Decreased Plaque Formation Research Articles

Drag reducing polymers may decrease atherosclerosis by increasing shear in areas normally exposed to low shear stress

Purpose: Drag reducing polymers (DRPs) have been shown to decrease plaque formation. Their mechanism of action is unknown. Atherosclerosis tends to develop in areas of low shear stress. This study investigates whether DRPs increase shear stress in areas normally exposed to low shear stress. Methods: Six dogs underwent surgical plication of the left half of the aorta. A specially modified 20-MHz Doppler ultrasound probe mounted at a 45-degree angle on a micromanipulator was used to measure blood flow velocity at six 4-mm intervals along both lateral sides of the aorta starting at the aortic wall and then at subsequent 0.1-mm depths moving into the lumen before and after administering DRP. Shear rates were calculated using linear regression and then compared using the paired t test. The blood viscosity remained constant at 0.04 poise during infusions of this amount of DRP. Results: The maximum shear rate occurring during the cardiac cycle on the side of the aortic stenosis (plication) was 9.96 ± 1.52/sec before the administration of the DRP and 14.27 ± 2.01/sec after the administration of the DRP ( P = .0240). The maximum shear rate on the side of the unstenosed aortic wall was 57.25 ± 7.93/sec before the administration of the DRP and 44.80 ± 6.23/sec after the administration of the DRP ( P = .0081). Conclusion: One of the ways that DRPs inhibit the development of atherosclerosis appears to be by increasing shear stress in areas normally exposed to low shear stress. Understanding this mechanism may lead to the development of pharmaceutical agents that inhibit the development of atherosclerosis. (J Vasc Surg 1999;30:761-4.)

Anti-idiotypic antibodies mimicking glycoprotein D of herpes simplex virus identify a cellular protein required for virus spread from cell to cell and virus-induced polykaryocytosis.

Glycoprotein D (gD) of herpes simplex virus 1 (HSV-1) is required for stable attachment and penetration of the virus into susceptible cells after initial binding. We derived anti-idiotypic antibodies to the neutralizing monoclonal antibody HD1 to gD of HSV-1. These antibodies have the properties expected of antibodies against a gD receptor. Specifically, they bind to the surface of HEp-2, Vero, and HeLa cells susceptible to HSV infection and specifically react with a Mr 62,000 protein in these and other (143TK- and BHK) cell lines. They neutralize virion infectivity, drastically decrease plaque formation by impairing cell-to-cell spread of virions, and reduce polykaryocytosis induced by strain HFEM, which carries a syncytial (syn-) mutation. They do not affect HSV growth in a single-step cycle and plaque formation by an unrelated virus, indicating that they specifically affect the interaction of HSV gD) with a cell surface receptor. We conclude that the Mr 62,000 cell surface protein interacts with gD to enable spread of HSV-1 from cell to cell and virus-induced polykaryocytosis.

Effects of puromycin aminonucleoside on excision repair and recombination repair inescherichia coli

Ultraviolet (UV) lethality was increased when puromycin aminonucleoside (PAN) (3.0 mM) was added to the postirradiation medium ofEscherichia coli strains. The extent of repair inhibition differed greatly for strains WP-2hcr+, B/r(λ)hcr+, WP-2hcr−, and Bs-1hcr−. The interaction between PAN and UV was synergistic in thehcr+ strains. PAN enhanced UV lethality in strain B/r (λ) to a greater degree than in WP-2hcr+. There was no UV lethality enhancement by PAN (3.0 mM) in thehcr− strains, but the interaction of PAN (8.0 mM) with UV was synergistic. PAN decreased plaque formation of T1 UV-irradiated phage plated onE. coli Bhcr+ but had no effect on phage plated on Bs-1 or WP-2hcr− strains. These results suggest that PAN interferes with thehcr function in UV-irradiated bacteria.

Spontaneous reverse haemolytic plaque formation. II. The role of T cells and monocytes in regulating immunoglobulin secretion by human peripheral blood B cells.

