Low viscosity silicone with less shrinkage for brain slices.

Plastination consists of replacing lipid and water with a curable polymer. This technique has numerous advantages, of which the production of non-toxic, inert, highly durable, dry, and easy maintenance and storage specimens stand out. Like all anatomical techniques, plastination also has disadvantages, and one of them is tissue shrinkage. The feasibility of using low viscosity domestic silicone (0,1Pa.s at 20°C) to plastinate brain slices was examined. Twenty humans, 10 millimeters (mm) brain slices were impregnated, ten slices each with two polymers [10 with domestic low viscosity polymer - P1 and 10 slices with Biodur® (0,45-0,6Pa.s at 20°C) S10]. Shrinkage was accessed by volume and area measurements. Volume shrinkage was significantly less in the slices impregnated with low viscosity domestic polymer, demonstrating the feasibility to plastinate brain slices with domestic low viscosity silicone polymer.

Muscle hypertrophy training does not suppress the GH/IGF axis in young adult males.

PURPOSE: This study aimed to analyze the expression of the IGF type-1 receptor gene (IGF-1r) and IGF-I, GH, testosterone, and IGFBP-3 concentrations in young people subjected to 10 weeks of muscle hypertrophy training. METHODS: IGF-1r expression, serum concentrations of IGF-I, IGFBP-3, GH, and total testosterone, as well as body composition, fat percentage, and body mass index, were determined for 22 healthy young males at three moments of resistance training (first, fifth, and tenth week of training). RESULTS: Throughout the 10 weeks of training, a reduction was observed in the relative expression of the IGF-1r gene (2-ΔΔCT) and an increase in IGF-I and GH concentrations. A reduction in total testosterone concentrations was detected during the recovery period in the fifth week. The IGFBP-3 concentrations did not change throughout the training. CONCLUSIONS: The resistance training protocol prescribed for muscle hypertrophy did not suppress the GH-IGF-I axis, but it did cause alterations in IGF-1r gene expression and in IGF-I kinetics compatible with increased IGF bioactivity.

Effects of aerobic exercise on molecular aspects of asthma: involvement of SOCS-JAK-STAT.

BACKGROUND: Aerobic training (AT) decreases airway inflammation in asthma, but the underlying cellular and molecular mechanisms are not completely understood. Thus, this study evaluated the participation of SOCS-JAK-STAT signaling in the effects of AT on airway inflammation, remodeling and hyperresponsiveness in a model of allergic airway inflammation. METHODS: C57Bl/6 mice were divided into Control (Co), Exercise (Ex), HDM (HDM), and HDM+Exercise (HDM+ Ex). Dermatophagoides pteronyssinus (100ug/mouse) were administered oro-tracheally on days 0, 7, 14, 21, 28, 35, 42 and 49. AT was performed in a treadmill during 4 weeks in moderate intensity, from day 24 until day 52. RESULTS: AT inhibited HDM-induced total cells (p<0.001), eosinophils (p<0.01), neutrophils (p<0.01) and lymphocytes (p<0.01) in BAL, and eosinophils (p<0.01), neutrophils (p<0.01) and lymphocytes (p<0.01) in peribronchial space. AT also reduced BAL levels of IL-4 (p<0.001), IL-5 (p<0.001), IL-13 (p<0.001), CXCL1 (p<0.01), IL-17 (p<0.01), IL-23 (p<0.05), IL-33 (p<0.05), while increased IL- 10 (p<0.05). Airway collagen fibers (p<0.01), elastic fibers p<0.01) and mucin (p<0.01) were also reduced by AT. AT also inhibited HDM-induced airway hyperresponsiveness (AHR) to methacholine 6,25mg/ml (p<0.01), 12,5mg/mL (p<0.01), 25mg/mL (p<0.01) and 50mg/mL (p<0.01). Mechanistically, AT reduced the expression of STAT6 (p<0.05), STAT3 (p<0.001), STAT5 (p<0.01) and JAK2 (p<0.001), similarly by peribronchial leukocytes and by airway epithelial cells. SOCS1 expression (p<0.001) was upregulated in leukocytes and in epithelial cells, SOCS2 (p<0.01) was upregulated in leukocytes and SOCS3 down-regulated in leukocytes (p<0.05) and in epithelial cells (p<0.001). CONCLUSIONS: AT reduces asthma phenotype involving SOCSJAK- STAT signaling.

