Histopatologia de la leishmaniasis cutánea causada por Leishmania (Leishmania) mexicana en la península de Yucatán, México

Localized Cutaneous Leishmaniasis (LCL) known as "chiclero's ulcer" in southeast Mexico, was described by SEIDELIN in 1912. Since then the sylvatic region of the Yucatan peninsula has been documented as an endemic focus of LCL. This study of 73 biopsies from parasitological confirmed lesions of LCL cases of Leishmania (Leishmania) mexicana infection was undertaken: 1) to examine host response at tissue level; and 2) to relate manifestations of this response to some characteristics of clinical presentation. Based on Magalhães' classification we found that the most common pattern in our LCL cases caused by L. (L.) mexicana was predominantly characterized by the presence of unorganized granuloma without necrosis, (43.8%). Another important finding to be highlighted is the fact that in 50/73 (68.5%) parasite identification was positive. There was direct relation between the size of the lesion and time of evolution (r s = 0.3079, p = 0.03), and inverse correlation between size of the lesion and abundance of amastigotes (r s = -0.2467, p = 0.03). In view of the complexity of clinical and histopathological findings, cell-mediated immune response of the disease related to clinical and histopathological features, as so genetic background should be studied.La Leishmaniosis Cutánea Localizada (LCL) mejor conocida como "úlcera del chiclero" en el sureste de México fue descrita por SEIDELIN en 1912. Desde entonces la región selvática de la península de Yucatán ha sido identificada como un área endémica de LCL. En el presente estudio se analizaron 73 biopsias de lesiones de casos de LCL causados por Leishmania (Leishmania) mexicana con el fin de: 1) examinar la respuesta a nivel tisular; y 2) relacionar las manifestaciones de esta respuesta con ciertas características de la presentación clínica. Con base en la clasificación histopatológica de Magalhães el patrón histopatológico más frecuente se caracterizó por la presencia de granuloma desorganizado y ausencia de necrosis (43.83%). Otro hallazgo importante a señalar fue la presencia de parásito en 50/73 (68.5%) de las biopsias estudiadas. Respecto a las posibles relaciones significativas hubo una relación directa entre el tamaño de la lesión y el tiempo de evolución (r s = 0.3079, p = 0.03); una correlación inversa entre el tamaño de la lesión y la abundancia de promastigostes (r s = -0.2467, p = 0.03). Con base en la complejidad de los hallazgos clínicos e histopatológicos, consideramos necesario estudiar la respuesta inmune mediada por células relacionada con los cambios histopatológicos, así como el papel de los factores genéticos

Development and Long-Term Follow-Up of an Experimental Model of Myocardial Infarction in Rabbits

[EN] A chronic model of acute myocardial infarction was developed to study the mechanisms involved in adverse postinfarction ventricular remodeling. In an acute myocardial infarction (AMI), the left circumflex coronary artery of New Zealand White rabbits (n = 9) was occluded by ligature for 1 h, followed by reperfusion. A specific care protocol was applied before, during, and after the intervention, and the results were compared with those of a sham operated group (n = 7). After 5 weeks, programmed stimulation and high-resolution mapping were performed on isolated and perfused hearts using the Langendorff technique. The infarct size determined by 2,3,5-triphenyltetrazolium chloride inside of the area at risk (thioflavin-S) was then determined. The area at risk was similar in both groups (54.33% (experimental infarct group) vs. 58.59% (sham group), ns). The infarct size was 73.16% as a percentage of the risk area. The experimental infarct group had a higher inducibility of ventricular arrhythmias (100% vs. 43% in the sham group, p = 0.009). A reproducible chronic experimental model of myocardial infarction is presented in which the extent and characteristics of the lesions enable the study of the vulnerability to develop ventricular arrhythmias because of the remodeling process that occurs during cardiac tissue repair.This research was funded by Generalitat Valenciana (PROMETEO/2018/078), Instituto de Salud Carlos III (CB16/11/00486; PI15/01408; PIE15/0001 3and PI18/01620) to F.J.C.Genovés, P.; Arias-Mutis, ÓJ.; Parra, G.; Such-Miquel, L.; Zarzoso, M.; Del Canto, I.; Soler, C.... (2020). Development and Long-Term Follow-Up of an Experimental Model of Myocardial Infarction in Rabbits. Animals. 10(9). https://doi.org/10.3390/ani1009157610

