Alexandru Busuioceanu en España: poeta y profesor

Romanian author, Alexandru Busuioceanu (1896-1961), had a long trajectory as poet, art historian and essayist in Romanian language when he was appointed cultural counselor in Madrid in 1942. The present article proposes an overview of his professional and literary trajectory in Spain, and also an account of the perception that the critics of this country had of him.El escritor rumano, Alexandru Busuioceanu (1896-1961), tras una larga trayectoria como poeta, historiador del arte y ensayista en lengua rumana, es nombrado consejero cultural en Madrid en 1942. Este artículo pretende hacer un repaso de su trayectoria profesional y literaria en España, así como dar cuenta de la percepción que de él tenía la crítica de este país

Viajeros rumanos en España, en busca de las raíces comunes

Flashed by The Alhambra Tales of Washington Irving, the Romanian writer Mihail Koga˘lniceanu made, in 1846, a travel to Spain which allowed him to see the parallelism between our country and the Balcanic one. He opened the way to traveller writers such as Nicolae Iorga (1927) or Mihai Tican (1929), which explored in the relationships between the two countries

Dime lo que comes y te diré quién eres. Alimentación y literatura en los Balcanes.

Sin resume

Alexandru Busuioceanu in Spain: poet and teacher

Romanian author, Alexandru Busuioceanu (1896-1961), had a long trajectory as poet, art historian and essayist in Romanian language when he was appointed cultural counselor in Madrid in 1942. The present article proposes an overview of his professional and literary trajectory in Spain, and also an account of the perception that the critics of this country had of him

Dime lo que comes y te diré quién eres. Alimentación y literatura en los Balcanes.

Sin resume

Dissociation of pulse wave velocity and aortic wall stiffness in diabetic db/db mice: The influence of blood pressure.

Introduction: Vascular stiffness is a predictor of cardiovascular disease and pulse wave velocity (PWV) is the current standard for measuring in vivo vascular stiffness. Mean arterial pressure is the largest confounding variable to PWV; therefore, in this study we aimed to test the hypothesis that increased aortic PWV in type 2 diabetic mice is driven by increased blood pressure rather than vascular biomechanics. Methods and Results: Using a combination of in vivo PWV and ex vivo pressure myography, our data demonstrate no difference in ex vivo passive mechanics, including outer diameter, inner diameter, compliance (Db/db: 0.0094 ± 0.0018 mm2/mmHg vs. db/db: 0.0080 ± 0.0008 mm2/mmHg, p \u3e 0.05 at 100 mmHg), and incremental modulus (Db/db: 801.52 ± 135.87 kPa vs. db/db: 838.12 ± 44.90 kPa, p \u3e 0.05 at 100 mmHg), in normal versus diabetic 16 week old mice. We further report no difference in basal or active aorta biomechanics in normal versus diabetic 16 week old mice. Finally, we show here that the increase in diabetic in vivo aortic pulse wave velocity at baseline was completely abolished when measured at equivalent pharmacologically-modulated blood pressures, indicating that the elevated PWV was attributed to the concomitant increase in blood pressure at baseline, and therefore stiffness. Conclusions: Together, these animal model data suggest an intimate regulation of blood pressure during collection of pulse wave velocity when determining in vivo vascular stiffness. These data further indicate caution should be exerted when interpreting elevated PWV as the pure marker of vascular stiffness

Phosphoinositide 3-kinase, Src, and Akt modulate acute ventilation-induced vascular permeability increases in mouse lungs

