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| 1 | Changed clinical aspects of primary liver cancer in China during the past 30 years显示文摘BACKGROUND: Primary liver cancer (PLC) is one of the most frequently seen tumors in China. Thirty years ago, patients with PLC were often detected at relatively late stage, with a palpable mass or marked clinical symptoms and poor prognosis. In the past 30 years, the diagnosis and treatment of PLC have been greatly improved with better prognosis. METHODS: In order to study the changes of PLC during the 30 years, the clinical data of 3250 patients with PLC from 10 medical institutions of China were collected, ana- lyzed , and compared with those of 3254 PLC patients be- fore the 30 years. RESULTS: In the 3250 patients aged 1-80 years, with an average age of 49.1 years, the male to female ratio (2.3:1) was lower than that before the 30 years. 73.5% of the 3250 patients sought medical advice within 3 months after the onset of the disease in contrast to 63.8% before the 30 years. Compared with those patients before the 30 years the symptoms and signs were alleviated generally. The HBsAg positive rate was 81.0%, but the HCV-Ab positive rate was 13.2%. The AFP level in 75% of patients was elevated, but in the remaining 25% was normal. 1912 patients (58.8%) were confirmed pathologically. Among them 1755 patients (91.8%) had hepatocellular carcinoma. The overall resec- tion rate was 46.3%. Those who had early, middle, late stage carcinoma accounted for 29.9%, 51.5%, and 18.6%respectively in contrast to 0.4%, 47.0%, and 52.6% repor- ted before the 30 years. The 1-, 3-, 5-year survival rates of the patients were 66.1%, 39.7%, and 32.5% respectively, whereas 93.5%, 70.1%, and 59.1% for the early stage pa- tients, and 65.3%, 30.5%, and 23.5% for the middle stage patients. The half and 1-year survival rates of the late stage patients were 52.5%, and 14.7%, respectively. CONCLUSION: Comparison with the clinical data before and after the 30 years show that PLC can be diagnosed ear- ly. More PLC patients tend to undergo resection while re- ceiving a better conservative treatment, which ensures a prognosis. | Bing-Hui Yang, Jing-Lin Xia, Li-Wen Huang, Zhao-You Tang, Ming-Shan Chen, Jin-Qing Li, An-Min Liang, Qin-Guo Mo, Hui-Shan Lu, Chao-Liu Dai, Lu-Nan Yan, Zhi-Jian Yu, Rong-Sheng Rao, Le-Qun Li, Zhi-Xiong Su, Zhuang-Wei Fang Shanghai, China Liver Cancer Institute & Zhongshan Hospital, Fudan University, Shanghai 200032, China Tumor Hospital, Zhongshan University, Guangzhou 510000, China Tumor Hospital, Guangxi Medical Universi- ty, Nanning 530000, China Xiehe Hospital, Fujian Medical University, Fuzhou 350000, China Second Hos- pital, Chinese Medical University, Shenyang 110000, China Huaxi Hospital, Sichuan University, Chengdu 610041, China Hospital Affiliated to Nantong Medical University, Nantong 226000 , China Second Hospital, Jiangxi Medical University, Nanchang 330000 , China First Hospital Affiliated to Guangxi Medical University, Nanning 530000 , China People’s Hospital of Hainan Province, Haikou 570000, China | 2004 | Hepatobiliary & Pancreatic Diseases International2004，3，2： | 20 |
| 2 | Olfactory ecto-mesenchymal stem cell-derived exosomes ameliorate murine Sjögren’s syndrome by modulating the function of myeloid-derived suppressor cells显示文摘Sjögren’s syndrome(SS)is a systemic autoimmune disease characterized by progressive inflammation and tissue damage in salivary glands and lacrimal glands.Our previous studies showed that myeloid-derived suppressor cells(MDSCs)exhibited impaired immunosuppressive function during disease progression in patients with SS and mice with experimental Sjögren’s syndrome(ESS),but it remains unclear whether restoring the function of MDSCs can effectively ameliorate the development of ESS.In this study,we found that murine olfactory ecto-mesenchymal stem cell-derived exosomes(OE-MSC-Exos)significantly