Objective To investigate the therapeutic effect of Jiangzhi Decoction(JD) for the treatment of disordered lipid metabolism.Methods With Zhibituo Capsule as the control capsule,a random,paralleled and positive controlled clinical trial was carried out.A total of 64 patients were equally randomized into the treatment group and control group,and the treatment lasted 4 weeks.Results After administration,the level of total cholesterol(TC),triglyceride(TG),and arteriosclerosis index(AI) were reduced,the high density lipoprotein cholesterol(HDL-C) level was increased,and the sum of the decrease of electrocardiogram(ECG) ST segment was markedly improved in the treatment group,the difference being significant compared with those before treatment.In the treatment group,oppressive pain in the chest and hypochondrium,dizziness,limb numbness,poor appetite and headache were much relieved,and the relief of oppressive pain in the chest and hypochondrium,dizziness,and poor appetite was obvious as compared with the control group.Conclusion JD has good curative effect on disordered lipid metabolism with stagnation of phlegm and blood-stasis,in particular on relieving the clinical symptoms.

Objective To investigate the relationship between the leptin level and neonatal weight and the expression of leptin in placenta. Methods The concentrations of leptin in 100 maternal blood and umbilical blood of the term pregnant women were examined by radioimmunoassay (RIA). According to the neonatal weight to divide into the large for gestational age (LGA) group 19 cases, the appropriate for gestational age (AGA) group 65 cases, the small for gestational age (SGA) 16 cases. The level of leptin mRNA in 41 placental tissue was examined by Reverse transcription polymerase chain reaction (RT PCR). Results (1) The expression level of leptin mRNA in placenta was 0 97?0 04, which was positively related to the neonatal weight significantly ( r =0 43, P 0 05).(3)The concentration of leptin in umbilical blood was (7 58? 5 15) ?g/L, which was positively related to the neonatal weight ( r =0 57, P

Objective To investigate the level of leptin in the serum of GDM mothers and their neonates and the variation of the leptin expression in placenta. Methods The concentrations of serum insulin and leptin in 24 GDM and 26 healthy mothers and neonates were examined by radioimmunoassay (RIA).The level of leptin mRNA in 50 placentas was examined by reverse transcription-polymerase chain reaction(RT-PCR). Results (1) The serum levels of leptin and insulin in GDM group [(18.62?7.86) ?g/L and (13.47?5.11) mIU/L] were significantly higher than those in control group [(14.21?7.59) ?g/L and (8.98?4.23) mIU/L,P 0.05) in both groups. But the leptin level in umbilical blood of the two group was positively related to the insulin level ( r=0.53,P

Animals ; Brain ; drug effects ; metabolism ; Calmodulin ; metabolism ; Female ; Lead ; toxicity ; Male ; Maternal Exposure ; Pregnancy ; Protein Kinase C ; metabolism ; Rats ; Rats, Wistar

Background Choroidal neovascularization (CNV) is one of the causes of blindness in multiple eye diseases.Researches showed that complement system participates in the pathogenesis of CNV.Objective This study was to construct the recombinant of complement factor B-small interference RNA (CFB-siRNA) expression vector and to observe its inhibitory effect on human umbilical vein endothelial cells (ECV-304).Methods CFB gene primers were designed based on human CFB gene,and an expression vector of CFB-siRNA was constructed by inserting CFB-siRNA into pRNAT-U6.1/Neo plasmid.Recombinant plasmids were confirmed by the digestion analysis of restriction endonuclease,and all inserted sequences were verified by DNA sequencing.The recombinant pRNAT-U6.1/CFB-siRNA plasmid and the blank plasmid were transfected into ECV-304 cells in the CFB-siRNA group and blank plasmid group by electroblot,respectively,and non-transfected cells served as the normal control group.The cells were observed under the fluorescence microscope 48 hours after transfection,and the transfective efficiency was calculated.The relative expression of CFB mRNA in the cells of different groups was detected by semi-quantitative reverse transcription PCR (RT-PCR).MTT was employed to calculated the growth inhibitory rates of the cells 24,48 and 72 hours after transfection.The percentages of the cells in different cell cycles were detected by flow cytometry.Results The sequence of the target vector was identical to the designed sequence.The green fluorescence protein (GFP) was seen in both the CFB-siRNA group and the blank plasmid group.The relative expression levels of CFB mRNA were 0.07 ±0.04,0.14 ±0.02 and 0.14 ±0.03 in the CFB-siRNA group,the blank plasmid group and the normal control group,respectively,a significant difference was obtained among the three groups (F=233.05,P =0.00);the expression level of CFB mRNA in the CFB-siRNA group was significantly declined in comparison with the blank plasmid group and the normal control group (both at P＜0.05).The growth inhibitory rates of the cells were (23.45 ±0.01) ％,(33.48 ±0.02) ％ and (45.49±0.01) ％ at 24,48 and 72 hours after transfection,respectively,a significant difference was obtained among the three groups (Fgroup =212.99,P =0.00);the growth inhibitory rates in CFB-siRNA group were significantly higher than that in the blank plasmid group and normal control group (all at P＜ 0.05).The percentages of G1 phase cells were (44.4 ±0.5) ％,(25.8 ±0.4) ％ and (27.9 ± 0.6) ％ in the CFB-siRNA group,the blank plasmid group and the normal control group respectively,a significant difference was obtained among the three groups (F=58.98,P=0.00).The percentages of G1 phase and G2 phase cells in the CFB-siRNA group were significantly higher than those in the blank plasmid group and the normal control group (all at P＜0.05).Conclusions Recombinant pRNAT-U6.1/CFB siRNA inhibits the proliferation of ECV-304 cells effectively by arresting the cells in G1 intermediate phase of the growth cycle.

