1.Prevention of unintentional child injuries.
Chinese Journal of Pediatrics 2003;41(11):876-879
2.Vitamin D, vitamin D receptor and clinical disease.
Wei XIANG ; Zong-yi DING ; Wei ZHENG
Chinese Journal of Pediatrics 2004;42(7):541-544
Bone Density
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Coronary Artery Disease
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metabolism
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physiopathology
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Diabetes Mellitus, Type 1
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metabolism
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physiopathology
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Humans
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Hypertension
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metabolism
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physiopathology
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Kidney Diseases
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metabolism
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physiopathology
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Macrophages
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metabolism
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Neoplasms
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metabolism
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physiopathology
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Receptors, Calcitriol
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physiology
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Risk Factors
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Skin Diseases
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metabolism
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physiopathology
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Vitamin D
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metabolism
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physiology
4.Protective effects of recombinant human thioredoxin on myocardium in mice with viral myocarditis
Zong-yan, TENG ; Xino-wei, WU ; Yi-na, ZHANG ; Jing, LI ; Ying-ying, CONG
Chinese Journal of Endemiology 2008;27(4):361-363
Objective To evaluate protective effects of recombinant human thioredoxin(TRX) in myocardial injury of mice with viral myocarditis. Methods We established viral myocarditis models by intraperitoneal injection with 0.1 ml 100TCID50 Coxsackie virus 3m(CVB3m), along with tail vein injection of recombinant human TRX (2 mg/kg) for protection. The control group was given equivalent volume of normal saline. The mice were killed 7 days following the injections. Serum lactate dehydrogenase (LDH) activity was determined and myocardial injury was examined with light microscopy. Results The somm LDH activity in Coxsackie virns-infected mice [(3130.50±390.57)U/L] was higher than that of animals in the control group[ (1617.86±155.42)U/L] and that of TRX protection group[ (1959.43±540.75)U/L], the difference being statistically significant (P<0.05); there was no significant difference between TRX protection group and the control group(P 0.05). Light microscopy showed that five of the eight Coxsackie rims-infected mice had myocardial lesions, including focal myocardial necrosis and inflammatory infiltration. There was no myocardial injury in the TRX protection group. Conclusions Recombinant human TRX can lessen myocardial injuries induced by infection with CVB3m, and so can protect myocardium.
5.Effect of recombinant human thioredoxin on Coxsackie virus 3m-induced cell injury
Zong-yan, TENG ; Yi-na, ZHANG ; Ying, FAN ; Xiao-wei, WU ; Ling-wang, ZHOU ; Tong, WANG
Chinese Journal of Endemiology 2010;29(4):367-370
Objective To observe the protective function of recombinant human thioredoxin(TRX) on HeLa cell injury induced by Coxsackie virus 3m(CVB3m) and to study the inhibiting effect of TRX on viral replication. Methods We infected HeLa cells with 10TCID50 CVB3m and then protected these cells with TRX (2,5,10 mg/L). The protective group of TRX, viral group, control group of TRX, and normal control group were included. Six parallel wells were set up in each group. The cell growth was observed by methyl thiazolyl tetrazolium(MTT) and contrast phase microscope. Results The results of contrast phase microscope revealed that HeLa cells were arranged tightly and polygon in normal control group; untightly, became circle and abscission in viral group; HeLa cells morphous improved by increasing TRX concentration in TRX protective group(2,5,10mg/L). MTT results of the inhibitory ratio on cell growth of TRX(2,5,10 mg/L) control group(1.2%,2.9%,6.3%) were compared with normal control group(0), there was no significant difference(all P > 0.05); and while the inhibitory ratio on cell growth of TRX(2,5,10 mg/L) protective group(32.0%,28.0%,27.0%) was compared with virus infective group(51.7%), there was a significant difference (all P < 0.05). The inhibition study of viral replication showed that compared the inhibitory ratio on cell growth of TRX(2,5,10 mg/L) protective group(26.0%,27.0%, 10.9%) with virus infective group(60.0%), there was a significant difference(all P < 0.05). In the protective groups, there was a significant difference (all P < 0.05) between low dose groups(2,5 mg/L) and high dose groups( 10 mg/L). Conclusions The recombinant TRX(2,5,10 mg/L) may alleviate HeLa cell's injury induced by virus and the construct has no significant toxicity. TRX(2,5,10 mg/L) is effective in inhibiting virus CVB3m replication.