enhanced the suppressive function of MDSCs by upregulating arginase expression and increasing ROS and NO levels.Moreover,treatment with OE-MSC-Exos via intravenous injection markedly attenuated disease progression and restored MDSC function in ESS mice.Mechanistically,OE-MSC-Exo-secreted IL-6 activated the Jak2/Stat3 pathway in MDSCs.In addition,the abundant S100A4 in OE-MSC-Exos acted as a key factor in mediating the endogenous production of IL-6 by MDSCs via TLR4 signaling,indicating an autocrine pathway of MDSC functional modulation by IL-6.Taken together,our results demonstrated that OE-MSC-Exos possess therapeutic potential to attenuate ESS progression by enhancing the immunosuppressive function of MDSCs,possibly constituting a new strategy for the treatment of Sjögren’s syndrome and other autoimmune diseases. | Ke Rui Yue Hong Qiugang Zhu Xiaofei Shi Fan Xiao Hailong Fu Qing Yin Yida Xing Xinfeng Wu Xiaodan Kong Huaxi Xu Jie Tian Shengjun Wang Liwei Lu | 2021 | Cellular & Molecular Immunology2021，18，2： | 12 |
| 3 | Induction of tryptase and histamine release from human colon mast cells by lgE dependent or independent mechanisms显示文摘AIM: To investigate the tryptase and histamine release ability of human colon mast cells upon IgE dependent or independent activation and the potential mechanisms.METHODS: Enzymatically dispersed cells from human colons were challenged with anti-IgE or calcium ionophore A23187, and the cell supernatants after challenge were collected. Both concentration dependent and time course studies with anti-IgE or calcium ionophore A23187 were performed. Tryptase release was determined with a sandwich ELISA procedure and histamine release was measured using a glass fibre-based fiuorometric assay.RESULTS:Both anti-IgE and calcium ionophore were able to induce dose dependent release of histamine from colon mast cells with up to approximately 60% and 25% net histamine release being achieved with 1μg/mL calcium ionophore and 10μg/mL anti-IgE, respectively. Dose dependent release of tryptase was also observed with up to approximately 19ng/mL and 21ng/mL release of tryptase being achieved with 10μg/mL anti-IgE and 1μg/mL calcium ionophore, respectively. Time course study revealed that both tryptase and histamine release from colon mast cells stimulated by anti-IgE initiated within 10 sec and reached their maximum release at 6 min following challenge. Pretreatment of cells with metabolic inhibitors abolished the actions of anti-IgE as well as calcium ionophore. Tryptase and histamine release, particularly that induced by calcium ionophore was inhibited by pretreatment of cells with pertussis toxin.CONCLUSION: Both anti-IgE and calcium ionophore are able to induce significant release of tryptase and histamine from colon mast cells, indicating that this cell type is likely to contribute to the pathogenesis of colitis and other mast cell associated intestinal diseases. | Shao-HengHe HuaXie Yong-SongHe | 2004 | World Journal of Gastroenterology2004，10，3： | 11 |
| 4 | Activation of human colon mast cells through proteinase activated receptor-2显示文摘AIM:To investigate the ability of agonists of PAR-2 to stimulate release of tryptase and histamine from human colon mast cells and the potential mechanisms.METHODS:Enzymatically dispersed cells from human colons were challenged with tc-LIGRLO, tc-OLRGIL, SLIGKV,VKGILS, trypsin, anti-IgE or calcium ionophore A23187,and the cell supematants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure and histamine release was measured using a glass fibrebased fluorometric assay.RESULTS: Both PAR-2 agonists tc-LIGRLO-NH2 and SLIGKVNH2 were able to induce dose dependent release of tryptase and histamine from colon mast cells. More than 2.5 fold increase in both tryptase and histamine release was provoked by 100μmol/mL tc-LIGRLO-NH2, in comparison with only 2.0 fold increase being stimulated by SLIGKV-NH2,The reverse peptides