Objective To discuss the clinical significance of fetal encephalic accumulated fluid revealed by prenatal ultrasonography.Methods Prenatal ultrasonography was performed on 8426 women at more than 20 weeks' gestation.Totally 150 women with fetal encephalic accumulated fluid more than 5 mm were included in this study.The changes of fetal encephalie accumulated fluid and the associated anomalies were observed regularly every 2 weeks until delivery.The live infants were followed up regularly.Results The incidence of fetal encephalic fluid was 1.8%,including 72 cases with fluid in the fetal anterior or posterior cornu of unilateral ventricle,46 cases with accumulated fluid in fetal posterior fossa,32 cases with fluid in more than 2 sites.Generally,the accumulated fluid in fetal encephalus was first diagnosed at 17-40 gestational weeks,with a median of(26?5)weeks.Most of them were found between 29-32 gestational weeks(63 cases,42.0%),and the maximum amount of accumulated fluid was also found between 29-32 weeks(70 cases,46.7%).Spontaneous regression of intracranial fluid could be seen in 111 fetuses (74.0%).The period of fluid regression ranged from 29 to 40 weeks of gestation,of which the average gestational week was(36?2)weeks.Additionally,the most frequent period of regression was in the first two thirds of the three trimesters of pregnancy.The incidence of defected infants was 3.8%,10.2% and 67.4%,respectively,when the amount of accumulated fluid was less than 10mm,10-14 mm and more than 15 mm.And the accumulated fluid in more than 2 sites was also a risk factor of defected fetuses,with an incidence of 60.0%.Conclusions Most cases could be diagnosed between 29-32 gestational weeks, and the maximum amount of accumulated fluid is also observed in this period.The more fluid in fetal encephalus,the more sites the fluid distributed in,the more defected fetuses or infants would be observed.So in cases of more than 15 mm of fluid,or accumulated fluid in more than 2 sites,anomalies should be observed extremely carefully.

In order to investigate the anti-leukemia effects of gambogic acid (GA) and its relation to the regulation of nucleoporin Nup88 in U937 cells in vitro, the inhibitory effect of GA on the growth of U937 cells was examined by using MTT assay. Apoptosis was detected by Annexin-V FITC/PI double-labeled cytometry. Cell cycle regulation was studied by propidium iodide method. Both flow cytometry (FCM) and RT-PCR were employed to assess the expression of Nup88, and the localization of Nup88 was determined by confocal microscopy. The results indicated that GA had strong inhibitory effect on cell proliferation and apoptosis induction activity in U937 cells in vitro in a time-and dose-dependent manner. The 24-h IC(50) value was (1.019+/-0.134) mg/L. Moreover, GA induced arrest of U937 cells in G(0)/G(1) phase. Over-expression of Nup88 was found in U937 cells, whereas GA could significantly down-regulate both the protein and mRNA levels of Nup88. Nup88 was diffusely distributed between nucleus and cytoplasm and was located at the cytoplasmic side of nuclear rim, and occasionally in cytoplasm. It is suggested that GA exerts its anti-leukemia effects by regulating the expression and distribution of nucleoporin Nup88. It promises to be new agent for the treatment of acute leukemia.
Antineoplastic Agents, Phytogenic/*pharmacology ; Apoptosis/drug effects ; Cell Proliferation/drug effects ; Nuclear Pore Complex Proteins/genetics ; Nuclear Pore Complex Proteins/*metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; U937 Cells ; Xanthones/*pharmacology

OBJECTIVETo study the association between Alzheimer' s disease (AD) and apolipoprotein E (apoE) polymorphism and apoE epsilon4 allele; and to investigate the role of apoE in senile plaque formation.

METHODSDuring the period from 1982 to 2003, 27 portmortem cases of AD from the archival files of Department of Pathology of Beijing Hospital, diagnosed according to the consortium to establish a registry for Alzheimer's disease (CERAD) criteria, were enrolled into this study. Among the 27 cases studied, there were 23 cases of definite AD and 4 cases of probable AD. Postmortem brain tissues from 67 neurologically unremarkable deceased were used as age-matched controls. Immunohistochemical study for beta-amyloid (Abeta) and Tau protein, as well as immunohistochemical study for Abeta/apoE, were performed in all AD cases using streptavidin-peroxidase (SP) and double immunostaining ( SP/ABC) methods, respectively. Senile plaques and neurofibrillary tangles in the 23 cases of definite AD were further quantified. The apoE genotypes in all cases were analyzed by polymerase chain reaction and restriction fragment length polymorphism technologies.

RESULTSImmunohistochemical study for Abeta distinguished 4 different types of senile plaques: diffuse non-neuritic plaques, diffuse neuritic plaques, dense-core neuritic plaques and dense-core non-neuritic plaques. Double immunohistochemistry for Abeta/apoE showed that some senile plaques were positive for both Abeta and apoE. The expression rates for Abeta and apoE in these 4 different types of senile plaques were 4. 28%, 84. 71%, 8.50% and 2.51%, respectively. The positivity rate for Abeta/apoE in diffuse neuritic plaques were significantly higher than those in other 3 types (P < 0.01). The frequency of occurrence of apoE epsilon4 allele in AD was significantly higher than that in the control group (P < 0.01). The numbers of senile plaques and neurofibrillary tangles in AD cases with apoE epsilon4 allele were also significantly higher than those in AD cases without apoE epsilon4 allele (P < 0.01).

