The was discharged after 10 days. Large foreign bodies can be retrieved by endoscopy and in selected cases gastrointestinal perforations secondary to foreign bodies can also be managed by endoscopy being surgery a

second line approach. “
“A 70-year old man with Parkinson’s disease, congestive heart failure, CABG surgery in 2005, hypertension, renal failure and a BMI of 39 presented with abdominal pain and increasing renal dysfunction. A CT scan was performed with normal findings. A gastroscopy was then performed. A junior doctor performed the endoscopy. He found a duodenal ulcer and a duodenal tumour. The patient experienced intense abdominal pain and abdominal distension immediately after the procedure. A senior surgeon was called GDC-0973 cost to the endoscopic unit. He realised that a perforation had occurred and relieved Ku-0059436 concentration the abdominal pressure placing four 16 G needles through the abdominal wall. The patient was taken to the OR. He was treated with a covered duodenal stent that sealed the perforation. He was allowed to drink immediately after the procedure and recovered. The patient was dismissed within one week. The stent was removed endoscopically in conscious sedation after three weeks. A diagnostic laparoscopy was performed. There was old fibrin and foul liquid above the liver indicating a 2-3 days

old perforation. Due to plentiful intra abdominal fat it was impossible to visualise the duodenum. A per-operative gastroscopy was performed and the duodenal ulcer was recognised. The previously described “tumour”

was found to be the liver surface. Air bubbles were seen on the laparoscopic view while insufflating with the gastroscope, verifying a perforation. It was possible to pass the gastroscope outside the duodenum into the subomental area under the liver. The gastroscope was retrieved and passed down the real duodenal lumen. A guide wire was placed into the distal portion Adenosine triphosphate of the duodenum. A 9 cm partially covered duodenal stent (Hanarostent, M.I Tech, Korea) was placed over the wire, through the scope with the covered portion reaching into the stomach. No air bubbles were seen at laparoscopy, indicating sealing of the perforation. An abdominal drain was placed. We believe that covered metal stents can be used as a treatment alternative for perforated duodenal ulcers, especially in patients with comorbidities. This treatment option has recently been used in several patients at our department with good results. Simultaneous drainage of the abdominal cavity at the site of leakage seems to be crucial in most cases. Stent treatment together with percutaneous drainage may even be a future alternative to surgery in all patients with perforated duodenal ulcers. “
“Postoperative delayed bleeding of submucosal tunnel is a rare complication after peroral endoscopic myotomy (POEM) for esophageal achalasia. However, once it occurs it can be fatal.

To achieve long term anti-inflammatory efficacy and new cell protection, a strategy of selective CB2 receptor stimulation was chosen, based on known coordinated responses of the endocannabinoid system to injury. Specifically, local endocannabinoid levels increase with tissue injury or inflammation (Franklin et al., 2003 and Walter et al., 2003) at the same time as CB2 receptors on inflammatory and some parenchymal cells are induced by immune cell transcription factors or soluble inflammatory factors. IFNγ and granulocyte macrophage-colony

stimulating factor (GM-CSF) promote CB2 expression in microglia ( Maresz et al., 2005 and Racz et al., 2008) while stimulation of CB2 receptors reduces microglia migration ( Romero-Sandoval et al., 2009) production of TNF-α ( Sagredo et al., 2009 and Zarruk this website et al., 2012), reactive oxygen species ( Han et al., Selleckchem Galunisertib 2009),

and regulates expression of iNOS and CCR2 ( Racz et al., 2008). This constant supply of CB2 receptors, renewed during microglia proliferation and action, represented a druggable potentially nontolerizing target for long term inflammation reduction. In our experiments, the anti-inflammatory action achieved with HU-308 was through mechanisms involving glial cells, mainly activated microglia, in which CB2 receptors were upregulated in response to neural injury. Finding CB2 receptor-like IR on microglia was altered by HU treatment in patterns consistent with receptor internalization, while lack of receptor Adenosine internalization by WIN maintained microglia and active morphology, raise the possibility of functional selectivity or

