infections. 75010 Paris 17 (85%) patients had hyperleukocytosis, 19 (95%) had leukaemic masses, and all 20 had France E-mail: [email protected] severe pancytopenia. All patients presented with respiratory symptoms and pulmonary infiltrates paris.fr prior to AML FAB-M5 diagnosis. Compared with historical controls, dexamethasone-treated patients had a significantly lower ICU mortality rate (20% versus 50%; p50.04) and a trend for less Received: respiratory deterioration (50% versus 80%; p50.07). There were no significant increases in the May 24 2011 Accepted after revision: rates of infections with dexamethasone. -
Corticosteroids in Terminal Cancer-A Prospective Analysis of Current Practice
Postgraduate Medical Journal (November 1983) 59, 702-706 Postgrad Med J: first published as 10.1136/pgmj.59.697.702 on 1 November 1983. Downloaded from Corticosteroids in terminal cancer-a prospective analysis of current practice G. W. HANKS* T. TRUEMAN B.Sc., M.B., B.S., M.R.C.P.(U.K.) S.R.N. R. G. TWYCROSS M.A., D.M., F.R.C.P. Sir Michael Sobell House, The Churchill Hospital, Headington, Oxford OX3 7LJ Summary Introduction Over half of a group of 373 inpatients with advanced Corticosteroids have a major role to play in the malignant disease were treated with corticosteroids control of symptoms in patients with advanced for a variety of reasons. They received either pred- malignant disease. They may be employed in a non- nisolone or dexamethasone, or replacement therapy specific way to improve mood and appetite; or they with cortisone acetate. Forty percent of those receiv- may be indicated as specific adjunctive therapy in the ing corticosteroids benefited from them. A higher relief of symptoms related to a large tumour mass or response rate was seen when corticosteroids were to nerve compression. The management of a numberProtected by copyright. prescribed for nerve compression pain, for raised of other symptoms and syndromes may also be intracranial pressure, and when used in conjunction facilitated by treatment with corticosteroids (Table with chemotherapy. No significant difference in 1). efficacy was noted between the 2 drugs. The results, The use of corticosteroids in patients with ad- however, suggest that with a larger sample, dexame- vanced cancer is empirical, as it is in other non- thasone would have been shown to be significantly endocrine indications. -
Dexamethasone and Fludrocortisone Inhibit Hedgehog Signaling In
This is an open access article published under an ACS AuthorChoice License, which permits copying and redistribution of the article or any adaptations for non-commercial purposes. Article Cite This: ACS Omega 2018, 3, 12019−12025 http://pubs.acs.org/journal/acsodf Dexamethasone and Fludrocortisone Inhibit Hedgehog Signaling in Embryonic Cells † ‡ † ‡ Kirti Kandhwal Chahal,*, , Milind Parle, and Ruben Abagyan*, † Department of Pharmaceutical Sciences, G. J. University of Science and Technology, Hisar 125001, India ‡ Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92037, United States ABSTRACT: The hedgehog (Hh) pathway plays a central role in the development and repair of our bodies. Therefore, dysregulation of the Hh pathway is responsible for many developmental diseases and cancers. Basal cell carcinoma and medulloblastoma have well- established links to the Hh pathway, as well as many other cancers with Hh-dysregulated subtypes. A smoothened (SMO) receptor plays a central role in regulating the Hh signaling in the cells. However, the complexities of the receptor structural mechanism of action and other pathway members make it difficult to find Hh pathway inhibitors efficient in a wide range. Recent crystal structure of SMO with cholesterol indicates that it may be a natural ligand for SMO activation. Structural similarity of fluorinated corticosterone derivatives to cholesterol motivated us to study the effect of dexamethasone, fludrocortisone, and corticosterone on the Hh pathway activity. We identified an inhibitory effect of these three drugs on the Hh pathway using a functional assay in NIH3T3 glioma response element cells. Studies using BODIPY-cyclopamine and 20(S)-hydroxy cholesterol [20(S)-OHC] as competitors for the transmembrane (TM) and extracellular cysteine-rich domain (CRD) binding sites showed a non-competitive effect and suggested an alternative or allosteric binding site for the three drugs. -
Ketoconazole Revisited: a Preoperative Or Postoperative Treatment in Cushing's Disease