tc-OLRGIL-NH2 and VKGILS-NH2 at the concentrations tested had no effect on the release of these two mediators.The maximum tryptase release elicited by tc-LIGRLO-NH2 was similar to that induced by anti-IgE(10μg/mL) or calcium ionophore (1μg/mL), though the latter was a more potent stimulus for histamine release.Both histamine and tryptase release in response to tc-LIGRLONH2 were completed within 3 rain. Trypsin at concentrations from 1.0 to 100μg/mL was capable of provoking a dose dependent release of tryptase as well as histamine with a maximum of 16ng/mL tryptase and 14ng/mL histamine release being achieved. An approximately 80% and 70% inhibition of trypsin induced release of tryptase and histamine were observed with SBTI, respectively. Pretreatment of cells with metabolic inhibitors or pertussis toxin abolished the actions of tc-LIGRLO-NH2, SLIGKV-NH2 and trypsin.CONCLUSION: The agonists of PAR-2 and trypsin are potent secretagogues of human colon mast cells, which are likely to contribute to the development of inflammatory disorders in human gut. | Shao-HengHe Yong-SongHe HuaXie | 2004 | World Journal of Gastroenterology2004，10，3： | 11 |
| 5 | Activation of human tonsil and skin mast cells by agonists of proteinase activated receptor-2显示文摘Aim: To investigate the effects of the agonists of proteinase activated receptor (PAR)-2,and histamine on degranulation of human mast cells. Methods: Human mast cells were enzymatically dispersed from tonsil and skin tissues. The dispersed cells were then cultured with various stimuli, and tryptase and histamine levels in cell supernatants collected from challenge tubes were measured. Results:PAR-2 agonist peptide SLIGKV provoked a dose-dependent release of histamine from skin mast cells. It also induced tryptase release from tonsil mast cells, tcLIGRLO appeared less potent than SLIGKV in induction of release of histamine and tryptase. Trypsin was able to induce a “bell” shape increase in tryptase release from tonsil mast cells. It was also able to induce a dose-dependent release of histamine from both tonsil and skin mast cells. The actions of trypsin on mast cells were inhibited by soy bean trypsin inhibitor (SBTI) or α1-antitrypsin (α1-AT).Time course study revealed that both stimulated tryptase or histamine release initiated within 10s and reached their peak release between 4 and 6min. Pretreatment of cells with metabolic inhibitors or pertussis toxin reduced the ability of mast cells to release tryptase or histamine. Conclusion: It was demonstrated that the in vitro tryptase release properties of human tonsil and skin mast cells suggested a novel type of mast cell heterogeneity. The activation of mast cells by PAR-2 agonists indicated a self-amplification mechanism of mast cell degranulation. | Shao-hengHE HuaXIE Yi-lingFU | 2005 | Acta Pharmacologica Sinica2005，26，5： | 11 |
| 6 | TLR-mediated metabolic reprogramming in the tumor microenvironment: potential novel strategies for cancer immunotherapy显示文摘Cellular energy metabolism not only promotes tumor cell growth and metastasis but also directs immune cell survival,proliferation and the ability to perform specific and functional immune responses within the tumor microenvironment.A better understanding of the molecular regulation of metabolism in different cell components in the tumor-suppressive microenvironment is critical for the development of effective strategies for human cancer treatments.Toll-like receptors(TLRs)have recently been recognized as critical factors involved in tumor pathogenesis,regulating both tumor cells and tumor-infiltrating innate and adaptive immune cells.However,little is known about the molecular crosstalk between TLR signaling and tumor or/and immune cell metabolism,although there is abundant expression of TLRs in these cells.In this review,we explore the functional role of TLR signaling in reprogramming cell metabolism in the tumor microenvironment.In