Temporal change in species and functional plant traits in the moist grassland on the Sete Cidades National Park, Piauí, Brazil.

The present study investigated the dynamic on a short-time scale in the vegetation in moist grassland of the Sete Cidades National Park, Piauí. Herb-subshrub layer samples was carried out in July 2007, 2009 and 2011. Changes in structural, floristic and functional traits in the community were assessed by species richness, diversity and similarity indices between those periods, as well as by hierarchical classification and ordination. Cluster and Principal Component Analyses identified functional groups according to 23 species trait state. To distinguish the contribution of space and time configuration in the community structure, we used the variance partition technique. The functional groups of chamaephytes and therophytes II were associated with wetter sites, while the groups of non-tussock hemicriptophytes I, tussock hemicriptophytes (FG4), and geophytes (FG5) were associated to the drier ones. We found a non-accelerated dynamics, at least on a short-time scale, represented by some descriptors in the community, such as the close similarity between the inventories and ordering of sampling transects in moist grassland. Therefore, besides considering the partition of the temporal niche as a mechanism for the co-existence of species, the heterogeneity of space dictated by environmental filters seems to determine the stability of the this grassland communities over time.

Exercise deactivates leukocytes in asthma.

Leukocytes play a central role in asthma physiopathology. Aerobic training (AT) reduces leukocytes recruitment to the airways, but the effects of AT on some aspects of leukocytes activation in asthma are unknown. Therefore, the effects of 4 weeks of AT on airway inflammation, pulmonary and systemic Th2 cytokines levels, leukocytes expression of pro and anti-inflammatory, pro-fibrotic, oxidants and anti-oxidants mediators in an experimental model of asthma was investigated. AT reduced the levels of IL-4, IL-5, IL-13 in bronchoalveolar lavage fluid (BALF) (p<0.001), serum levels of IL-5, while increased BALF and serum levels of IL-10 (p<0.001). In addition, AT reduced leukocytes activation, showed through decreased expression of Th2 cytokines (IL-4, IL-5, IL-13; p<0.001), chemokines (CCL5, CCL10; p<0.001), adhesion molecules (VCAM-1, ICAM-1; p<0.05), reactive oxygen and nitrogen species (GP91phox and 3-nitrotyrosine; p<0.001), inducible nitric oxide synthase (iNOS; p<0.001), nuclear factor kB (NF-kB; p<0.001) while increased the expression of anti-inflammatory cytokine (IL-10; p<0.001). AT also decreased the expression of growth factors (TGF-beta, IGF-1, VEGF and EGFr; p<0.001). We conclude that AT reduces the activation of peribronchial leukocytes in a mouse model of allergic asthma, resulting in decreased airway inflammation and Th2 response.

Interleukin-18 and interferon-gamma polymorphisms are implicated on proviral load and susceptibility to human T-lymphotropic virus type 1 infection.

Interleukin-18 (IL-18) and interferon-gamma (IFN-γ) exert important functions in both innate and adaptive immune responses against intracellular pathogens and viruses. Previous studies suggested that host genetic factors, including cytokines gene polymorphisms, could be involved in the pathogenesis of human T-cell leukemia virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Thus, we analyzed -137C/G and -607A/C of the IL-18 promoter and +874T/A of the IFN-γ in DNA samples from 98 HTLV-1-infected individuals exhibiting or not clinical symptoms and 150 healthy control individuals. The IL-18 promoter -607CC genotype was significantly lower in HTLV-1 asymptomatic carriers (HAC) and HTLV-1-infected individuals (HAC + HAM/TSP) than healthy control group. In contrast, the -607AC genotype was significantly higher in HAC and HTLV-1-infected individuals group compared to the healthy control group. The -137G/-607A IL-18 haplotype was higher in infected group than healthy control group, and the -137C/-607C IL-18 haplotype was increased in the healthy control group compared to the others. Finally, the IFN-γ polymorphism analysis showed that the HTLV-1-infected individuals with +874AT genotype presented higher proviral load than +874AA genotype. These data indicate that the IL-18-607AC genotype and -137G/-607A haplotype could be a risk factor for HTLV-1 infection, whereas the protective effect could be conferred by -607CC genotype and -137C/-607C haplotype. Also, the IFN-γ could be implicated on the proviral load levels.