RPMI 1640 Medium was developed at Roswell Park Memorial Institute in 1966 by Moore and his co-workers. A modification of McCoy′s 5A Medium, it was formulated to support lymphoblastoid cells in suspension culture, but it has since been shown to support a wide variety of cells that are anchorage-dependent. Originally intended to be used with a serum supplement, RPMI 1640 has been shown to support several cell lines in the absence of serum. It has also been widely used in fusion protocols and in the growth of hybrid cells. This medium is suitable for culturing human normal and neoplastic leukocytes.
Reconstitution
Supplement with 0.3 g/L L-glutamine, 2.0 g/L sodium bicarbonate, 0.001 g/L folic acid at 1×.
At the site of microbial infections, the significant influx of immune effector cells and the necrosis of tissue by the invading pathogen generate hypoxic microenvironments in which both the pathogen and host cells must survive. Currently, whether hypoxia adaptation is
The American journal of tropical medicine and hygiene, 81(6), 1041-1049 (2009-12-10)
Trypanosoma cruzi, the agent of Chagas disease, can be subdivided into six discrete typing units (DTUs), TcI, TcIIa, TcIIb, TcIIc, TcIId or TcIIe, each having distinct epidemiologically important features. Dozens of genetic markers are available to determine the DTU to
Genetic and environmental factors modulate the susceptibility to diabetic nephropathy, as initiating and/or progression factors. The objective of the European Rational Approach for the Genetics of Diabetic Complications (EURAGEDIC) study is to identify nephropathy susceptibility genes. We report molecular genetic
Infection and immunity, 77(7), 2908-2918 (2009-04-29)
We analyzed the defensive role of the cytosolic innate recognition receptor nucleotide oligomerization domain 1 (NOD1) during infection with Listeria monocytogenes. Mice lacking NOD1 showed increased susceptibility to systemic intraperitoneal and intravenous infection with high or low doses of L.
Recent studies suggest that SOCS2 is involved in the regulation of TLR signaling. In this study, we found that the expression of SOCS2 is regulated in human monocyte-derived DC by ligands stimulating TLR2, 3, 4, 5, 8 and 9 signaling.
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