Per la corretta attribuzione del "Romanzo delle donne contemporanee in Italia" (1863)

The use of free energy simulation techniques in the study of protein stability is critically evaluated. Results from two simulations of the thermostability mutation Asn218 to Ser218 in Subtilisin are presented. It is shown that components of the free energy change can be highly sensitive to the computational details of the simulation leading to the conclusion that free energy calculations cannot currently be used to reliably predict protein stability. The different factors that undermine the reliability are discussed

Reactive Oxygen Species, Endoplasmic Reticulum Stress and Mitochondrial Dysfunction: The Link with Cardiac Arrhythmogenesis.

This is the final version of the article. It first appeared from Frontiers via http://dx.doi.org/10.3389/fphys.2016.00313BACKGROUND: Cardiac arrhythmias represent a significant problem globally, leading to cerebrovascular accidents, myocardial infarction, and sudden cardiac death. There is increasing evidence to suggest that increased oxidative stress from reactive oxygen species (ROS), which is elevated in conditions such as diabetes and hypertension, can lead to arrhythmogenesis. METHOD: A literature review was undertaken to screen for articles that investigated the effects of ROS on cardiac ion channel function, remodeling and arrhythmogenesis. RESULTS: Prolonged endoplasmic reticulum stress is observed in heart failure, leading to increased production of ROS. Mitochondrial ROS, which is elevated in diabetes and hypertension, can stimulate its own production in a positive feedback loop, termed ROS-induced ROS release. Together with activation of mitochondrial inner membrane anion channels, it leads to mitochondrial depolarization. Abnormal function of these organelles can then activate downstream signaling pathways, ultimately culminating in altered function or expression of cardiac ion channels responsible for generating the cardiac action potential (AP). Vascular and cardiac endothelial cells become dysfunctional, leading to altered paracrine signaling to influence the electrophysiology of adjacent cardiomyocytes. All of these changes can in turn produce abnormalities in AP repolarization or conduction, thereby increasing likelihood of triggered activity and reentry. CONCLUSION: ROS plays a significant role in producing arrhythmic substrate. Therapeutic strategies targeting upstream events include production of a strong reducing environment or the use of pharmacological agents that target organelle-specific proteins and ion channels. These may relieve oxidative stress and in turn prevent arrhythmic complications in patients with diabetes, hypertension, and heart failure.Biotechnology and Biological Sciences Research Council (Doctoral Training Award), Croucher Foundation of Hong Kon

Expression of Avian Influenza Virus Receptors and H5N1 Virus Infection In Human Respiratory Tract

Oral Presentations - Virus Structure/Function and Receptor BindingReceptor specificity restricts influenza virus cross species transmission, with SAα2,6 Gal and SAα2,3 Gal sialic acids recognized by human and avian influenza viruses, respectively. This study investigated the distribution of these two species of sialic acids in the human respiratory tract. The SAα2,3 Gal species was infrequently detected in the upper respiratory tract, but prevalent in the lower part, while the SAα2,6 Gal species is more common in the upper respiratory tract. Though alveolus cells are more susceptible than trachea and bronchus epithelial cells to avian influenza H5N1 virus infection in the ex vivo experiment, H5N1 virus was found to infect the upper respiratory tract epithelial cells of a human case. It was also found that H5N1 virus infection occurs in the epithelial cells of the respiratory tract which do not express detectable SA α2,3Gal. These observations may be important to investigate further if the currently-observed limited human to human transmission by H5N1 virus is associated with the differential expression of SAα2,3 Gal in human upper respiratory tract among individuals.postprin

Battery management system and control strategy for hybrid and electric vehicle

Author name used in this publication: K. W. E. ChengAuthor name used in this publication: K. DingAuthor name used in this publication: W. TingVersion of RecordPublishe

Diclofenac Prolongs Repolarization in Ventricular Muscle with Impaired Repolarization Reserve

