Limited-Access Bioremediation in a Factory Setting

A factory in New Hampshire had a volatile organic compound (VOC) release detected in a storm-water outfall pipe. Hydrogen Release Compound (HRC) injection was determined to be the best remedial solution. Tight soils, shallow water table, access limitations, and pending property sale complicated remediation. Groundwater was directly below the floor slab. The plume was centered on the storm-water drain which carries runoff from the upgradient parking lot under the building. The VOCs are believed to have entered the subsurface in the central area of the building through spillage; the storm drain system was a preferential pathway. The groundwater contamination was addressed through bioremediation using HRC. Application required many injection points and applications, due to the low permeability of the soil. Due to interference with operations and property sale, repeated openings of the floor for injections using a drill rig were not feasible. Permanent injection points were installed, but would not be accessible for direct injection. Therefore, a trench was cut into the concrete floor slab between each point and the wall. Piping ran from the injection point to the wall, terminating at a standpipe with a quick-connect fitting. Each trench was then fillled with concrete to restore the floor slab. Since starting HRC treatment, VOC levels at the outfall have dropped to below the state regulatory standard. One well had levels of 1800 ug/L and 1200 ug/L of Cis-1,2 Dichloroethene and Vinyl Chloride in April, 2008. By January, 2009, both were below MCLs. Site closure is expected to be completed in a reasonable timeframe. The treatment has not interfered with Site activities or with sale of the Site

Mutants of Cochliobolus heterostrophus deficient in extracellular enzymes

Mutants with altered production and/or activity of certain extracellular enzymes have been obtained in Cochliobolus heterostrophus, a leaf spot pathogen of maize. The mutations should serve as useful phenotypic markers and can also be employed in studying the enzymes, their regulation, and their effect on other phenotypic traits, such as pathogenicity

Phylogenetics and Genetic Variation of Heligmosomoides thomomyos in Western Pocket Gophers (Thomomys spp.)

The host specificities and systematics of North American Heligmosomoides species remain particularly uncertain. The primary aim of this study was to verify that a species described previously based only on morphology, H. thomomyos, from pocket gopher (Rodentia: Geomyidae) hosts in Oregon represented a monophyletic lineage. In order to address this aspect, as well as to further understand relationships and geographic patterns, we carried out phylogenetic, genetic diversity, and population dynamic analyses using partial 18S rRNA and COI mtDNA sequences of Heligmosomoides specimens. Phylogenetic analyses suggested that there are likely multiple Heligmosomoides species present in these hosts. This was supported by the high degree of divergence and differentiation found among populations, significant population structure between locations, and a modest positive association between geographic and genetic distances. This study serves as the first molecular characterization and first phylogenetic report of H. thomomyos, and documents two new host records for this parasite. The relationship of H. thomomyos among pocket gopher hosts and to other Heligmosomoides species, however, warrants continued study

Linkage among melanin biosynthetic mutations in Cochliobolus heterostrophus

Melanin is synthesized by C. heterostrophus from acetate via pentaketide and several dihydroxynaphthalene intermediates (Tanaka et al. 1991 Mycol. Res. 95:49-56), as it is for certain other fungi (Bell and Wheeler 1986 Ann. Rev. Phytopathol. 24:411-451; Kubo et al. 1989 Exp. Mycol 13:77-84; Chumley and Valent 1990 Mol. Plant-Microbe Int. 3:135-143). Previously, five melanin deficient mutants of C. heterostrophus were analyzed by Tanaka et al. (Mycol. Res. 95:49-56), who were unable to establish complete linkage relationships because three of the mutations (alb1, alb3, and brn1) showed no recombination when crossed to each other, and were unlinked to the other two (sal1 and pgr1), which mapped about 12 cM apart. A sixth color mutation, scr1, represented a third linkage group, but there was no evidence of its involvement in melanin biosynthesis. Independently, we have recovered six melanin-deficient mutants, one of which (alb1, Leach et al. 1982 J. Gen. Microbiol. 128:1719-1729) was included in the study of Tanaka et al. and maps to chromosome 1 on the C. heterostrophus RFLP map (Tzeng et al. 1992 Genetics 130:81-96). We report here that our remaining five melanin-deficient mutants [crm1 (light cream), crm2 (dark cream), brn1 (brown), rsy1 (rose), and probably gra3 (gray)] are linked to, but are not allelic with, alb1 (white) and constitute a gene cluster on chromosome

A New Greenhouse Method to Assay Soybean Resistance to Brown Stem Rot

Greenhouse, growth chamber, and field experiments were conducted to develop a method to assess resistance of soybeans to Cadophora gregata (Phialophora gregata), causal agent of brown stem rot (BSR). In the new method, C. gregata is introduced at the base of the stems of 2-week-old soybeans, and the presence of the fungus is assessed in the tips of the stems 5 weeks later. To test the effectiveness of the method, two populations of soybeans and 10 checks were inoculated at the stem base and then assayed for fungal colonization of the stem tips, percentage of symptomatic leaflets, and percent internal stem length discolored. The lines also were planted in naturally infested fields to assess for percent internal stem length discolored, and were tested for the presence/absence of a BSR-resistant molecular marker. Greenhouse, field, and molecular marker data were compared. Linear regression analysis suggested that percentage of plants with colonized stem tips explained 41 to 64% of the variability (P \u3c 0.0001) in percent stem length discolored in the field and 58 to 85% of the variability (P \u3c 0.0001) in molecular marker data for BSR resistance. Percent stem length discolored assessed in the greenhouse had the lowest correlation with percent stem length discolored in the field and with the molecular marker. Of three incubation temperatures tested, 22°C was the most conducive for distinguishing resistant/susceptible soybeans using the colonization method

