Humans ; Post and Core Technique

Objective:To determine the plasma level of apelin in patients of maintenance hemodialysis (MHD) and to explore the relationship between apelin level and carotid atherosclerosis (AS) in MHD patients.Methods:A total of 92 MHD patients and 36 sex-and age-matched healthy subjects were enrolled in this study.The plasma level of apelin was evaluated by radiation immunoassay;serum endothelial injury markers including thrombomodulin,von Willebrand factor (vWF),and CD 146,and inflammatory factors including high sensitive C-reactive protein (hsCRP),IL-6 and TNF-α were determined by ELISA.Common Carotid arteries intima media thickness (CCA-IMT),cross-sectional calculated intima-media area (cIM area) area and atherosclerotic plaque were measured by non-invasive high-resolution B-mode ultrasonography.Results:The plasma levels of apelin was significantly decreased in MHD patients compared with healthy subjects (P＜0.01),accompanied with elevated plasma levels of thrombomodulin,vWF,CD 146,hsCRP,IL-6 and TNF-α (all P＜0.01).The plasma levels of apelinin in MHD patients with carotid artery plaques were obviously lower than those without plaques [(43.16± 10.12) pg/mL vs (61.43±16.25) pg/mL,P＜0.01].Plasma level of apelin was inversely related with CCA-IMT and cIM area (r=-0.355 and r=-0.297 respectively,all P＜0.01).Multiple stepwise regression analysis showed that plasma level of apelin was an independent risk factor for CCA-IMT and cIM area.Conclusion:The plasma apelin in MHD patients might take part in vascular endothelial injury and the progress of atherosclerosis.It plays an important role in the initiation and development of uremia associated atherosclerosis through elevating inflammatory factors including hsCRP,IL-6 and TNF-α levels.

Objective:To study the autoimmune response against self myocardial tissue in an experimental rats model of acute myocardial infarction (AMI) and reveal a potential role of autoimmune mediated myocardial injury involved in ventricular remodeling after AMI.Methods:An experimental animal model of AMI was adopted by in vivo ligation of left anterior descending branch (LAD) in Wistar rats After six weeks, spleens were removed and splenocytes were collected About 100?10 6～150?10 6 splenocytes were freshly transferred to syngeneic inbred rats Four weeks later, these recipient rats were anesthetized for hemodynamics analysis by catheter technique Antibody against cardiac myosin heavy chain (MHC) was screened by enzyme linked immunosorbent assay Histopathological studies were performed on all hearts Results:The antibody against cardiac MHC was positive in 8 of 22 AMI rats and recipient rats, and in 0 of 20 sham operation and recipient rats,P

Dentin-Bonding Agents

Dentin-Bonding Agents ; Water

Objective To investigate the effect of solute cartier organic anion transporter family, member 1B1 (SLCOIBI) gene variants on the response to therapy with repaglinide in type 2 diabetes. Methods 100 newly-diagnosed type 2 diabetic patients were treated with repaglinide during a course of 48 weeks. Anthropometrie parameters and indices related to glucose metabolism were measured periodically. Genotypes of SLCO1B1 D130N and V174A were detected by PCR-restriction fragment length polymorphism (RFLP) and sequencing respectively. Results Eighty-nine patients accomplished the 48-week follow-up visits. D130N variant in SLCO1B1 gene was associated with repaglinide treatment, DD genotype had better HbA1C lowering effect than N allele carrier [△HbA1C: (-2.29±0.23) % vs (-1.49±0.21)%, P<0.05]. No association was detected between D130N and the other effects of repaglinide on glucose metabolism related phenotypes. Conclusion D130N variant in SLCO1B1 gene is associated with the response to repaglinide treatment in patients with type 2 diabetes. DD homozygotes had a better effect than N allele carriers.

AIM: The study was designed to explore the autoimmune mechanism of myocardial injury and ventricular remodeling after acute myocardial infarction (AMI). METHODS: An experimental animal model of AMI was adopted in Wistar rats. After 6 weeks, splenocytes were freshly transferred to syngeneic inbred rats. Four weeks later, these recipient rats were anesthetized for hemodynamics analysis by catheter technique. Serum antibody against cardiac myosin heavy chanin (MHC) was screened by ELISA. Histopathological studies were performed on all hearts. The phenotypes of T lymphocytes in myocardium were analyzed by histocytochemistry stain. RESULTS: Histopathological studies showed the lymphocytes infiltration in non-infarction myocardium in AMI rats and the organ specific inflammation of myocardium in all succedent recipient (AMI-T) rats. Histocytochemistry stain revealed the predominant CD4+T cells infiltration in myocardium. The antibody against MHC was examined in 8/22 cases of AMI rats and AMI-T rats, but none in sham-T rats. The left ventricular dysfunction was found in AMI-T rats, which was characterized by slight decline of ~+dp/dt_~max. CONCLUSIONS: The study showed inflammatory response of non-infarction myocardium in AMI rats and demonstrated the lymphocytes-mediated myocardial injury and cardiac dysfunction by adoptive transfer of splenocytes of AMI rats. The autoimmune-mediated myocardial injury might be a novel mechanism of ventricular remodeling after AMI. [

