Ecological resilience indicators for salt marsh ecosystems

Salt marshes are coastal ecosystems within the intertidal zone, characterized by hypoxic, saline, soil conditions and low biodiversity. Low diversity arises from frequent disturbance and stressful conditions (i.e., high salinity and hypoxia), where vegetative reproduction and low competition result in mostly monotypic stands, with some differences in plant community influenced by flooding regime (described below). While there are several types of salt marshes in the Northern Gulf of Mexico (NGoM), ranging from low to high salt marshes and salt flats (Tiner, 2013), Spartina alterniflora–dominated salt marshes in the Coastal and Marine Ecological Classification Standard (CMECS) Low and Intermediate Salt Marsh Biotic Group (FGDC, 2012) are the most extensive and are the focus of this project. These salt marshes are classified as “Gulf Coast Cordgrass Salt Marsh” (CEGL004190; USNVC, 2016). Within the NGoM region, some salt marsh areas are dominated by other species such as Spartina patens and Juncus roemerianus, which both occupy higher elevations in high-precipitation zones (e.g., Louisiana, Alabama, Mississippi, and Florida). In lower precipitation regions (southern Texas), hypersaline conditions often develop yielding communities of succulent salt marsh plants (Batis and Salicornia spp.). In climatic zones with warmer winter temperatures, temperate salt marshes naturally transition to mangrove (generally in the southern Gulf of Mexico range) or, in areas with lower precipitation, to salt flats (generally in western part of the study area)

Risk and protective factors at age 10: Psychological adjustment in children with a cleft lip and/or Palate

© Copyright 2016 American Cleft Palate-Craniofacial Association. Objective: To explore psychological functioning in children with a cleft at age 10 from a broad perspective, including cognitive, emotional, behavioral, appearance-related, and social adjustment. High-risk groups were identified within each area of adjustment to investigate whether vulnerable children were found across domains or whether risk was limited to specific areas of adjustment. Methods: Retrospective chart review from psychological assessments at age 10 (N = 845). The effects of gender, cleft visibility, and the presence of an additional condition were investigated. Results were compared with large national samples. Measures: Personality Inventory for Children, Child Experience Questionnaire, Strengths and Difficulties Questionnaire, Satisfaction With Appearance scale. Results: The factor affecting psychological adjustment on most domains was the presence of an associated condition in addition to the cleft. As expected, no support was found for cleft visibility as a risk factor, while there were some gender differences related to emotional difficulties and attention. Correlation analyses of risk groups pointed to an association between social experiences and emotional adjustment and between social and behavioral adjustment; whereas, dissatisfaction with appearance was not related to any other domains of risk at age 10. Conclusions: The results point to the importance of early screening and assessment of children born with a cleft to identify possible associated conditions and offer adapted and appropriate treatment and care. Future research should investigate how protective factors could counteract potential risk in children with a cleft

Tandem E2F Binding Sites in the Promoter of the p107 Cell Cycle Regulator Control p107 Expression and Its Cellular Functions

The retinoblastoma tumor suppressor (Rb) is a potent and ubiquitously expressed cell cycle regulator, but patients with a germline Rb mutation develop a very specific tumor spectrum. This surprising observation raises the possibility that mechanisms that compensate for loss of Rb function are present or activated in many cell types. In particular, p107, a protein related to Rb, has been shown to functionally overlap for loss of Rb in several cellular contexts. To investigate the mechanisms underlying this functional redundancy between Rb and p107 in vivo, we used gene targeting in embryonic stem cells to engineer point mutations in two consensus E2F binding sites in the endogenous p107 promoter. Analysis of normal and mutant cells by gene expression and chromatin immunoprecipitation assays showed that members of the Rb and E2F families directly bound these two sites. Furthermore, we found that these two E2F sites controlled both the repression of p107 in quiescent cells and also its activation in cycling cells, as well as in Rb mutant cells. Cell cycle assays further indicated that activation of p107 transcription during S phase through the two E2F binding sites was critical for controlled cell cycle progression, uncovering a specific role for p107 to slow proliferation in mammalian cells. Direct transcriptional repression of p107 by Rb and E2F family members provides a molecular mechanism for a critical negative feedback loop during cell cycle progression and tumorigenesis. These experiments also suggest novel therapeutic strategies to increase the p107 levels in tumor cells

Evaluation of a health promotion program in children: Study protocol and design of the cluster-randomized Baden-Württemberg primary school study [DRKS-ID: DRKS00000494]

