Fish and Invertebrate Use of Restored vs. Natural Oyster Reefs in a Shallow Temperate Latitude Estuary

Coastal marine habitats continue to be degraded, thereby compelling largescale restoration in many parts of the world. Whether restored habitats function similarly to natural habitats and fully recover lost ecosystem services is unclear. In estuaries, oyster reefs have been degraded by multiple anthropogenic activities including destructive fishing practices and reduced water quality, motivating restoration to maintain oyster fisheries and other ecosystem services, often at relatively high cost. We compared fish and invertebrate communities on recently restored (0–1 year post-restoration), older restored (3–4 years post-restoration), and natural oyster reefs to determine if and when restored reefs support functionally similar faunal communities. To test the influence of landscape setting on the faunal communities, the restored and natural reefs, as well as a control without reef present, were distributed among three landscapes (on the edge of salt marsh away from seagrass [salt marsh landscape], on mudflats [mudflat landscape], and near to seagrass and salt marsh [seagrass landscape]). Oyster density and biomass were greatest on restored reef habitat, as were those of non-oyster bivalve species. Total abundance of invertebrates was much greater on oyster reefs than in control plots, regardless of reef or landscape type, yet were frequently highest on older restored reefs. Meanwhile, juvenile fish densities were greatest on natural reefs, at intermediate densities on older restored reefs, and least abundant on controls. When comparing the effects of reef age and landscape setting, juvenile fish densities were greatest on younger reefs within the mudflat landscape. Collectively, these results indicate that oyster reefs harbor higher densities of resident invertebrate prey, which may explain why reef habitat is also important for juvenile fish. Laboratory and field experiments supported the notion that gag grouper (a predatory demersal fish) forage more effectively on oyster reefs than on unstructured mud bottom, whereas our experiments suggest that flounders that utilize oyster reefs likely forage on adjacent mud bottom. Because landscape setting influenced fish and invertebrate communities on restored reefs, the ecological consequences of landscape setting should be incorporated into restoration decision making and site selection to enhance the recovery of ecosystem goods and services

Biotic resistance to invasion along an estuarine gradient

Biotic resistance is the ability of native communities to repel the establishment of invasive species. Predation by native species may confer biotic resistance to communities, but the environmental context under which this form of biotic resistance occurs is not well understood. We evaluated several factors that influence the distribution of invasive Asian mussels (Musculista senhousia) in Mission Bay, a southern California estuary containing an extensive eelgrass (Zostera marina) habitat. Asian mussels exhibit a distinct spatial pattern of invasion, with extremely high densities towards the back of Mission Bay (up to 4,000 m−2) in contrast with near-complete absence at sites towards the front of the bay. We established that recruits arrived at sites where adult mussels were absent and found that dense eelgrass does not appear to preclude Asian mussel growth and survival. Mussel survival and growth were high in predator-exclusion plots throughout the bay, but mussel survival was low in the front of the bay when plots were open to predators. Additional experiments revealed that consumption by spiny lobsters (Panulirus interruptus) and a gastropod (Pteropurpura festiva) likely are the primary factors responsible for resistance to Asian mussel invasion. However, biotic resistance was dependent on location within the estuary (for both species) and also on the availability of a hard substratum (for P. festiva). Our findings indicate that biotic resistance in the form of predation may be conferred by higher order predators, but that the strength of resistance may strongly vary across estuarine gradients and depend on the nature of the locally available habitat

Interaction among apoptosis-associated sequence variants and joint effects on aggressive prostate cancer

