ATP-Binding Cassette Transporters ; metabolism ; Adenocarcinoma ; genetics ; metabolism ; pathology ; Adult ; Aged ; Blotting, Western ; Female ; Humans ; Immunohistochemistry ; Lung ; metabolism ; pathology ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Male ; Middle Aged ; Neoplasm Staging ; RNA, Messenger ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

The leaves and fruits of Ginkgo biloba L.are embodied in Pharmacopoeia of People's Republic of China,mainly contain ginkgo flavonoids,terpene lactones,phenolic acids,isopentenyl alcohol,steroids and other chemical compositions.The extract and active ingredients can be made into tablets,capsules,granules,oral liquid,injection,dripping pills,syrup,tincture and other formulations,clinically used for cardiovascular and cerebrovascular disease treatment.The adverse reactions are allergies,diarrhea,bleeding,liver and kidney toxicity.This review contains the chemical composition,dosage form and clinical adverse reactions of Ginkgo biloba in recent years,for providing a reference of further development and rational utilization of this plant resource.

Objective To identify interleukin (IL)-17-producing T cells and Foxp3 positive CD4 positive T ceils from patients with rheumatoid arthritis (RA), and investigate their cytokine levels as well as their correlations. Methods Flow cytometry was used to analyze the subsets of T cells in peripheral blood from 39 RA patients and 40 healthy donors. IL-17, IL-6, IL-23 and transforming growth factor (TGF)-beta levels in sera of these subjects were tested by ELISA. Results IL-17+CD4+ T cells increased significantly and IL-17, IL-6 and IL-23 elevated markedly in peripheral blood of RA patients compared to healthy donors (P< 0.01 ). However,Foxp3+CD4+T cells decreased evidently (P<0.01) and TGF-beta did not increase in RA pati-ents when compared to healthy donors (P>0.05). Conclusion This study suggests that Th17 cells predomin-ance coupled with relatively insufficient CD4+ regulatory T cells in RA is mainly caused by alterations of rela-ted cytokines.

OBJECTIVETo demonstrate the myocardial lesion associated with long-term administration of methamphetamine in rats.

METHODSThe experimental models of intoxication of methamphetamine were established in Sprague-Dawley rats. Methamphetamine hydrochloride (3 mg x kg(-1) x d(-1)) was subcutaneously injected to rats in methamphetamine-treated group (n = 16), and normal saline at the same dose was injected to rats in control group (n = 16). After 1 week and 8 weeks of injection, 8 rats in each group were sacrificed and their hearts were examined with light microscopy and electron microscopy, respectively.

RESULTSAfter 1 week of methamphetamine exposure, foci of contraction band and cellular degeneration were present in subendocardial myocardium. Cellular degeneration, myocytolysis, and contraction band necrosis became prominent and extensive in methamphetamine-treated rats after 8 weeks. Hypertrophy, intracellular vacuolization, and fibrosis were also observed. The ultrastructural feature showed marked swelling and degeneration of mitochondria, enlargement of sarcoplasmic reticulum, and dissolution of myofilaments. No obvious cardiac myocyte lesions were observed in rats of control group.

CONCLUSIONMethamphetamine abuse daily for a long time may result in an increased risk of cardiovascular lesions similar to cardiomyopathy.

Adolescent ; Adult ; Animals ; Heart ; drug effects ; Humans ; Male ; Methamphetamine ; administration & dosage ; adverse effects ; Myocardium ; pathology ; ultrastructure ; Rats ; Rats, Sprague-Dawley

OBJECTIVEDisturbances of the synthesis and breakdown of the extracellular matrix of arterial walls have emerged as key features of the atherosclerotic process. We observed the changes of circulating procollagen marker for type III collagen turnover rate, the N-terminal propeptide P III NP and vascular resistance in hypertensive patients treated with various antihypertensive regimens.

METHODA total of 130 light to moderate hypertensive patients were randomly assigned to receive enalapril (group B, n = 43), enalapril + spirolactone (20 mg/d, group A, n = 44) and anti-hypertensive drugs not directly affecting RAAS (calcium antagonist, beta-blocker, group C, n = 43) for 1 year. Target blood pressure is < 130/80 mm Hg.

