Atrial compartment operation for atrial fibrillation: to isolate the left atrium or not?

BACKGROUND: The atrial compartment operation was designed to convert atrial fibrillation (AF) to sinus rhythm with intentional preservation of the electrical connection between adjacent atrial compartments. However, incidental left atrial isolation was observed in some patients. This study compared the long-term clinical outcomes of left atrial isolation for AF with those with right and left atrial connection. METHODS: Twenty patients with mitral valve disease and chronic AF who underwent atrial compartment operation with successful sinus conversion were studied. Left atrial isolation was documented by local electrogram recording. When there were no signs of electrical connection between the left atrium and the rest of the heart, either during sinus rhythm or during stimulation from various atrial compartments, left atrial isolation was confirmed. All patients were followed by electrocardiogram and echocardiogram serial recordings. Clinical signs and symptoms of cardiac performance and thromboembolism were also examined. RESULTS: Seven patients showed an isolated left atrium and 13 patients had electrical connection between the right and left atria. The age, gender, AF duration, and underlying disease were not different between the two groups of patients. During a mean follow-up period of 66 +/- 15 months, none of the patients with left atrial isolation showed recurrence of AF, although one experienced paroxysmal atrial flutter. However, 8 of the 13 patients with right and left atrial connection experienced recurrent atrial flutter/fibrillation (6 atrial flutter and 5 AF) (p = 0.058). The propensity for recurrent atrial flutter/fibrillation in these patients may be related to the conduction delay between the two atrial compartments, measured at 142 +/- 48 ms. At the end of the follow-up period, all patients with left atrial isolation remained in normal sinus rhythm without antiarrhythmic drugs. Of the patients who had right and left atrial connection, 2 developed sustained AF and 1 developed atrial flutter. Patients with left atrial isolation showed a decreased transmitral "A" flow compared with those with right and left atrial connection. Postoperative left atrial diameter and clinical functional class did not differ between patients with and without left atrial isolation. The incidence of embolization observed in both treatment groups did not differ significantly: 14% (1/7) in patients with left atrial isolation and 8% (1/13) in patients with right and left atrial connection (p > 0.05 between the groups). CONCLUSIONS: Left atrial isolation confers a better arrhythmia outcome but at the expense of poorer mechanical performance as compared with preserved electrical connection between the two atria. Nonetheless, all patients remain at risk for systemic embolization. Therefore, modifications of current surgical incisions for AF are needed.     

Sphingosylphosphorylcholine,a naturally occurring lipid mediator,inhibits human platelet function

1 The lysophospholipids, lysophosphatidic acid and sphingosine 1-phosphate, have been reported to activate platelets. Here we examined effects of the naturally occurring related sphingosylphosphorylcholine (SPC) on human platelet function. 2 Platelet activation was determined as aggregation, elevation of intracellular Ca(2+) concentrations, surface expression of P-selectin, GP 53, and GP IIb/IIIa neoepitope PAC-1, and of fibrinogen binding to the platelet surface. 3 Platelets were activated by ADP (5 and 20 micro M), the thrombin receptor-activating peptide TRAP-6 (5 and 20 micro M), the thromboxane A(2) mimetic U-46619 (1 micro M) and collagen (20 and 50 micro g ml(-1)) but not by SPC (up to 20 micro M). 4 SPC concentration-dependently (IC(50) approximately 1-10 micro M) inhibited activation of washed human platelets in response to all of the above agonists, with almost complete inhibition occurring at 20 micro M SPC. 5 The SPC stereoisomers, D-erythro SPC and L-threo SPC, exhibited similar concentration-response curves in inhibiting 20 micro M ADP-induced platelet aggregation, suggesting that SPC did not act via specific lysophospholipid receptors. 6 Although SPC slightly activated platelet protein kinase A (as assessed by VASP phosphorylation), this effect could not explain the marked platelet inhibition. Possible protein kinase C inhibition also did not explain the inhibition of platelet activation by SPC. On the other hand, SPC suppressed agonist-induced Ca(2+) mobilization and phospholipase C stimulation. 7 These results indicate that the lysophospholipid SPC is an effective inhibitor of human platelet activation, apparently primarily by uncoupling agonist-activated receptors from their effectors.     

Ultrasound bone densitometry of the calcaneus in healthy Chinese children and adolescents

Introduction We evaluate reference data to examine whether there are sex-, age-, height-, weight- and BMI-related differences of quantitative ultrasound parameters (QUS) for healthy Chinese children and adolescents. Methods A total of 726 healthy children and adolescents (360 male and 366 female) aged from 10–21 years were examined with a Lunar Achilles Express densitometer. The measurements on the right heel included speed of sound (SOS), broadband ultrasound attenuation (BUA), and a calculated stiffness index (SI). Results Our results found that there were no significant differences for BUA, SOS and SI between males and females, except in the age range of 12 to 13 years. The values of all parameters were significantly higher in the 12-year-old females compared to males, and BUA values were significantly higher in 13-year-old females compared to males. A spurt in QUS parameters were observed at 12 years in females and at 14 years in males. A steady increase of BUA, SOS, and SI was seen with increasing body height and weight in both sexes. Conclusion In conclusion, the present results can be used as reference data for children and adolescents in China.     