Effect of chronic exercise on myocardial electrophysiological heterogeneity and stability. Role of intrinsic cholinergic neurons: A study in the isolated rabbit heart

[EN] A study has been made of the effect of chronic exercise on myocardial electrophysiological heterogeneity and stability, as well as of the role of cholinergic neurons in these changes. Determinations in hearts from untrained and trained rabbits on a treadmill were performed. The hearts were isolated and perfused. A pacing electrode and a recording multielectrode were located in the left ventricle. The parameters determined during induced VF, before and after atropine (1 mu M), were: fibrillatory cycle length (VV), ventricular functional refractory period (FRPVF), normalized energy (NE) of the fibrillatory signal and its coefficient of variation (CV), and electrical ventricular activation complexity, as an approach to myocardial heterogeneity and stability. The VV interval was longer in the trained group than in the control group both prior to atropine (78 +/- 10 vs. 68 +/- 10 ms) and after atropine (76 +/- 8 vs. 67 +/- 10 ms). Likewise, FRPVF was longer in the trained group than in the control group both prior to and after atropine (53 +/- 8 vs. 42 +/- 7 ms and 50 +/- 6 vs. 40 +/- 6 ms, respectively), and atropine did not modify FRPVF. The CV of FRPVF was lower in the trained group than in the control group prior to atropine (12.5 +/- 1.5% vs. 15.1 +/- 3.8%) and, decreased after atropine (15.1 +/- 3.8% vs. 12.2 +/- 2.4%) in the control group. The trained group showed higher NE values before (0.40 +/- 0.04 vs. 0.36 +/- 0.05) and after atropine (0.37 +/- 0.04 vs. 0.34 +/- 0.06; p = 0.08). Training decreased the CV of NE both before (23.3 +/- 2% vs. 25.2 +/- 4%; p = 0.08) and after parasympathetic blockade (22.6 +/- 1% vs. 26.1 +/- 5%). Cholinergic blockade did not modify these parameters within the control and trained groups. Activation complexity was lower in the trained than in the control animals before atropine (34 +/- 8 vs. 41 +/- 5), and increased after atropine in the control group (41 +/- 5 vs. 48 +/- 9, respectively). Thus, training decreases the intrinsic heterogeneity of the myocardium, increases electrophysiological stability, and prevents some modifications due to muscarinic block.This research was supported by the Spanish Ministry of Education and Science, (DEP2007-73234-C03-01 to AMA), http://www.mecd.gob.es/portada-mecd/; and the Generalitat Valenciana (PROMETEO 2010/093 to FJC, and FPI/2008/003 to MZ), http://www.gva.es/va/inicio/presentacion; jsessionid=ydprbDQZTsCTz85W1Such-Miquel, L.; Brines-Ferrando, L.; Alberola, A.; Zarzoso Muñoz, M.; Chorro Gasco, FJ.; Guerrero-Martínez, JF.; Parra-Giraldo, G.... (2018). Effect of chronic exercise on myocardial electrophysiological heterogeneity and stability. Role of intrinsic cholinergic neurons: A study in the isolated rabbit heart. PLoS ONE. 13(12). https://doi.org/10.1371/journal.pone.0209085S1312Billman, G. E. (2002). Aerobic exercise conditioning: a nonpharmacological antiarrhythmic intervention. Journal of Applied Physiology, 92(2), 446-454. doi:10.1152/japplphysiol.00874.2001Billman, G. E. (2006). A comprehensive review and analysis of 25 years of data from an in vivo canine model of sudden cardiac death: Implications for future anti-arrhythmic drug development. Pharmacology & Therapeutics, 111(3), 808-835. doi:10.1016/j.pharmthera.2006.01.002Dor-Haim, H., Berenfeld, O., Horowitz, M., Lotan, C., & Swissa, M. (2013). Reduced Ventricular Arrhythmogeneity and Increased Electrical Complexity in Normal Exercised Rats. PLoS ONE, 8(6), e66658. doi:10.1371/journal.pone.0066658Hamer, M., & Stamatakis, E. (2008). Physical Activity and Cardiovascular Disease: Directions for Future Research. The Open Sports Sciences Journal, 1(1), 1-2. doi:10.2174/1875399x00801010001Powers, S. K., Smuder, A. J., Kavazis, A. N., & Quindry, J. C. (2014). Mechanisms of Exercise-Induced Cardioprotection. Physiology, 29(1), 27-38. doi:10.1152/physiol.00030.2013Hull, S. S., Vanoli, E., Adamson, P. B., Verrier, R. L., Foreman, R. D., & Schwartz, P. J. (1994). Exercise training confers anticipatory protection from sudden death during acute myocardial ischemia. Circulation, 89(2), 548-552. doi:10.1161/01.cir.89.2.548Hajnal, Á., Nagy, O., Litvai, Á., Papp, J., Parratt, J. R., & Végh, Á. (2005). Nitric oxide involvement in the delayed antiarrhythmic effect of treadmill exercise