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Antecedentes / Objetivos: Caracterizar a los pacientes heterosexuales con diagnóstico de sífilis y/o gonococia atribuidos a relaciones anales (RA). Métodos: Estudio descriptivo en 15 centros de ITS e IIPP (julio 2005-diciembre 2007). Se recogieron variables sociodemográficas y situaciones de riesgo (ejercicio y contacto con prostitución, relación con contacto ocasional, con pareja estable, con pareja estable u ocasional infectada por el VIH). Se ha realizado un análisis descriptivo, bivariante y multivariado de regresión logística para evaluar, en heterosexuales, los factores asociados a tener RA frente a otras prácticas sexuales. Resultados: Se identificaron 1.891 diagnósticos, de los cuales 591 (31,3%) se habían infectado a través de relaciones heterosexuales no protegidas. De estos, 70 (11,8%) tuvieron RA, exclusivamente o en combinación con otras prácticas; el 61,4% fueron hombres, con edad media de 32,9 años (DE:10,3), 45,7% eran extranjeros y el 42,9% no tenía estudios o sólo primarios. El 62,9% (44 pacientes) tenían gonococia, 35,7% (25) sífilis y 1,4% (1) ambas. Entre los 70 casos con RA, el 18,6% refiere haberlas mantenido sólo con su pareja estable, un 71,4% con contactos esporádicos o prostitución, con o sin su pareja estable, y un 10% con contactos esporádicos y prostitución teniendo o no pareja estable; el 38,6% había tenido de 3-5 parejas en el último año. En el modelo de regresión logística, ajustado por sexo, edad, estudios, país de origen y situación de riesgo, la probabilidad tener RA fue mayor en los pacientes que tuvieron de 3 a 5 parejas (OR: 5,7; IC95%: 2,3-14,3) y en los que tuvieron de 6 a 20 (OR: 3,0; IC95%: 1,0-9,1) comparados con los referían 1 a 2 parejas en los últimos 12 meses. Conclusiones: En torno al 12% de los casos con sífilis y/o gonococia que atribuyen su infección a relaciones heterosexuales, referían tener RA. La probabilidad de tener RA en esta población aumenta con el número de parejas sexuales.

The aim of this work was the modification of the composition and surface microstructure of powder metallurgy titanium to improve the wear resistance and reduce the elastic modulus while maintaining the corrosion behavior, characteristics needed for biomedical applications. For this purpose, Mo and Nb coatings were produced by colloidal techniques. Stable aqueous suspensions were prepared from micro-sized powder of Mo and Nb particles, deposited onto the powder metallurgy titanium substrates (green or sintered). After a heat treatment to promote the diffusion and the consolidation of the layers, microstructural changes were obtained. In the case of green substrates, the co-sintering process provides a diffusion depth of 85-100 micron. In the as-sintered case, a uniform depth of 40-65 microns was reached. The surfaces were characterised by micro-hardness, corrosion and tribocorrosion testing, and the results showed that hardened surfaces presented lower tendency to corrosion both under static conditions and under sliding., Funds were provided by Spanish Government (programme MINECO, ref. MAT2012-38650-C02-01), Regional Government of Madrid (programme MULTIMAT-CHALLENGE, ref. S2013/MIT-2862) and Institute of Alvaro Alonso Barba (IAAB) for the research stay in CMEMS-UMINHO (University of Minho)., info:eu-repo/semantics/publishedVersion

T-type Ca(2+) channels are expressed in the ventricular myocytes of the fetal and perinatal heart, but are normally downregulated as development progresses. Interestingly, however, these channels are re-expressed in adult cardiomyocytes under pathological conditions. We investigated low voltage-activated T-type Ca(2+) channel regulation in hypoxia in rat cardiomyocytes. Molecular studies revealed that hypoxia induces the upregulation of Cav 3.2 mRNA, whereas Cav 3.1 mRNA is not significantly altered. The effect of hypoxia on Cav 3.2 mRNA was time- and dose-dependent, and required hypoxia inducible factor-1α (HIF-1α) stabilization. Patch-clamp recordings confirmed that T-type Ca(2+) channel currents were upregulated in hypoxic conditions, and the addition of 50 μm NiCl2 (a T-type channel blocker) demonstrated that the Cav 3.2 channel is responsible for this upregulation. This increase in current density was not accompanied by significant changes in the Cav 3.2 channel electrophysiological properties. The small monomeric G-protein RhoA and its effector Rho-associated kinase I (ROCKI), which are known to play important roles in cardiovascular physiology, were also upregulated in neonatal rat ventricular myocytes subjected to hypoxia. Pharmacological experiments indicated that both proteins were involved in the observed upregulation of the Cav 3.2 channel and the stabilization of HIF-1α that occurred in response to hypoxia. These results suggest a possible role for Cav 3.2 channels in the increased probability of developing arrhythmias observed in ischaemic situations, and in the pathogenesis of diseases associated with hypoxic Ca(2+) overload.

Some sensor systems are characterized by multiple simultaneous aperiodic emissions, with low signal-to-noise ratio and asynchronous detection. In these systems, complementary sets of sequences can be used to encode emissions, due to their suitable auto-correlation and cross-correlation properties. The transmission of a complementary set can be accomplished by interleaving the sequences of the set, generating a macro-sequence which is easily transmitted by a BPSK modulation. The detection of the macrosequence can be performed by means of efficient correlation algorithms with a notably decreased computational load and hardware complexity. This work presents a new hardware design in configurable logic of an efficient correlator for macrosequences generated from complementary sets of sequences. A generic implementation has been achieved, so the configuration can be changed according to the requirements of the application. The developed correlator has been tested in an ultrasonic pulse compression system in which real-time is needed. However, it is applicable in any multi-sensor or communication system where the goal is to make simultaneous emissions from different independent sources, minimizing mutual interference.

1. Tight control of cellular growth is essential to ensure normal tissue patterning and prevent pathological responses. Excessive vascular smooth muscle cell (VSMC) proliferation is associated with the pathophysiology of atherosclerosis and restenosis post-angioplasty. Thus, drug targeting of pathological VSMC growth may be a suitable therapeutic intervention in vascular proliferative diseases. 2. In the present study, we investigated the mechanisms underlying VSMC growth arrest induced by the pharmacological agent PCA-4230. Addition of PCA-4230 to cultured VSMCs blocked the induction of cyclin D1 and cyclin A expression normally seen in serum-restimulated cells. Moreover, PCA-4230 inhibited cyclin-dependent kinase 2 (CDK2) activity and abrogated hyperphosphorylation of the retinoblastoma (Rb) gene product. Similarly, PCA-4230-dependent growth arrest of transformed cell lines correlated with reduced level of cyclin D1 protein and inhibition of CDK2 activity. Consistent with these findings, PCA-4230 repressed serum-inducible cyclin A promoter activity, and overexpression of either cyclin D1 or E2F1 efficiently circumvented this inhibitory effect. Importantly, adenovirus-mediated overexpression of E2F1 restored S-phase entry in PCA-4230-treated VSMCs, demonstrating that PCA-4230 represses cyclin A gene expression and VSMC growth via inhibition of the cyclin D1/E2F pathway. 3. Because of its ability to inhibit the growth of human VSMCs and transformed cell lines, future studies are warranted to assess whether PCA-4230 may be a suitable therapeutic intervention for the treatment of hyperproliferative disorders, including cardiovascular disease and cancer.