A couple of weeks ago, I was looking for a new design of drawings. So now, here is my new style of creations !!. More definition and more design with a new concept. Enjoy ! I will accept observations !.
This Blog was created to present drawing of models to papers, thesis, presentations, posters or any info related to science (specially in biological science). I am Biologist and I prepare drawings for delivery.
24.3.13
Neurogenesis Re-Loaded !!
Neurogenesis in the Sub-Granular Zone (SGZ) of the hippocampus Reloaded!!. This drawing was created in comparison with one of my firsts design in the neurogenesis. Thanks to the creativity and patience to make everyday a nice work !
(Hace un tiempo había realizado este dibujo pero sin los conocimientos que he ido adquiriendo en el tiempo. Hoy año 2013 Graphique-science esta a la vanguardia!!!)
20.3.13
First drawing in a review !!
http://link.springer.com/article/10.1007%2Fs12035-013-8435-5
Peroxisome Proliferator-activated Receptors and Alzheimer's Disease: Hitting the Blood–Brain Barrier
Juan M. Zolezzi and Nibaldo C. Inestrosa
The blood–brain barrier (BBB) is often affected in several neurodegenerative disorders, such as Alzheimer's disease (AD). Integrity and proper functionality of the neurovascular unit are recognized to be critical for maintenance of the BBB. Research has traditionally focused on structural integrity more than functionality, and BBB alteration has usually been explained more as a consequence than a cause. However, ongoing evidence suggests that at the early stages, the BBB of a diseased brain often shows distinct expression patterns of specific carriers such as members of the ATP-binding cassette (ABC) transport protein family, which alter BBB traffic. In AD, amyloid-β (Aβ) deposits are a pathological hallmark and, as recently highlighted by Cramer et al. (2012), Aβ clearance is quite fundamental and is a less studied approach. Current knowledge suggests that BBB traffic plays a more important role than previously believed and that pharmacological modulation of the BBB may offer new therapeutic alternatives for AD. Recent investigations carried out in our laboratory indicate that peroxisome proliferator-activated receptor (PPAR) agonists are able to prevent Aβ-induced neurotoxicity in hippocampal neurons and cognitive impairment in a double transgenic mouse model of AD. However, even when enough literature about PPAR agonists and neurodegenerative disorders is available, the problem of how they exert their functions and help to prevent and rescue Aβ-induced neurotoxicity is poorly understood. In this review, along with highlighting the main features of the BBB and its role in AD, we will discuss information regarding the modulation of BBB components, including the possible role of PPAR agonists as BBB traffic modulators.
First paper with drawings !
http://iospress.metapress.com/content/y05258137g173l5v/
Transforming Growth Factor β1 Modulates Amyloid β-Induced Glial Activation through the Smad3-Dependent Induction of MAPK Phosphatase-1
B Flores and R von Bernhardi
Chronic neuroinflammation has been proposed as a driving force for Alzheimer's disease (AD), which is characterized by amyloid-β (Aβ) deposition, neurofibrillary tangles, neuronal loss, and activation of glial cells. Persistent activation of mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB) pathway has been reported, which induces an increased expression of inflammatory mediators. Transforming growth factor β1 (TGFβ1) is an inflammation modulator whose levels are increased in AD. However, its canonical signaling pathway, Smad, appears to be impaired. Our previous findings indicate that TGFβ1 plays a key role in the pathogenesis of neuroinflammation, but the molecular mechanisms underlying its effects are not completely elucidated. Here, we studied the potential role of MKP-1, a phosphatase that exerts negative regulation on MAPK signaling, in the modulatory actions of TGFβ1. Using rat primary glial cultures, we found that pretreatment with TGFβ1 for 48 h reduced the production of inflammatory mediators induced by Aβ42, a result that was associated with prevention of MAPK p38 activation, attenuation of NF-κB p65 nuclear translocation, and an increase in MKP-1 levels. Moreover, suppression of MKP-1 expression by siRNA and inhibition of Smad3 reversed the modulation of inflammatory response exerted by TGFβ1. These results indicate that TGFβ1 induces the expression of MKP-1 in glial cells through the Smad pathway and inhibits MAPK and NF-κB signaling, thus revealing a novel mechanism for the neuroprotective actions of TGFβ1. Further research would be important in order to characterize the role of this mechanism in the pathogenesis of AD.
7.3.13
4.3.13
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