No abstract

In the recent decades, systemic inflammation, as a clinical phenomenon, has been the focus of extensive research particularly with regard to its potential association with a variety of cardiovascular diseases including atherogenesis and acute coronary syndromes. Within this context, there also exists a potential link between systemic inflammation and cardiac arrhythmogenesis in various aspects. Accordingly, systemic inflammation response as measured with inflammation markers (cytokines, etc) has been investigated in the setting of well-known cardiac arrhythmias including atrial fibrillation and ventricular tachycardia. Based on current literature, clinical utility of these markers might potentially yield important prognostic implications in the setting of certain arrhythmogenic conditions. On the other hand, there exists limited data regarding therapeutic implications including clinical benefit of primary anti-inflammatory agents (corticosteroids, colchicine, etc) in the setting of arrhythmia management. The present review primarily aims to discuss potential triggers and fundamental mechanisms of inflammation-related arrhythmias along with a particular emphasis on clinical implications of systemic inflammation in the setting of cardiac arrhythmogenesis.

The present study aimed to investigate the effects of apelin and leptin on renal functions following renal ischemia/reperfusion (I/R). A total of 32 rats were divided into four groups. The control group was not induced with ischemia, but was administered normal saline intraperitoneally. Normal saline, apelin and leptin were administered intraperitoneally to the I/R, ischemia/reperfusion and apelin (I/R+A) and ischemia/reperfusion and leptin (I/R+L) groups, in turn for three days prior to the surgical procedure. Blood and urine samples were obtained after 24 h of reperfusion, and scintigraphic examination was performed. Renal damage was evaluated histopathologically. Urea levels of the I/R+L and I/R+A groups were comparable, but were higher compared to that of the control group. The I/R group had the highest urea levels (control, 27±2; I/R, 120±15; I/R+A, 75±10; I/R+L, 80±11; p<0.001). Creatinine levels were higher in all three ischemic groups compared to the control group. Glomerular filtration rate values of the I/R+A and I/R+L groups were not significantly, but numerically higher compared to that of the I/R group. No pathological damage was observed in any of the animals in the control group. In the I/R group, two animals had moderate and six had severe renal damage, while three had moderate and one had severe renal damage in the I/R+L group. In the I/R+A group, moderate renal damage was found in one animal, while none had severe renal damage. This study demonstrates the functional and histopathological protective effects of leptin and apelin against renal I/R injury.

In the setting of acute myocardial infarction (AMI), adverse myocardial remodeling (AMR) has been universally regarded as an early-onset phenomenon generally arising within the first few weeks (usually within days in the infarct zone) following myocardial injury. On the other hand, onset of cardiac morphological changes in this setting may potentially extend far beyond this time frame (usually beyond several months after the index AMI), suggesting a prolonged latent period in certain cases. In clinical practice, this delayed form of post-AMI remodeling, namely late AMR, has emerged as an interesting and underrecognized phenomenon with poorly understood mechanisms. Notably, systemic inflammation and associated growth factors seem to play a pivotal role in this setting. Accordingly, the present article primarily aims to discuss potential mechanisms and clinical implications of late AMR (in a comparative manner with its classical early counterpart) among AMI survivors along with a particular emphasis on potential benefits of certain anti-inflammatory strategies in this setting.

This study examined the frequency of E-cadherin expression in endometrial biopsy or hysterectomy specimens from patients diagnosed with endometrial adenocarcinoma and in normal endometrial tissue specimens. E-cadherin expression was detected by immunohistochemistry using monoclonal antibody to E-cadherin. Specimens were classified as positive when >or= 5% of the tumour cells showed staining for E-cadherin, irrespective of the pattern of staining. Twenty-three endometrioid carcinomas and nine non-endometrioid (four papillary serous and five clear cell) carcinomas were studied, along with 10 normal endometrial tissue specimens as controls. E-cadherin expression was significantly less frequent in non-endometrioid carcinomas compared with endometrioid carcinomas and controls. There was no statistically significant difference in the frequency of E-cadherin expression between endometrioid carcinomas and controls. In conclusion, this study demonstrated that uterine non-endometrioid (papillary serous and clear cell) carcinomas were less likely to express E-cadherin compared with endometrioid carcinomas and normal endometrial tissue. This may help to explain the more aggressive behaviour of non-endometrioid carcinomas.