Biosensors have become powerful tools for real-time monitoring of specific small molecules and precise control of gene expression in biological systems. High-throughput sensors for 1, 4-butanediamine biosynthesis can greatly improve the screening efficiency of high-yielding 1, 4-butanediamine strains. However, the strategies for adapting the characteristics of biosensors are still rarely studied, which limits the applicability of 1, 4-butanediamine biosensors. In this paper, we propose the development of a 1, 4-butanediamine biosensor based on the transcriptional regulator PuuR, whose homologous operator puuO is installed in the constitutive promoter P_gapA of Escherichia coli to control the expression of the downstream superfolder green fluorescent protein (sfGFP) as the reporter protein. Finally, the biosensor showed a stable linear relationship between the GFP/OD₆₀₀ value and the concentration of 1, 4-butanediamine when the concentration of 1, 4-butanediamine was 0-50 mmol/L. The promoters with different strengths in the E. coli genome were used to modify the 1, 4-butanediamine biosensor, and the functional properties of the PuuR-based 1, 4-butanediamine biosensor were explored and improved, which laid the groundwork for high-throughput screening of engineered strains highly producing 1, 4-butanediamine.
Biosensing Techniques/methods* ; Escherichia coli/metabolism* ; Promoter Regions, Genetic/genetics* ; Green Fluorescent Proteins/metabolism* ; Transcription Factors/genetics* ; Escherichia coli Proteins/genetics* ; Diamines/metabolism* ; Gene Expression Regulation, Bacterial

Beta-thalassemia major(β-TM)is an inherited disease caused by a defect in the synthesis of globin. The disease requires long-term blood transfusion and iron chelator treatment, which can cause various secondary changes in the body and eye tissues. Compared with normal peers, β-TM patients will show changes in the eye such as steeper corneal curvature, shallower anterior chamber, increased lens thickness, shorter axial length, and reduced tear secretion. At the same time, nutritional deficiencies and the use of iron chelator drugs will increase the risk of complicated cataract and retinal degeneration, thus affecting the quality of life of β-TM patients.This article combines relevant domestic and foreign literatures to explore and review the changes in the eye of β-TM patients, with a view to providing valuable insights for clinical practice.

β thalassemia is a hereditary hemolytic disease caused by the defect of β globin gene. Transfusion-dependent β thalassemia patients need long-term blood transfusion to survive, and a series of systemic and ocular complications will occur in the disease itself and long-term blood transfusion. Retinal blood vessel density decreases, retinal thickness thinned and elastic pseudoxanthoxanoma syndrome are found in fundus due to long-term anemia and side effects of iron chelating agent. At present, there are few reports about eye changes in thalassemia patients, and the cognition is relatively scarce. Therefore, it is necessary to be vigilant for physicians, deeply explore the cause and symptomatic treatment, combined with individual disease characteristics, to provide a more scientific and accurate plan for clinical treatment.

Objective To study the proliferation inhibition effect by silencing PLCε gene expression with RNA interference in BIU-87 cells. Methods The specific short hairpin RNA recombinant plasmids were constructed by gene clone technology.The expression level of PLCε protein and mRNA were detected by Western blot and RT-PCR respectively after transfected recombinant plasmids into BIU-87 cells.The influence on proliferation was check by MTT.The changes of proliferating cell nuclear antigen(PCNA)were analyzed by immunocytochemical method,and the distribution of cell cycle was analyzed using flow cytometry. Results After transfected with the specific recombinant plasmids,PCNA expression was decreased 33.08%,and the analysis of cell cycle indicated that cells of G0/G1 phase were increased comparision with(40.75±2.30)%and(40.00±1.76)0A,and its G2/M phase cells(8.16±0.51)%were decreased strikingly compared with group control(31.20±1.76)%and group NP(35.94±1.58)%.Cells were blocked at G0/G1 phase,the cell proliferation was inhibited obviously. Conclusion PLCε may play an important role in proliferation of bladder cancer cells,which could be a potential target of biological treatment on bladder cancer in the future.