<p>Abstract</p> <p>Background</p> <p>Increasing prevalences of overweight and obesity in children are known problems in industrialized countries. Early prevention is important as overweight and obesity persist over time and are related with health problems later in adulthood. "Komm mit in das gesunde Boot - Grundschule" is a school-based program to promote a healthier lifestyle. Main goals of the intervention are to increase physical activity, decrease the consumption of sugar-sweetened beverages, and to decrease time spent sedentary by promoting active choices for healthy lifestyle. The program to date is distributed by 34 project delivery consultants in the state of Baden-Württemberg and is currently implemented in 427 primary schools. The efficacy of this large scale intervention is examined via the Baden-Württemberg Study.</p> <p>Methods/Design</p> <p>The Baden-Württemberg Study is a prospective, stratified, cluster-randomized, and longitudinal study with two groups (intervention group and control group). Measurements were taken at the beginning of the academic years 2010/2011 and 2011/2012. Efficacy of the intervention is being assessed using three main outcomes: changes in waist circumference, skinfold thickness and 6 minutes run. Stratified cluster-randomization (according to class grade level) was performed for primary schools; pupils, teachers/principals, and parents were investigated. An approximately balanced number of classes in intervention group and control group could be reached by stratified randomization and was maintained at follow-up.</p> <p>Discussion</p> <p>At present, "Komm mit in das Gesunde Boot - Grundschule" is the largest school-based health promotion program in Germany. Comparative objective main outcomes are used for the evaluation of efficacy. Simulations showed sufficient power with the existing sample size. Therefore, the results will show whether the promotion of a healthier lifestyle in primary school children is possible using a relatively low effort within a school-based program involving children, teachers and parents. The research team anticipates that not only efficacy will be proven in this study but also expects many other positive effects of the program.</p> <p>Trial registration</p> <p>German Clinical Trials Register (DRKS), DRKS-ID: DRKS00000494</p

Critical Role of the Rb Family in Myoblast Survival and Fusion

The tumor suppressor Rb is thought to control cell proliferation, survival and differentiation. We recently showed that differentiating Rb-deficient mouse myoblasts can fuse to form short myotubes that quickly collapse through a mechanism involving autophagy, and that autophagy inhibitors or hypoxia could rescue the defect leading to long, twitching myotubes. Here we determined the contribution of pRb relatives, p107 and p130, to this process. We show that chronic or acute inactivation of Rb plus p107 or p130 increased myoblast cell death and reduced myotube formation relative to Rb loss alone. Treatment with autophagy antagonists or hypoxia extended survival of double-knockout myotubes, which appeared indistinguishable from control fibers. In contrast, triple mutations in Rb, p107 and p130, led to substantial increase in myoblast death and to elongated bi-nuclear myocytes, which seem to derive from nuclear duplication, as opposed to cell fusion. Under hypoxia, some rare, abnormally thin triple knockout myotubes survived and twitched. Thus, mutation of p107 or p130 reduces survival of Rb-deficient myoblasts during differentiation but does not preclude myoblast fusion or necessitate myotube degeneration, whereas combined inactivation of the entire Rb family produces a distinct phenotype, with drastically impaired myoblast fusion and survival

Functional Interactions between Retinoblastoma and c-MYC in a Mouse Model of Hepatocellular Carcinoma

Inactivation of the RB tumor suppressor and activation of the MYC family of oncogenes are frequent events in a large spectrum of human cancers. Loss of RB function and MYC activation are thought to control both overlapping and distinct cellular processes during cell cycle progression. However, how these two major cancer genes functionally interact during tumorigenesis is still unclear. Here, we sought to test whether loss of RB function would affect cancer development in a mouse model of c-MYC-induced hepatocellular carcinoma (HCC), a deadly cancer type in which RB is frequently inactivated and c-MYC often activated. We found that RB inactivation has minimal effects on the cell cycle, cell death, and differentiation features of liver tumors driven by increased levels of c-MYC. However, combined loss of RB and activation of c-MYC led to an increase in polyploidy in mature hepatocytes before the development of tumors. There was a trend for decreased survival in double mutant animals compared to mice developing c-MYC-induced tumors. Thus, loss of RB function does not provide a proliferative advantage to c-MYC-expressing HCC cells but the RB and c-MYC pathways may cooperate to control the polyploidy of mature hepatocytes