Child ; Dystonia Musculorum Deformans ; diagnosis ; etiology ; genetics ; Humans ; Magnetic Resonance Imaging ; Male

Child ; Diagnosis, Differential ; Humans ; Male ; Paragonimiasis ; diagnosis ; Tuberculosis ; diagnosis

The opening of laboratories in universities is one of important parts in teaching reform and it is necessary for bringing up high-qualified students.Combined with the practical teaching,we have a primary discussion with the problems of the laborato- ry opening and put forward some suggestions and measures.

Background and purpose:Remarkable advances have been made in cancer chemotherapy by developing new anticancer drugs and therapy strategies.However,multidrug resistance in human cancers remains a major clinical challenge for cancer treatment.Attempts in several clinical studies to reverse multidrug resistance protein (MDR) by using MDR modulators have not yet generated promising results.Our aim was to explored the mechanism of reversal of multidrug resistance in human leukemia K562 cells by PI3-K inhibitor.Methods:Trypanblue dye exclusion method was used to observe the drug sensitivity and the effect of LY294002 on the drug resistance.Western blot to analyze P-gp and p-Akt phenotypes,and flow cytometer was used to measure the intracellular drug accumulation. Results:K562/D induced by DNR was cross resistant to DNR,ADR,VCR and VP16 (Resistance Index:65,52,134 and 50 respectively).DNR induced over-expressions of P-gp and p-Akt in K562/D cells;LY294002 increased the intracellular drug accumulation,and then reversed the drug resistance to DNR,ADR,VCR and VPI6 in K562/D cells(Resistance Index:23,21,63 and 29 respectively),but not in the sensitive cells (K562/S).Conclusion:The multidrug resistance of K562/D cells can be induced by DNR which is related to the P-gp and p-Akt over-expressions, and LY294002 can reverse multidrug resistance in human leukemia cells in vitro via inhibits PI3-K/Akt pathway.

Objective To discuss the clinical performance of ICARE rebound tonometer.Methods Intraocular pressure measurements were performed on 112 cases(224 eyes)with non-contact tonometer and ICARE rebound tonometer respectively.Results The intraocular pressure of right eyes which measured by ICARE rebound tonometer was(15.4 ±3.4)mm Hg,and the left eyes' was(15.6 ±3.2)mm Hg on average,but they were(13.5 ±2.7)mm Hg and(13.6 ±2.6)mm Hg respectively measured by non-contact tonometer There was significant difference between the two tonometer(t =4.384,4.535;P ＜0.01).Conclusions lOP measured by ICARE rebound tonometer is higher than that of non-contact tonometer when IOP is in the normal range.ICARE rebound and non-contact tonometer have a good consistency.

OBJECTIVEThe activity of deer serum albumin on proliferation of rat osteogenic-like cells UMR-106 and the IGF-I secretion were investigated in order to elucidate pilose antler's bone-strengthening mechanism.

METHODDeer serum albumin was isolated from freeze-dry pilose antler powder extract. The methods were Sephacryl S-200HR gel filtration, POROS 20QE ion-exchange and TSK G3000SW chromatographies. The effect of deer serum albumin on proliferatio of UMR-106 cells was assaied by MTT, and the secretion of IGF-I of UMR-106 cells was assaied by RIA.

RESULTDeer serum albumin, with the molecular weight of 56.3 kDa, significantly increased the proliferation rate of the osteoblast-like UMR-106 cell and IGF-I secretion. When concentration of deer serum albumin reached 0.149 microg x mL(-1), UMR-106 cell proliferation rate was 241.03% and IGF-I secretion was 66.89 ng x mL(-1).

CONCLUSIONThe concentration of deer serum albumin, from 14.9 ng x mL(-1) to 14.90 microg x mL(-1), significantly increased the proliferation rate of the osteoblast-like UMR-106 cell and IGF- I secretion.