BACKGROUND:Arsenic trioxide is considered to inhibit the proliferation of vascular smooth muscle cel s and promote cel apoptosis. Therefore, we wondered whether the arsenic can inhibit the hyperplasia of vascular smooth muscle cel s, an arsenic-coated stent can be compatible with the vascular tissue, and a better vascular intimal coverage as early as possible can reduce intimal hyperplasia.
OBJECTIVE:To observe the vascular histocompatibility of the arsenic-coated stent.
METHODS:Fourteen white rabbits were randomized into two groups and respectively subject to the implantation of arsenic-coated 316 L stainless steel stents and bare 316 L stainless steel stents into the abdominal aorta. After 28 days, the distal and proximal parts of the vessel at the implantation site were ligated and the ligated vessel was taken for hematoxylin-eosin staining and light microscope observation.
RESULTS AND CONCLUSION:(1) Gross observation:the vessel at the stent site was a little larger than the adjacent vessels in the outer diameter, which was expanded but had no visible thrombus. After cutting the stent, the neointima formed smoothly on the stent surface. (2) Light microscope observation:the stent was located in the middle of the vessel, the medial smooth muscle was pressed, and vascular intimal smooth muscle hyperplasia was found around the stent, thereby thickening the vascular intima. The vascular neointima formed and covered the stent, and there was a thin black layer between the stent and the vascular tissue, which consisted of arsenic and its compounds. These findings suggest that the arsenic-coated stents can be covered with vascular tissues, possessing good vascular histocompatibility.

Objective To study the prenatal diagnosis and clinical significance of fetal hyperechogenic kidneys.Methods Thirty one cases with fetal hyperechogenic kidneys were prenatally diagnosed with ultrasound.Autopsy was conducted and histological examination of the kidney was performed when pregnancy was terminated.A close follow-up was given for cases continuing pregnancy.Umbilical cord blood was collected for fetal chromosome analysis after delivery.Results(1)6 fetuses were complicated with other organ abnormalities,3 fetuses had abnormal chromosome,and 2 cases had a family history.(2) 12 cases chose to terminate pregnancy,10 of whom were oligohydromnios.Causes for fetal hyperechogenic kidneys were infantile polycystic kidney disease(IPKD,10 cases),adult polycystic kidney disease (APKD,1 case),polycystic kidney dysplasia(PKD,1 case)after postmortem histological examination. (3)Nineteen cases continued pregnancy,2 neonates with oligohydramnios died during neonatal period,both of them were IPKD;3 cases that were IPKD,IPKD and KPD respectively died 3 months,8 months and 1 year after birth,respectively;one case presented with hypertension symptom 26 months after birth,which was diagnosed as IPKD.The other 13 cases had no clinical manifestation and a close following-up is being undertaken for them at present.Conclusions(1)Fetal hyperechogenic kidneys could be caused by IPKD, APKD,or PKD,and are sometimes a normal variant.(2)Aminotic fluid volume is a key factor for prognosis;a suggestion for termination would be given to cases with fetal hyperechogenic kidneys and oligohydromnios.(3)For cases with fetal hyperechogenic kidneys,a complete and careful ultrasonography should be given to both parents and fetus,and fetal chromosomal analysis is suggested prenatally.