A sensitive reverse haemolytic plaque assay was used on freshly isolated blood cells from normal human subjects to show that T lymphocytes and monocytes were both necessary for immunoglobulin production by unstimulated B cells cultured only for the time necessary to form plaques. When lymphocyte preparations were fully depleted of T cells by E-rosette formation overnight on ice followed by Ficoll-Hypaque centrifugation, the number of plaque-forming cells was reduced by up to 94%; this reduction was reversed by the replacement of T cells, although excess T cells suppressed plaque formation. Moreover, when T-cell function was blocked by 10-1000 ng of two monoclonal anti-T-cell antibodies, OKT3 or UCHT1, this significantly reduced or abolished spontaneous IgG plaques, and higher concentrations of either OKT3 or UCHT1 reduced the numbers of IgA and IgM plaques formed by B cells. The role of monocytes in spontaneous plaque formation was investigated. The removal of plastic-adherent cells from mononuclear cell preparations did not consistently result in a reduction in the numbers of plaques, but complement-mediated lysis of monocytes with either of two monoclonal antibodies with specificity for monocytes, OKM1 and FMC17, reduced by 50% the number of IgG, IgA and IgM plaques. This effect was reversed by addition of as few as 1% plastic-adherent cells. Decreased plaque formation by B cells, resulting from either blocking of T-cell function with monoclonal antibody or complement-mediated lysis of monocytes, or both, was fully reversed by soluble factors present in cell-free conditioned medium from lectin-activated T cells. Thus spontaneous plaque formation by human peripheral blood B cells requires T cells and a small number of monocytes, and the major function of these cells is to help B cells by the production of soluble factors.

Loss on serial passage of rhesus monkey kidney cells of proteolytic activity required for Sendai virus activation

Primary and secondary cultures of rhesus monkey kidney cells supported multiple-cycle replication of Sendai virus, but later passages lost this ability, and this was reflected in decreased plaque formation. Multiple-cycle replication also did not occur in LLC-MK2 cells, a continuous line of RMK cells. Failure of replication in serially passed cells was correlated with a decrease in proteolytic cleavage of a viral surface glycoprotein (Fo), and the ability of cells to support multiple-cycle replication and plaque formation could be restored by the addition of trypsin (0.3 microgram/ml) to the overlay medium. The use of wild-type virus, which requires trypsin, and protease activation mutants that require chymotrypsin or elastase for activation has provided evidence that the activating protease supplied by primary or secondary cells has trypsin-like activity. Inactive virus, with uncleaved Fo glycoprotein, absorbed to primary or secondary cells but did not infect them, even though such cells possess the enzyme that is capable of cleaving the Fo glycoprotein of virus synthesized in these cells. The inability of these cells to activate adsorbed virus indicates that the activating protease that they possess is inacessible to adsorbed virus, although it can act on the Fo glycoprotein during virus maturation in these cells. These data provide a biochemical explanation for the failure of later passages of a cell strain or a continuous cell line to support the replication of a paramyxovirus.

The Effect of Disaccharides on the Plaque-Forming Potential of Streptococcus mutans

The comparative and combined effects of sucrose, maltose, and lactose as factors on the plaque-forming potential of Streptococcus mutans were assessed. With increasing additions of maltose to sucrose-supplemented medium there was decreasing plaque formation. Lactose additions slightly increased plaque formation, but when combined with maltose they significantly enhanced the maltose inhibition of plaque formation.

Growth of plaque while chewing sucrose and sorbitol flavoured gum

The aim of the study was to assess the claimed toothcleansing effect of sorbitol and sucrose flavoured chewing gums. A total of 24 dental students participated in a double-blind, four times crossed over clinical trial during which each student chewed both types of gum for 4 days each. No other means to clean the teeth were allowed during the test periods. Two 4-day periods of no oral hygiene and no chewing were used as controls indicating the normal growth rate of plaque. The results confirmed earlier observations that sorbitol flavoured gum does neither increase or decrease plaque formation. Chewing of sucrose gum, however, was found to promote the growth rate of plaque. The cleansing effect of the gums was also tested on the plaque formed during the 4-day no-oral-hygiene periods. In this part of the study the chewing of 10 pieces of sorbitol flavoured gum during a time period of 3 h did not significantly reduce the plaque scores, while the sucrose flavoured gum, correspondingly used, again resulted in a statistically significant increase in the amount of bacterial deposits. Because of the rapid reaction of the plaque to sucrose flavoured gum, so-called sugarless substitutes were recommended for those who insist on chewing.