Thus, the present study provides new insights into the genes/pathways in CD4 T-cells that collectively might play a role in diabetes development – resistance in NOR mice or susceptibility in NOD mice. The BCL2L1 pathway and the genes within Idd13, Idd9/11 and Idd27 that are altered at all 3 ages (Pldn, Trp53bp1, Tmem87a, Ctdspl2,

Gatm, Raly, Khdrbs1, and Trim12a and Trim5/12c) make particularly interesting candidate genes/pathways as they most likely represent basic genetic defects in the NOD mouse. While our find more study has highlighted prime candidate genes, future studies will confirm which of the NOD altered genes and/or their interacting partners or regulators act interactively to effect the diabetogenic activity of NOD CD4 T-cells. In our lab, we are investigating the genetic loci underlying the expression of the altered CD4 T-cell molecular network to define key regulatory loci. The majority of the CD4 T-cell NOD altered CHIR-99021 supplier genes were repressed, similar to the results of the spleen leukocyte study [25] and supported by many other studies

in both mice and humans [[36], [37], [38], [39], [40], [41] and [42]]. Kodama et al. [36] reported global repression of genes in various tissues of NOD mice (including spleen cells) in comparison to NOD.B10 controls, a strain in which the NOD MHC haplotype is replaced with that from the nondiabetic B10 mice. Liston et al. [37] also found a global dampening in gene expression in NOD thymocytes of the genes involved in T cell negative selection. They identified several differentially expressed type 1 diabetes candidate

genes, among them four genes (Ly6c, Prim2, Trim12, and Trim30) whose expression was also dampened in our study, thus providing supporting evidence for possible involvement of these candidate genes in CD4 T-cells as well. Heinig et al. [38], in a systems-genetics study investigating rat tissues and macrophages and human monocytes, discovered that the IRF7-driven inflammatory network (which is enriched for innate immune response genes) is associated with type 1 diabetes risk. Interestingly, homologs of 9 of the genes belonging to this network (Lcp2, Oas1a, Rtp4, Ifit1l, Ifit1, Ly6c1, Ifit3, Sp110, and Trim21) were also repressed in NOD mice, for suggesting a similar network may also be altered in CD4 T-cells of NOD mice and might contribute to diabetes development in the mouse. Similarly, in human T1D studies, Elo et al. [39] found early suppression of immune response gene expression in whole blood samples of children in the prediabetic phase who eventually developed clinical diabetes. Furthermore, Orban et al. [40] also found repression of all genes that were differentially expressed in whole untreated human peripheral blood CD4 T-cells from new onset T1D patients, including genes involved in key immune functions, such as adhesion molecules lymphocyte function-associated antigen 1 (LFA-1) and P-selectin.

This method not only effectively seals the restoration margins in the long term, but also protects the more vulnerable bonds to dentin against degradation EGFR inhibitor [2]. The strength of the

micromechanical attachment of resin to etched enamel has proven adequate for retention in most clinical applications. Enamel is composed mainly of crystalline hydroxyapatite. The inorganic crystals are arranged in an orderly microstructure, which allows selective acid etching to produce a pattern into which the resin can penetrate and interlock [3]. Reliable adhesion to enamel can be achieved, but the bonding performance with dentin has been less consistent. On the other hand, it has been advocated that even with the good sealing of enamel margins with phosphoric acid etching, resin–dentin interface produced by the etch and rinse adhesive showed signs of degradation [4]. So one

should consider that the limitation of enamel sealing in terms of durability of dentin bonding. Dentin has a significant organic content that varies with depth, and lacks the orderly microstructure of enamel. Its structure is characterized by dentinal tubules, the spacing and orientation of which depend on the location and depth of the dentin surface [5]. In vital teeth, these tubules provide direct access to living processes and, ultimately, the pulp (Fig. 1). Opening up the dentin tubules by acid etching significantly increases the dentin permeability [6]. Leakage of pulpal