particular,we discuss how malignant tumors regulate metabolism to support their growth and survival,summarize more recently identified metabolic profiles of different immune cell subsets and TLR-mediated regulation of cellular metabolism in both tumor and immune cells,and further explore potential strategies targeting cell metabolism for TLR-based cancer therapy.An improved understanding of these issues should open new avenues for the development of novel strategies via TLR-mediated metabolic reprogramming of the tumor microenvironment for cancer immunotherapy. | Lan Huang Huaxi Xu Guangyong Peng | 2018 | Cellular & Molecular Immunology2018，15，5： | 11 |
| 7 | M1 muscarinic acetylcholine receptor in Alzheimer's disease显示文摘The degeneration of cholinergic neurons and cholinergic hypofunction are pathologies associated with Alzheimer's disease(AD). Muscarinic acetylcholine receptors(mAChRs) mediate acetylcholine-induced neurotransmission and five mAChR subtypes(M1–M5) have been identified. Among them, M1 mAChR is widely expressed in the central nervous system and has been implicated in many physiological and pathological brain functions. In addition, M1 mAChR is postulated to be an important therapeutic target for AD and several other neurodegenerative diseases. In this article, we review recent progress in understanding the functional involvement of M1 mAChR in AD pathology and in developing M1 mAChR agonists for AD treatment. | Shangtong Jiang Yanfang Li Cuilin Zhang Yingjun Zhao Guojun Bu Huaxi Xu Yun-Wu Zhang | 2014 | Neuroscience Bulletin2014，30，2： | 10 |
| 8 | Roles of histamine and its receptors in allergic and inflammatory bowel diseases显示文摘Mast cell has a long history of being recognized as an important mediator-secreting cell in allergic diseases, and has been discovered to be involved in IBD in last two decades. Histamine is a major mediator in allergic diseases, and has multiple effects that are mediated by specific surface receptors on target cells. Four types of histamine receptors have now been recognized pharmacologically and the first three are located in the gut. The ability of histamine receptor antagonists to inhibit mast cell degranulation suggests that they might be developed as a group of mast cell stabilizers. Recently, a series of experiments with dispersed colon mast cells suggested that there should be at least two pathways in man for mast cells to amplify their own activation-degranulation signals in an autocrine or paracrine manner. In a word, histamine is an important mediator in allergic diseases and IBD, its antagonists may be developed as a group of mast cell stabilizers to treat these diseases. | HuaXie Shao-HengHe | 2005 | World Journal of Gastroenterology2005，11，19： | 9 |
| 9 | Inhibition of histamine release from human mast cells by natural chymase inhibitors显示文摘AIM: To investigate the ability of natural chymase inhibitors to modulate histamine release from human mast cells. METHODS: Enzymatically dispersed cells from human lung, tonsil, and skin were challenged with anti-IgE or calcium ionphore A23187 in the absence or presence of the natural chymase inhibitors secretory leukocyte pro- tease inhibitor (SLPI) and α1-antitrypsin, then histamine release was determined. RESULTS: IgE-dependent hista- mine release from lung, tonsil, and skin mast cells were inhibited by up to 70%, 61%, and 62%, respectively following incubation with α1-antitrypsin (5000 nmol/L).SLPI 5000 nmol/L was also able to inhibit anti-IgE- dependent histamine released from lung, tonsil and skin mast cells by up to approximately 72%, 67%, and 58%, respectively. While neither α1-antitrypsin nor SLPI by themselves altered histamine release from lung, tonsil and skin mast cells, they were able to inhibit calcium ionophore-induced histamine release from lung and tonsil mast cells. CONCLUSION: Both α1-antitrypsinand SLPIcould potently inhibit IgE-dependent and calcium ionophore- induced histamine release from dispersed human lung, tonsil, and skin mast cells in a concentration-dependent manner, which suggested that they were likely to play a protective role in mast cell associated diseases including allergy. | Shao-hengHE HuaXIE Xiao-junZHANG Xian-jieWANG | 2004 | Acta Pharmacologica Sinica2004，25，6： | 9 |
