Background-The purpose of this study was to test the hypothesis that periodontal pathogens associated with aggressive periodontitis persist in extracrevicular locations following scaling and root planing, systemic antibiotics, and anti-microbial rinses.

No abstract

Fluids co-produced with methane from hydraulically fractured organic-rich shales of the Marcellus Formation (USA) are characterized by high total dissolved solids (TDS), including elevated levels of Ba, Sr and Br. To investigate the source and geologic history of these high-TDS fluids and their dissolved constituents, we carried out a series of sequential extraction experiments on dry-drilled cuttings extracted within, below and above the Marcellus Shale from a well in Tioga County, New York State. The experiments were designed to extract (1) water soluble components, (2) exchangeable cations, (3) carbonate minerals, and (4) hydrochloric acidsoluble constituents. The geochemistry of the resultant leachates highlights the different geochemical reservoirs for extractable elements within the shale; notably, Na and Br were largely water-soluble, while Ba was extracted primarily from exchangeable sites, and Ca and Sr were found both in exchangeable sites and carbonate. Strontium isotope ratios measured on the leachates indicate that each of the element reservoirs has a distinct value. Measured 87 Sr/ 86 Sr ratios in the water soluble component are similar to those of Marcellus produced water, while the ion exchange reservoir yields lower ratios, and carbonate Sr is lower still, approaching Devonian-Silurian seawater values. Despite the isotopic similarity of water leachates and produced water, the total water chemistry argues against generation of produced water by interaction of hydraulic fracturing fluid with "dry" shale. The high-TDS produced water is most likely trapped formation water (within and/or adjacent to the shale) that is released by hydraulic fracturing. The formation water was affected by multiple processes, possibly including basin scale, tectonically-driven fluid flow. Significant chemical and isotopic differences between Marcellus Shale produced water and overlying Upper Devonian/Lower Mississippian produced waters suggests a hydrologic barrier has been maintained in parts of the Appalachian Basin since the late Paleozoic.

Endothelin-1 (ET-1) was originally characterized as a potent vasoconstrictor secreted by the endothelium and participating in the regulation of vascular tone. Subsequent analysis has revealed ET-1 to be a multifunctional peptide produced by a wide variety of cells and tissues under normal and pathologic conditions. The importance of macrophages as a source of ET-1 during infection and inflammation is supported by clinical observations in humans and in animal models of inflammation. We hypothesize that the production of ET-1 is part of the characteristic macrophage response to infection, and have begun to investigate the ability of various classes of microbes or microbial products to induce macrophage ET-1 production. We report the production of ET-1 by murine macrophages in response to stimulation with both gram-positive and gram-negative bacteria. Stimulation of macrophages with yeast (Candida albicans or Saccharomyces cerevisiae) or the protozoan parasite Leishmania major, elicited no significant release of ET-1. The production of ET-1 in response to lipopolysaccharide (LPS) was dose and time dependent, and required the expression of a functional toll-like receptor 4 (TLR4). Pharmacologic inhibition of the transcription factor, nuclear factor-kappaB (NF-kappaB) suppressed LPS-induced ET-1 production. Our findings complement the growing body of literature implicating a role for macrophage-derived ET-1 in inflammatory pathologies. The production of ET-1 by macrophages during infection and inflammation has the potential to affect tissue perfusion, leukocyte extravasation, and immune cell function.

No abstract

Paul RJ, Bowman PS, Johnson J, Martin AF. Effects of sex and estrogen on myosin COOH-terminal isoforms and contractility in rat aorta. Am J Physiol Regul Integr Comp Physiol 292: R751-R757, 2007. First published August 17, 2006; doi:10.1152/ajpregu.00167.2006.-We reported that estrogen treatment of ovariectomized rats increased uterine smooth muscle contractility and the ratio of the COOH-terminal myosin heavy chain isoform SM1 (204 kDa) and SM2 [200 kDa; Hewett TE, Martin AF, Paul RJ. J Physiol (Lond) 460: 351-364, 1993]. We extended this model to study sex and estrogen effects on vascular contractility. Experimental groups included 10-to 14-wk-old male (M), female (F), ovariectomized female (OF), and OF treated with estrogen (OF&E) for 7 days with a subcutaneous pellet delivery system, resulting in 17␤-estradiol of 85 (OF&E) vs. 5 (OF or M) pg/ml. The SM1-to-SM2 ratio increased from 1.8 to 2.6 in thoracic aorta, similar to uterine muscle. Isometric force was measured in 5-mm segments of intact and endothelium-denuded (Ϫendo) aorta. With KCl, the maximum forces were in the order OF Ϸ M Ͼ OF&E, and ED50 OF&E Ͼ OF Ϸ M. Differences in ED50 with estrogen persisted after endothelial denudation. The decreased force in Ϫendo OF aorta was not seen in OF&E, suggesting that estrogen altered an endothelium-dependent effect. No differences in maximum forces were noted with norepinephrine: ED50 OF Ͼ OF&E Ͼ M. Estrogen treatment, in contrast to KCl, increased sensitivity. Endothelial denudation increased sensitivity but reduced the differences between groups. With ACh relaxation, males were more sensitive than females, and estrogen had no effect. In the abdominal aorta, there were no changes in SM1/SM2 with 17␤-estradiol, and differences in contractility were blunted. In summary, estrogen treatment decreased responses to KCl but increased sensitivity to norepinephrine; male rats always demonstrated the highest contractility. An increase in the COOH-terminal myosin heavy chain isoform SM1-to-SM2 ratio with 17␤-estradiol treatment may underlie the changes observed in contractility.estrogen; vascular sensitivity; isometric force; myosin isoforms; ovariectomy THE OCCURRENCE OF CARDIOVASCULAR diseases is greater in men aged 30 -50 yr compared with women of similar age (15, 16). The incidence of cardiovascular diseases is also greater in postmenopausal compared with premenopausal women, and vascular protective effects of female sex hormones have been proposed (15,16,18,31). Currently, estrogen replacement therapy to postmenopausal women is in widespread use, but its validity is questioned (14,17,23,27,34,36). The mechanism by which sex and/or estrogen may affect the heart is unknown; it is likely to be multifactorial and has been reviewed in detail (30, 40). Estrogen receptors have been identified on both vascular endothelial (4, 10) and smooth muscle cells (5, 21, 22, 29), providing two potential pathways by which estrogen could affect vascular function. In addition, non-receptor-mediated mechanisms may play a role (35). Estroge...

No abstract

No abstract