Objective To screen the optimized Buyang Huanwu Decoction (BYHWD);To verify it. Methods H2O2 was used to induce PC12 cell oxidative stress models. MTT method was used to determine the prevention effects of BYHWD at different concentrations (0.1, 0.2, 0.5, 1.0, 2.0, 3.5 mg/mL) on in vitro oxidative stress cell models to define the optimized concentration. Orthogonal design was used to divide BYHWD single medicine into decomposed BYHWD groups, control group (only with DMEM), normal group (without H2O2 and medicine processing), and model group, to investigate the protective effects on PC12 cells. Optimized BYHWD was screened to decide the compatibility ratio of each medicine. MTT was used to detect the cell survival rate in each group. Middle cerebral artery occlusion was used to replicate MACO rat models. SD rats were randomly divided into sham-operation group, model group, BYHWD group and optimized BYHWD high-, medium-and low-dose groups. Each medication group was given relevant medicine for gavage. The screened results were verified. Results Compared with other decomposed BYHWD groups, the protective effects of the compatibility of Astragali Radix+Chuanxiong Rhizoma+Pheretima on PC12 cells was the best (P<0.05), which was nearly equaled to BYHWD. Compared with the model group, BYHWD and the optimized one could evidently reduce cerebral cortex infarction area and improve the impaired brain edema (P<0.05), and the medium-dose group was the best. Conclusion The optimized BYHWD ratio is:Astragali Radix:Chuanxiong Rhizoma:Pheretima=10:3:1.

Aim To investigate the effect of aloe-emodin on lipopolysaccharide(LPS)-induced production of nitric oxide and expression of inducible nitric oxide synthase in RAW264.7 cells.Methods RAW264.7 macrophage line in mice was induced by LPS to set up the inflammatory model.Nitric oxide(NO)production was examined by Griess reaction;the expression of iNOS mRNA was detected by RT-PCR analysis;NO radical generation was tested by sodium nitroprusside method.Results Aloe-emodin at the dose of 0.69～2.5 mg·L~(-1) exhibited the inhibitory effect on LPS-induced NO production in a dose-dependent and time-dependent manner;aloe-emodin at the dose of 0.63～5.00 mg·L~(-1) suppressed LPS-induced iNOS mRNA expression in RAW 264.7 cells.However,aloe-emodin had no scavenging effect on sodium nitroprusside-triggered NO production,and didn't affect iNOS enzyme activity.Conclusion Aloe-emodin inhibited signifi-cantly LPS-induced NO production through suppressing inducible NO synthase(iNOS)expression at mRNA level in a dose-dependent and time-dependent manner,but failed to affect sodium nitroprusside-triggered NO production and iNOS enzyme activity.

Background Presbyopia is one of primary causes affecting the visual and life qualities of the agings,and its mechanism is associated with the oxidative damage of lens epithelial cells with ageing.SS31 is a mitochondria-targeted antioxidant peptide.To study the effect of SS31 on oxidative damage of lens epithelial cells has an important significance for the prevention and treatment of presbyopia.Objective This study was to investigate the effect of SS31 on in vitro oxidative damaged human lens epithelial cells.Methods Human lens epithelial cell line (HLEB-3) was cultured using DMEM with low glucose and 10％ fetal bovine serum(FBS).The cell model of oxidative damage was established by adding 200 μmol/L tea-butyl hydropeoxide (t-BHP) into DMEM for 18 hours.The cells were divided into blank control group,t-BHP model group,10 nmol/L SS31 +t-BHP group,100 nmol/L SS31 +t-BHP group,1 μmol/L SS31 +t-BHP group,10 μmol/L SS31 +t-BHP group and 100 pμmol/L t-BHP group,and then MTT assay was used to detect the survival rate of the cells and evaluate the optimal SS31 concentration for sequential study.The cells then were divided into blank control group,t-BHP model group and 1 μmol/L SS31 +t-BHP co-culture group.The change of mitochondrial membrane potential of the cells was tested by JC-1 dye and flow cytometry.Reactive oxygen species (ROS) level in the mitochondria was determined using MitoSOX staining.Results The cell survival rate in the t-BHP model group was (53.42±2.52)％,and that in the blank control group was 100％.The cell survival rate was considerably increased in various concentrations of SS31 groups,showing a significant difference among different groups (F=58.349,P＜0.01).A highest survival rate was (82.13 ±3.15) ％ in the 1 μmol/L SS31 +t-BHP co-culture group,which was statistically significant in comparison with the t-BHP model group (t =28.710,P＜0.05).JC-1 dye and flow cytometry assay showed that the ratio between red and green fluorescence intensity was 7.07 ±0.06 in the blank control group,4.46±0.14 in the t-BHP model group and 5.76±0.26 in the 1 μmol/L SS31 +tBHP co-culture group,showing significant difference among the 3 groups (F=172.332,P＜0.01).The ratios between red and green fluorescence intensity in the blank control group and 1 μmol/L SS31 +t-BHP co-culture group were higher than that in the t-BHP model (t =2.609,1.303,both at P＜0.001).ROS fluorescence cells were much more in the t-BHP model group compared with blank control group and 1 μmol/L SS31 + t-BHP co-culture group.Conclusions SS31 can protect HLEB-3 cells from oxidative stress.SS31 may serve as a potential new approach to the treatment of presbyopia and other age-related diseases of lens.

