Objective:To investigate the method with good sensitivity,specificity,reliability for diagnosis of Chlamydia trachomatis.Methods:Inoculate the nasopharyngeal swabs to detect the Chlamydia trachomatis(CT) with McCoy cell culture and plasmid gene probes labeled with biotin ligase-chain reaction.Then calculate the sensitivity,specificity,positive predicative value(PPV) and negative predicative value(NPV) of both TC and G-LCR respectively.Compare the difference of the two methods.Results:There were 49 positive specimens and 344 negative by enlarged gold standard.There was significant difference with cell culture,G-LCR-PAGE,G-LCR-ELISA by two-related-samples ? 2 tests( P

Objective To investigate the role of connective tissue growth factor (CTGF) in transdifferentiation of human renal tubular epithelial cells (HKC).Methods Cultured HKC were divided into 3 groups: (1) negative control; (2) low dose CTGF treated (rhCTGF 2. 5 ng/ml); (3) high dose CTGF treated (rhCTGF,5. 0 ng/ml). Expression of ?-smooth muscle actin (?-SMA) and fibronectin(FN) mRNA were measured by RT-PCR. Indirect immunofluorescence and flow cytometry methods were used to assess the level of intracellular ?-SMA protein. Concentration of FN secreted into the media was determined by ELBA. Results Upon the stimulations of different concentrations of rhCTGF,expression of ?-SMA and FN mRNA increased markedly(P

To investigate the role of connective tissue growth factor (CTGF) in transdifferentiation of human renal tubular epithelial cell (HKC), in vitro cultured HKC cells were divided into 3 groups: negtive control, low dose CTGF-treated group (rh CTGF, 2.5 ng/ml) and high dose CTGF-treated (rhCTGF, 5.0 ng/ml). Then the expression of alpha-smooth muscle actin (alpha-SMA) were assessed by indirect immuno-fluorescence, and the percentage of alpha-SMA positive cells were assessed by flow cytometry. RT-PCR were also performed to examine the mRNA level of alpha-SMA. Upon the stimulation of different concentrations of rhCTGF, the expression of alpha-SMA were markedly stronger than that in negative controls. The percentages of alpha-SMA positive cells were significantly higher in the stimulated groups than that of negative controls (38.9%, 65.5% vs 2.4%, P<0.01). alpha-SMA mRNA levels were also up-regulated by the stimulation of rhCTGF (P<0.01). These results suggest that CTGF can promote the transdifferentiation of human renal tubular epithelial cells towards myofibroblast (Myo-F).
Actins/metabolism ; Cell Differentiation/*drug effects ; Cells, Cultured ; Epithelial Cells/*cytology ; Immediate-Early Proteins/*pharmacology ; Insulin-Like Growth Factor Binding Proteins/pharmacology ; Intercellular Signaling Peptides and Proteins/*pharmacology ; Kidney Tubules/*cytology

BACKGROUND: Researchers in China and abroad have done a lot of experiments to study the bond strength of dentine adhesives from generation one to six,which have received satisfied results. However,there are still no reports about the bond strength of the seventh generation adhesive (Adper EasyTM one). OBJECTIVE: To evaluate the bond strength of the Adper EasyTM one to normal dentine and caries-affected dentine,and to compare the results with total-etching adhesives. METHODS: A total of 12 healthy posterior teeth were randomly divided into group A and B; 12 posterior teeth with chronic occlusal caries were divided into group C and D. Adper EasyTM one was applied for group A and C,while Single bond 2 for group B and D. The modes of group A,B,C,D were subjected to microtensile bond strength test. Interfacial morphologies were analyzed by Stereo-Microscopy. RESULTS AND CONCLUSION: The microtensile bond strength of group A and B was (21.84±3.98),(27.10±4.85) MPa,which was (16.44±3.46) and (21.48±4.85) MPa in the group C and D. The differences between group A and B,group C and D,group A and C,as well as group B and D were statistical significant (P < 0.05). Failures mostly occur along the resin-dentine interface. The total-etching adhesives performed more effectively to both normal dentine and caries-affected dentine than Adper EasyTM one. For the same adhesive,the healthy dentine yielded higher bond strength than the caries-affected dentine.

