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Riverside, CT, United States

Goodwin College is a private, nonprofit, four-year institution located on One Riverside Drive, East Hartford, Connecticut. The college offers a variety of certificate and associate degree programs along with bachelor degree programs in child study, health science, organizational studies,RN-BSN and the newest public safety. Goodwin College began as Data Institute Business School in 1962. In 2004, the college transitioned to not-for-profit status and was granted accreditation by the New England Association of Schools and Colleges . In 2008, the Connecticut Board of Governors for Higher Education authorized Goodwin College to offer baccalaureate programs.In 2005, Goodwin College initiated a major project to construct a new campus along the Connecticut River in East Hartford. The college had purchased riverfront property that was home to a defunct oil terminal, and took steps to redevelop the site in partnership with state and federal environmental agencies and the Connecticut Development Authority . The site had been designated as a brown field, or contaminated area, by the Environmental Protection Agency, and the college removed 30 large oil storage tanks and conducted soil remediation with the help of state and federal funding. Goodwin College is accredited by the New England Association of Schools and Colleges through its Commission on Institutions of Higher Education. The Goodwin College nursing degree is accredited by the National League for Nursing Accreditation Commission .Connecticut River Academy is located at the same campus as Goodwin College. Wikipedia.

Olson K.R.,Goodwin College | Al-Kaisi M.M.,Iowa State University | Lal R.,Ohio State University | Lowery B.,University of Wisconsin - Madison
Soil Science Society of America Journal | Year: 2014

In agricultural land areas, no-tillage (NT) farming systems have been practiced to replace intensive tillage practices such as, moldboard plow (MP), chisel plow (CP), and other systems to improve many soil health indicators, and specifically to increase soil organic carbon (SOC) sequestration and reduce soil erosion. Numerous approaches to estimate the amounts and rates of SOC sequestration as a result of a switch to NT systems have been published, but there is a concern regarding protocol for assessing SOC especially for different tillage systems. Therefore, the objectives of this paper are to: (i) define and understand concepts of SOC sequestration, (ii) quantify SOC distribution and the methodology of measurements, (iii) address soil spatial variability at field- or landscape-scale for potential SOC sequestration, and (iv) consider proper field experimental design, including pretreatments baseline for SOC sequestration determination. For SOC sequestration to occur, as a result of a treatment applied to a land unit, all of the SOC sequestered must originate from the atmospheric CO2 pool and be transferred into the soil humus through land unit plants, plant residues, and other organic solids. The SOC stock present in soil humus at end of a study must be greater than the pretreatment SOC stock levels in the same land unit. However, one should recognize that a continuity equation showing drawdown in atmospheric concentration of CO2 may be difficult, if not impossible, to quantify. Therefore, SOC sequestration results of paired comparisons of NT to other conventional tillage systems with no pretreatments SOC baseline, and if the conventional system is not at a steady state, will likely be inaccurate where the potential for SOC loss exists in both systems. To unequivocally demonstrate that the SOC sequestration has occurred at a specific site, a temporal increase must be documented relative to pretreatment SOC content and linked attendant changes in soil properties and ecosystem services and functions with proper consideration given to soil spatial variability. Also, a standardized methodology that includes proper experimental design, pretreatment baseline, root zone soil depth consideration, and consistent method of SOC analysis must be used when determining SOC sequestration. © Soil Science Society of America. Source

Tikekar R.V.,University of California at Davis | Tikekar R.V.,Goodwin College | Nitin N.,University of California at Davis
Langmuir | Year: 2012

The oxidative stability of encapsulated product is a critical parameter in many products from food to pharmaceutical to cosmetic industries. The overall objective of this study was to correlate differences in the distribution pattern of encapsulated material within solid lipid nanoparticles (SLNs) and nanostructured lipid carriers (NLCs) with the relative susceptibility of these materials to undergo oxidation. The distribution of an encapsulated lipid soluble dye (Nile Red) in SLNs and NLCs was quantitatively measured using fluorescence imaging. The relative susceptibility of the encapsulated material to react with free radicals generated in the aqueous phase and oxygen from the ambient environment was measured using peroxyl radical and oxygen sensitive fluorescent dyes encapsulated in the lipid phase of colloidal particles respectively. Imaging measurements demonstrate a significant exclusion of the encapsulated dye molecules from the lipid core of SLNs as compared to NLCs. Imaging results also showed significant differences in the intraparticle distribution of encapsulated dye between NLCs containing 1 and 10% liquid lipid. On the basis of these differences in distribution, we hypothesized that the relative susceptibility of encapsulated material to peroxyl radicals and oxygen would be in the order SLNs > 1% NLC > 10% NLC. Measurement of relative susceptibility of peroxyl radical sensitive dye encapsulated in SLNs and NLCs to peroxyl radicals generated in the aqueous phase validated the proposed hypotheses. However, the susceptibility of encapsulated oxygen sensitive dye to ambient oxygen was not significantly different between SLNs and NLCs. The results of this study demonstrate that difference in distribution pattern of encapsulated material within colloidal particles can significantly influence the susceptibility of encapsulated material to react with free radicals. Overall, this study demonstrates a comprehensive approach to characterize the susceptibility of encapsulated materials in colloidal particles to oxidation processes. © 2012 American Chemical Society. Source