biased agonism between these 2 synthetic cannabinoid ligands. Internalization of CB2 receptors to different extents with different agonists, differential activation of specific downstream signaling pathways, and the inability of WIN stimulation to internalize CB2 receptors, are all effects that have been shown in vitro ( Atwood et al., 2012). The differential effects of WIN and HU also may relate to the mixed or more promiscuous pharmacologic effects of WIN. Although WIN and HU have similar in vitro binding affinity to CB2 (Pertwee, 2010), WIN is an aminoalkylindole with significant agonist activity at CB1, CB2, and the vanilloid receptor VR1; HU-308 is a bicyclic compound and a selective CB2 agonist (Pertwee, 2010); and TRPV1 (transient receptor potential vanilloid 1 receptor) activation is proinflammatory. Neuronal TRPV1 cation channels are best known as mediators of inflammatory pain in dorsal spinal cord, with a role in neuron-mediated glial activation in primary sensory ganglia of rodents (Chen et al., 2009 and Cavanaugh et al., 2011). In rat TRPV1 is also expressed in astrocytes and microglia (Doly et al., 2004 and Kim et al., 2006).

Such heuristic genetic patterns may correlate with ASD endophenotypes and/or overlap with other brain and developmental disorders. The incremental advances

in discovery of genes associated with ASD risk are already influencing clinical progress in early detection and intervention. Moreover, as a more definitive catalogue of ASD risk variants is generated – in particular through genome sequencing projects MAPK Inhibitor Library order – it is our opinion a platform will emerge for the proper design to dissect the roles of gene–gene and potential gene–environment interactions in ASD. Papers of particular interest, published within the period of review, have been highlighted as: • of special interest The authors wish to thank Anath C. Lionel

for assistance. BD is supported by MH057881. SWS holds the GlaxoSmithKline Canadian Institutes of Health Research (CIHR) Endowed Chair in Genome Sciences. “
“Current Opinion in Genetics & Development 2012, 22:283–289 This review comes from a themed issue on Molecular and genetic bases of disease Edited by Beverly Emanuel and Steve Warren For a complete overview see the Issue and the Editorial 0959-437X/$ – see front matter, © 2012 Elsevier Ltd. All rights reserved. DOI 10.1016/j.gde.2012.02.005 Genomic selleck compound imprinting is an epigenetic process that controls parent-of-origin expression of an estimated selleck kinase inhibitor 1–2% of genes in the mammalian genome [1 and 2•]. Although few in number, many imprinted genes play important roles in development and growth, often in a dose-dependent manner [3]. Imprinted genes mostly occur in

clusters in the genome controlled by a CpG rich region known as an Imprint Control Element (ICE). This ICE shows differential DNA methylation, which is established in the germ cells of one parent and maintained on this parental chromosome throughout life. The ICE on the other parental allele remains unmethylated. The unmethylated ICE activates a macro non-coding (nc) RNA in cis, while methylation prevents activation on the other allele. Macro ncRNAs are inefficiently processed long ncRNAs whose main product is unspliced [ 1]. In three of four cases where the function of the imprinted macro ncRNA has been tested, it acts as a cis-silencer to prevent upregulation of flanking imprinted genes in the cluster [ 4, 5, 6 and 7••]. A hallmark of imprinted genes is that they show developmental and tissue-specific regulation of imprinted expression [ 8]. For example, the Dlk1 gene is paternally expressed and plays a dose-dependent role in regulating growth of the embryo, but switches to biallelic expression in neural stem cells and niche astrocytes where it is required for normal postnatal neurogenesis [ 9 and 10••].

The advances

in vaccine technology have initiated a future of novel and innovative vaccine designs based on new knowledge of the antigenic properties of pathogens and the ways in which a protective immune response might be induced. “
“Key concepts ■ Adjuvantation of vaccines is a well-established concept and practice The adjuvant concept is more than 80 years old with the first adjuvant present in human vaccines, an aluminium salt (aluminium potassium sulphate, also known as alum), appearing in the 1920s. About 70 years later a licensed vaccine with an alternative adjuvant to aluminium salt was developed ( Figure 4.1). The addition of components other than the pathogen or antigen to vaccine learn more preparations represents one of the original attempts to improve vaccine efficacy. Adjuvants are substances that can enhance and modulate the immunogenicity of the vaccine antigen. In a vaccine, the specificity of the immune response is provided by the antigen and the role of the adjuvant is to MAPK Inhibitor Library manufacturer amplify this immune response. Live vaccines

usually do not require adjuvants as they mimic natural infection and are therefore ‘naturally adjuvanted’. Most inactivated (whole or subunit) vaccines do require adjuvants since the inactivation processes remove, in part or totally, the pathogenic features of the microorganisms that are responsible for triggering the immune response. Inactivated vaccines may retain some of the characteristics that stimulate the innate

