Objective To evaluate the efficacy of a new micro-bubble contrast agent of C_3F_8 in the opacification of the left ventricle. Methods Seven pigs received a bolus injection of C_3F_8 (0.002) and (0.02) (ml/kg) intravenously. Left ventricular opacification grades and number of endocardial border delineation segments were observed and left ventricular ejection fraction(LVEF) were measured using modified Simpson method after each intravenous contrast injection. Heart rate and respiration rate were recorded before and after each injection. Results There was a significant improvement for every measurement of contrast enhancement in each intravenous injection. In addition, part of myocardial tissue could be enhanced after contrast injection. There was no difference in heart rate and respiration rate between pre- and post-injection. Conclusions This new contrast agent is safe and helpful in delineating endocardial border of the left ventricle.

Objective To determine the accuracy and usefulness of dobutamine stress echocardiography(DSE) in detecting restenosis after percutaneous coronary intervention (PCI). Methods DSE was conducted in 47 patients before coronary angiography, 6 months to 18 months after PCI. The standard protocol of DSE was 5,10,20,30 ?g?kg~(-1)?min~(-1) with subsequent incremental increases every 3 minutes to a maximum dose of 40 ?g?kg~(-1)?min~(-1). Consistency of the results was compared between DSE and coronary angiography.Results Compared with coronary angiographic results, DSE had a low sensitivity(64%) but high specificity(86%) for detection of restenosis after PCI. The total accuracy was 72%. Conclusions DSE can assess restenosis after PCI with lower cost and safety.

Objective To evaluate the role of transeso phageal echocardiography(TEE) before chemical or electric cardioversion for non-vulvular atrial fibrillation. Methods Forty-three patients, confirmed non-vulvular atrial fibrillation, undertook anticoagulation or anti-platelet therapy and transthoracic echocardiography and TEE less than 24-48 hours prior to cardioversion. Results Two thrombi in the left atrial appendage and three spontaneous echo contrasts in the left atrium were evidenced. After anticoagulation or anti-platelet therapy, 39 patients undertook cardioversion therapy. Among them,31 patients received drug cardioversion,success in 19,and failure in 12;8 patients received electric cardioversion,success in 6,and failure in 2. There were no thromboembolic events during the hospitalization. Conclusions TEE performed before cardioversion for atrial fibrillation is necessary to reduce the risks of thromboembolic events and to guide for anticoagulation therapy.

The most radiation exposure for children arises from the medical process, and due to their characteristics such as relatively immature,organ development,they are more sensitive to the radiation than a-dults,and have higher risk of radiation related diseases,so medical radiation exposure should not be ignored.

Protein arginine methyltransferase 5 (PRMT5) has been implicated as an important regulator of many cellular processes and signaling pathways,including chromatin remodeling,RNA splicing,DNA transcription,and cell proliferation.Therefore,structural and functional studies on PRMT5 are quite important.The full length ofPRMT5 gene was cloned into vector pGEX-4T-1,resulting in only low expression levels in Escherichia coli (E.colO.Here,it was showed that the several N-terminal amino acids deletions could result in a significant increase in the amount of soluble ft"action,while one of them did not affect the protein-arginine methyltransferase activity.And it was also found that the N-terminal 15 amino acids region of PRMT5 may be important for the catalytic activity.

