OBJECTIVE:To study the protective effects of Danshen injection on 5/6 nephrectomiy induced model rats with in-flammatory renal injury. METHODS:50 rats were equally randomized into a sham-operation (isometric distilled water) group,a model (isometric distilled water) group,a positive control [captopril 5 mg/(kg·d)] group and Danshen injection low-dose and high-dose [1.6,4.8 ml/(kg·d)] groups. Models were established by performing 5/6 nephrectomy on the rats in all groups except the sham-operation group. The rats were given drugs for 4 consecutive weeks from the 6th week. 24 h urine protein was determined for all rats every week. After the last administration,the contents of creatinine,urea nitrogen and interleukins 1β(IL-1β),IL-2 and IL-10 in rats’serum were determined. Pathological changes and infiltration of macrophages CD68 in rats’kidney tissues were ob-served. RESULTS:Compared to the sham-operation group,those in the model group had more 24 h urine protein and more obvi-ous renal pathologic changes during 1-4 weeks of administration,and higher contents of creatinine,urea nitrogen,IL-1β,IL-2 and IL-10 and CD68 positive expression in serum. Compared to the model group,during 2-4 weeks of administration,those in the posi-tive control group and Danshen injection low-dose and high-dose groups had less 24 h urine protein,milder renal pathologic chang-es,and lower contents of creatinine,urea nitrogen,IL-1β and CD68 positive expression in serum,and higher content of IL-10, and only the rats in the positive control group demonstrated lower IL-2 content. There of the above were statistical differences(P<0.01 or P<0.05). CONCLUSIONS:Danshen injection can alleviate renal pathologic changes and reduce inflammatory injury of the kidneys of 5/6 nephrectomiy induced model rats.

AIM: To explore the antitumor mechanisms of bifidobacteria adolescence in vivo. METHODS: The activity of NF-?B and its inhibiting protein I ?B? of large bowel carcinoma tissues was detected by using laser scanning confocal microscope and immunohistochemistry. RESULTS: The positive cell density of NF-?B of large bowel carcinoma transplantation tumors in bifidobacterium injection group was markedly lower than that in tumor control group( P

Objective To prepare a novel extravascular human epithelial growth factor receptor 2 (HER2)-targeted polylactic-co-glycolic acid (PLGA)-COOH ultrasound contrast agent with liquid perfluorocarbons(PFH-PLGA-tra),and to observe it's general properties and it's effects on ultrasound imaging in vitro.Methods Polymeric nanocapsules of liquid perfluorocarbons were prepared by the single emulsion technique and conjugated with trastuzumab monoclonal antibody by EDC/NHS.The general characteristics were observed.The conjugation was demonstrated by immunofluorescence and the targeting performance of the agent was checked in human MCF-7 cells line in vitro.The encapsulation of liquid fluorocarbons was detected by heating in vitro.The effects on ultrasound imaging were observed in vitro.Results The mean diameter of agents was (261 ± 28)nm.The targeted nanocapsules were positive in immunofluorescence.In the targeted study,it was shown that a number of targeted nanocapsules conjugated with MCF-7 cells in vitro.Droplet-to-bubble transition experiment in vitro showed that there were no nano/microbubbles formed by heating in control groups at 80℃,while there were a lot of nano/microbubbles appeared in nanocapsules formulations at 80 ℃.The agents presented a good ultrasound imaging in vitro.Conclusions The HER2-targeted polymeric nanocapsules of liquid perfluorocarbons are successfully prepared,which may become a novel extravascular targeted ultrasound contrast agents.

