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Infectious Diseases	1
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bradykinin receptor(Bradykinin receptors)	1
B2 receptor(Bradykinin B2 receptor)	1

A review with 61 referencesTopics include: the structure and subtypes of trimeric G proteins; the working cycle of G proteins; the structure of G protein activators, specifically those of transmembrane receptors, amphipathic peptides and polyamines; and activation of G proteins by amphipathic peptides and polyamines.

01 Apr 2009·Arteriosclerosis, Thrombosis, and Vascular BiologyQ1 · MEDICINE

Certain Progestins Prevent the Enhancing Effect of 17β-Estradiol on NO-Mediated Inhibition of Platelet Aggregation by Endothelial Cells

Q1 · MEDICINE

Article

Author: Jourdain, Marie ; Bronner, Christian ; Zerr-Fouineau, Murielle ; Hecker, Markus ; Boesch, Caroline ; Schini-Kerth, Valérie B.

Objectives— Estro-progestin treatments have been associated with an increased risk of thromboembolic events in postmenopausal women. This study examined whether progestins affect the stimulatory effect of estrogens on the endothelial formation of nitric oxide (NO), a potent antithrombotic factor. Methods and Results— Experiments were performed with human endothelial cells. Endothelial NO synthase (eNOS) and GTP cyclohydrolase I (GTPCH I) mRNA expression was assessed by RT-PCR, eNOS protein by Western blotting, NO formation by electron spin resonance spectroscopy, and platelet aggregation by an aggregometer. Medroxyprogesterone acetate (MPA), progesterone, levonorgestrel, and nomegestrol acetate prevented the 17β-estradiol (17β-E)-induced expression of eNOS mRNA and protein. MPA and progesterone reduced the 17β-E-induced formation of NO and potentiation of the inhibitory effect of endothelial cells on platelet aggregation whereas levonorgestrel and nomegestrol acetate were without effect. Moreover, MPA and progesterone prevented the 17β-E-induced expression of GTPCH I mRNA. Mifepristone, a glucocorticoid and progesterone receptor antagonist, and L-sepiapterin prevented the inhibitory effect of MPA and progesterone on platelet aggregation. Conclusions— Certain progestins, including MPA, attenuate the 17β-E-induced NO-mediated inhibition of platelet aggregation by endothelial cells through preventing both eNOS and GTPCH I expression most likely via activation of glucocorticoid receptors.

03 Feb 2009·Proceedings of the National Academy of SciencesQ1 · CROSS-FIELD

Thymic stromal lymphopoietin overproduced by keratinocytes in mouse skin aggravates experimental asthma

Q1 · CROSS-FIELD

Article

Author: Frossard, Nelly ; Hener, Pierre ; Zhang, Zhikun ; Metzger, Daniel ; Kato, Shigeaki ; Chambon, Pierre ; Li, Mei

Atopic dermatitis (AD) is often the initial step in the “atopic march,” given that more than half of AD patients with moderate to severe AD develop asthma later in life. Both AD and asthma share a similar “atopy” phenotype that includes T helper type 2 inflammation with eosinophilia and hyper-IgE immunoglobulinemia, but the molecular mechanisms underlying the “atopic march” remain elusive. In the present study, we show that induced expression of thymic stromal lymphopoietin (TSLP) in mouse epidermal keratinocytes upon topical application of MC903 (a low calcemic analogue of vitamin D3) not only triggers AD as we previously reported but also aggravates experimental allergic asthma induced by ovalbumin sensitization and challenge. Our study, which provides a mouse model to study human “atopic march,” indicates that keratinocyte-produced TSLP may represent an important factor in the link of atopic dermatitis to asthma.

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Pipeline

Pipeline Snapshot as of 02 Feb 2025

The statistics for drugs in the Pipeline is the current organization and its subsidiaries are counted as organizations,Early Phase 1 is incorporated into Phase 1, Phase 1/2 is incorporated into phase 2, and phase 2/3 is incorporated into phase 3

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