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Ye C.,Huazhong University of Science and Technology | Geng Z.,Hubei Maternity and Child Health Hospital
Chinese Journal of Cancer Prevention and Treatment | Year: 2016

OBJECTIVE: The antitumor function of Difuloromethylornithine (DFMO), especially in solid tumors, has been paid renewed attention in recent years. The purpose of this study was to summarize the research progress of chemoprevention and chemotherapy by DFMO. METHODS: The PubMed and CNKI database from Jan 2000 to Jan 2016 were filtered using “Difuloromethylornithine, neoplasms, chemoprevention, chemotherapy” as keywords. A total of 175 English papers and 16 Chinese papers were obtained. Inclusion criteria: basic research of DFMO as a chemopreventive and/or chemotherapeutic drug; clinical trials of DFMO as a chemopreventive and/or chemotherapeutic agent. Exclusion criteria: progress on preparation of DFMO; research on other ornithine decarboxylase (ODC) inhibitors. Eventually 33 papers were analyzed. RESULTS: The chemopreventive or chemotherapeutic mechanisms of DFMO include decreasing polyamine by inhibiting ODC activity and reversing immunosuppression in the tumor microenvironment. And other mechanisms underlying the DFMO effect are still being explored. The results of the recent studies indicated that DFMO, as a single agent or in combination with other therapy, has remarkable preventive or therapeutic effect on multiple solid neoplasms, especially cancers of epithelial origin, such as colon cancer. Compared with other chemotherapeutic drugs, DFMO is endowed with a high degree of safety and tolerability and is relatively inexpensive. Moreover, since DFMO is a FDA approved agent, the rapid translation of preclinical findings into the clinic can therefore be expected. CONCLUSIONS: It is promising to use DFMO alone and in combination in effective prevention or treatment of neoplasms, although further studies are still needed for repurposing of this “old agent” for new cancer indications. © 2016, Editorial Board of Chinese Journal of Cancer Prevention and Treatment. All right reserved.


PubMed | Fudan University, People's Care, Nanjing Medical University, Zhengzhou University and 8 more.
Type: | Journal: Patient preference and adherence | Year: 2014

Although surveys conducted in Western countries have shown that the levonorgestrel-releasing intrauterine system (LNG-IUS; Mirena()) is well accepted by European women, its acceptance by Chinese women is not yet clearly known. The purpose of this study was to analyze the experiences and levels of satisfaction with Mirena among Chinese women living in 12 different cities.In total, 1,021 women who attended 21 medical centers for insertion of Mirena were invited to complete a questionnaire regarding their contraceptive decision at baseline (preinsertion), and two further questionnaires on their experience and satisfaction with Mirena at 3-6 months and 1 year after insertion.At baseline, 36% of women self-reported heavy or very heavy menstrual bleeding, while 41% reported normal bleeding. The majority of women (98%) were satisfied with the preinsertion counseling, during which contraceptive reliability was identified as the most important reason for considering Mirena. Continuation rates for Mirena were 99% at 3-6 months and 93% at 12 months after insertion, and most women (92% and 93%, respectively) had less bleeding at these times. The percentage of women who rated Mirena as better than their previous contraceptive method was 63%. Overall, around 90% of respondents were very satisfied or rather satisfied with Mirena, and 64% stated that they would recommend it to their friends.These data suggest that continuation and satisfaction rates with Mirena were very high, and that the device is well accepted by Chinese women.


Xia H.,Shanghai JiaoTong University | Wu H.,Jilin University | Xia S.,Hubei Maternity and Child Health Hospital | Zhu X.,Shenzhen Maternity Hospital | And 8 more authors.
Pediatric Infectious Disease Journal | Year: 2014