CONCLUSIONSApoE polymorphism is associated with AD. The presence of apoE epsilon4 allele carries a higher risk for the development of AD. ApoE may also play an important role in the transformation of diffuse non-neuritic plaques to diffuse neuritic plaques.

Aged ; Aged, 80 and over ; Alleles ; Alzheimer Disease ; metabolism ; pathology ; Amyloid beta-Peptides ; metabolism ; Apolipoproteins E ; genetics ; metabolism ; Brain ; metabolism ; pathology ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Neurofibrillary Tangles ; pathology ; Plaque, Amyloid ; pathology ; tau Proteins ; metabolism

A total of 159 patients with acute coronary syndrome(ACS)were enrolled from December 2006 to June 2008 and divided into the percutaneous coronary intervention(PCI)group and the internal medicine treatment group.The participants in the two groups were further assigned to the Tirofiban or the placebo control group.The change in electrocardiograph within 48 hours,major adverse cardiac events (MACE)during hospital stay and 30 days' follow-up,and bleeding were compared between the sub-groups.As a result,in comparison with the placebo control groups,the Tirofiban sub-groups showed significant improvement in electrocardiography(P＜0.01).In the internal medicine treatment group,the rate of MACE during 30 days' follow-up was significantly decreased in patients treated with Tirofiban(P＜0.05),although no significant difference in bleeding rate was found.Our data suggest that Tirofiban may be safe and effective in the treatment of ACS.

Objective To observe therapeutic effects of HuGanJieXian decoction on rats hepatic fibrosis induced by tetrachloride. Methods Rat models of hepatic fibrosis were constructed by intraperitoneal injection of tetrachloride.HuGanJieXian decoction composed of low, middle, and high dose curcumin were given to these rats respectively at the same time. Sho-saiko-to compound treatment group and Fufangbiejiarangan Tablets treatment group were made as positive control groups. After twelve weeks, all rats were executed. Serum samples were kept for measuring serum levels of PC-Ⅲ, LN, and HA. Left livers were extirpated for pathologic examination including H.E and Masson stainings. Grade of hepatic fibrosis were evaluated according to SSS system. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) of supematant centrifugated from hepatic tissue homogenate were detected. Results Serum levels of PC-Ⅲ, LN, and HA were depressed obviously in decoction groups compared with those of fibrotic group (P<0.05) , especially in the low-dose curcumin group.HuGanJieXian Decoction could increase the level of SOD and decrease the level of MDA (P<0.05) , especially in the low-dose curcumin group. Staining of H. E and Masson showed that degrees of hepatic fibrosis in decoction groups were improved obviously compared with that of the fibrotic group. Conclusion HuGanJieXian Decoction can improve rat hepatic fibrosis, the mechanism of this effect may be associated with protecting hepatic cell membrane and anti- peroxidative damage.

Objective To choose zebrafish as the experimental animal model for studying the spatiotemporal expression rule of rap1 gen in zebrafish embryo early development process .Methods The Rap1 gene fragment was cloned from the zebrafish emby‐oscDNA ,then the Rap1 gene fragment and pCS2+ plasmid were performed the in vitro connetion and recombination was extracted , the combinant plasmid was correct after the double enzyme digestion ,colony PCR and sequencing identification .T3 RNA polymer‐ase in vitro transcription system was used to obtain the digoxin (DIG)‐labeled anti‐sense mRNA probe of Rap1 gene .The whole mount in situ hybridization method was adopted to detect the Rap1 expression in zebrafish embryo early development process . Results The positive hybridization signal of Rap1 gene was detected at the cell division junction region of 0 .75 hpf ,animal pole of 3 .70 hpf and 6 .00 hpf ,and notochord of 12 .00 -72 .00 hpf .Conclusion Rap1 gene might be involved in the early development process of notochord nervous system in zebrafish .

