Direct support and general support maintenance : fighting vehicle, infantry, M2 (2350-01-048-5920) and fighting vehicle, cavalry, M3 (2350-01-049-2695), hull.

Includes index.

Technical manual, operator's manual : fighting vehicle, infantry, M2 (2350-01-048-5920) and fighting vehicle, cavalry, M3 (2350-01-049-2695), turret.

At head of title: Advance copy.

Technical manual organizational maintenance : fighting vehicle, infantry, M2 (2350-01-048-5920) and fighting vehicle, cavalry, M3 (2350-01-049-2695) turret.

Includes indexes.

Hand receipt covering content of Components of End Item (COEI), Basic Issue Items (BII), and Additional Authorization List (AAL) for fighting vehicle, infantry, M2, (2350-01-048-5920) and fighting vehicle, cavalry, M3, (2350-01-049-2695).

"August 1984."

Direct support and general support maintenance : fighting vehicle, Infantry, M2 (2350-01-048-5920) and fighting vehicle, Cavalry, M3 (2350-01-049-2695) turret.

Includes index.

Unit support, intermediate direct support, and intermediate general support maintenance repair parts and special tools list (including depot maintenance repair parts and special tools) for fighting vehicle, infantry, M2, (2350-01-048-5920), fighting vehicle, infantry, M2A1, (2350-01-179-1027), fighting vehicle, cavalry, M3, (2350-01-049-2695) ....

"9 February 1987."

Unit maintenance : fighting vehicle, infantry, M2, (2350-01-048-5920), M2A1 (2350-01-179-1027), and fighting vehicle, cavalry, M3 (2350-01-049-2695), M3A1 (2350-01-179-1028), turret.

"December 1986"--Vol. 3.

Unit maintenance : fighting vehicle, infantry, M2, (2350-01-048-5920), M2A1 (2350-01-179-1027), and fighting vehicle, cavalry, M3 (2350-01-049-2695), M3A1 (2350-01-179-1028), turret.

"December 1986"--Vol. 3.

DS, GS, and depot maintenance repair parts and special tools list : borescope, M1 (20mm-40mm) 6650-318-4426 and borescope, M2 (57mm-8 inch) 6650-587-0986.

"December 1968."

The experimental production of macrophages in the circulating blood

Reprinted from "The Journal of medical research, vol. XLIII, no. 2, April-May 1922."

Runx2 and Vascular Calcification

Thesis (Ph.D.)--University of Washington, 2016-06

Replication of Norovirus in cell culture reveals a tropism for dendritic cells and macrophages.

Noroviruses are understudied because these important enteric pathogens have not been cultured to date. We found that the norovirus murine norovirus 1 (MNV-1) infects macrophage-like cells in vivo and replicates in cultured primary dendritic cells and macrophages. MNV-1 growth was inhibited by the interferon-alphabeta receptor and STAT-1, and was associated with extensive rearrangements of intracellular membranes. An amino acid substitution in the capsid protein of serially passaged MNV-1 was associated with virulence attenuation in vivo. This is the first report of replication of a norovirus in cell culture. The capacity of MNV-1 to replicate in a STAT-1-regulated fashion and the unexpected tropism of a norovirus for cells of the hematopoietic lineage provide important insights into norovirus biology.

Comparison of taurine- and glycine-induced conformational changes in the M2-M3 domain of the glycine receptor

In the ionotropic glutamate receptor, the global conformational changes induced by partial agonists are smaller than those induced by full agonists. However, in the pentameric ligand-gated ion channel receptor family, the structural basis of partial agonism is not understood. This study investigated whether full and partial agonists induce different conformation changes in the glycine receptor chloride channel ( GlyR). A substituted cysteine accessibility analysis demonstrated previously that glycine binding induced an increase in surface accessibility of all residues from Arg(271) to Lys(276) in the M2-M3 domain of the homomeric alpha1 GlyR. Here we compare the surface accessibility changes induced by the full agonist, glycine, and the partial agonist, taurine. In GlyRs incorporating the A272C, S273C, L274C, or P275C mutation, the reaction rate of the cysteine-specific compound, methanethiosulfonate ethyltrimethylammonium, depended on how strongly the receptors were activated but was agonist-independent. Reaction rates could not be compared in the R271C and K276C mutant GlyRs because methanethiosulfonate ethyltrimethylammonium did not modify the extremely small currents induced by saturating taurine or equivalent low glycine concentrations. The results indicate that bound taurine and glycine molecules impose identical conformational changes to the M2-M3 domain. We therefore conclude that the higher efficacy of glycine is due to an increased ability to stabilize a common activated configuration.

LPS regulates a set of genes in primary murine macrophages by antagonising CSF-1 action

We previously reported that bacterial products such as LPS and CpG DNA down-modulated cell surface levels of the Colony Stimulating Factor (CSF)-1 receptor (CSF-1R) on primary murine macrophages in an all-or-nothing manner. Here we show that the ability of bacterial products to down-modulate the CSF-IR rendered bone marrow-derived macrophages (BMM) unresponsive to CSF-1 as assessed by Akt and ERK 1/2 phosphorylation. Using toll-like receptor (th-)9 as a model CSF-1-repressed gene, we show that LPS induced tlr9 expression in BMM only when CSF-1 was present, suggesting that LPS relieves CSF-1-mediated inhibition to induce gene expression. Using cDNA microarrays, we identified a cluster of similarly CSF-1 repressed genes in BMM. By real time PCR we confirmed that the expression of a selection of these genes, including integral membrane protein 2B (itm2b), receptor activity-modifying protein 2 (ramp2) and macrophage-specific gene 1 (mpg-1), were repressed by CSF-1 and were induced by LPS only in the presence of CSF-1. This pattern of gene regulation was also apparent in thioglycollate-elicited peritoneal macrophages (TEPM). LPS also counteracted CSF-1 action to induce mRNA expression of a number of transcription factors including interferon consensus sequence binding protein 1 (Icsbp1), suggesting that this mechanism leads to transcriptional reprogramming in macrophages. Since the majority of in vitro studies on macrophage biology do not include CSF-1, these genes represent a set of previously uncharacterised LPS-inducible genes. This study identifies a new mechanism of macrophage activation, in which LPS (and other toll-like receptor agonists) regulate gene expression by switching off the CSF-1R signal. This finding also provides a biological relevance to the well-documented ability of macrophage activators to down-modulate surface expression of the CSF-1R. (C) 2005 Elsevier GmbH. All rights reserved.