Objective To investigate the effect of the dihydroartemisinin (DHA) on the human low-differentiated lung adenocarcinoma cell line A549 and to explore its mechanism. Methods The A549 cells at logarithmic growth phase were divided into control group and DHA group. The cells in the control group were incubated with conventional reagent, and the cells in DHA group were incubated with 500 nmol/L of DHA. After incubation for 72 hours, methyl thiazolyl tetrazolium (MTT) assay was used to examine the proliferation of A549 cells in the two groups. Gene expression of p85, Akt, Bax and Bcl-2 was detected by real-time fluorescence quantitative polymerase chain reaction (PCR) . The protein expression of p85, Akt, p-p85, p-Akt, Bax and Bcl-2 was detected by Western blotting method. The activity of Caspase3 was measured by Caspase3 colorimetric assay kit. Results Compared with the control group, the proliferation rate of A549 cells in DHA group was significantly decreased ( P<0.01) . The RT-PCR results showed that the mRNA expression levels of p85 and AKT had no obvious difference between the two groups, but the mRNA expressien level of Bax was increased ( P<0.001), and the mRNA expressien level of Bcl-2 was decreased ( P<0.05) . The Western blotting results showed that there was no significant changes of p85 and Akt proteins between the two groups (P>0.05), but p-p85, p-Akt and Bcl-2 protein expression levels were significantly decreased ( P<0.01) , and Bax protein expression was increased ( P<0.01). Moreover, the activity of Caspase3 was also enhanced ( P<0.001). Conclusion DHA can reduce the proliferation of A549 cells and increase the apoptosis of A549 cells, and its mechanism probably has relationship with the inhibition of PI3K/Akt signaling pathway.

Background and purpose:Breast cancer has the highest morbidity and mortality rate in women worldwide. Triple-negative breast cancer (TNBC) has no speciifc target and has low survival rate. Recent studies have veriifed BRD4 could promote tumor progression. This study aimed to detect the expression level of BRD4 in TNBC after treatment with gemcitabine, and to reveal the effect ofBRD4 silencing plus gemcitabine as a treatment for TNBC. Methods:The expression ofBRD4 in TNBC cell lines treated with gemcitabine was detected by reverse transcription PCR (RT-PCR) and Western blot. The effect of BRD4 silencing plus gemcitabine in TNBC was illustratedin vitro and in vivo.Results:The expression ofBRD4 in TNBC was signiifcantly increased after treatment with gemcitabine.In vitro,BRD4 knockdown signiifcantly lowered the IC50 value. The apoptotic rate of TNBC was signiifcantly increased in theBRD4 silencing plus gemcitabine group compared to the other. The growth rate of tumorin vivo was signiifcantly lowered in the BRD4 silencing plus gemcitabine group.Conclusion:BRD4 may play an important role in the drug resistance to gemcitabine in TNBC.BRD4 silencing plus gemcitabine may be a novel treatment strategy for TNBC.

Objective To explore the effects and mechanism of atrovastatin on the expression of the NF-κB in renal tissues of diabetic rats.Methods A total of 60 male SD rats was randomly taken out 40 rats to make diabetic model by injection of 65mg streptozotoein (STZ) into enterocoelia,the rest of 20 rats were normal control group.After the model made,atrovastatin (2 mg/kg/d) was given to the treated group,and the normal control group and diabetic rats without treatment group were given equivalent water.After 12 weeks,the rats were killed.Total RNA of the renal tissues was isolated from one kidney for each rat,and the renal tissues from the another kidney was prepared for immunohistochemistry (IHC) analysis.The NF-κB mRNA expressions among three groups were determined by RT-PCR.The distribution of NF-κB in the renal tissues was observed,and compared its difference among three groups.ResultsPCR showed that NF-κB mRNA was increased in the renal tissues of diabetic rats compared to control rats ( P ＜ 0.05 ).Drug-treated rats showed significantly decreased levels of NF-κB mRNA in the renal tissues compared to the untreated diabetic group( P ＜0.05).The results were also observed in protein lelel of NF-κB expression.IHC showed that there existed positive cells in the glomerular and renal tubulointerstitum.Conclusions Atrovastatin can down-regulate the expression of NF-κB and suppress the increased level of NF-κB protein in the renal tissue of diabetic rats,and slow the progress of retinopathy.

