Angwin, CA, United States

Pacific Union College

www.puc.edu
Angwin, CA, United States

Pacific Union College is a private liberal arts college located in Napa Valley, California. The campus is located in the upper valley town of Angwin, eight miles north of St. Helena, California and within the Howell Mountain wine appellation. It is the only four-year college in Napa County. A coeducational residential college, it serves an almost exclusively undergraduate student body, the overwhelming majority of which live on campus.PUC maintains full regional accreditation from the Western Association of Schools and Colleges and various programmatic accreditations. It is the only liberal arts college affiliated with the Adventist Church. It was the 12th college or university founded in the state of California. In the fall of 2011, enrollment at Pacific Union College stood at over 1,500 students. Students study a variety of courses offered by the school's 20 academic departments. The school offers over 70 undergraduate majors and one master's program. The campus occupies 150 acres of the college's 1,900 acres in property. Wikipedia.


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News Article | May 2, 2017
Site: www.prweb.com

LearnHowToBecome.org, a leading resource provider for higher education and career information, has evaluated the best colleges and universities in California for 2017. Of the 50 four-year schools who made the list, Stanford University, University of Southern California, California Institute of Technology, University of California Los Angeles and University of California Berkeley came in as the top five. Of the 50 two-year schools ranked, Santa Rosa Junior College, Pasadena City College, Ohlone College, College of San Mateo and Mission College were the top five. A full list of schools is included below. “California offers students some of the highest-quality academic opportunities in the country, and the schools on our list are the best of the best,” said Wes Ricketts, senior vice president of LearnHowToBecome.org. “Not only do these colleges and universities offer outstanding degree programs, they also provide their students with career resources and counseling services that equip them for post-college success.” To be included on the “Best Colleges in California” list, institutions must be regionally accredited, not-for-profit schools. Each college is ranked on additional statistics including the number of degree programs offered, the availability of career and academic resources, the opportunity for financial aid, graduation rates and annual alumni earnings 10 years after entering college. Complete details on each college, their individual scores and the data and methodology used to determine the LearnHowToBecome.org “Best Colleges in California” list, visit: The Best Four-Year Colleges in California for 2017 include: Art Center College of Design Azusa Pacific University California Baptist University California Institute of Technology California Lutheran University California Polytechnic State University-San Luis Obispo California State University-Long Beach Chapman University Claremont McKenna College Concordia University-Irvine Dominican University of California Fresno Pacific University Harvey Mudd College Holy Names University Loma Linda University Loyola Marymount University Mills College Mount Saint Mary's University National University Notre Dame de Namur University Occidental College Pacific Union College Pepperdine University Pitzer College Point Loma Nazarene University Pomona College Saint Mary's College of California San Diego State University San Francisco State University San Jose State University Santa Clara University Scripps College Stanford University University of California-Berkeley University of California-Davis University of California-Irvine University of California-Los Angeles University of California-Riverside University of California-San Diego University of California-Santa Barbara University of California-Santa Cruz University of La Verne University of Redlands University of San Diego University of San Francisco University of Southern California University of the Pacific Westmont College Whittier College Woodbury University The Best Two-Year Colleges in California for 2017 include: Allan Hancock College American River College Bakersfield College Butte College Cabrillo College Canada College Chabot College Chaffey College Citrus College City College of San Francisco College of San Mateo College of the Canyons College of the Siskiyous Contra Costa College Copper Mountain College Crafton Hills College Cuesta College Cypress College De Anza College Diablo Valley College Feather River College Foothill College Fresno City College Las Positas College Lassen Community College Long Beach City College MiraCosta College Mission College Modesto Junior College Monterey Peninsula College Mt. San Antonio College Napa Valley College Ohlone College Orange Coast College Palomar College Pasadena City College Riverside City College Sacramento City College Saddleback College San Bernardino Valley College San Diego Mesa College Santa Ana College Santa Barbara City College Santa Rosa Junior College Shasta College Skyline College Solano Community College Southwestern College West Valley College Yuba College ### About Us: LearnHowtoBecome.org was founded in 2013 to provide data and expert driven information about employment opportunities and the education needed to land the perfect career. Our materials cover a wide range of professions, industries and degree programs, and are designed for people who want to choose, change or advance their careers. We also provide helpful resources and guides that address social issues, financial aid and other special interest in higher education. Information from LearnHowtoBecome.org has proudly been featured by more than 700 educational institutions.