Objective To copy the mouse aging model with D-galactose,and to investigate the role of Schisandra total lignin (SCL)in the mouse brain tissue aging and its mechanism.Methods 50 mice were radomly divided into control group,model group (100 mg·kg-1 ·d-1),low dose (35 mg·kg-1 ·d-1)of SCL group (SCL-L), middle dose (70 mg· kg-1 · d-1 )of SCL group (SCL-M)and high dose (140 mg· kg-1 · d-1 )of SCL group (SCL-H)(n=10).D-galactose (100 mg·kg-1 ·d-1 )was injected into the mice hypodermically for 10 weeks to induce aging models in all the groups except control group,and 35,70,and 140 mg· kg-1 · d-1 SCL were administered for 10 weeks in SCL groups.The learning and memory abilities were measured by the Water Maze test.The expression levels of Bax,Bcl-2,ubiquitin (Ub),microtubule-associated protein light chain 3 (LC3)in the brain tissue of the mice in various groups were observed by Western blotting method. The LC3 protein expressions in mouse brain cortex and hippocampus were observed by immunohistochemistry.Results In learning and memory test,compared with control group,the swimming time of the mice in model group was increased (P<0.05),and the number of errors was increased (P<0.05);compared with model group,the swimming time in SCL-L,SCL-M and SCL-H groups was decreased (P<0.05)and the number of errors was also decreased (P<0.05). Compared with control group,the expression level of Bax was increased (P<0.05),the expression level of Bcl-2 was decreased (P<0.05),the expression levels of Ub and LC3-Ⅱ/LC3-Ⅰ proteins were increased (P<0.05)in model group;compared with model group,the expression level of Bax was decreased (P<0.05),the expression level of Bcl-2 was incerased (P<0.05),and the expression levels of Ub and LC3-Ⅱ/LC3-Ⅰ proteins were decreased (P<0.05)in SCL-L,SCL-M and SCL-H groups.In control group,the neuronal morphology was normal,and none of brown granules were visible in the cytoplasm of mouse brain cortex and hippocampus and the expression of LC3 protein was negative.In model group,the neurons were degeneration,and the number of LC3 protein positive cells in the cerebral cortex and hippocamptal tissue was increased (P<0.05).In SCL-L,SCL-M and SCL-H groups,the number of degenerative neurons was decreased,and the number of LC3 protein positive cells was decreased (P<0.05).Conclusion SCL can inhibit the D-galactose-induced brain tissue aging in the mice, and the mechanism is related to regulating autophagy and inhibiting apoptosis.

Objective To investigate clinical effects of Deanxit in non-erosive gastroesophageal re-flux disease ( NERD) with anxiety and depression.Methods A total of 76 patients diagnosed NERD with anxiety and depression by endoscopy and hospital anxiety and depression scale ( HAD) were randomly divid-ed into regular treatment group and Deanxit treatment group.Clinical efficacy, symptom score, and anxiety and depression score were observed after one week, four weeks, and eight weeks.Results Deanxit signifi-cantly increased the clinical efficacy after one week ( P <0.01) and remission rate after one week ( P <0.05), four and eight weeks ( P <0.01).It improved symptoms, depression, and anxiety, which showed significant differences ( P <0.01) compared to control group after one week, four and eight weeks adminis-tration.Conclusions Deanxit can be applied in NERD with anxiety and depression treatment, which has quick effect and high remission rate, and improve patient's reflux symptoms and anxiety depression.

To explore the protective effects of trimetazidine on vascular endothelial cells injury induced by hydrogen peroxide (H2O2) and its pharmacological mechanisms of anti-oxidation.Methods Human umbilical vein endothelial cells (HUVECs) were injured by H2O2.Next,the cells were treated with three different concentrations of trimetazidine (1 μmol/L,10 μmol/L,100μmol/L,respectively).The viability of cells was detected by methyl thiazoeyl tetrazolium (MTT) assay.In addition,malondialdehyde (MDA)contents,superoxide dismutase (SOD) and secretion of NO were measured.Results Trimetazidine could enhance the viability of the injured HUVECs induced by oxidation,decrease the level of MDA,enhance the SOD activity,and increase the secretion of nitrogen monoxide.These effects were in a certain dose-dependent manner and the difference was significant among the three concentrations (P＜0.05).Conclusions Our results suggest that trimctazidine may protect lipid peroxidation and prevent oxidation-induced cellular dysfunction of HUVECs (J Geriatr Cardiol 2008;5:248-251)

In this study, the effect of heparin-derived oligosaccharide (HDO) on platelet-derived growth factor (PDGF) induced vascular smooth muscle cells (VSMCs) proliferation and the related signal transduction mechanisms were investigated. MTT assays were used to measure VSMCs proliferation. Cell cycle distribution was analyzed by flow cytometry. The level of key regulatory proteins in PKC, MAPK and Akt/PI3K pathways were determined by RT-PCR, Western blot and immunocytochemical methods. Meanwhile, mRNA expressions of some proto-oncogenes were assayed by RT-PCR method. Our data showed that HDO (0.01, 0.1 and 1 μmol · L(-1)) inhibited 30 ng · mL(-1) PDGF-induced VSMCs proliferation in a dose-dependent manner, blocked the G1/S transition and inhibited the level of key regulatory proteins and some proto-oncogenes (P < 0.05). The results showed that HDO may decrease the key regulatory proteins expression, hence suppress the transcription of proto-oncogene and G1/S transition, finally inhibiting VSMCs proliferation.
Cell Cycle ; Cell Proliferation ; drug effects ; Cells, Cultured ; Flow Cytometry ; Heparin ; pharmacology ; Humans ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Oligosaccharides ; pharmacology ; Platelet-Derived Growth Factor ; pharmacology ; Signal Transduction