Feasibility of Using a Novel 2.45 GHz Double Short Distance Slot Coaxial Antenna for Minimally Invasive Cancer Breast Microwave Ablation Therapy: Computational Model, Phantom, and In Vivo Swine Experimentation.

Microwave ablation (MWA) by using coaxial antennas is a promising alternative for breast cancer treatment. A double short distance slot coaxial antenna as a newly optimized applicator for minimally invasive treatment of breast cancer is proposed. To validate and to analyze the feasibility of using this method in clinical treatment, a computational model, phantom, and breast swine in vivo experimentation were carried out, by using four microwave powers (50 W, 30 W, 20 W, and 10 W). The finite element method (FEM) was used to develop the computational model. Phantom experimentation was carried out in breast phantom. The in vivo experimentation was carried out in a 90 kg swine sow. Tissue damage was estimated by comparing control and treated micrographs of the porcine mammary gland samples. The coaxial slot antenna was inserted in swine breast glands by using image-guided ultrasound. In all cases, modeling, in vivo and phantom experimentation, and ablation temperatures (above 60°C) were reached. The in vivo experiments suggest that this new MWA applicator could be successfully used to eliminate precise and small areas of tissue (around 20-30 mm2). By modulating the power and time applied, it may be possible to increase/decrease the ablation area.

Atrial natriuretic peptide reduces inflammation and enhances apoptosis in rat acute pancreatitis.

AIM: We previously reported that atrial natriuretic peptide (ANP) reduces serum amylase and intrapancreatic trypsinogen activation in the onset of acute pancreatitis whereas secretin increases them. In the present work, we sought to establish the effect of ANP and secretin on the inflammatory response and cell death in experimental acute pancreatitis. METHODS: The expression and activity of key inflammatory mediators and apoptosis were evaluated in the presence or absence of the atrial peptide, secretin or both in cerulein-induced acute pancreatitis in rats. Also, ultrastructural changes in pancreatic acinar cells were assessed by transmission electron microscopy. RESULTS: ANP significantly reduced NF-κB activation and TNF-α intrapancreatic levels. Furthermore, it decreased inducible nitric oxide synthase and cyclooxygenase 2 expression and activity while it diminished myeloperoxidase activity. ANP also stimulated apoptosis as shown by caspase-3 expression and activation as well as TUNEL assay. These findings correlated well with the ultrastructural changes observed in the exocrine pancreas. Although secretin reduced various inflammatory markers, it also diminished caspase-3 activation and the overall response was the aggravation of the disease as reflected by the ultrastructural alterations of pancreatic acinar cells. In the presence of ANP, various effects evoked by secretin were antagonized. CONCLUSION: Present findings show that ANP significantly attenuated the severity of acute pancreatitis in the rat by inducing apoptosis and reducing the inflammatory response and further suggest that ANP may have eventual therapeutic implications in the disease and/or in medical interventions at risk of its developing like endoscopic retrograde cholangiopancreatography.

RAC3 more than a nuclear receptor coactivator: a key inhibitor of senescence that is downregulated in aging.

Receptor-associated coactivator 3 (RAC3) is a nuclear receptor coactivator usually overexpressed in tumors that exerts oncogenic functions in the cytoplasm and the nucleus. Although as part of its oncogenic actions it was previously identified as an inhibitor of apoptosis and autophagy, its expression is required in order to preserve the pluripotency and embryonic stem cell self-renewal. In this work we investigated its role in cellular senescence. We found that RAC3 overexpression in the nontumoral HEK293 cells inhibits the premature senescence induced by hydrogen peroxide or rapamycin. The mechanism involves not only the inhibition of autophagy early induced by these stimuli in the pathway to senescence, but also the increase in levels and nuclear localization of both the cell cycle suppressors p53/p21 and the longevity promoters FOXO1A, FOXO3A and SIRT1. Furthermore, we found that RAC3 overexpression is required in order to maintain the telomerase activity. In tumoral HeLa cells its activity was inhibited by depletion of RAC3 inducing replicative senescence. Moreover, we demonstrated that in vivo, levels of RAC3 are downregulated in the liver from aged as compared with young rats, whereas the levels of p21 are increased, correlating with the expected senescent cell contents in aged tissues. A similar downregulation of RAC3 was observed in the premature and replicative senescence of human fetal WI-38 cells and premature senescence of hepatocyte HepG2 cell line. Taken together, all these results demonstrate that RAC3 is an inhibitor of senescence whose downregulation in aged individuals could be probably a tumor suppressor mechanism, avoiding the clonal expansion of risky old cells having damaged DNA.

The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action.

