Glaucoma in Patients with Eyes Close to Areas Affected by Port-wine Stain has Lateral and Gender Predilection / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The location of facial port-wine stain (PWS) may be helpful for predicting some associated anomalies; high glaucoma incidence is found in patients with eyes close to PWS-affected areas (V1, ophthalmic branch area of the trigeminal nerve). This study aimed to investigate the characteristics of glaucoma in V1-affected PWS.</p><p><b>METHODS</b>A total of 569 patients with V1 area-affected PWS were reviewed in the study. The large series was based on the referral system between the Department of Plastic and Reconstructive Surgery and the Department of Ophthalmology. All patients were screened for glaucoma with assessments of intraocular pressure, cup-to-disc ratio, corneal diameter (only for infants), and axial length.</p><p><b>RESULTS</b>Of the 569 patients, 110 (19.3%) patients had glaucoma. Among the patients, 18.1% (76/420) had early-onset glaucoma (under 4-year-old group). In the 4 to 18-year-old age group, 29.3% (29/99) of the patients had glaucoma. Compared with right lateral and bilateral PWS, left-sided PWS had a lower risk of glaucoma in this study (odds ratio = 0.432 [95% confidence interval, 0.264-0.706], P = 0.01). The under 4-year-old group showed a slight predominance of males (61.8%) in glaucoma.</p><p><b>CONCLUSIONS</b>High glaucoma incidence was observed in patients with eyes close to PWS. More attention should be paid to glaucoma screening for right lateral and bilateral PWS patients. The predominance of males in Sturge-Weber syndrome (SWS) early-onset glaucoma patients might be due to the limitation of the case number; however, it might also provide us a new clue of potential relationship between SWS and PCG.</p>

Akt-centered amplification loop plays a critical role in vascular endothelial growth factor/stromal cell-derived factor 1-α cross-talk and cardioprotection / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Vascular endothelial growth factor (VEGF) is one of major mediators of angiogenesis and survival factor in some tissue, however, its direct effects on cardiomyocytes remain poorly understood.</p><p><b>METHODS</b>Rat neonatal ventricular myocytes were cultured in vitro. Akt phosphorylation was measured by Western blotting; the expression of stromal cell-derived factor α (SDF-1α)/CXCR4 axis was evaluated by real-time PCR and Western blotting. LY294002 and AMD3100 were used to interfere with the signaling of VEGF and SDF-1α/CXCR4 axis. Cardiac myocytes viability and injury were evaluated by trypan blue staining and lactate dehydrogenase (LDH) release.</p><p><b>RESULTS</b>Treatment of neonatal rat ventricular myocytes with VEGF induced phosphorylation of Akt in a dose and Flk-1 dependent manner. VEGF attenuated H2O2 induced cardiac myocyte death. The phosphoinositol-3-kinase (PI3K) inhibitor, LY294002 and Flk-1 antibody abolished the beneficial effects of VEGF on H2O2 induced cell death. In the mean time SDF-1α-CXCR4 axis was up-regulated by VEGF through PI3K-Akt signaling and contributed to the protective effects of VEGF on H2O2 induced cell death. Interestingly, SDF-1α also promoted production of VEGF in cultured cardiac myocytes and LY294002 reversed the up-regulation of VEGF induced by SDF-1α.</p><p><b>CONCLUSION</b>VEGF has direct protective effects on cardiomyocytes; a crosstalk between VEGF and SDF-1α through PI3K-Akt serves a survival role in cardiomyocytes in vitro.</p>

Reposition of coronary sinus lead dislocation only using pre-shaped stylet and guidewire: a case report / 中华医学杂志(英文版)

Technologies associated with cardiac resynchronization therapy (CRT) devices and lead systems have progressed. However, dislocation after coronary sinus (CS) lead placement continues to be a problem. We reported on the patient treated with CRT, in whom dislocation of CS lead occurred. In the case, we tried to reposition the CS lead without the left heart delivery system only using pre-shaped stylet and guidewire, and the dislocated CS lead could be successfully repositioned by the method. The method of only using a pre-shaped stylet and guidewire is easier than the conventional way, and it can shorten procedure duration and fluoroscopy time, as well as reduce the cost of treatment, but it is not always feasible.