fluids from the tubules under hydrostatic pressure might disrupt attempts at chemical bonding to the dentin surface. Early attempts to achieve bonding GSK1210151A chemical structure to dentin by extending the enamel acid-etching technique were unsuccessful [7]. As mechanical attachment to etched dentin is not a viable alternative, research has instead focused on forming some type of chemical bond to one or both of the main constituents of dentin (that is, organic collagen and inorganic hydroxyapatite) [8]. It has been proposed that the removal of mineral phase from the dentin by acid etching exposes the dentinal collagen matrix as a bonding substrate, thinking as a practical approach to improve bonding Bay 11-7085 to dentin [9]. The hydrophilic functionality of the adhesion monomer helps facilitate permeation of itself into the exposed collagen fibrils leading to the formation of hybridized layer, whereas the hydrophobic functionality facilitates bonding to the resin composites. The process of hybridization is believed to result from the infiltration of the resin monomer into the collagen fibrils exposed by dentin demineralization, and in situ polymerization. The presence of cutting debris on instrumented dental surfaces in the form of a smear layer and smear plugs that obstruct the dentin tubules is also a significant cofactor [10]. The smear layer should be removed before chemical bonding to the dentin surface is attempted.

Endothelial cells, which are positive for Tie-2, have been reported to differentiate NLG919 molecular weight into chondrocytes and osteoblasts heterotopic cartilaginous and bone tissues in FOP but not in normal skeletal tissue [74] and [75]. In endothelial cells, over-expression of mutant ALK2 found in FOP induced their endothelial-to-mesenchymal transition and differentiation into chondrocytes, osteoblasts and adipocytes [75]. Treatment with BMP-4 or TGF-β1

also induced similar changes in human endothelial cells in vitro [75]. However, lineage-tracing experiments reveal that endothelial cells failed to contribute to either the chondrocytic or osteoblastic populations within the BMP-2-induced ectopic skeletal tissues in mice [76]. Both chondrocytes and osteoblasts induced by BMP-2 developed

from the non-myogenic Sca-1+ and PDGFRα+ residential mesenchymal cells of the skeletal muscle [76]. Taken together, the results suggest that both myogenic and non-myogenic skeletal muscle cells have functional BMP receptors, but only non-myogenic mesenchymal cells contribute to heterotopic bone formation in vivo. Myostatin (also called GDF-8) is a member of the TGF-β family that is specifically expressed in skeletal muscle tissue [77]. Myostatin−/− mice are larger than wild-type Paclitaxel mice due to the increased size of their hypertrophic skeletal muscles [77]. From zebrafish to humans, an increase in skeletal muscle mass in response to a loss-of-function mutation of myostatin has been demonstrated, indicating that myostatin acts as a negative regulator of skeletal muscle mass. Myostatin

binds to ActR-IIA and ActR-IIB type II receptors similarly to several BMPs, whereas, in contrast to osteogenic BMPs, myostatin binds to ALK4 and ALK5/TβR-I type I receptors similarly to non-osteogenic members of the TGF-β family [78]. Phosphorylated Smad1/5/8 was found in normal skeletal muscle tissue in mice, suggesting that BMP-like activity is physiologically activated in the muscles [79]. Over-expression of noggin, an antagonist of BMPs but not of myostatin, prevented the hypertrophy of skeletal muscle in myostatin-deficient mice, suggesting that BMP signaling plays a role in the myostatin-deficient phenotype [79]. BMP signaling via Smad1/5/8 and Smad4 suppresses the expression Vitamin B12 of MUSA-1, a ubiquitin ligase that induces the atrophy of skeletal muscle, and myostatin signaling via Smad2/3 inhibits the expression of MUSA-1 by competing with Smad4 [79]. Thus, BMPs are important physiological regulators of the skeletal muscle mass [80]. Since the original “BMP” activity was discovered a half century ago, BMPs have been shown to be critical factors in the development and regeneration of bone and cartilage. As Urist suggested in 1965, clinicians have repeatedly attempted to induce bone formation using BMPs. Recent findings suggested that BMPs are also involved in maintaining a normal skeletal muscle mass.

However, in this work, the addition of LiCl to the coffee husk did not affect the mycelial growth nor the BE of P. ostreatus mushrooms (P > 0.05, Table 1). The fact that BE was not reduced by the addition of different concentrations of LiCl may indicate (a) a resistance or tolerance of the fungus to the metal or (b) that the amount OSI-906 purchase of LiCl added to the substrate was not sufficient to cause inhibition or any toxic effect to the fungus. Some fungal mechanisms may have contributed to this tolerance, for example, a reduction of absorption or an increase in the efflux of metals through cell wall adsorption, the precipitation

