Keratorefractive surgery changes the central corneal thickness (CCT) and corneal curvature, which could influence the Goldmann applanation tonometer (GAT) and non-contact tonometer (NCT) measurements of intraocular pressure (IOP), but not dynamic contour tonometer(DCT). During the procedure of LASIK, there is a transient rise of IOP, which increases the risks of optic nerve damage. Meanwhile, the presence of functioning filtering blebs may affect the choice and outcome of refractive surgery, or even becomes a contraindication of surgery. Steroids are typically used after keratorefractive surgery, which could lead to IOP elevation. Hence it is important to monitor IOP after LASIK and to be aware of inaccurate IOP readings due to corneal flap interface fluid. Treating patients with postoperative elevated IOP after keratorefractive surgery is similar to that for patients with glaucoma. This review will address the issues surrounding the safety, relevant complications and implications of keratorefractive surgeries on glaucoma and relevant diagnostic tests.

miR-200c has been shown to regulate the epithelial-mesenchymal transition (EMT) by inhibiting ZEB1 and ZEB2 expression in breast cancer cells. This study further examined the role of miR-200c in the invasion and metastasis of breast cancer that goes beyond the regulation on ZEB1 and ZEB2 expression. In this study, the bioinformatics software (miRanda) was used to predict the target gene of miR-200c and Renilla luciferase assay to verify the result. The metastatic breast cancer cells MDA-MB-231 were cultured and transfected with the miR-200c mimic or inhibitor. The expressions of miR-200c and HMGB1 were detected by RT-PCR and Western blotting, respectively. Transwell assay and wound healing assay were employed to examine the invasive and migrating ability of transfected cells. Target prediction and Renilla luciferase analysis revealed that HMGB1 was a putative target gene of miR-200c. After transfection of MDA-MB-231 cells with the miR-200c mimic or inhibitor, the expression of miR-200c was significantly increased or decreased when compared with cells transfected with the miR-200c mimic NC or inhibitor NC. Moreover, the expression of HMGB1 was reversely correlated with that of miR-200c in transfected cells. Tranwell assay showed that the number of invasive cells was significantly reduced in miR-200c mimic group when compared with miR-200c inhibitor group. It was also found that the migrating ability of cells transfected with miR-200c mimics was much lower than that of cells transfected with miR-200c inhibitors. It was suggested that miR-200c can suppress the invasion and migration of breast cancer cells by regulating the expression of HMGB1. miR-200c and HMGB1 may become useful biomarkers for progression of breast cancer and targets of gene therapy.

Objective To explore the changes of plasma angiotensinⅡ (AngⅡ) and cardiac function,and the curative effect of children with acute viral myocarditis (VMC) treated with captopril(CAP).Methods Concentrations of plasma AngⅡ were measured with radio-immunity and cardiac function was detected by Doppler echocardiography for the VMC group (n=60) before and after treatment [the CAP group (n=30), the routine group (n=30) and the control group (n=30)].Results 1. The level of plasma AngⅡ significantly increased and the contractive and diastolic function obviously declined in children with acute VMC. There was a significant difference between VMC group and control group, with a significant correlation between the level of AngⅡand the contractive diastolic function.2. Compared with the level before treatment, the level of AngⅡ decreased and the contractive function obviously ameliorated in two groups; the diastolic function obviously ameliorated in the CAP group and did not ameliorate in the routine group after treatment. In CAP group the level of AngⅡ and the cardiac function significantly improved; there were statistical differences between the two groups after treatment.Conclusions 1.The increase of the plasma AngⅡ was an important factor for decrements of the contractive and diastolic function in acute viral myocarditis.2.It could decrease the concentration of plasma AngⅡ and ameliorate cardiac function in children with acute VMC treated with captopril,which was an effective therapy for acute VMC.

0.05).Conclusions SNP of 2350G→A in ACE gene is associated with MI,AA genotype is probably a genetic marker of MI in Han nationality.