European Journal of Endocrinology (2008) 158 91–99 ISSN 0804-4643 CLINICAL STUDY Ketoconazole revisited: a preoperative or postoperative treatment in Cushing’s disease F Castinetti, I Morange, P Jaquet, B Conte-Devolx and T Brue Department of Endocrinology, Diabetes, Metabolic Diseases and Nutrition, Hoˆpital de la Timone, Centre Hospitalier Universitaire de Marseille and Faculte´ de Me´decine, Universite´ de la Me´diterrane´e, 264 rue St Pierre, Cedex 5, 13385 Marseille, France (Correspondence should be addressed to T Brue; Email: [email protected]) Abstract Context: Although transsphenoidal surgery remains the first-line treatment in Cushing’s disease (CD), recurrence is observed in about 20% of cases. Adjunctive treatments each have specific drawbacks. Despite its inhibitory effects on steroidogenesis, the antifungal drug ketoconazole was only evaluated in series with few patients and/or short-term follow-up. Objective: Analysis of long-term hormonal effects and tolerance of ketoconazole in CD. Design: A total of 38 patients were retrospectively studied with a mean follow-up of 23 months (6–72). Setting: All patients were treated at the same Department of Endocrinology in Marseille, France. Patients: The 38 patients with CD, of whom 17 had previous transsphenoidal surgery. Intervention: Ketoconazole was begun at 200–400 mg/day and titrated up to 1200 mg/day until biochemical remission. Main outcome measures: Patients were considered controlled if 24-h urinary free cortisol was normalized. Results: Five patients stopped ketoconazole during the first week because of clinical or biological intolerance. On an intention to treat basis, 45% of the patients were controlled as were 51% of those treated long term. -
18-Dehydrogenase Deficiency W
Arch Dis Child: first published as 10.1136/adc.51.8.576 on 1 August 1976. Downloaded from Archives of Disease in Childhood, 1976, 51, 576. Hypoaldosteronism in three sibs due to 18-dehydrogenase deficiency W. HAMILTON, A. E. McCANDLESS, J. T. IRELAND, and C. E. GRAY From the University Departments of Child Health, Liverpool and Glasgow Hamilton, W., McCandless, A. E., Ireland, J. T., and Gray, C. E. (1976). Archives of Disease in Childhood, 51, 576. Hypoaldosteronism in three sibs due to 18-dehydrogenase deficiency. Three sibs all presented in the early neonatal period with a salt-losing syndrome. The salt-losing form of congenital adrenal hyperplasia was diagnosed and appropriate treatment with glucocorticosteroids, mineralocorticosteroids, and additional dietary salt started. Although early life was maintained with difficulty, with age all3 children required decreasingamounts ofreplace- ment steroids to maintain normal plasma electrolyte balance. They were reinvestigated at the ages of 15 years and 8 years (twins), when cortisol synthesis and metabolism proved normal, but aldosterone synthesis was blocked by deficiency of 18-dehydro- genase. Rational treatment of these cases of a salt-losing syndrome in which aldo- sterone synthesis alone is blocked due to lack of the enzyme 18-dehydrogenase requires the administration of a mineralocorticosteroid drug only. Since deoxycor- ticosterone (acetate or pivalate) requires intramuscular administration, as life-long therapy oral fludrocortisone is preferable. Although fludrocortisone has glucocorti- coid activity, the 'hydrocortisone equivalent' effect of the small dosage used was un- likely to inhibit either pituitary corticotrophin or growth hormone production. Salt-loss of adrenal origin is recognized as a female external genitalia or macrogenitosomia http://adc.bmj.com/ feature of 3/1-hydroxysteroid dehydrogenase de- praecox in the male. -
Mitigations in Selected Haemostatic Parameters in Administration of Graded Doses of Dexamethasone and Its Blockers in Wister
ogy iol : Cu ys r h re P n t & R Anatomy & Physiology: Current y e s m e o a t Nwangwa et al., Anat Physiol 2018, 8:2 r a c n h A Research DOI: 10.4172/2161-0940.1000297 ISSN: 2161-0940 Research Article Open Access Mitigations in Selected Haemostatic Parameters in Administration of Graded Doses of Dexamethasone and its Blockers in Wister Rats Nwangwa EK and Odigie OM* Department of Human Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria *Corresponding author: Odigie OM, Department of Human Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria, E-mail: [email protected] Received date: May 07, 2018; Accepted date: May 25, 2018; Published date: May 29, 2018 Copyright: © 2018 Nwangwa EK, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Clinical trials have shown that an even newer compound, dexamethasone (Dex), might be more potent and less likely to cause side-effects than any other known corticosteroid medication. This study investigated the possible changes in selected haemostatic parameters [clotting time, bleeding time, platelets count and fibrinogen level] in albino wistar rats, following administration of graded doses of Dex. Forty-two male albino Wistar rats were randomly grouped into seven of six rats each. With Group A receiving normal diets (Control), Groups B-G were respectively given 0.1 mg/Kg of Dex, 0.3 mg/Kg of Dex, 0.1 mg/Kg of Dex +33 mg/Kg of Ketokonazol (Keto), 0.3 mg/Kg of Dex +33 mg/Kg of Keto, 0.1 mg/Kg of Dex+Vitamin (Vit) E and 0.1 mg/Kg of Dex.