OBJECTIVETo evaluate the effect of different auxiliary resistance forms on the resistance and marginal fitness of complete crowns for short molar preparations.

METHODSA total of 70 Nissin resin teeth were prepared with 20° total occlusal convergence, 2.5 mm of occlusocervical height, and a shallow finish line on a milling machine. The milled preparations were then randomly assigned to 7 groups of 10. The first group was used as the control group. A total of 30 dies were modified by preparing interproximal grooves with angles of 0°, 6°, and 20° centered on the mesial and distal surfaces of the dies. The rest of the teeth were prepared with occlusal holes in the center of the occlusal surface milled with the same burs to form 0°, 6°, and 20° holes. Cobalt-chromium copings were fabricated for all specimens. The marginal gap of specific points on the axial surface was measured before and after cementation. The resistance of each specimen was evaluated by applying an external force at an angle of 45° to the long axis of the die by using a universal testing machine in a lingual to buccal direction. The maximum force applied before crown dislodgement was measured. Data were analyzed using the SAS 9.2 software.

RESULTSThe results showed that the 0° groove, 0° hole, and 6° hole were effective in improving the resistance of the complete crowns (P<0.05). The 0° groove, 6° groove, 0° hole, 6° hole, and 20° hole had significant difference with the control group in terms of marginal discrepancies (P<0.05).

CONCLUSIONAuxiliary resistance forms with less degree indicate greater resistance force but worse marginal fitness. In clinical practice, if the resistance of a preparation is enough, the auxiliary resistance forms should be avoided from being used.

Cementation ; Crowns ; Dental Prosthesis Design ; Dental Prosthesis Retention ; Humans ; Molar ; Tooth Crown

OBJECTIVETo evaluate the influence of eugenol-containing and resin-containing endodontic sealers on the bond strength of fiber posts using different strategies of root canal irrigation.

METHODSForty-eight mandibular premolars were endodontically treated. The specimens were randomly assigned into two groups according to different endodontic sealers. Group A used Endofil (eugenol-containing endodontic sealer), and group B used AH-plus (resin-containing endodontic sealer). After post space preparation, each group was randomly assigned into three subgroups according to the strategies of root canal irrigation (eight premolars in each subgroup). Group Al and B1: 0.9%NaCl irrigation; Group A2 and B2: 17% ethylene diamine tetraacetic acid (EDTA)+5.25%NaClO+0.9%NaCl irrigation; Group A3 and B3: ultrasonic agitation associated with 1 7%EDTA+5.25%NaClO+0.9%NaCl. One week after the cementation of fiber posts using RelyX™ Unicem, a push-out test was performed to measure the bond strength of the posts. The microstructure of the root canal surface was examined under scanning electron microscope (SEM).

RESULTSThe bond strengths of the six groups were as follows: Al (7.96±2.23) MPa, A2 (9.95±2.89) MPa, A3 (18.88±3.69) MPa, B1 (11.41±3.71) MPa, B2 (14.00±4.04) MPa, and B3 (19.14±3.27) MPa. Statistical analysis revealed a significant interaction between the different endodontic sealers and the strategies of root canal irrigation (P<0.05). Lower bond strength was found in group Al but not in group BI (P<0.05), and the same result was revealed when comparing group A2 and B2. No significant difference was observed between group A3 and B3 (P>0.05). SEM showed that the root canal in group A3 and B3 achieved the cleanest surface with nearly all dentine tubules opened.

CONCLUSIONThe eugenol-containing endodontic sealer can impair the bond strength of fiber posts compared with the resin-containing sealer when the root canal is irrigated by 0.9% NaCl or 17%EDTA+5.25%NaClO+0.9%NaC. No difference was observed between the two sealers when using 17%EDTA+5.25% NaCIO+0.9%NaCl combined with ultrasonic irrigation.

Bicuspid ; Cementation ; Dental Bonding ; Dental Pulp Cavity ; Dental Stress Analysis ; Dentin ; Humans ; Post and Core Technique ; Root Canal Filling Materials ; Root Canal Irrigants ; Root Canal Therapy

Objective To investigate the effect of low 1evel laser treatment (LLLT) on periodontal clinical index,high-sensitivity C-reactive protein (hs-CRP) and metabolic control in patients of type 2 diabetes mellitus combined chronic peridontitis.Methods Nighty patients with type 2 diabetes combined chronic peridontitis were divided into three groups:initial periodontal therapy (group A),initial therapy combined with LLLT (group B) and control group (group C).The periodontal clinical parameters including periodontal probing depth (PD),clinical attachment loss (CAL),sulcus bleeding index (SBI),hs-CRP,HbA1c and fasting blood glucose (FBG) were tested before and at three months after therapy.Results The periodontal clinical parameters (PD,CAL,SBI) and hsCRP in group A and B improved significantly compared with that of group C after therapy (P＜0.05),with group B had more significant difference (P＜0.01).For the levels of HbA1c and FPG,group A and B showed downtrend,and more obvious outcome was detected in group B (P＜0.05).Conclusions LLLT can effectively improve periodontal status,hs-CRP levels and metabolic control of patients with type 2 diabetes combined with chronic peridontitis,and thus to prevent the occurrence of diabetes complications.

