Considerations for Developing a Closure Plan for Inactive Swine Waste Lagoons in North Carolina

Environmental impacts and regulations in North Carolina related to closing unused swine waste lagoons were examined. There are over 3,000 swine operations in North Carolina, each raising more than 250 hogs, which use anaerobic waste lagoons to treat and store their waste. Most of the facilities in the state with populations of 1, 000 or more hogs began operation after 1990. Environmental and public health risks, although not as yet quantified, are associated with anaerobic lagoons and until these impoundments are closed the risks remain. Four county health boards and one county commission in the state have adopted rules mandating lagoon closure of certain swine operations within their jurisdiction when the facility ceases production. Four of these counties also have bonding requirements to ensure funds for completing the closure. One hundred-two of the existing swine operations in the state are subject to these county provisions. All other swine operations in the state rasing more than 250 hogs are subject only to state requirements - which allow facilities that are going out of business to either close their lagoon or maintain it under a waste management plan. The North Carolina Agriculture Cost Share Program is the only program in the state which provides financial assistance for closing lagoons and is restricted to closing lagoons which are abandoned or located at operations going out of business. This program will not be able to fund closure of all inactive swine waste lagoons in the state. Based on the information reviewed, the state should develop a plan to address the issues related to closing unused lagoons. Specific items which deserve consideration include options for holding swine operations financial responsible for closure, evaluating current closure standards, refining cost-shared expenditures, and providing clear statutory authority for mandating lagoon closure.Master of Science in Public Healt

Social disorganization and history of child sexual abuse against girls in sub-Saharan Africa : a multilevel analysis

Background: Child sexual abuse (CSA) is a considerable public health problem. Less focus has been paid to the role of community level factors associated with CSA. The aim of this study was to examine the association between neighbourhood-level measures of social disorganization and CSA. Methods: We applied multiple multilevel logistic regression analysis on Demographic and Health Survey data for 6,351 adolescents from six countries in sub-Saharan Africa between 2006 and 2008. Results: The percentage of adolescents that had experienced CSA ranged from 1.04% to 5.84%. There was a significant variation in the odds of reporting CSA across the communities, suggesting 18% of the variation in CSA could be attributed to community level factors. Respondents currently employed were more likely to have reported CSA than those who were unemployed (odds ratio [OR] = 2.05, 95% confidence interval [CI] 1.48 to 2.83). Respondents from communities with a high family disruption rate were 57% more likely to have reported CSA (OR=1.57, 95% CI 1.14 to 2.16). Conclusion: We found that exposure to CSA was associated with high community level of family disruption, thus suggesting that neighbourhoods may indeed have significant important effects on exposure to CSA. Further studies are needed to explore pathways that connect the individual and neighbourhood levels, that is, means through which deleterious neighbourhood effects are transmitted to individuals

A bacterial antirepressor with SH3 domain topology mimics operator DNA in sequestering the repressor DNA recognition helix

Direct targeting of critical DNA-binding elements of a repressor by its cognate antirepressor is an effective means to sequester the repressor and remove a transcription initiation block. Structural descriptions for this, though often proposed for bacterial and phage repressor–antirepressor systems, are unavailable. Here, we describe the structural and functional basis of how the Myxococcus xanthus CarS antirepressor recognizes and neutralizes its cognate repressors to turn on a photo-inducible promoter. CarA and CarH repress the carB operon in the dark. CarS, produced in the light, physically interacts with the MerR-type winged-helix DNA-binding domain of these repressors leading to activation of carB. The NMR structure of CarS1, a functional CarS variant, reveals a five-stranded, antiparallel β-sheet fold resembling SH3 domains, protein–protein interaction modules prevalent in eukaryotes but rare in prokaryotes. NMR studies and analysis of site-directed mutants in vivo and in vitro unveil a solvent-exposed hydrophobic pocket lined by acidic residues in CarS, where the CarA DNA recognition helix docks with high affinity in an atypical ligand-recognition mode for SH3 domains. Our findings uncover an unprecedented use of the SH3 domain-like fold for protein–protein recognition whereby an antirepressor mimics operator DNA in sequestering the repressor DNA recognition helix to activate transcription

Ligation of newly replicated DNA controls the timing of DNA mismatch repair

Acknowledgments We would like to thank to Dr. Michael Knop for sharing plasmids and infrastructure, for critical comments to the manuscript, and generous support. Thanks to Dr. Hannah Zhao and Dr. Tobias Schmidt for constructing some plasmids/strains used in this study, Dr. Helle Ulrich for valuable discussions and for sharing plasmids (auxin-degron system), and Sandra Ruf and Dr. Nina Papavasiliou for technical support/infrastructure with radioisotopes. R.D.K. and C.D.P. were supported by the NIH grant R01 GM50006 and the Ludwig Institute for Cancer Research. G.X.R., A.K., and H.H. were supported by the Deutsches Krebsforschungszentrum and the Deutsche Forschungsgemeinschaft grant HO-5501-1.Peer reviewedPublisher PD

Tools for Risk and Emergency Communication (Panel)

After the welcoming remarks, Dr. Kain introduced the first panel theme of communication and introduced the speakers. Her presentation, Social Media Management Systems (not included in the video), overviews the tools that social media managers can use on multiple platforms and apps. She demonstrates the software managers Tweetdeck and Hootsuite

Ligation of newly replicated DNA controls the timing of DNA mismatch repair.

Mismatch repair (MMR) safeguards genome stability through recognition and excision of DNA replication errors.1-4 How eukaryotic MMR targets the newly replicated strand in vivo has not been established. MMR reactions reconstituted in vitro are directed to the strand containing a preexisting nick or gap,5-8 suggesting that strand discontinuities could act as discrimination signals. Another candidate is the proliferating cell nuclear antigen (PCNA) that is loaded at replication forks and is required for the activation of Mlh1-Pms1 endonuclease.7-9 Here, we discovered that overexpression of DNA ligase I (Cdc9) in Saccharomyces cerevisiae causes elevated mutation rates and increased chromatin-bound PCNA levels and accumulation of Pms1 foci that are MMR intermediates, suggesting that premature ligation of replication-associated nicks interferes with MMR. We showed that yeast Pms1 expression is mainly restricted to S phase, in agreement with the temporal coupling between MMR and DNA replication.10 Restricting Pms1 expression to the G2/M phase caused a mutator phenotype that was exacerbated in the absence of the exonuclease Exo1. This mutator phenotype was largely suppressed by increasing the lifetime of replication-associated DNA nicks, either by reducing or delaying Cdc9 ligase activity in vivo. Therefore, Cdc9 dictates a window of time for MMR determined by transient DNA nicks that direct the Mlh1-Pms1 in a strand-specific manner. Because DNA nicks occur on both newly synthesized leading and lagging strands,11 these results establish a general mechanism for targeting MMR to the newly synthesized DNA, thus preventing the accumulation of mutations that underlie the development of human cancer