of minerals and polysaccharides or extracellular binding by intracellular sequestration of metallothionein ( Gadd, 2007). The levels of minerals and the percentage of crude protein found in the mushrooms enriched with Li were consistent with data from the literature (Gençcelep et al., 2009, Kalac, 2009, Petrovska, 2001 and Sturion and Ranzani, 2000) and, therefore, the enrichment of the substrate with LiCl did not affect the nutritional quality of the mushrooms according to the parameters observed in this work (Table 2). The high concentration of Li in mushroom without enrichment (Fig. 1) can be due to the presence of Li in substrate without addition LGK-974 cell line of the lithium chloride (Table 2). In different vegetables concentrations of Li greater

than 200 ppm have been found (Schrauzer, 2002). Vetter (2005) observed concentrations less than those found in this work, when investigating wild mushroom growing in Hungary. This may be due to the low concentration of lithium in the soil. As shown in Fig. 1, the increase in the accumulation of Li in P. ostreatus mushrooms was directly dependent on the concentration of LiCl that was added to the coffee husk. This result shows the potential to use mushrooms enriched with

the desired concentration of Li to obtain a positive effect when administered to patients for psychiatric treatment. Although accessibility of a mineral cannot be considered Mannose-binding protein-associated serine protease synonymous with bioavailability, it is an important factor that affects bioavailability. In addition, for an element to be absorbed and possibly used by an organism, it must be in an accessible form in the intestinal fluid: (a) as a free ion or (b) as a complex with other nutrients (Elless et al., 2000). The chemical forms of highly accessible minerals are also considered more bioavailable. It can be seen, therefore, that minerals present in non-residual fractions (water-soluble, exchangeable, acid-soluble or reduced bound) are potentially more bioavailable than those present in the residual fraction (Rabinovich et al., 2007). The residual fraction is only solubilised chemically using a very aggressive extraction, which suggests that the mineral is not bioavailable.

These Dactolisib supplier are associated with vascular congestion and hypersensitivity pneumonitis resulting in extensive diffuse alveolar damage and ultimately ARDS.3 Most patients develop clinical signs within the first 24 h of silicone administration and the onset of symptoms has been linked to a higher mortality rate (20%).4 The most frequent symptoms include hypoxemia, dyspnea, fever, chest pain, cough and hemoptysis.1 Bronchoalveolar lavage (BAL) commonly reveals alveolar hemorrhage, and a restrictive

pattern is usually observed on pulmonary function studies. While the acute presentation is typical for the majority of patients, delayed-onset pneumonitis and injection-site inflammation occurring years after silicone administration has been described. Migration of micro-droplets of silicone could also assume a delayed presentation in the form of pulmonary fibrosis.4 Occasionally, pulmonary toxicity has been described to lag behind CNS manifestations especially when initial chest radiography and pulmonary this website examinations are benign in the presence of lethargy. Increasing release of silicone emboli from the source results in a slow progression to ARDS similar to the manifestation of heroin induced pulmonary

edema.5 Neurologic sequelae of silicone embolism vary from mild alteration in levels of consciousness to frank coma. Interestingly, the absence of underlying cardiac septal defects does not preclude the occurrence of neurologic manifestations, as microinfarcts in white matter

following cerebral silicone embolism has been described in these individuals and PJ34 HCl observed to be uniformly fatal.2 Large volume injections, high pressure infiltrations and prior exposure to silicone have been associated with a worse prognosis and increased rapidity of symptom onset.2 The presence of an IgG polydimethylsiloxane antibody which selectively binds to the silicone polymers has been implicated in this inflammatory process. Histology typically reveals multi-organ involvement with granulomas diffusely dispersed within the cardiopulmonary, renal, hepatic and gastrointestinal organ systems. Histopathologic analysis with the aid of infrared spectrophotometry and atomic absorption reveals these granulomas to consist of silicone vacuoles, tissue macrophages, neutrophils, eosinophils and fibrin deposits. Pulmonary silicone embolism characteristically results in a consistent chest CT imaging pattern of bilateral peripheral ground-glass opacities and interlobular septal thickening as portrayed by the present patient.4 The mechanism of silicone injury to pulmonary capillaries closely mimics fat embolism with the occurrence of bilateral alveolar hemorrhages and diffuse presence of silicone droplets in pulmonary alveolar macrophages and lung capillaries.

