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Liu Z.,Chinese Institute of Basic Medical Sciences | Qie S.,Chinese Institute of Basic Medical Sciences | Li L.,Institute for Medical Devices Control | Xiu B.,Chinese Institute of Basic Medical Sciences | And 9 more authors.
BioMed Research International | Year: 2016

Rapid and accurate diagnosis of pulmonary tuberculosis (PTB) is an unresolved problem worldwide, especially for sputum smear- (S-) cases. In this study, five antigen genes including Rv3871, Rv3874, Rv3875, Rv3876, and Rv3879 were cloned from Mycobacterium tuberculosis (Mtb) RD1 and overexpressed to generate antigen fragments. These antigens and their combinations were investigated for PTB serodiagnosis. 298 serum samples were collected from active PTB patients, including 117 sputum smear+ (S+) and sputum culture+ (C+) cases, 101 S-/C+ cases, and 80 S-/C- cases. The serum IgG levels of the five antigens were measured by ELISA. Based on IgG levels, the sensitivity/specificity of Rv3871, Rv3874, Rv3875, Rv3876, and Rv3879 for PTB detection was 81.21%/74.74%, 63.09%/94.78%, 32.21%/87.37%, 62.42%/85.26%, and 83.56%/83.16%, respectively. Furthermore, the optimal result for PTB diagnosis was achieved by combining antigens Rv3871, Rv3876, and Rv3879. In addition, the IgG levels of Rv3871, Rv3876, and Rv3879 were found to be higher in S-/C+ PTB patients than in other PTB populations. More importantly, combination of the three antigens demonstrated superior diagnostic performance for both S-/C+ and S-/C- PTB. In conclusion, the combination of Rv3871, Rv3876, and Rv3879 induced higher IgG response in sputum S-/C+ PTB patients and represents a promising biomarker combination for diagnosing of PTB. © 2016 Zhiqiang Liu et al.

Xu L.,Institute for Medical Devices Control | Xu L.,Inner Mongolia University of Science and Technology | Li X.,Inner Mongolia University of Science and Technology | Takemura T.,Japan National Institute of Materials Science | And 3 more authors.
Journal of Nanobiotechnology | Year: 2012

Background: Since silver-nanoparticles (NPs) possess an antibacterial activity, they were commonly used in medical products and devices, food storage materials, cosmetics, various health care products, and industrial products. Various silver-NP based medical devices are available for clinical uses, such as silver-NP based dressing and silver-NP based hydrogel (silver-NP-hydrogel) for medical applications. Although the previous data have suggested silver-NPs induced toxicity in vivo and in vitro, there is lack information about the mechanisms of biological response and potential toxicity of silver-NP-hydrogel.Methods: In this study, the genotoxicity of silver-NP-hydrogel was assayed using cytokinesis-block micronucleus (CBMN). The molecular response was studied using DNA microarray and GO pathway analysis.Results and discussion: The results of global gene expression analysis in HeLa cells showed that thousands of genes were up- or down-regulated at 48 h of silver-NP-hydrogel exposure. Further GO pathway analysis suggested that fourteen theoretical activating signaling pathways were attributed to up-regulated genes; and three signal pathways were attributed to down-regulated genes. It was discussed that the cells protect themselves against silver NP-mediated toxicity through up-regulating metallothionein genes and anti-oxidative stress genes. The changes in DNA damage, apoptosis and mitosis pathway were closely related to silver-NP-induced cytotoxicity and chromosome damage. The down-regulation of CDC14A via mitosis pathway might play a role in potential genotoxicity induced by silver-NPs.Conclusions: The silver-NP-hydrogel induced micronuclei formation in cellular level and broad spectrum molecular responses in gene expression level. The results of signal pathway analysis suggested that the balances between anti-ROS response and DNA damage, chromosome instability, mitosis inhibition might play important roles in silver-NP induced toxicity. The inflammatory factors were likely involved in silver-NP-hydrogel complex-induced toxic effects via JAK-STAT signal transduction pathway and immune response pathway. These biological responses eventually decide the future of the cells, survival or apoptosis. © 2012 Xu et al.; licensee BioMed Central Ltd.

