Optimization of Cost–Carbon Reduction–Technology Solution for Existing Office Parks Based on Genetic Algorithm

With limited investment costs, how to fully utilize the carbon-reduction capacity of a campus in terms of buildings, equipment, and energy is an important issue when realizing the low-carbon retrofit of office parks. To this end, this paper establishes a mathematical optimization model for the decarbonization-based retrofit of existing office parks, based on the genetic algorithm, taking into account the relationship between cost, energy-consumption, and carbon-emissions, and taking the maximum carbon reduction of the park over its whole life as the optimization goal. The validity of the model was verified in conjunction with a case study of an office park in Nanchang, China. The case study shows that, compared with current typical parks, the carbon reduction through an office park’s decarbonization retrofit has a non-linear correlation with the investment cost, and when the total investment cost of the park is above CNY 60 million, the increase in carbon reduction with the increase in the investment cost is gradually weakened, and the park achieves the maximum carbon reduction of 236,087 t when the investment cost reaches CNY 103 million. Under the current technical and economic conditions, the investment-cost–carbon-reduction benefits of different carbon-reduction technologies are different, the carbon-reduction benefit of increasing renewable energy utilization is the best, and the carbon-reduction benefit of upgrading the energy efficiency of the park’s supply-and-use system is lower than that of renewable energy utilization, but better than that of upgrading the performance of the building envelope system. In addition, the configuration of the parameters of the same low-carbon technology in different forms of buildings varies significantly, due to differences in the building form and daily use. The model established in this paper is able to give a comprehensive optimized building–equipment–energy configuration plan for existing office parks, when maximizing carbon reduction under different investment costs, which guides the park’s decarbonization retrofit

The Antitumor Activity of the Novel Compound Jesridonin on Human Esophageal Carcinoma Cells

<div><p>Jesridonin, a small molecule obtained through the structural modification of Oridonin, has extensive antitumor activity. In this study, we evaluated both its in vitro activity in the cancer cell line EC109 and its in vivo effect on tumor xenografts in nude mice. Apoptosis induced by Jesridonin was determined using an MTT assay, Annexin-V FITC assay and Hoechest 33258 staining. Apoptosis via mitochondrial and death receptor pathways were confirmed by detecting the regulation of MDM2, p53, and Bcl-2 family members and by activation of caspase-3/-8/-9. In addition, vena caudalis injection of Jesridonin showed significant inhibition of tumor growth in the xenograft model, and Jesridonin-induced cell apoptosis in tumor tissues was determined using TUNEL. Biochemical serum analysis of alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), gamma-glutamyl transferase (GGT), total protein (TP) and albumin (ALB) indicated no obvious effects on liver function. Histopathological examination of the liver, kidney, lung, heart and spleen revealed no signs of JD-induced toxicity. Taken together, these results demonstrated that Jesridonin exhibits antitumor activity in human esophageal carcinomas EC109 cells both in vitro and in vivo and demonstrated no adverse effects on major organs in nude mice. These studies provide support for new drug development.</p></div

Effect of JD and oridonin treatment on cell morphology and nuclei of EC109 cells.

<p>EC109 cells were treated with JD or Oridonin (15 μM or 30 μM) for 16 h and observed for changes in cell morphology and nuclei. A. An inverted microscope (200X) was used to observe the morphology of EC109 cells treated by JD or Oridonin. B. EC109 cells treated by JD or Oridonin were stained with Hoechst 33258 and observed under a fluorescence microscope (200X). A representative result of 3 independent experiments is shown.</p

Effect of caspase-8/9 inhibitor on JD induced cell apoptosis.

<p>A. Apoptosis induced by JD or/with Caspase-8 inhibitor (Z-IETD-FMK) or Caspase-9 inhibitor (Z-LEHD-FMK). A representative result of 3 independent experiments is shown. B. The percentage of FITC-positive cells of 3 independent experiments is shown as Mean ± SD. *p < 0.05 versus control; **p < 0.01 versus control.</p

Biochemical serum analysis of JD treated mice.

<p>A. Concentration of ALT (U/L) in serum of the mice shown as Mean ± SD. B. Concentration of AST (U/L) in serum of the mice shown as Mean ± SD. C. Concentration of ALP (U/L) in serum of the mice shown as Mean ± SD. D. Concentration of GGT (U/L) in serum of the mice shown as Mean ± SD. E. Concentration of TP (g/L) in serum of the mice shown as Mean ± SD. F. Concentration of ALB (g/L) in serum of the mice shown as Mean ± SD. *p < 0.05 versus control; **p < 0.01 versus control.</p

Histopathological examination of major organs in JD treated mice.

<p>When the mice were sacrificed, major organs (heart, liver, spleen, lung, kidney) were collected and fixed in 4% buffered paraformaldehyde and paraffin embedded for H&E staining. Pictures were original captured at 200× magnification. The bar represents 100μm.</p

Effect of JD treatment on caspase-8, 9,3 protein expression in EC109 cells.

<p>A. Western blot of proteins extracted from EC109 cells following 24 h treatment with JD (15μM and 30μM). A representative result of 3 independent experiments is shown. B. The pro-caspase-8/GAPDH ratio is shown as Mean ± SD. C. The cleaved-caspase-8/GAPDH ratio is shown as Mean ± SD. D. The pro-caspase-9/GAPDH ratio is shown as Mean ± SD. E. The cleaved-caspase-9/GAPDH ratio is shown as Mean ± SD. F. The pro-caspase-3/GAPDH ratio is shown as Mean ± SD. G. The cleaved-caspase-3/GAPDH ratio is shown as Mean ± SD.*p < 0.05 versus control; **p < 0.01 versus control.</p

JD or Oridonin treatment stimulates apoptosis.

<p>A. EC109 cells were treated with JD or oridoin (15 μM and 30 μM) for 24 h followed by annexin V-FITC/PI staining. Annexin V-FITC/PI double staining differentiates the following groups: live cells (annexin V^-/PI^-), early apoptotic cells (annexin V⁺/PI^-), late apoptotic or necrotic cells (annexin V⁺/PI⁺) and dead cells (annexin V^-/PI⁺). A representative result of 3 independent experiments is shown. B. The percentage of FITC-positive cells of treated by JD or Oridonin. Three independent experiments is shown as Mean ± SD. *p < 0.05 versus control; **p < 0.01 versus control.</p

Jesridonin synthesis.

<p>Jesridonin synthesis.</p

Cell viability treated by JD and Oridonin.

<p>A. EC109 cells were treated for 24 h, 48 h and 72 h with 5-FU as a positive control. B-F. JD treatment of 24h, 48h and 72h to human esophageal cell lines EC109, EC9706, KYSE450, KYSE750 and TE-1, respectively. G-K. Oridonin treatment of 24h, 48h and 72h to human esophageal cell lines EC109, EC9706, KYSE450, KYSE750 and TE-1, respectively. L. JD treatment of 24h, 48h and 72h on normal cell line GES-1. M. JD treatment of 24h, 48h and 72h on normal cell line HL7702. Cell viability was determined by MTT assay and results are shown as the Mean ± SD of 3 independent experiments.</p