Fernhall B.,Goodwin College
European Journal of Applied Physiology | Year: 2011

This study compared the validity of reported equations as predictors of peak VO2 in 8-10-year-old children. Participants (90 boys and girls aged 8-10 years) performed the multistage-shuttle-run-test (MSRT) and peak VO2 was measured in field using a portable gas analyser. The equations that estimated peak VO2 from the MSRT performance were chosen according to the age range of this study. As follows, the FITNESSGRAM reports and the equations of Leger et al. (Can J Appl Sport Sci 5: 77-84, 1988), Barnett et al. (Pediatr Exerc Sci 5:42-50, 1993), Matsuzaka et al. (Pediatr Exerc Sci 16:113-125, 2004) and Fernhall et al. (Am J Ment Retard 102:602-612, 1998) were used to estimate the peak VO2 and compared with the directly measured value. The equation of Leger et al. (Can J Appl Sport Sci 5: 77-84, 1988) provided a mean difference (d) of 4.7 ml kg-1 min -1 and a 1.0 slope. The equation of Matsuzaka et al. (Pediatr Exerc Sci 16:113-125, 2004)(a) using maximal speed (MS) showed a higher d (5.4) than the remaining using total laps d (4.2). The equation of Barnett et al. (Pediatr Exerc Sci 5:42-50, 1993)(a) that includes triceps skinfold and MS showed the highest d (6.1) but the smallest range (24.1) and slope (0.6). Data from the FITNESSGRAM had the smallest d (1.8 ml kg-1 min-1), but also had the highest range between limits of agreement (28.6 ml kg-1 min-1) and a 1.2 slope. The lowest slope (0.4) and range (22.2 ml kg-1 min-1) were observed using the equation of Fernhall et al. (Am J Ment Retard 102:602-612, 1998). Log transformation of the data revealed that the equations of Matsuzaka et al. (Pediatr Exerc Sci 16:113-125, 2004)(a) (1.1*/÷1.25) and Fernhall et al. (Am J Ment Retard 102:602-612, 1998) (1.17*/÷1.25) showed the closest agreement among all, but they still yield unsatisfactory accuracy. © Springer-Verlag 2010. Source

Kumar B.,Rapidsoft Systems, Inc. | Katsinis C.,Goodwin College
2012 IEEE Consumer Communications and Networking Conference, CCNC'2012 | Year: 2012

With the proliferation of digital contents and the expanding variety of connected and IP-enabled consumer electronics (CE) devices, consumers are increasingly seeking ways to efficiently integrate their mobile devices with home networked devices. Expanding wireless coverage is enabling exciting new set of consumer-focused applications between CE devices, mobile handsets, home appliances and personal computers. In this paper, we discuss an architectural framework for mobile device interaction with consumer home network appliances and devices. A number of technological elements such as service discovery, addressing and numbering, control and data transport protocols and security requirements are presented and discussed. A realization of this framework will allow mobile devices to interact with home appliances and other consumer electronic devices in a heterogeneous network from remote locations. © 2012 IEEE. Source

Dasmahapatra G.,Virginia Commonwealth University | Patel H.,Virginia Commonwealth University | Nguyen T.,Virginia Commonwealth University | Attkisson E.,Virginia Commonwealth University | And 2 more authors.
Clinical Cancer Research | Year: 2013

Purpose: To determine whether Polo-like kinase 1 (PLK1) inhibitors (e.g., BI2536) and histone deacetylase (HDAC) inhibitors (e.g., vorinostat) interact synergistically in the BCR/ABL+ leukemia cells sensitive or resistant to imatinib mesylate (IM) in vitro and in vivo. Experimental Design: K562 and LAMA84 cells sensitive or resistant to imatinib mesylate and primary CML cells were exposed to BI2536 and vorinostat. Effects on cell viability and signaling pathways were determined using flow cytometry, Western blotting, and gene transfection. K562 and BV173/E255K animal models were used to test in vivo efficacy. Results: Cotreatment with BI2536 and vorinostat synergistically induced cell death in parental or imatinib mesylate-resistant BCR/ABL + cells and primaryCD34+ bone marrow cells but was minimally toxic to normal cells. BI2536/vorinostat cotreatment triggered pronounced mitochondrial dysfunction, inhibition of p-BCR/ABL, caspase activation, PARP cleavage, reactive oxygen species (ROS) generation, and DNA damage (manifest by increased expression of γH2A.X, p-ATM, p-ATR), events attenuated by the antioxidant TBAP. PLK1 short hairpin RNA (shRNA) knockdown significantly increased HDACI lethality, whereas HDAC1-3 shRNA knockdown reciprocally increased BI2536-induced apoptosis. Genetic interruption of theDNAdamage linker H1.2 partially but significantly reduced PLK1/HDAC inhibitor-mediated cell death, suggesting a functional role for DNA damage in lethality. Finally, BI2536/vorinostat cotreatment dramatically reduced tumor growth in both subcutaneous and systemic BCR/ABL+ leukemia xenograft models and significantly enhanced animal survival. Conclusions: These findings suggest that concomitant PLK1 and HDAC inhibition is active against imatinib mesylate-sensitive or refractory CML and ALL cells both in vitro and in vivo and that this strategy warrants further evaluation in the setting of BCR/ABL+ leukemias. © 2012 AACR. Source

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