上颌骨切除后即刻修复的研究

本文研究上颌骨肿瘤切除术后用带蒂组织瓣即刻修复的方法,并对瓣的解剖学基础及手术应用优缺点进行讨论说明。结论带组织瓣是即刻修即上颌骨缺损的较好办法;颞肌筋膜瓣是修复较大面积的上颌骨缺损的最简便有效的方法之一。     

Erratum

To evaluate the effect of estrogen and androgen levels on erythrocyte deformability in endocrinological erectile dysfunction patients. Methods: The estrogen level, androgen level, IR of 30 psychogenic and 15 endocriological ED were studied and the correlation between the estrogen and androgen levels and RI were analyzed. Results: There is a negative correlation between the androgen and estrogen levels and IR;     

彩色多普勒血流显像在肾脏占位病变中的应用

应用彩色多普勒血流显像检查肾脏占位病变３６例，其中肾脏恶性肿瘤２７例，良性占位病变９例，与周围肾实质对比，肾脏恶性肿瘤显示肾脏轮廊失常，边缘不整，中等强度水平回声。彩色多普勒血流显像示肿块内部及周边血流检出率为９３％（２５／２７），肾脏良性占位血流检出率为１１％（１／９），经统计学处理，相差显著（Ｐ＜０．０１）。彩色多普勒血流显像为临床提供了更多有益的鉴别诊断资料，提高了肾脏占位病变的诊断水平。     

Alpha5 nicotinic acetylcholine receptor mediates nicotine-induced HIF-1α and VEGF expression in non-small cell lung cancer

By binding to nicotinic acetylcholine receptors (nAChRs), nicotine induces the proliferation and apoptosis of non-small cell lung cancer (NSCLC). Previous studies have indicated that α5-nAChR is highly associated with lung cancer risk and nicotine dependence. However, the mechanisms through which α5-nAChRs may influence lung carcinogenesis are far from clear. In the present study, we investigated the roles of α5-nAChR in the nicotine-induced expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF). Immunohistochemistry was used to detect the expression of α5-nAChR and HIF-1α in 60 specimens of lung cancer and para-carcinoma tissue. The correlations between the expression levels of α5-nAChR and HIF-1α and other clinicopathological data were analyzed. In a cell line that highly expressed α5-nAChR, the loss of α5-nAChR function by siRNA was used to study whether α5-nAChR is involved in the nicotine-induced expression of HIF-1α and VEGF through the activation of the ERK1/2 and PI3K/Akt signaling pathways. Cell growth was detected using the cell counting kit-8 (CCK-8). α5-nAChR (78.3%) and HIF-1α (88.3%) were both overexpressed in NSCLC, and their expression levels were found to be correlated with each other (P < 0.05). In the A549 cell line, α5-nAChR and HIF-1α were found to be expressed under normal conditions, and their expression levels were significantly increased in response to nicotine treatment. The silencing of α5-nAChR significantly inhibited the nicotine-induced cell proliferation compared with the control group and attenuated the nicotine-induced upregulation of HIF-1α and VEGF, and these effects required the cooperation of the ERK1/2 and PI3K/Akt signaling pathways. These results show that the α5-nAChR/HIF-1α/VEGF axis is involved in nicotine-induced tumor cell proliferation, which suggests that α5-nAChR may serve as a potential anticancer target in nicotine-associated lung cancer.     

Weight-of-evidence evaluation of long-term ozone exposure and cardiovascular effects

We conducted a weight-of-evidence (WoE) analysis to assess whether the current body of research supports a causal relationship between long-term ozone exposure (defined by EPA as at least 30 days in duration) at ambient levels and cardiovascular (CV) effects. We used a novel WoE framework based on the United States Environmental Protection Agency's National Ambient Air Quality Standards causal framework for this analysis. Specifically, we critically evaluated and integrated the relevant epidemiology and experimental animal data and classified a causal determination based on categories proposed by the Institute of Medicine's 2008 report, Improving the Presumptive Disability Decision-making Process for Veterans. We found that the risks of CV effects are largely null across human and experimental animal studies. The few positive associations reported in studies of CV morbidity and mortality are very small in magnitude, mainly reported in single-pollutant models, and likely attributable to bias, chance, or confounding. The few positive effects in experimental animal studies were observed mainly in ex vivo studies at high exposures, and even the in vivo findings are not likely relevant to humans. The available data also do not support a biologically plausible mechanism for the effects of ozone on the CV system. Overall, the current WoE provides no convincing case for a causal relationship between long-term exposure to ambient ozone and adverse effects on the CV system in humans, but the limitations of the available studies preclude definitive conclusions regarding a lack of causation; thus, we categorize the strength of evidence for a causal relationship between long-term exposure to ozone and CV effects as “below equipoise.”