AIM: To elucidate the anti-inflammatory mechanism of cholecystokinin octapeptide (CCK-8). METHODS: The pulmonary interstitial macrophages (PIMs) from rats were stimulated with LPS (1 mg?L~(-1)) in the presence or absence of CCK-8 (10~(-8)-10~(-6) mol?L~(-1)) or/and CCK receptor antagonist proglumide (2 mg?L~(-1)). The expression of TNF-? mRNA was assayed by reverse transcription polymerase chain reaction (RT-PCR) at 3 h of the stimulation, and nuclear factor-?B (NF-?B) binding activity was analyzed by electrophoretic mobility shift assay (EMSA) at 1 h of stimulation. The I?B? protein level in the cytoplasma at 30 min of the stimulation was detected by Western blot. RESULTS: CCK-8, at concentrations from 10~(-8) mol?L~(-1) to 10~(-6) mol?L~(-1) obviously inhibited LPS-induced TNF-? mRNA expression and NF-?B binding activity in a dose-dependent manner. Stimulation with LPS resulted in a reduction of I?B? protein level in PIMs, which was elevated by CCK-8. The effects of CCK-8 on NF-?B activity and I?B protein level were attenuated by CCK receptor antagonist proglumide. CONCLUSION: CCK-8 inhibits LPS-induced TNF-? mRNA expression by regulating NF-?B activity in rat PIMs, which is mediated through CCK receptors and inhibition of I?B? degradation. This represents one of the anti-inflammatory mechanisms of CCK-8.

AIM：The mechanism of tumor necrosis factor-alpha (TNF-α) induced pulmonary artery hypertension(PAH) in endotoxic shock (ES) is not clear. Cholecystokinin-octapeptide (CCK-8) had anti-ES and anti-PAH effects. The impact of CCK-8 on changes in vascular reactivity and endothelial ultrastructure induced by TNF-α was studied. The role of nitric oxide (NO) was preliminarily studied. METHODS：Rabbit pulmonary artery rings were divided into four groups: TNF-α, TNF-α+CCK-8, CCK-8 and Vehicle. The rings were incubated for 2 h, 7 h or 14 h. Relaxative responses to ACh(10-8-10-5 mol/L)， SNP (10-9-10-6 mol/L) and contractile responses to PE(10-8-10-5 mol/L) were generated seperately. The NOS activity of rings was detected and the ultrastructure of endothelium was observed in the groups that incubated for 7 h.RESULTS:The relaxative responses to ACh were not affected by TNF-α and CCK-8 after incubation for 2 h. TNF-α(7 h,14 h) significantly reduced ACh-induced endothelium-dependent relaxation response of pulmonary artery. CCK-8 reversed the effect. CCK-8 itself had no effect on responses of normal pulmonary artery. Contraction to PE and relaxation to SNP were unaffected by TNF-α, CCK-8. The NOS activity increased in the TNF-α and the TNF-α+CCK-8 groups. While no significant difference was obseved between the Vehicle and the CCK-8 groups. Endothelial injury in TNF-α group and alleviated changes in TNF-α+CCK-8 group were observed. CONCLUSION:TNF-α significantly inhibits endothelium-dependent relaxation, which be one of the mechanisms of PAH induced by TNF-α during ES. It was found for the first time that CCK-8 reversed TNF-α induced impairment of endothelium-dependent relaxation and alleviated structural injury of endothelium, which might be one of the mechanisms of anti-PAH effect by CCK-8 during ES. The effects of TNF-α and CCK-8 might be related to NO.

AIM and METHODS: To elucidate the mechanism of anti-endotoxic shock of cholecystokinin octapeptide(CCK-8), the effects of CCK-8 on changes in rabbit thoracic aortic reactivities induced by lipopolysaccharides(LPS) in vitro were studied, and the ultrastructure of the endothelial cells was observed under scanning electron microscope. RESULTS: Incubation of thoracic aortic rings(TARs) with LPS(100 mg/L) resulted in an time-dependent impairment of the endothelium-dependent relaxations to acetylcholine(incubation for 3, 7, 14 h), a reduction of contractive response to phenylphrine(incubation for 14 h) and ultrastructural injury in endothelial cells(incubation for 7 h), all of which were alleviated by concomitant incubation with CCK-8(1 mg/L). In contrast, neither the vascular contractions nor the relaxations were affected by CCK-8 (1 mg/L) alone. CONCLUSION: CCK-8 improved the vascular reactivities in the presence of LPS, which may be one of the anti-endotoxic shock mechanisms of CCK.

