ObjectiveTo investigate the effect of volume embolization ratio(VER) in evaluating the embolization efficacy of aneurysms.MethodsFifty-three patients who received intracranial aneurysm embolization surgery were all treated with detachable coils endovascular embolization,While fifty-seven intracranial aneurysms were treated.The VER was calculated and the relationships between the VER values and the size,the neck,embolization degree of intracranial aneurysm were analyzed.ResultsThe VER of small,medium,large,and giant aneurysms were (40.8 ± 26.5 )％,( 18.6 ± 16.1 )％,(2.3 ± 2.1 )％,(0.4 ±0.1 )％,respectively,which had statistical significance (F =7.091,P ＜ 0.01 ).The VER of wide-necked and narrow-necked aneurysms were (27.5 ± 23.1 )％,(29.4 ± 26.6)％,which had no statistical significance(P ＞0.05 ).The VER of complete embolization,neck residual and partial embolization were (41.8 ± 29.3 )％,(31.4 ± 21.2)％,( 12.3 ± 15.1 )％,respectively,which had statistical differences (F =7.970,P ＜ 0.01 ).ConclusionsThe VER is an objective index to evaluate the embolization degree of aneurysms.It has certain prediction significance for the efficacy judgement of embolization of aneurysms.

Animals ; Atherosclerosis ; diet therapy ; physiopathology ; Humans ; Plaque, Atherosclerotic ; drug therapy

BACKGROUND:Bone marrow mesenchymal stem cels (BMSCs) have the ability of multi-directional differentiation. Polygonatum sibiricum polysaccharide can promote osteogenetic differentiation of mouse BMSCs by activating Wnt/β-catenin signaling pathway, which is expected to become a new drug for the treatment of osteoporosis.
OBJECTIVE:To investigate the effects of Polygonatum sibiricum polysaccharide on Wnt/β-catenin signaling pathway in the osteogenic differentiation of mouse BMSCs.
METHODS:The mouse BMSCs were cultured and induced in osteoblast medium containing final concentrations (5, 10, 25, 50mg/L) of Polygonatum sibiricum polysaccharide. The mouse BMSCs treated without Polygonatum sibiricum polysaccharide was set as the negative control group. The morphological changes of cels were observed under an inverted microscope. Alkaline phosphatase (ALP) activity assay was performed by PNPP method. The mineralization nodules were observed and stained with alizarin red S and the number and area fraction were recorded under an inverted microscope. The mRNA expressions of osteogenesis-related genes ALP, Runx2, and osteocalcin were evaluated by quantitative real-time PCR (qRT-PCR). qRT-PCR and western blot were used to determine the expression level of β-catenin. The downstream β-catenin/TCF transcriptional activity was evaluated with the Dual-Luciferase Reporter Assay System.
RESULTS AND CONCLUSION: Compared with the control group, polygonatum sibiricum polysaccharide significantly enhanced the alkaline phosphatase activity, the mineralization ability of cels, and the mRNA expression of ALP, Runx2 and osteocalcin in the differentiated BMSCs in a dose dependent manner (P <0.05). After induction, the mRNA expression of β-catenin was the highest on the 3rd day. Polygonatum sibiricum polysaccharide significantly increased the expression of β-catenin (P < 0.05) in the process of promoting the differentiation of BMSCs into osteoblasts, and also promoted the high-level expression of luciferase reporter gene (TOPFlash) which contains wild type TCF binding sites (P < 0.05). These results demonstrate that Polygonatum sibiricum polysaccharide can promote the osteoblast differentiation of mouse BMSCs by activating the Wnt/β-catenin signaling pathway.

OBJECTIVETo explore the potential effect of Guizhi plus Gegen Decoction (GGD) in improving learning and memory of lipopolysaccharides (LPS) induced neuroinflammatory mice and its possible mechanisms.

METHODSTotally 63 male ICR mice were randomly divided into 5 groups, i.e., the normal control (n = 13), the model group (n = 13), the low dose GGD group (n = 10), the high dose GGD group (n = 14), and the positive control group (n = 13). Mice were intraperitoneally injected with LPS (0.33 mg/kg) to induce Alzheimer's disease (AD) model. Mice in the high and the low dose GGD groups were administered with 12 g/kg or 6 g/kg by gastrogavage for 4 successive weeks. Mice in the control group were intraperitoneally injected with minocycline (50 mg/kg) for 3 days. By the end of treatment LPS were injected 4 h before behavior test each day, and then behavior test was conducted in mice of each group. Effect of GGD on learning and memory of AD mice was observed by using open field test, novel object recognition task, and Morris water maze.