immune system (ie pathogen-associated molecular patterns [PAMPs], see Chapter 2 – Vaccine immunology), but the amount and context of these PAMPs may be insufficient to provoke long-lasting immunity. Aluminium salts have been sufficient to induce an adequate immune response for most of the licensed inactivated and subunit vaccines. However, many of the modern vaccines consist of highly purified antigens for which the natural innate immune triggers are not present. These refined formulations often show reduced immunogenicity and therefore require adjuvantation. Classic aluminium salts are not always capable of eliciting Rho the desired immune response and more complex adjuvantation may be required. One of the promising approaches to improve efficacy of newly developed prophylactic and therapeutic vaccines is the use of innovative adjuvants including the technique of combining different types of adjuvants into single formulations. Adjuvant selection There is no universal adjuvant to cover all vaccine needs. The appropriate selection of adjuvants to match the antigens is key to the formulation of novel and efficacious vaccines. For example, different aluminium salts (phosphate or hydroxide) are used depending on the ion charge required for binding to the antigen.

Deaths in hospital: The number of deaths in hospital by age and clinical risk group was estimated by counting inpatient admissions with an acute respiratory illness code extracted from the Hospital Episode Statistics database with death recorded as the discharge method. Only deaths within 30 days of admission were included in the analysis. General practitioner consultations: The age-stratified weekly numbers of consultations in general

practice for acute respiratory illness were obtained from the Royal College of General DZNeP Practitioners Weekly Returns Service. The population monitored by the Royal College of General Practitioners is closely matched to the national population in terms of age, gender, deprivation index and prescribing patterns. 16 Consultation numbers were scaled by the size of the population covered by the Royal College LY294002 mw of General Practitioners practices (1.44% of population of England and Wales) in 2010 16 to give weekly consultation rates per 100,000 people.

These rates were then multiplied by the population of England during the corresponding season to give estimated weekly numbers of episodes. The data were not available by clinical risk group. Population by age and clinical risk group: The population of England in clinical risk groups indicated for seasonal influenza vaccination was estimated using the proportion of patients identified in the Royal College of General Practitioners practices as having a READ code indicating an influenza high-risk condition, averaged between 2003 and 2010. Weekly counts in the laboratory reports for pathogens potentially responsible for acute respiratory illness were used as explanatory variables to estimate the proportion of health care outcomes (acute respiratory illness episodes leading

to GP consultations, hospital admissions and deaths in hospital) attributable to influenza. We used an adaptation of a generalised linear model for negative www.selleck.co.jp/products/Metformin-hydrochloride(Glucophage).html binomial outcome distributions with an identity link function. The negative binomial distribution was used to account for overdispersion in many of the outcome variables and the identity link function to ensure contributions from different pathogens were additive (see Supporting Text Section 1 for model equations). The models were constructed by allowing for the incorporation of i) a moving average to smooth fluctuations in laboratory reports; ii) a secular trend in outcomes iii) the separation of influenza A into its subtypes; iv) the effects of interactions between co-circulating pathogens and v) a temporal offset between pathogen testing and the onset of clinical effect. Details are provided in Sections 1 and 2 of the Supporting Text. The best fitting model was selected using the Akaike Information Criterion.

, 2012 and Zinser et al., 2009), protein accumulation ( Waldbauer et al., 2012), cell cycling (e.g. Bruyant et al., 2001, Holtzendorff et al., 2001, Holtzendorff et

al., 2008, Liu et al., 1997, Partensky et al., 1996, Vaulot et al., 1995 and Vaulot and Marie, 1999), amino acid uptake ( Mary et al., 2008) as well as carbon fixation and other photosynthetic parameters ( Bruyant and Babin, 2005, Claustre et al., 2002 and Zinser et al., 2009) have been reported. Omic analyses of MED4 revealed that the diel gene expression patterns hold true for nearly the entire transcriptome and proteome ( Waldbauer et al., 2012 and Zinser et al., 2009). For most of the periodic genes RNA accumulation peaked around dawn or dusk. Transcript maxima of at least few genes were