At pH 1.0 the anthocyanins were predominantly in the flavylium cation form, whereas the proportion of this form significantly decreased at pH 3.0 and

almost disappeared at pH 5.0. In fact, at pH 5.0 the absence of absorption bands in the visible spectrum indicates that the http://www.selleckchem.com/products/ABT-888.html anthocyanins present in the functional extract were mostly in the colourless forms of hemiacetals and/or chalcones (Table 5). Colour parameters are consistent with the results obtained by UV–Vis, considering that at pH 1 the hue (h  ab) value was in the red-purple region, and the chroma value was 2–20 times higher than those obtained at other pH conditions ( Table 5). In addition, the FE had the lowest values of C∗C∗ at pH 3 and 5 (1.4 and 0.5, respectively) due to high concentration of the colourless forms. Finally, the bathochromic shift in the UV–Vis spectra observed at pH 7.0 and 9.0 as compared to pH 1.0, along with the colour characteristics at pH 7 (C∗=5.1C∗=5.1 and hab in blue region) indicated a shift in the equilibrium towards formation of the quinonoidal bases. The values of the decay constants (kDMA and kDMA+FE), used to calculate the percentage of protection against the 1O2 ( Table 5), were obtained from exponential fits

for the first-order decay curves of DMA at 375 nm, in the presence and absence of jambolão FE at pH 1.0 and 3.0 conditions (data not shown). The proportion of functional extract used in these analyses (2.45%v/v) was equivalent to monomeric anthocyanin concentration of 2.1 μg/ml. The results obtained (about 60%

of protection at both pH conditions) corresponds MAPK inhibitor to an activity Selleckchem Vorinostat higher than those reported by Wang and Jiao (2000), where percentages of protection against the 1O2 between 8% (blueberry) and 15% (strawberry) were obtained when a juice proportion of 5%v/v was used. Regarding the ABTS + scavenging capacity, the TEAC value at pH 5 was 2.2–2.7 times higher when compared to TEAC values at pH 1.0 and 3.0 (Table 5). These results indicated that the colourless forms of anthocyanins tend to have a greater free radical scavenging capacity than the flavylium cation form. Since the TEAC values under pH 7.0 and 9.0 conditions were similar to the one obtained at pH 5.0, both hemiacetals/chalcones and quinonoidal base forms show similar ABTS + scavenging capacities. The increase in the free radical scavenging capacity of anthocyanins with increasing pH was due to the higher reducing capacity showed by the colourless (hemiacetals/chalcones) and quinonoidal base forms of anthocyanins as compared to the flavylium cation species (Vieyra et al., 2009). TEAC values obtained at pH 5.0–9.0 (9.7–12.7 μmol Trolox/g fruit) are in the same range as the ones reported for jambolão fruits (15 μmol Trolox/g fruit, unbuffered aqueous solution) (Luximon-Ramma et al., 2003).

A major flaw in all the studies Selleck SCH772984 reviewed was the lack of any definition of toxicity or signs of pathology. Of all the studies generally assessing rat health on a GM diet, not one explained how the study would adequately show that the crop is safe for human and/or animal consumption. Furthermore, all the studies reviewed failed to justify or give reason for the choice of methods used. Yet, most studies concluded that the investigation did not reveal any meaningful differences between animals fed the GM or non-GM feed. One study even stated that “since no meaningful differences were observed, no further microscopic examinations were deemed necessary” (Hammond et al., 2004). However,

the absence of meaningful differences in a preliminary investigation does not mean that further analysis would not find meaningful differences. In addition, the authors did not small molecule library screening support this statement with proof since they provided few details as to what their microscopic examinations entailed or found. Therefore, they give very little evidence that their study adequately

assessed the safety of consuming the GM crop. Another common remark in these publications was that all changes observed were not diagnostically significant, were within the normal range, or are common to this strain and age of rat. The six studies that made this remark gave little evidence to support this conclusion (Hammond et al., 2004, Hammond et al., 2006a, Hammond et al., 2006b, Healy et al., 2008,

Qi et al., 2012 and Teshima et al., 2000). Most gave no evidence at all. For example, Qi et al. (2012) referenced a study by Tang et al. (2012) to support their notion that “microscopic observations occurred spontaneously in Sprague–Dawley rats of this age.” However, the referenced study made no mention of microscopic observations occurring spontaneously and the study did not even use Sprague–Dawley rats. A very common statement found in the reviewed studies was that since the lesions or changes were observed in both groups, they were not deemed to be diet-related (Healy et al., 2008, Sakamoto et al., 2007, Sakamoto et al., 2008 and Wang et al., 2002). For example, in two studies (Hammond et al., 2006b and Sakamoto et al., 2007), there was Meloxicam a brief mention of gastric gland dilatations being observed in both the GM and non-GM fed groups. Gland dilatations can occur in aged rats (Frantz et al., 1991), but they can also be a pathological occurrence for example in alendronate-induced injury (Şener et al., 2004), ulcer healing (Tarnawski et al., 1991) or underlying neoplastic lesions (Frantz et al., 1991). In these pathologies, the dilatations are large, they may sometimes extend into the submucosa and they may become dysplastic (Kikuchi et al., 2010). In the two publications (Hammond et al., 2006b and Sakamoto et al.