6.Inhibition effect of B7-H1 gene-modified regulatory dendritic cells on thyroid -associated ophthalmopathy in mice
Hua-Xin, CHEN ; Bo-Zong, SHAO ; Xuan-Chen, CHEN ; Wei-Ming, ZHOU ; Yi, ZHANG
International Eye Science 2014;(10):1765-1769
AIM:To construct adenovirus vector expressing mice B7-H1 gene, transfect dendritic cells ( DCs ) , and to study the therapeutic effect of modified DC on thyroid-associated ophthalmopathy ( TAO) in mice.
METHODS: We designed and constructed B7-H1 gene adenovirus expression vector, and transfected DCs from mouse bone marrow, tested the phenotype and function of modified DCs, identificated its negative regulation to immune responses. The modified DCs were infected the sicked mice. And then the immunotherapeutic effect of modified DCs to TAO were tested.
RESULTS: B7 - H1 gene adenovirus vector was constructed and transfected DCs from bone marrow. The titer of the recombinant adenovirus was 1. 8í109 PFU/mL. B7-H1 gene modified DCs characteristics of regulatory DCs, could inhibit positive immune responses. The inhibition proceeding of TAO into mice infected modified DCs, was obviously prior to the control mice. The gene modified DCs, maybe become the new immunotherapy biological agent to thy TAO.
CONCLUSION: We constructed the expression of mouse B7 - H1 gene adenovirus expressed vector successfully, transfected DCs, by vector have properties of regulatory DCs, inhibiting positive immune response and the occurrence and development of thyroid eye disease. Gene modified DCs, reveal potent to the treatment of thyroid eye disease.
7.The effects of protein phosphatase 2A inhibitors on the viability of pancreatic cancer cell and its mechanism
Wei LI ; Zheng CHEN ; Feiran GONG ; Yang ZONG ; Yi MIAO ; Min TAO ; Zekuan XU
Chinese Journal of Digestion 2012;32(1):42-45
ObjectiveTo investigate the effects of protein phosphatase 2A (PP2A) inhibitors on the viability of pancreatic cancer cell line PANC-1 and its mechanism.MethodsPANC-1 cells were treated with PP2A inhibitors Cantharidin or Okadiac acid.The activity degree of NF-κB pathway was tested by Western blot.NF-κB pathway was blocked from all sectors by PP2Acα plamid transfection,NF-κB inhibition of protein kinase α (IKKα) and NF-κB inhibitor α (IκBα) dominant negative mutant and p65 interfering plasmid.Cell viability was determined by MTT.ResultsPP2A inhibitors could induce phosphorylation of IKKα,further phosphorylation of IκBα and degradation and followed by the release of p65 into nucleus.When PP2Acα,IKKα dominant negative mutant and IκBα dominant negative mutant were overexpressed,or p65 was interfered,the inhibition rate of Cantharidin on cell viability decreased (31.85±13.37) %,(23.48±8.98)%,(22.63±5.81)% and (20.88±3.24)%respectively,and the inhibition rate of Okadiac acid on cell viability decreased (40.17 ± 11.65)%,(27.34±14.28)%,(24.85±3.39)% and (27.08±3.81)% respectively.ConclusionsPP2Ainhibitors play a role in preventing pancreatic cancer through PP2Acα/IKKα/IκBα/p65 pathway.
