Ear, Middle ; pathology ; Female ; Granuloma, Plasma Cell ; pathology ; Humans ; Mastoiditis ; pathology ; Middle Aged

Objective Evaluate the immunotoxicity of Ginenoside Compound K Injection.Methods Active Systemic Anaphylaxis (ASA)tests and Passive Cutaneous Anaphylaxis (PCA)tests were used to evaluate Ginenoside Compound K Injection.Results In the ASA tests,positive control group showed pole-strength anapbylaxis,both the high-dose group and the low-dose group of Ginenoside Compound K Injection didn't produce allergic reaction and the body weights of all groups showed no significant differences.In the PCA tests,all rats of positive control group caused blue spots with their diameters bigger than 5 mm (diameters on the left side of blue spots was (10.1± 3.34) mm and diameters on the right side of blue spots was(7.57± 1.94)mm.Serum IgE was significantly increased.While both high dose and low dose of Ginenoside Compound K Injection group didn't show blue spots with their diameters greater than 5 mm and their IgE levels showed no significant differences compared with negative control group.Conclusion Ginenoside Compound K Injection showed no immunotoxicity under these experimental conditions.

Objective To evaluate the effects of different kinds of fluorides and their loading on the fluoride releasing characteristics of fluoride containing composite resins. Methods Two paste type of composite resin, containing NaF and K 2TiF 6 respectively, were prepared. The composite resins were based on Bis GMA/TEGDMA resin and loaded with fluoride at 5%, 10%, 15% and 20% by weight, and a non fluoridated composite resin was prepared as the control. Six standardized discs (6 mm?3 mm) were made of each material, and three discs of each material were stored in plastic vials containing 5 ml deionized water at 37 ℃ respectively and the others in artificial saliva. The water and the artificial saliva were changed every 24 hours. An ion selective electrode (9606BN Orion) connected to an ion analyzer (720A Orion) was used to determine the amount of fluoride released on days 8, 15, 22, 29 and 62. The data were analyzed using t tests. Results All of the fluoride containing materials demonstrated a higher fluoride release than that from non fluoride control materials. The composite resin containing NaF released significantly more fluoride than that of K 2TiF 6. All materials showed a significantly higher release of fluoride in water than in artificial saliva ( P

Objective To establish a euglycemic clamp technique in beagle dogs. Methods The euglycemic clamp technique was applied in healthy beagle dogs and the blood glucose, insulin, C-peptide, insulin and glucagon were monitored during the clamp. Results The blood glucose was controlled within the basal level.The coefficient of variation was less than 5% during the clamp. The serum insulin concentration finally reached(40.0±3.8)mIU/L stably and a significant inhibition was shown in endogenous insulin by the determination of C-peptide. But there was no significant increase in serum glucagon compared with basal values.Conclusion Methodology confirmed that the euglycemic clamp technique is successful in beagle dogs and can be applied in the study of pharmacodynamics of insulin preparations.

Adult ; Bone Marrow ; pathology ; Female ; Humans ; Leg ; Neoplasm Invasiveness ; Rhabdomyosarcoma, Embryonal ; pathology ; therapy

OBJECTIVE To explore the effect of clofenotane (DDT) on epithelial-mesenchymal transition (EMT) and the relevant molecular mechanism in human colorectal cancer cells. METHODS Human colorectal cancer cells DLD1 were treated with DDT 0.01, 0.1, 1.0, 10.0 and 100.0 nmol·L-1 for 48 h. Then, the morphology of DLD1 cells was observed. mRNA levels of E-cadherin, N-cadherin, vimentin and Snail1 were detected by real-time PCR. Protein expression of STAT3 signaling pathway of proteins STAT3 and p-STAT3 was detected by Western blotting. STAT3 inhibitor WP1006 (5μmol · L-1) was added to determine its impact on DDT-induced alternation of STAT3/Snail1 signaling and EMT-related molecules. Protein expression of STAT3 and p-STAT3 was detected by Western blotting and mRNA levels of E-cadherin, N-cadherin, Vimentin and Snail1 were detected by real-time PCR. RESULTS DLD1 cell morphology was changed after exposure to DDT 0.01-100.0 nmol · L- 1. Meanwhile, real-time PCR showed that the mRNA level of E-cadherin was significantly decreased compared with normal cell control (P<0.01), which was 42.4±2.8%of that in the normal control group. The mRNA levels of N-cadherin, Vimentin and Snail1 were significantly increased (P<0.01), which were 1.91±0.1, 1.5±0.2 and 1.5±0.1 times that of the normal control group. DDT 0.1, 1.0 and 10.0 nmol · L-1 exposure induced up-regulation of STAT3 and p-STAT3 protein levels (P<0.01), which were 2.1 and 1.8 times that of the normal control group. The addition of STAT3 inhibitor WP1066 (5 μmol · L-1) prevented STAT3 from phosphorylation as well as the up-regulation of Snail1(P<0.01), which was (56.3 ± 0.9)% that of the DDT 1.0 nmol · L-1 treat?ment group. Compared with DDT treatment alone, the mRNA levels of EMT-related molecules were remarkably reversed by WP1066 (5 μmol · L- 1) co-treatment, increasing E-cadherin but decreasing N-cadherin and vimentin in DLD1 cells(P<0.01), which were 50.2±2.9%and 61.6±6.1%of those in the DDT 1.0 nmol · L- 1 treatment group, respectively. CONCLUSION DDT alters the expressions of EMT-related molecules including E-cadherin, N-cadherin and vimentin via STAT3/Snail1 signaling, thus promoting the EMT process in human colorectal cancer cells. This progress may be closely related to DDT-induced colorectal cancer development.

