Therefore, determining when to splint and selecting the most appr

Therefore, determining when to splint and selecting the most appropriate technique remains a difficult decision for clinicians. The aim of this study was to assess the biomechanical response in the anterior region of a mandible to bone loss and to different types of periodontal splints by measuring strains. Strains represent deformation, and thus indicate the biomechanical response of the mandible. Strains have previously been measured using strain gauges to analyse the biomechanical response of mandibular bone and tooth structures19 during masticatory loading in vivo18 and in cadavers with

natural teeth after implant insertion.20 Bone deformation has also been estimated indirectly by measuring strains on mandible replicas made of

epoxy resin21 or autopolymerized acrylic resin.19 In this study, it was hypothesized selleck that bone loss and splint type affect the strains in the mandible, and that the strain values depend on mandible surface (buccal or lingual), region (central or lateral incisor), and load level. Eighty mandibular human teeth (approved by the Federal University of Uberlândia Ethics Committee, protocol #112/06), extracted for periodontal or orthodontic treatment, were selected in this study: 20 central incisors, 20 lateral incisors, 20 canines and 20 first premolars (being half of the right side and half of the left side). Teeth of similar size were selected, where LEE011 mouse the buccolingual and mesiodistal widths had a maximum deviation of 10% from the mean. Soft tissue and calculus deposits were removed with a periodontal curette (Hu-Friedy, Chicago, IL, USA). The teeth were cleaned using a rubber cup and fine pumice water slurry and stored in 0.2% thymol solution (Pharmacia Biopharma Ltda, Uberlândia, Brazil). The teeth were randomly Coproporphyrinogen III oxidase divided into 10 groups. The teeth were stored in distilled water at 4 °C. To reproduce the

anatomy of the anterior mandible, an intact dentate human mandible was obtained from the Laboratory of Human Anatomy at Federal University of Uberlândia. A wax barrier (Wilson, Polidental Indústria e Comércio Ltda, Cotia, Brazil) was made around the anterior mandibular region up to the first molars (Fig. 1). A vinyl polysiloxane impression material (Aerojet, São Paulo, Brazil) was prepared according to the manufacturer’s instructions and inserted into the wax barrier. After 24 h the mandible was removed, leaving its impression in the vinyl polysiloxane mould. Melted wax was inserted into this mould to create a wax model. From the wax model, all teeth were removed at the level of the alveolar bone crest. An impression was made from the wax model using vinyl polysiloxane material. After 24 h the wax model was removed, creating a mould of the external anatomy of the anterior mandible. Ten wax (Epoxiglass, Diadema, SP, Brazil) replicas were made. Eight alveoli were created in the wax models. Before the teeth were inserted in the created alveoli, their roots were dipped into melted wax up to 2.

showed malignant transformation associated with depressed SAM lev

showed malignant transformation associated with depressed SAM levels and global DNA hypomethylation (Zhao et al., 1997). An in vitro study on mammalian cells directly demonstrated that arsenic induces DNA hypomethylation that was associated with chromosomal instability (Sciandrello et al., 2004). In addition, arsenite has been shown to increase both the levels of the repressive histone mark dimethylated

H3K9 and the activating mark trimethylated H3K4, and decreases the repressive mark trimethylated H3K27 in human lung carcinoma A549 cells (Zhou et al., 2008). An unexpected finding was recently reported in vivo, as a global dose-dependent hypermethylation of blood DNA was observed in learn more Bangladeshi adults with chronic arsenic exposure (Pilsner et al., 2007). This effect was modified by folate, suggesting that arsenic-induced increases Lumacaftor nmr in DNA methylation were dependent from methyl availability (Pilsner et al., 2007). The same group, however, reported that lower blood DNA methylation was a risk factor for arsenic-induced skin lesions in a related Bangladeshi population (Pilsner et al., 2009). In a human study from India, significant DNA hypermethylation of p53 and p16 promoter regions was observed in blood DNA of subjects exposed to toxic level of arsenic compared to controls

