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INSM - Insmed - 2009 draadje
Volgen
Muurvast sinds half drie. Ben benieuwd.
Het volume bevalt mij niet
vrij vogeltje schreef:
Het volume bevalt mij niet
Zie het positief, niet veel mensen willen verkopen zelfs nu het vrijwel zeker is dat er geen buyout komt . We wachten af
"I am pleased to be joining the Insmed management team and look forward to significantly contributing to the strategic review," said Mr. LaBella. then the company will be sold soon to Merck and/or Roche. che. toch steeds meer geluiden betreffende een overname!!!! Yok
yokyok schreef:
"I am pleased to be joining the Insmed management team and look forward to significantly contributing to the strategic review," said Mr. LaBella.
then the company will be sold soon to Merck and/or Roche. che.
toch steeds meer geluiden betreffende een overname!!!!
Yok
Ach ja, verschil van mening zal er altijd zijn (gelukkig) Maar volgens mij komt er geen algehele verkoop. Volgens mij een fase III ALS trial in samen werking met merck & co
Hoop het ook niet mag van mij tie ook terug naar de 18, maar ja tis wel een hapklare brok! Yok
Toch een heel sterk slot weer, kan niet anders zeggen.
J Clin Endocrinol Metab. 2010 Mar 16. [Epub ahead of print] Treatment with Recombinant Human Insulin-Like Growth Factor (rhIGF)-I/rhIGF Binding Protein-3 Complex Improves Metabolic Control in Subjects with Severe Insulin Resistance. Regan FM, Williams RM, McDonald A, Umpleby AM, Acerini CL, O'Rahilly S, Hovorka R, Semple RK, Dunger DB. Department of Paediatrics (F.M.R., R.M.W., A.M., C.L.A., R.H., D.B.D.), and Institute of Metabolic Science (C.L.A., S.O., R.H., R.K.S., D.B.D.), The University of Cambridge, Cambridge CB2 0QQ, United Kingdom; and Diabetes and Endocrinology (A.M.U.), Postgraduate Medical School, University of Surrey, Guildford GU2 7WG, United Kingdom. Objective: Diabetes in the context of severe insulin resistance (SIR) presents a major therapeutic challenge because conventional therapies including insulin and insulin sensitizers often fail to achieve adequate metabolic control. Adjunctive therapy with recombinant human IGF-I (rhIGF-I)/recombinant human IGF binding protein-3 (rhIGFBP-3) has been shown to improve insulin sensitivity in both type 1 and type 2 diabetes and may have a role in the treatment of SIR. We report clinical and physiological outcomes after adjunctive therapy with rhIGF-I/rhIGFBP-3 in five subjects with SIR. Research Design and Methods: Five females (median age, 17 yr; range, 5-37) with SIR (two with pathogenic insulin receptor mutations) were treated with 0.5-2.0 mg/kg rhIGF-I/rhIGFBP-3 using a 16-wk dose escalation protocol. Glycosylated hemoglobin was recorded monthly. At baseline and end of treatment all patients were evaluated using continuous glucose monitoring sensing and admitted for overnight GH profiling and insulin-modified stable-label iv glucose tolerance test. Changes in body composition were assessed using dual-energy x-ray absorptiometry and magnetic resonance imaging. Results: Treatment with rhIGF-I/rhIGFBP-3 was well tolerated, and all subjects reported clinical improvements with reduction in acanthosis nigricans. Glycosylated hemoglobin was reduced (8.5% pretreatment to 7.1%; P < 0.03) with a trend toward reduction in mean continuous glucose monitoring sensing glucose (10.7 vs. 8.5 mmol/liter; P = 0.08). Effects of treatment on other biochemical measures were variable, but there was a trend toward improved C-peptide responses during the iv glucose tolerance test. Conclusions: rhIGF-I/rhIGFBP-3 is well tolerated and clinically effective in subjects with SIR.www.ncbi.nlm.nih.gov/pubmed/20233784