Objective:It has been proposed that blood pressure variability(BPV) is positively related to end-organ damage(EOD) in hypertension.The present work was designed to observe the effects of long-term treatment with nitrendipine and hydralazine on BPV and EOD in spontaneously hypertensive rats(SHR),to examine the hypothesis that lowering BPV with an antihypertensive drug is an important factor in organ protection.Design and methods:Drugs were mixed in rat chow.After 4 months of drug administration,blood pressure was recorded continuously in conscious freely moving rats for 24 h.The heart,kidneys,and brain were then isolated and examined.Results:It was found that nitrendipine significantly decreased blood pressure and BPV,and significantly decreased EOD score in SHR.Hydralazine decreased blood pressure,but did not lower BPV.No effect on EOD was found in hydralazine-treated rats.In control rat(n=38),EOD score was weakly related to systolic blood pressure(r=0.331,P<0.05) and closely related to long-term systolic BPV(r=0.551,P<0.01).In nitrendipine-treated rats,EOD score was closely related to long-term systolic BPV(r=0.602,P<0.01),but not to blood pressure level(r=0.174,P>0.05).Conclusion:BPV plays an important role in the organ-protecting effects of nitrendipine.

Objective:It has been proposed that blood pressure variability(BPV) is positively related to end-organ damage(EOD) in hypertension.The present work was designed to observe the effects of long-term treatment with nitrendipine and hydralazine on BPV and EOD in spontaneously hypertensive rats(SHR),to examine the hypothesis that lowering BPV with an antihypertensive drug is an important factor in organ protection.Design and methods:Drugs were mixed in rat chow.After 4 months of drug administration,blood pressure was recorded continuously in conscious freely moving rats for 24 h.The heart,kidneys,and brain were then isolated and examined.Results:It was found that nitrendipine significantly decreased blood pressure and BPV,and significantly decreased EOD score in SHR.Hydralazine decreased blood pressure,but did not lower BPV.No effect on EOD was found in hydralazine-treated rats.In control rat(n=38),EOD score was weakly related to systolic blood pressure(r=0.331,P<0.05) and closely related to long-term systolic BPV(r=0.551,P<0.01).In nitrendipine-treated rats,EOD score was closely related to long-term systolic BPV(r=0.602,P<0.01),but not to blood pressure level(r=0.174,P>0.05).Conclusion:BPV plays an important role in the organ-protecting effects of nitrendipine.

OBJECTIVETo investigate the effects and mechanisms of high glucose on the phenotype transformation of rat vascular smooth muscle cells (VSMCs).

METHODSVSMCs ere isolated from rat thoracic aorta and the 3rd-5th VSMCs were incubated with normal glucose (5.5 mmol/L), high glucose (25 mmol/L), or high glucose (25 mmol/L) + P38 inhibitor (25 mmol/L +SB203580) for another 24 hours. Then the gene expression of osteopontin (OPN), alpha smooth-actin (alpha-SMA), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9(MMP-9) were assayed by real time RT-PCR, the protein expression of P38 were assayed by Western blot.

RESULTS(1) High glucose promoted the phenotype transformation of VSMCs and up-regulated the expression of MMP-2 and MMP-9. (2) High glucose promoted the phosphorylation of P38. (3) SB203580, the inhibitor of P38/MAPK signal pathway, inhibited the effects of high glucose on phenotype transformation and expression of MMP-2 and MMP-9.

CONCLUSIONHigh glucose may promote phenotype transformation of VSMCs via the signal pathway of P38/MAPK.

Actins ; metabolism ; Animals ; Aorta, Thoracic ; cytology ; Blotting, Western ; Cells, Cultured ; Glucose ; pharmacology ; Imidazoles ; pharmacology ; MAP Kinase Signaling System ; Matrix Metalloproteinase 2 ; Matrix Metalloproteinase 9 ; metabolism ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Osteopontin ; metabolism ; Phenotype ; Pyridines ; pharmacology ; Rats ; p38 Mitogen-Activated Protein Kinases ; metabolism