distributed http://www.selleckchem.com/products/Adriamycin.html over the complete day ( Waldbauer et al., 2012 and Zinser et al., 2009). Maximal abundance of the majority of oscillating proteins peaked between 2 and 8 h after their respective mRNAs ( Waldbauer et al., 2012). However, a high divergence of transcript–protein relationships regarding timing and magnitude of expression was observed. The kaiB and kaiC genes of MED4 exhibit periodic expression during the day–night cycle as observed in S. elongatus. Moreover, they appear to possess only one transcription initiation Navitoclax research buy start site upstream of kaiB, which would lead to a dicistronic mRNA like in S. elongatus as well. However, unequivocal evidence is still lacking ( Holtzendorff et al., 2008 and Vogel et al., 2003). In fact, transcription analyses have shown different results so far. While kaiB and kaiC peak in phase in one study (in late night) ( Holtzendorff et al., 2008), Zinser et al. (2009) showed that kaiC peaks around sunset. The reason for this difference (e.g. experimental setup) remains to be solved. Expression profiles of several genes peaking in the dark phase suggest anticipation of light changes, which would indicate an internal timing mechanism (Holtzendorff et al., 2008 and Zinser et al., 2009). However, MED4

does not exhibit find more self-sustained oscillations: When cells are shifted from light–dark cycles to constant light, cell cycle and psbA expression rhythms vanish. Therefore, it was suggested that MED4 harbors a core oscillatory mechanism that requires a daily resetting by environmental stimuli ( Holtzendorff et al., 2008). Biochemical analysis provided first evidence that the core of the hourglass-like timing mechanism in MED4 might be constituted by the remaining Kai proteins ( Axmann et al., 2009): KaiC from MED4, which shows 75% sequence identity to S. elongatus-KaiC, was proven to be an autokinase and ATPase in vitro. Thus MED4-KaiC displays at least two of the key enzymatic activities described for the well-studied S. elongatus counterpart. Intrinsic phosphorylation of the residues S427 and T428 (aligning with the known phosphorylation sites of S. elongatus-KaiC, see Fig. 2) occurred at high level and independently of S. elongatus-KaiA or MED4-KaiB.

Similarly, the imaginary component varies from −2τcpNcycε1 to 2τcpNcycε1, which can be expressed as ±Trel(f00I − f11I)/2. The

two imaginary limiting values correspond to magnetisation that ‘swaps’ ensembles after each 180° pulse, spending equal time in the ground and excited state ensembles. The imaginary limiting values correspond to the least refocused magnetisation. All four frequency limits are proportional to Trel. This provides a strong justification for performing constant time CPMG experiments, as this means that the relaxation for each term, and the maximum phase that any one term can accrue will be constant for all values of Ncyc. The complete set of discrete frequencies that can potentially contribute to the signal intensity, parameterised in terms of the indices j and k: equation(59) Fk,j=k-2j+1Ncycf11R-f00R+2f00R+f11R+i-k-2j+3Ncyc+2f00I-f11ITrel4with the index k running from 1 to 1 + 2Ncyc describing the trinomial expansion

in selleck products ε0 − ε1, and j running from 1 to 1 + Ncyc describing the binomial expansion in ε0 + ε1. The geometric distribution of these the real and imaginary components of these frequencies is illustrated in Figs. 3B and 4A, where the real component has been normalised by a factor of f11RTrel, and the imaginary terms by (f00I − f11I)Trel. Using these normalisations, the range of frequencies are independent on Ncyc and take the form of a diamond with limits in the imaginary dimension of (−0.5, 0.5) and in the real dimension of (f00R/f11R) to 1. As f00R ≪ f11R, on this scale the

first term appears to be very close to zero, and the terms ‘higher’ up the diamond on the real axis have significantly AZD6738 supplier larger relaxation rates. In the constant time CPMG experiment, the range of the resolvable frequencies is identical. The spectral resolution is limited by the density of frequencies which increases substantially with increasing Ncyc ( Fig. 4A). The simultaneous binomial and trinomial expansions result in there being many different pathways that can lead to the Grape seed extract same final net evolution frequency. The total number of individual pathways that will contribute at each frequency is given by the product of the coefficients of the two series, written here in terms of the Gamma function, a generalisation of the factorial, Γ(x+1)=x!Γ(x+1)=x!: equation(60) χk,j=χk,jbiχk,jtri=Γ(n+1)Γ(n-k+1)Γ(k+1)∑j=0nΓ(n+1)Γ(j+k+1)Γ(n-2j-k+1) The degeneracies of each frequency are strongly dependent on Ncyc. Initially, each of the six frequencies has equal degeneracy (Ncyc = 1, Fig. 3B). At successively higher values of Ncyc, there exists a strong combinatorial preference for terms to converge on the central frequency ( Fig. 4A). This combinatorial factor effectively describes the additional mixing between ground and excited ensembles that occur at increased νCPMG. It is important to note however that the frequencies emerging from the CPMG block are not equally weighted, and using Eq.

