Radiotherapy is an important part of the standard treatment regimen for rectal cancer, bringing survival benefits and improved quality of life to patients with rectal cancer. However, the radiotherapy resistance of rectal cancer patients greatly limits the effectiveness of treatment and affects the prognosis of patients. The emergence of nanoparticles provides a new way to improve radiotherapy resistance of rectal cancer, which can overcome radiotherapy resistance by inhibiting DNA damage repair, affecting cell cycle, targeting delivery, enhancing DNA damage, and regulating tumor microenvironment, etc. In this article, complex coordination mechanism leading to radiotherapy resistance in rectal cancer was reviewed, current relevant studies on nanoparticles in improving radiotherapy response in rectal cancer were summarized, and the feasibility and future research direction of the combination of nanoparticles and radiotherapy in clinical treatment of rectal cancer were discussed.

Radiotherapy is an important part of the standard treatment regimen for rectal cancer, bringing survival benefits and improved quality of life to patients with rectal cancer. However, the radiotherapy resistance of rectal cancer patients greatly limits the effectiveness of treatment and affects the prognosis of patients. The emergence of nanoparticles provides a new way to improve radiotherapy resistance of rectal cancer, which can overcome radiotherapy resistance by inhibiting DNA damage repair, affecting cell cycle, targeting delivery, enhancing DNA damage, and regulating tumor microenvironment, etc. In this article, complex coordination mechanism leading to radiotherapy resistance in rectal cancer was reviewed, current relevant studies on nanoparticles in improving radiotherapy response in rectal cancer were summarized, and the feasibility and future research direction of the combination of nanoparticles and radiotherapy in clinical treatment of rectal cancer were discussed.

Objective To explore the expression changes of SIRT1 and related inflammatory regula-tors in peripheral blood of patients with major depressive disorder and analyze the correlation between SIRT1, depression and inflammatory regulators. Methods Forty patients with major depressive disorder and forty healthy controls were selected. Hamilton Depression Scale (HAMD-17) was used to assess the degree of de- pression in patients with depressive disorder. Quantitative Real-time PCR( RT-PCR) was used to detect the relative expression levels of SIRT1,Elf-1,NF-κB,IL-1β,GM-CSF mRNA,and enzyme linked immunosorbent assay(ELISA) was used to detect the expression levels of SIRT1,Elf-1,NF-κB,IL-1β,GM-CSF proteins. The correlation between the severity of depression disorder and SIRT1 and the correlation between SIRT1 and Elf-1 and NF-κB were analyzed. Results (1)Compared with the control group,SIRT1 mRNA expression significantly decreased in the case group (P<0. 01),while Elf-1,NF-κB,IL-1β,GM-CSF mRNA expression significantly increased in the case group (P<0. 01). ( 2) The expression of plasma SIRT1 protein((8. 23± 1. 78)ng/ml) in the case group was lower than that in the control group (P<0. 01). The expressions of plas-ma Elf-1 protein((1 921. 67±271. 07)pg/ml),NF-κB protein((2 057. 29±260. 44)pg/ml),IL-1β protein ((186. 60±31. 00) pg/ml) and GM-CSF protein((183. 69±28. 87) pg/ml) were higher than those in the control group((1 512. 92±284. 54)pg/ml,(1537. 18±313. 82) pg/ml,(144. 79±31. 48) pg/ml,(162. 82± 27. 90) pg/ml,respectively,all P<0. 01). (3) SIRT1 mRNA expression level was negatively correlated with the severity of major depressive disorder (r=-0. 51, P<0. 01) and was negatively correlated with the mRNA expression levels of Elf-1 and NF-κB (r=-0. 66,P<0. 01,r=-0. 64,P<0. 01). Conclusion The expres-sion level of SIRT1 in peripheral blood of patients with major depressive disorder is correlated with the sever-ity of depression. This may be related to the decrease of SIRT1 expression in peripheral blood leukocytes of patients with major depressive disorder,which activates the pathway of NF-κB and Elf-1 and increase expres-sion of GM-CSF and IL-1β.

γ-glutamyltranspeptidase was detected from the cultured mycelia of Cordyceps sinensis (CSGT). Km and Vmax of CSGT was 2.54×10-4 mol/L and 0.1808 mol/L·min respectively when L-glutamic acid 5-(4-nitroanilide) (GpNA) and glycyglycine was used as its substrate. CSGT was stable from pH 8.0 to 11.0 and at or below 20℃. It was optimally active at pH 9.0～10.0 and 30℃. A series of reducing reagents could activate CSGT, and metal cations such as Zn2+, Cu2+, Hg2+ , Mn2+ inhibited strongly activity of the enzyme, but K+, Ca2+, Mg2+ and Na+ at high concentrations had no effect on its activity, indicating that its active center could contain -SH.

Genistein is a high specific and noncompetitive inhibitor of epidermal growth factor receptor tyramine kinase domain (EGFR-TK). In the paper, a molecular docking between genistein and EGFR-TK was studied to explore the mechanism of their interaction and antitumor mechanism of genistein by AUTODOCK 3.05 program. The results indicated that genistein located in the active cavity of EGFR-TK by high affinity (deltaG = -31.2 kJ/mol), and genistein inhibited EGFR-TK by interfering with forming of Lys721/Glu738 ion pair. The inhibition belonged to noncompetitive interaction, in which hydrophobic force and hydrogen bond played key roles.
Catalytic Domain ; Genistein ; metabolism ; pharmacology ; Models, Molecular ; Receptor, Epidermal Growth Factor ; antagonists & inhibitors ; metabolism