In order to improve its dispersion condition in dental composite resin and enhance its interaction with the matrix, single-walled carbon nanotubes(SWNTs) were refluxed and oxidized, then treated by APTE. Their outer surface were coated by nano-SiO2 particles using sol-gel process, then further treated by organosilanes ATES. IR and TEM were used to analyze modification results. TEM pictures showed nano-particles were on the surface of SWNTs; IR showed characteristic adsorbing bands of SiO2. Composite resin specimen with modified SWNTs was prepared and examined by TEM. SWNTs were detected in composite resin matrix among other inorganic fillers.
Composite Resins ; chemistry ; Dental Materials ; chemistry ; Humans ; Nanotubes, Carbon ; chemistry ; Resin Cements ; chemistry ; Silicon Dioxide ; chemistry ; Surface Properties ; Tensile Strength

Objective To investigate the injury of nonsteroidal anti-inflammatory drug (NSAID) in small intestinal mucosa and the protective role of muscovite.Methods From December 2012 to June 2013,28 healthy volunteers without intestinal mucosal injury showed by capsule endoscopy were selected as objects of this study.Based on computer-generated random number table,the subjects were divided into muscovite group and control group.Subjects of muscovite group orally took muscovite 3 g twice daily,diclofenac 75 mg twice daily and omeprazole 20 mg once a day.The medicine for control group were as same as muscovite group but no muscovite.Patient in both groups took medicines for two weeks.All subjects underwent capsule endoscopy examination after the medication.Before and after the medication,the clinical symptoms of subjects and the changes of small intestinal mucosa under endoscopy were compared.The t-test was performed for comparison between the groups in normally distributed measurement data.For non-normal distributed measurement data,Wilcoxon rank sum test was used for comparison between the groups.Chi-square test or Fisher's exact test was implemented for comparison between the groups of count data.Results There were no differences in the incidences of the injury of the intestinal mucosa,ulceration,petechiae and (or) erythema,mucosal exposure between muscovite group (5/14,4/14,3/14 and 1/14,respectively) and control group (10/14,8/14,7/14 and 3/14,respectively) (all P＞0.05).Both the incidences of intestinal mucosal erosions and lymphangiectasis of muscovite group (4/14 and 1/14) were lower than those of control group (10/14 and 8/14) and the differences were statistically significant (x2 =5.143,Fisher's exact test,both P＜0.05).All the number of injury of the intestinal mucosa,ulceration and erosions of muscovite group (0.00(2.00),0.00(1.00),0.00(1.25),respectively) were lower than those of control group (5.50(17.25),2.00(9.75),3.00(5.00),respectively) and the differences were statistically significant (Z=-2.156,-1.988 and -2.338,all P＜0.05).There was no statistically significant difference in the number of petechiae and (or) erythema between muscovite group and control group (P＞0.05).In muscovite group,the number of grade zero,one,two,three and four intestinal mucosa injury was nine,zero,one,three and one; in control group was four,zero,two,two and six.There was statistically significant difference between the two groups (Z=-2.108,P＜0.05).In muscovite group,the number of mucosa injury in the upper,middle and lower sections of small intestine was 0.00(0.25),0.00(0.25),0.00(0.75),respectively,and there was no significant difference in the distribution of small intestinal mucosa injury in the group (all P＞ 0.05).In control group,the number of mucosa injury in the upper,middle and lower sections of small intestine was 2.00(4.00),0.00(4.25),3.00(9.75),respectively,and there was statistically significant difference in the distribution of small intestinal mucosa injury in the group (x2 =7.189,P＜0.05).The number of small intestinal mucosa injury in the upper and lower sections of control group was more than that of muscovite group and the difference was statistically significant (Z=-2.087 and-2.502,both P＜ 0.05).Conclusion Short-term orally taking NSAID lead to small intestinal mucosal injury and muscovite could reduce NSAID-related small intestinal mucosal injury.