Superoxide radicals are normally produced by the enzyme NADPH oxidase in order to activate Everolimus supplier the defense mechanisms against invading pathogens (Halliwell and Gutteridge, 2007). Superoxide is produced by the electron transport chain from oxygen occupying the final position and acting as the terminal electron acceptor. Some electrons can randomly “leak” from the electron transport chain (Campian et al., 2004) and interact with oxygen

to produce superoxide radicals. Thus under physiological conditions, about 1–3% of the oxygen molecules in the mitochondria are converted into superoxide radicals. Superoxide radical is normally present mainly in the form of an anion radical and is removed by a dismutation reaction (Liochev and Fridovich, 2000): equation(1) 2O2−·+2H+⟶SODH2O2+O2 While without SOD this reaction PCI-32765 mw proceeds very slowly (k ∼ 0.2 M−1 s−1), the reaction becomes biologically relevant

when it is catalyzed by the SOD. The kinetic constant of the SOD-catalyzed superoxide depletion dismutation reaction has been estimated to be 2.5 × 109 M−1 s−1 ( Liochev and Fridovich, 2003). A mutual link between superoxide radicals and iron shows, that under in vivo stress conditions, an excess of superoxide releases “free iron” from iron-containing molecules (e.g. ferritin). The release of iron by superoxide has also been demonstrated for the [4Fe–4S] cluster-containing enzymes. Inactivation of these enzymes by O2− is a rapid process that leads to oxidation of the iron-sulphur cluster. The native clusters contain two Fe(II) and two Fe(III) ions, and the oxidation [one Fe(II) is oxidized to Fe(III)] may be denoted as follows (Liochev and Fridovich, 1994): equation(2) [2Fe(II) 2Fe(III)–4S]2+ + O2−  + 2H+ → [Fe(II) 3Fe(III)–4S]3+ + H2O2 The rate constant for reaction PtdIns(3,4)P2 (2) has been estimated in the range of 108 to 109 M−1 s−1. Since the oxidized protein binds the Fe(III) more firmly, Fe(II) ions are released from protein

according to the following reaction: equation(3) [Fe(II) 3Fe(III)–4S]3+ → [3Fe(III)–4S]+ + Fe(II) The released Fe(II) can participate in the Fenton reaction, generating highly reactive hydroxyl radicals ( OH) (Prousek, 2007) equation(4) Fe(II) + H2O2 → Fe(III) +  OH + OH−  (Fenton reaction) The Fenton reaction has its in vivo significance mainly under state of an organisms overloaded by iron (as in the conditions of hemochromatosis, b-thalassemia, hemodialysis). Thus high amounts of “free available iron” can have deleterious effects (Kakhlon and Cabantchik, 2002). The superoxide radical participates in the Haber–Weiss reaction (Liochev and Fridovich, 2002): equation(5) O2−  + H2O2 → O2 +  OH + OH−which is a combination of Fenton reaction and the reduction of Fe(III) by superoxide: equation(6) Fe(III) + O2−  → Fe(II) + O2 The hydroxyl radical is highly reactive with a half-life in aqueous solution of less than 1 ns (Pastor et al., 2000).

After extrusion the samples were collected, cooled to room temperature under natural convection conditions. The samples were then milled to a 0.149 mm granule size. They were labeled as extruded amaranth flours

and kept at 10 °C until analysis. Untreated flours were stored in the same manner as the extruded samples. In order to assess possible effects of flour particle size on the analysis, granule sizes were checked using a Malvern Mastersizer S-MAN 5005 (Malvern Instruments Ltda, Malvern, UK). (data not shown). The chemical composition of the flours including the moisture, fat, protein and ash content, were determined by the method described in AOAC (1997). The dietary fiber was analyzed using the enzymatic and gravimetric method according to Prosky, Asp, Schwiser, Devries, and Furnas (1988); starch was determined according to the MLN0128 chemical structure method of Rickard and Behn (1987). Starch was quantified

