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Summary: Following severe injury, biomineralization is disrupted and limited therapeutic options exist to correct these pathologic changes. This study utilized a clinically relevant murine model of polytrauma including a severe injury with concomitant musculoskeletal injuries to identify when bisphosphonate administration can prevent the paradoxical decrease of biomineralization in bone and increased biomineralization in soft tissues, yet not interfere with musculoskeletal repair. Introduction: Systemic and intrinsic mechanisms in bone and soft tissues help promote biomineralization to the skeleton, while preventing it in soft tissues. However, severe injury can disrupt this homeostatic biomineralization tropism, leading to adverse patient outcomes due to a paradoxical decrease of biomineralization in bone and increased biomineralization in soft tissues. There remains a need for therapeutics that restore the natural tropism of biomineralization in severely injured patients. Bisphosphonates can elicit potent effects on biomineralization, though with variable impact on musculoskeletal repair. Thus, a critical clinical question remains as to the optimal time to initiate bisphosphonate therapy in patients following a polytrauma, in which bone and muscle are injured in combination with a severe injury, such as a burn. Methods: To test the hypothesis that the dichotomous effects of bisphosphonates are dependent upon the time of administration relative to the ongoing biomineralization in reparative bone and soft tissues, this study utilized murine models of isolated injury or polytrauma with a severe injury, in conjunction with sensitive, longitudinal measure of musculoskeletal repair. Results: This study demonstrated that if administered at the time of injury, bisphosphonates prevented severe injury-induced bone loss and soft tissue calcification, but did not interfere with bone repair or remodeling. However, if administered between 7 and 21 days post-injury, bisphosphonates temporally and spatially localized to sites of active biomineralization, leading to impaired fracture callus remodeling and permanence of soft tissue calcification. Conclusion: There is a specific pharmacologic window following polytrauma that bisphosphonates can prevent the consequences of dysregulated biomineralization, yet not impair musculoskeletal regeneration. [ABSTRACT FROM AUTHOR]

Natural sensory environments, despite strong potential for structuring systems, have been neglected in ecological theory. Here, we test the hypothesis that intense natural acoustic environments shape animal distributions and behavior by broadcasting whitewater river noise in montane riparian zones for two summers. Additionally, we use spectrally-altered river noise to explicitly test the effects of masking as a mechanism driving patterns. Using data from abundance and activity surveys across 60 locations, over two full breeding seasons, we find that both birds and bats avoid areas with high sound levels, while birds avoid frequencies that overlap with birdsong, and bats avoid higher frequencies more generally. We place 720 clay caterpillars in willows, and find that intense sound levels decrease foraging behavior in birds. For bats, we deploy foraging tests across 144 nights, consisting of robotic insect-wing mimics, and speakers broadcasting bat prey sounds, and find that bats appear to switch hunting strategies from passive listening to aerial hawking as sound levels increase. Natural acoustic environments are an underappreciated niche axis, a conclusion that serves to escalate the urgency of mitigating human-created noise. An experimental study finds that birds and bats avoid whitewater river noise, and that intense noise reduces bird foraging activity and causes bats to switch hunting strategies. Overlap between noise and song frequency predicts bird declines until high levels where other mechanisms appear important. [ABSTRACT FROM AUTHOR]

Rapid urbanization is a key driver of the unique set of health risks facing urban populations. One of the most critical health hazards facing urban women is intimate partner violence (IPV). In post-conflict urban areas, women may face an even greater risk of IPV. Yet, few studies have examined the IPV experiences of urban-dwelling, conflict-affected women, including those who have been internally displaced. This study qualitatively examined the social and structural characteristics of the urban environment that contributed to the IPV experiences of women residing in post-conflict Abidjan, Côte d'Ivoire. Ten focus groups were conducted with men and women, both internally displaced (IDPs) and non-displaced. Lack of support networks, changing gender roles, and tensions between traditional gender norms and those of the "modern" city were reported as key contributors to IPV. Urban poverty and with it unemployment, food insecurity, and housing instability also played a role. Finally, IDPs faced heightened vulnerability to IPV as a result of displacement and discrimination. The relationship between economic strains and IPV are similar to other conflict-affected settings, but Abidjan's urban environment presented other unique characteristics contributing to IPV. Understanding these factors is crucial to designing appropriate services for women and for implementing IPV reduction interventions in urban areas. Strengthening formal and informal mechanisms for help-seeking, utilizing multi-modal interventions that address economic stress and challenge inequitable gender norms, as well as tailoring programs specifically for IDPs, are some considerations for IPV program planning focused on conflict-affected women in urban areas. [ABSTRACT FROM AUTHOR]