Report from the National Society of Genetic Counselors Service Delivery Model Task Force: A Proposal to Define Models, Components, and Modes of Referral

The Service Delivery Model Task Force (SDMTF) was appointed in 2009 by the leadership of the National Society of Genetic Counselors (NSGC) with a charge to research and assess the capacity of all existing service delivery models to improve access to genetic counseling services in the context of increasing demand for genetic testing and counseling. In approaching this charge, the SDMTF found that there were varying interpretations of what was meant by “service delivery models” and the group held extensive discussions about current practices to arrive at consensus of proposed definitions for current genetic service delivery models, modes of referral and components of service delivery. The major goal of these proposed definitions is to allow for conversations to begin to address the charge to the committee. We propose that current models of service delivery can be defined by: 1) the methods in which genetic counseling services are delivered (In‐person, Telephone, Group and Telegenetics), 2) the way they are accessed by patients (Traditional referral, Tandem, Triage, Rescue and Self‐referral) and 3) the variable components that depend upon multiple factors unique to each service setting. This report by the SDMTF provides a starting point whereby standardized terminology can be used in future studies that assess the effectiveness of these described models to overcome barriers to access to genetic counseling services.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146876/1/jgc40645.pd

Prdx1 inhibits tumorigenesis via regulating PTEN/AKT activity

It is widely accepted that reactive oxygen species (ROS) promote tumorigenesis. However, the exact mechanisms are still unclear. As mice lacking the peroxidase peroxiredoxin1 (Prdx1) produce more cellular ROS and die prematurely of cancer, they offer an ideal model system to study ROS-induced tumorigenesis. Prdx1 ablation increased the susceptibility to Ras-induced breast cancer. We, therefore, investigated the role of Prdx1 in regulating oncogenic Ras effector pathways. We found Akt hyperactive in fibroblasts and mammary epithelial cells lacking Prdx1. Investigating the nature of such elevated Akt activation established a novel role for Prdx1 as a safeguard for the lipid phosphatase activity of PTEN, which is essential for its tumour suppressive function. We found binding of the peroxidase Prdx1 to PTEN essential for protecting PTEN from oxidation-induced inactivation. Along those lines, Prdx1 tumour suppression of Ras- or ErbB-2-induced transformation was mediated mainly via PTEN

DOK2 inhibits EGFR-mutated lung adenocarcinoma

Somatic mutations in the EGFR proto-oncogene occur in ~15% of human lung adenocarcinomas and the importance of EGFR mutations for the initiation and maintenance of lung cancer is well established from mouse models and cancer therapy trials in human lung cancer patients. Recently, we identified DOK2 as a lung adenocarcinoma tumor suppressor gene. Here we show that genomic loss of DOK2 is associated with EGFR mutations in human lung adenocarcinoma, and we hypothesized that loss of DOK2 might therefore cooperate with EGFR mutations to promote lung tumorigenesis. We tested this hypothesis using genetically engineered mouse models and find that loss of Dok2 in the mouse accelerates lung tumorigenesis initiated by oncogenic EGFR, but not that initiated by mutated Kras. Moreover, we find that DOK2 participates in a negative feedback loop that opposes mutated EGFR; EGFR mutation leads to recruitment of DOK2 to EGFR and DOK2-mediated inhibition of downstream activation of RAS. These data identify DOK2 as a tumor suppressor in EGFR-mutant lung adenocarcinoma

Melatonin Chimeras Alter Reproductive Development and Photorefractoriness in Siberian Hamsters

Nightly melatonin (MEL) durations > 8 h provoke gonadal regression and decreases in body mass, whereas signals < 7 h stimulate gonadal and somatic growth in male Siberian hamsters. The authors sought to determine the minimum frequency of short MEL signals sufficient to induce the long-day phenotype in several photoperiodic traits. D,L-propranolol (hereafter propranolol) injections shortened MEL signals on the night of treatment without altering MEL on the subsequent night; this permitted interpolation of short MEL signals at variable frequencies against a background of long MEL signals (chimeras). Hamsters kept in short days (10 h light/day, 10L) were injected with propranolol 6 h after dark onset for 28 consecutive weeks beginning at 30 days of age (Week 0) either every other day or once every 3, 6, or 9 days. Control animals were injected with saline or with propranolol during the light phase or were transferred to long days (16L) at Week 0. Hamsters in 16L underwent rapid gonadal development and increases in body mass and displayed summer pelage color, as did hamsters treated with propranolol every other day. Animals treated with propranolol less frequently than every other day uniformly maintained undeveloped gonads and winter-like body weights, but pelage color becameproportionately darker with increased frequency of propranolol treatments. The onset of spontaneous testicular development in 10L was unaffected by propranolol injections. After termination of injections at Week 28, testicular regression was not observed in most 10L animals that previously had undergone spontaneous testicular development; however, 40% of hamsters that had been injected with propranolol every 3rd night did manifest the winter phenotype after Week 28. In an alternating sequence, short MEL signals completely override long signals and induce the summer phenotype. Threshold frequencies differ for MEL stimulation of long-day pelage and gonadal phenotypes. The timing and development of refractoriness to MEL does not depend in any simple manner on the number of long MEL signals or on the accumulation of a reaction product produced by long, and depleted by short, MEL signals.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/67291/2/10.1177_074873098129000345.pd