<p>Abstract</p> <p>Background</p> <p>Molecular and epidemiological evidence demonstrate that altered gene expression and single nucleotide polymorphisms in the apoptotic pathway are linked to many cancers. Yet, few studies emphasize the interaction of variant apoptotic genes and their joint modifying effects on prostate cancer (PCA) outcomes. An exhaustive assessment of all the possible two-, three- and four-way gene-gene interactions is computationally burdensome. This statistical conundrum stems from the prohibitive amount of data needed to account for multiple hypothesis testing.</p> <p>Methods</p> <p>To address this issue, we systematically prioritized and evaluated individual effects and complex interactions among 172 apoptotic SNPs in relation to PCA risk and aggressive disease (i.e., Gleason score ≥ 7 and tumor stages III/IV). Single and joint modifying effects on PCA outcomes among European-American men were analyzed using statistical epistasis networks coupled with multi-factor dimensionality reduction (SEN-guided MDR). The case-control study design included 1,175 incident PCA cases and 1,111 controls from the prostate, lung, colo-rectal, and ovarian (PLCO) cancer screening trial. Moreover, a subset analysis of PCA cases consisted of 688 aggressive and 488 non-aggressive PCA cases. SNP profiles were obtained using the NCI Cancer Genetic Markers of Susceptibility (CGEMS) data portal. Main effects were assessed using logistic regression (LR) models. Prior to modeling interactions, SEN was used to pre-process our genetic data. SEN used network science to reduce our analysis from > 36 million to < 13,000 SNP interactions. Interactions were visualized, evaluated, and validated using entropy-based MDR. All parametric and non-parametric models were adjusted for age, family history of PCA, and multiple hypothesis testing.</p> <p>Results</p> <p>Following LR modeling, eleven and thirteen sequence variants were associated with PCA risk and aggressive disease, respectively. However, none of these markers remained significant after we adjusted for multiple comparisons. Nevertheless, we detected a modest synergistic interaction between <it>AKT3 rs2125230-PRKCQ rs571715 </it>and disease aggressiveness using SEN-guided MDR (p = 0.011).</p> <p>Conclusions</p> <p>In summary, entropy-based SEN-guided MDR facilitated the logical prioritization and evaluation of apoptotic SNPs in relation to aggressive PCA. The suggestive interaction between <it>AKT3-PRKCQ </it>and aggressive PCA requires further validation using independent observational studies.</p

Chemokine Ligand 5 (CCL5) and chemokine receptor (CCR5) genetic variants and prostate cancer risk among men of African Descent: a case-control study

<p>Abstract</p> <p>Background</p> <p>Chemokine and chemokine receptors play an essential role in tumorigenesis. Although chemokine-associated single nucleotide polymorphisms (SNPs) are associated with various cancers, their impact on prostate cancer (PCA) among men of African descent is unknown. Consequently, this study evaluated 43 chemokine-associated SNPs in relation to PCA risk. We hypothesized inheritance of variant chemokine-associated alleles may lead to alterations in PCA susceptibility, presumably due to variations in antitumor immune responses.</p> <p>Methods</p> <p>Sequence variants were evaluated in germ-line DNA samples from 814 African-American and Jamaican men (279 PCA cases and 535 controls) using Illumina’s Goldengate genotyping system.</p> <p>Results</p> <p>Inheritance of <it>CCL5</it> rs2107538 (AA, GA+AA) and rs3817655 (AA, AG, AG+AA) genotypes were linked with a 34-48% reduction in PCA risk. Additionally, the recessive and dominant models for <it>CCR5</it> rs1799988 and <it>CCR7</it> rs3136685 were associated with a 1.52-1.73 fold increase in PCA risk. Upon stratification, only <it>CCL5</it> rs3817655 and <it>CCR7</it> rs3136685 remained significant for the Jamaican and U.S. subgroups, respectively.</p> <p>Conclusions</p> <p>In summary, <it>CCL5</it> (rs2107538, rs3817655) and <it>CCR5</it> (rs1799988) sequence variants significantly modified PCA susceptibility among men of African descent, even after adjusting for age and multiple comparisons. Our findings are only suggestive and require further evaluation and validation in relation to prostate cancer risk and ultimately disease progression, biochemical/disease recurrence and mortality in larger high-risk subgroups. Such efforts will help to identify genetic markers capable of explaining disproportionately high prostate cancer incidence, mortality, and morbidity rates among men of African descent.</p