| 10 | Olfactory ecto-mesenchymal stem cells possess immunoregulatory function and suppress autoimmune arthritis显示文摘最近的研究在嗅觉的薄板 propria 作为居民干细胞的一种新类型识别了嗅觉的 ecto 间充质的干细胞(OE-MSCs ) 。然而,它仍然保持不清楚是否 OE-MSCs 拥有任何 immunoregulatory 功能。在这研究,我们发现老鼠 OE-MSCs 比骨头表示了更高转变的生长因素贝它和 interleukin-10 层次导出髓的 MSC。在文化, OE-MSCs 经由直接压制受动器 T 房间增长并且增加规章的 T (Treg ) 房间扩大施加了他们的抑制免疫力的能力。在有导致骨胶原的关节炎的老鼠, OE-MSCs 的采纳转移显著地压制了关节炎发作和疾病严厉,它被增加的 Treg 房间伴随并且在 vivo 减少了 Th1/Th17 房间回答。一起拿,我们的调查结果在调整 T 房间回答识别了 OE-MSCs 的新奇功能,显示那 OE-MSCs 可以为风湿性关节炎和另外的自体免疫的疾病的处理代表新房间治疗。 | Ke Rui Zhijiang Zhang Jie Tian Xiang Lin Xiaohui Wang Jie Ma Xinyi Tang Huaxi Xu Liwei Lu Shengjun Wang | 2016 | Cellular & Molecular Immunology2016，13，3： | 8 |
| 11 | Modulation of histamine release from human colon mast cells by protease inhibitors显示文摘AIM:To investigate the ability of protease inhibitors to modulate histamine release from human colon mast cells.METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophore A23187 in the absence or presence of tryptase and chymase inhibitors, and histamine release was determined.RESULTS: IgE dependent histamine release from colon mast ceils was inhibited by up to approximately 37%, 26% and 36.8% by chymase inhibitors Z-Ile-Glu-Pro-Phe-CO2 Me(ZIGPFM), N-TosyI-L-phenylalanyl-chloromethyl ketone (TPCK), and C^l-antitrypsin, respectively. Similarly, inhibitors of tryptase leupeptin, N-tosyI-L-lysine chloromethyl ketone (TLCK), lactoferrin and protamine were also able to inhibit anti-IgE induced histamine release by a maximum of some 48%,37%,40% and 34%, respectively. Preincubation of these inhibitors with cells for 20 rain before challenged with anti-IgE had small effect on the inhibitory actions of these inhibitors on colon mast cells. A specific inhibitor of aminopeptidase amastatin had no effect on anti-IgE induced histamine release. The significant inhibition of calcium ionophore induced histamine release was also observed with the inhibitors of tryptase and chymase examined. Apart from leupeptin and protamine, the inhibitors tested by themselves did not stimulate colon mast cells.CONCLUSION: It was demonstrated that both tryptase and chymase inhibitors could inhibit IgE dependent and calcium ionophore induced histamine release from dispersed colon mast cells in a concentration dependent of manner, which suggest that they are likely to be developed as a novel class of anti-inflammatory drugs to treat chronic of colitis in man. | Shao-HengHe HuaXie | 2004 | World Journal of Gastroenterology2004，10，3： | 7 |
| 12 | Modulation of tryptase secretion from human colon mast cells by histamine显示文摘AIM: TOtryptasepotentialinvestigate the ability of histamine to modulate release from human colon mast cells and the mechanisms.METHODS: Enzymatically dispersed cells from human colons were challenged with histamine, anti-IgE or calcium ionophore A23187 (CI), and the cell supernatants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure.RESULTS:Histamine at concentrations from 1ng/mL was able to induce a “bell” shape dose related release of tryptase from colon mast cells. The maximum release of tryptase was approximately 3.5 fold more than spontaneous release. As little as 10ng/ml histamine showed a similar potency to 10μg/mL anti-IgE in induction of tryptase release. Histamine induced release of tryptase initiated at 10s when histamine (100ng/mL) was added to cells, gradually increased thereafter, and completed at 5 rain.Both pertussis toxin or metabolic inhibitors were able to inhibit histamine induced tryptase release. When histamine and anti-IgE were added to colon mast