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The ground water-source heat pump system for the plant factory lacks a scientific operation strategy to solve the problem of high energy consumption in winter and summer. It is very difficult and uneconomical to change the operation conditions by experimental means to obtain actual operation data. The current study aims to build a TRNSYS simulation model of the ground water-source heat pump system of Shanghai Chongming Natural Light Plant Factory. For the heating season, the simulation of energy consumption was 2315 GJ. Compared with the actual energy consumption, the relative error is -0.98%, which indicates that the simulation results are accurate and the simulation model developed is appropriate and usable. Numerical simulations for the whole year on this basis yielded that the plant factory energy supply system operates from November to March with a heating energy consumption of 3530.84 GJ and from June to September with a cooling energy consumption of 1126.24 GJ. In most cases, the indoor temperature fluctuates within a reasonable range, but in the summer high-temperature season, the plant factory temperature will reach above 40℃, which seriously affects plant growth. After optimization, the plant factory stops production in July and August, and the system stops running, the results are that the optimized system can save 56% of the annual cooling energy consumption, totalling 767.48 GJ, which can reduce the costs by 160,318.05 RMB.

Acne vulgaris is a chronic inflammatory cutaneous disease. 5‐Aminolaevulinic acid photodynamic therapy (ALA‐PDT) is a novel and effective approach for severe acne vulgaris treatment. However, its specific treatment mechanism still remains unclear. In the present study, we investigated the potential mechanism of how ALA‐PDT regulated intense inflammatory response in acne vulgaris. It appeared that ALA‐PDT suppresses proliferation and lipid secretion of primary human sebocytes. Besides, ALA‐PDT could up‐regulate the expression of CXCL8 in vivo and in vitro, amplifying the inflammatory response by recruiting T cells, B cells, neutrophils and macrophages. We also found that ALA‐PDT elevated the expression of CXCL8 via p38 pathway. SB203580, a p38 pathway inhibitor, decreased the expression of CXCL8 in sebocytes after ALA‐PDT. These findings indicate that ALA‐PDT amplifies the intense inflammatory response in the treatment of acne vulgaris via CXCL8. Our data decipher the mechanism of intense inflammatory response after ALA‐PDT for acne vulgaris. [ABSTRACT FROM AUTHOR]