Research Triangle Park

About: Research Triangle Park is a nonprofit organization based out in Durham, North Carolina, United States. It is known for research contribution in the topics: Population & Environmental exposure. The organization has 24961 authors who have published 35800 publications receiving 1684504 citations. The organization is also known as: RTP.

Isothermal in vitro amplification of DNA by a restriction enzyme/DNA polymerase system.

Abstract: An isothermal in vitro DNA amplification method was developed based upon the following sequence of reaction events. Restriction enzyme cleavage and subsequent heat denaturation of a DNA sample generates two single-stranded target DNA fragments (T1 and T2). Present in excess are two DNA amplification primers (P1 and P2). The 3' end of P1 binds to the 3' end of T1, forming a duplex with 5' overhangs. Likewise, P2 binds to T2. The 5' overhangs of P1 and P2 contain a recognition sequence (5'-GTTGAC-3') for the restriction enzyme HincII. An exonuclease-deficient form of the large fragment of Escherichia coli DNA polymerase I (exo- Klenow polymerase) [Derbyshire, V., Freemont, P. S., Sanderson, M. R., Beese, L., Friedman, J. M., Joyce, C. M. & Steitz, T. A. (1988) Science 240, 199-201] extends the 3' ends of the duplexes using dGTP, dCTP, TTP, and deoxyadenosine 5'-[alpha-thio]triphosphate, which produces hemiphosphorothioate recognition sites on P1.T1 and P2.T2. HincII nicks the unprotected primer strands of the hemiphosphorothioate recognition sites, leaving intact the modified complementary strands. The exo- Klenow polymerase extends the 3' end at the nick on P1.T1 and displaces the downstream strand that is functionally equivalent to T2. Likewise, extension at the nick on P2.T2 results in displacement of a downstream strand functionally equivalent to T1. Nicking and polymerization/displacement steps cycle continuously on P1.T1 and P2.T2 because extension at a nick regenerates a nickable HincII recognition site. Target amplification is exponential because strands displaced from P1.T1 serve as targets for P2 and strands displaced from P2.T2 serve as targets for P1. A 10(6)-fold amplification of a genomic sequence from Mycobacterium tuberculosis or Mycobacterium bovis was achieved in 4 h at 37 degrees C.

Models‐3 Community Multiscale Air Quality (CMAQ) model aerosol component 1. Model description

Abstract: [1] An initial evaluation of the Models-3 Community Multiscale Air Quality (CMAQ) model aerosol component reveals CMAQ's varying ability to simulate observed visibility indices and aerosol species concentrations. The visibility evaluation, using National Weather Service observations from 139 airports for 11–15 July 1995, shows that CMAQ reasonably captured the general spatial and temporal patterns of visibility degradation, including major gradients, maxima and minima. However, CMAQ's two visibility prediction methods, Mie theory approximation and mass reconstruction, both underpredict visibility degradation (i.e., overpredict visibility). The mean bias, normalized mean bias (NMB), mean error and normalized mean error (NME) for the Mie calculations are −5.9 dv, −21.7%, 7.0 dv and 25.4%, respectively. For the reconstruction simulations, these statistics are −9.8 dv, −35.5%, 10.0 dv and 36.2%, respectively. Most simulated values (∼90% Mie and ∼85% reconstruction) fall within a factor of two of the observations, although r2 = 0.25 (Mie) and r2 = 0.24 (reconstruction). The speciated aerosol evaluation uses observations of sulfate, nitrate, PM2.5, PM10 and organic carbon obtained from 18 stations of the Interagency Monitoring of Protected Visual Environments (IMPROVE) network in June 1995. This evaluation reveals that, with the exception of sulfate (mean bias: 0.15 μg/m3, NMB: 3.1%), the model consistently underpredicts aerosol concentrations of nitrate (−0.10 μg/m3, −33.1%), PM2.5 (−3.9 μg/m3, −30.1%), PM10 (−5.66 μg/m3, −29.2%) and organic carbon (−0.78 μg/m3, −33.7%). Sulfate was simulated best by the model (r2 = 0.63, mean error = 1.75 μg/m3, NME = 36.2%), followed by PM2.5 (0.55, 5.00 μg/m3, 38.5%), organic carbon (0.25, 0.94 μg/m3, 40.6%), PM10 (0.13, 9.85 μg/m3, 50.8%) and nitrate (0.01, 0.33 μg/m3, 104.3%). Except for nitrate, 75–80% of simulated concentrations fall within a factor of two of the IMPROVE observations.

Benzothiadiazole induces disease resistance in Arabidopsis by activation of the systemic acquired resistance signal transduction pathway

Abstract: Summary Benzothiadiazole (BTH) is a novel chemical activator of disease resistance in tobacco, wheat and other important agricultural plants. In this report, it is shown that BTH works by activating SAR in Arabidopsis thaliana. BTH-treated plants were resistant to infection by turnip crinkle virus, Pseudomonas syringae pv ‘tomato’ DC3000 and Peronospora parasitica. Chemical treatment induced accumulation of mRNAs from the SAR-associated genes, PR-1, PR-2 and PR-5. BTH treatment induced both PR-1 mRNA accumulation and resistance against P. parasitica in the ethylene response mutants, etr1 and ein2, and in the methyl jasmonate-insensitive mutant, jar1, suggesting that BTH action is independent of these plant hormones. BTH treatment also induced both PR-1 mRNA accumulation and P. parasitica resistance in transgenic Arabidopsis plants expressing the nahG gene, suggesting that BTH action does not require salicylic acid accumulation. However, because BTH-treatment failed to induce either PR-1 mRNA accumulation or P. parasitica resistance in the non-inducible immunity mutant, nim1, it appears that BTH activates the SAR signal transduction pathway.

Cellular senescence promotes adverse effects of chemotherapy and cancer relapse

Abstract: Cellular senescence suppresses cancer by irreversibly arresting cell proliferation. Senescent cells acquire a proinflammatory senescence-associated secretory phenotype. Many genotoxic chemotherapies target proliferating cells nonspecifically, often with adverse reactions. In accord with prior work, we show that several chemotherapeutic drugs induce senescence of primary murine and human cells. Using a transgenic mouse that permits tracking and eliminating senescent cells, we show that therapy-induced senescent (TIS) cells persist and contribute to local and systemic inflammation. Eliminating TIS cells reduced several short- and long-term effects of the drugs, including bone marrow suppression, cardiac dysfunction, cancer recurrence, and physical activity and strength. Consistent with our findings in mice, the risk of chemotherapy-induced fatigue was significantly greater in humans with increased expression of a senescence marker in T cells prior to chemotherapy. These findings suggest that senescent cells can cause certain chemotherapy side effects, providing a new target to reduce the toxicity of anticancer treatments. Significance: Many genotoxic chemotherapies have debilitating side effects and also induce cellular senescence in normal tissues. The senescent cells remain chronically present where they can promote local and systemic inflammation that causes or exacerbates many side effects of the chemotherapy. Cancer Discov; 7(2); 165–76. ©2016 AACR. This article is highlighted in the In This Issue feature, p. 115