8.Cantharidin induces apoptosis in pancreatic cancer cell lines PANC1 and CFPAC-1
Wei LI ; Zheng CHEN ; Yang ZONG ; Feiran GONG ; Yi ZHU ; Hong YIN ; Zekuan XU ; Min TAO ; Yi MIAO
Chinese Journal of Pancreatology 2011;11(4):255-258
Objective To investigate the apoptosis induction effect of Cantharidin on pancreatic cancer cell line PANC1 and CFPAC-1 and possible mechanism. Methods PANC1 and CFPAC-1 was treated with Cantharidin. Cell growth was determined by MTT. Apoptosis was measured by flow cytometry. Caspase activity was measured by using enzyme chemical method. Apoptosis-related gene expressions were determined by using RT-PCR and Western blotting. Results Cantharidin significantly inhibited the growth of pancreatic cancer cells PANC1, CFPAC-1 and induced apoptosis in a dose-dependent manner. Seventy-two hours after 10 μmol/L Cantharidin treatment, the inhibitory rates of PANC1, CFPAC-1 were (52.95 ± 6.34)% and (71.21 ±6.30)%. Twenty-four hours after treatment, the early and later period apoptotic cell of PANC1 was increased from 7.35% to 24.89%, from 6.36% to 17.73%. The early and later period apoptotic cell of CFPAC was increased from 6.39% to 24.70%, from 9.21% to 12.58% (P<0.01). Activity of caspase 8 and caspase 9 in PANC1 cells was (155.8 + 11.5)% and (194.6 ± 14.7)% when compared with that of control group. Activity of caspase 8 and caspase 9 in CFPAC- 1 was ( 182.5 ± 24.3 ) % and ( 215.8 ± 12.2) %when compared with that of control group ( P < 0. 01 ). The expression of pro-apoptotic genes, TNF-α,TRAILR1, TRAILR2, Bad, Bak and Bid was elevated, the expression of anti-apoptotic Bcl-2 gene was decreased. Conclusions Cantharidin can induce apoptosis in pancreatic cancer cell lines by activating caspase,up-regulating the expression of pro-apoptotic genes and down-regulating the expression of anti-apoptotic genes.
9.Isolation,incubation and identification of parenchymal neural stem cells in adult mouse spinal cord
Hui ZHANG ; Zong-Sheng YIN ; Sheng-Quan ZHANG ; Wei WANG ; Xing-Yi HUA ; Yong HU ; Guang-Wu LI ;
Chinese Journal of Trauma 2003;0(07):-
Objective To isolate and identify the adult neural stem cells from the parenchyma of spinal cord in adult mouse.Methods The parenchymal spinal cord from adult mouse was dissected and dissociated by mechanical trituration.The tissue suspension was cultured in serum-free DMEM/F12 medium supplemented with EGF and B27.The cell colonies generated from a single cell were screened by limited dilution and incubated with BrdU.The cell colonies were transferred into medium with serum to induce differentiation.The cells were identified with antibodies to Nestin,BrdU,MAP2 and GFAP by immunofluorescence staining.Results The cells were cultured for seven days to generate proliferative neurospheres.The majority of cells in these neurospheres expressed Nestin and were differentiated into MAP2-positive cells and GFAP-positive cells in medium containing with fetal bovine serum.Conclusion A significant number of neural stem cells are present in the parenchymal adult mouse spinal cord and can proliferate and also give rise to neurons and glia in vitro.
10.Depression contributed a dissatisfied cervical surgery outcome of the posterior decompression in cervical spondylotic myelopathy
Yaqi ZONG ; Yuan XUE ; Ying ZHAO ; Wei LIN ; Huairong DING ; Dong HE ; Zhiyang LI ; Yanming TANG ; Yi WANG
Chinese Journal of Orthopaedics 2015;(8):854-858
Objective To investigate the effect of depression symptoms on surgical outcome of posterior decompression among cervical spondylotic myelopathy (CSM) patients. Methods Between October 2006 and October 2011 in our hospital, lami?nectomy or laminoplasty was performed in 396 cases that were enrolled in the study. There were 132 males and 264 females with an average age of 60.2 years(ranged,39-84 years). All patients were divided into depression group and non?depressed group by the 21?item Beck Depression Inventory (BDI). There were no statistically significant differences between groups in age, sex, smok?ing status, duration of symptoms, and employment status (whether in the current working). The Japanese Orthopedic Association (JOA) scores, Neck disability index (NDI) and visual analogue scale (VAS) were compared after 1.5 months postoperatively. Re?sults All of 396 cases were followed up. The mean follow up duration was 32 months (range,24-50 months). There were no statistically significant differences in the CCI decline (7.1%±2.1% versus 6.8%±1.5%), expansion degree[(130.9±7.0) mm2 versus (150.8 ± 5.2) mm2] and the drift?back distance of the spinal cord [(5.7 ± 1.2) mm versus (6.2 ± 0.8) mm]. However, pa?tients with continuous depression showed poorer improvement than non?depressed patients in the surgery outcome: JOA im?proved (1.42±0.56 versus 6.76±3.12); NDI declined (7.31±2.18 versus 21.11±11.36); and VAS lightened (16.08±19.76 versus 23.85±20.79). Conclusion Depression contributed a dissatisfied surgery outcome after posterior decompression on functional re?covery, disability index and pain scores among patients of the cervical spondylotic myelopathy.