BACKGROUND: Candida species is an important cause of nosocomial infection in neonatal intensive care units (NICUs). However, most reports in China have been limited to single institutions. The aim of this study is to investigate the epidemiology of invasive candidiasis in multiple NICUs across China. METHODS: We retrospectively collected demographic data, clinical characteristics, microbiological results and outcome of preterm infants with invasive candidiasis discharged from 11 academic tertiary NICUs during January 2009 to December 2011. RESULTS: There were 30,045 preterm infants discharged from 11 NICUs during the study period. We detected 223 infants with invasive candidiasis, resulting in an incidence of 0.74 cases per 100 preterm discharges from NICUs. In very low birth weight infants, the incidence was 3.42 cases per 100 very low birth weight discharges. Mean gestational age of infected infants was 31.4 weeks and median birth weight was 1410 gram. Among the cohort of infants with invasive candidiasis, 214 (96.0%) infants had positive blood culture for fungus, 5 infants had positive urine culture, 3 from cerebrospinal fluid and 1 from articular effusion in the shoulder joint. Among the cohort of infants with candidemia, 48 (22.4%) infants had fungal meningitis. Candida albicans accounted for 57.4% of total positive cultures. Overall mortality attributable to invasive candidiasis was 19.3%. CONCLUSIONS: Invasive candidiasis is a common problem among preterm neonates in China, especially among very low birth weight infants and it is associated with a high mortality. The preponderance of infections was due to Candida albicans. Copyright © 2013 by Lippincott Williams & Wilkins.


Cheng H.,Xi'an Jiaotong University | Zhan N.,Wuhan University | Ding D.,Hubei Maternity and Child Health Hospital | Liu X.,Soochow University of China | And 3 more authors.
Journal of Investigative Dermatology | Year: 2015

Previously, tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) had been known to be an inducer of apoptosis of keratinocytes by engaging the Fn14 receptor. However, the high-risk human papillomavirus (HPV) infection confers a proliferation advantage on keratinocytes that may consequently harbor tumorigenicity. This study was designed to investigate the cross-talk in keratinocytes between TWEAK/Fn14 signaling and HPV type 16 infection, which may cooperate in regulating cell-cycle progression. TWEAK and Fn14 expression was determined in anogenital warts and normal skin. Both primary keratinocytes and HaCaT cells were transfected with HPV16 E6/E7 genes. The results showed that Fn14 is highly expressed upon HPV16 transfection and accompanied by an increase in Ras GTPase activity and TNF-receptor-associated factor 2 (TRAF2) expression. Moreover, the E6/E7-transfected keratinocytes exhibit a shift of TNF receptor profile from type 1 to type 2 and weakened apoptotic response to TNF-α stimuli, when compared with the normal control. Surprisingly, significant increase in proliferation but not apoptosis was seen in E6/E7-positive keratinocytes, as TWEAK was additionally supplemented. In conclusion, the HPV16 infection in keratinocytes causes a switch of apoptotic to proliferative fate under TWEAK/Fn14 interaction, possibly by favoring Ras and TRAF2 activation and modulating TNF receptor expression.


Zou X.,Wuhan University | Zou X.,Hubei Maternity and Child Health Hospital | Cheng H.,Wuhan University | Zhang Y.,Wuhan University | And 3 more authors.
Experimental Biology and Medicine | Year: 2012

Anti-double-stranded DNA (dsDNA) IgG causes renal damage in patients with lupus nephritis by cross-reacting with multiple autoantigens, including alpha-actinin-4, in mesangial cells (MCs). However, how the cross-reactions play a role in mesangial phenotypic abnormalities is not well understood. Here, we investigated the effects of the fragment antigen-binding (Fab) of anti-dsDNA IgG3 on the biochemical properties of alpha-actinin-4. Experiments revealed that anti-dsDNA Fab specifically binds to alpha-actinin-4, but not G-actin. The binding by anti-dsDNA Fab sequentially increases the positive charge of alpha-actinin-4 and inhibits the affinity of alpha-actinin-4 to calcium ions. By the low shear viscosity and a co-sedimentation assay, we found that the alpha-actinin-4-induced F-actin gelation improves when anti-dsDNA Fab is added. However, the Fab control has no such effect on F-actin gelation. Furthermore, the in vitro cultured MCs exhibit higher F-actin expression and transforming growth factor-b1 synthesis after the incubation with anti-dsDNA Fab. Therefore, our results indicated that anti-dsDNA Fab may enhance F-actin formation by the proprietary modification of alpha-actinin-4, which could partially explain the myofibroblast-like phenotype of MCs in anti-dsDNA-positive lupus nephritis. © 2008 Society for Experimental Biology and Medicine.


