in the Japanese Dental Science Review is an interesting and unique paper comprehensively describing the classical and recent publications on the mandibular condylar cartilage, containing 98 references, covering a wide range from clinical Nivolumab supplier to biological studies [1]. Mandibular condylar cartilage is termed secondary cartilage because of its characteristic developmental process, emerging from the distal and lateral part of the mesenchymal cell aggregate (the anlage of mandibular condyle), apart from Meckel’s cartilage, and unites

with the anlage of the mandible (the mandibular ramus) [2]. In terms of the anatomical localization, the principal function of this cartilage is to provide a smooth lubricated surface for articulation and to facilitate the absorption and transmission of the mechanical load with a low frictional coefficient during jaw movement, i.e. chewing. In addition, a distinct feature of the mandibular condylar cartilage is to undergo endochondral ossification, regulated by pleitropic hormones, such as growth hormones, parathyroid hormone-related protein, basic fibroblast growth factor, and insulin-like growth factor-1 during

the developmental process [3] and [4], thereby serving as the growth center of the mandible, similar to the growth plate in the long bone. The mandibular condylar cartilage has characteristic features in its cellular components, extracellular matrix composition and degrading enzymes, and hormonal and mechanical regulation. PD0332991 chemical structure Generally, cartilage below tissue consists of a relatively small number of cells and an abundant extracellular matrix consisting of collagen types II, VI, IX, X, and XI and

aggrecan. For example, the growth plate cartilage of the long bone contains mostly type II collagen, while the mandibular condylar cartilage contains type I collagen, usually lacking in most cartilages. Reportedly, the mandibular condylar cartilage cells, but not the long bone cartilage cells, express cathepsin L, which degrades type I collagen and proteoglycan aggregates at low pH as well as collagen types II, IV, IX, and XI, even at pH values close to neutrality [5]. Further elucidation of these unique biological properties may clarify not only mandibular growth and development, but also help in developing new treatment strategies for deformities of the orofacial complex caused by impaired mandibular growth. “
“Periodontal diseases are the most common inflammatory diseases caused by plaque biofilm in the oral cavity. During the progression of periodontal diseases, the pathological change of gingivitis to periodontitis is characterized by the irreversible loss of tooth supporting apparatus, ultimately leading to the loss of the tooth. It includes the progressive destruction of whole periodontal tissue: the gingiva, periodontal ligament (PDL), cementum, and alveolar bone, as well as the connective tissue attachment between the root surface and alveolar bone [1].

Thermocycling showed no significant effects on the bond strength of 3-step etch and rinse system to caries-affected dentin, although there were significant reductions in bond strength to sound dentin. Moreover, for 1-step and 2-step self-etch adhesives, no significant effect on bond strength was detected when bonded to sound and caries-affected dentin [46]. Fluid penetration into the resin–dentin interface occurs via dentinal tubules under constant hydrostatic pulpal pressure, as well as via the dentin margin. Therefore, the presence of mineral LGK-974 datasheet deposits in dentinal tubules may alter the bonding durability between normal and caries-affected dentin. Nakajima et al. [47] reported that constant

hydrostatic pulpal pressure during 1-month storage significantly decreased the bond strength of 2-step self-etch system to normal dentin, but did not affect the bond strength to caries-affected dentin. The lower dentin permeability of caries-affected dentin may therefore reduce water penetration into the interface, leading to long-term stability of the interface when there is no direct exposure to water in presence of the surrounding bonded enamel. Tubular occlusion may prevent water entrapment,

this website being manifestations of evaporative and convective water flux from dentin, at the resin–dentin interface [49]. Current one-step self-etch adhesives show higher hydrophilicity, and attract water from the hydrated dentin substrate during application on the adhesive surface and absorb water even after polymerization. Ultrastructurally, water entrapment in the 1-step self-etch adhesive layer is observed in the bonded normal dentin specimen as water-filled channels (i.e. water-tree, water-droplet), however water-treeing and water-droplet formation can be eliminated in the bonded caries-affected dentin specimen [49]. In the absent of water fluxes from caries-affected dentin, a one-step self-etch adhesives might initially establish a better seal along the interface. Cobimetinib supplier However, the absorbed water in the adhesive

layer would cause hydrolytic degradation of resinous materials over time, compromising the integrity of the resin–dentin interface. Some researchers have evaluated the effect of caries removal method on bonding to caries-affected dentin [50] and [51]. Using etch and rinse system of Single Bond (3M), caries removal methods (steel bur in a slow-speed handpiece, air abrasion with aluminum oxide particle, partially diamond-coated oscillating tip with airscaler, hand excavator with Carisolv) did not affect the bond strength to caries-affected dentin [50]. This result is in agreement with another study using etch and rinse system of OptiBond Solo Plus Total-Etch (Kerr), in which there were no significant differences in bond strength to caries-affected dentin between excavation by a steel round bur in a slow-speed handpiece, Er:YAG laser and 600-grit SiC paper [51].