RESULTSTarget blood pressure was reached in all treated patients and was similar among various groups. Under the same blood pressure controlling precondition, serum P III NP were similar at baseline among various groups and remained unchanged in group B [(3.4 +/- 0.3) microg/L vs. (3.7 +/- 0.3) microg/L, P > 0.05] and significantly decreased in group A [(2.3 +/- 0.2) microg/L vs. (3.8 +/- 0.2) microg/L, P < 0.05] while significantly increased in group C [(3.9 +/- 2.0) microg/L vs. (3.2 +/- 1.5) microg/L, P < 0.05]. Vascular resistance was similar among groups before therapy and all significantly decreased after 1 year antihypertensive therapy and the decrease was more significant in group A [(1064.3 +/- 158.6) dyn.s(-1).cm(-5)] than that in group B [(1200.8 +/- 298.7) dyn.s(-1).cm(-5)] and group C [(1205.1 +/- 206.4) dyn.s(-1).cm(-5)].

CONCLUSIONSpironolactone in conjunction with enalapril is a more favorable antihypertensive regimen in decreasing P III NP and improving vascular resistance than enalapril alone or antihypertensive drug regimens not directly affecting RAAS.

Adult ; Aged ; Angiotensin-Converting Enzyme Inhibitors ; therapeutic use ; Antihypertensive Agents ; therapeutic use ; Biomarkers ; Enalapril ; therapeutic use ; Humans ; Hypertension ; drug therapy ; metabolism ; physiopathology ; Middle Aged ; Procollagen ; blood ; Spironolactone ; therapeutic use ; Vascular Resistance

OBJECTIVETo determine the expression of S100-beta protein and glial fibrillary acidic protein (GFAP) in hippocampal astrocytes of rats with Alzheimer disease (AD) model rats, and observe the effect of butylphthalide on their expression.

METHODSSixty male adult rats were randomized equally into model group, butylphthalide group, and control group, and in the former two groups, AD models were established by injecting beta-amyloid protein 1-40 into the hippocampus. Sixty days later, the rats were sacrificed and the bilateral hippocampuses were taken for immunohistochemistry.

RESULTSThe number of cells positive for S100 and GFAP in the hippocampus in butylphthalide group were significantly higher than that in the control group (P/0.01), but lower than that in the model group (P/0.05).

CONCLUSIONThe expression of S100 protein and glial fibrillary acidic protein increased significantly in the hippocampal astrocytes of rats with AD, and butylphthalide can inhibit the increase of their expression.

Alzheimer Disease ; chemically induced ; metabolism ; Amyloid beta-Peptides ; Animals ; Benzofurans ; pharmacology ; Disease Models, Animal ; Glial Fibrillary Acidic Protein ; metabolism ; Hippocampus ; metabolism ; Male ; Nerve Growth Factors ; metabolism ; Neuroprotective Agents ; pharmacology ; Peptide Fragments ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; S100 Calcium Binding Protein beta Subunit ; S100 Proteins ; metabolism

OBJECTIVETo determine the effect of butylphthalide on the expressions of p38 mitogen-activated protein kinase and extra-cellular signal regulated kinases (ERKs) in the brain tissue of rats with Alzheimer's disease (AD).

METHODSSixty male adult rats were randomly divided to AD model group, butylphthalide group, and control group (n=20). AD models were established by injecting beta-amyloid protein 1-42 into the hippocampus of rats. Sixty days later, the learning and memory abilities of the rats were evaluated using Y-maze test, and the expressions of p38 and ERKs in the brain tissue of the rats were measured by immunohistochemistry. RESULTS Compared with the control group, the rats in AD model group exhibited significantly reduced learning and memory abilities, increased expressions of P38 in the hippocampus and lowered expression of ERK in the cortex (P<0.01). In comparison with the model group, the rats in the butylphthalide group showed significantly decreased P38-positive cells in the hippocampus and increased expression of ERK in the cortex (P<0.01).

CONCLUSIONSButylphthalide improves the learning and memory abilities of rats with experimental AD, the mechanism of which may involve inhibition of P38 expression and enhancement of ERK expression in the brain tissues.

Alzheimer Disease ; enzymology ; metabolism ; physiopathology ; Animals ; Benzofurans ; pharmacology ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Gene Expression Regulation, Enzymologic ; drug effects ; Hippocampus ; drug effects ; metabolism ; Male ; Memory ; drug effects ; Neuroprotective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley ; p38 Mitogen-Activated Protein Kinases ; antagonists & inhibitors

OBJECTIVETo compare plasma and red blood cell folate levels among women in their first trimester of pregnancy from rural areas with high or low prevalence of neural tube defects.

METHODSA cross-sectional study was performed, among women in their first trimester of pregnancy from rural areas with high or low prevalence of neural tube defects in 2003. Non-fasting blood sample were collected and analyzed for plasma and red blood cell folate concentrations for 688 women.