Dit dateert van 2007-Ipsenwww.eje-online.org/cgi/content/abstra... -------------------------------------------------------------------------------- ARTICLE IGF-I treatment of insulin resistance Anna McDonald, Rachel M Williams, Fiona M Regan, Robert K Semple1 and David B Dunger University of Cambridge, Department of Paediatrics, Box 116, Addenbrookes Hospital, Hills Road, Cambridge, CB2 2QQ, UK and 1 Department of Clinical Biochemistry, Box 232, Addenbrooks Hospital, Hills Road, Cambridge, CB2 2QQ, UK (Correspondence should be addressed to D B Dunger; Email: dbd25@cam.ac.uk ) This paper was presented at the Ipsen symposium, ‘The evolving biology of growth and metabolism’, Lisbon, Portugal, 16–18 March 2007. Ipsen has supported the publication of these proceedings. Abstract Severe insulin resistance resulting from known or putative genetic defects affecting the insulin receptor or post-insulin receptor signalling represents a clinical spectrum ranging from Donohue’s and Rabson–Mendenhall syndrome, where the genetic defect is identified, through to the milder phenotype of type A insulin resistance, where a genetic defect can only be detected in around 10% of cases. Paradoxically, subjects with these conditions may present with hypoglycaemia due to mismatch of post-prandial glucose excursion and compensatory hyperinsulinaemia. Ultimately, treatment with insulin and insulin sensitisers will be unsuccessful and subjects may succumb to diabetes or its complications. Recombinant human IGF-I alone or combined with its binding protein (IGFBP-3) provides an alternative therapy as IGF-I receptor shares structural and functional homology with the insulin receptor and recombinant human insulin-like growth factor I (rhIGF-I) therapy could improve glucose disposal by signalling through the IGF-I receptor, whilst reducing the adverse effects of high insulin concentrations. There are also data which indicate that IGF-I signalling through the IGF-I receptor on the pancreatic ß-cell may be important in maintaining insulin secretion. Pilot studies confirmed that rhIGF-I could reduce glucose and insulin levels in subjects with type A insulin resistance and those with Rabson–Mendenhall syndrome with sustained beneficial effects on HbA1c. Continued study has confirmed efficacy of rhIGF-I when combined with IGFBP-3 in the treatment of Donohue’s and type A insulin resistance subjects. Observations that IGF-I treatment can improve C-peptide levels in these subjects may indicate that it might be more valuable as a first line intervention to preserve ß-cell function, rather than its current use as a medication of last resort in subjects where all other therapies have failed.
yokyok schreef:
Hoop het ook niet mag van mij tie ook terug naar de 18, maar ja tis wel een hapklare brok!
Yok
tie? is toch heel anders ......
En weer terug naar de 1.15, schiet ook niet op, ben benieuwd waar de koers eind 2011 staat!!
yokyok schreef:
En weer terug naar de 1.15, schiet ook niet op, ben benieuwd waar de koers eind 2011 staat!!
Met een paar aandelen naar de 1,15 gezet bij slot. Wordt niet veel verkocht op het moment.
Wat kunnen we dit jaar nog verwachten van insm?? Yok
yokyok schreef:
Wat kunnen we dit jaar nog verwachten van insm??
Yok
nee.. verkoop maar
Als jij dat zegt dan hou ik ze maar vast!!! PW Yok
We gaan weer lekker onder de dollar, let maar op
21:16 Koers ARCA biopharma schiet 210% omhoog na toewijzing patent Zoiets moet bij ons gebeuren
CHart Broke channel, but many support levels just beneath, RSI went over 70 and whenever it turns prior to reaching about 30 , still bullish. (did not break RSI 50 so far, which is good) So currently just some consolidation from the sharp rise we have had (which indeed goes with some decline)
Wat een vreemd slot weer, wel fijn natuurlijk.
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