Objective To evaluate the protective effect of epigallocatechin gallate (EGCG) against interleukin (IL)-17-induced injury to keratinocytes,and to explore its mechanism.Methods Some cultured HaCaT cells were divided into 3 groups to be treated with IL-17 alone at concentrations of 50,70,90 μg/L,respectively,with those receiving no treatment as the blank control group.Some HaCaT cells were divided into 5 groups:IL-17 group treated with 90 μg/L IL-17 alone,IL-17 + EGCG group treated with 90 μg/L IL-17 and 60 μmol/L EGCG,IL-17 + SP600125 group treated with 90 μg/L IL-17 and SP600125 (a JAK signaling pathway inhibitor),IL-17+ EGCG + anisomycin group treated with 90μg/L IL-17,60xmol/L EGCG and anisomycin (a Janus kinase signaling pathway activator),and blank control group receiving no treatment.After different durations of treatment,CCK-8 assay was performed to evaluate cellular proliferative activity,flow cytometry to detect cell apoptosis,enzyme-linked immunosorbent assay (ELISA) to measure expression levels of IL-6,IL-23 and IL-8,and Western-blot analysis to determine protein expressions of c-Jun N-terminal kinase (JNK) and phosphorylated JNK (P-JNK).Results IL-17 promoted cellular proliferation of HaCaT cells,and the proliferation rate,which was correlated with the concentration of IL-17,reached the maximum in the 90-μg/L IL-17 group (P ＜ 0.05).EGCG at 60 μmol/L significantly inhibited cellular proliferation of,promoted apoptosis in,and reduced IL-6,IL-23 and IL-8 expressions in,HaCaT cells induced by 90 μg/L IL-17 (all P ＜ 0.05).Compared with the IL-17 group,the IL-17 + EGCG group and IL-17 + SP600125 group both showed significantly decreased P-JNK expression,cell proliferation rate and IL-6,IL-23 and IL-8 expression levels (all P ＜ 0.05).However,compared with the IL-17 + EGCG group,the IL-17 + EGCG + anisomycin group showed significantly increased protein expression of P-JNK,cell proliferation rate and IL-6,IL-23 and IL-8 expression levels (all P ＜ 0.05).Conclusion EGCG protected against IL-17-induced injury to HaCaT cells,such as abnormal cell proliferation,apoptosis and inflammatory response,likely by inhibiting the JNK signaling pathway.

Objective To study the effect of fund support on cited times of Chinese papers on AIDS by controlling the influence of confounding factors.Methods The effect of publication time of fund-supported papers and non fund-supported papers, h-index of authors, IF of journals on accumulated cited times of each academic paper was controlled by propensity score matching.The cited times of matched fund-supported papers and non fund-supported papers were compared by paired t test.Results The balance of confounding factors which were unbalanced before matching was achieved between fund-supported papers and non fund-supported papers after matching.No significant difference was found between fund-supported papers and non fund-supported papers after matching.Conclusion Fund support does not affect the cited times of Chinese papers on AIDS, which shows that fund support can not noticeably improve the academic level and impact of Chinese papers on AIDS.

Objective:To study the effects of ~(125)I-(α_v)ASODN on the in vitro invasive ability of heptocellular carcino-ma cell line(HepG2) through PEI-RGD-mediated receptor process. Methods: Intergrin α_v-specific antisense oligonucle-otide was labeled with ~(125)I, and PEI-RGD/~(125)I-(α_v)ASODN complex was prepared by combining ~(125)I-(α_v)ASODN with polyethyleneimine derivative PEI-RGD. PEI-RGD/~(125)I-(α_v)ASODN complex was transferred into HepG2 cells through the receptor-mediated process. The effect of PEI-RGD/~(125)I-(α_v)ASODN complex on the invasive ability of HepG2 cells was examined by Boyden chamber invasive assay. Results: (1) The labeling yield and radiochemical purity of ~(125)I-(α_v) ASODN were(73.78±4.09)% and(96.68±1.38)%, respectively, and the labeled compound had a good stability in vitro after 48 h at 37℃; (2) The ability of HepG2 cells to uptake PEI-RGD/~(125)I-(α_v)ASODN reached its peek ([12.77±0.85] % ) when PEI-RGD/~(125)I-(α_v)ASODN was at 4 μl/2 μg ([12.77±0.85] %), and then gredually decreased thereafter. So the dosage of PEI-RGD/~(125)I-(α_v)ASODN for the following experiment was chosen as 2 μl/1 μg; (3) The invasive capacity of HepG2 cells was significantly reduced in PEI-RGD/~(125)I-(α_v)ASODN group compared with those in other experiment and control groups (P <0.01 ). Conclusion: ~(125)I-(α_v)ASODN mediated by PEI-RGD can effectively inhibit the invasive capacity of HepG2 cells.

