1.MR-guided percutaneous sclerotherapy of venous vascular malformations of the extremities
Xianjin ZHU ; Wu WANG ; Wen HONG ; Zhenguo HUANG ; Xuezhe ZHANG
Chinese Journal of Radiology 2009;43(5):531-534
Objective To prospectively assess the therapeutic procedure and outcome of MR-guided percutaneous sclerotherapy in patients with venous vascular malformations of the extremities. Methods Fifty-seven percutaneous sclerotherapy treatments were performed under MR guidance in 28 patients with venous vascular malformation. Assessment was conducted to analyze (1) individual success of therapy, (2) improvement of clinical symptoms, ( 3 ) occurrence of complications, (4) volume changes at follow-up examinations, (5) contrast-to -noise ration (CNR) changes. Paired-t test was used to compare the volume and CNR of pre- and postintervention. Results All MR-guided percutaneous sclerotherapy were performed successfully and without serious complications. Individual predominant symptoms were improved, especially about the pain and functional impairment. The mean lesion volumes of pre- and post-intervention were (56. 8 ± 11.7 ) cm3 and ( 27.0 ± 7.2 ) cm3 respectively, which showed significant difference ( t = 8. 90, P < 0. 01 ). The percentage of volume shrinkage ranged from 28. 5% to 74. 4% [ mean ( 54. 4 ± 5. 3 ) % ]. The CNR of the pre and post-interventional images were 21.9 ± 2. 0 and 8.4 ± 0. 9 respectively. There was significant difference(t = 21.76, P < 0.01 ) between them, and the percentages of CNR decrease were 40.0% to 78. 0% [ the mean(61.0 ± 3.6)%]. Conclusion MR-guided sclerotherapy of venous vascular malformations of the extremities is a safe and efficient technique.
2.Effect of iridoid glycosides from Boschniakia rossica on epithelial-mesenchymal transition of HepG2 cells induced by transforming growth factor-beta 1
Aihua JIN ; Jiebo ZHU ; Xuezhe YIN ; Jishu QUAN
Journal of Clinical Hepatology 2024;40(6):1175-1182
ObjectiveTo investigate the effect of iridoid glycosides from Boschniakia rossica (IGBR) on epithelial-mesenchymal transition (EMT) of HepG2 hepatoma cells induced by transforming growth factor-beta 1 (TGF-β1). MethodsHepG2 hepatoma cells were induced by 10 μg/L TGF-β1 to construct an EMT model of hepatoma cells. The cells were divided into control group (treated with serum-free DMEM), model group (treated with 10 μg/L TGF-β1), and IGBR group (treated with 10 μg/L TGF-β1 and 500 mg/L IGBR), and all cells were cultured for 48 hours. Cell adhesion assay, wound healing assay, and Transwell chamber assay were used to observe the migration and invasion abilities of cells. RT-PCR and Western blot were used to measure the mRNA and protein expression levels of E-cadherin, N-cadherin, and vimentin in cells, and Western blot was used to measure the protein expression levels of Slug, Twist1, ZEB1, p-STAT3, and STAT3. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups; the independent-samples t test was used for comparison between two groups. ResultsAfter TGF-β1 induction, HepG2 cells in the model group showed long spindle-shape changes, while those in the control group showed polygonal epithelia-like changes. Compared with the model group, the IGBR group had a significant reduction in cell adhesion rate and significant inhibition of cell migration and invasion abilities (all P<0.05), as well as significant increases in the mRNA and protein expression levels of E-cadherin (P<0.05), significant reductions in the mRNA and protein expression levels of N-cadherin and vimentin (all P<0.05), and significant reductions in the protein expression levels of Slug, Twist1, ZEB1, and p-STAT3 (all P<0.05). ConclusionIGBR can inhibit TGF-β1-induced EMT process in HepG2 cells, thereby attenuating cell adhesion, migration, and invasion abilities, and it can also upregulate E-cadherin, downregulate N-cadherin and vimentin, and upregulate the protein expression of Slug, Twist1, ZEB1, and STAT3, possibly by inhibiting the STAT3 pathway to downregulate the EMT transcription factors such as Slug, Twist1, and ZEB1.
3.Advances in microbial remediation of the re-dissolved chromium contaminated sites.
Xiao YAN ; Jianlei WANG ; Mingjiang ZHANG ; Xuezhe ZHU ; Xingyu LIU
Chinese Journal of Biotechnology 2021;37(10):3591-3603
Wet detoxification has traditionally been seen as the most promising technology for treating chromium-contaminated sites. However, the addition of chemicals in the wet detoxification process not only increases the cost but also introduces extra pollutants. Moreover, the chromium-containing slag may be re-dissolved in the form of Cr(VI), and the increased concentration of Cr(VI) results in a serious "returning to yellow" phenomenon in the chromium-contaminated sites, causing undesirable secondary pollution. Microbial remediation is a promising technology to address the re-dissolution of chromium-containing slag after wet detoxification, and this article reviews the advances in this area. Firstly, the toxicity, current situation and conventional technologies for treating the chromium-containing slag were briefly summarized. The mechanisms of the inevitable re-dissolution of chromium-containing slag after wet detoxification were summarized. Three main mechanisms, namely bioreduction, biosorption and biomineralization, which are involved in the environmental-friendly and efficient microbial remediation technology, were reviewed. The variation of microbial species and the succession of microbial community during the bioremediation of chromium-contaminated sites were discussed. Finally, future research directions were prospected with the aim to develop long-term, stable and sustainable technologies for remediating the chromium-contaminated sites.
Biodegradation, Environmental
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Chromium/toxicity*
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Environmental Pollutants/toxicity*
4.Consensus for the management of severe acute respiratory syndrome.
Nanshang ZHONG ; Yanqing DING ; Yuanli MAO ; Qian WANG ; Guangfa WANG ; Dewen WANG ; Yulong CONG ; Qun LI ; Youning LIU ; Li RUAN ; Baoyuan CHEN ; Xiangke DU ; Yonghong YANG ; Zheng ZHANG ; Xuezhe ZHANG ; Jiangtao LIN ; Jie ZHENG ; Qingyu ZHU ; Daxin NI ; Xiuming XI ; Guang ZENG ; Daqing MA ; Chen WANG ; Wei WANG ; Beining WANG ; Jianwei WANG ; Dawei LIU ; Xingwang LI ; Xiaoqing LIU ; Jie CHEN ; Rongchang CHEN ; Fuyuan MIN ; Peiying YANG ; Yuanchun ZHANG ; Huiming LUO ; Zhenwei LANG ; Yonghua HU ; Anping NI ; Wuchun CAO ; Jie LEI ; Shuchen WANG ; Yuguang WANG ; Xioalin TONG ; Weisheng LIU ; Min ZHU ; Yunling ZHANG ; Zhongde ZHANG ; Xiaomei ZHANG ; Xuihui LI ; Wei CHEN ; Xuihua XHEN ; Lin LIN ; Yunjian LUO ; Jiaxi ZHONG ; Weilang WENG ; Shengquan PENG ; Zhiheng PAN ; Yongyan WANG ; Rongbing WANG ; Junling ZUO ; Baoyan LIU ; Ning ZHANG ; Junping ZHANG ; Binghou ZHANG ; Zengying ZHANG ; Weidong WANG ; Lixin CHEN ; Pingan ZHOU ; Yi LUO ; Liangduo JIANG ; Enxiang CHAO ; Liping GUO ; Xuechun TAN ; Junhui PAN ; null ; null
Chinese Medical Journal 2003;116(11):1603-1635