Discharge of methylmercury-enriched hypolimnetic water from a stratified reservoir

A study conducted from July 1995 to June 1996 examining spatial and temporal distribution of mercury (Hg) at the Caballo Reservoir, New Mexico, revealed that the highest levels of methylmercury (MMHg) occurred in both the inlet and the Rio Grande upstream of the reservoir. As a result, a second study was designed to identify possible sources of the elevated levels of MMHg, and to determine if water discharged from the Elephant Butte Reservoir upstream could be a primary source. In July 1996, as anoxia began to develop in the hypolimnion of the Elephant Butte Reservoir, surface water MMHg concentrations were below the MDL of 0.018 ng/l while water discharged into the tailrace was 0.149 ng/l MMHg. By September 1996, when the anoxic hypolimnion spanned 60% of the total reservoir depth, surface water MMHg was still below the MDL, while discharge water had increased to 1.144 ng/l MMHg. Following reservoir turnover in November 1996, surface water increased to 0.264 ng/l MMHg while discharge water decreased to 0.420 ng/l MMHg. By January 1997, MMHg in the tailrace decreased to pre-stratification levels, and both surface water and discharge water reached similar MMHg levels until the onset of summer stratification in July 1997. This trend was repeated the following year when MMHg concentrations in the tailrace increased from 0.190 ng/l in August 1997 to 1.240 ng/l in September 1997. In addition, vertical profile sampling of the reservoir from August 1997 to September 1997 showed a buildup of MMHg in the anoxic hypolimnion which coincided with increasing levels of MMHg discharged into the tailrace. During the course of this study the single largest contribution of MMHg to the river below the reservoir was from water released through the dam during the fall months of the year.     

Co-occurrence of toxic bacterial and fungal secondary metabolites in moisture-damaged indoor environments

Toxic microbial secondary metabolites have been proposed to be related to adverse health effects observed in moisture-damaged buildings. Initial steps in assessing the actual risk include the characterization of the exposure. In our study, we applied a multi-analyte tandem mass spectrometry-based methodology on sample materials of severely moisture-damaged homes, aiming to qualitatively and quantitatively describe the variety of microbial metabolites occurring in building materials and different dust sample types. From 69 indoor samples, all were positive for at least one of the 186 analytes targeted and as many as 33 different microbial metabolites were found. For the first time, the presence of toxic bacterial metabolites and their co-occurrence with mycotoxins were shown for indoor samples. The bacterial compounds monactin, nonactin, staurosporin and valinomycin were exclusively detected in building materials from moist structures, while chloramphenicol was particularly prevalent in house dusts, including settled airborne dust. These bacterial metabolites are highly bioactive compounds produced by Streptomyces spp., a group of microbes that is considered a moisture damage indicator in indoor environments. We show that toxic bacterial metabolites need to be considered as being part of very complex and diverse microbial exposures in 'moldy' buildings. PRACTICAL IMPLICATIONS: Bacterial toxins co-occur with mycotoxins in moisture-damaged indoor environments. These compounds are measurable also in settled airborne dust, indicating that inhalation exposure takes place. In attempts to characterize exposures to microbial metabolites not only mycotoxins but also bacterial metabolites have to be targeted by the analytical methods applied. We recommend including analysis of samples of outdoor air in the course of future indoor assessments, in an effort to better understand the outdoor contribution to the indoor presence of microbial toxins. There is a need for a sound risk assessment concerning the exposure to indoor microbial toxins at concentrations detectable in moisture-damaged indoor environments.     

Heterogeneity of tachykinin receptors in the rabbit lung

The tachykinins, substance P (SP) and neurokinin A (NKA), are agonists for the NK(1) and NK(2) receptors, respectively. Tachykinins have various respiratory effects, including bronchoconstriction. This study characterizes tachykinin binding sites in the rabbit lung. We hypothesize that (2-[(125)I]iodohistidyl(1))Neurokinin A ([(125)I]NKA) interacts with NK1 and NK2 binding sites in the rabbit lung. The K d determined from saturation isotherms was 0.69 times/divided by 1.14 nM (geometric mean times/divided by SEM) and the B max was 4.15 + or - 0.22 femtomole/mg protein (arithmetic mean + or - SEM). Competitive inhibition studies with NKA, SP and various selective tachykinin agonists showed the rank order of potency; [beta-Ala(8)]-Neurokinin A 4-10 = SP > NKA > [Sar(9),Met(02)11]-Substance P. [beta-Ala(8)]-Neurokinin A 4-10, a selective NK(2) agonist, and SP inhibition of [(125)I]NKA binding were best described using a two-site model. Competitive inhibition studies using the selective nonpeptide NK(2) antagonist (SR 48968) and the selective nonpeptide NK(1) antagonist (CP 96,345) revealed Ki's of 5.5 nM and 8.1 nM, respectively. Our data therefore suggest that [(125)I]NKA binds to both the NK(1) and NK(2) receptors in the lung.     

Localization using nonindividualized head-related transfer functions

The HPV proteins encoded by the early viral genes, including E6 and E7, are thought to subvert the normal regulatory pathways of infected cells to accommodate viral replication. Mechanistically some of this is accomplished by protein-protein interactions between viral proteins and a number of key cellular regulatory proteins that include tumor suppressor gene products. By undermining cellular regulatory pathways the HPV oncogenes cause hyperproliferation and the perturbation of normal cellular differentiation pathways. Although expression of the high-risk HPV-encoded E6 and E7 oncoproteins may be important prerequisites for cellular transformation, it is very likely that additional cellular changes are necessary for carcinogenic progression. The elucidation of the role of the early HPV genes in the initiation and/or maintenance of carcinogenic progression will continue to be a fascinating area of investigation and may reveal new opportunities for antiviral therapy and antitumor intervention.     

Technical Opportunities for International Collaborations by the U.S. Fusion Program

This report was prepared by a Working Group at the request of the U.S. Department of Energy, Office of Fusion Energy Sciences in 1997. The report addresses technical opportunities for mutually beneficial collaboration between the United States and other international fusion research programs. A number of outstanding opportunities are discussed.