Angiotensin Receptor Antagonists ; Atrial Fibrillation ; physiopathology ; Heart Atria ; cytology ; physiopathology ; Humans ; Membrane Potentials ; Receptors, Angiotensin ; agonists

Objective To investigate the expressions of transforming growth factor-?1(TGF-?1)and ?-smooth muscle actin(?-SMA)in the lungs of mice with intra-amniotic endotoxin priming and exposed to 60% hyperoxia after born in order to elucidate the possible relationship with bronchopulmonary dysplasia(BPD).MethodsFifty C57 pregnant mice were divided into 2 groups:lipopolysaccharide(LPS,40 ?g/L)group and saline solution group,and then received an intra-amniotic injection of corresponding solution on E15.The neonatal mice of each group were randomized to be set in 60% oxygen exposure or in room air.So there were 4 subgroups,LPS+air,LPS+hyperoxia,saline+air and saline+hyperoxia groups.On days 1,3,7,10 and 14 after birth(8 rats each time point),the lung histological changes was assessed with hematoxylin and eosin(HE)staining for radial alveolar counting(RAC).The expressions of TGF-?1 and ?-SMA proteins were detected by immunohistochemical and immunofluorescence staining,and the expressions of TGF-?1 and ?-SMA mRNA by real-time polymerase chain reaction(RT-PCR).ResultsIn the LPS+hyperoxia group and saline+hyperoxia group,RAC began to decrease on day 3,and then further declined in a time-dependent manner.Compared with saline+hyperoxia group,LPS+hyperoxia group had significantly lower RAC(P

AIM:To observe the expression of connective tissue growth factor(CTGF)in unilateral ureteral obstruction(UUO)rats,and to explore its pathogenic role in renal tubulointerstitial fibrosis.METHODS:48 Wistar rats were randomly divided into sham-operated and UUO group.The rats were sacrificed at day 1,3,7,and 14.The degree of tubulointerstitial damage was scored according to the Masson staining.The mRNA and protein levels of CTGF,transforming growth factor-?1(TGF-?1),collagen Ⅰ(Col Ⅰ),and plasminogen activator inhibitor-1(PAI-1)were detected by reverse transcriptional-polymerase chain reaction(RT-PCR)and immunohistochemistry,respectively.Expression of CTGF protein in the kidney was also assessed using Western blotting.RESULTS:TGF-?1 mRNA level began to increase as early as 1 day after UUO.This increase was followed by the elevation of CTGF mRNA level,which began to increase at third days after UUO(P

Objective To investigate the possible mechanism of the gap junctional influence on the change in permeability of the blood-brain barrier(BBB)after reperfusion subsequent to cerebral ischemia.Methods In the test laser scanning confocal microscope(LSCM)was used to investigate the change of Cx43 levels and distribution.The MCAO/R model was induced using intraluminal suture technique first described by Longa with a little modification.A total of 60 Wistar rats were divided into 4 groups:the sham-operation group,control group,octanol-treatment group and DMSO vehicle control group. Control group were further divided into seven subgroups at different time points of reperfusion after middle cerebral artery occlusion.To observe the change in permeability of BBB,Evans blue(EB)in the brain tissue was surveyed by the means of EB fluorescent quantitation.Octanol-treatment group and DMSO vehicle control group were done at the point of the peak of permeability of BBB.Octanol,the specific blocker for gap junctions(GJ)was used in an intervention study.To compare the amount of EB with the same point of groups,the influence of octanol on BBB permeability was investigated.Results At 3 h of reperfusion after cerebral ischemia for 2 h,the permeability of BBB began to increase,reached the peak at 24 h of reperfusion and was still elevated at 72 h.The Cx43 expression formed into bigger plague and remained linear disposition in the penumbra after reperfusion subsequent to cerebral ischemia.Octanol group was done at 24 h of reperfusion after cerebral ischemia.The amount of EB of octanol group((4.924?0.296)?g/g)was significantly lower than that of corresponding operation control group(5.543?0.506)?g/g.Conclusions (1)Cx43 expression is concentrated around vessels in brain.The Cx43 forms into bigger plague and the function maybe strengthens after reperfusion.Gap junction might aggravate the disruption of BBB.(2) Octanol,the specific blocker of gap junctions,could effectively prevent the permeability of BBB from increasing and has a protective effect on BBB.