In vivo extracellular recordings were made in the subthalamic nucleus (STN) of intact control rats and rats with 5,7-dihydroxytryptamine (5,7-DHT) -produced lesion of dorsal raphe nucleus (DRN). The results showed that the firing rate of STN neurons in control rats and DRN-lesioned rats were (6.93+/-6.55) Hz and (11.27+/-9.31) Hz, respectively, and the firing rate of DRN-lesioned rats significantly increased when compared to the control rats (P<0.01). In control rats, 13% of STN neurons discharged regularly, 46% irregularly and 41% in bursts. In DRN-lesioned rats, 9% of STN neurons discharged regularly, 14% irregularly and 77% in bursts, the percentage of STN neurons firing in bursts was obviously higher than that of the control rats (P<0.01). In addition, the mean interspike interval coefficient of variation of STN neurons in control rats and DRN-lesioned rats were (0.05+/-0.04) and (0.11+/-0.09), respectively. The mean interspike interval coefficient of variation of DRN-lesioned rats was significantly higher than that of the control rats (P<0.001). These results show that the firing rate and the bursting pattern rate of neurons in STN of DRN-lesioned rats increase significantly, suggesting that DRN inhibits the neuronal activity of the subthalamic neurons in the intact rat.
5,7-Dihydroxytryptamine ; pharmacology ; Adrenergic Agents ; pharmacology ; Animals ; Electrophysiological Phenomena ; Male ; Neurons ; physiology ; Random Allocation ; Raphe Nuclei ; drug effects ; pathology ; Rats ; Rats, Sprague-Dawley ; Subthalamic Nucleus ; physiopathology

AIMTo investigate the in vitro and in vivo stability of 9-nitrocamptothecin lactone form in rat plasma.

METHODSThe specific and accurate HPLC method was developed for quantifying 9-nitrocamptothecin lactone form and the total lactone and carboxylate forms simultaneously. By using of this method, the ratios of lactone form to the total in rat plasma at different time were determined in vitro and in vivo. The results were compared to determine which was the main factor influencing the stability of 9-nitrocamptothecin lactone form in rat plasma in vivo.

RESULTSThe stability of lactone form in rat plasma was much higher in vivo than that in vitro.

CONCLUSIONBlood cells help to increase the stability of 9-nitrocamptothecin lactone form. Clearance from blood in vivo is the primary factor which influences the plasma stability of 9-nitrocamptothecin lactone form. The kinetic process of 9-nitrocamptothecin lactone form and total drug in rats were both best fitted to a two-compartment model. However, the process of 9-nitrocamptothecin carboxylate form in vivo was best fitted to a one-compartment model.

Animals ; Antineoplastic Agents ; blood ; pharmacokinetics ; Area Under Curve ; Camptothecin ; analogs & derivatives ; blood ; pharmacokinetics ; Carboxylic Acids ; blood ; pharmacokinetics ; Chromatography, High Pressure Liquid ; methods ; Drug Stability ; Lactones ; blood ; pharmacokinetics ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo evaluate surgical methods and results of extracardiac conduit total cavopulmonary anastomosis (EC-TCPA) without cardiopulmonary bypass (CPB).

METHODSFrom May 2000 to April 2003, 11 patients with functional univentricle underwent off-pump EC-TCPA (no-CPB group). Their postoperative outcome was retrospectively compared with a 17-patient group who underwent EC-TCPA with cardiopulmonary bypass (CPB group) over a concurrent time period.

RESULTSThere was 1 operative death in no-CPB group and 2 in CPB group; early postoperative hemodynamics appeared to significantly improve in no-CPB group. Blood and platelet transfusions decreased and blood plasma transfusion significantly lowered in no-CPB group compared with CPB group (P = 0.036). Postoperative courses of patients in no-CPB group were smooth and event free, and extubation time was substantially short Intensive cares unit stay (P = 0.04) and hospital stay (P = 0.02) postoperation were significantly shorter, hospital costs were significantly reduced (P = 0.004) in no-CPB group compared with CPB group.

CONCLUSIONSEC-TCPA without use of CPB is not a difficult procedure; the procedure results in improvement in postoperative hemodynamics, and decreased use of blood and blood products. It is a more efficient operation with more short recovery time and reduced hospital stay.

Adolescent ; Blood Pressure ; Cardiopulmonary Bypass ; Child ; Child, Preschool ; Female ; Follow-Up Studies ; Heart Bypass, Right ; methods ; Heart Defects, Congenital ; physiopathology ; surgery ; Humans ; Male ; Retrospective Studies