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Ana (70112-2699) USA Email: David G Nielsen - dnielsen@tulane.eduPublished: 27 November 2009 Virology Journal 2009, 6:211 doi:10.1186/1743-422X-6-Received: 27 October 2009 Accepted: 27 NovemberThis article is available from: http://www.virologyj.com/content/6/1/211 ?2009 Nielsen; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribu
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Mpled sequences are likely CRF02_AG (accounting for 50 of HIV-1M infections), with the other "pure" subtypes (G, D, A, and F) and CRFs (CRF11_cpx, 36_cpx, 37_cpx, and CRF01_AE) accounting for the remainder of infections. CRF02_AG and clade G viruses are broadly distributed across west central Africa and have apparently been circulating stably there for many years [3,17-19], consistent with the pr
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Cell lines from primary alveolar macrophages from MS-/- mice. Results: We used in vitro infection of the primary AMs with the J2 retrovirus carrying the v-raf and v-myc oncogenes. Following initial isolation in media supplemented with murine macrophage colony-stimulating factor (M-CSF), we subcloned three AM cell lines, designated ZK-1, ZK-2 and ZK-6. These cell lines grow well in RPMI-1640-10 FB
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L antibodies made also rapidly clear to the clinicians that a reliable predictive factor for outcome was, in fact, lacking [3-7]. The introduction of K-RAS mutational status analysis allowed a reliable selection of resistant patients (i.e. those with mutated K-RAS). However not all K-RAS wildtype cases were also responders to anti-EGFR monoclonal antibodies. This observation made the need for furt
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D. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractBackground: Alveolar macrophages (AM) avidly bind and ingest unopsonized inhaled particles and bacteria through class
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Surface expression of the macrophage-associated differentiation Ags was assessed by direct immunofluorescence (thick lines). ZK1 cells were incubated with FITC-labeled anti-mouse F4/80 or FITC-labeled anti-mouse CD11b. Mouse IgG2a and IgG2b were used as isotype controls (light lines). Staining of cells with FITC-labeled anti-mouse Ig compared to unstained cells detects the of cells expressing su
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R macrophages which was derived from brochoalveolar lavage (BAL) obtained from MS-/- mice [31]. Immortalization was conducted by infection of the primary AMs from MS/- mice with a retrovirus J2. The immortalized AMs were cloned by limiting dilution method. Three of the clones, designated as ZK-1, ZK-2 and ZK-6 were chosen for further characterization of macrophage phenotype and phagocytic function
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Om neutrophils, eosinophiles, and basophiles. C3a and C5a act on specific receptors to produce local inflammatory responses and when secreted in concentrations high enough to invoke a general systemic response, they cause circulatory collapse similar to an IgE mediated allergic response. ATs modulate the secretion of IL-6, and TNF from B cells and serve as potent chemoattractants[52]. C5a also wor

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