142 research outputs found
Akadémiai Kiadó levele Lukács Györgynek
<p>Ketamine has been found to have rapid, long-lasting antidepressant effects in treatment-resistant (TR) patients with major depressive disorder (MDD). Recently, we have also shown that ketamine acts as a prophylactic to protect against the development of stress-induced depressive-like behavior in mice, indicating that a preventative treatment against mental illness using ketamine is possible. While there is significant investigation into ketamine’s antidepressant mechanism of action, little is known about ketamine’s underlying prophylactic mechanism. More specifically, whether ketamine’s prophylactic action is molecularly similar to or divergent from its antidepressant action is entirely unknown. Here, we sought to characterize immunohistochemical signatures of cell populations governing ketamine’s antidepressant and prophylactic effects. 129S6/SvEv mice were treated with saline (Sal) or ketamine (K) either before a social defeat (SD) stressor as a prophylactic, or after SD as an antidepressant, then subsequently assessed for depressive-like behavior. Post-fixed brains were processed for doublecortin (DCX), calretinin (CR) and calbindin (CB) expression. The number of DCX<sup>+</sup> neurons in the dentate gyrus (DG) of the hippocampus (HPC) was not affected by prophylactic or antidepressant ketamine treatment, while the number of CR<sup>+</sup> neurons in the ventral hilus increased with antidepressant ketamine under SD conditions. Moreover, antidepressant, but not prophylactic ketamine administration significantly altered CR and CB expression in the ventral HPC (vHPC). These data show that while antidepressant ketamine treatment mediates some of its effects via adult hippocampal markers, prophylactic ketamine administration does not, at least in 129S6/SvEv mice. These data suggest that long-lasting behavioral effects of prophylactic ketamine are independent of hippocampal DCX, CR and CB expression in stress-susceptible mice.</p
ADEPT - Abnormal Doppler Enteral Prescription Trial
<p>Abstract</p> <p>Background</p> <p>Pregnancies complicated by abnormal umbilical artery Doppler blood flow patterns often result in the baby being born both preterm and growth-restricted. These babies are at high risk of milk intolerance and necrotising enterocolitis, as well as post-natal growth failure, and there is no clinical consensus about how best to feed them. Policies of both early milk feeding and late milk feeding are widely used. This randomised controlled trial aims to determine whether a policy of early initiation of milk feeds is beneficial compared with late initiation. Optimising neonatal feeding for this group of babies may have long-term health implications and if either of these policies is shown to be beneficial it can be immediately adopted into clinical practice.</p> <p>Methods and Design</p> <p>Babies with gestational age below 35 weeks, and with birth weight below 10th centile for gestational age, will be randomly allocated to an "early" or "late" enteral feeding regimen, commencing milk feeds on day 2 and day 6 after birth, respectively. Feeds will be gradually increased over 9-13 days (depending on gestational age) using a schedule derived from those used in hospitals in the Eastern and South Western Regions of England, based on surveys of feeding practice. Primary outcome measures are time to establish full enteral feeding and necrotising enterocolitis; secondary outcomes include sepsis and growth. The target sample size is 400 babies. This sample size is large enough to detect a clinically meaningful difference of 3 days in time to establish full enteral feeds between the two feeding policies, with 90% power and a 5% 2-sided significance level. Initial recruitment period was 24 months, subsequently extended to 38 months.</p> <p>Discussion</p> <p>There is limited evidence from randomised controlled trials on which to base decisions regarding feeding policy in high risk preterm infants. This multicentre trial will help to guide clinical practice and may also provide pointers for future research.</p> <p>Trial registration</p> <p>Current Controlled Trials ISRCTN: 87351483</p
Vaca Muerta y Argentina: ¿riqueza energética o maldición holandesa?
La enfermedad holandesa es un fenómeno que surge en una economía
cuando ocurre un shock positivo en lo que se denomina el sector de los
transables exitosos de un país, el cual está asociado a los recursos naturales.
Dicho shock genera una apreciación real del tipo de cambio la cual tiene como
consecuencia un proceso de desindustrialización en el sector del resto de los
transables, conocido como transable tradicional.
Este modelo teórico surge en los Países Bajos en la década de 1960, cuando
a raíz del descubrimiento de grandes yacimientos de gas natural en la ciudad
de Slochteren, se desencadenaron los efectos previamente mencionados. De
esta manera, el modelo de enfermedad holandesa busca explicar el motivo de
dichos efectos y le da un rol sumamente relevante a las políticas económicas
que se deben llevar a cabo para atenuarlos.
Debido a que Argentina basa su crecimiento económico principalmente en
la explotación de recursos naturales, se considera pertinente analizar los
posibles riesgos que tiene el país de sufrir la enfermedad holandesa. Para esto,
se estudia el caso puntual de la explotación de Vaca Muerta, cuya potencialidad
tomó relevancia a partir del año 2010.
A su vez, se analiza el caso de Noruega, país que pudo atenuar los efectos
de la enfermedad holandesa gracias a su institucionalidad y prudencia en el
marco de las medidas económicas tomadas.
Para este trabajo, la importancia del análisis radica no solo en la
identificación de la enfermedad holandesa en cuanto a sus síntomas y efectos,
sino también en el posterior planeamiento de políticas de prevención para que
dicho fenómeno no afecte el crecimiento económico del país en cuestión.
El rol de las políticas económicas e instituciones resulta clave a la hora de
evitar los efectos nocivos que puede tener la enfermedad holandesa, así como
también para aprovechar el boom y lograr un crecimiento sostenible en el largo
plazo a través de, por ejemplo, inversión en capital humano y tecnología
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