Kooperativer Bibliotheksverbund

Berlin Brandenburg

and
and

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
Year
  • 1
    Language: English
    In: European Journal of Pharmacology, 15 August 2013, Vol.714(1-3), pp.498-506
    Description: Macrophage migration inhibitory factor (MIF)-deficient mice develop glucose intolerance and hyperglycemia, but remain entirely responsive to exogenous insulin in adult age. Furthermore, as a consequence of MIF deficiency, the immune response in these mice is predominantly anti-inflammatory. Since MIF is a natural counter-regulator of glucocorticoid action, and it is known that excessive concentration of glucocorticoids contribute both to beta cell dysfunction and immunosuppression, we hypothesized that MIF absence enables elevation of glucocorticoids which in turn caused the observed condition. Our results confirm that MIF-knockout (MIF-KO) mice possess higher levels of circulating corticosterone, but lower expression of glucocorticoid receptor in pancreatic islets, liver and adipose tissue to the one observed in wild type (WT) mice. A significant up-regulation of glucocorticoid receptor expression was however noticed in MIF-deficient lymph node cells. The inhibition of glucocorticoid receptor by RU486 improved tolerance to glucose in MIF-KO mice and restored euglycemia. Although RU486 treatment did not alter the level of glucose receptor GLUT2, it enhanced insulin secretion and up-regulated insulin-triggered Akt phosphorylation within hepatic tissue. Finally, inhibition of glucocorticoid receptor changed anti-inflammatory phenotype of MIF-KO lymphocytes toward a physiological profile. Our results indicate that deregulated glucocorticoid secretion and glucocorticoid receptor expression in the absence of MIF possibly contributes to the development of glucose intolerance and immunosuppression in MIF-KO mice. However, since MIF-KO mice respond normally to insulin and their beta cell function is within physiological range, additional cause for glucose intolerance could be sought in the possible malfunction of their insulin.
    Keywords: Macrophage Migration Inhibitory Factor ; Glucocorticoids ; Diabetes ; Insulin ; Inflammation ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0014-2999
    E-ISSN: 1879-0712
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Language: English
    In: Diabetologia, 2014, Vol.57(5), pp.980-990
    Description: Byline: Ivana Nikolic (1), Tamara Saksida (1), Katia Mangano (2), Milica Vujicic (1), Ivana Stojanovic (1), Ferdinando Nicoletti (2), Stanislava Stosic-Grujicic (1) Keywords: Beta cell apoptosis; Carbon monoxide-releasing molecule-A1; Cytokines; Type 1 diabetes Abstract: Aims/hypothesis Recent studies have identified carbon monoxide (CO) as a potential therapeutic molecule for the treatment of autoimmune diseases owing to its anti-inflammatory and anti-apoptotic properties. We explored the efficacy and the mechanisms of action of the CO-releasing molecule (CORM)-A1 in preclinical models of type 1 diabetes. Methods The impact of CORM-A1 on diabetes development was evaluated in models of spontaneous diabetes in NOD mice and in diabetes induced in C57BL/6 mice by multiple low-dose streptozotocin (MLDS). Ex vivo analysis was performed to determine the impact of CORM-A1 both on T helper (Th) cell and macrophage differentiation and on their production of soluble mediators in peripheral tissues and in infiltrates of pancreatic islets. The potential effect of CORM-A1 on cytokine-induced apoptosis in pancreatic islets or beta cells was evaluated in vitro. Results CORM-A1 conferred protection from diabetes in MLDS-induced mice and reduced diabetes incidence in NOD mice as confirmed by preserved insulin secretion and improved histological signs of the disease. In MLDS-challenged mice, CORM-A1 attenuated Th1, Th17, and M1 macrophage response and facilitated Th2 cell differentiation. In addition, CORM-A1 treatment in NOD mice upregulated the regulatory arm of the immune response (M2 macrophages and FoxP3.sup.+ regulatory T cells). Importantly, CORM-A1 interfered with in vitro cytokine-induced beta cell apoptosis through the reduction of cytochrome c and caspase 3 levels. Conclusions/interpretation The ability of CORM-A1 to protect mice from developing type 1 diabetes provides a valuable proof of concept for the potential exploitation of controlled CO delivery in clinical settings for the treatment of autoimmune diabetes. Author Affiliation: (1) Department of Immunology, Institute for Biological Research 'Sinisa Stankovic', University of Belgrade, Bul. Despota Stefana 142, 11060, Belgrade, Serbia (2) Department of Biomedical Sciences, School of Medicine, University of Catania, Via Androne 83, 95124, Catania, Italy Article History: Registration Date: 10/01/2014 Received Date: 19/07/2013 Accepted Date: 18/12/2013 Online Date: 02/02/2014 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00125-014-3170-7) contains peer-reviewed but unedited supplementary material, which is available to authorised users.