RESULTSThe median plasma (10.53 nmol/L) and red blood cell folate (389.2 nmol/L) among women from the high prevalence rural area were lower than those of women from the low prevalence rural area (plasma folate: 30.39 nmol/L, red blood cell level folate: 926.0 nmol/L). Among women from the high prevalence area, about 50% and 43% were respectively, deficient for plasma and red blood cell folate, compared with 6% and 4% respectively, for women from the low prevalence area. The median plasma folate levels among women who took periconceptional folic acid supplements in both high and low prevalence areas were about twice higher than those who did not take the folic acid. The median red blood cell folate level of the folic acid users was 40% higher than those of the non-users. Among those who took folic acid, women in the low prevalence area had 70%-90% higher plasma folate concentration and twice higher red cell folate concentration than women in the high prevalence area.

CONCLUSIONWomen from the rural area with a high prevalence of neural tube defects had low plasma and red blood cell folate levels. Periconceptional supplementation with folic acid could substantially improve folate status of reproductive-aged women. However, supplementation with 0.4 mg of folic acid per day might be inadequate for women in the high prevalence rural area.

Dietary Supplements ; Erythrocytes ; chemistry ; Female ; Folic Acid ; administration & dosage ; blood ; Humans ; Neural Tube Defects ; epidemiology ; prevention & control ; Preconception Care ; Pregnancy ; Pregnancy Trimester, First ; Prevalence ; Rural Health

OBJECTIVETo explore the influences of Mycobacterium tuberculosis on the levels of human acute monocytic leukemia cell line THP-1 apoptosis and death.

METHODSHuman acute monocytic leukemia cell line THP-1 were infected with Mycobacterium tuberculosis strains H37Ra, H37Rv, or Beijing genotype (BJTB), respectively, to construct the infection models. Cell apoptosis was detected using flow cytometry. The distribution of the apoptotic proteins was detected using immunofluorescent staining assays. The cells late apoptosis was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining assays. The change of cell death was determined by Tyrpan blue staining assays.

RESULTSTHP-1 apoptosis was induced by Mycobacterium tuberculosis strains H37Ra, H37Rv, and BJTB. H37Ra strongly induced THP-1 apoptosis, H37Rv weakly induced THP-1 apoptosis, and BJTB induced THP-1 apoptosis at the lowest level among these three Mycobacterium tuberculosis strains. On the contrary, BJTB strongly induced THP-1 death, H37Rv weakly induced THP-1 death, and H37Ra induced THP-1 death at the lowest level.

CONCLUSIONSMycobacterial strains with different virulence induce different levels of apoptosis and death of THP-1 cells. Compared with highly virulent strains, attenuated strains induce more apoptosis and less death.

Apoptosis ; Cell Line, Tumor ; Humans ; In Situ Nick-End Labeling ; Leukemia, Monocytic, Acute ; Mycobacterium tuberculosis ; pathogenicity ; Virulence

OBJECTIVETo investigate the role of Gemin3 in cell proliferation and its regulation pathway.

METHODSUsing co-immunoprecipitation and GST pull-down assay to determine the domain of Gemin3 and p53 binding and interaction in vitro and in vivo. To check the effect of Gemin3 on p53 by luciferase reporter assay. Stable Gemin3 knock-down cell lines were generated by lentivirus-delivered small hairpin RNA then puromycin selection. Real-time PCR was used to confirm the effect of Gemin3 level on p53 and its downstream genes, and flow cytometry was used to analyze the effect of Gemin3 on apoptosis.

RESULTSThe C-terminal of Gemin3 interacted with the DNA binding domain of p53. The p53 reporter gene, PA3M-p53 and increasing amount of GFP-Gemin3 were co-transfected into Saos-2 cells. Gemin3 repressed p53 expression at transcription level. Real-time PCR indicated that the expression of p53, p21 and Bax in Gemin3 knock-down cells was higher than that in the control cells. Western blot showed Gemin3 knock-down cells had a higher p53 espression. Flow cytometric assay showed that knock-down Gemin3 expression led to an increased cell apoptosis.

CONCLUSIONGemin3 binds with p53 forming a complex and plays an anti-apoptotic role by repressing the p53 expression.

Apoptosis ; B-Lymphocytes ; cytology ; Cell Line, Tumor ; DEAD Box Protein 20 ; genetics ; metabolism ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Genes, Reporter ; Humans ; Immunoprecipitation ; Lentivirus ; genetics ; Osteosarcoma ; genetics ; metabolism ; pathology ; Plasmids ; Protein Binding ; RNA, Messenger ; metabolism ; RNA, Small Interfering ; genetics ; Transfection ; Tumor Suppressor Protein p53 ; genetics ; metabolism ; bcl-2-Associated X Protein ; genetics ; metabolism