Objective To observe the role and related mechanism of chemerin and its receptor ChemR23 in glomerular endothelial cells (GEnCs) stimulated by high glucose.Methods Mouse GEnCs were cultured and divided into control group,20.0 mmol/L high glucose group,40.0 mmol/L high glucose group and mannitol control group.Then the expressions of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in cell culture supematant as well as the expressions of intracellular protein and mRNA of chemerin,ChemR23,IL-6 and TNF-α were detected.Lentiviral transfection targeting ChemR23 was applied before high glucose-or Chemerin-stimulated,and expressions of supernatant and intracellular mRNA of IL-6 and TNF-α were measured.Meanwhile whether p38 mitogen-activated protein kinase (p38 MAPK) pathway was activated by high glucose was detected.The specific inhibitor of p38 MAPK was added prior to high glucose-stimulated,then supernatant and intracellular mRNA expressions of IL-6 and TNF-α was detected.The supernatant expressions of IL-6 and TNF-α were measured by ELISA.The intracellular protein expression and p38 MAPK phosphorylation activity were detected by Western blotting.The mRNA expression was detected by real time PCR.Results Compared with those in the control group,in high glucose groups the expressions of IL-6,TNF-α and chemerin were significantly increased (all P ＜ 0.05),however,the expressions of ChemR23 did not change (all P ＞ 0.05);the supernatant and mRNA expressions of IL-6 and TNF-α were also elevated in the chemerin group (all P ＜ 0.05).Lentivirus baring shRNA could efficiently suppress ChemR23 expression,and the Chemerin-or high glucose-induced expressions of IL-6 and TNF-α were reduced (all P ＜ 0.05).Also it could significantly reduce the expression of phosphorylated-p38 MAPK (p-p38 MAPK) induced by high glucose (P ＜ 0.05),as high glucose group had higher p-p38 MAPK than control group (P ＜ 0.05).While the high glucose-elevated expressions of IL-6 and TNF-α were significantly attenuated by p38 MAPK inhibitor (all P ＜ 0.05).Conclusions High glucose stimulation can induce the expression of chemerin in GEnCs.By binding to ChemR23,chemerin activates p38 MAPK signaling pathway,and then promotes the expressions of IL-6 and TNF-α.These inflammatory cytokines aggravate inflammation of GEnCs.

OBJECTIVE: To carry out genetic testing and prenatal diagnosis for 29 Chinese pedigrees affected with tuberous sclerosis complex (TSC) and assess efficacy of combined next generation sequencing (NGS) and multiple ligation-dependent probe amplification (MLPA) for the diagnosis. METHODS: NGS and MLPA were used in conjunct to detect variants of TSC1 and TSC2 genes among the probands of the pedigrees. Paternity test was carried out to exclude maternal DNA contamination. Prenatal diagnosis was provided to 14 couples based on the discoveries in the probands. RESULTS: Twenty-seven variants were identified in the TSC1 and TSC2 genes among the 29 pedigrees, which yielded a detection rate of 93.1%. Respectively, 5 (18.5%) and 22 (81.5%) variants were identified in the TSC1 and TSC2 genes. Twelve variants were unreported previously. Prenatal diagnosis showed that five fetuses were affected with TSC, whilst the remaining nine were unaffected. CONCLUSION Above finding has expanded the spectrum of TSC1 and TSC2 gene variants. Combined NGS and MLPA has enabled diagnosis of TSC with efficiency and accuracy.
DNA Mutational Analysis ; Female ; Genetic Testing ; Humans ; Mutation ; Pregnancy ; Prenatal Diagnosis ; Tuberous Sclerosis/genetics* ; Tuberous Sclerosis Complex 1 Protein/genetics* ; Tuberous Sclerosis Complex 2 Protein/genetics*

OBJECTIVE: To explore the genetic basis for a girl with febrile convulsion as the main manifestation. METHODS: The child was subjected to whole exome sequencing (WES) and copy number variation sequencing(CNV-seq). Fluorescence quantitative PCR was carried out to validate the microdeletion in her family. RESULTS: The 7-year-old girl was diagnosed with febrile convulsion (complex type) for having fever for 3 days, mild cough and low thermal convulsion once. Her father, mother and aunt also had a history of febrile convulsion. A heterozygous deletion with a size of approximately 1.5 Mb was detected in the 16p13.11 region by WES and CNV-seq. The deletion has derived from her father and was confirmed by fluorescence quantitative PCR. CONCLUSION 16p13.11 microdeletion syndrome has significant clinical heterogeneity. Different from those with epilepsy, mental retardation, autism, multiple malformations, carriers of 16p13.11 deletion may only manifest with febrile convulsion. Deletion of certain gene(s) from the region may be related to febrile convulsion and underlay the symptom of this child.
Child ; DNA Copy Number Variations ; Epilepsy ; Female ; Humans ; Seizures/genetics* ; Seizures, Febrile/genetics* ; Whole Exome Sequencing