The interest has increased in part due to the introduction of the sequential sampling framework (for reviews, see Bogacz et al., 2006 and Ratcliff and Smith, 2004). To make a decision, it is assumed that the brain accumulates samples of sensory evidence IOX1 price until an absorbing choice boundary is reached. The inherent noise in both the physical stimulus and the neural signal makes the process stochastic, potentially leading to an incorrect choice. The rate of approach to a boundary is called drift rate, and depends on the quality

of the extracted sensory evidence. The boundary is hypothesized to be under subjective control, and can be modulated depending on timing demands. A higher boundary criterion will require greater evidence accumulation, leading to slower and more accurate decisions. The interaction between drift rate and choice criteria has an obvious property: it provides an integrated account www.selleckchem.com/products/fg-4592.html of both response time (RT) and accuracy in choice laboratory experiments. The drift diffusion model (DDM) developed by Ratcliff and coworkers (Ratcliff, 1978 and Ratcliff and Rouder, 1998) belongs to

this theoretical frame. The model was originally developed to explain simple two-choice decisions in terms of psychologically plausible processing mechanisms, and has proven to account for a large range of paradigms (for a review, see Ratcliff & McKoon, 2008). However, its extension to more complex decisions is not straightforward and is currently the object of an intense field of research in both experimental psychology (e.g., Hübner et al., 2010, Leite and Ratcliff, 2010, Smith and Ratcliff, 2009, Stafford et al., 2011, White et al., 2011 and White et al., 2011) and neuroscience (e.g., Churchland et al., 2008 and Resulaj et al., 2009). The present study aims to evaluate whether the DDM can be extended to conflicting situations, and contributes to this emerging field. As other sequential sampling models, the DDM posits that RT is the sum of two components, a non-decision time and a decision-related

time. The decision process takes the form of an accumulation PJ34 HCl of evidence delimited by two boundaries representing alternative choices. The starting point of the diffusion depends on prior expectations, and can be located everywhere on the axis joining the two alternatives, being closer to the more expected alternative. In each moment, the incremental evidence is the difference between sensory inputs supporting choice 1 versus 2. This difference is a random variable which follows a Gaussian distribution, with mean μ (drift rate) and variance σ2 (diffusion coefficient). The combination of sensory evidence into a single variable and its linear stochastic accumulation over time present an interesting property.

Fraction C4 (100 mg) was passed over a Sephadex LH-20 column (30 mm × 800 mm, 80 g) and then eluted with MeOH (500 mL) to obtain compound 20 (15 mg). Fraction E3 (1 g) was subjected to chromatography on ODS (30 mm × 150 mm, 50 g) and then eluted successively with solvents selleck kinase inhibitor of decreasing polarity (MeOH/H2O, 4:6 600 mL−6:4 600 mL−7:3 600 mL−9:1 600 mL−1:0 600 mL) to yield seven fractions, E3-1−E3-7. Compound 21 (8 mg) was obtained as granulated crystal from E3-6. Fractions F (18 g), G (15 g), H (20 g), and I (20 g) were subjected to chromatography on ODS (50 mm ×

250 mm, 250 g) and then eluted successively with solvents of decreasing polarity (MeOH/H2O, 3:7 3 L−5:5 3 L−7:3 3 L−9:1 3 L−1:0 3 L) to yield 11 fractions, F1−F11, eight fractions, G1−G8, seven fractions, H1−H7, and

eight fractions, I1−I8. Compound 1 (10 mg) was obtained as granulated crystal from F-5. Isolation of the following 15 compounds was performed by preparative HPLC: compounds find more 2 (18 mg; tR 75.0 min), 12 (30 mg; tR 38.9 min), 13 (20 mg; tR 46.8 min), and 14 (60 mg; tR 53.5 min) were isolated from fraction D3 (500 mg) by HPLC system I; compound 18 (4 mg; tR 41.8 min) was isolated from fraction A2 (60 mg) by HPLC system VI; compounds 3 (15 mg; tR 70.3 min), 4 (15 mg; tR 45.8 min), 5 (14 mg; tR 58.9 min), and 6 (14 mg; tR 65.9 min) were isolated from fraction I4 (200 mg) by HPLC system II; compounds 7 (40 mg; tR 33.5 min) and 8 (60 mg; tR 49.6 min) were isolated from