cells at the same time, the quantity of tryptase released was similar to that induced by anti-IgE alone.The similar results were observed with CI. However, when various concentrations of histamine were incubated with cells for 20min before adding anti-IgE or CI, the quantity of tryptase released was similar to that was induced by histamine alone.CONCLUSION:Histamine is a potent activator of human colon mast cells, which represents a novel and pivotal selfamplification mechanism of mast cell degranulation. | Shao-HengHe HuaXie | 2004 | World Journal of Gastroenterology2004，10，3： | 5 |
| 13 | The C-terminal 17 amino acids of the photoreceptor UVR8 is involved in the fine-tuning of UV-B signaling^FA显示文摘Plant UV-B responses are mediated by the photoreceptor UV RESISTANCE LOCUS 8 (UVR8). In re-sponse to UV-B irradiation, UVR8 homodimers dissociate into monomers that bind to the E3 ubiquitin ligase CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1). The in-teraction of the C27 domain in the C-terminal tail of UVR8 with the WD40 domain of COP1 is critical for UV-B sig-naling. However, the function of the last 17 amino acids (C17) of the C-terminus of UVR8, which are adjacent to C27, is unknown, although they are largely conserved in land plants. In this study, we established that Arabidopsis thaliana UVR8 C17 binds to full-length UVR8, but not to COP1, and reduces COP1 binding to the remaining portion of UVR8, including C27. We hypothesized that overexpression of C17 in a wild-type background would have a dominant negative effect on UVR8 activity;however, C17 overexpression caused strong silencing of endogenous UVR8, precluding a detailed analysis. We therefore generated YFP-UVR8N423 transgenic lines, in which C17 was deleted, to examine C17 function in-directly. YFP-UVR8N423 was more active than YFP-UVR8, suggesting that C17 inhibits UV-B signaling by attenuating binding between C27 and COP1. Our study reveals an inhibitory role for UVR8 C17 in fine-tuning UVR8–COP1 interactions during UV-B signaling. | Li Lin Huaxi Dong Guoqian Yang Ruohe Yin | 2020 | Journal of Integrative Plant Biology2020，62，9： | 3 |
| 14 | Inhibition of tryptase release from human colon mast cells by protease inhibitors显示文摘AIM: To investigate the ability of protease inhibitors to modulate tryptase release from human colon mast cells.METHODS: Enzymatically dispersed cells from human colon were challenged with anti-IgE or calcium ionophore A23187 in the absence or presence of tryptase and chymase inhibitors,and tryptase release was determined.RESULTS:IgE dependent tryptase release from colon mast cells was inhibited by up to approximately 37%, 40% and 36.6% by chymase inhibitors Z-Ile-Glu-Pro-Phe-CO2Me (ZIGPFM), N-tosyI-L-phenylalanyl-chloromethyl ketone (TPCK), and α1-antitrypsin, respectively. Similarly, the inhibitors of tryptase leupeptin, N-tosyI-L-lysine chloromethyl ketone (TLCK) and lactoferrin were also able to inhibit anti-IgE induced tryptase release by a maximum of 39.4%,47.6% and 36.6%, respectively. The inhibitory actions of chymase inhibitors, but not tryptase inhibitors on colon mast cells were enhanced by preincubation of them with cells for 20min before challenged with anti-IgE. At a concentration of 10μg/mL, protamine was able to inhibit anti-IgE and calcium ionophore induced tryptase release. However, at 100μg/mL, protamine elevated tryptase levels in supematants.A specific inhibitor of aminopeptidase amastatin had no effect on anti-IgE induced tryptase release. The significant inhibition of calcium ionophore induced tryptase release was also observed with the inhibitors of tryptase and chymase examined. The inhibitors tested by themselves did not stimulate tryptase release from colon mast cells.CONCLUSION:It was demonstrated for the first time that both tryptase and chymase inhibitors could inhibit IgE dependent and calcium ionophore induced tryptase release from dispersed colon mast cells in a concentration dependent of manner, which suggest that they are likely to be developed as a novel class of anti-inflammatory drugs to treat chronic of colitis in man. | Shao-HengHe HuaXie | 2004 | World Journal of Gastroenterology2004，10，3： | 3 |
