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[This corrects the article DOI: 10.1371/journal.pone.0050281.].

OBJECTIVES/GOALS: Our goal is to explore and collaboratively identify the team science competencies essential for Clinical Research Professionals at all experience levels and how these competencies relate to the Joint Task Force for Clinical Translational Research Professionals Competencies. METHODS/STUDY POPULATION: Team science competencies for clinical research professionals are poorly defined. The JTF Clinical Trial Competencies lack sufficient emphasis on team science, though it is briefly included in two JTF competency domains: Leadership & Professionalism, and Communication & Teamwork. The competencies primarily focus on tasks related to clinical research and basic knowledge of product development; however, a conceptual model for applying the competencies using a team science lens is needed. Currently, the JTF competency figure is often thought of as sequential, given the competencies are numbered, creating the misconception that the last competencies are less important. We support a new figure showing the permeability of team science across competencies and the connectedness and equality of the competencies. RESULTS/ANTICIPATED RESULTS: Our anticipated results are to show the integral nature of team science in clinical research professional communities of practice. Once complete, we will have identified measurable team science competency-based skills essential for clinical research professionals at various levels of expertise. Understanding the multi-dimensional team science competencies will inform targeted team science education and training for clinical research professionals. Our revised competency framework provides an improved team science conceptual model for clinical translational science. DISCUSSION/SIGNIFICANCE: Our work will define team science competencies as related to clinical research professionals at all experience levels. The interdependence of teams across clinical trial activities necessitates a consideration of an improved conceptual framework for clinical translational team science competencies.

Versa sobre o campo da sociologia rural. Dividido em: Ênfase na pesquisa; Tendências dos métodos de estudo; Alteração de método; Estudos de Grupos; Estudo sobre a população; Problemas a serem resolvidos.

Background and Objective: Type I diabetes is a chronic disorder of pancreas. This disorder occurs as a result of autoimmune destruction of insulin producing beta-cells. Long duration before the onset of clinical symptoms, the autoimmune reactions develop. Therefore, a molecular marker to indicate the initiation of immunological reaction is very critical to identify the people at risk and to take appropriate measures. Since Hsp60 is an antigen involved in the pathogenesis of type I diabetes, this investigation was conducted on detecting anti Hsp60 antibody in various immunoglobulin classes and sub-classes. Methods: In this study 49 recently manifested type I diabetes patients (50 normal control subjects, 23 individuals with high and 22 with low risk for type I diabetes, as deduced from islet antibody status) were included. Seventeen recently manifested type I patients and 15 normal control subjects were analyzed twice with a three-month interval. The serum samples of patients and normal subjects were collected and stored at 20°C until measurement time. Total anti human Hsp60 antibody was determined in serum samples by ELISA, positive sera were analyzed for IgG or IgA antibody as well as for IgG1 and IgG4 sub-classes by ELISA. Findings: The mean concentration of total anti Hsp60 antibody in recently manifested patients and normal subjects were 182.8±218.5 and 142.5±146.6 Au/ml, respectively (P>0.05). Anti Hsp60 antibody concentration means in type I diabetes relative at high risk and relatives at low risk were 83.6 and 133.4 Au/ml, respectively. There was a significant difference between these two mean values. However, the difference between these two values and mean concentration of total anti Hsp60 antibody in normal subjects was not significant. Moreover, the mean of antibody levels determined for IgG, IgA, IgG1 and IgG4 to be considered statistically significant. Conclusion: According to the results, there is significant spontaneous humoral immunity to autologous Hsp60 without detectable association to type I diabetes.

Al-Zn-Mg-Cu alloys are widely used in aircraft applications because of their superior mechanical properties and strength/weight ratios. Commercial Al-Zn-Mg-Cu alloys have been intensively studied over the last few decades. However, well-considered thermodynamic calculations, via the CALPHAD approach, on a variation of alloying elements can guide the fine-tuning of known alloy systems and the development of optimized heat treatments. In this study, a comparison was made of the solidus temperatures of different Al-Zn-Mg-Cu alloys determined from thermodynamic predictions and differential scanning calorimetry (DSC) measurements. A variation of the main alloying elements Zn, Mg, and Cu generated 38 experimentally produced alloys. An experimental determination of the solidus temperature via DSC was carried out according to a user-defined method, because the broad melting interval present in Al-Zn-Mg-Cu alloys does not allow the use of the classical onset method for pure substances. The software algorithms implemented in FactSage®, Pandat™, and MatCalc with corresponding commercially available databases were deployed for thermodynamic predictions. Based on these investigations, the predictive power of the commercially available CALPHAD databases and software packages was critically reviewed.

Topo II poisons, which target topoisomerase II (topo II) to generate enzyme mediated DNA damage, have been commonly used for anti-cancer treatment. While clinical evidence demonstrate a capability of topo II poisons in inducing apoptosis in cancer cells, accumulating evidence also show that topo II poison treatment frequently results in cell cycle arrest in cancer cells, which was associated with subsequent resistance to these treatments. Results in this report indicate that treatment of MCF-7 and T47D breast cancer cells with topo II poisons resulted in an increased phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and an subsequent induction of G2/M cell cycle arrest. Furthermore, inhibition of ERK1/2 activation using specific inhibitors markedly attenuated the topo II poison-induced G2/M arrest and diminished the topo II poison-induced activation of ATR and Chk1 kinases. Moreover, decreased expression of ATR by specific shRNA diminished topo II poison-induced G2/M arrest but had no effect on topo II poison-induced ERK1/2 activation. In contrast, inhibition of ERK1/2 signaling had little, if any, effect on topo II poison-induced ATM activation. In addition, ATM inhibition by either incubation of cells with ATM specific inhibitor or transfection of cells with ATM specific siRNA did not block topo II poison-induced G2/M arrest. Ultimately, inhibition of ERK1/2 signaling greatly enhanced topo II poison-induced apoptosis. These results implicate a critical role for ERK1/2 signaling in the activation of G2/M checkpoint response following topo II poison treatment, which protects cells from topo II poison-induced apoptosis.