    Keywords: Beta cell apoptosis ; Carbon monoxide-releasing molecule-A1 ; Cytokines ; Type 1 diabetes
    ISSN: 0012-186X
    E-ISSN: 1432-0428
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Language: English
    In: Biochemical and Biophysical Research Communications, 2010, Vol.395(2), pp.225-231
    Description: Proteins of the BCL-2 family are important regulators of apoptosis. The BCL-2 family includes three main subgroups: the anti-apoptotic group, such as BCL-2, BCL-XL, BCL-W, and MCL-1; multi-domain pro-apoptotic BAX, BAK; and pro-apoptotic “BH3-only” BIK, PUMA, NOXA, BID, BAD, and SPIKE. SPIKE, a rare pro-apoptotic protein, is highly conserved throughout the evolution, including , whose expression is downregulated in certain tumors, including kidney, lung, and breast. In the literature, SPIKE was proposed to interact with BAP31 and prevent BCL-XL from binding to BAP31. Here, we utilized the Position Weight Matrix method to identify SPIKE to be a BH3-only pro-apoptotic protein mainly localized in the cytosol of all cancer cell lines tested. Overexpression of SPIKE weakly induced apoptosis in comparison to the known BH3-only pro-apoptotic protein BIK. SPIKE promoted mitochondrial cytochrome release, the activation of caspase 3, and the caspase cleavage of caspase’s downstream substrates BAP31 and p130CAS. Although the informatics analysis of SPIKE implicates this protein as a member of the BH3-only BCL-2 subfamily, its role in apoptosis remains to be elucidated.
    Keywords: Apoptosis ; Spike ; Cytochrome C ; Caspase 3 ; Bcl-2 Family ; Biology ; Chemistry ; Anatomy & Physiology
    ISSN: 0006-291X
    E-ISSN: 1090-2104
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    In: Vjesnik bibliotekara Hrvatske, 03/19/2018, Vol.60(4), p.181
    Description: Cilj. Rad analizira suradnju između knjižnica i aktera civilnoga društva koji se bave problematikom beskućništva kao primjer pomoći ugroženim društvenim skupinama. Također utvrđuje koliku je medijsku pozornost tema dobila. Pristup. Prvi dio rada analizira suradnju između knjižnica i civilnoga društva, naglašavajući potencijale knjižnica i aktivan pristup kako bi se pružila konkretna pomoć potrebitima. Drugi dio rada, kvantitativna analiza sadržaja novinarskih tekstova triju internetskih portala u razdoblju duljem od godine dana, utvrđuje kolika je medijska zainteresiranost za temu. Rezultati. U konačnici, rezultati pokazuju nedostatnu medijsku zainteresiranost za suradnju između knjižnica i civilnoga društva te problematiku beskućništva općenito. Ipak, zamjetni su pozitivni primjeri koji pokazuju kako su mediji dali svojevrstan poticaj suradnji i doprinijeli rješavanju problema. Originalnost/vrijednost. Rad naglašava temelje novinarstva koje je potrebno poštovati kako bi se pridonijelo rješavanju gorućih društvenih problema. U radu je također naglašena važnost strateškoga razmišljanja o ulozi knjižnica, imajući na umu njihovu otvorenost prema ugroženim društvenim skupinama i upotrebu njihovih potencijala za dobrobit cjelokupna društva.
