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12篇 您的检索式：作者名="Jan Frystyk"

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		题名	作者	年代	出处	被引量
	1	Comparison of Osteoprotegerin to Traditional Atherosclerotic Risk Factors and High-Sensitivity C-Reactive Protein for Diagnosis of Atherosclerosis显示文摘	Rasmus Mogelvang Sune H. Pedersen Allan Flyvbjerg Mette Bjerre Allan Z. Iversen Soren Galatius Jan Frystyk Jan S. Jensen	2012	The American Journal of Cardiology2012，，4：	3
	2	Insulin-like growth factor-I serum concentrations and patterns of insulin-like growth factor binding proteins in patients with chronic liver disease显示文摘	Jens-Gerd Scharf Frank Schmitz Jan Frystyk Christian Skjaerbaek Heidrun Moesus Werner F. Blum Giuliano Ramadori Heinz Hartmann	1996	Journal of Hepatology1996，，：	2
	3	The insulin-like growth factor (IGF) system and its relation to infliximab treatment in adult patients with Crohn’s disease显示文摘	Martin Eivindson Henning Gr?nb?k Kristin Skogstrand Poul Thorsen Jan Frystyk Allan Flyvbjerg Jens F. Dahlerup	2007	Scandinavian Journal of Gastroenterology2007，，4：	1
	4	The insulin-like growth factor (IGF)-system in active ulcerative colitis and Crohn’s disease: Relations to disease activity and corticosteroid treatment显示文摘	Martin Eivindson Henning Gr?nb?k Allan Flyvbjerg Jan Frystyk Erik Zimmermann-Nielsen Jens Frederik Dahlerup	2006	Growth Hormone & IGF Research2006，，1：	1
	5	Insulin-like growth factor I (IGF-I) replacement therapy increases albumin concentration in liver cirrhosis: Results of a pilot randomized controlled clinical trial显示文摘	Mariam Conchillo Robert J. de Knegt Marina Payeras Jorge Quiroga Bruno Sangro Jose-Ignacio Herrero Inma Castilla-Cortazar Jan Frystyk Allan Flyvbjerg Carl Yoshizawa Peter L.M. Jansen Bruce Scharschmidt Jesús Prieto	2005	Journal of Hepatology2005，，4：	1
	6	Obesity and cancer risk: the role of the insulin–IGF axis显示文摘	Andrew G. Renehan Jan Frystyk Allan Flyvbjerg	2006	Trends in Endocrinology & Metabolism2006，，8：	1
	7	Adiponectin isoforms, insulin resistance and liver histology in nonalcoholic fatty liver disease显示文摘	Giampaolo Bianchi Elisabetta Bugianesi Jan Frystyk Lise Tarnow Allan Flyvbjerg Giulio Marchesini	2010	Digestive and Liver Disease2010，，1：	1
	8	Serum Adiponectin Is a Predictor of Coronary Heart Disease: A Population-Based 10-Year Follow-Up Study in Elderly Men显示文摘	Jan Frystyk Christian Berne Lars Berglund Karin Jensevik Allan Flyvbjerg Bj?rn Zethelius	2007	The Journal of Clinical Endocrinology & Metabolism2007，，2：	1
	9	Adiponectin isoforms, insulin resistance and liver histology in nonalcoholic fatty liver disease显示文摘	Giampaolo B Elisabetta B Jan Frystyk		0，，01：	1
	10	Cardiovascular disease and insulin - like growth factor 1 显示文摘	Frystyk Jan MD PhD	2002	American Heart Association2002，106，8：	1
	11	Free insulin-like growth factors – measurements and relationships to growth hormone secretion and glucose homeostasis显示文摘	Jan Frystyk	2004	Growth Hormone & IGF Research2004，，5：	1
	12	Soluble membrane attack complex in ascites in patients with liver cirrhosis without infections显示文摘AIM: To study complement activation in 46 patients with alcoholic cirrhosis and ascites but no spontaneous bacterial peritonitis (SBP) and 10 healthy controls. METHODS: Complement activation was determined by the measurement of soluble membrane attack complex (sMAC) concentrations in ascites and plasma. In patients, metabolic liver function was determined by the galactose elimination capacity and the clinical status assessed by the Model of End-Stage Liver Disease and Child-Pugh scores. RESULTS: Ascites sMAC levels were markedly higherthan in the corresponding plasma sample (median (range): 596 (170 - 1519) vs 160 (77 - 848) μg/L; P < 0.01). Ascites sMAC levels correlated positively with liver status. There was no relationship between ascites sMAC and leukocyte count. No relationship between ascites sMAC and blood C-reactive protein, albumin or neutrophile count was found. Plasma sMAC concentrations were slightly higher in patients than in controls [130 μg/L (70 - 204); P = 0.04]. Neither sMAC in ascites nor plasma was related to mortality. CONCLUSION: The increased sMAC concentration in ascites and plasma indicate an activation of the complement system in cirrhosis even in the absence of SBP. This was particularly evident in the peritoneal fluid and most marked in patients with preserved liver status. The high ascites sMAC levels may reflect transudation of membrane attack complexes from the liver. Whether this complement activation has any clinical implications remains to be clarified.	Mette Bjerre Peter Holland-Fischer Henning Grφnbk Jan Frystyk Troels K Hansen Hendrik Vilstrup Allan Flyvbjerg	2010	World Journal of Hepatology2010，2，6：	0

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