Objectlve To explore the effect of Qibai Pingfei capsule on the right ventricular hypertrophy index (RVHI)of rats with phlegm and blood stasis of COPD.Methods 60 rats were randomly divided into 6 groups,a control group,a model group,a Ligustrazine group,a Nifedipine group,a high dose Qibai Pingfei capsule group and a low dose Qibai Pingfei capsule group.Composite factors method was adopted to establish phlegm and blood stasis COPD rat model.At the same time of modeling.Qibai Pingfei capsule,Ligustrazine,Nifedipine were also given to these rats.Observed the changes of RVHI in each group.Results RVHI did not show statistic difierence between high dose of the Qibai Pingfei capsule group and the control group(P＞0.05).and between the Nifedipine group and the model group(P＞0.05).RVHI manifested significant diffbrencc between the Ligustrazine group and the low dose Qibai Pingfei capsule group(P＜0.01),and between the Ligustrazine group and the control group(P＜0.01).Conclusion High dose Qibai Pingfei capsule can effectively prevent the right ventricular hypertrophy of model rats with the phlegm and blood stasis of COPD.Ligustrazine has certain effects but not as good as high dose Qibai Pingfei capsule.Nifedipine can not prevent the right ventricular hypertrophy of model rats.

Objective To investigate the expression of inflammatory mediators in renal tubular epithelial cells in patients with diabetic nephropathy (DN) and to explore the possible clinicopathological significance. Methods Twenty-three patients with DN diagnosed by renal biopsy and 10 patients with renal cell carcinoma undergone nephrectomy were allocated into DN group and control group, respectively. The renal expression of NF-κB p50, NF-κB p65, NF-κB p65 mRNA, MCP-1, OPN, α-SMA, and FN was detected by immunohistochemical or in situ hybridization assay. Serum creatinine, urinary N-acetylglucosaminedase (NAG), urinary albumin and 24-hour urinary protein were detected. The correlation between these inflmmnatory markers and clinicopathological data were analyzed. Results (1)Among all the 23 DN patients, granular degeneration of the renal tubular epithelium, focal tubular atrophy, infiltration of inflammatory cells and interstitial fibrosis were apparent, and none of these were found in control group. (2) Immunohistochemical and in situ hybridization assay showed that, compared with control group, expression of these factors increased significantly in renal tubular cells or interstitium in DN patients, and expression of α-SMA or FN was not found in tubular epithelial cells. (3)Statistics assay showed the tubular NF-κB p65 protein expression was correlated with all of the following factors: NF-κB p50 protein (r=0.792) and NF-κB p65 mRNA (r=0.763), tubular MCP-1 (r=0.825) and OPN (r=0.869) expression, interstitial α-SMA (r=0.327) and FN (r=0.432) expression, proteinuria(r=0.710), estimated glomerular filtration rate (eGFR) (r=-0.728), and urinary NAG (r= 0.930), P<0.01 respectively. Conclusion Tubular inflammation may play a role in the pathogenesis and progression of DN.

Objective • To investigate the effect of Toll-like receptor 4 (TLR4) in the pathological injury in fat embolism mice model. Methods • One hundred and twenty male C57BL/6 mice were randomly divided into 10 groups. One group was set as blank control group, and others were injected separately with 1, 2…9 μL/g of allogeneic perirenal fat via tail vein, respectively. The mortality of each group was counted, median lethal dose (LD50) of fat injection in mice was calculated by Bliss method, and the fat embolism LD50 mice model was established. The TLR4 protein expression in the pulmonary tissue of surviving mice was detected by Western blotting. Sixty male C57BL/6 mice were randomly divided into the control group (the same dose of saline was given via tail vein) and the experimental groups (group 2 h, group 8 h, group 24 h and group 48 h, the LD50 fat was given via tail vein). The TLR4 protein expression at different time after fat injection was detected by Western blotting. The mortality of 20 TLR4 gene-knockout mice (TLR4-/- mice) was recorded and compared with 60 wild-type mice after LD50 fat injection. Results • The LD50 of fat embolism mice model was (3.93±0.78) μL/g. After the injection of 1-7 μL/g fat, the expressions of TLR4 protein in the pulmonary tissue of all seven groups were significantly increased, compared with the control group (all P=0.000). In the fat embolism LD50 mice model, compared with the control group, the expressions of TLR4 protein in group 2 h were significantly increased (P=0.005). Then, expression level of TLR4 protein was gradually reduced after 2 h, and there was no significant difference between the control group and group 48 h. The mortality of TLR4-/- mice injected with LD50 fat was lower than that of wild-type mice (P=0.043). Conclusion • TLR4 protein involves in the pathologic process of fat embolism syndrome. The knockout of TLR4 gene can reduce the mortality of fat embolism mice. TLR4 and its correlated non-infectious inflammatory response may be an important molecular mechanism of biochemical injury in fat embolism syndrome. Blocking the activation of TLR4-mediated signaling pathway can significantly improve the prognosis, which provides new basis for the prevention, evaluation and treatment of fat embolism syndrome.