ABSTRACT
We use direct-write laser micromachining technology to fabricate the microfluidic chip, and to establish a microfluidic chemiluminescence immunoassay system based on superparamagnetic microbeads, for detecting alpha- fetoprotein (AFP). The AFP analysis can be completed in 20 minutes with 5 microl sample and 5 microl reagent, and there is a good linear correlation in the range of 1-800 ng/ml.
Subject(s)
Humans , Equipment Design , Immunoassay , Methods , Luminescent Measurements , Methods , Microfluidic Analytical Techniques , alpha-FetoproteinsABSTRACT
Objective To investigate the significance of TGF-β1, TGFRl and TGFR2 in the pathogenesis and prognosis in patients with myelofibrosis. Methods The expression of TGF-β1 and its receptors (TGFR1 and TGFR2 ) in bone marrow tissues and the level of TGF-β1 in the blood of 23 patients with myelofibrosis were detected by SABC immunocytochemistry and ELISA repectively. Results Expression of TGF-β1 and TGFR 1 was significantly higher in primary and secondary myelofibrosis patients than that of the control. No significant difference of TGFR2 expression was found between the groups of myelofibrosis and the control (P>0.05). The level of TGF-β1 in the blood of the patients with myelofibrosis was significantly higher than that of the control (P<0.01) and more obvious in secondary cases while TGF-β1 decreased nearly to the normal level when patients were in clinical remission. Conclusion TGF-β1 and it's receptors may be involved in the pathogenesis of myelofibrosis and might be of importance for the prognosis of the patients with myelofibrosis.
ABSTRACT
Objective To investigate the significance of TGF-β1, TGFRl and TGFR2 in the pathogenesis and prognosis in patients with myelofibrosis. Methods The expression of TGF-β1 and its receptors (TGFR1 and TGFR2 ) in bone marrow tissues and the level of TGF-β1 in the blood of 23 patients with myelofibrosis were detected by SABC immunocytochemistry and ELISA repectively. Results Expression of TGF-β1 and TGFR 1 was significantly higher in primary and secondary myelofibrosis patients than that of the control. No significant difference of TGFR2 expression was found between the groups of myelofibrosis and the control (P>0.05). The level of TGF-β1 in the blood of the patients with myelofibrosis was significantly higher than that of the control (P<0.01) and more obvious in secondary cases while TGF-β1 decreased nearly to the normal level when patients were in clinical remission. Conclusion TGF-β1 and it's receptors may be involved in the pathogenesis of myelofibrosis and might be of importance for the prognosis of the patients with myelofibrosis.