Objective To invstigate the effect of high dose X-ray irradiation on the expression of multidrug resistance-1 (MDR1), Bcl-2, MMP7 genes. Methods A nasopharyngeal carcinoma cell line,CNE1, were irradiated with a total dose of 50 Gy. The resistance to the cisplatin of CNE1 cells and the irradiated CNE1 (CNE1 R) cells was detected by MTT. mRNAs expression of MDR1 , Bcl-2 and MMP7 was measured by quantitative RT-PCR. Results The expression of MDR1 increased in CNE1 R cells. The semiquantitative A value of MDR1 mRNA was 0.47 ±0.04, and the value of CNE1R cells (1st, 7th, 21st,28th, 35th, 42nd and 49th days after irradiation) were 0.67 ± 0. 06 (t = -5.44, P = 0. 003) ,0.70 ± 0. 01(t=-5.90,P=0. 002),0.73±0. 01(t= -6. 45,P=0. 001) ,0. 67 ± 0. 03 (t= -3.97,P=0.011),0.65 ±0.01(t = -4.43,P=0. 007),0. 62±0. 05(t= -2. 64,P=0.046) and 0.62 ±0.02(t = -3.34,P=0.021), respectively. Bcl-2 mRNA expression were 0.55 ±0.02 and 1.05 ±0.04(t = -9.93,P=0. 000) and MMP7 mRNA expression were 0.51 ±0.01 and 0.82 ±0.02(t = -8.51,P=0.000) in CNE1and CNE1 R cells. Conclusions The MDR1 expression was increased after a total dose of50 Gy irradiation,which may be related to the synchronous change of Bcl-2 and MMP7 genes.

Objectives: To investigate the distribution of common pathogens and their antibiotic resistance from patiens with catheter related sepsis (CRS).Methods: Catheter bacteria cultrure and antibiotic sensitivity test were performed from 69 patiens with CRS.Results: The common pathogens in CRS were fungi (41.1%),Gram-positive cocci (35.6%)and Gram-negtive bacilli (23.3%). Non-C. albicans species were major pathogen (19/30 stranins).The most strains were staphylococcus epidermidis in Gram-positive cocci and the most of them were Methicillin resistant.No vancomycin resistant strains were found. The Gram negative bacilli were often resistant to third generation cephalosporens.Conclusions: The dorminant pathogens of CRS are fungi and gram positive cocci and we should pay more attention to pathogens of resistence to antibiotics. In order to control CRS, CVC must be used reasonably and shorten the duration of retention.

AIM: To investigate the effect of adalimumab combined with dexamethasone intravitreal implant in the treatment of refractory non-infectious uveitis macular edema(UME).METHODS: A total of 92 cases(131 eyes)of refractory non-infectious UME patients admitted to our hospital from January 2020 to January 2022 were selected and randomly divided into control group, with 46 cases(63 eyes)treated with dexamethasone intravitreal implant and observation group, with 46 cases(68 eyes)treated with adalimumab subcutaneous injection combined with dexamethasone intravitreal implant. The best corrected visual acuity(BCVA), central retinal thickness(CRT), vitreous opacity and Th17/Treg cytokines were measured before and after treatment, and the occurrence of adverse reactions was recorded.RESULTS: Totally 3 cases(4 eyes)were lost to follow-up. After treatment for 1, 3, 6 and 12 mo, BCVA was improved in both groups compared with that before treatment, and CRT, vitreous opacity score, serum interleukin(IL)-17 and IL-22 levels were decreased compared with those before treatment, and serum transforming growth factor-β(TGF-β)and IL-10 levels were increased compared with those before treatment. BCVA in the observation group was better than that in the control group, and CRT, vitreous opacity score, serum IL-17 and IL-22 levels were lower than those in the control group, and serum TGF-β and IL-10 levels were higher than those in the control group(all P<0.05). During treatment and follow-up, no serious adverse reactions occurred in both groups.CONCLUSION: Adalimumab combined with dexamethasone intravitreal implants in the treatment of refractory non-infectious UME can significantly subside the macular edema, reduce vitreous opacity and improve visual acuity.