in dogs. Life Sciences, 77(16), 1960-1971. doi:10.1016/j.lfs.2005.02.015Such, L., Alberola, A. M., Such-Miquel, L., López, L., Trapero, I., Pelechano, F., … Chorro, F. J. (2008). Effects of chronic exercise on myocardial refractoriness: a study on isolated rabbit heart. Acta Physiologica, 193(4), 331-339. doi:10.1111/j.1748-1716.2008.01851.xZarzoso, M., Such-Miquel, L., Parra, G., Brines-Ferrando, L., Such, L., Chorro, F. J., … Alberola, A. (2011). The training-induced changes on automatism, conduction and myocardial refractoriness are not mediated by parasympathetic postganglionic neurons activity. European Journal of Applied Physiology, 112(6), 2185-2193. doi:10.1007/s00421-011-2189-4Billman, G. E. (2009). Cardiac autonomic neural remodeling and susceptibility to sudden cardiac death: effect of endurance exercise training. American Journal of Physiology-Heart and Circulatory Physiology, 297(4), H1171-H1193. doi:10.1152/ajpheart.00534.2009HAN, J., & MOE, G. K. (1964). Nonuniform Recovery of Excitability in Ventricular Muscle. Circulation Research, 14(1), 44-60. doi:10.1161/01.res.14.1.44Beaumont, E., Salavatian, S., Southerland, E. M., Vinet, A., Jacquemet, V., Armour, J. A., & Ardell, J. L. (2013). Network interactions within the canine intrinsic cardiac nervous system: implications for reflex control of regional cardiac function. The Journal of Physiology, 591(18), 4515-4533. doi:10.1113/jphysiol.2013.259382Armour, J. A. (2008). Potential clinical relevance of the ‘little brain’ on the mammalian heart. Experimental Physiology, 93(2), 165-176. doi:10.1113/expphysiol.2007.041178Abramochkin, D. V., Nurullin, L. F., Borodinova, A. A., Tarasova, N. V., Sukhova, G. S., Nikolsky, E. E., & Rosenshtraukh, L. V. (2009). Non-quantal release of acetylcholine from parasympathetic nerve terminals in the right atrium of rats. Experimental Physiology, 95(2), 265-273. doi:10.1113/expphysiol.2009.050302CHORRO, F. J., CANOVES, J., GUERRERO, J., MAINAR, L., SANCHIS, J., SORIA, E., … LOPEZ-MERINO, V. (2000). Opposite Effects of Myocardial Stretch and Verapamil on the Complexity of the Ventricular Fibrillatory Pattern: An Experimental Study. Pacing and Clinical Electrophysiology, 23(11), 1594-1603. doi:10.1046/j.1460-9592.2000.01594.xSuch, L., Rodriguez, A., Alberola, A., Lopez, L., Ruiz, R., Artal, L., … Chorro, F. J. (2002). Intrinsic changes on automatism, conduction, and refractoriness by exercise in isolated rabbit heart. Journal of Applied Physiology, 92(1), 225-229. doi:10.1152/jappl.2002.92.1.225Duytschaever, M., Mast, F., Killian, M., Blaauw, Y., Wijffels, M., & Allessie, M. (2001). Methods for Determining the Refractory Period and Excitable Gap During Persistent Atrial Fibrillation in the Goat. Circulation, 104(8), 957-962. doi:10.1161/hc3401.093156Wijffels, M. C. E. F., Kirchhof, C. J. H. J., Dorland, R., & Allessie, M. A. (1995). Atrial Fibrillation Begets Atrial Fibrillation. Circulation, 92(7), 1954-1968. doi:10.1161/01.cir.92.7.1954Zaitsev, A. V., Berenfeld, O., Mironov, S. F., Jalife, J., & Pertsov, A. M. (2000). Distribution of Excitation Frequencies on the Epicardial and Endocardial Surfaces of Fibrillating Ventricular Wall of the Sheep Heart. Circulation Research, 86(4), 408-417. doi:10.1161/01.res.86.4.408Armour, J. A., Collier, K., Kember, G., & Ardell, J. L. (1998). Differential selectivity of cardiac neurons in separate intrathoracic autonomic ganglia. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 274(4), R939-R949. doi:10.1152/ajpregu.1998.274.4.r939Armour, J. A., & Hopkins, D. A. (1990). Activity of in vivo canine ventricular neurons. American Journal of Physiology-Heart and Circulatory Physiology, 258(2), H326-H336. doi:10.1152/ajpheart.1990.258.2.h326D’Souza, A., Bucchi, A., Johnsen, A. B., Logantha, S. J. R. J., Monfredi, O., Yanni, J., … Boyett, M. R. (2014). Exercise training reduces resting heart rate via downregulation of the funny channel HCN4. Nature Communications, 5(1). doi:10.1038/ncomms4775Sartiani, L., Romanelli, M., Mugelli, A., & Cerbai, E. (2015). Updates on HCN Channels in the Heart: Function, Dysfunction and Pharmacology. Current Drug Targets, 16(8), 868-876. doi:10.2174/1389450116666150531152047Herrmann, S., Layh, B., & Ludwig, A. (2011). 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GEMINI 3D spectroscopy of BAL+IR+Fe II QSOs: II. IRAS 04505-2958 an explosive QSO with hypershell and a new scenario for galaxy formation and galaxy end