fraction H5 (500 mg) by HPLC system III; compounds 9 (8 mg; tR 17.5 min), 10 (70 mg; tR 26.5 min), and 11 (65 mg; tR 33.7 min) were isolated from fraction G6 (1 g) by HPLC system IV; compound 19 (6 mg; tR 122.9 min) was isolated from fraction B2 (40 mg) by HPLC system V. (20S,23R)-3β-hydroxy-12β,23-epoxy-dammar-24-ene 3-mercaptopyruvate sulfurtransferase 3-O-β-D-glucopyranoside-20-O-α-L-arabinofuranosyl-(1→6)-β-D-glucopyranoside (notoginsenoside-LX): white amorphous powder; [α]20 D = −20.8 (c = 0.30, MeOH); IR νmax 3425, 2930, 1637, 1452, 1384, 1079, 620 cm−1; Libermann-Burchard and Molish reactions were positive; 1H and 13C NMR: see Table 1; HRESIMS m/z 937.5097 [M+Na]+ (calculated for C47H78O17Na, 937.5137). (20S,23R)-3β-hydroxy-12β,23-epoxy-dammar-24-ene 20-O-α-L-arabinofuranosyl -(1→6)-β-D-glucopyranoside (notoginsenoside-LY): white granulated crystal; [α]20 D = −11.4 (c = 0.45, MeOH); IR νmax 3419, 2942, 1637, 1452, 1384, 1043, 621 cm−1; Libermann-Burchard and Molish reactions were positive; 1H and 13C NMR: see Table 1; HRESIMS m/z 775.4577 (calculated for C41H68O12Na, 775.4608). 20(S)-protopanaxadiol 3-O-β-D-xylopyranosyl-(1→2)-β-D-glucopyranosyl -(1→2)-β-D-glucopyranoside-20-O-α-L-arabinopyranosyl-(1→6)-β-D-glucopyranoside (notoginsenoside-FZ): white granulated crystal; [α]20 D = −12.2 (c = 0.

Consequently, the fractured file is the only metal susceptible to dissolve at the polarization conditions used during the process. Because the root canals present limited dimensions, an inert microelectrode must be used to guarantee the contact with the fragment without creating a barrier to the solution. The results presented here showed current values of up to 2.25 mA, indicating that the platinum

tip with diameter equal to 0.1 mm is able to promote the proper contact to conduct the electrical current. The total electrical charge values generated during the polarization tests evidence a statistical difference among the 3 groups of fragments (ANOVA, P < .05). The larger is the diameter of the cross section of the exposed surface, the higher selleck kinase inhibitor is the total value of the electrical charge. These results showed that the current generated during the polarization depends on the surface area exposed to the solution. The results presented Galunisertib mw by Ormiga et al (28) also suggested that the current values depend on the area exposed to the solution, once the reduction of the area exposed to the solution was followed

by the decline of the current values during the entire test. It is important to note that the exposed area can be affected by the thickness of the platinum tip used as anode. The smaller is the point thickness, the higher is the area of the fragment exposed to the solution and faster is the dissolution. This factor points that the microelectrode to be developed must have the minimum possible thickness, even when promoting dissolution in large surfaces. In the present study, a platinum tip was manufactured from a wire of 0.1 mm in diameter. This diameter was selected by considering the minimum thickness necessary to maintain acceptable mechanical resistance. According to the results from the 360-minute polarization of fragments from group

Metalloexopeptidase D3, the cross-section area correspondent to the D3 of the K3 30.06 files is sufficient to generate current values of up to 1.50 mA. These current values indicate a significant dissolution of the fragment, which can be confirmed by the radiographic images obtained before and after the tests. However, because the current generated depends on the surface area exposed to the solution, other studies should be developed to test fragments with smaller cross-section diameter, like the D3 of a 25.04 file for example. During the tests, the current peaks showed a gradual reduction during the initial 120 minutes and did not surpass 0.30 mA from this moment. This gradual decrease can be related to the reduction of the area exposed to the solution during the test, once the active portion of the files presents a taper. However, the current decrease was concentrated in the initial 120 minutes of the test, and the constant taper of the K3 files should have caused a gradual decrease of current during the entire test.