OBJECTIVE To investigate enhanced immune function of methionine encephalin (MENK) and its anti-tumor mechanism in CT26 colon cancer mouse model. METHODS 3×106 CT26 cells were implanted subcutaneously in BALB/c mice. Four days after, MENK was peritoneally administrated at the concentration of 20 mg·kg-1 for 14 d. The percentage of MDSCs in bone marrow, spleen, blood, tumor and liver were detected by flow cytometry. Non- esterified fatty acid (NEFA), triglycerides (TG) and total cholesterol (T-CHO) in liver homogenate were tested by a NEFA test kit, a TG test kit and a T- CHO test kit respectively. qRT- PCR and Western blot were used to measure mRNA and protein levels of inflammation-, glycometabolsim- and lipometabolsim-associated indexes in liver. RESULTS MENK decreased percentages of MDSCs in bone marrow, spleen, blood and tumor in colon cancer mice. MENK-treated mice displayed elevated ratio of CD4+T and CD8+T cells in spleen as well as increased T and B lymphocytes proliferation. Meanwhile, MENK also ameliorated liver damage reflected by lower levels of GPT and GOT in serum and reduced risks of cancer- associated index including inflammation, high lipid and high glucose. Furthermore, MENK lowered down the levels of NEFA, TG and T- CHO in liver homogenate. MENK treatment decreased expression of p- STAT3, increased expression of p-AKT, IRS1 and Glut4 at protein level as well as reduced lipogenesis-associated genes and elevated glycolysis-associated genes in liver of tumor bearing mice. Also, abated expression of genes associated with MDSCs generation (M-CSF, GM-CSF, IL-6, IL-1β) and migration (S100A9, KC) was observed within shrunken subcutaneous tumor by MENK intervention. CONCLUSION MENK has the ability to strength immune function against colon cancer by reducing MDSCs and improving liver metabolism.

Objective To evaluate the using of either 225 or 150 microgrammes of mifepristone combined with misoprostol for termination of second-trimester gestation(16～24 weeks).Methods 180 women requesting voluntary induced abortion during gestation 16～24 weeks were randomised to three groups,group 1:oral mifepris- tone 225rag,group 2:oral mifepristone 150mg,and group 3:injected 100rag rivanot by amniocentestis.The total suc- cess rate,once success rate,the interval of having-medicine to uterine-constraction,the volume of bleeding within 2 hours after labour and cervical laceration rate were observed.Results The once success rate of induced labour in group 1 was higher than that in group 2 and group 3(P

Lycii Cortex, a popular herb medicine in traditional Chinese medicine, is used to treat different inflammation-related diseases. The aim of our work is to find the key constituents inhibiting NF-kappaB, a key regulator of inflammation. In the investigations of cell-based in vitro assays of extracts, we found that both ethyl acetate extract and methanol extract of Lycii Cortex inhibited the TNF-alpha-induced activation of NF-kappaB. Through bioassay-guided fractionation, we identified 4 phenolic amides including trans-N-(p-coumaroyl) tyramine (1), trans-N-feruloyltyramine (2), trans-N-caffeoyltyramine (3), and dihydro-N-caffeoyltyramine (4). Four phenolic amides showed differently inhibitory activities on TNF-alpha-induced NF-kappaB activation. Trans-N-caffeoyltyramine (3) was identified as the key component with an IC50 of 18.41 micromol x L(-1). It was suggested that the hydroxyl group at C-3 in trans-N-caffeoyltyramine might be a key binding site and its C-7,8-double bond might play an important role on NF-kappaB inhibitory activities as the link of the conjugation of pi electrons leading to a partial planar conformation. It might be inferred that the biological activity of compound 3 is attributed to the structure of Michael reaction acceptor containing alpha, beta-unsaturated ketones and benzene along with hydroxyl group in o-diphenol.
Biological Assay ; Cell Line ; Drugs, Chinese Herbal ; chemistry ; isolation & purification ; pharmacology ; Humans ; Inflammation Mediators ; antagonists & inhibitors ; immunology ; Lycium ; chemistry ; Molecular Structure ; NF-kappa B ; antagonists & inhibitors ; immunology