| 15 | Effects of reduction temperature and content of Pd loading on the performance Pd/CeO2 catalyst for CO oxidation显示文摘The content of noble metal loading and the reduction process of the catalysts are important factors influence the economic indicator and catalytic performance for industrial catalysis. In the present work, Pd/CeO2NT (Pd supported on the CeO2 nanotubes) catalysts are prepared with the hydrothermal synthesized CeO2NT and glutathione (GSH) reduced Pd nanoparticles via impregnation. The content of Pd loading as well as the catalysts reduction temperature are optimized to the CO oxidation reduction. Our results show that the best Pd loading is 1.5%Pd/CeO2NT. The catalysts reduced at 350 ℃ for 2 h prior to catalytic reaction perform the best toward CO oxidation, which reaches completely CO conversion at 70 ℃. The XRD, Raman, H2-TPR, TEM, BET and XPS characterization reveal that the excellent catalytic performance of 350 °C 1.5%Pd/CeO2NT sample can be attributed the high Pd^0 species and oxygen vacancy in the sample, which are important factors influence the activity of the catalysts. | Yue Yan Huaxi Li Zhanghui Lu Xuewen Wang Rongbin Zhang Gang Feng | 2019 | Chinese Chemical Letters2019，30，6： | 2 |
| 16 | Expression of the human fast-twitch skeletal muscle troponin I cDNA in a human ovarian carcinoma suppresses tumor growth显示文摘To explore the efficiency and mechanism of ovarian carcinoma gene therapy with the human fast-twitch skeletal muscle troponin I gene (TnI-fast), TnI-fast cDNA was transferred into human ovarian adeno-carcinoma cell-line SK-OV-3. In vitro, the cell growth and cell cycle of TnI-fast-, vector-, and mock-transfected cells were determined by MTT and flow cytometry assay, respectively. The condi-tioned media of TnI-fast-, vector-, and mock-transfected SK-OV-3 cells were collected, and the cell pro-liferation inhibiting rates of human umbilical cord venous endothelial cells (HUVECs) by the three conditioned media were assayed. All the three cell lines were implanted into node mice, and the tumor growth, cell apoptosis, angiogenesis, and expression of TnI-fast were observed or analyzed, respec-tively. In vitro, expression of TnI-fast protein had no inhibiting effect on the growth of the dominant and stable transfectant cells, but endothelium, when compared with vector-transfected cells and nontrans-fected parental SK-OV-3 cells. Implantation of stable clone expressing TnI-fast in the female BALB/c nude mice inhibits primary tumor growth by an average of 73%. The nude mice grafts expressing TnI-fast exhibit a significant decrease of microvascular density, a higher rate of tumor cells apoptosis and a comparable proliferation rate as control. Our study, to our knowledge, shows the slowed down growth of the primary ovarian carcinoma, suggested that grafts were self-inhibitory by halting angio-genesis. Our data might also provide a novel useful strategy for cancer therapy by antiangiogenic gene therapy with a specific angiogenesis inhibitor TnI-fast. | XIONG GuangWu1,3, YANG Li2, WEI YuQuan2, WANG ShiLang1, TIAN Ling2, LEI Song2, KAN Bing2 & MAO YongQiu2 1 Department of Obstetrics and Gynecology, Second Huaxi Hospital, Sichuan University, Chengdu 610041, China 2 State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China 3 Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100083, China | 2007 | Science China(Life Sciences)2007，50，1： | 2 |