(Chanda et al., 2006). In this study, hypermethylation showed a dose–response relationship with arsenic measured in drinking water. Environmental factors can alter gene expression by epigenetic mechanisms and lead to late-onset neurodegenerative diseases. Exposure to environmental neurotoxic metals, pesticides and other chemicals is increasingly recognized as a key risk factor in the pathogenesis of chronic neurodegenerative disorders such as Parkinson’s and Alzheimer’s

diseases (Kanthasamy et al., 2012, Kwok, 2010 and Migliore and Coppede, 2009). Kanthasamy et al. (2012) described the role of acetylation of histones and non-histone proteins in neurotoxicant-induced neurodegenerative processes in the nigral dopaminergic neuronal system. Paraquat, a widely used herbicide, and the organochlorine insecticide Dieldrin, are Alanine-glyoxylate transaminase among the environmental chemicals potentially linked with Parkinson’s disease. Histone acetylation may represent the key epigenetic change in dopaminergic neuronal cells during neurotoxic insults. Experimental evidence comes from the research conducted by Song et al. on N27 dopaminergic cells. Exposure to Paraquat induced histone H3 acetylation in a time-dependent manner and decreased total histone deacetylase (HDAC) activity (Song et al., 2010 and Song et al., 2011). In mesencephalic dopaminergic neuronal cells, Dieldrin lead to a time-dependent increase in the acetylation of core histones H3 and H4 by a Dieldrin-induced proteasomal dysfunction, resulting in accumulation of a key histone acetyltransferase (HAT).

Cell cycle arrest at these checkpoints

Cell cycle arrest at these checkpoints AG-014699 research buy prevents DNA replication and mitosis in the presence of

DNA damage. For this reason, no dose-response effect could be observed. The inactivation of these cell cycle checkpoints results in genomic instability, which is closely associated with cell transformation and tumorigenesis. It is widely accepted that the mutagenic action of nitrosamines is mediated via their immediate metabolic product (Verna et al., 1996). The metabolism of NDEA in vivo results in the formation of electrophilic reactive intermediates, free radicals, and associated oxidative stress ( Parke, 1987 and Shiota et al., 2002), which are in turn able to alkylate lipids, proteins, and genetic materials. Among its many effects as a potent tumor promoting agent, PB can cause oxidative damage to livers in response to the induction of certain cytochrome P450 enzymes ( Imaoka et al., 2004).

Wastl et al. (1998) demonstrate in preneoplastic and neoplastic INCB024360 mouse liver lesions that PB is a potent inducer of CYP2A5, and is likewise involved in NDEA metabolism, suggesting that it may play an important role in the development of liver cancer and may be used as a marker for spontaneous and NDEA-induced mouse liver foci. In the present work we did not investigate the effects on mouse CYP2A5 (an ortholog of human CYP2A6). Several genetic models of carcinogenesis indicate that progression to carcinoma involves the activation of proto-oncogenes and an additional event involving the deletion or inactivation of a suppressor gene ( Osanai et al., 1997).

The described mechanisms of proto-oncogene Smoothened activation include point mutations and gross DNA rearrangements, such as translocations and gene amplification ( Slenman and Sager, 1987 and Sargent et al., 1996). In the present study an increasing number of dicentric chromosomes was observed for both treatments, especially involving the largest chromosomes. This might suggest that the ras proto-oncogene, located on chromosome 1, is involved in the carcinogenic process ( Sargent et al., 1996). NDEA was also found to induce more CYP2B2 than CYP2B1, but when PB was used as a CYP inducer, the levels of CYP2B1 were higher than those of CYP2B2. The results obtained for the phenobarbital-induction of CYP2B1 and CYP2B2 mRNAs in cultured rat hepatocytes reflect the situation found in vivo, in that CYP2B1 mRNAs are more inducible than CYP2B2. The same was already described for Valproate, an anti-epileptic drug ( Rogiers et al., 1995). Measurements of cell viability are very important when the objective is RNA expression, since a decrease in the number of cells can be problematic for down-regulated genes. Another problem correlated to cytotoxic effects is the decrease in the micronucleus index, and the absence of any dose-response, as related before.

For example, the incidence of device-associated HAI is two- to th

For example, the incidence of device-associated HAI is two- to three-fold higher in low-resources countries than in high-resources countries (Table