The number of animals and intensity of noxious this website stimuli used were the minimum necessary to demonstrate consistent effects of the drug treatments. The animals were intraperitoneally (i.p.) pre-treated with vehicle (saline, 10 ml/kg) and STK-1000R (0.01, 0.1, 1 and 10 mg/kg), 30 min before the i.p. injection of 0.6% aqueous acetic acid (0.45 ml/mouse, made up in saline). The abdominal constrictions were counted over a period of 20 min (Rodrigues et al., 2012). The mice received 20 μl of a 2.5% formalin solution (0.92% formaldehyde, in saline) intraplantarly under the ventral surface of the right hindpaw. Animals were observed from 0 to 5 min (early phase) and 15

to 30 min (late phase) and the time that they spent licking the injected paw was considered as indicative of nociception (Rodrigues et al., 2012). Animals were treated with vehicle (saline, 10 ml/kg, i.p.) and STK-1000R (0.01, 0.1 and 1.0 mg/kg, i.p), 30 min before the formalin injection. Data were expressed as means ± standard error of mean (S.E.M.) with 6–8 animals per group. Comparisons between experimental and control groups were performed by one-way analysis of variance (ANOVA)

followed by Newman–Keul’s test. P values less than 0.05 were considered as indicative of significance. The pulp of tamarillo fruits was freeze–dried (yielding buy E7080 a moisture content of approximately 80%). The dried pulp powder (235 g) was then de-fatted with chloroform–methanol (1:1) in a Sohxlet apparatus, yielding nonpolar compounds at a content of approximately 26%. The defatted residue was then submitted to successive extraction with water and 10%

aq. KOH, both at 100 °C, and the extracted polysaccharides (fraction TW and TK, respectively) recovered Dolichyl-phosphate-mannose-protein mannosyltransferase by EtOH precipitation and dialysis, respectively (Fig. 1B). The fraction TW was obtained in 9.0% yield, while fraction TK was a polysaccharide obtained in only 1.0% yield. Both fractions were submitted to freeze–thaw treatment, giving rise to precipitates (PTW, 0.5% yield and PTK, 0.1% yield, each) and supernatants (STW, 6.0% yield and STK, 0.9% yield). The monosaccharide analysis of PTW revealed only arabinose (32.0%) and glucose (68.0%). The glucose content was due to starch, with typical 13C NMR signals at δ 100.6 (C-1), 72.1 (C-2), 73.2 (C-3), 78.9 (C-4), 71.7 (C-5) and 60.7 (C-6). To remove this polysaccharide, an α-amylase digestion was performed. Thereafter, only arabinose was detected on monosaccharide analysis, indicating the presence of an arabinan. The HSQC spectrum of the arabinan is given in Fig. 2A. The data suggested that the arabinan contained a linear structure and (1 → 5)-linked α-l-arabinofuranosyl units, due to the presence of exclusively five signals in the spectrum. The assignments of the signals were done by COSY and HSQC experiments and are shown in Fig. 2A. The C-5 O-substitution was confirmed with DEPT-135 experiment ( Fig.

In the last stage of the purification process, the active fractions were eluted from a phenyl-sepharose column when the salt gradient had been exhausted. This procedure resulted in a purification factor of 99.3 with 8% recovery of the original β-glucosidase activity. The GSK1120212 price electrophoretic profile of the enzyme in SDS–PAGE confirmed the presence of a single protein band with an estimated molecular mass of

65.15 kDa ( Fig. 1). Substantial activity against pNPβGlc was observed for the purified enzyme within a pH range of 5.5–7.0 and temperature range of 30–50 °C. The optimum pH for the enzyme was 6.0 ( Fig. 2A) and the β-glucosidase achieved maximal substrate hydrolysis at 45 °C ( Fig. 2B). This optimum pH value is the same as those reported for hydrolysis of pNPβGlc by the β-glucosidase from apple seed ( Yu, Xu,