1:16) of the relative serum antibody has been observed in 80%, while none of this high level was observed in patients with Echovirus-25 and adenovirus dermatitis (

Objective To explore the mutagenic effect of sodium pentachlorophenate (NaPCP) on zebrafish p53 gene coding sequence(CDS) in somatic cell.Methods The experiment was carried out using tuebingen strain of zebrafish, according to the results of acute toxicity test to determine the exposure levels in zebrafish.Zebrafish were randomly divided into blank control group and exposed groups, each containing 10 zebrafish.After exposing for 45d of NaPCP, the RNA was extracted from liver of zebra fish, and the p53 gene including a complete coding sequence of was obtained by RT-PCR.Results LC50 of NaPCP was 18.4 μg/L.Sequence analysis showed that the p53 gene CDS length of 1125bp, encoding 374 amino acids.The percent identity between the published zebrafish sequence of p53 (GI:425876786)and ours was 99.2%,with the other biological sequence of p53 existing some differences.After 45d exposure, zebrafish p53 gene of NaPCP exposure group had mutated at the concentration of 1.8 μg /L.The base substitution of GAG→AAG at codon 8,CAT→CAG at codon 148 and CAG→CAA at codon 229 were detected by PCR-directed sequencing.This may result in the Glu→Lys and His→Gln of expressed p53 protein.Conclusion NaPCP is a kind of gene mutation, which can induce the mutation of p53 gene in zebrafish somatic cells, that has the potential mutagenic risk for humans.

Objective To study maternal toxicity, embryotoxicity and teratogenecity of Chimonanthus salicifolius S. Y. Hu in SD rats.Methods A total of 64 successfully mated female SD rats were randomly divided in to 4 groups (16 per group), in which 3 experimental groups were daily treated with 3.75, 7.5 and 15.0 g/kg. bw test substance by lavage from 7th to 16th day during gestation respectively. Body weight and general conditions of the pregnant rats were recorded during the study. On the 20th day in pregnancy, the rats were anatomized and examined grossly, the fetuses were removed and counted, weight, length, visceral and skeletal changes were then examined. Results There was no significant difference in the conception rate, total weight gain during the pregnancy and the number of living, dead and resorbed fetuses between each dosage groups and the control group (P>0.05) . The number of the rib, sternum, the fifth sternum punctated and the parietal bone which were ossified defectively all showed no difference among the four groups (P>0.05) . Conclusion Chimonanthus salicifolius S. Y. Hu extract had no obvious maternal toxicity, embryotoxicity and teratogenecity in SD rats under this experiment condition.

OBJECTIVETo compare the differences between bone-length measurements on human head and to probe proportion relation of the position of head points.

METHODSOne hundred healthy adult volunteers, aged between 18-25 years, 50 males and 50 females, were randomly selected, and their height, body weight, the distances from Shenting (GV 24) to Toulinqi (GB 15), from Shenting to Touwei (ST 8), between bilateral Touwei (ST 8), between the two Mastoid, from Yintang (EX-HN 3) to front hairline, front hairline to Naohu (GV 17), Naohu to Fengfu (GV 16), Fengfu to the middle of rear hairline were measured respectively with standard measure instruments, and the proportion relation between bone-length measurement location and the point position were compared.

RESULTSThere was a significant difference between the distance of bilateral Touwei and the distance of the two Wangu (P<0.05). The proportion relation of Shenting-Toulinqi, Shenting-Touwei, bilateral Touwei distances basically conformed to the bone-length measurement location, while in the proportion relation of the distances of Yintang-front hairline, front hairline-Naohu, Naohu-Fengfu, Fengfu-the middle of rear hairline and the bone-length measurement location there were some differences.

CONCLUSIONBilateral Touwei distance is not same as the bone-length measurements between two Mastoid, and Toulinqi can be located at the middle point of the connecting line of Shenting and Touwei. There is a certain deviation between marker location of Naohu, Fengfu and other points on body surface and the bone-length measurements.

