Permeation of human plasma lipoproteins in human carotid endarterectomy tissues: measurement by optical coherence tomography

Atherosclerosis is an inflammatory process occurring in arterial tissue, involving the subintimal accumulation of LDL. Measurement of the rate at which LDL and other lipoproteins, such as HDL and VLDL, enter and exit the tissue can provide insight into the mechanisms involved in the development of atherosclerotic lesions. Permeation of VLDL, LDL, HDL, and glucose was measured for both normal and atherosclerotic human carotid endarterectomy tissues (CEA) at 20°C and 37°C using optical coherence tomography (OCT). The rates for LDL permeation through normal CEA tissue were (3.16 ± 0.37) × 10(-5) cm/s at 20°C and (4.77 ± 0.48) × 10(-5) cm/s at 37°C, significantly greater (P < 0.05) than the rates for atherosclerotic CEA tissue at these temperatures [(1.97 ± 0.34) × 10(-5) cm/s at 20°C and (2.01 ± 0.23) × 10(-5) cm/s at 37°C]. This study effectively used OCT to measure the rates at which naturally occurring lipoproteins enter both normal and diseased carotid intimal tissue.     

Effect of thiochrome capronate on lipid metabolism in rats

Thiochrome caproate modified by the oxyethyl radical of the thiochrome derivative was studied for its effect on different indices of lipid metabolism in the liver and blood of albino rats. It was shown that when animals were fed on a standard laboratory diet, thiochrome caproate changed the amount of total and free fatty acids in the studied tissues and the fatty acid composition in the liver to a greater extent than thiochrome and hydroxythiamine.     

Fanconi anemia signaling and Mus81 cooperate to safeguard development and crosslink repair

Individuals with Fanconi anemia (FA) are susceptible to bone marrow failure, congenital abnormalities, cancer predisposition and exhibit defective DNA crosslink repair. The relationship of this repair defect to disease traits remains unclear, given that crosslink sensitivity is recapitulated in FA mouse models without most of the other disease-related features. Mice deficient in Mus81 are also defective in crosslink repair, yet MUS81 mutations have not been linked to FA. Using mice deficient in both Mus81 and the FA pathway protein FancC, we show both proteins cooperate in parallel pathways, as concomitant loss of FancC and Mus81 triggered cell-type-specific proliferation arrest, apoptosis and DNA damage accumulation in utero. Mice deficient in both FancC and Mus81 that survived to birth exhibited growth defects and an increased incidence of congenital abnormalities. This cooperativity of FancC and Mus81 in developmental outcome was also mirrored in response to crosslink damage and chromosomal integrity. Thus, our findings reveal that both pathways safeguard against DNA damage from exceeding a critical threshold that triggers proliferation arrest and apoptosis, leading to compromised in utero development.     

tag7 Gene and gene therapy of cancer

Modern gene therapeutic approaches towards the treatment of malignant neoplasms are discussed. Specifically, results of the first experiments on the development of vaccines on the basis of tumor cells modified with various cytokines and activation molecules are described. We compare effectiveness of different cytokines used for modification of tumor cells are made and consider possible mechanisms of vaccine action. The reasons for impossibility of the development of effective endogenous antitumor immunity are examined. The results of comparative analysis of the Tag7 protein antitumor activity are presented. This evidence clearly shows that Tag7 is a promising agent for anticancer therapy.