The p160 nuclear receptor co-activators represent a family of molecules, which are recruited by steroid nuclear receptors as well as other transcription factors that are overexpressed in several tumors. We investigated the role of one member of this family on the sensitivity of cells to apoptosis. We observed that overexpression of the RAC3 (receptor-associated co-activator-3) p160 co-activator inhibits hydrogen peroxide-induced cell death in human embryonic kidney 293 (HEK293) cells. The mechanism involves the activation of anti-apoptotic pathways mediated through enhanced nuclear factor kappa B (NF-kappaB) activity, inhibition of caspase-9 activation, diminished apoptotic-inducing factor (AIF) nuclear localization and a change in the activation pattern of several kinases, including an increase in both AKT and p38 kinase activities, and inhibition of ERK2. Moreover, RAC3 has been found associated with a protein complex containing AIF, Hsp90 and dynein, suggesting a role for the co-activator in the cytoplasmatic nuclear transport of these proteins associated with cytoskeleton. These results demonstrate that there are several molecular pathways that could be affected by their overexpression, including those not restricted to steroid regulation or the nuclear action of co-activators, which results in diminished sensitivity to apoptosis. Furthermore, this could represent one mechanism by which co-activators contribute to tumor development.

Secondary serological response of patients with chronic hepatosplenic suppurative brucellosis.

Chronic hepatosplenic suppurative brucellosis (CHSB) is a local reactivation of a previous brucellosis, coursing with an immunoglobulin G (IgG) and IgA secondary immunological response. The observation of two cases of CHSB with an apparent IgM response gave rise to a detailed serological study of three of our patients. We studied the first sample from all three patients and successive samples from two of them. In cases 1 and 2, we found samples with positive IgM lateral flow and IgM enzyme-linked immunosorbent assay results concomitantly with rheumatoid factor (RF); after absorption with anti-RF serum, these results were rendered negative. In patients 2 and 3 the diagnosis of brucellosis was delayed, because none of the test results were initially very significant. However, a clear seroconversion of IgG antibodies was observed in subsequent months; titers of the Brucellacapt and Coombs tests increased in similar ways, although Brucellacapt decreased more rapidly than Coombs, which persisted at high titers for years. In patient 3 a relapse was observed in the fourth year of follow-up, detected by Coombs and also by IgG lateral flow and counterimmunoelectrophoresis (CIEP), although not by the rose bengal, agglutination, or Brucellacapt tests. Serological changes in CHSB may sometimes be mild and are detected mainly by the Coombs test. Brucellacapt does not offer additional information, although IgG lateral flow and CIEP may be of some use. Careful surveillance of titer changes in the Coombs test is the best marker of infection activity. As the disease progresses, an intense IgG response may develop and RF sometimes appears, simulating an IgM response.

Intrinsic viscosity of SiO2, Al2O3 and TiO2 aqueous suspensions.

The viscosity of dilute suspensions of several metal oxides (SiO2, Al2O3 and TiO2) was measured at different pH values. The intrinsic viscosity, [eta], was derived from the concentration dependence of the viscosity. This magnitude was pH-dependent. A correlation with the shape of the kinetic unity has been proposed.

TNF-alpha enhances estrogen-induced cell proliferation of estrogen-dependent breast tumor cells through a complex containing nuclear factor-kappa B.

Breast tumors are usually classified according to their response to estrogens as hormone-dependent or -independent. In this work, we investigated the role of the proinflammatory cytokine TNF-alpha on the estrogen-receptor-positive T47D breast ductal tumor cells. We have found that TNF-alpha exerts a mitogenic effect, inducing cyclin D1 expression and activation of the transcription factor NF-kappaB. Importantly, activation of NF-kappaB was required for estrogen-induced proliferation and cyclin D1 expression. TNF-alpha enhanced the estrogen response by increasing the levels and availability of NF-kappaB. Chromatin immunoprecipitation analysis suggested that the action of estrogens is mediated by a protein complex that contains the activated estrogen receptor, the nuclear receptor coactivator RAC3 and a member of the NF-kappaB family. Finally, our results demonstrate that activation of this transcription factor could be one of the key signals for estrogen-mediated response.

Aplicacion de un metodo inmunoenzimatico (ELISA) al diagnostico de la hidatidosis humana. / Application of an immunoenzimatic method (ELISA) to the diagnosis of human hydatidosis

En el presente estudio, se realiza una evaluacion de un nuevo metodo de ELISA, en el diagnostico inmunologico de la hidatidosis humana. Asimismo se comparan los resultados con los obtenidos con otras tecnicas, tales como aglutinacion del latex e inmunoelectroforesis, y se analizan segun la localizacion de los quistes. Por otra parte, se discuten las ventajas del metodo de ELISA, en relacion con la utilidad de su empleo en casos aislados de hidatidosis y estudios seroepidemiologicos