Objective:To evaluate the effect of preoperative panel reactive antibody(PRA)levels on long-term survival after kidney transplantation. Methods:Data on 1 162 patients underwent first kidney transplantation performed between January 2001 and June 2014 were included in our center. According to the preoperative PRA levels,the patients were divided into negative group( PRA≤10%) and positive group( PRA>10%) ,which were retrospectively analyzed. Results: The 1-,5-,10-year patient survival rates of the negative group calculated by Kaplan-Meier were 96. 8%,89. 4%,78. 6%,respectively,while the positive group were 93. 5%,81. 6%, 65. 4%. The 1-,5-,10 -year death-censored graft survival rates of the negative group were 95. 9%,84. 8%,63. 1%,respectively,while the positive group were 92. 3%,74. 1%,51. 9%. The log-rank test revealed that there was significant difference between the patient and graft survival curves (χ2 =9. 623/11. 019, P=0. 002/0. 001 ) . Cox multivariate analysis found that preoperative PRA levels were independent risk factors for reducing the patient or graft survival rates(P<0. 001). Logistic multivariate regression analysis confirmed the significant association between preoperative PRA levels and the risk of acute rejection ( OR=8. 25,95% CI=2. 86-5. 72, P<0. 001). The 5-,10-year creatinine values were significantly lower in the negative group compared to the positive group(all P<0. 05), while there was no difference in the 1-year. In addition, Logistic multivariate regression analysis confirmed the significant association between preoperative PRA levels and the production of donor specific antibody(DSA)(OR=6. 89,95% CI=4. 52-9. 17,P<0. 05). Conclusion: The detection of preoperative PRA is an important indictor predicting the sensitivity status of the recipients. The preoperative PRA positive recipients need careful monitoring and diagnosis of acute rejection and DSA after kidney transplantation.

OBJECTIVE:To explore the genome-wide methylation differences between coronary heart disease (CHD) patients and healthy volunteers,and to investigate the relationsip of DNA methylation with CHD from epigenetics. METHODS:In case-control study,subjects were divided into CHD group(50 cases)and health control group(50 cases). DNA of 2 groups were sequenced with methylated DNA immunoprecipitation sequencing technology. The genome-wide methylation differences were analyzed and compared between 2 groups. RESULTS:The number of methylation peak in CHD group was higher than health group,with statistical signfi-cance(P<0.05). The methylation peak mainly distributed in 5'UTR,Intron functional elements. The number of reads in AQP1,SHB and other gene promoters in CHD group were lower than health group,and its methylation level decreased. The number of reads in GRK5 and serveal gene promoters on chrX in CHD group were higher than helath group,and its methylation level increased,with sta-tistical significance(P<0.01). CONCLUSIONS:The genome-wide methylation level of CHD patients are higher than those of healthy volunteers. The occurence of CHD is possibly associated with the change of methylation level of related gene promoters.

Insufficient remyelination due to impaired oligodendrocyte precursor cell (OPC) differentiation and maturation is strongly associated with irreversible white matter injury (WMI) and neurological deficits. We analyzed whole transcriptome expression to elucidate the potential role and underlying mechanism of action of lipocalin-2 (LCN2) in OPC differentiation and WMI and identified the receptor SCL22A17 and downstream transcription factor early growth response protein 1 (EGR1) as the key signals contributing to LCN2-mediated insufficient OPC remyelination. In LCN-knockdown and OPC EGR1 conditional-knockout mice, we discovered enhanced OPC differentiation in developing and injured white matter (WM); consistent with this, the specific inactivation of LCN2/SCl22A17/EGR1 signaling promoted remyelination and neurological recovery in both atypical, acute WMI due to subarachnoid hemorrhage and typical, chronic WMI due to multiple sclerosis. This potentially represents a novel strategy to enhance differentiation and remyelination in patients with white matter injury.
Mice ; Animals ; Remyelination/physiology* ; Oligodendrocyte Precursor Cells/metabolism* ; White Matter ; Subarachnoid Hemorrhage/metabolism* ; Lipocalin-2/metabolism* ; Early Growth Response Protein 1/metabolism* ; Oligodendroglia/metabolism* ; Mice, Knockout ; Cell Differentiation/physiology* ; Brain Injuries/metabolism*