Adult ; Heart Diseases ; etiology ; Hemorrhagic Fever with Renal Syndrome ; complications ; Humans ; Male

Abstract? AlM: To explore the effect of Danshen injection iontophoresis combined with lumbrukinase on early patients with retinal vein occlusion ( RVO ) , and observe the prognosis to provide objective basis for clinical?METHODS: Eighty-two patients ( 117 eyes ) with early RVO were randomly selected in our hospital from January, 2011 to April, 2014, 41 cases (59 eyes) of control group treated with Lumbrokinase. Forty-one cases ( 58 eyes) of the observation group, treated with Danshen injection iontophoresis combined with lumbrokinase. The main indexes were the treatment effect, visual acuity and retinal circulation time.?RESULTS: The total effective rate of the observation group was 85. 4% ( 35/41 ), more than that of control group 68. 3% ( 28/41 ), the difference was statistically significant (P<0. 05). The invalid rate of the observation group was 14. 6% (6/41), lower than that of the control group 31. 7% ( 13/41 ), the difference was statistically significant (P<0. 05). The vision of the observation group 4. 8 ~5. 0 was 53. 7% (22/41), more than that of control group 41. 5% ( 17/41 ), the difference was statistically significant ( P < 0. 05 ). The restore vision of the observation group 4. 3 ~ 4. 7 was 31. 7% (13/41), lower than that of the control group 41. 5% ( 17/41 ), the difference was statistically significant ( P<0. 05 ). After treatment, retinal circulation time of two groups were lower than before treatment, the difference was statistically significant (P<0. 05). After treatment of retinal vein circulation time of the observation group was 8. 15 ± 1. 30s, 9. 70 ± 1. 28s lower than that of the control group, the difference was statistically significant (P<0. 05).?CONCLUSlON: There is better effective on Danshen injection iontophoresis combined with Lumbrokinase for early retinal vein occlusion, and can improve the patient's visual acuity, promote the rehabilitation of patients.

Aim To investigate the effect of CD44 anti-body-A3 D8 on the expression of IL-3 Rα and down-stream PI3K/Akt in NB4 cells. Methods The ex-pression of IL-3 Rα mRNA was detected by real-time quantitative RT-PCR, the IL-3Rα protein expression and changes of PI3 K/Akt signal pathway in NB4 cells treated with A3D8 were analyzed by Western blot. An-nexin-V-FITC/PI double staining flow cytometry was u-tilized to detect the apoptotic cells. The inhibitor of PI3 K/Akt signaling LY294002 combined with A3 D8 was used to inhibit the PI3K/Akt in NB4 cells. Re-sults After treated with A3 D8 , both the transcription-al level and translational level of IL-3 Rα were remark-ably reduced, and the PI3K/Akt pathway was inhibi-ted. LY294002 improved the inhibitory and apoptotic effects of A3D8 on NB4 cells. Conclusion CD44 antibody A3 D8 can downregulate the expression of IL-3Rα and inhibit the downstream PI3K/Akt pathway.

Objective To study the effects of Rhizoma Acori Tatarinowii (RAT) on amino acids neurotransmitter in mice brain and to explore its mechanisms. Methods After treated by different parts of RAT,the cerebral contents of the amino acids neurotransmitter in rats were detected by high performance liquid chromatography (HPLC) Results Volatile oil, fluid extract and defatted decoction of RAT could significantly lower cerebral glutamic acid level. Volatile oil and fluid extract decreased the content of aspartic acid, and volatile oil could also reduce the taurine content in brain tissue. Conclusion RAT can lower the contents of excitatory amino acids(EAA ) and has protective effect on the brain.

Objective To establish a tandem affinity purification(TAP) system of innate immune-regulatory protein PKR and analyze PKR function, for the future screen and identification of novel PKR-interaction proteins. Methods PKR gene was amplified by PCR, and then cloned into a mammalian expression vector pcTAP-A. Recombinant pcTAP-PKR was transfected into PKR knock-down(PKRkd) HeLa cells by LipofectAMINE 2000,and the PKR overexpressed HeLa cells were harvested for mitogen-activated protein kinases(MAPK) activation analysis. Cell extracts of PKR overexpressed cells were purified using TAP kit and examined by Western blot. Results Cal modulin resin(CBP) and streptavidin resin(SBP) tagged PKR was detected in PKRkd HeLa cells as early as 24 h upon transfection with pcTAP-PKR, and its expression decreased at later time points. The overexpression of PKR was autophosphorylated, and thus involved in the regulation of MAPK actviation. After small-scale TAP kit purification, PKR protein was detectable by Western blot. Conclusion We have successfully established a TAP system that over-expresses functional PKR, providing a useful tool for the future study on the identification of PKR interacting proteins.