Lu, & Lin, 2007), from Pyrococcus furiosus ( Yeom et al., 2012) and from the endophytic bacterium Pseudomonas ZD-8 ( Yang, Ning, Shi, Chang, & Huan, 2004). The β-glucosidase from Termitomyces clypeatus also exhibited maximal activity against pNPβGlc at 45 °C ( Pal et al., 2010). The purified D. hansenii UFV-1 β-glucosidase maintained approximately 51% of its original activity after 6 h www.selleckchem.com/products/chir-99021-ct99021-hcl.html of pre-incubation at 45 °C and 30% after 60 min at 50 °C ( Fig. 2C). The half-life of D. hansenii UFV-1 β-glicosidase at 45 and 50 °C was 312 and 73 min, respectively. Stability of this enzyme was also evaluated at 4 °C and through at room temperature (25 °C). The enzyme maintained 97% and 62% of its original activity after 30 and 90 days of incubation at 4 °C, respectively. When kept at room temperature, the enzyme maintained 67% and 47% of its original activity after 5 and 15 days, respectively. The D. hansenii UFV-1 β-glicosidase showed significant stability over a

wide pH range. This enzyme retained more than 90% of its activity after incubation for 30 min in a pH range of 5.5–8.0. About 85% and 64% of its activity was maintained after incubation at pH 4.5 and 4.0, respectively, and enzymatic activity was null after incubation at pH values below 3.5 ( Fig. 2A). The enzyme showed significant stability for a wide pH range and reasonable temperature levels which is desirable for industrial applications, especially for hydrolysis of isoflavones in soybean products. Immobilised D. hansenii UFV-1 cells containing β-glucosidase showed substantial activity within the same pH range of the free enzyme (5.5–7.0) and over an even larger temperature range (20–55 °C). In this case, the optimum pH was 5.5 ( Fig. 2D), lightly more acidic than the optimum pH of the free enzyme, which was 6.0. This decrease in optimum pH after immobilisation in calcium alginate can be partially explained by the effect of the micro-environment in the calcium alginate gel matrix, particularly due to the presence of positively charged Ca2+ ions ( Adami, Cavazzomi, Trezzi, & Craveri, 1998).

7 N to 6.9 N. This decline was expected and widely documented due to the action of cell wall degrading enzymes ( Civello et al., 1999, Ferreyra et al., 2007, Salentijn et al., 2003 and Trainotti et al., 2001). The highest transcript accumulation of Exp2 and Exp5 occurred in stages 1 and

2 ( Fig. 1B and C), while the fruit Ku-0059436 in vitro was immature and flesh firmness was high ( Fig. 1A). Expansins, non-enzymatic proteins, are known to act during early stages of fruit development in the process of cell wall polysaccharide solubilisation ( Civello et al., 1999 and Harrison et al., 2001). Therefore, the high transcript accumulation prior to fruit softening confirmed Exp2 and Exp5 as precursors in the softening process in strawberries ( Civello et al., 1999 and Harrison et al., 2001). Transcript accumulation of PLa and PLb was also high at early stages of fruit development (1 and 2) and followed a down-regulation when fruit were turning red ( Fasudil Fig. 1D and E). On the other hand, PLc transcripts accumulated at higher levels during strawberry maturation (stages 4 and 5) ( Fig. 1F). Probably, PLa and PLb are associated with cell division processes while PLc is involved in cell wall disassembly during fruit maturation. PME ( Fig, 1G) and PG ( Fig.

1H), known to be involved in fruit softening ( Castillejo et al., 2004 and Redondo-Nevado et al., 2001), had high transcript accumulation after stage 3, which means that their transcript level during stage 2, although lower than the following

stages, was enough to induce softening, or that the dramatic decline in firmness was not entirely dependent on these two genes. β-Gal transcript accumulation was relatively low, apart from stage 5 (fully ripe stage) ( Fig. 1I). Trainotti et al. (2001) characterised three β-Gal genes; Faßgal1, expressed Fenbendazole during maturation, and Faßgal2 and Faßgal3 expressed in green fruit and other tissues. In the current work, β-Gal primers corresponded to Faßgal1, which encode an enzyme acting on galactose, generated from pectin hydrolysis. This way, higher transcript accumulation of β-Gal was expected in an advanced maturation stage, when higher concentration of pectin hydrolysis products is present. Generated from PME and PG action, pectin hydrolysis products serve as substrate for β-galactosidases demonstrating a coordinated process, in which, peaks of transcription occur in order: first Exp2, Exp5, PLa and PLb, then PLc, PME and PG, then β-Gal. Total anthocyanin content increased significantly (P ⩽ 0.05) with fruit development reaching 23.4 mg 100 g−1 during stage 5 ( Table 2). The onset of red colour was correlated with an increase in total anthocyanin content, as expected. The highest total phenolic content was observed during stage 1 (965.5 mg GAE100 g−1) and its levels dropped at stage 2 (628.2 mg 100 g−1), then increased over time reaching 752 mg GAE100 g−1 during stage 5.