RESULTSOpen field test showed there was no statistical difference in the movement time and the movement distance among all groups (P > 0.05), suggesting that LPS and GGD had no effect on locomotor activities of mice. In novel object recognition test, AD mice spent significantly shorter time to explore novel object after they were induced by LPS (P < 0.05), while for AD mice in the low and high dose GGD groups, their capacities for exploration and memory were significantly improved (P < 0. 05, P < 0.01). Results of Morris water maze showed that AD mice exhibited increased escape latency (P < 0.05) and spent much less time in swimming across the original platform (both P < 0.05). However, AD mice in the low and high dose GGD groups had obvious shortened latency and increased time percentage for swimming (P < 0.05, P < 0.01).

CONCLUSIONGGD possessed certain improvement in learning and memory disorder of LPS induced AD mice.

Alzheimer Disease ; chemically induced ; drug therapy ; psychology ; Animals ; Drugs, Chinese Herbal ; therapeutic use ; Lipopolysaccharides ; adverse effects ; Male ; Memory Disorders ; prevention & control ; Mice ; Mice, Inbred ICR ; Neuritis ; chemically induced ; drug therapy ; psychology ; Phytotherapy

The study aims to investigate the embryo-fetus development toxicity of the novel PPAR-δ agonist HS060098 on SD rats. The pregnant rats that were randomly divided into the solvent control group (1% hydroxypropyl methyl cellulose water solution) and HS060098 suspension groups (10, 30 and 100 mg x kg(-1) xd(-1)) were orally administered with HS060098 suspension or vehicle during the gestation of 6 -15 days (GD6-15). At termination (GD20), female rats were sacrificed. The pregnant females were evaluated by corpora lutea count, implantation sites, existence and death of embryos. Fetal sex, weight, externals, variations and malformations of viscus and skeleton were observed. The results show that there were no significant abnormality in maternal general conditions and fetal appearance as well as viscera, but in the 100 mg x kg(-1) x d(-1) group, the maternal weight gain decreased greatly (P < 0.01) and the skeletal ossification delayed remarkably (P < 0.01); in the 30 mg x kg(-1) xd(-1) group, the fatal and litter number of incompletely ossified sternebrae II was higher than those of the control group (P < 0.05); the skeletal malformations occurred in all dose groups, which indicate that the novel PPAR-δ agonist HS060098 had maternal toxicity and adversely effected fetal skeletal development under the experimental conditions.
Animals ; Bone and Bones ; drug effects ; Embryonic Development ; drug effects ; Female ; Fetal Weight ; PPAR delta ; agonists ; Pregnancy ; Rats ; Toxicity Tests

Both sides of the picornavirus genome have 5'-untranslated region (5'UTR) and 3'- untranslated region (3'UTR). This study demontrated that both the 5'-and 3'-UTR can form complex structures, such as stem-loop, clover and pseudoknot structure, These structures play an important role in the regulaton of the replication and translation of the viruses. This article reviewed the progress of research on the structure and function of picornavirus' 3'-UTR over recent years.
3' Untranslated Regions ; Animals ; Humans ; Nucleic Acid Conformation ; Picornaviridae ; chemistry ; genetics ; metabolism ; Picornaviridae Infections ; virology ; RNA, Viral ; chemistry ; genetics ; metabolism

OBJECTIVETo study the effect and mechanism of methyl protodioscin (MPD), an active ingredients of yamogenin, in protecting cardiomyocytes (CMC) against anoxia/reoxygenation (A/R) injury.

METHODSCultured CMCs of neonatal SD rats were randomly divided into three groups, cells in Group A were untreated normal cells, cells in Group B and C were made to injury CMC model by A/R, and only those in Group C were treated with MPD. Levels of ATPase activity and lactate dehydrogenase (LDH) in cell membrane of CMCs were determined. Besides, the mRNA expression of sodium-calcium exchanger (NCX) in MPD treated CMCs was detected.

RESULTSAs compared with Group B, the degree of CMC injury was significantly milder and the activities of Na+ -K+ -ATPase and Ca2+ -Mg2+ -ATPase were higher in Group C after cells were treated with MPD in concentration of 10 microg/mL and 50 microg/mL. The mRNA expression of NCX in CMCs was down-regulated after MPD treatment (P < 0.05).

CONCLUSIONMPD could maintain the low calcium internal environment in CMCs by way of protecting the membranous function of Na+ -pump and Ca2+ -pump, and influencing the Ca2+ transmembrane transportation in CMCs.