Background: The aim of the present work was to characterize the electrophysiological effects of the non-steroidal anti- inflammatory drug diclofenac and to study the possible proarrhythmic potency of the drug in ventricular muscle. Methods: Ion currents were recorded using voltage clamp technique in canine single ventricular cells and action potentials were obtained from canine ventricular preparations using microelectrodes. The proarrhythmic potency of the drug was investigated in an anaesthetized rabbit proarrhythmia model. Results: Action potentials were slightly lengthened in ventricular muscle but were shortened in Purkinje fibers by diclofenac (20 mM). The maximum upstroke velocity was decreased in both preparations. Larger repolarization prolongation was observed when repolarization reserve was impaired by previous BaCl 2 application. Diclofenac (3 mg/kg) did not prolong while dofetilide (25 mg/kg) significantly lengthened the QT c interval in anaesthetized rabbits. The addition of diclofenac following reduction of repolarization reserve by dofetilide further prolonged QT c . Diclofenac alone did not induce Torsades de Pointes ventricular tachycardia (TdP) while TdP incidence following dofetilide was 20%. However, the combination of diclofenac and dofetilide significantly increased TdP incidence (62%). In single ventricular cells diclofenac (30 mM) decreased the amplitude of rapid (I Kr ) and slow (I Ks ) delayed rectifier currents thereby attenuating repolarization reserve. L-type calcium current (I Ca ) was slightly diminished, but the transient outward (I to ) and inward rectifier (I K1 ) potassium currents were not influenced. Conclusions: Diclofenac at therapeutic concentrations and even at high dose does not prolong repolarization markedly and does not increase the risk of arrhythmia in normal heart. However, high dose diclofenac treatment may lengthen repolarization and enhance proarrhythmic risk in hearts with reduced repolarization reserve

Quantifying measures to limit wind driven resuspension of sediments for improvement of the ecological quality in some shallow Dutch lakes

Although phosphorus loadings are considered the main pressure for most shallow lakes, wind-driven resuspension can cause additional problems for these aquatic ecosystems. We quantified the potential effectiveness of measures to reduce the contribution of resuspended sediments, resulting from wind action, to the overall light attenuation for three comparable shallow peat lakes with poor ecological status in the Netherlands: Loosdrecht, Nieuwkoop, and Reeuwijk (1.8–2.7 m depth, 1.6–2.5 km fetch). These measures are: 1. wave reducing barriers, 2. water level fluctuations, 3. capping of the sediment with sand, and 4. combinations of above. Critical shear stress of the sediments for resuspension (Vcrit), size distribution, and optical properties of the suspended material were quantified in the field (June 2009) and laboratory. Water quality monitoring data (2002–2009) showed that light attenuation by organic suspended matter in all lakes is high. Spatial modeling of the impact of these measures showed that in Lake Loosdrecht limiting wave action can have significant effects (reductions from 6% exceedance to 2% exceedance of Vcrit), whereas in Lake Nieuwkoop and Lake Reeuwijk this is less effective. The depth distribution and shape of Lake Nieuwkoop and Lake Reeuwijk limit the role of wind-driven resuspension in the total suspended matter concentration. Although the lakes are similar in general appearance (origin, size, and depth range) measures suitable to improve their ecological status differ. This calls for care when defining the programme of measures to improve the ecological status of a specific lake based on experience from other lakes.

Genes Suggest Ancestral Colour Polymorphisms Are Shared across Morphologically Cryptic Species in Arctic Bumblebees

email Suzanne orcd idCopyright: © 2015 Williams et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Vanadium

International audienceVanadium (chemical symbol, V) is a d-block transition metal,silver in color, appearing in the first long period of the peri-odic table between titanium and chromium. Vanadium hastwo stable isotopes: 50V and 51V, with atomic abundance of0.25 % and 99.75 %, respectively. Vanadium has several oxidation forms (between 2+ and 5+). In the lithosphere, Voccurs as reducing V(III) form, whereas in oxidizing con- ditions V prevails under V(IV) form. Vanadium(II) is partic- ularly unstable in the environment. Vanadium(III) is more stable than V(II), but it is also gradually oxidized by the air or dissolved oxygen. Vanadium(V) is expected to be the prevailing form in waters exposed to atmospheric oxygen, whereas V(IV) may be present in reducing environments. Depending upon geometry and environment, V ionic radii vary between 36 pm and 79 pm. Vanadium has a high melting point of 1910 42 C and is a mildly incompatible, refractory,lithophile (siderophile in the iron core and chondrites) ele- ment. Vanadium has an electronegativity of 1.63 on the Pau- ling scale and displays a first ionization potential of 6.74 eV. More details can be found in Richards (2006) and Haynes (2015)