Ren X.,Peking University | Xu L.,Peking University | Xu J.,Institute for Medical Devices Control | Zhu P.,Peking University | And 3 more authors.
Journal of Biomaterials Science, Polymer Edition | Year: 2013

Polysulfone has been widely used as hemodialysis membrane material because of its excellent physiochemical performance. There is still a need to further improve its anti-coagulation property in clinical practice. In this work, we covalently immobilized heparin onto polysulfone membrane to improve its anti-coagulation performance. Low temperature plasma technique with environmentally friendly nitrogen as the gas source, as well as N-ethyl-N′-[3-dimethylaminopropy] carbodiimide hydrochloride/hydroxy-2,5-dioxopyrolidine-3-sulfonicacid sodium chemistry were utilized to immobilize heparin onto the surface of polysulfone membrane. X-ray photoelectron spectroscopy, attenuated total reflectance Fourier-transform infrared spectroscopy, as well as water contact angle results confirmed successful binding of heparin to the membrane surface. Only slight permeability differences were observed between the immobilized surface and the unmodified surface, while the polysulfone membrane had become more hydrophilic after immobilization. The blood coagulation time was greatly prolonged after modification and less platelets adhesion was observed on the heparin immobilized surface. Also, compared with heparin injection doses in clinical, the heparinized process in our work consumed less heparin. Our study suggests that the immobilized heparin has local anti-coagulation effect, while reducing the doses. © 2013 Taylor and Francis.

Xu L.,Institute for Medical Devices Control | Xu L.,Wenzhou University | Shao A.,Institute for Medical Devices Control | Zhao Y.,Institute for Medical Devices Control | And 7 more authors.
Journal of Nanoscience and Nanotechnology | Year: 2015

It is known that the biological half-life of silver in the central nervous system is longer than in other organs. However, the potential toxicity of silver nanoparticles (NPs) on brain tissue and the underlying mechanism(s) of action are not well understood. In this study, neurotoxicity of silver NPs was examined in rat after intragastric administration. After a two-week exposure to low-dose (1 mg/kg, body weight) or high-dose (10 mg/kg) silver NPs, the pathological and ultrastructural changes in brain tissue were evaluated with H&E staining and transmission electron microscopy. The mRNA expression levels of key tight junction proteins of the blood-brain barrier (BBB) were analyzed by real-time RT-PCR, and several inflammatory factors were assessed in blood using ELISA assay. We observed neuron shrinkage, cytoplasmic or foot swelling of astrocytes, and extra-vascular lymphocytes in silver NP exposure groups. The cadherin 1 (2 -ΔΔCt: 1.45-fold/control) and Claudin-1 (2 -ΔΔCt: 2.77-fold/control) were slightly increase in mRNA expression levels, and IL-4 significantly increased after silver NP exposure. It was suggest that silver NP can induce neuronal degeneration and astrocyte swelling, even with a low-dose (1 mg/kg) oral exposure. One potential mechanism for the effects of silver NPs to the nervous cells is involved in inflammatory effects. Copyright © 2015 American Scientific Publishers

Zhao Y.-H.,Institute for Medical Devices Control | Zhao Y.-H.,Center for Medical Device Evaluation | Ding W.-Y.,Dalian Medical University | Wu J.-B.,CAS Institute of Biophysics | Wang C.-R.,Institute for Medical Devices Control
Journal of Dalian Medical University | Year: 2012

[Objective] To study the correlation of ΔNp63α expression with cigarette smoking-induced lung cancer. [Methods] We cultured exposed human normal bronchial epithelial cells (HBE cells) to cigarette smoke extracts and detected the protein and mRNA levels of ΔNp63α with Western blot and realtime PCR respectively. We also cloned the genomic promoter of ΔNp63α and determined its transcriptional activity after exposure to cigarette smoke extracts. [Results] The cigarette smoke extracts induced the expression of ΔNp63α both at protein and mRNA levels significantly in a dose dependent manner. The cigarette smoke extracts at 50 μg/mL induced 93% and 311% increasing of mRNA and protein levels respectively. The transcriptional activity of the ΔNp63α promoter was also enhanced by cigarette smoke extracts in a dose dependent manner. The extracts at 50 μg/mL induced 140% increasing of transcriptional activity. [Conclusion] Cigarette smoke extracts could induce the expression of ΔNp63α by enhancing its transcriptional activity and this finding indicated that ΔNp63α might be involved in cigarette smoking-induced lung cancer.

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