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The metabolic syndrome (MetS) is a cluster of cardiometabolic disorders that result from the increasing prevalence of obesity. The major components of MetS include insulin resistance, central obesity, dyslipidemia, and hypertension. MetS identifies the central obesity with increased risk for cardiovascular diseases (CVDs) and type-2 diabetes mellitus (T2DM). Patients with rheumatic diseases, such as rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, and ankylosing spondylitis, have increased prevalence of CVDs. Moreover, CVD risk is increased when obesity is present in these patients. However, traditional cardiovascular risk factors do not completely explain the enhanced cardiovascular risk in this population. Thus, MetS and the altered secretion patterns of proinflammatory adipokines present in obesity could be the link between CVDs and rheumatic diseases. Furthermore, adipokines have been linked to the pathogenesis of MetS and its comorbidities through their effects on vascular function and inflammation. In the present paper, we review recent evidence of the role played by adipokines in the modulation of MetS in the general population, and in patients with rheumatic diseases.

Epithelial-to-mesenchymal transition (EMT), one of the crucial steps for carcinoma cells to acquire invasive capacity, results from the disruption of cell-cell contacts and the acquisition of a motile mesenchymal phenotype. Although the transcriptional events controlling EMT have been extensively studied, in recent years, several posttranscriptional mechanisms have emerged as critical in the regulation of EMT during tumor progression. In this review, we highlight the regulation of posttranscriptional events in EMT by RNA-binding proteins (RBPs). RBPs are responsible for controlling pre-mRNA splicing, capping, and polyadenylation, as well as mRNA export, turnover, localization, and translation. We discuss the most relevant aspects of RBPs controlling the metabolism of EMT-related mRNAs, and describe the implication of novel posttranscriptional mechanisms regulating EMT in response to different signaling pathways. Novel insight into posttranscriptional regulation of EMT by RBPs is uncovering new therapeutic targets in cancer invasion and metastasis.

Gene expression is potently regulated through the action of microRNAs (miRNAs). Here, we present evidence of a miRNA regulating Hakai protein. Hakai was discovered as an E3 ubiquitin-ligase that mediates the posttranslational downregulation of E-cadherin, a major component of adherens junctions in epithelial cells and a potent tumour suppressor. Recent data have provided evidence that Hakai affects cell proliferation in an E-cadherin-independent manner, thus revealing a role for Hakai in the early stages of tumour progression. Furthermore, Hakai is highly up-regulated in human colon adenocarcinomas compared to normal tissues. However, the molecular mechanisms that regulate Hakai abundance are unknown. We identified two putative sites of miR-203 interaction on the Hakai mRNA, in its 3'-untranslated region (UTR). In several human carcinoma cell lines tested, overexpression of a miR-203 precursor (Pre-miR-203) reduced Hakai abundance, while inhibiting miR-203 by using an antisense RNA (Anti-miR-203) elevated Hakai levels. The repressive influence of miR-203 on the Hakai 3'-UTR was confirmed using heterologous reporter constructs. In keeping with Hakai's proliferative influence, Anti-miR-203 significantly increased cell number and BrdU incorporation, while Pre-miR-203 reduced these parameters. Importantly, the growth-promoting effects of anti-miR-203 required the presence of Hakai, because downregulation of Hakai by siRNA suppressed its proliferative action. Finally, in situ hybridization showed that miR-203 expression is attenuated in colon tumour tissues compared to normal colon tissues, suggesting that miR-203 could be a potential new prognostic marker and therapeutic target to explore in colon cancer. In conclusion, our findings reveal, for the first time, a post-transcriptional regulator of Hakai expression. Furthermore, by lowering Hakai abundance, miR-203 also reduces Hakai-regulated-cell division.

The purpose of this paper is to provide a comparison between the different methods utilized for building up anthropomorphic phantoms in Radiotherapy Treatment Plans. A simplified model of the Snyder Head Phantom was used in order to construct an analytical, voxelized and volumized phantom, throughout a segmentation program and different algorithms programmed in Matlab code. The irradiation of the resulting phantoms was simulated with the MCNP5 (Monte Carlo N-Particle) transport code, version 5, and the calculations presented in particle flux maps inside the phantoms by utilizing the FMESH tool, superimposed mesh tally. The different variables involved in the simulation were analyzed, like particle flux, MCNP standard deviation and real simulation CPU time cost. In the end the volumized model resulted to have the largest computer time cost and bigger discrepancies in the particle flux distribution.

Renal cell carcinoma with inferior vena cava thrombus is relatively uncommon and complicates radical nefrectomy. During the past twenty years our hospital have substantially contributed to the surgical stratification of renal cell carcinoma with extension into inferior vena cava through different techniques. The reason for this article is to discuss the mote efficient and appropiate surgical technique for this pathology. We believe that the diagnosis of vena caval invasion and level of tumoral extension is based on radiological examinations and it is crucial for the success of the surgery. We consider that the use of vena caval filter applied preoperatively could prevent the risk of thromboembolism during and after the surgery. The use of prosthetic grafts is unusual, because the long standing obstruction caused by the tumor thrombus will develope extensive collateral circulation which works as a natural veno-venous bypass. Finally, we try to avoid the use of veno-venous and cardiopulmonar bypass with or without complete hypothermic circulatory arrest due to the high association with adverse outcomes and mortality.

A case of pseudomonas endocarditis of biliary origin with impairment of the mitral and tricuspid heart valves is reported. Former history of the patient did not reveal narcotic addiction or previous open-heart surgery. Osteomyelitis is an uncommon complication of pseudomonas endocarditis. Echocardiography was a useful diagnostic method in the present case, showing the vegetation on the tricuspid valve. The poor prognosis of cases with left valvular heart disease which are resistant to medical treatment is emphasized. Differential count of the colonies did not localize the affected heart valve in this case.