Reports of PFBS in wild mammalian tissues are relatively uncommon in the international literature and has only recently

been found in harbor seals from the Dutch Wadden Sea (1.74–3.28 ng/g spleen) (Van de Vijver et al., 2005), in harbor seals from the German Bight (up to 3.1 ng/g liver) (Ahrens et al., 2009) and in gray seals from the Baltic Sea (up to 3.5 ng/g liver) (Kratzer et al., 2011). The concentrations were approximately the same as in INCB024360 the mink in our study (Table 1), although PFBS was only found in 27–55% of the samples (compared to 89% in our study). In addition, PFBS has been found in sea turtles from the east coast of USA (< 0.02–0.846 and < 0.01–0.195 ng/g serum) (Keller et al., 2012 and O'Connell et al., 2010). In contrast, PFBS was below detection limit in all samples of Arctic and North Atlantic pilot whale, ringed seal, minke whale, harbor porpoise, hooded seal, white-sided dolphin and fin whales (Rotander et al., 2012). Also, PFBS was not detected in ringed seal populations in the Canadian Arctic (Butt et al., 2007 and Butt et al., 2008), nor in common guillemot from the Baltic Sea (Berger, 2008) or harbor porpoise in the North and Baltic Sea (Huber et al., 2012). PFBS is persistent (Quinete et al., 2010), but not expected to be as bioaccumulative as PFAAs with longer carbon chains (Conder et al., 2008). However, as a replacement

for PFOS, the use of this compound will probably increase in the future. Selleck Cobimetinib Mink, with its wide geographical distribution and the proximity of its habitat to human activities, could be a suitable sentinel species for monitoring PFBS exposure to mammals. The sampling areas in this study were selected because of their assumed differences in contamination and this was confirmed by the multiple regression Cytidine deaminase model,

which showed that area of sampling was significantly influencing the concentrations of PFHxS, PFOS, PFNA, PFDA and PFUnDA (p = < 0.001–0.01). The multiple regression models explained 18–53% of the variation in the tissue concentrations. Pairwise comparisons of least squares between the areas are given in Table 1. To visualize the variation in contaminant concentrations in the four areas, a PCA model (R2 = 0.52, Q2 = 0.119) containing 3 significant principal components according to cross validation was calculated. Scores and loadings plots of component 1 versus component 2 are given in Fig. 1 and Fig. 2, explaining 23% and 15% of the variance, respectively. The scores plot is a summary of the relationships among the observations (mink). The loadings plot can be used to interpret the patterns seen in the scores plot, as the plots are superimposable. Plots of component 2 versus 3, the descriptive data for the components and the R2 and Q2 calculated for each variable are found in the Supplementary data. In the PCA scores plot (Fig.

The crown ratio model is an important submodel that influences the predictions of diameter increment. It is therefore interesting to know how well the predictions of this submodel agree with observed values. The highest crown ratios would be expected for

open-grown trees. Typically, crown ratios of open-grown Akt inhibitors in clinical trials spruce range from 0.91 to 0.94 (Lässig, 1988 and Stampfer, 1995), and crown ratio of open-grown pine is 0.86 (Stampfer, 1995). The light demanding pine trees can have a number of dying branches even on open-grown trees (Stampfer, 1995), due to self-shading. For stand grown trees, crown ratios would be high in sparse stands and low in dense stands. For open-grown tree, the find more simulated crown ratios of Moses (always 1.0) and Prognaus (>0.96 for spruce, >0.67 for pine) agree well with observations on open-grown trees. Crown ratios

predicted by BWIN and Moses were more variable but they could be as low as 0.5 for spruce and 0.3 for pine. This is clearly too low for open-grown trees and rather corresponds to crown ratios of dominant stand grown trees. Abetz and Künstle (1982) reported crown ratios of 0.3–0.7 for dominant spruce. The high crown ratios of open-grown trees might be underestimated because sparse stands are often lacking in the data sets. BWIN and Silva were both fit from permanent research plots, which are usually fully stocked. On the other hand, Prognaus was fit from Forest Inventory data, which covers a larger variety of stocking degrees. Moses uses a function that forces a crown ratio of 1, if the competition index is 0. For stand-grown

