The demand for high performance “green” or “sustainable” buildings is rapidly becoming the most significant trend in the building industry. As the Architecture, Engineering, and Construction (AEC) industry develops the strategies and technologies for these projects, an increased emphasis must be placed on the processes and competencies required to deliver high performance buildings. This paper defines an emerging research and education program at Penn State called the Lean and Green Initiative. Focused on understanding all aspects of the delivery of high performance projects, this program is underpinned by established process-based theories and structured around a systematic methodology designed to minimize waste, maximize value, and reduce cost. Current research and educational activities are described in the paper including nine primary research thrusts and their respective goals. Initial results of each research thrust are also provided, providing an early look at the benefits of a process improvement approach to the delivery of high performance buildings.
Background miR-429 and TLN1 have been shown to affect the biological behaviours of many carcinomas. However, their effects in nasopharyngeal carcinoma (NPC) are not yet clear. Here, we investigated their regulatory relationships and effects on NPC cells. Methods TargetScan was used to predict the regulatory relationships of miR-429 and TLN1 in NPC cells. Then, Western blotting and quantitative real-time PCR (qPCR) were performed to examine TLN1 levels, and qPCR was used to determine miR-429 levels in NPC cell lines with different metastatic characteristics (5-8F, CNE-2, CNE-1, 6-10B and NP69), to investigate whether TLN1 and miR-429 are correlated with the metastatic characteristics of these cells. Next, we upregulated or downregulated miR-429 in 5-8F and 6-10B cells, which have different tumourigenicity and transferability, and examined TLN1 expression by western blotting and qPCR after transfection. QPCR was also performed to confirm successful transfection of miR-429 mimic into 5-8F and 6-10B cells. Dual luciferase reporter gene assay was performed to investigate whether miR-429 regulates TLN1 by binding to its 3′UTR. After transfection, Cell Counting Kit-8 (CCK8) and IncuCyte were used to examine the proliferation of these cells, and wound-healing assay, Transwell migration assay, and invasion assays were performed to investigate the changes in migration and invasion after transfection. Results Western blotting and qPCR analyses showed that the protein level of TLN1 was negatively correlated with miR-429 in NPC cell lines ( P < 0.05), while the mRNA level showed no relation with miR429 expression ( P > 0.05). In addition, cells with high transferability showed high TLN1 expression at the protein level, while miR429 expression showed the opposite trend ( P < 0.05), but there were no differences at the mRNA level between the different cell lines. Overexpression of miR429 in 5-8F and 6-10B cells was accompanied by downregulation of TLN1 at the protein level ( P < 0.05), while there were no significant differences at the mRNA level ( P > 0.05). In addition, transferability, proliferation, and invasion were downregulated by miR429 overexpression ( P < 0.05). However, dual-luciferase reporter gene assay indicated that TLN1 was not a direct target of miR-429. Conclusion This study showed that miR-429 functions as a tumour suppressor in NPC by downregulation of TLN1, although the relationship is not direct.
Background: Acquired resistance is a challenge for epidermal growth factor receptor (EGFR) mutant nonsmall cell lung cancer. Here, we propose a novel treatment strategy based on recent lipid metabolism work. Methods:We applied a variety of experimental methods such as immunoblotting, MTT, si-RNA, and animal models, to demonstrate the relationship between EGFR and low-density lipoprotein receptor (LDLR) and the effects of statin monotherapy, and TKI monotherapy, and their combination on cell proliferation at the cell level and animal level.Results: LDLR has a positive correlation with EGFR, EGFR signaling upregulates LDLR expression through the SREBP-1 dependent pathway, EGFR mutation cells count on lipids to survive and grow.Combined with a molecule-targeted drug, atorvastatin not only enhances the treatment effect in vitro, but also mitigates the growth of NSCLC in vivo. In this animal experiment, the combination medicine (atorvastatin with TKI) has a better tumor suppression effect on NSCLC. In HCC827 cell line, the average tumor shrinkage is about 68% in Gefitinib group, and about 49% in atorvastatin group, but about 89% in combination group. In H1975 cell line, the average tumor shrinkage is about 18% in Osimertinib group, and about 8% in atorvastatin group, but about 44% in combination group.Conclusions: the combination of an EGFR-TKI and a statin for EGFR mutant NSCLC may be a novel tumor inhibiting treatment.
We used the atomic force microscope to determine the distributions of 150–200 nm diameter styrene-butadiene (SB) latex spheres with TR. = 45 °C deposited at sub monolayer coverages from water suspensions onto mica, glass, calcite and cellophane surfaces. Two deposition methods are used: drying of μl drops and dipping. For drop drying, the distributions are extremely inhomogeneous. A high density ring forms at the boundary of the area wet by the drop. At low suspension densities on cellophane, the ring is a close-packed monolayer several micrometers wide. Thicker rings form on calcite and glass. Inside the rings, the particle density is very low and non uniform; e.g., monolayer thick islands form on mica, short chains are predominant on calcite, small clusters form on glass, and isolated spheres occur on cellophane. Particle densities are substantially reduced near some substrate defects but are enhanced near others. For the dipping method, homogeneous distributions are obtained on glass and cellophane. The density of adsorbed particles increases linearly with immersion time and the distribution of monomers, dimers, and trimers is not characteristic of random adsorption.
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