by enzymatic hydrolysis as described by Rickard and Behn (1987). Amylose content was determined following the method ISO 6647 (International Organization for Standardization, 1987). Amylopectin content was equal to the value obtained by subtraction of amylose from total starch. The color of the samples was determined in triplicate using the equipment ColorQuest XE (Hunter Lab, ColorQuest, USA). The CIE L∗a∗b∗ system was employed. This system determines the L∗, a∗ and b∗ values, where L∗ represents lightness with 0 for black and 100 for white;

a∗ represents the opposition between green and GDC-0068 in vitro red colors ranging from positive (green) to negative (red) values; and b∗ is the yellow/blue opposition also ranging from positive (yellow) to negative (blues) values. In the CIE L∗a∗b∗ color space a∗ and b∗ values exhibit minima and maxima values that depend on L∗ value. To determine the water absorption Ergoloid (WAI) and the water solubility indexes (WSI), the methodology proposed by Anderson, Conway, and Griffin (1969) was followed. Pasting properties of amaranth flours were determined using a Rapid Visco Analyzer (RVA-4, Newport Scientific, Warriewood, Australia) according to Ragaee and Abdel-Aal (2006). The pasting temperature (PT), peak viscosity (PV, the maximum hot paste viscosity), holding strength or trough viscosity (the trough at the minimum hot paste viscosity), final viscosity (FV, the viscosity at the end of test after cooling to 50 °C and holding at this temperature), breakdown (BD, peak viscosity − holding strength or trough viscosity) and setback (SB, final viscosity − holding strength) were determined with Thermocline for Windows software (Version 2.0). The viscosities are presented in Rapid Visco Units (RVU). Thermal properties were analyzed using a Differential Scanning Calorimeter (DSC822, Mettler Toledo, Schwerzenbach, Switzerland) according to González, Carrara, Tosi, Añón, and Pilosof (2007) with some modifications. Amaranth flour (13.0 ± 0.

“
“Physical exercise has beneficial effects on brain health and cognition. It uses the processes of energy metabolism and synaptic plasticity to promote brain health, upregulating proteins related to cognitive (Ding et al., 2006) and mitochondrial function (Kirchner et al., 2008). Exercise has also protective effects against several neurological diseases including Parkinson’s

selleck chemicals disease (Smith and Zigmond, 2003), Alzheimer’s disease (Mirochnic et al., 2009), and ischemic stroke (Stummer et al., 1994). In addition, exercise has been associated with a reduced risk of cognitive impairment and dementia with age (Laurin et al., 2001). Both acute and chronic exercises increase hippocampal activity (Holschneider et al., 2003 and Holschneider et al., 2007). Exercise induces hippocampal synaptic plasticity mainly by enhancing synaptic efficacy and the expression of molecules involved in learning and memory (Farmer et al., 2004, Vaynman et al., 2003 and Vaynman et al., 2004). Increase of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and fibroblast growth factor (FGF), and their mRNAs have been widely reported after exercise (Berchtold et al., 2010, Gomez-Pinilla et al., 1997 and Neeper et al., 1996). Components of the presynaptic vesicle membrane, such as synapsin I (SYN) Gemcitabine in vivo and synaptophysin (SYP) are also found to be increased

after exercise training (Vaynman et al., 2006). Exercise induces long-term potentiation (LTP) (van Praag et al., 1999a) and increased glutamatergic activity (Leung et al., 2006), but the simultaneous increase

of the expression of neurotrophic factors, such as BDNF, promotes neuroprotection against the excitotoxic effects of glutamate in cell cultures (Jiang et al., 2005). There is evidence that treadmill exercise increases the number of astrocytes and the level of glial fibrillary acidic protein (GFAP) in the frontoparietal cortex and dorsolateral striatum C1GALT1 of exercised rats (Li et al., 2005) and stimulates the proliferation of astrocytes in the subgranular zone (SGZ) (Uda et al., 2006). Voluntary physical activity is also known to induce adult hippocampal neurogenesis, increasing cell proliferation and survival (Ehninger and Kempermann, 2003, van Praag et al., 1999a and van Praag et al., 1999b). In addition, structural neuronal proteins may also be affected by exercise due to their plastic characteristics in face of various stimuli (for reviews, see Sánchez et al., 2000 and Julien, 1999). Considering that for humans the recommended guideline for the practice of physical activity states at least 30 min of moderate-intensity activity on most days of the week (Hillman et al., 2008), here we used an animal model of short-term, moderate intensity treadmill exercise protocol (Ferreira et al.