trees, the average crown ratios were predicted well by all four simulators, with deviations being mostly less than 0.06, and IKBKE only in some cases as high as 0.22. This agrees well with differences of 0.018, 0.02, and 0.246 in crown ratio after a 20-year simulation ( Sterba et al., 2001). The variability in crown ratio is best predicted by a dynamic model, as implemented in Moses. We expected that individual-tree growth models would correctly predict height:diameter ratios. The findings of our investigation generally support these expectations. Height:diameter ratios predicted by all four growth models are within the bounds defined by open-grown trees and very dense stands. Furthermore, all models show an increase of height:diameter ratios with increasing density, a decrease with age, and lower height:diameter ratios for dominant trees than for mean trees. A word about misclassification costs: the cost of under-estimating height:diameter ratios can greatly exceed costs of overestimation. Consider a collection of stands near the 80:1 threshold of stability.

Thus, to determine the upstream

signaling pathway involved in KRG-mediated COX-2 inhibition, we measured the activation of p38 and CREB by detecting increased phospho-p38 and phospho-CREB levels in acrolein-stimulated cells and found that phosphorylation of p38 and CREB was strongly reduced by KRG in acrolein-stimulated cells (Fig. 4). These results demonstrate the role of p38 and CREB signaling in the inhibition of acrolein-mediated COX-2 induction. Fluorescence-activated cell sorting showed that while the number of apoptotic cells increased following INCB024360 in vitro treatment with acrolein, pretreatment with KRG reduced the number of apoptotic cells (Fig. 5A). To confirm this result, we evaluated the presence of dead cells by TUNEL staining, which is widely used in detecting DNA fragmentations in situ. The TUNEL assay indicates cell death, including apoptosis, by detection of the appearance of intensely stained nuclei, which indicates incorporation of labeled dUTP into the 3′-end of fragmented DNA derived from apoptotic nuclei. As illustrated GPCR Compound Library in Fig. 5B, acrolein treatment significantly increased the proportion of TUNEL-positive cells, which was restored by KRG pretreatment. These results revealed that the vascular protective effect

of KRG is mediated by the inhibition of COX-2 expression in acrolein-stimulated HUVECs. In this study, we explored the inhibition of an inflammatory mediator, COX-2, by KRG water extract in HUVECs. We found that KRG inhibited both mRNA and the protein level of COX-2 and its cytoprotective effect in acrolein-stimulated HUVECs. There is increasing evidence that α,β-unsaturated aldehydes in CS, including

acrolein and crotonaldehyde play an important pathophysiological role in vascular diseases such as atherosclerosis and Alzheimer’s disease. Exposure to α,β-unsaturated aldehydes is critical to the inflammatory response via activation of the proinflammatory signaling pathway and redox-sensitive transcription factors [27] and [28]. Furthermore, α,β-unsaturated aldehydes increase oxidative stress [29], which plays a crucial role in the pathogenesis of vascular diseases via direct injury to the endothelium [30]. COX-2, a key enzyme for prostaglandin biosynthesis, is an inducible enzyme that is rapidly induced during inflammatory reactions. Regorafenib solubility dmso Numerous studies have reported the involvement of CS in vascular diseases through COX-2 and endothelial NO synthase activity [31] and [32]. Increase of COX-2 expression was reported to promote atherosclerotic inflammation [33]. Chronic inflammation plays an important role in vascular diseases, therefore, COX-2 may participate in the development of inflammation-related diseases, including vascular diseases. Ginseng has been used as a general tonic for >2000 years in East Asia, and it has become a famous herbal medicine for treatment of various diseases, including vascular disorders.