Inhibition of spore germination of selected isolates of Cochliobolus carbonum was studied with increasing concentrations of thiram. Isolate differences were detected for the 'TMTD' polymodal curve. This difference was shown to be heritable and independent of tolerance to thiram as indicated by vegetative growth. The polymodal 'TMTD' curve of spore germination inhibition in C. carbonum may result from two (or more) thiram sensitive loci each genetically conditioned independently. [ABSTRACT FROM AUTHOR]

We previously demonstrated that treatments with rIL-1 B accelerated the onset and progression of CIA in mice. In the present study, it was observed that IL-1 also enhanced the development of CIA in rats. Like the mouse model, maximal incidence (80-100%) of arthritis occurred within 7 days after the first treatment with IL-1 in rats. Thus, the acceleration of CIA by IL-1 (IL-1 CIA) may be an improved model for the rapid screening of anti-inflammatory and/or anti-arthritic drugs. As a first step to determining the utility of the IL-1 CIA model as a drug screen, we examined the ability of various known anti-inflammatory and anti-arthritic drugs to modify the IL-1 mediated enhancement of CIA in both rats and mice. The results of these studies showed that when analyzed in the IL-1 CIA model, rats and mice exhibited differences in their responses to several of these drugs. For example, dexamethasone, cyclophosphamide, azathioprine, various non-steroidal anti-inflammatory drugs (NSAIDs) as well as methotrexate were found active in the IL-1 CIA of rats. By contrast, the NSAIDs were found to be less effective in suppressing the IL-1 accelerated disease in mice. In both rats and mice, cyclosporine A and several disease modifying anti-arthritic drugs failed to the prevent the development of CIA that was potentiated by IL-1. Thus, in the IL-1 CIA model NSAIDs appeared to be less active in mice than rats. In conclusion, because of the shorter latent period required for the development of arthritis in the IL-1 treated animals, the IL-1 accelerated CIA model in both mice and rats may be useful for screening anti-inflammatory or anti-arthritic compounds. [ABSTRACT FROM AUTHOR]

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Experiments were conducted in 1969 and 1970 to determine the influence of chemical treatments of seed pieces and soil on the development of Verticillium wilt as measured by tuber yield increases and reduction in severity of tuber defects. The influence of storage on Verticillium-induced tuber defects was evaluated. Seed treatment chemicals tested included zinc ion maneb, maneb, maneb-chloroneb, Polyram, benomyl, and thiabendazole. Soil treatment chemicals included O-Diethyl (O-methyl-sulfinyl) phenyl phosphoro-thioate, disulfoton, phorate, carbofuran, aldicarb, ethyl 4 (methyl- thio)-m-tolyl isopropyl phosphor amidate, benomyl, and thiabendazole. Inoculated seed pieces and artificially infested plot areas were used the first year while the second year natural inoculum from a previous crop was the source of infection. Kennebec and Katahdin cultivars were tested in 1969 and Kennebec alone in 1970. Verticillium-induced yield reductions and tuber defects were more severe in all respects with Kennebec than with Katahdin. With Katahdin the only significant evidence of infection was stem end discoloration. Seed treatments, with the exception of benomyl or thiabendazole, which were erratically phytotoxic, resulted in consistent yield increases and reduction in pink eye severity. In 1969 seed treatment reduced stem end browning in Kennebec. Soil treatment with disulfoton, carbofuran, and aldicarb, both alone and in combination with seed treatments resulted in consistent yield increases with Kennebec. The seed piece and soil treatment combinations tested in 1970 appeared to have an additive effect on yield increase from combination treatments equivalent to the gain from soil treatment alone plus seed treatment alone. The nematicide soil treatment materials did not influence yield. Tuber stem-end browning and pink eye defects in Kennebec did not increase in severity over a five month storage period. [ABSTRACT FROM AUTHOR]