Nitric oxide induces heat shock protein 72 production and delayed protection against myocardial ischemia in rabbits via activating protein kinase C / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Nitric oxide (NO) is a biologically active molecule which has been reported to protect the heart against ischemia and reperfusion injury in different species. This study aimed to test the hypothesis that nitric oxide may induce the expression of heat shock protein 72 (HSP72) which may protect the heart against ischemia.</p><p><b>METHODS</b>Rabbits were given intravenous saline or S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide donor, or Zaprinast, an inhibitor of cyclic guanosine monophosphate (GMP)-phosphodiesterase, which may increase myocardial cyclic GMP content. Twenty-four hours later, the rabbits were either sampled to measure HSP72, or induced with a 30-minute coronary occlusion followed by a 120-minute reperfusion, and then the infarct size was measured. Meanwhile, chelerythrine (CHE, an inhibitor of protein kinase C) was given intravenously 5 minutes before SNAP injection and the effect on HSP72 expression and infarct size was determined.</p><p><b>RESULTS</b>Twenty-four hours after pretreatment, immunoblotting showed HSP72 expression increased in the SNAP group compared with control groups, and this was blocked by CHE. Myocardial infarct size in the SNAP group was smaller than that of the control group ((32.4 +/- 5.8)% vs (51.1 +/- 4.7)%, P < 0.05). Pretreated with CHE abolished the infarct size-limiting effect of SNAP ((46.0 +/- 5.1)%). Pretreatment with Zaprinast neither induced HSP72 expression nor reduced infarct size ((55.4 +/- 5.4)%).</p><p><b>CONCLUSION</b>NO induced HSP72 expression and a delayed protection to the heart via the activities of protein kinase C by a cyclic GMP-independent pathway.</p>

Insulin protects isolated hearts from ischemia/reperfusion injury: cross-talk between PI3-K/Akt and JNKs / 生理学报

Our previous results have demonstrated that insulin reduces myocardial ischemia/reperfusion (MI/R) injury and increases the postischemic myocardial functions via activating the cellular survival signaling, i.e., phosphatidylinositol 3-kinase (PI3-K)-Akt-endothelial nitric oxide synthase (eNOS)-nitric oxide (NO) cascade. However, it remains largely controversial whether c-Jun NH2-terminal kinase (JNK) is involved in the effects of insulin on MI/R injury. Therefore, the aims of the present study were to investigate the role of JNK, especially the cross-talk between JNK and previously expatiated Akt signaling, in the protective effect of insulin on I/R myocardium. Isolated hearts from adult Sprague-Dawley rats were subjected to 30 min of regional ischemia and followed by 2 or 4 h of reperfusion (n=6). The hearts were pretreated with PI3-K inhibitor LY294002, or phosphorylated-JNK inhibitor SP600125, respectively, then perfused retrogradely with insulin, and the mechanical functions of hearts, including the heart rate (HR), left ventricular developed pressure (LVDP) and instantaneous first derivation of left ventricular pressure (+/-LVdp/dt(max)) were measured. At the end of reperfusion, the infarct size (IS) and apoptotic index (AI) were examined. MI/R caused significant cardiac dysfunction and myocardial apoptosis (strong TUNEL-positive staining). Compared with the control group, insulin treatment in MI/R rats exerted protective effects as evidenced by reduced myocardial IS [(28.9 +/- 2.0)% vs (45.0 +/- 4.0) %, n=6, P<0.01], inhibited cardiomyocyte apoptosis [decreased AI: (16.0 +/- 0.7) % vs (27.6 +/- 1.3) %, n=6, P<0.01] and improved recovery of cardiac systolic/diastolic function (including LVDP and +/-LVdp/dt(max)) at the end of reperfusion. Moreover, insulin resulted in 1.7-fold and 1.5-fold increases in Akt and JNK phosphorylation in I/R myocardium, respectively (n=6, P<0.05). Inhibition of Akt activation with LY294002 abolished, and inhibition of JNK activation with SP600125 enhanced the cardioprotection by insulin, respectively. And the abolishment by LY294002 could be partly converted by SP600125 pretreatment. In addition, SP600125 also decreased the Akt phosphorylation (n=6, P<0.05). These results demonstrate that insulin simultaneously activates both Akt and JNK, and the latter further increases the phosphorylation of Akt which attenuates MI/R injury and improves heart function; this cross-talk between Akt and JNK in the insulin signaling is involved in insulin-induced cardioprotective effect.