From a study of BAL + IR + Fe II QSOs (using deep Gemini GMOS-IFU spectroscopy) new results are presented: for IRAS 04505-2958. Specifically, we have studied in detail the out flow (OF) process and their associated structures, mainly at two large galactic scales: (i) two blobs/shells (S1, S2) at radius r = 1.1 and 2.2 kpc; and (ii) an external hypergiant shell (S3) at r = 11 kpc. In addition, the presence of two very extended hypergiant shells (S4, S5) at r = 80 kpc is discussed. From this GMOS study the following main results were obtained: (i) For the external hypergiant shell S3 the kinematics GMOS maps of the ionized gas show very similar features to those observed for the prototype of exploding external supergiant shell: in NGC 5514. (ii) The main knots K1, K2 and K3 -of this hypergiant shell S3- show a stellar population and emission line ratios associated with the presence of a starburst + OF/shocks. (iii) The internal shells S1 and S2 show structures, OF components and properties very similar to those detected in the nuclear shells of Mrk 231. (iv) The shells S1+S2 and S3 are aligned at PA = 131: i.e. suggesting that the OF process is in the blow-out phase with bipolar structure. In addition, the shells S4 and S5 (at 80-100 kpc scale) are aligned at PA = 40, i.e.: a bipolar OF perpendicular to the internal OF. Finally, the generation of UHE cosmic rays and neutrino/ dark-matter -associated with HyNe in BAL + IR + Fe II QSOs- is discussed.Comment: Submitted MNRAS, 81 pages, 25 Figure