Animals ; Antlers ; chemistry ; Bone Neoplasms ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Deer ; Insulin-Like Growth Factor I ; secretion ; Materia Medica ; isolation & purification ; pharmacology ; Osteoblasts ; metabolism ; pathology ; Osteosarcoma ; pathology ; Rats ; Serum Albumin ; isolation & purification ; pharmacology

OBJECTIVETo identify the mutation in transforming growth factor-beta1 gene (TGF beta1) in a Chinese patient with Camurati-Engelmann disease(CED).

METHODSDenaturing high-performance liquid chromatography (DHPLC) analysis was performed on the whole seven coding exons and exon-intron boundaries, then the mutation was identified by direct sequencing.

RESULTSMutation screening of TGF beta1 in this patient revealed a heterozygous missense mutation R218H in exon 4.

CONCLUSIONThe identification of the mutation could provide essential data for subsequent therapy and genetic counseling.

Base Sequence ; Camurati-Engelmann Syndrome ; genetics ; China ; Chromatography, High Pressure Liquid ; DNA Mutational Analysis ; Humans ; Male ; Mutation ; Polymerase Chain Reaction ; Transforming Growth Factor beta1 ; genetics ; Young Adult

OBJECTIVETo study the clinical efficacy of the endobutton in the treatment of acute acromioclavicular joint dislocation by reconstructing coracoclavicular ligaments.

METHODSFrom October 2008 to January 2010,12 patients with acute acromioclavicular joint dislocation were immobilized with the endobutton. All the patients had the dislocations of or above type III according to Rockwood classification. Among the patients, 9 patients were male and 3 patients were female, with an average age of 55 years (ranged from 31 to 83 years). Eight patients had injuries in the left, and 4 patients in the right. Four patients had accompanied injuries of rib fractures, 2 patients had brain injuries,and 1 patient had femoral fracture. Seven patients were injured by traffic accident, 4 patients were injured by falling down,and 1 patient was sports injuries. All the patients had pain and tenderness at the shoulder, positive piano sign, and shoulder confined activity. The duration from injury to operation ranged from 2 days to 10 days (averaged 6 days). The therapeutic effects were evaluated by Karlsson criteria based on range of motion of acromioclavicular joint, subjective feeling,and postoperative X-ray.

RESULTSAll the patients were followed up, and the duration ranged from 4 months to 19 months (averaged 11 months). The motion of the shoulder joint recovered to normal about 15 to 35 days after operation. There were no displacement, dislocation and redislocation occurred. All the patients got A degree results according to Karlsson criteria.

CONCLUSIONReconstruction of coracoclavicular ligament by using the endobutton to treat acute acromioclavicular dislocation of or above type III is a perfect method with advantage of rigid fixation, micro-injury, and early functional exercise.

Acromioclavicular Joint ; diagnostic imaging ; injuries ; physiopathology ; surgery ; Adult ; Aged ; Aged, 80 and over ; External Fixators ; Female ; Humans ; Joint Dislocations ; diagnostic imaging ; physiopathology ; surgery ; Male ; Middle Aged ; Orthopedic Procedures ; instrumentation ; Tomography, X-Ray Computed ; Treatment Outcome

OBJECTIVEGastric cancer cells are insensitive to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). To sensitize gastric cancer cells to TRAIL, we treated gastric cancer MGC803 cells with TRAIL and cisplatin.

METHODSCell proliferation was measured using MTT assay. Cell apoptosis was determined by flow cytometry. Expression of proteins was analyzed by Western blot. The distribution of lipid rafts and death receptors was analyzed by immunofluorescence microscopy. MGC803 cells were pretreated with 50 mg/L nystatin for 1 h, and followed by the treatment of cisplatin and TRAIL.