2). Additionally, even within high-resource countries, the incidence of SSIs is considerably different, as the incidence is lower in the NHSN than the ECDC for many procedures (Table 3). Moreover, the change in HAI incidence in consecutive reports from the same benchmark organization (Fig. 1) and the underlying Cobimetinib in vitro contributing causes may complicate the selection and interpretation of the benchmarking process [14], [16], [26], [37], [38], [39], [40], [41] and [42]. For example, several causes that may affect fair comparisons were hypothesized to explain the downward trend in device-associated HAI rates in consecutive NHSN reports, including (1) changes in HAI definitions to reduce the percentage of non-objective diagnoses (e.g., abandoning clinical sepsis as an acceptable diagnosis for CALBSI); (2) complying with regulations for mandatory HAI reporting in many states (this represented 70% of contributing hospitals in the 2010 data); (3) enrollment of many hospitals with smaller bed numbers, which generally have a lower risk of HAIs (this represented two-thirds of contributing hospitals in the 2010 data); and (4) implementation of multiple infection control strategies by many hospitals, which may have resulted in an actual

decrease in HAI incidence. Benchmarking local GCC

data is challenging, although benchmarking to NHSN reports learn more is preferred because the case definitions and methodologies are similar and differences in HAI rates will likely encourage improvements. However, differences in surveillance environments, including regulations in GCC and NHSN hospitals, should be taken into consideration. Additionally, delays in implementing frequent NHSN changes in case definitions and methodologies could further complicate interpretation of the data. Benchmarking to INICC seems legitimate because of similar methodologies and challenges, as well as the availability Farnesyltransferase of unique data on mortality, length of stay, and prevention. However, the use of aggregate data from enrolled hospitals does not account for the variability in surveillance adjudication between and within participating countries. Moreover, the benchmarking process is expected to improve infection control practices when using a benchmark of a higher standard. ECDC may be an alternative benchmark to GCC hospitals for SSIs and antimicrobial use and resistance. However, the considerable differences in device-associated HAI definitions likely limit its use as a benchmark for that purpose. WHO estimates for high-resources countries are driven by NHSN and ECDC data, while the estimates for low-resources countries are largely fragmented and not derived from a clear source.

The insects were reared in plastic beakers, covered with smooth g

The insects were reared in plastic beakers, covered with smooth gauze and fed on rabbit blood through latex membranes

2 weeks after molting ( Garcia et al., 1989 and Mello et al., 1996). Only fully engorged insects were used for further experiments. For sequence identification and RT-PCR, the salivary glands, anterior midgut (stomach), posterior midgut (small intestine) and fat body of always ten unfed fifth instar nymphs, fifth instar nymphs at 3, 5, 10, and 15 days after feeding (daf) and the same tissues from adult insects at 5 daf including the gonads were dissected. The respective tissues were frozen, pooled in liquid nitrogen and stored at −80 °C. The pH-values of the whole midgut and rectum of unfed fifth instar nymphs were estimated using a universal indicator solution (Merck, Darmstadt, Germany). Guts were entirely submerged in indicator solution and the resulting coloration of the tissue was compared with the supplied color card. Linsitinib price Total RNA was isolated using the RNeasy Mini Kit (Qiagen, Hilden, Germany), following the manufacturers’ protocols. Nucleic acid concentrations were measured by a Bio Photometer (Eppendorf, Hamburg, Germany). Reverse transcription was carried out as described previously (Araújo et al., 2006). Degenerate cathepsin forward and reverse primers, Cat-Deg-F 5′-TGYGGNWSNTGYTGGGCNTT-3′ and Cat-Def-R 5′-CCCCANSWRTTYTTNAYDATCCA-3′, were designed according to the highly conserved

cathepsin L regions, CGSCWSF and WLVKNSWG, respectively (Fig. 2). For the first strand amplification, cDNA from the small intestine at 5 daf was used. The cycling parameters in an iCycler Thermal Cycler (BioRad, Hercules, CA, USA) were carried out as described previously and differed only in the annealing temperatures of 51.5 °C (Araújo et ADAMTS5 al., 2006). Gene amplification products of the predicted size, approximately 500 bp, were cloned into pGEM T-Easy vector (Promega, Madison, WI, USA), following the manufactures’ instructions and sequenced at least twice from both directions (Plataforma Genômica – Sequenciamento de DNA/PDTIS-FIOCRUZ/IOC). 5′-

and 3′-RACE procedures were carried out using commercial kits (Invitrogen, Carlsbad, CA, USA) following the manufacturer’s instructions. Total RNA from the small intestine of fifth instar nymphs at 5 daf was used for both methods. For the 5′-ends RACE amplification of the tbcatL-1 and tbcatL-2 cDNA, the GSP1 primers Cat1-R 5′-AGCTTTTTCATCTCCT-3′ and Cat2-R 5′-TGATGATTCAGTATCTA-3′ were used for the first strand synthesis. For the subsequent PCR amplifications, the GSP2 primers Cat3-R 5′-GCTTCATAGGGGTATGATGATTC-3′ and Cat4-R 5′-CTAACATATTGGAACGCTTTATCC-3′ with a forward abridged anchor primer were used. A second PCR was carried out using the GSP3 primers Cat5-R 5′-GTCCACCTTCACAGCCATTGT-3′ and Cat6-R 5′-CCATATTCCTTGGAGCAGTCCATT-3′ with a nested abridged universal amplification forward primer (Invitrogen).