0 (five instances) to 0.76 with the mode in the 0.6–0.65 interval (Supplemental Fig. S1). Figure options Download full-size image Download high-quality image (354 K) Download as PowerPoint slide We selected loci that have multiple alleles in most to all of the 54 populations and are independent at the population level, i.e., that are on separate chromosomes or sufficiently far apart on the same chromosome to show minimal linkage disequilibrium. When two syntenic candidate microhaps were sufficiently close to show significant LD in several populations, we selected the locus with higher average heterozygosity in more or all of the eight major geographical regions into

which the populations cluster (see Table S1). Our development of this panel has been undertaken to demonstrate Selleck Androgen Receptor Antagonist that such a SNP-based resource can be developed and be of value in lineage/familial identification. By the very nature of these 31 multiallelic Everolimus supplier loci that we have documented, proof of principle now exists. We also find the microhap loci have value for ancestry inference and individual identification. The SNP and haplotype

frequencies for the microhaps in this study are available from the authors. They are also available in the web-accessible ALFRED database (http://alfred.med.yale.edu) where they can be retrieved in a search by using the key word “microhap”. The size (molecular extent) range of the 31 microhaps is 18 bp to 201 bp with an average of 107.5 bp and a median value of 97 bp. The overall levels of heterozygosity and genotype resolvability are very good. A locus with only two alleles (e.g., a single SNP) can have heterozygosity no greater than 0.5, while a locus with three alleles can have heterozygosity of 0.667.

In general, the maximum heterozygosity occurs when all alleles have the same frequency. The median heterozygosity for these 31 loci is 0.55 for the 54 populations studied and ranges from 0.40 to 0.63. GNA12 26 of the 31 microhaps have heterozygosity greater than 0.5. Heterozygosity levels and genotype resolvability are also very good when examined for each of the eight major geographical regions into which the populations are grouped. The native populations of the Pacific Islands (4 populations) and the Americas (7 populations) have the lowest (but still very good) median heterozygosities of 0.53 and 0.54, respectively. Most of the 31 microhaps are on separate chromosomes or separated by molecular distances (>95 Mb) at which linkage is unlikely to exist. Eleven inter-microhap distances among syntenic loci are smaller (up to 67 Mb, cf. Table 1) and cannot be assumed to be segregating independently in families. However, the molecular extent of linkage disequilibrium (LD) varies greatly around the genome and occasionally exceeds 100 kb.

Nicholas Hopkinson was also funded by The Wellcome Trust and Mark Dayer by The British Heart Foundation. The study was supported by the NIHR Respiratory Biomedical Research Unit at Royal Brompton and Harefield NHS Foundation Trust and Imperial College, London. “
“Aluminum refinery workers are constantly exposed to aluminum oxide (Al2O3) obtained from bauxite (Musk et al., 2000), MK-2206 price reporting respiratory symptoms. Decreased lung function and lung inflammation have been observed

in epidemiologic (Kraus et al., 2000 and Fritschi et al., 2003) and experimental (Halatek et al., 2005, Ichinose et al., 2008 and Mazzoli-Rocha et al., 2010) studies. Neighborhoods of the aluminum oxide industry are also exposed to concentrations of alumina dust, making these communities susceptible to develop respiratory

alterations (Chattopadhyay et al., 2007). High intensity exercise practiced under stressed conditions triggers a transitory state of low immunity (Brenner et al., 1994). On the other hand, while regular exercise can be beneficial to health, a sedentary style of life is detrimental to it (Brines et al., 1996). Daily physical activity may be able to modulate the immune system (Brines et al., 1996), increasing the resistance to respiratory infections (Oliveira et al., 2007 and Malm, 2006). Regular exercise improves histology, decreases free radical production Rigosertib concentration and increases the activity of anti-oxidant enzymes in mice exposed to cigarette smoke (Menegali et al., 2009). Recently, Toledo et al. (2012) demonstrated that physical training minimized the reduction in lung elastance and

reduced oxidative stress in mice exposed to cigarette smoke. Hence, the aim of this study Ureohydrolase was to evaluate whether regular exercising prevents pulmonary alterations induced in a murine model of acute exposure to alumina dust. Twenty-three female BALB/c mice (20–25 g) were randomly divided into 2 groups: control (C, n = 10) and exercise (E, n = 13) that swam for 15 min/day, 5 days per week during 4 consecutive weeks (E), or remained sedentary (C). After a 4-week training, all animals were exposed for 1 h in a whole-body chamber to either sterile saline (CS, n = 6 or ES, n = 4) or to a suspension of 8 mg/m3 of alumina dust (CA, n = 6 or EA, n = 7) collected in an aluminum refinery, both delivered by an ultrasonic nebulizer. Each animal rested in a container, which was made of high clarity polypropylene falcon tubes whose conical tips were cut off and replaced by metal meshes and whose lids were perforated; the containers rested side by side inside the exposure chamber ( Mazzoli-Rocha et al., 2010). All animals were analyzed 24 h after saline or alumina dust exposure.