Reconstructing Native American Population History

The peopling of the Americas has been the subject of extensive genetic, archaeological and linguistic research; however, central questions remain unresolved1–5. One contentious issue is whether the settlement occurred via a single6–8 or multiple streams of migration from Siberia9–15. The pattern of dispersals within the Americas is also poorly understood. To address these questions at higher resolution than was previously possible, we assembled data from 52 Native American and 17 Siberian groups genotyped at 364,470 single nucleotide polymorphisms. We show that Native Americans descend from at least three streams of Asian gene flow. Most descend entirely from a single ancestral population that we call “First American”. However, speakers of Eskimo-Aleut languages from the Arctic inherit almost half their ancestry from a second stream of Asian gene flow, and the Na-Dene-speaking Chipewyan from Canada inherit roughly one-tenth of their ancestry from a third stream. We show that the initial peopling followed a southward expansion facilitated by the coast, with sequential population splits and little gene flow after divergence, especially in South America. A major exception is in Chibchan-speakers on both sides of the Panama Isthmus, who have ancestry from both North and South America

7th Drug hypersensitivity meeting: part two

No abstract availabl

Modelling of the effect of ELMs on fuel retention at the bulk W divertor of JET

Effect of ELMs on fuel retention at the bulk W target of JET ITER-Like Wall was studied with multi-scale calculations. Plasma input parameters were taken from ELMy H-mode plasma experiment. The energetic intra-ELM fuel particles get implanted and create near-surface defects up to depths of few tens of nm, which act as the main fuel trapping sites during ELMs. Clustering of implantation-induced vacancies were found to take place. The incoming flux of inter-ELM plasma particles increases the different filling levels of trapped fuel in defects. The temperature increase of the W target during the pulse increases the fuel detrapping rate. The inter-ELM fuel particle flux refills the partially emptied trapping sites and fills new sites. This leads to a competing effect on the retention and release rates of the implanted particles. At high temperatures the main retention appeared in larger vacancy clusters due to increased clustering rate

Impact of fast ions on density peaking in JET: fluid and gyrokinetic modeling

The effect of fast ions on turbulent particle transport, driven by ion temperature gradient (ITG)/ trapped electron mode turbulence, is studied. Two neutral beam injection (NBI) heated JET discharges in different regimes are analyzed at the radial position ρ$_{t}$=0.6, one of them an L-mode and the other one an H-mode discharge. Results obtained from the computationally efficient fluid model EDWM and the gyro-fluid model TGLF are compared to linear and nonlinear gyrokinetic GENE simulations as well as the experimentally obtained density peaking. In these models, the fast ions are treated as a dynamic species with a Maxwellian background distribution. The dependence of the zero particle flux density gradient (peaking factor) on fast ion density, temperature and corresponding gradients, is investigated. The simulations show that the inclusion of a fast ion species has a stabilizing influence on the ITG mode and reduces the peaking of the main ion and electron density profiles in the absence of sources. The models mostly reproduce the experimentally obtained density peaking for the L-mode discharge whereas the H-mode density peaking is significantly underpredicted, indicating the importance of the NBI particle source for the H-mode density profile

Current Research into Applications of Tomography for Fusion Diagnostics

Retrieving spatial distribution of plasma emissivity from line integrated measurements on tokamaks presents a challenging task due to ill-posedness of the tomography problem and limited number of the lines of sight. Modern methods of plasma tomography therefore implement a-priori information as well as constraints, in particular some form of penalisation of complexity. In this contribution, the current tomography methods under development (Tikhonov regularisation, Bayesian methods and neural networks) are briefly explained taking into account their potential for integration into the fusion reactor diagnostics. In particular, current development of the Minimum Fisher Regularisation method is exemplified with respect to real-time reconstruction capability, combination with spectral unfolding and other prospective tasks