Tsai C.-Y.,Chang Gung University | Wang C.-S.,Chang Gung Memorial Hospital | Tsai M.-M.,Chang Gung University | Chi H.-C.,Chang Gung University | And 7 more authors.
Clinical Cancer Research | Year: 2014

Purpose: The proinflammatory cytokine interleukin-32 (IL-32) is a novel tumor marker highly expressed in various human carcinomas, including gastric cancer. However, its effects on prognosis of patients with gastric cancer and cancer metastasis are virtually unknown at present. The main aim of this study was to explore the clinical significance of IL-32 in gastric cancer and further elucidate the molecular mechanisms underlying IL-32-mediated migration and invasion. Experimental Design: Gastric cancer cells with ectopic expression or silencing of IL-32 were examined to identify downstream molecules and establish their effects on cell motility, invasion, and lung metastasis in vivo. Results: IL-32 was significantly upregulated in gastric cancer and positively correlated with aggressiveness of cancer and poor prognosis. Ectopic expression of IL-32 induced elongated morphology and increased cell migration and invasion via induction of IL-8, VEGF, matrix metalloproteinase 2 (MMP2), and MMP9 expression via phosphor-AKT/phospho-glycogen synthase kinase 3β/active β-catenin as well as hypoxiainducible factor 1α (HIF-1α) signaling pathways. Conversely, depletion of IL-32 in gastric cancer cells reversed these effects and decreased lung colonization in vivo. Examination of gene expression datasets in oncomine and staining of gastric cancer specimens demonstrated the clinical significance of IL-32 and its downstream molecules by providing information on their coexpression patterns. Conclusions: IL-32 contributes to gastric cancer progression by increasing the metastatic potential resulting from AKT, β-catenin, and HIF-1α activation. Our results clearly suggest that IL-32 is an important mediator for gastric cancer metastasis and independent prognostic predictor of gastric cancer. © 2014 AACR.


Huang Y.-H.,Chang Gung Memorial Hospital | Lin Y.-H.,Chang Gung University | Chi H.-C.,Chang Gung University | Liao C.-H.,Chang Gung University | And 10 more authors.
Cancer Research | Year: 2013

Thyroid hormone (T3) signaling through the thyroid hormone receptor (TRα1) regulates hepatoma cell growth and pathophysiology, but the underlying mechanisms are unclear at present. Here, we have shown that the oncomir microRNA-21 (miR-21) is activated by T3 through a native T3 response element in the primary miR-21 promoter. Overexpression of miR-21 promoted hepatoma cell migration and invasion, similar to that observed with T3 stimulation in hepatoma cells. In addition, anti-miR-21-induced suppression of cell migration was rescued by T3. The Rac-controlled regulator of invasion and metastasis, T-cell lymphoma invasion and metastasis 1 (TIAM1), was identified as a miR-21 target additionally downregulated by T3. Attenuation and overexpression of miR-21 induced upregulation and downregulation of TIAM1, respectively. TIAM1 attenuation, in turn, enhanced migration and invasion via the upregulation of β-catenin, vimentin, and matrix metalloproteinase-2 in hepatoma cells. Notably, correlations between TRa1, miR-21, and TIAM1 expression patterns in animal models paralleled those observed in vitro. In the clinic, we observed a positive correlation (P=0.005) between the tumor/nontumor ratios of TRa1 and miR-21 expression, whereas a negative correlation (P = 0.019) was seen between miR-21 and TIAM1 expression in patients with hepatoma. Our findings collectively indicate that miR-21 stimulation by T3 and subsequent TIAM1 suppression promotes hepatoma cell migration and invasion. Cancer Res; 73(8); 2505-17. © 2013 American Association for Cancer Research.


Lin Y.-H.,Chang Gung University | Liao C.-J.,Chang Gung University | Huang Y.-H.,Chang Gung Memorial Hospital | Wu M.-H.,Chang Gung University | And 10 more authors.
Oncogene | Year: 2013

MicroRNAs (miRNAs) are thought to control tumor metastasis through direct interactions with target genes. Thyroid hormone (T 3) and its receptor (TR) are involved in cell growth and cancer progression. However, the issue of whether miRNAs participate in T 3 /TR-mediated tumor migration is yet to be established. In the current study, we demonstrated that T 3 /TR negatively regulates mature miR-17 transcript expression, both in vitro and in vivo. Luciferase reporter and chromatin immunoprecipitation (ChIP) assays localized the regions responding to TR-mediated repression to positions -2234/-2000 of the miR-17 promoter sequence. Overexpression of miR-17 markedly inhibited cell migration and invasion in vitro and in vivo, mediated via suppression of matrix metalloproteinases (MMP)-3. Moreover, p-AKT expression was increased in miR-17-knockdown cells that led to enhanced cell invasion, which was blocked by LY294002. Notably, low miR-17 expression was evident in highly metastatic cells. The cell migration ability was increased by T 3, but partially reduced upon miR-17 overexpression. Notably, TRα1 was frequently upregulated in hepatocellular carcinoma (HCC) samples and associated with low overall survival (P=0.023). miR-17 expression was significantly negatively associated with TRα1 (P=0.033) and MMP3 (P=0.043) in HCC specimens. Data from our study suggest that T 3 /TR, miR-17, p-AKT and MMP3 activities are interlinked in the regulation of cancer cell metastasis. © 2013 Macmillan Publishers Limited.


News Article | February 15, 2017
Site: www.businesswire.com

SANTA CLARA, Calif.--(BUSINESS WIRE)--Green Charge today announced that Pacific Union College will install a 1MW/2MWh commercial energy storage system on its Napa Valley campus. Pacific Union College is expected to save nearly $800,000 dollars over the 10-year agreement with revenues generated through demand charge reduction and demand response programs through Pacific Gas and Electric Company. Pacific Union College is located 70 miles north of San Francisco in the heart of Napa Valley. The campus hosts more than 1,600 undergraduate students and 90 full time professors. The Green Charge energy storage system will also provide resiliency for the College’s cogeneration (cogen) plant. “We see daily the many challenges organizations such as colleges, universities, manufacturers, transit systems, and utility suppliers have from variations in grid-provided power quality,” said Vic Shao, CEO at Green Charge. “Commercial energy storage is a viable solution to provide quality power to our customers located toward the end of distribution lines while providing substantial savings.” “While our main motivation for installing energy storage is saving money through peak demand shaving, we are pleased that energy storage is a way to enhance the reliability and performance of our power supply,” said Dale Withers, the facilities director at Pacific Union College. “We look forward to both benefits as a result of our work with Green Charge.” Controlled by GridSynergy Software, the storage systems are part of a proven industry solution that allow customers to see additional revenues and reduce costs associated with surges in demand. Customized algorithms direct the battery storage systems to discharge enough power to prevent spikes in the amount of energy drawn from the grid. During off-peak hours, the batteries recharge minimizing the cost of covering peaks in demand. Green Charge has been designing and deploying commercial energy storage since 2009, with systems installed throughout the United States. Part of ENGIE, the largest independent power producer in the world, Green Charge’s mission is to use energy storage to power the world efficiently and sustainably. Our team consists of top energy storage industry experts, who provide performance-based solutions to optimize the value of energy for our customers. Our ecosystem of solar, EV charging, and energy efficiency experts allows our customers to combine energy storage and renewables easily and economically. Delivering all these capabilities with the least possible risk is the Green Charge Power Efficiency Agreement—a shared-savings model that puts the power of energy storage in customers’ hands with no capital outlay. Visit www.greencharge.net for more information.


Urbain X.,Catholic University of Leuven | De Ruette N.,Columbia University | Andrianarijaona V.M.,Pacific Union College | Martin M.F.,Pacific Union College | And 5 more authors.
Physical Review Letters | Year: 2013

There is no consensus on the magnitude and shape of the charge transfer cross section in low-energy H++H2 collisions, in spite of the fundamental importance of these collisions. Experiments have thus been carried out in the energy range 15≤E≤5000 eV. The measurements invalidate previous recommended data for E≤200 eV and confirm the existence of a local maximum around 45 eV, which was predicted theoretically. Additionally, vibrationally resolved cross sections allow us to investigate the evolution of the underlying charge transfer mechanism as a function of E. © 2013 American Physical Society.


Wu S.-M.,Chang Gung University | Cheng W.-L.,Chang Gung University | Lin C.D.,Pacific Union College | Lin K.-H.,Chang Gung University
Cellular and Molecular Life Sciences | Year: 2013

The thyroid hormone 3,3′,5-triiodo-l-thyronine (T3) mediates several physiological processes, including embryonic development, cellular differentiation, metabolism, and the regulation of cell proliferation. Thyroid hormone receptors (TRs) generally act as heterodimers with the retinoid X receptor (RXR) to regulate target genes. In addition to their developmental and metabolic functions, TRs have been shown to play a tumor suppressor role, suggesting that their aberrant expression can lead to tumor transformation. Conversely, recent reports have shown an association between overexpression of wild-type TRs and tumor metastasis. Signaling crosstalk between T3/TR and other pathways or specific TR coregulators appear to affect tumor development. Since TR actions are complex as well as cell context-, tissue- and time-specific, aberrant expression of the various TR isoforms has different effects during diverse tumorigenesis. Therefore, elucidation of the T 3/TR signaling mechanisms in cancers should facilitate the identification of novel therapeutic targets. This review provides a summary of recent studies focusing on the role of TRs in hepatocellular carcinomas (HCCs). © 2012 Springer Basel AG.

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