Photo-trichromatic printing, in theory and practice.

Mode of access: Internet.

Saturday half holiday at the Government Printing Office : hearing before the Committee on Printing, House of Representatives, Seventieth Congress, second session, on S.2440..., January 18, 1929.

Mode of access: Internet.

Mackenzie's five thousand receipts in all the useful and domestic arts : constituting a complete practical library relative to agriculture, bees, bleaching, brewing, calico printing, carving at table, cements, confectionary, cookery ...

Includes index.

A complete history of the several translations of the Holy Bible, and New Testament, into English, : both in ms. and in print: and of the most remarkable editions of them since the invention of printing. /

Pages 49-64, 112 are misnumbered 65-80, 512 respectively.

The triumph of the English language; a survey of opinions concerning the vernacular from the introduction of printing to the Restoration.

Mode of access: Internet.

Style manual of the California State Printing Office.

Mode of access: Internet.

Specimen book of printing types ...

At head of title: New York type foundry.

The South Australian system of conveyancing by registration of title, with instructions for the guidance of parties dealing, illustrated by copies of the books and forms in use in the Land Titles Office. To which is added the South Australian Real Property Act as amended in the sessions of 1858, with a copious index by Henry Gawler. Adelaide, Printed at the Register and Observer Printing Offices, 1859.

Mode of access: Internet.

Cellular targets of carcinogens.

"Conducted by the Interdisciplinary Communications Program of the Smithsonian Institution."

Printing and Publishing

Successively Issued by: U.S. Business and Defense Services Administration. Printing and Publishing Industries Division; U.S. Bureau of Domestic Commerce. Printing and Publishing Division; U.S. Bureau of Domestic Commerce. Forest Products More

Defining the chemotherapeutic targets of Histone Deacetylase inhibitors

The use of many conventional chemotherapeutic drugs is often severely restricted due to dose-limiting toxicities, as these drugs target the destruction of the proliferating fraction of cells, often with little specificity for tumor cells over proliferating normal body tissue. Many newer drugs attempt to overcome this shortcoming by targeting defective gene products or cellular mechanisms that are specific to the tumor, thereby minimizing the toxicity to normal tissue. Histone deacetylase inhibitors are an example of this type of tumor-directed drug, having significant toxicity for tumors but minimal effects on normal tissue. These drugs can affect the transcriptional program by modifying chromatin structure, but it is not yet clear whether specific transcriptional changes are directly responsible for their tumor-selective toxicity. Recent evidence suggests that transcriptional changes underlie their cytostatic activity, although this is not tumor-selective and affects all proliferating cells. Here we present evidence that supports an alternative mechanism for the tumor-selective cytotoxicity of histone deacetylase inhibitors. The target is still likely to be the chromatin histones, but rather than transcriptional changes due to modification of the transcriptionally active euchromatin, we propose that hyperacetylation and disruption of the transcriptionally inactive heterochromatin, particularly the centromeric heterochromatin, and the inability of tumor cells to cell cycle arrest in response to a specific checkpoint, underlies the tumor-selective cytotoxicity of these drugs.

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.