AIM: To investigate the effect of cholecystokinin octapeptide(CCK-8) on the L-arginine-nitric oxide(NO) pathway in rabbit thoracic aortae treated with lipopolysaccharide(LPS). METHODS: The isolated thoracic aortic rings(TARs) from rabbits were incubated with LPS, LPS+CCK or vehicle for 14 h. Then the contractility to phenylephrine(PE) by TARs and the response to L-arginine(L-Arg) by pre-contractile TARs were measured. In addition, we added NO synthase(NOS) inhibitors aminoguanidine(AG)and N ?-nitro-L-arginine(L-NNA) into organ baths to observe the changes of vascular contractility to PE. NOS activity in isolated TARs were also detected. RESULTS: Incubation of TARs with LPS for 14 h resulted in an increase of NOS activity and a reduction of contractility to PE. Treatment with CCK-8 significantly inhibited the increased NOS activity in thoracic aortae and improved the hypocontractility of TARs to the same degree as AG. CONCLUSION: CCK-8 may improve the hypocontractility of TARs induced by LPS by inhibiting the activity of NOS.

Objective To investigate the role of nuclear factor-kappa B(NF-?B)in the modulation of diallyl trisulfide(DATS)on interleukin-1?(IL-1?)expression induced by lipopolysaccharide(LPS)in mice with acute lung injury(ALI).Methods Mice were randomly divided into Control group,ALI group,DATS group,DATS prevention group and DATS treatment group.The expression of IL-1? mRNA in the lung tissue was detected by reverse transcription PCR(RT-PCR).NF-?B activity in the lung tissue was detected by electrophoresis mobility shift assay(EMSA).The expression of phospho-I?B and I?B were assayed by Western blot.Results The expression of IL-1? mRNA,NF-?B activity and the phospho-I?B expression in lung tissues increased significantly at ALI group(P

Objective To survey the resistance profile of clinical isolates to antibiotics across the hospitals in Dongguan,Guangdong Province during 2015.Methods Kirby-Bauer method or automated system was used to test the susceptibility of clinical isolates to selected antimicrobial agents.Results were analyzed according to CLSI 2015 breakpoints.The susceptibility data were analyzed using WHONET 5.6 software.Results A total of 29 665 strains of microorganisms were isolated,of which gram positive cocci accounted for 32.1％ (9 509/29 665) and gram negative bacilli accounted for 67.9％ (20 156/29 665),respectively.The prevalence of methicillinresistant Staphylococcus was 23.3％ (705/3 024) in S.aureus and 43.6％ (1 054/2 419) in coagulase-negative Staphylococcus.No vancomycin-resistant staphylococcal strain was found.ESBLs-producing strains accounted for 36.4％ (2 554/7 020) in E.coli and 24.5％(792/3 227) in Klebsiella isolates.The prevalence of carbapenem-resistant Enterobacteriaceae was 0.2％ (30/13 077).The prevalence of carbapenem-resistant Pseudomonas aeruginosa (CRPA) and carbapenem-resistant Acinetobacter baumannii (CRAB) was 16.0％ (500/3 116) and 53.9％ (827/1 533),respectively.The prevalence of penicillin-resistant S.pneumoniae (PRSP) strains was 10.1％ (142/1 404).Beta-lactamase was produced in 30.6％ (276/902) of the H.influenzae strains.The prevalence of vancomycin-resistant Enterococcus (VRE) strains was 0.7％ (10/1 441).Conclusions Periodic surveillance of antimicrobial resistance is valuable for rational antimicrobial therapy,formulation of treatment guidelines and infection control and prevention measures,as well as preventing the spread of drug-resistant strains.

AIM: To investigate in vitro effects of cholecystokinin octapeptide(CCK-8) on the expressions of B7.1 and B7.2 and the costimulatory activity of T lymphocytes in unstimulated macrophages.METHODS: Mouse peritoneal macrophages were isolated and incubated with CCK-8(10-12-10-6 mol/L) for indicated time.The B7.1 and B7.2 expressions of murine peritoneal macrophages were analyzed by flow cytometry.CD4+T cells were isolated from mouse spleen using immunomagnetic beads,and cultured with 1/4 numbers of macrophages which were pretreated with CCK-8 and/or anti-B7.1 antibody,anti-B7.2 antibody,CCK1R antagonist CR1409,CCK2R antagonist CR2945 for 24 h.ConA was added into the culture medium to stimulate CD4+T cell proliferation.The proliferation was determined by measuring -TdR incorporation in a ?-scintillation counter.RESULTS: B7.1 and B7.2 expressions and costimulatory activity of peritoneal macrophages were enhanced by CCK-8 in a dose-dependent manner,and the maximal effects occurred at the concentrations of 10-9 mol/L to 10-7 mol/L.Anti-B7.2 antibody,but not anti-B7.1 antibody,reduced the modulatory role of CCK-8 on costimulatory activity.Both CR1409 and CR2945 reversed the effect of CCK-8 on costimulation,and the role of CR1409 was more significant.CONCLUSION: CCK-8 enhances macrophage costimulatory activity by upregulating B7.2 expression,which is mediated by CCK1R and CCK2R.CCK1R might be the major receptor responsible for the modulation of CCK-8 on costimulation.