    Keywords: Library & Information Science;
    ISSN: 0507-1925
    E-ISSN: 1334-6938
    Source: CrossRef
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Language: English
    In: Circulation, Nov 25, 2014, Vol.130(22)
    Keywords: Pulmonary Hypertension -- Risk Factors ; Pulmonary Hypertension -- Care And Treatment ; Hemodynamics -- Research ; Biological Markers -- Research ; Cellular Signal Transduction -- Research
    ISSN: 0009-7322
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    In: Circulation, 2016, Vol.134(Suppl_1 Suppl 1), pp.A19307-A19307
    Description: Introduction: Transforming Growth Factor-β (TGFβ) ligands signal via type I and type II serine-threonine kinase receptors to regulate broad transcriptional programs. Excessive TGFβ-mediated signaling is implicated in the pathogenesis of pulmonary arterial hypertension (PAH), based in part on the ability of broad inhibitors of TGFβ/Activin/GDF/Nodal receptors ALK4/5/7 to attenuate experimental pulmonary hypertension (PH). These broad inhibition strategies do not delineate the specific contribution of TGFβ vs. a multitude of other ligands, and their translation is limited by cardiovascular and systemic toxicity.Hypothesis: We tested whether or not TGFBRII-Fc, a selective TGFβ1/3 ligand trap, reverses PH and vascular remodeling in experimental PH models.Methods: Signaling studies utilized cultured human pulmonary artery smooth muscle cells. PH was studied in monocrotaline-treated Sprague-Dawley rats, SUGEN/hypoxia-treated Sprague-Dawley rats and SUGEN/hypoxia-treated C57BL/6 mice. PH, cardiac function, vascular remodeling, and valve structure were assessed by ultrasound, invasive hemodynamic measurements, and histomorphometry.Results: TGFBRII-Fc is an inhibitor of TGFβ1 and TGFβ3 but not TGFβ2 signaling. In vivo, treatment with TGFBRII-Fc attenuated Smad2 phosphorylation, normalized expression of Pai-1, and mitigated PH and pulmonary vascular remodeling in monocrotaline-treated rats, SUGEN/hypoxia-treated rats and SUGEN/hypoxia-treated mice. Administration of TGFBRII-Fc to monocrotaline-treated or SUGEN/hypoxia-treated rats with established PH improved right ventricular systolic pressures, right ventricular function, and survival. No cardiac structural or valvular abnormalities were observed following treatment with TGFBRII-Fc.Conclusions: Our findings are consistent with a pathogenetic role of TGFβ1/3, demonstrating the efficacy and tolerability of selective TGFβ ligand blockade for improving hemodynamics, remodeling, and survival in multiple experimental PH models.
    ISSN: 0009-7322
    Source: Copyright © 2013 Lippincott Williams & Wilkins. All rights reserved.〈img src=http://exlibris-pub.s3.amazonaws.com/LWW%20logo.png style="vertical-align:middle;margin-left:7px"〉
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Language: English
    In: Circulation, Nov 8, 2016, Vol.134(19)
    Keywords: Transforming Growth Factors -- Research ; Pulmonary Hypertension -- Care And Treatment ; Treatment Outcome -- Analysis
    ISSN: 0009-7322
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Language: English
    In: Липар - часопис за књижевност, језик, уметност и културу, 2015, Vol.XVI(58), pp.45-60
    Description: The paper investigates the reach of thoughts and linguistic attitudes of Wilhelm von Humboldt in Spanish linguistics and determines to what extent and in which aspects his work is present in papers of eminent Spanish linguists. Special chapters were dedicated to the theoretical aspects of reception...
    Keywords: Language and Literature Studies ; Translation Studies ; Reception ; Wilhelm Von Humboldt ; the Inner Form of Language ; the Outer Form of Language ; Weltansicht ; History & Archaeology
    ISSN: 1450-8338
    Source: Central and Eastern European Online Library (C.E.E.O.L.)
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    Language: English
    In: Circulation, Nov 25, 2014, Vol.130(22)
    Keywords: Biological Markers -- Research ; Pulmonary Hypertension -- Risk Factors ; Pulmonary Hypertension -- Care And Treatment ; Bone Morphogenetic Proteins -- Research
    ISSN: 0009-7322
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    Language: English
    In: The Journal of Thoracic and Cardiovascular Surgery, July 2015, Vol.150(1), pp.266-266
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2015.03.004 Byline: Igor Gosev, Ivana Nikolic, Sary F. Aranki Author Affiliation: Division of Cardiac Surgery, Brigham and Women's Hospital, Boston, Mass
    Keywords: Surgery ; Hospital Patients;
    ISSN: 0022-5223
    E-ISSN: 1097-685X
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages