Xaverian Brothers High School

Westwood, MA, United States

Xaverian Brothers High School

Westwood, MA, United States

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Of the Xaverian Brothers High School project, Ms. Doyle said, "The school is securing its power prices on a long-term basis and has already begun generating clean, renewable energy, achieving greater energy independence now and in the future. A system of this size will generate over 9,410,450 kilowatt hours (kWhs) over its lifetime of 25 years. That is equal to avoiding the emission of 6,613 metric tons of carbon dioxide, or the burning of 744,170 gallons of gasoline. Brother Daniel Skala, Headmaster of Xaverian Brothers High School, is excited about the newly installed solar array. His enthusiasm stems from the fact that his institution is reducing its carbon footprint and demonstrating leadership in sustainability. By installing a solar array on the rooftop of their esteemed institution, Brother Dan and the trustees of Xaverian Brothers High School are keeping with the recent comments of Pope Francis regarding the environment and how The Holy Father wants our planet's inhabitants to 'care for our common home'.  Brother Dan would like to implement a program to educate the 950 students currently enrolled in the school on the daily environmental benefits of the solar array. The Xaverian Brothers High School solar array is net metered and interconnected to the grid, generating renewable power with an estimated annual market value of over $152,000.  Additionally, the sale of Solar Renewable Energy Certificates (SRECs), created by the state to help incentivize solar development in Massachusetts, will generate income to help finance the system for the high school. MassAmerican Energy, the installation vendor for this project, is a leading full-service solar energy provider.  MassAmerican was a key player in the design and installation of the new solar array, completing this project on time and on budget. FireFlower Alternative Energy helps businesses profitably invest in America's energy independence.  With a focus on the numbers, FireFlower invests in and develops renewable energy in the Northeast and can help site owners, commercial energy users, and the financial community collaborate to get real projects built.  For more information about FireFlower Alternative Energy, visit http://www.fireflower-ae.com. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/fireflower-alternative-energy-and-xaverian-brothers-high-school-complete-solar-development-300448702.html


Sun L.,Sun Yat Sen University | Liu B.,Sun Yat Sen University | Lin Z.,Sun Yat Sen University | Yao Y.,Sun Yat Sen University | And 12 more authors.
Molecular Cancer | Year: 2015

Background: Salivary Adenoid cystic carcinoma (SACC) patients with local invasion and lung metastasis are often resistant to conventional therapy such as operation, chemotherapy and radiotherapy. To explore the underling mechanisms, we studied the roles of miRNA in regulating invasiveness of SACC cells. Methods: MicroRNA profiling was done in SACC cells with microarray. MiRNA mimics or antisense oligonucleotide was transfected and invasiveness of SACC cells was evaluated by adhesion assay and transwell assay. The target gene of miRNA was identified by luciferase reporter assay and "rescue" experiment. Tumor metastasis was evaluated by BALB/c-nu mice xenografts. MiRNA and its target gene expression were identified by in-situ hybridization and immunohistochemistry respectively, in 302 patients from affiliated hospitals of Sun Yat-sen University and in 148 patients from affiliated hospitals of Central South University, and correlated to the clinicopathological status of the patients. Results: MiR-320a was down-regulated in high lung metastatic ACCM and SACC-LM cells compared with the corresponding low metastatic ACC2 and SACC-83 cells, and inhibited adhesion, invasion and migration of SACC cells by targeting integrin beta 3 (ITGB3). In vivo, enforced miR-320a expression suppressed metastasis of SACC xenografts. In the two independent sets, miR-320a was downregulated in primary SACCs with metastasis compared to those without metastasis, and low expression of this miRNA predicts poor patient survival and rapid metastasis. Multivariate analysis showed that miR-320a expression was an independent indicator of lung metastasis. Conclusions: MiR-320a inhibits metastasis in SACCs by targeting ITGB3 and may serve as a therapeutic target and prognostic marker in salivary cancers. © 2015 Sun et al.; licensee BioMed Central.


Sun L.,Sun Yat Sen University | Liu B.,Sun Yat Sen University | Lin Z.,Sun Yat Sen University | Yao Y.,Sun Yat Sen University | And 12 more authors.
Molecular Cancer | Year: 2015

Background: Salivary Adenoid cystic carcinoma (SACC) patients with local invasion and lung metastasis are often resistant to conventional therapy such as operation, chemotherapy and radiotherapy. To explore the underling mechanisms, we studied the roles of miRNA in regulating invasiveness of SACC cells. Methods: MicroRNA profiling was done in SACC cells with microarray. MiRNA mimics or antisense oligonucleotide was transfected and invasiveness of SACC cells was evaluated by adhesion assay and transwell assay. The target gene of miRNA was identified by luciferase reporter assay and "rescue" experiment. Tumor metastasis was evaluated by BALB/c-nu mice xenografts. MiRNA and its target gene expression were identified by in-situ hybridization and immunohistochemistry respectively, in 302 patients from affiliated hospitals of Sun Yat-sen University and in 148 patients from affiliated hospitals of Central South University, and correlated to the clinicopathological status of the patients. Results: MiR-320a was down-regulated in high lung metastatic ACCM and SACC-LM cells compared with the corresponding low metastatic ACC2 and SACC-83 cells, and inhibited adhesion, invasion and migration of SACC cells by targeting integrin beta 3 (ITGB3). In vivo, enforced miR-320a expression suppressed metastasis of SACC xenografts. In the two independent sets, miR-320a was downregulated in primary SACCs with metastasis compared to those without metastasis, and low expression of this miRNA predicts poor patient survival and rapid metastasis. Multivariate analysis showed that miR-320a expression was an independent indicator of lung metastasis. Conclusions: MiR-320a inhibits metastasis in SACCs by targeting ITGB3 and may serve as a therapeutic target and prognostic marker in salivary cancers. © 2015 Sun et al.


Lin Z.,Sun Yat Sen University | Sun L.,Sun Yat Sen University | Chen W.,Sun Yat Sen University | Liu B.,Sun Yat Sen University | And 4 more authors.
Cancer Science | Year: 2014

Epithelial-to-mesenchymal transition (EMT) is implicated in embryonic development and various pathological events. Transforming growth factor beta (TGFβ) has been reported to induce EMT in tumor cells, which is a critical step in the process of metastasis leading to cancer spreading and treatment failure. However, the involvement of microRNA during the EMT process in tongue squamous cell carcinoma (TSCC) remains to be determined. To address this question, TSCC cell lines SCC9 and CAL27 were treated with human recombinant TGFβ1 for 48 h. miRNA microarray illustrated that miR-639 was significantly downregulated in TGFβ-treated SCC9 cells. Ectopic expression of miR-639 with miRNA mimics effectively blocked TGFβ-induced EMT in SCC9 and CAL27 cells, but inhibition of miR-639 in SCC9 and CAL27 cells with antisense oligonucleotides induced EMT. Computational microRNA target predictions detected a conserved sequence matching to the seed region of miR-639 in the 3′-UTR of FOXC1 mRNA. Luciferase reporter assays revealed that miR-639 targets FOXC1. Ectopic expression of FOXC1 induces EMT in TSCC cells. Silencing FOXC1 expression blocked TGFβ-induced EMT in SCC9 cells. Clinically, reduced miR-639 expression was associated with metastasis in TSCC and poor patient survival. The data from the present study suggest that reduced expression of miR-639 underscores the mechanism of TGFβ-induced EMT in TSCC by targeting FOXC1 and may serve as therapeutic targets in the process of metastasis. © 2014 The Authors.


Fan S.,Sun Yat Sen University | Chen W.-X.,Sun Yat Sen University | Lv X.-B.,Sun Yat Sen University | Tang Q.-L.,Sun Yat Sen University | And 13 more authors.
Cancer Letters | Year: 2015

Mitochondria play an important role in the initiation of apoptosis. However, whether cisplatin can induce apoptosis by initiating a mitochondrial fission pathway and the mechanism underlying this effect remain poorly understood. In this study, we show that the mitochondrial fission protein FIS1 is upregulated upon cisplatin treatment in tongue squamous cell carcinoma (TSCC) cells. FIS1 knockdown can attenuate mitochondrial fission and cisplatin sensitivity. We found that FIS1 is a direct target of miR-483-5p and that miR-483-5p can inhibit mitochondrial fission and cisplatin sensitivity in vitro and in vivo. Furthermore, we found that miR-483-5p and FIS1 are significantly associated with cisplatin sensitivity and with overall survival in patients with TSCC in a retrospective analysis of multiple centers. This study revealed that a novel mitochondrial fission pathway composed of miR-483-5p and FIS1 regulates cisplatin sensitivity. The modulation of miR-483-5p and FIS1 levels may provide a new approach for increasing cisplatin sensitivity. © 2015 Elsevier Ireland Ltd.


Fan S.,Sun Yat Sen University | Liu B.,Sun Yat Sen University | Sun L.,Sun Yat Sen University | Lv X.,Sun Yat Sen University | And 24 more authors.
Oncotarget | Year: 2015

Cisplatin has been widely employed as a cornerstone chemotherapy treatment for a wide spectrum of solid neoplasms; increasing tumor responsiveness to cisplatin has been a topic of interest for the past 30 years. Strong evidence has indicated that mitochondrial fission participates in the regulation of apoptosis in many diseases; however, whether mitochondrial fission regulates cisplatin sensitivity remains poorly understood. Here, we show that MFF mediated mitochondrial fission and apoptosis in tongue squamous cell carcinoma (TSCC) cells after cisplatin treatment and that miR-593-5p was downregulated in this process. miR-593-5p attenuated mitochondrial fission and cisplatin sensitivity by targeting the 3' untranslated region sequence of MFF and inhibiting its translation. In exploring the underlying mechanism of miR-593-5p downregulation, we observed that BRCA1 transactivated miR-593-5p expression and attenuated cisplatin sensitivity in vitro. The BRCA1-miR-593-5p-MFF axis also affected cisplatin sensitivity in vivo. Importantly, in a retrospective analysis of multiple centers, we further found that the BRCA1-miR-593-5p-MFF axis was significantly associated with cisplatin sensitivity and the survival of patients with TSCC. Together, our data reveal a model for mitochondrial fission regulation at the transcriptional and post-transcriptional levels; we also reveal a new pathway for BRCA1 in determining cisplatin sensitivity through the mitochondrial fission program.


PubMed | Xaverian Brothers High School, North Sichuan Medical College, Sun Yat Sen University and University of Sichuan
Type: Journal Article | Journal: Cancer letters | Year: 2015

Mitochondria play an important role in the initiation of apoptosis. However, whether cisplatin can induce apoptosis by initiating a mitochondrial fission pathway and the mechanism underlying this effect remain poorly understood. In this study, we show that the mitochondrial fission protein FIS1 is upregulated upon cisplatin treatment in tongue squamous cell carcinoma (TSCC) cells. FIS1 knockdown can attenuate mitochondrial fission and cisplatin sensitivity. We found that FIS1 is a direct target of miR-483-5p and that miR-483-5p can inhibit mitochondrial fission and cisplatin sensitivity in vitro and in vivo. Furthermore, we found that miR-483-5p and FIS1 are significantly associated with cisplatin sensitivity and with overall survival in patients with TSCC in a retrospective analysis of multiple centers. This study revealed that a novel mitochondrial fission pathway composed of miR-483-5p and FIS1 regulates cisplatin sensitivity. The modulation of miR-483-5p and FIS1 levels may provide a new approach for increasing cisplatin sensitivity.

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