1.The recent effect of professional instruction On patients with type 2 diabetes mellitus
Lei LI ; Qiaoying HAN ; Aijuan LIN ; Guangxiu WANG ; Qiaohong HE
Chinese Journal of Practical Nursing 2008;24(8):10-13
Objective To discuss the recent effect of professional instruction on patients with type 2 diabetes mellitus. Methods 200 patients with type 2 diabetes mellitus were divided into the observation group and the control group. The observation group received professional instruction while the control group only got doctors'simple advice about the characteristic, results and attentions of diabetes mellitus. Various in dices were determined before and 3 months after intervention and patients compliance was evaluated 3 months after intervention. Results The indices such as blood glucose,glycosylated hemoglobin, urine trace protein, blood lipid, weight index, blood pressue and waistline were different between the two groups(P<0.05) after intervention although no difference was seen between them before intervention(P>0.05).The patients compliance in the observation was better compared with the control group(P<0.01). Conclusion Application of professional instruction proved to be an effective method to alleviate the symptoms of patients with type 2 diabetes mellitus.
2.Effect of elicitors on induction and manipulation of secondary metabolic effective ingredients in Salvia miltiorrhiza.
Wenyuan LI ; Wei GAO ; Aijuan SHAO ; Yunfei HE ; Luqi HUANG
China Journal of Chinese Materia Medica 2011;36(3):258-262
The application of elicitors, which is currently the focus of research, has been considered as one of the most effective methods to improve the synthesis of secondary metabolites in medicinal plants. Biotic and abiotic elicitors can regulate the secondary metabolic pathways of effective ingredients in Salvia miltiorrhiza. This paper has introduced the research progress about the induction and the regulation mechanism of S. miltiorrhiza by elicitors.
Biosynthetic Pathways
;
drug effects
;
Drugs, Chinese Herbal
;
pharmacology
;
Salvia miltiorrhiza
;
drug effects
;
metabolism
3.LGR5 Modulates Differentiated Phenotypes of Chondrocytes Through PI3K/AKT Signaling Pathway
Xu WU ; Yaoyao FU ; Jing MA ; Chenlong LI ; Aijuan HE ; Tianyu ZHANG
Tissue Engineering and Regenerative Medicine 2024;21(5):791-807
BACKGROUND:
Tissue engineering is increasingly viewed as a promising avenue for functional cartilage reconstruction.However, chondrocyte dedifferentiation during in vitro culture remains an obstacle for clinical translation of tissue engineered cartilage. Re-differentiated induction have been employed to induce dedifferentiated chondrocytes back to their original phenotype. Regrettably, these strategies have been proven to be only moderately effective.
METHODS:
To explore underlying mechanism, RNA transcriptome sequencing was conducted on primary chondrocytes (P0), dedifferentiated chondrocytes (P5), and redifferentiated chondrocytes (redifferentiation-induction of P5, P5.R). Based on multiple bioinformatics analysis, LGR5 was identified as a target gene. Subsequently, stable cell lines with LGR5 knocking-down and overexpression were established using P0 chondrocytes. The phenotypic changes in P1 and P5 chondrocytes with either LGR5 knockdown or overexpression were assessed to ascertain the potential influence of LGR5 dysregulation on chondrocyte phenotypes. Regulatory mechanism was then investigated using bioinformatic analysis, protein–protein docking, immunofluorescence co-localization and immunoprecipitation.
RESULTS:
The current study found that dysregulation of LGR5 can significantly impact the dedifferentiated phenotypes of chondrocytes (P5). Upregulation of LGR5 appears to activate the PI3K/AKT signal via increasing the phosphorylation levels of AKT (p-AKT1). Moreover, the increase of p-AKT1 may stabilize b-catenin and enhance the intensity of Wnt/b-catenin signal, and help to restore the dedifferentated phenotype of chondrocytes.
CONCLUSION
LGR5 can modulate the phenotypes of chondrocytes in P5 passage through PI3K/AKT signaling pathway.