Animals ; Cell Hypoxia ; Cells, Cultured ; Diosgenin ; analogs & derivatives ; pharmacology ; Myocardial Reperfusion Injury ; metabolism ; Myocytes, Cardiac ; drug effects ; metabolism ; Oxygen ; adverse effects ; Rats ; Rats, Sprague-Dawley ; Saponins ; pharmacology

AIM To explore the mechanism of amyloid β-protein fragment 25-35(Aβ25-35)-induced inflammation and apoptosis in rat hippocampus in vivo by studying mitogen-activated protein kinase (MAPK) signaling pathway and the protective effect of anti-inflammatory drug ibuprofen. METHODS Rats were given ibuprofen (7.5 mg·kg-1 daily, ig) for 3 weeks prior to and 1 week after icv single dose of Aβ25-35 (10 μL, 1 mmol·L-1). Seven days after injection, Nissl staining and immunocytochemical technique were employed to determine the morphology of pyramidal neurons and astrocyte infiltration in hippocampal CA1. The expressions of IL-1β, extracellular signal-regulated kinase (ERK), p38 MAPK, PKC, and caspase-3 were determined by Western blot. Reverse transcription-PCR analysis showed changes in IL-1β mRNA level. RESULTS Intracerebroventricular injection of Aβ25-35 elicited astrocyte activation and infiltration and caused a strong inflammatory reaction characterized by increased IL-1β production and elevated IL-1β mRNA level. The inflammatory reaction was accompanied by the loss of pyramidal neurons in hippocampal CA1. The phosphorylation of p38 MAPK was significantly increased, on the other hand, the phosphorylation of ERK was significantly reduced and these were coupled with the increase of caspase-3 expression in hippocampal CA1. Ibuprofen (7.5 mg·kg-1 daily, 4 weeks) significantly reduced Aβ-induced IL-1β expression, caspase-3 expression and p38 MAPK activation. The loss of pyramidal neurons was also significantly attenuated by treatment with ibuprofen. CONCLUSION The activation of p38 MAPK and the down-regulation of ERK play a pivotal role in the inflam-matory response and apoptosis evoked by Aβ25-35 in vivo, which can be prevented by ibuprofen.

Objective To analyze comprehensively the monitoring data of iodized salt in Zhangjiakou city during 2001 to 2009, and to provide basic information for working out control strategies of the iodine deficiency disorders. Methods According to the iodized salt monitoring requirements in National Iodine Deficiency Disorders Monitoring Program of Ministry of Health, a batch of nine salt samples were taken from each processing (wholesale)company of each county or district of the seventeen counties(districts) of Zhangjiakou once a month. Two townships (towns, street offices) were selected by their location of east, south, west and north in each county(district), and a township in central area each year. Four villages(neighborhoods) were selected in each township(town, street office),and eight household salt samples were collected in each village(neighborhood), and quantitatively determined by direct titration of iodine. Results Iodized salt processing(wholesale) : during 2001 to 2009, a total of 1728 batches was monitored, 1689 batch qualified, batch qualification rate 97.74%;15552 salt samples were tested, 15 357 qualified, iodized salt qualification rate 98.75 %. Household salt levels : 5297 villages (neighborhoods) of 1305 townships(towns, street offices) were monitored, 44 316 salt samples were collected, 43 274 qualified, iodized salt qualification rate 98.04%(43 274/44 141 ), iodized salt coverage rate 99.61%(44 141/44 316), qualified iodized salt consumption rate 97.65%(43 274/44 316). Rate of non-iodized salt was 0.40%(260/44 316), and salt median iodine was 30.02 mg/kg. Conclusions The iodized salt quality indicators are within the state-controlled range in Zhangjiakou city for nine years which remaines at relatively stable levels with a smaller range of annual fluctuations.Detection of non-iodized salt over the years has become the main factors affecting the effectiveness of the prevention and control measures.We should increase monitoring,supervision,and universal health education,and prevent the spread of non-iodized salt.

Objective To evaluate protective effects of recombinant human thioredoxin(TRX) in myocardial injury of mice with viral myocarditis. Methods We established viral myocarditis models by intraperitoneal injection with 0.1 ml 100TCID50 Coxsackie virus 3m(CVB3m), along with tail vein injection of recombinant human TRX (2 mg/kg) for protection. The control group was given equivalent volume of normal saline. The mice were killed 7 days following the injections. Serum lactate dehydrogenase (LDH) activity was determined and myocardial injury was examined with light microscopy. Results The somm LDH activity in Coxsackie virns-infected mice [(3130.50±390.57)U/L] was higher than that of animals in the control group[ (1617.86±155.42)U/L] and that of TRX protection group[ (1959.43±540.75)U/L], the difference being statistically significant (P<0.05); there was no significant difference between TRX protection group and the control group(P 0.05). Light microscopy showed that five of the eight Coxsackie rims-infected mice had myocardial lesions, including focal myocardial necrosis and inflammatory infiltration. There was no myocardial injury in the TRX protection group. Conclusions Recombinant human TRX can lessen myocardial injuries induced by infection with CVB3m, and so can protect myocardium.