Cheng H.,Xi'an Jiaotong University | Xu M.,Xi'an Jiaotong University | Liu X.,Soochow University of China | Zou X.,Hubei Maternity and Child Health Hospital | And 2 more authors.
Experimental Dermatology | Year: 2016

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) has been reported to induce keratinocyte apoptosis in vitro by engaging its sole receptor of fibroblast growth factor-inducible 14 (Fn14). In this study, we explored the role of TWEAK/Fn14 pathway in the growth of psoriatic keratinocytes that is, however, characterized by suppressed apoptotic cell death. Skin tissues from the patients with psoriasis or healthy donors were determined for TWEAK and Fn14 expression, and primary keratinocytes were evaluated under the stimulation of psoriatic proinflammatory cytokines or plus TWEAK. The results showed that both TWEAK and Fn14 were highly expressed in psoriatic skins. Moreover, the stimulation of psoriatic cytokines enhanced Fn14 expression by keratinocytes in vitro, which expressed TNF receptor 2 predominantly and proliferated increasingly with the addition of TWEAK. Furthermore, TWEAK stimulation enhanced the synthesis of survivin, inhibitor of apoptosis protein 2 and cellular FLICE-inhibitory protein in lesional keratinocytes. Therefore, TWEAK/Fn14 interaction prefers to enhance proliferation but not apoptosis of keratinocytes under psoriatic inflammation. The activation of nuclear factor-κB signalling-dependent anti-apoptotic proteins and biased expression of TNF receptors may be responsible for such a novel principle in keratinocytes under psoriatic inflammation. © 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.


Zou X.-Y.,Hubei Maternity and Child Health Hospital | Ding D.,Hubei Maternity and Child Health Hospital | Zhan N.,Wuhan University | Liu X.-M.,Soochow University of China | And 2 more authors.
Journal of Investigative Dermatology | Year: 2015

Glyoxalase I (GLO1) is a methylglyoxal detoxification enzyme being implicated in the progression of multiple malignancies. However, currently, the role of GLO1 in human nonmelanoma skin tumors remains unclear. To explore the expression of GLO1 in cutaneous neoplasms and its role in the pathogenesis of skin cancers, we determined the GLO1 expression in multiple subtypes of cutaneous neoplasms and cell lines harboring different tumorigenicity. Also, the GLO1 siRNA transfection was performed in squamous cell carcinoma (SCC)-13 cells or SCC in the xenograft model. The results show that GLO1 was overexpressed by SCC, basal cell carcinoma, and verrucous carcinoma but weakly expressed by several benign neoplasms. Human papilloma virus 16 E6/E7-transfected keratinocytes expressed more GLO1 than did normal keratinocytes, although both of them had lower levels of GLO1 than SCC-13 cells. Moreover, the knockdown of GLO1 by siRNA was related to enhanced apoptosis of SCC-13 cells in the presence of tumor necrosis factor-related apoptosis-inducing ligand and inhibited cell invasion and migration, which was mirrored by the suppressed growth of SCC xenografts in mice. Finally, the GLO1 regulation of SCC-13 cells might be relevant to methylglyoxal-induced p53 translocation. Therefore, GLO1 is prevailingly expressed in cutaneous neoplasms of higher malignancy and contributes to the progression of SCC. © 2015 The Society for Investigative Dermatology.


