Direct support and general support maintenance manual (including repair parts and special tools list) for pump, fuel, metering and distributing, assembly 2910-178-1185, 2910-759-5410, 2910-908-6320, 2910-968-6317, and 2910-116-8241.

"June 1984."

Direct support and general support, maintenance : engine, diesel, 8 cylinder, naturally aspirated, fuel-injected, water cooled, DDA model, 6.2 liter (NSN 2815-01-168-7892).

"June 1985."

Direct support and general support maintenance repair parts and special tools lists (including depot maintenance repair parts and special tools) : engine, with container, turbosupercharged, diesel, fuel injection, 90-degree "V" type, air-cooled, 12-cylinder, assembly; models AVDS-1790-2C, 2815-00-410-1203 and AVDS-1790-2D, 2815-00-410-1204 and AVDS-1790-2DR, 2815-00-124-5387.

"December 1977."

Direct support and general support maintenance manual for truck, cargo, 8 ton, 4 x 4, M520 w/winch (NSN 2320-00-873-5422) ... truck, tanker, fuel servicing: 2500 gallon, 4 x 4, M559 w/o winch (NSN 2320-00-445-7250).

Includes index.

Organizational, direct support, and general support maintenance repair parts and special tools list : hammer, pile-driver, self-powered; diesel engine driven, w/fuel oil tank and lubricating oil tank, NSN 3895-00-854-4150, link-belt speeder model 440.

"This publication supersedes TM 5-3895-333-25P dated 18 February 1969 and all changes"--P. i.

Operator, organizational, direct support, general support, and depot maintenance manual : hammer, pile-driver, self-powered, w/fuel oil tank and lubricating oil tank (Link-Belt Speeder mdl 440) FSN 3895-854-4150.

"December 1968."

Operator, organizational, direct and general support maintenance manual : heater, space, multi-fuel, with blower, 60,000 BTU/hr, (Hunter model UH-68[[D), FSN 4520-114-1055.

"June 1969."

Operator's, organizational, direct and general support maintenance manual : heater, space, multi-fuel, with blower, 60,000 BTU/HR, (Hunter model UH-68F), NSN 4520-01-050-5628.

Includes index.

Organizational, direct support, and general support maintenance repair parts and special tools list for pumping assembly, diesel engine driven, wheel mtd, 350 gpm, 275 ft. head, model 350PAF (fuel use only), NSN 4320-01-092-3551 ....

"23 July 1990."

Operator, organizational, and direct support maintenance manual including repair parts and special tools lists : heaters, space, radiant type, portable (type I, model M1941, solid fuel) FSN 4520-257-4877, (type II, model M1941, liquid fuel) FSN 4520-927-4214, (Yukon model M1950, solid or liquid fuel) FSN 4520-287-3353 : heaters, immersion, liquid fuel fired, for corrugated cans ....

"December 1969."

ROR alpha regulates the expression of genes involved in lipid homeostasis in skeletal muscle cells - Caveolin-3 and CPT-1 are direct targets of ROR

The staggerer mice carry a deletion in the RORalpha gene and have a prolonged humoral response, overproduce inflammatory cytokines, and are immunodeficient. Furthermore, the staggerer mice display lowered plasma apoA-I/-II, decreased plasma high density lipoprotein cholesterol and triglycerides, and develop hypo-alpha-lipoproteinemia and atherosclerosis. However, relatively little is known about RORalpha in the context of target tissues, target genes, and lipid homeostasis. For example, RORalpha is abundantly expressed in skeletal muscle, a major mass peripheral tissue that accounts for similar to40% of total body weight and 50% of energy expenditure. This lean tissue is a primary site of glucose disposal and fatty acid oxidation. Consequently, muscle has a significant role in insulin sensitivity, obesity, and the blood-lipid profile. In particular, the role of RORalpha in skeletal muscle metabolism has not been investigated, and the contribution of skeletal muscle to the ROR-/- phenotype has not been resolved. We utilize ectopic dominant negative RORalpha expression in skeletal muscle cells to understand the regulatory role of RORs in this major mass peripheral tissue. Exogenous dominant negative RORalpha expression in skeletal muscle cells represses the endogenous levels of RORalpha and -gamma mRNAs and ROR-dependent gene expression. Moreover, we observed attenuated expression of many genes involved in lipid homeostasis. Furthermore, we show that the muscle carnitine palmitoyltransferase-1 and caveolin-3 promoters are directly regulated by ROR and coactivated by p300 and PGC-1. This study implicates RORs in the control of lipid homeostasis in skeletal muscle. In conclusion, we speculate that ROR agonists would increase fatty acid catabolism in muscle and suggest selective activators of ROR may have therapeutic utility in the treatment of obesity and atherosclerosis.

Direct continuities between cisternae at different levels of the Golgi complex in glucose-stimulated mouse islet beta cells

Direct continuity between the membranes of cisternae in the Golgi complex in mammalian cells rarely has been observed; when seen, its documentation has been equivocal. Here we have used dual-axis electron microscope tomography to examine the architecture of the Golgi in three dimensions at approximate to6-nm resolution in rapidly frozen, freeze-substituted murine cells that make and secrete insulin in response to glucose challenge. Our data show three types of direct connections between Golgi cisternae that are normally distinct from one another. These connections all bypass interceding cisternae. We propose that when pancreatic beta cells are stimulated to synthesize and secrete insulin rapidly in vivo, such connections provide a continuous lumen that facilitates the rapid transit of large amounts of newly made protein for secretion. The heterotypic fusion of cisternae, even transiently, raises important questions about the molecular mechanisms that (i) facilitate the fusion/fission of cisternal membranes and control the directionality and specificity of such events, and (it) retain Golgi processing enzymes at specific places within individual cisternae when two cisternae at different levels in the Golgi have fused, maintaining the sequential processing hierarchy that is a hallmark of Golgi organization.

The effects of ethanol on PPARS in MCF-7 human breast cancer cells

Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors involved in various metabolic diseases. In the liver, PPARα is involved in alcohol metabolism and may lead to the development of alcoholic fatty liver and other alcohol mediated liver injuries. PPARβ modulation by ethanol induces abnormal myelin production by oligodendrocytes. PPARα and PPARβ are PPAR isoforms expressed in the human breast cell lines. Epidemiological studies show a positive correlation between alcohol intake and breast cancer risk, however, the molecular mechanisms involved are unclear. We hypothesized that ethanol would affect the expression and transactivation of human PPAR isoforms in estrogen receptor (ER) positive and ER negative breast cancer cells. Using real time RT-PCR we looked at the transcription of PPAR isoforms in the presence of increasing concentrations of ethanol and saw isoform and time dependent specific effects. Gene reporter assays enabled us to ascertain the effects of ethanol on ligand-mediated activation of human PPARα and PPARβ at concentrations equivalent to both moderate and chronic alcohol consumption. Ethanol differentially blocked the ligand-mediated activation of both PPARα and PPARβ. Since PPARα and PPARβ are involved in the differentiation and proliferation of breast cancer cells, PPARs may be a possible mechanism involved in the effect of ethanol in breast cancer.