Objective To evaluate the effects of sevoflurane anesthesia on the sleep architecture of rats.Methods Sixteen pathogen-free healthy male Sprague-Dawley rats,aged 10-12 weeks,weighing 300-350 g,were divided into 2 groups (n=8 each) using a random number table:control group (group C) and sevoflurane group (group S).Each rat was implanted with a transmitter for recording electromyogram and electroencephalogram via telemetry.The rats were exposed to 2.4％ sevoflurane and pure oxygen 1.5 L/min for 5.5 h followed by 0.5 h washout with pure oxygen in group S,and the rats were exposed to pure oxygen 1.5 L/min for 6 h in group C.Then the rats were taken into the sleep monitoring box,and the 24 h after anesthesia was divided into 4 time periods according to the circadian rhythm:L1 (14:00-20:00),D1 (20:00-02:00),D2 (02:00-08:00) and L2 (08:00-14:00).The total time spent on wakefulness,on non-rapid eye movement (NREM) sleep and on REM sleep,the number of wakefulness,NREM sleep and REM sleep,and the time spent on wakefulness,on NREM sleep and on REM sleep during each time period were recorded using Version 3.0 Neurosore software.Results Compared with group C,the total time spent on wakefulness was significantly shortened,the total time spent on REM sleep was prolonged,the number of NREM sleep was increased,the time spent on REM sleep in L1 and D1 time periods was prolonged,the time spent on wakefulness in D2 time period was shortened,the time spent on NREM sleep was prolonged (P＜0.05),and no significant change was found in the total time spent on NREM sleep or the number of REM sleep and wakefulness in group S (P＞0.05).Conclusion Sevoflurane anesthesia can change the stability of sleep architecture,increase REM sleep and reduce wakefulness in rats.

Acupuncture Therapy ; Humans ; Infant ; Klinefelter Syndrome ; genetics ; therapy ; Male

Adult ; Ear Canal ; Foreign Bodies ; Humans ; Male ; Mandibular Condyle

AIM: To investigate the role of HGF/c-Met signaling pathway in crizotinib-induced apoptosis of different lung carcinoma cell lines and to analyze its potential regulatory mechanisms .METHODS: EML4-ALK positive cell line H2228, c-Met proliferation cell line H1993 and control cell line A549 were treated with crizotinib at different doses for different time periods .The viability of the cell lines was measured by MTT assay .The apoptosis was analyzed by flow cytometry with PI staining.The protein levels of MET and phosphorylated MET (p-MET) of HGF/c-Met signaling pathway as well as its down-stream key proteins AKT , ERK, p-AKT and p-ERK in the cell lines before and after crizotinib treatment were examined by Western blot .RESULTS:The growth of H1993, H2228 and A549 cell lines was inhibited after crizoti-nib treatment for 72 h in a dose-dependent manner .Apoptotic rates of H1993 cells and H2228 cells were increased with the crizotinib concentration and exposure time .Down-regulation of p-MET, p-AKT and p-ERK at protein levels in H1993 cells and H2228 cells after exposure to crizotinib for 72 h was confirmed by Western blot .No obvious change of the related-pro-teins of HGF/c-Met signaling pathway was found in A 549 cell line.CONCLUSION: HGF/c-Met signaling pathway may contribute to crizotinib-induced apoptosis of H1993 cells and H2228 cells, which provides the experimental basis for MET-targeting treatment of lung cancer .