PubMed | Hubei Maternity and Child Health Hospital, Wuhan University, Xi'an Jiaotong University and Soochow University of China
Type: Journal Article | Journal: The Journal of investigative dermatology | Year: 2015

Glyoxalase I (GLO1) is a methylglyoxal detoxification enzyme being implicated in the progression of multiple malignancies. However, currently, the role of GLO1 in human nonmelanoma skin tumors remains unclear. To explore the expression of GLO1 in cutaneous neoplasms and its role in the pathogenesis of skin cancers, we determined the GLO1 expression in multiple subtypes of cutaneous neoplasms and cell lines harboring different tumorigenicity. Also, the GLO1 siRNA transfection was performed in squamous cell carcinoma (SCC)-13 cells or SCC in the xenograft model. The results show that GLO1 was overexpressed by SCC, basal cell carcinoma, and verrucous carcinoma but weakly expressed by several benign neoplasms. Human papilloma virus 16 E6/E7-transfected keratinocytes expressed more GLO1 than did normal keratinocytes, although both of them had lower levels of GLO1 than SCC-13 cells. Moreover, the knockdown of GLO1 by siRNA was related to enhanced apoptosis of SCC-13 cells in the presence of tumor necrosis factor-related apoptosis-inducing ligand and inhibited cell invasion and migration, which was mirrored by the suppressed growth of SCC xenografts in mice. Finally, the GLO1 regulation of SCC-13 cells might be relevant to methylglyoxal-induced p53 translocation. Therefore, GLO1 is prevailingly expressed in cutaneous neoplasms of higher malignancy and contributes to the progression of SCC.


PubMed | Hubei Maternity and Child Health Hospital, Xi'an Jiaotong University, Wuhan University and Soochow University of China
Type: Journal Article | Journal: Experimental dermatology | Year: 2016

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) has been reported to induce keratinocyte apoptosis in vitro by engaging its sole receptor of fibroblast growth factor-inducible 14 (Fn14). In this study, we explored the role of TWEAK/Fn14 pathway in the growth of psoriatic keratinocytes that is, however, characterized by suppressed apoptotic cell death. Skin tissues from the patients with psoriasis or healthy donors were determined for TWEAK and Fn14 expression, and primary keratinocytes were evaluated under the stimulation of psoriatic proinflammatory cytokines or plus TWEAK. The results showed that both TWEAK and Fn14 were highly expressed in psoriatic skins. Moreover, the stimulation of psoriatic cytokines enhanced Fn14 expression by keratinocytes in vitro, which expressed TNF receptor 2 predominantly and proliferated increasingly with the addition of TWEAK. Furthermore, TWEAK stimulation enhanced the synthesis of survivin, inhibitor of apoptosis protein 2 and cellular FLICE-inhibitory protein in lesional keratinocytes. Therefore, TWEAK/Fn14 interaction prefers to enhance proliferation but not apoptosis of keratinocytes under psoriatic inflammation. The activation of nuclear factor-B signalling-dependent anti-apoptotic proteins and biased expression of TNF receptors may be responsible for such a novel principle in keratinocytes under psoriatic inflammation.


PubMed | Wuhan University, Xi'an Jiaotong University, Hubei Maternity and Child Health Hospital and Soochow University of China
Type: Comparative Study | Journal: The Journal of investigative dermatology | Year: 2015

Previously, tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) had been known to be an inducer of apoptosis of keratinocytes by engaging the Fn14 receptor. However, the high-risk human papillomavirus (HPV) infection confers a proliferation advantage on keratinocytes that may consequently harbor tumorigenicity. This study was designed to investigate the cross-talk in keratinocytes between TWEAK/Fn14 signaling and HPV type 16 infection, which may cooperate in regulating cell-cycle progression. TWEAK and Fn14 expression was determined in anogenital warts and normal skin. Both primary keratinocytes and HaCaT cells were transfected with HPV16 E6/E7 genes. The results showed that Fn14 is highly expressed upon HPV16 transfection and accompanied by an increase in Ras GTPase activity and TNF-receptor-associated factor 2 (TRAF2) expression. Moreover, the E6/E7-transfected keratinocytes exhibit a shift of TNF receptor profile from type 1 to type 2 and weakened apoptotic response to TNF- stimuli, when compared with the normal control. Surprisingly, significant increase in proliferation but not apoptosis was seen in E6/E7-positive keratinocytes, as TWEAK was additionally supplemented. In conclusion, the HPV16 infection in keratinocytes causes a switch of apoptotic to proliferative fate under TWEAK/Fn14 interaction, possibly by favoring Ras and TRAF2 activation and modulating TNF receptor expression.

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