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- Roila, F., et al.
(författare)
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Prevention of chemotherapy- and radiotherapy-induced emesis : Results of the 2004 Perugia International Antiemetic Consensus Conference
- 2006
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Ingår i: Annals of Oncology. - : Elsevier BV. - 0923-7534 .- 1569-8041. ; 17:1, s. 20-28
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Forskningsöversikt (refereegranskat)abstract
- Background: In the late 1990s, several professional organizations convened antiemetic guideline groups and published the findings of these expert panels. Each of these documents was based on analyses of the available published trials and provided nearly similar recommendations. Nonetheless, small differences in emetic risk categories and treatment recommendations led to confusion in antiemetics selection. With the emergence of new findings and agents since the guidelines were initially published, many of the oncology professional societies have updated the antiemetic guidelines. Materials and methods: A literature review up to March 2004 was carried out using MEDLINE with evaluation of the evidence by an expert panel composed of 23 oncology professionals in clinical medicine, medical oncology, radiation oncology, oncology nursing, statistics, pharmacy, medical policy and decision making, and pharmacology. The experts represented nine oncology professional societies and came from 11 different countries on four continents. Results: Recommendations on antiemetic regimens to prevent emesis induced by high, moderate, low and minimal risk chemotherapy were suggested as well as management of anticipatory emesis. Furthermore, recommendations for refractory emesis, emesis induced by high-dose chemotherapy and radiotherapy and for antiemetics in children receiving chemotherapy were elaborated. Conclusions: Recommendations about antiemetic prophylaxis in patients receiving treatment with chemo- and radiotherapy have been updated by representatives of nine oncological organizations. © 2005 European Society for Medical Oncology.
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- Grünberg, John, 1985, et al.
(författare)
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Overexpressing the novel autocrine/endocrine adipokine WISP2 induces hyperplasia of the heart, white and brown adipose tissues and prevents insulin resistance.
- 2017
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Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 7
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Tidskriftsartikel (refereegranskat)abstract
- WISP2 is a novel adipokine, most highly expressed in the adipose tissue and primarily in undifferentiated mesenchymal cells. As a secreted protein, it is an autocrine/paracrine activator of canonical WNT signaling and, as an intracellular protein, it helps to maintain precursor cells undifferentiated. To examine effects of increased WISP2 in vivo, we generated an aP2-WISP2 transgenic (Tg) mouse. These mice had increased serum levels of WISP2, increased lean body mass and whole body energy expenditure, hyperplastic brown/white adipose tissues and larger hyperplastic hearts. Obese Tg mice remained insulin sensitive, had increased glucose uptake by adipose cells and skeletal muscle in vivo and ex vivo, increased GLUT4, increased ChREBP and markers of adipose tissue lipogenesis. Serum levels of the novel fatty acid esters of hydroxy fatty acids (FAHFAs) were increased and transplantation of Tg adipose tissue improved glucose tolerance in recipient mice supporting a role of secreted FAHFAs. The growth-promoting effect of WISP2 was shown by increased BrdU incorporation in vivo and Tg serum increased mesenchymal precursor cell proliferation in vitro. In contrast to conventional canonical WNT ligands, WISP2 expression was inhibited by BMP4 thereby allowing normal induction of adipogenesis. WISP2 is a novel secreted regulator of mesenchymal tissue cellularity.
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- Hammarstedt, Ann, 1975, et al.
(författare)
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WISP2 Regulates Preadipocyte Commitment and PPARgamma Activation by BMP4
- 2013
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Ingår i: Proceedings of the National Academy of Science of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 110:7, s. 2563-2568
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Tidskriftsartikel (refereegranskat)abstract
- Inability to recruit new adipose cells following weight gain leads to inappropriate enlargement of existing cells (hypertrophic obesity) associated with inflammation and a dysfunctional adipose tissue. We found increased expression of WNT1 inducible signaling pathway protein 2 (WISP2) and other markers of WNT activation in human abdominal s.c. adipose tissue characterized by hypertrophic obesity combined with increased visceral fat accumulation and insulin resistance. WISP2 activation in the s.c. adipose tissue, but not in visceral fat, identified the metabolic syndrome in equally obese individuals. WISP2 is a novel adipokine, highly expressed and secreted by adipose precursor cells. Knocking down WISP2 induced spontaneous differentiation of 3T3-L1 and human preadipocytes and allowed NIH 3T3 fibroblasts to become committed to the adipose lineage by bone morphogenetic protein 4 (BMP4). WISP2 forms a cytosolic complex with the peroxisome proliferator-activated receptor γ (PPARγ) transcriptional activator zinc finger protein 423 (Zfp423), and this complex is dissociated by BMP4 in a SMAD-dependent manner, thereby allowing Zfp423 to enter the nucleus, activatePPARγ, and commit the cells to the adipose lineage. The importance of intracellularWisp2 protein for BMP4-induced adipogenic commitment and PPARγ activationwas verified by expressing a mutant Wisp2 protein lacking the endoplasmic reticulum signal and secretion sequence. Secreted Wnt/Wisp2 also inhibits differentiation and PPARγ activation, albeit not through Zfp423 nuclear translocation. Thus adipogenic commitment and differentiation is regulated by the cross-talk between BMP4 and canonical WNT signaling and where WISP2 plays a key role. Furthermore, they link WISP2 with hypertrophic obesity and the metabolic syndrome.
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