Objective To investigate the mechanism of HSP70 that inhibits myocardial cell apoptosis in sepsis.Methods Myocardial cells in primary culture were randomly divided into control group,normal serum group,sepsis serum group,transported empty vector group and transported HSP70 group.The myocardial cells in transported HSP70 group have been transported by pcDNA3.1-HSP70 for 36 hours.The myocardial cells in every group have been cultured by respective serum for 2 hours and dyed by Hoechst 33258,and then calculate the rate of myocardial cells apoptosis.Using Western-blot to investigate the effect of overexpression of HSP70 on Caspase-3,8,9's activation and Bid's cracking.Results The rate of myocardial cells apoptosis after dealing in transported HSP70 group [ ( 12.48 ± 2.39 ) ％,( 23.96 ± 3.12 ) ％,( 25.40 ± 3.96) ％ ] is lower than in sepsis serum group [ ( 28.66 ± 2.24 ) ％,( 55.76 ± 5.69 ) ％,( 46.89±8.74)％,t =5.856,5.932,6.027,P ＜0.01,n =3] and lower than in transported empty vector group [(34.25±3.42)％,(50.71±6.38)％,(47.62+5.74)％,t =5.876,5.903,6.122,P ＜0.01,n =3],is higher than in control group,and in normal serum group(3.13％ ～ 6.75％ ,t =6.324,6.578,6.137,5.987,6.032,6.871,P ＜ 0.01,n =3 ).When Caspase-3,8,9 activating,the gray-scale of P11,P20 and P10 in transported HSP70 group( 12.5276 ± 2.1247,9.3481 ± 4.5423,16.1349 ± 6.0641 ) is lighter than that in sepsis serum group ( 27.1324 ± 2.1564,25.5643 ± 4.3018,36.5647 ± 6.7135,t =5.856,5.902,5.891,P ＜ 0.01,n =3 ) and lighter than in transported empty vector group (28.0314 ±2.0367,25.6413 ±4.1356,34.5648 ±5.9473,t =3.861,3.933,4.281,P ＜0.05,n =3),is deeper than in control group(8.0324 ± 1.5234,5.1246 ± 1.3274,2.0314 ±0.6423,t =3.286,3.867,4.031,P＜0.05,n =3) and in normal serum group(8.5649 ± 1.2136,6.0324 ± 1.0214,3.2146 ±0.1325,t =5.898,5.969,6.879,P ＜0.01,n =3).The gray-scale of tBid in transported HSP70 group( 12.0316 ±2.3641 ) is lighter than in sepsis serum group(27.0536 ± 5.3214),t =3.274 ( P ＜ 0.05,n =3 ) and lighter than in transported empty vector group(27.1034 ± 3.6741,t =3.301,P ＜ 0.05,n =3 ),is deeper than in control group ( 6.0347 ± 2.1304,t =5.924,P ＜ 0.01,n =3 ) and in normal serum group ( 7.3121± 1.3021,t =5.871,P ＜ 0.01,n =3 ).Conclusions HSP70 inhibit myocardial cells apoptosis in sepsis by intervened the death receptor pathway and mitochondrial pathway.