_ Objective_ To evaluate the efficacy of unilateral subtotal adrenalectomy in the treatment of bilateral adrenal solitary neoplasma causing Cushing's syndrome and to elaborate the therapeutic principle. Methods From 2007 to 2013, a total of ten patients were diagnosed with Cushing's syndrome caused by bilateral solitary adrenal neoplasma. We compared patients'clinical symptoms, hormone profiles, biochemical and metabolic parameters, and imaging data before and after the surgery. Five of them chose the optimal neoplasma based on the lateralization ratio of adrenal venous sampling result and the other 5 patients chose the optimal neoplasma based on the diameter of the mass reflected by the computed tomography result and were then operated. Results After the unilateral subtotal adrenalectomy,the24-hour urinary free cortisol decreased significantly(P<0.05)and the midnight serum cortisol level also significantly reduced(P<0. 01). Plasma adrenocorticotropic hormone level increased significantly(P<0. 01). Nine patients of them did not need contralateral adrenalectomy and one patient received contralateral adrelectomy because of the remnant of Cushingnoid symptoms. Conclusion Unilateral subtotal adrenalectomy is an effective and safe way to treat Cushing's syndrome caused by bilateral solitary neoplasma.

Objective To evaluate effects of ursolic acid (UA) on interleukin?33 (IL?33) expression in HaCaT cells induced by interferon?γ(IFN?γ), and to explore their mechanism. Methods Some HaCaT cells were treated with UA at different concentrations(0, 0.1, 1, 5, 10, 20, 40 and 80μmol/L)for 24, 48 and 72 hours separately. Then, methyl thiazolyl tetrazolium(MTT)assay was conducted to evaluate cell proliferative activity. A cell model of inflammation was established by culture of HaCaT cells with the presence of 200μg/L IFN?γ. Some HaCaT cells were classified into several groups to be treated with IFN?γ(200μg/L)and UA(10 and 15μmol/L)alone or in combination (firstly treated with IFN?γ followed by UA treatment), and those receiving no treatment served as the blank control group. Reverse transcription PCR (RT?PCR) was performed to detect mRNA expressions of IL?6 and IL?33, and Western?blot analysis to measure IL?33 protein expression after 12?hour culture. The expressions of extracelluar signal?regulated kinase 1/2(ERK1/2)and phosphorylated ERK1/2(p?ERK1/2)were also measured by Western?blot analysis after 5?and 60?minute treatments with IFN?γand UA alone or in combination. Results MTT assay showed that the treatments with 5-20μmol/L UA for 24 hours had no effects on cell proliferative activity, while 40-80μmol/L UA could significantly inhibit it at 24, 48 and 72 hours (all P < 0.05). Thus, 10 and 15 μmol/L were chosen as the concentrations of UA for further study. After the treatment with 200μg/L IFN?γ, there was a significant increase in the expressions of IL?33 mRNA(0.812 ± 0.036 vs. 0.412 ± 0.021), IL?6 mRNA(0.947 ± 0.091 vs. 0.595 ± 0.030)and IL?33 protein(1.317 ± 0.119 vs. 0.147 ± 0.036)in HaCaT cells compared with the blank control group(all P<0.05). Compared with the IFN?γgroup, the IFN?γ+10?μmol/L UA group and IFN?γ+15?μmol/L UA group both showed significantly decreased expressions of IL?33 mRNA(0.447 ± 0.042 and 0.438 ± 0.028 respectively, both P<0.05), IL?6 mRNA(0.437 ± 0.099 and 0.350 ± 0.075 respectively, both P<0.05)and IL?33 protein(0.923 ± 0.058 and 0.564 ± 0.113 respectively, both P<0.05). There were no significant differences in IL?33 mRNA expression between the IFN?γ+10?or 15?μmol/L UA group and blank control group(P>0.05), while IL?33 protein expression was significantly lower in the IFN?γ+15?μmol/L UA group than in the IFN?γ+10?μmol/L UA group(P<0.05). The p?ERK1/2 protein expression significantly increased in HaCaT cells treated with IFN?γ for 5 and 60 minutes compared with the blank control group, but significantly decreased in the IFN?γ+15?μmol/L UA group compared with the IFN?γgroup(0.458 ± 0.053 vs. 0.941 ± 0.042 at 5 minutes, 0.302 ± 0.054 vs. 0.509 ± 0.032 at 60 minutes, both P < 0.05). However, no significant differences were observed in the total ERK1/2 protein expression between the IFN?γ+15?μmol/L UA group and IFN?γgroup at 5 or 60 minutes. Conclusion UA can suppress IL?33 expression in HaCaT cells induced by IFN?γ, likely by regulating expressions of the ERK signaling pathway?related proteins.