| 17 | Effect of Zinc on Bone Metabolism in Fetal Mouse Limb Culture显示文摘Objective To determine the effects of zinc-deficiency and zinc-excess on bone metabolism. Methods We developed the culture model of fetal mouse limbs (16th day) cultivated in self-made rotator with continuing flow of mixed gas for six days in vitro. The cultured limbs were examined by the techniques of 45Ca tracer and X-roentgenography. Results The right limbs cultivated had longer bone length, higher bone density than the left limbs uncultivated from the same embryo; and histologically, the right limbs had active bone cell differentiation, proliferation, increased bone trabecula, clearly calcified cartilage matrix, and osteogenic tissue. Compared with the control group,the zinc-deficient group and zinc-excess (Zn2+120 μmol/L) group contained less osteocalcin (BGP) and 45Ca content, and lower AKP activity; whereas zinc-normal (Zn2+45 μmol/L and Zn2+70 μmol/L)groups contained more BGP and 45Ca contents, and higher AKP (alkaline phosphatase) activity.Conclusion Both zinc-deficiency and zinc-excess can alter bone growth and normal metabolism.The results indicate that the culture model of fetal mouse limbs (16th day) in vitro can be used as a research model of bone growth and development. | LI YUN AND YU ZENG-LIDepartment of Nutrition and Food Hygiene, Huaxi School of Public Health, Sichuan University, Chengdu 610041. China | 2002 | Biomedical and Environmental Sciences2002，15，4： | 2 |
| 18 | Leptin Signaling Protects NK Cells from Apoptosis During Development in Mouse Bone Marrow显示文摘增加的证据在有免疫力的反应显示 leptin 的一个角色,但是发信号的 leptin 是否涉及在骨头髓(BM ) 调整 NK 房间开发,仍然保持大部分不清楚。在这研究,我们在在 prediabetic 的缺乏的 db/db 老鼠上演的 leptin 受体的 BM 描绘了 NK 房间区别和成熟。尽管 BM 细胞质类似于控制值, NK 房间的全部的数字严重地在变异的鼠标被减少。db/db BM 房间的流动 cytometric 分析揭示了在区别的各种各样的阶段开发 NK 房间的显著地减少的频率。显著地显示的 BM db/db NK 房间增加了 apoptosis,但是维持了正常房间骑车地位和 proliferative 能力。而且, recombinant leptin 能显著地在文化从野类型的老鼠提高 NK 房间的幸存。NK 房间上的进一步的检查功能的活动证明 db/db NK 房间与显著地增加的 IL-10 展出了正常内在的 cytotoxicity 生产。一起拿,我们的调查结果建议发信号的 leptin 经由在老鼠 BM 提高不成熟的 NK 房间的幸存调整 NK 房间开发。 | Cherry Kam Chun Lo Queenie Lai Kwan Lam Min Yang King-Hung Ko Lingyun Sun Rui Ma Shengjun Wang Huaxi Xu Sidney Tam Chang-You Wu Bo-Jiang Zheng Liwei Lu | 2009 | Cellular & Molecular Immunology2009，6，5： | 2 |
| 19 | Physicochemical properties of porous starches from different botanical origin显示文摘 | Xiao Huaxi Lin Qinlu Wu Yue | 2011 | Advanced Materials Research2011，159，： | 1 |
| 20 | SNX14 deficiency-induced defective axonal mitochondrial transport in Purkinje cells underlies cerebellar ataxia and can be reversed by valproate显示文摘Loss-of-function mutations in sorting nexin 14(SNX14)cause autosomal recessive spinocerebellar ataxia 20,which is a form of early-onset cerebellar ataxia that lacks molecular mechanisms and mouse models.We generated Snx14-deficient mouse models and observed severe motor deficits and cell-autonomous Purkinje cell degeneration.SNX14 deficiency disrupted microtubule organization and mitochondrial transport in axons by destabilizing the microtubule-severing enzyme spastin,which is implicated in dominant hereditary spastic paraplegia with cerebellar ataxia,and compromised axonal integrity and mitochondrial function.Axonal transport disruption and mitochondrial dysfunction further led to degeneration of high-energy-demanding Purkinje cells,which resulted in the pathogenesis of cerebellar ataxia.The antiepileptic drug valproate ameliorated motor deficits and cerebellar degeneration in Snx14-deficient mice via the restoration of mitochondrial transport and function in Purkinje cells.Our study revealed an unprecedented role for SNX14-dependent axonal transport in cerebellar ataxia,demonstrated the convergence of SNX14 and spastin in mitochondrial dysfunction,and suggested valproate as a potential therapeutic agent. | Hongfeng Zhang Yujuan Hong Weijie Yang Ruimin Wang Ting Yao Jian Wang Ke Liu Huilong Yuan Chaoqun Xu Yuanyuan Zhou Guanxian Li Lishan Zhang Hong Luo Xian Zhang Dan Du Hao Sun Qiuyang Zheng Yun-Wu Zhang Yingjun Zhao Ying Zhou Huaxi Xu Xin Wang | 2021 | National Science Review2021，8，7： | 1 |
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