RESULTS100 µg/L TRAIL resulted in (8.51 ± 3.45)% inhibition of cell proliferation and caused (3.26 ± 0.89)% cell apoptosis in MGC803 cells. Compared with the treatment with cisplatin alone, treatment with TRAIL (100 µg/L) and cisplatin (8.49 mg/L, IC(50) dose of 24 h) led to a dramatic increase in both inhibition of cell proliferation [(52.58 ± 4.57)% vs. (76.43 ± 5.35)%, P < 0.05] and cell apoptosis [(23.10 ± 3.41)% vs. (42.56 ± 4.11)%, P < 0.05]. Moreover, cleavage of caspase-8 and caspase-3 was detected. TRAIL (100 µg/L) did not induce obvious lipid rafts aggregation and death receptor 4 (DR4) clustering, while cisplatin (8.49 mg/L) significantly promoted the localization of DR4 in aggregated lipid rafts. Pretreatment with 50 mg/L nystatin, a cholesterol-sequestering agent, triggered (3.66 ± 0.52)% cell apoptosis after 24 h. Pretreatment with nystatin for 1 h before the addition of 8.49 mg/L cisplatin for 24 h caused a decreased tendency to cell apoptosis [(25.74 ± 3.28)% vs. (22.76 ± 2.97)%]. While, pretreatment with nystatin before the addition of cisplatin and TRAIL, the proportion of apoptotic cells decreased from (43.16 ± 4.26)% to (31.52 ± 3.99)% (P < 0.05).

CONCLUSIONCisplatin enhances TRAIL-induced apoptosis in gastric cancer MGC803 cells through clustering death receptors into lipid rafts.

Antineoplastic Agents ; administration & dosage ; pharmacology ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cisplatin ; administration & dosage ; pharmacology ; Dose-Response Relationship, Drug ; Humans ; Membrane Microdomains ; metabolism ; Nystatin ; pharmacology ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; metabolism ; Stomach Neoplasms ; metabolism ; pathology ; TNF-Related Apoptosis-Inducing Ligand ; pharmacology

Objective To study the effect of intestinal flora on the pharmacokinetics of ticagrelor in rats.Methods A total of 45 SD rats were randomly divided into control group,test A group and test B group.Rats of test groups were orally given live combined bifidobacterium and lactobacillus tablets for 7 days,respectively;rats of control group were given the same volume distilled water.On day 8,ticagrelor was orally administered to all rats.Blood samples were obtained at 0.08,0.25,0.50,1,1.5,2,3,4,6,8,12,24 h after ticagrelor administration.The plasma concentration of ticagrelor was determined by LC-MS/MS.The pharmacokinetic parameters were determined by DAS 2.1.1 software and the statistic analysis was processed with SPSS 21.0 software.Results The pharmacokinetic parameters of ticagrelor in the test A group,test B group and control group were as follows:AUC0-t were (6336.24 ± 1840.46),(4444.05± 1033.43) and (4469.32 ±928.47) ng· mL-1 · h-1;AUC0-∞ were (6841.98 ± 1975.95),(4656.66 ± 1083.78) and (4736.47 ± 897.42) ng · mL-1 · h;Cmax were (858.65 ± 275.98),648.81 ± 215.59) and (617.49 ± 168.95)ng · mL-1;t1/2 were (6.40 ± 2.18),(5.25 ± 1.39) and (5.68 ± 2.08) h;tmax were (0.88 ± 0.23),(0.90 ± 0.21) and (1.30 ± 0.59) h;clearance (CL) were (2.82±0.72) (4.07±0.99) and (3.95±0.91) L·h-1 ·kg-1;apparent volume of distribution (Ⅴ) were (26.07 ± 12.00),(31.45 ± 14.65) and (32.95 ± 14.17) L · kg-1.There were significant differences in AUC0-t,AUC0-∞,Cmax,tmax and CL between test A group and control group (P ＜ 0.05).On the contrary,no significant differences were observed on the pharmacokinetic parameters between test B group and control group.Conclusion Increased intestinal probiotics can increase the AUC0-t,AUC0-∞,and Cmax of ticagrelor,while decrease the CL of ticagrelor.