This paper is to explore changes of intestinal mucosal barrier, intestinal flora, and bacterial translocation in rats with severe acute pancreatitis (SAP). Twenty four male SD rats were randomly divided into the control group (n = 10) and the experimental group (n = 14). The model of severe acute pancreatitis of rats was induced by the method of injecting adversely 5% sodium taurocholate into the common biliary-pancreatic duct. All of the rats were killed after 24 hours and the level of the serum amylase and the plasma endotoxin was determined after that. The pathological changes of pancreas and small intestine were observed through hematoxylin-eosin staining (HE staining) and the abdominal viscera bacterial translocation rates were tested. With the method of real-time polymerase chain reaction (RT-PCR) the quantity of the intestinal flora was analyzed. In the control group, the level of Escherichia coli, Lactobacillus and Bifidobacterium were 2.08 ± 1.29, 11.04 ± 7.55 and 12.21 ± 4.95, respectively. On the contrast, the level of Escherichia coli in the cecum contents was much higher (9.72 ± 3.58, P < 0.01), while the Lactobacillus number was decreased significantly (0.67 ± 0.34, P < 0.01), and the Bifidobacterium number was also decreased (4.59 ± 3.42, P < 0.05) in the experimental group, so the ratio of Bifidobacterium/Escherichia coli was reversed. Besides, in the experimental group, the plasma endotoxin positive rates and the bacterial translocation rates were much higher (P < 0.01 or P < 0.05) and the pathology scores of pancreas and small intestines were also significantly higher (P < 0.01) than those in the control group. These results indicated that in severe acute pancreatitis rats, the intestinal mucosal barrier was severely damaged and the dysbacteriosis occurs in the intestinal canal. And these might relate to the occurrence and development of multiple organ infection.
Animals ; Bacterial Translocation ; Endotoxins ; Intestinal Mucosa ; pathology ; Intestines ; microbiology ; Male ; Pancreas ; pathology ; Pancreatitis ; microbiology ; pathology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the inhibitory effect of cinnamaldehyde on invasion capacities of human breast cancer cell line MDA-MB-435S and its relation with regulating the expression of miR-27a.

METHODSThe effect of cinnamaldehyde on invasive capacities of MDA-MB-435S was measured by Transwell matrigel invasion assay. The effect of miR-27a expression on invasive capabilities of MDA-MB-435S, the intervention of cinnamaldehyde in the miR-27a expression, and its relation with its effect on invasive capabilities were defected with liposome 2000 transinfection miRNA27a mimics/inhibitors, real time-polymerase chain reaction (Real-time PCR), and Transwell chamber model.

RESULTSCompared with the control group, the number of cells passing through the transwell chamber was more significantly reduced after treated by cinnamaldehyde for 12 h (P < 0.05). The miR-27a expression was 962.07 times and 40% of that of the control group after transinfected by miR-27a mimics and miR-27a inhibitors. After transinfected by miR-27a inhibitors, the number of cells passing through the transwell chamber was more significantly reduced (P < 0.05). The miR-27a expression of MDA-MB-435S was down-regulated by 12-h treatment of cinnamaldehyde (2(-deltaCt) = 0.56, 0.18, 0.18, respectively). The number of miR-27a mimics transinfection pretreated MDA-MB-435S cells passing through the transwell chamber increased more obviously than the number of un-pretreated MDA-MB-435S cells in the control group (P < 0.05).

CONCLUSIONSCinnamaldehyde could inhibit invasive capabilities of human breast cancer cell line MDA-MB-435S. The over-expression of miR-27a played an important role in the invasive capability of MDA-MB-435S. The inhibition of cinnamaldehyde on invasive capabilities of MDA-MB-435S cells was correlated with down-regulating the expression of miR-27a.

Acrolein ; analogs & derivatives ; pharmacology ; Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Female ; Humans ; MicroRNAs ; genetics

OBJECTIVETo compare right atrial structural remodeling and the expression of matrix metalloproteinase (MMP) and tissue inhibitors (TIMP) between patients with unstable angina (UA) and myocardial infarction (MI).

METHODSRight atrial appendages were obtained from 18 patients with UA and 22 patients with MI undergoing coronary artery bypass grafting (CABG) operations. MMP-1, -3, -7, -9 and TIMP-1 protein expressions were detected by immunohistochemistry and RT-PCR. Echocardiography was performed before CABG.