The effects of pulsed electromagnetic fields on proliferation and differentiation of endothelial progenitor cells / 中华物理医学与康复杂志

Objective To investigate the effects of pulsed electromagnetic fields(PEMFs)on proliferation and differentiation of endothelial progenitor cells(EPCs).Methods EPCs were isolated from rat bone marrow by density gradient centrifugation.EPCs were exposed to PEMFs from the 5th day to the end of culture.MTT was used to measure the proliferation of EPCs.The expression ofⅧ-related antigen and NOS_3 was evaluated by flow cytometry. Results Compared with the control,the proliferating ability of EPCs exposed to PEMFs was stronger;the number ofⅧ-related antigen and NOS_3 positive cells increased significantly in EPCs exposed in PEMFs.Conclusion PEMFs promotes the proliferation and differentiation of rat bone marrow EPCs.

Correlative multifactor analysis on frequency of ventricular premature beats in coronary heart disease / 第三军医大学学报

Objective　To investigate the prognosis in risk of ventricular arrhythmia in coronary heart disease with heart rate variability (H RV), left ventricular ejection fraction (LVEF) and other clinical background dat a. Methods　A total of 81 patients were divided into ventricular premature beats (VPBs)≥30/h group and VPBs<30/h group. Their LVEF, HRV and cli nical data were studied and analyzed. Results　The age and blood pressure between 2 groups had no significant difference. LVEF, standard deviati on of all normal RR intervals (SDNN), SD of the average of NN interval (SDANN) a nd HRV triangular index (HRVI) were significant less in VPBs≥30/h group than in VPBs<30/h group (43.29±15.38 vs 67.33±11.47，P＜0.01；90.05±22.2 9 vs 117.90±30.32，P＜0.05；77.43±17.78 vs 105.69±28.79，P＜0.05 ；24.54±8.70 vs 32.70±10.87，P＜0.05, respectively). Incidence of myo cardial infarction (MI) was larger in VPBs≥30/h group than VPBs<30/h group. LVE F was the independent predictable factor in risk of ventricular arrhythmia with multinomial regression logistic analysis（B=0.119, P=0.032）. Co nclusion 　Our findings indicate that LVEF is an independent predictable factor i n risk of ventricular arrhythmia in coronary heart disease. Although HRV and MI history can not be used to predict VPB, significant difference is found between 2 groups. High-risk patients could be selected successfully when these data are considered in combination.

Correlative multifactor analysis on frequency of ventricular premature beats in coronary heart disease / 第三军医大学学报

Objective　To investigate the prognosis in risk of ventricular arrhythmia in coronary heart disease with heart rate variability (H RV), left ventricular ejection fraction (LVEF) and other clinical background dat a. Methods　A total of 81 patients were divided into ventricular premature beats (VPBs)≥30/h group and VPBs<30/h group. Their LVEF, HRV and cli nical data were studied and analyzed. Results　The age and blood pressure between 2 groups had no significant difference. LVEF, standard deviati on of all normal RR intervals (SDNN), SD of the average of NN interval (SDANN) a nd HRV triangular index (HRVI) were significant less in VPBs≥30/h group than in VPBs<30/h group (43.29±15.38 vs 67.33±11.47，P＜0.01；90.05±22.2 9 vs 117.90±30.32，P＜0.05；77.43±17.78 vs 105.69±28.79，P＜0.05 ；24.54±8.70 vs 32.70±10.87，P＜0.05, respectively). Incidence of myo cardial infarction (MI) was larger in VPBs≥30/h group than VPBs<30/h group. LVE F was the independent predictable factor in risk of ventricular arrhythmia with multinomial regression logistic analysis（B=0.119, P=0.032）. Co nclusion 　Our findings indicate that LVEF is an independent predictable factor i n risk of ventricular arrhythmia in coronary heart disease. Although HRV and MI history can not be used to predict VPB, significant difference is found between 2 groups. High-risk patients could be selected successfully when these data are considered in combination.