Acupuncture Points ; Adolescent ; Adult ; Bone and Bones ; anatomy & histology ; Female ; Head ; anatomy & histology ; Humans ; Male ; Medicine, Chinese Traditional

Avidin layer was bound on the substrate surface of Silicon wafer modified with aldehyde. The interaction between avidin and biotin was adopted for the immobilization of mouse monoclonal biotin-anti-M13 (antibody GP3)-labeled biotin. The surface was incubated in a solution containing phage M13KO7, which was trapped by the antibody GP3 with the interaction between phage M13KO7 and antibody GP3, resulting in a variation of layer thickness that was detected by imaging ellipsometry. The results showed a saturated layer of antibody GP3 with a thickness about 6.9 nm on the surface of the silicon wafer. The specific interaction between phage M13KO7 and antibody GP3 resulted in a variation of the layer thickness. The layer of phage M13KO7 bound with antibody GP3 was 17.5 nm in the concentration of 1.1 x 10(10) pfu/mL. Each variation of layer thickness corresponded to a concentration of phage M13KO7 in the range of 0.1 x 10(10) approximately 2.5 x 10(10) pfu/mL, with the sensitivity of 10(9) pfu/mL. Compared with other methods, the optical protein-chip requires only short measurement time, is label free, is a quantitative test, and can be visualized. This study could be significant on the investigation of interactions between the antibody and virus, and shows potential in the early diagnosis of virosis.
Animals ; Antibodies, Viral ; immunology ; Bacteriophage M13 ; immunology ; isolation & purification ; Mice ; Protein Array Analysis ; methods

OBJECTIVETo explore operative method in the treatment of syndesmosis injury of ankle fractures.

METHODSTwenty-four patients with ankle fractures and syndesmosis diastasis were treated with shape memory fracture staples, including 10 males and 14 females ranging in age from 19 to 71 years, with an average of 43 years. All patients were diagnosised with history, body examination and image data and were operated according to classification of Lauge-Hansen.

RESULTSAll patients were followed up from 6 to 28 months with an average of 16 months, and all fractures healed, with a mean time 9.2 (8 to 14) weeks. Only one case had radiological and clinical manifestations of traumatic arthritis, but no breakage of shape memory fracture staple in all cases. Sixteen patients got excellent results, good in 5, fair in 2, poor in 1.

CONCLUSIONShape memory staple fixation for the treatment of syndesmosis diastasis in ankle fractures not only can perseve the physical motion of ankles, but also be remove earlier before weight bearing.

Adult ; Aged ; Ankle Fractures ; Ankle Injuries ; complications ; diagnostic imaging ; surgery ; Ankle Joint ; diagnostic imaging ; surgery ; Female ; Fracture Fixation, Internal ; instrumentation ; Humans ; Male ; Middle Aged ; Radiography ; Treatment Outcome ; Young Adult

OBJECTIVETo investigate the effect of bortezomib alone or combined with harringtonine (HT) or arsenic trioxide (As2O3) on the proliferation capacity and apoptosis of HL-60/ADM cell line and fresh cells from refractory/relapse acute leukemia patients.

METHODSHL-60/ADM cells or refractory/relapse leukemia cells were incubated with bortezomib at different doses alone and in combination with HT or As2O3. The proliferation capacity was observed by MTT assay, cell apoptosis by fluorescence microscopy and flow cytometry. Intracellular concentration of daunorubicin (DNR) was determined by flow cytometry.

RESULTSIn bortezomib-treated HL-60/ADM cells, the proliferation inhibition rate and apoptotic cells increased in a time- and dose-dependent manner. 40 nmol/L bortezomib could maximally inhibit the proliferation of HL-60/ADM cells at 48 hours. 15 micromol/L As2O3 or 752 nmol/L HT combined with different doses of bortezomib could inhibit proliferation and induce apoptosis of HL-60/ADM cells. The As2O3 plus bortezomib or HT plus bortezomib showed a greater anticancer efficacy than either of the drugs alone (P < 0.05, P < 0.01). Bortezomib (10 nmol/L) could markedly enhance the intracellular accumulation of DNR in HL-60/ADM cells (P < 0.05).

CONCLUSIONSBortezomib can inhibit proliferation and induce apoptosis of HL-60/ADM cells and fresh refractory/relapse acute leukemia cells, especially combined with HT or As2O3.

Adolescent ; Adult ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Boronic Acids ; pharmacology ; Bortezomib ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Child ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Female ; HL-60 Cells ; Harringtonines ; pharmacology ; Humans ; Male ; Oxides ; pharmacology ; Pyrazines ; pharmacology ; Young Adult