RESULTSThe left and right atrial diameter, left ventricular diameter and mRNA levels of MMP-3, MMP-9 and TIMP-1 were significantly higher in MI group than those in UA group [LAD: (40.8 +/- 4.2) mm vs. (33.1 +/- 5.1) mm, P < 0.01; RAD: (44.1 +/- 6.8) mm vs. (28.8 +/- 6.0) mm, P < 0.01; LVEDD: (48.9 +/- 6.0) mm vs. (39.7 +/- 7.1) mm, P < 0.05; MMP-3: 0.39 +/- 0.18 vs. 0.28 +/- 0.07, P < 0.05; MMP-9: 0.81 +/- 0.21 vs. 0.55 +/- 0.20, P < 0.01; TIMP-1: 1.79 +/- 0.89 vs. 0.94 +/- 0.47, P < 0.01]. MMP-1, MMP-7 levels were similar between the 2 groups (MMP-1: 0.14 +/- 0.06 vs. 0.10 +/- 0.08, P > 0.05; MMP-7: 0.25 +/- 0.05 vs. 0.23 +/- 0.06, P > 0.05).

CONCLUSIONRight atrial up-regulation of MMP-3, MMP-9 and TIMP-1 levels may contribute to the right atrial structural remodeling in MI patients.

Adult ; Aged ; Angina, Unstable ; metabolism ; Female ; Gene Expression Regulation ; Heart Atria ; metabolism ; Humans ; Male ; Matrix Metalloproteinase 1 ; metabolism ; Matrix Metalloproteinase 3 ; metabolism ; Matrix Metalloproteinase 7 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Middle Aged ; Myocardial Infarction ; metabolism ; Tissue Inhibitor of Metalloproteinase-1 ; metabolism ; Up-Regulation

Adult ; Aged ; Aged, 80 and over ; Female ; Follow-Up Studies ; Hepatic Encephalopathy ; blood ; diagnosis ; etiology ; Humans ; Insulin-Like Growth Factor Binding Protein 1 ; Insulin-Like Growth Factor Binding Proteins ; blood ; Liver Cirrhosis ; complications ; Male ; Middle Aged ; Neuropsychological Tests ; Pregnancy Proteins ; blood

OBJECTIVEIt has been known that the intrahepatic renin-angiotensin-aldosterone system (RAAS) plays a key role in the fibrogenesis in livers. Aldosterone (Aldo), the principal effector molecule of the RAAS, exerts local effects on cell growth and fibrogenesis. However, the signal transduction mechanisms underlying the effects of Aldo on hepatic fibrogenesis remain to be fully elucidated. The present study aims to investigate the signal transduction mechanism underlying the effects of Aldo on the signal passageway of active protein-1 (AP-1).

METHODSIn vitro, HSCs-T6 cell line was treated with Aldo for 10 min, 30 min, 60 min, 120 min and 180 min, and protein expression of Phospho-P42/44 was detected by Western blot. In addition, HSCs-T6 cell line was preincubated for 60 min or not with U0126 (an inhibitor of the MAPK/ERK kinase), and also with antioxidant-N-acetylcysteine (NAC) prior to exposure to Aldo for the indicated times. Protein expression of Phospho-P42/44 was measured by Western blot. DNA biding activity of AP-1 was analyzed by electrophoretic gel mobility shift assay (EMSA). By means of RT-PCR, expression of alpha1(1) procollagen mRNA was detected.

RESULTSAldo stimulated HSC via extracellular signal-regulated kinase (ERK1/2) pathway. Time course experiments showed that Aldo induced Phospho-P42/44 expression, which was abrogated by U0126, reaching a maximum at 10 minutes, and then declined progressively. NAC inhibited the Phospho-P42/44 expression. EMSA showed that stimulation of HSC by Aldo markedly increased AP-1 DNA binding activity. U0126 markedly reduced AP-1 DNA binding activity induced by Aldo; NAC partly decreased AP-1 activity induced by Aldo. Aldo up-regulated expression of alpha1(1) procollagen mRNA, which was attenuated by U0126 and NAC.

CONCLUSIONStimulation of HSC by Aldo results in activation of AP-1 via ERK1/2 pathway, leading to up-regulation of AP-1 target gene alpha1(1) procollagen mRNA expression.

Aldosterone ; pharmacology ; Cell Line ; Collagen Type I ; biosynthesis ; genetics ; Hepatocytes ; cytology ; metabolism ; Humans ; Mitogen-Activated Protein Kinase 3 ; metabolism ; RNA, Messenger ; biosynthesis ; genetics ; Transcription Factor AP-1 ; metabolism