To determine the role of phosphoinositide 3-OH kinase (PI3K) pathways in the acute vascular permeability increase associated with ventilator-induced lung injury, we ventilated isolated perfused lungs and intact C57BL/6 mice with low and high peak inflation pressures (PIP). In isolated lungs, filtration coefficients (Kf) increased significantly after ventilation at 30 cmH2O (high PIP) for successive periods of 15, 30 (4.1-fold), and 50 (5.4-fold) min. Pretreatment with 50 µM of the PI3K inhibitor, LY-294002, or 20 µMPP2, a Src kinase inhibitor, significantly attenuated the increase in Kf, whereas 10 µM Akt inhibitor IV significantly augmented the increased Kf. There were no significant differences in Kf or lung wet-to-dry weight (W/D) ratios between groups ventilated with 9 cmH 2O PIP (low PIP), with or without inhibitor treatment. Total lung ß-catenin was unchanged in any low PIP isolated lung group, but Akt inhibition during high PIP ventilation significantly decreased total ß-catenin by 86%. Ventilation of intact mice with 55 cmH2O PIP for up to 60 min also increased lung vascular permeability, indicated by increases in lung lavage albumin concentration and lung W/D ratios. In these lungs, tyrosine phosphorylation of ß-catenin and serine/threonine phosphorylation of Akt, glycogen synthase kinase 3ß (GSK3ß), and ERK1/2 increased significantly with peak effects at 60 min. Thus mechanical stress activation of PI3K and Src may increase lung vascular permeability through tyrosine phosphorylation, but simultaneous activation of the PI3K-Akt-GSK3ß pathway tends to limit this permeability response, possibly by preserving cellular ß-catenin. Copyright © 2007 the American Physiological Society

Vascular Mechanics in Decellularized Aortas and Coronary Resistance Microvessels in Type 2 Diabetic db/db Mice

We previously reported differences in stiffness between macro- and micro-vessels in type 2 diabetes (T2DM). The aim of this study was to define the mechanical properties of the ECM independent of vascular cells in coronary resistance micro-vessels (CRMs) and macro-vessels (aorta) in control Db/db and T2DM db/db mice. Passive vascular remodeling and mechanics were measured in both intact and decellularized CRMs and aortas from 0 to 125 mmHg. We observed no differences in intact control and diabetic aortic diameters, wall thicknesses, or stiffnesses (p \u3e 0.05). Aortic decellularization caused a significant increase in internal and external diameters and incremental modulus over a range of pressures that occurred to a similar degree in T2DM. Differences in aortic diameters due to decellularization occurred at lower pressures (0–75 mmHg) and converged with intact aortas at higher, physiological pressures (100–125 mmHg). In contrast, CRM decellularization caused increased internal diameter and incremental modulus only in the db/db mice, but unlike the aorta, the intact and decellularized CRM curves were more parallel. These data suggest that (1) micro-vessels may be more sensitive to early adverse consequences of diabetes than macro-vessels and (2) the ECM is a structural limit in aortas, but not CRMs. © 2015 Biomedical Engineering Societ

Clara cell secretory protein and phospholipase A2 activity modulate acute ventilator-induced lung injury in mice

Lung vascular permeability is acutely increased by high-pressure and high-volume ventilation. To determine the roles of mechanically activated cytosolic PLA2 (cPLA2) and Clara cell secretory protein (CCSP), a modulator of cPLA2 activity, we compared lung injury with and without a PLA2 inhibitor in wild-type mice and CCSP-null mice (CCSP-/-) ventilated with high and low peak inflation pressures (PIP) for 2- or 4-h periods. After ventilation with high PIP, we observed significant increases in the bronchoalveolar lavage albumin concentrations, lung wet-to-dry weight ratios, and lung myeloperoxidase in both genotypes compared with unventilated controls and low-PIP ventilated mice. All injury variables except myeloperoxidase were significantly greater in the CCSP-/- mice relative to wild-type mice. Inhibition of cPLA2 in wild-type and CCSP-/- mice ventilated at high PIP for 4 h significantly reduced bronchoalveolar lavage albumin and total protein and lung wet-to-dry weight ratios compared with vehicle-treated mice of the same genotype. Membrane phospho-cPLA2 and cPLA2 activities were significantly elevated in lung homogenates of high-PIP ventilated mice of both genotypes but were significantly higher in the CCSP-/- mice relative to the wild-type mice. Inhibition of cPLA2 significantly attenuated both the phospho-cPLA2 increase and increased cPLA2 activity due to high-PIP ventilation. We propose that mechanical activation of the cPLA 2 pathway contributes to acute high PIP-induced lung injury and that CCSP may reduce this injury through inhibition of the cPLA2 pathway and reduction of proinflammatory products produced by this pathway. Copyright © 2005 the American Physiological Society