, 2007 and Oka et al , 2003) which would relief the tonic inhibit

, 2007 and Oka et al., 2003) which would relief the tonic inhibition that these neurons exert over the dorsomedial hypothalamus to activate brown adipose tissue thermogenesis and over the rostral raphe pallidus to elicit cutaneous vasoconstriction (Nakamura et al., 2005, Rathner

et al., 2008 and Yoshida et al., 2009) probably through two separate pathways (Nakamura et al., 2009 and Ootsuka and McAllen, 2006). Nonetheless, how the other central mediators RG7204 interact with these neurons in the hypothalamus to produce fever is less known. There is also the possibility that different central mediators are involved in different pathways for fever induction. For example, endogenous opioids are involved in the febrile response induced by LPS and several cytokines but not by IL-1β (Fraga et al., 2008), while ET-1 is involved in the febrile response induced only by LPS and pre-formed pyrogenic factor (Fabricio et al., 2006), but not in the fever induced by other cytokines. Meanwhile, both endogenous opioids and ET-1 induce fever by prostaglandin-independent mechanisms (Fabricio et al., 2005 and Fraga et al., 2008). Although substance P may be involved in mediating certain febrile responses, its actions are not well understood. Substance P (SP: Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gli-Leu-Met-NH2) is found in primary afferent fibers [A-δ, C and capsaicin-sensitive fibers (Cahill and Coderre, 2002)] as well as in the CNS

(Hurd et al., 1999), and there are several studies showing BMS354825 its participation in inflammatory processes and, to a lesser extent, in the febrile response. In the CNS, SP is present in several structures, including the POA [for review see (Otsuka and Yoshioka, 1993)]. Although the main source of SP is neuronal cells, some studies with rodents have shown that SP can also be synthesized by macrophages, eosinophils, lymphocytes, dendritic cells, and others (Bost, 2004, Ho et al., 1997 and Satake and Kawada, 2006). SP effects are mediated almost exclusively by

the metabotropic NK1R, which is expressed in several structures of the CNS, including the putamen, caudate nucleus and hypothalamus, and in the peripheral nervous system, where it is found in dorsal root ganglia and intestinal intrinsic neurons [for Methamphetamine review see (Harrison and Geppetti, 2001 and Tuluc et al., 2009)]. Furthermore, the NK1R can also be expressed by immune cells such as macrophages, neutrophils, lymphocytes and mast cells (Cooke et al., 1998, Ho et al., 1997, Lai et al., 1998 and Lambrecht et al., 1999). The administration of NK1R antagonists reduced neutrophil migration induced by P. nigriventer venom ( Costa et al., 2002) or formalin ( Santos et al., 2004), when systemically injected, and reduced the febrile response to LPS when administered centrally ( Balasko et al., 2000 and Szelenyi et al., 1997) in laboratory animals, highlighting the participation of SP in these events.

One μL was injected by a split injector (50:1) at an inlet temper

One μL was injected by a split injector (50:1) at an inlet temperature of 250 °C. The oven temperature was programmed as follows: started at 80 °C, heating rate 5 °C/min up to 175 °C, followed by another gradient of 3 °C/min to 230 °C, and hold at this temperature for 5 min. Detection was carried out by an FID set to 280 °C. The fatty acids were identified by comparing the retention times

with those of four purified standard mixtures of fatty acid methyl esters (4-7801; 47085-U; 49453-U and 47885-U from Sigma Chemical Co.). Peak areas were calculated as area % of total fatty acids. PS content was determined according to Laakso (2005). Lipids extracts containing about 1–2 mg of PS were mixed with 2 mg of internal standard (5β-cholestan-3α-ol; epicoprostanol) and evaporated to dryness under a nitrogen stream.

VX-809 datasheet A hot saponification was carried out by adding 2.5 mL of KOH 2.0 M in methanol followed by extraction with heptane. Sterols were derivatized with 200 μL of bis(trimethylsilyl)-trifluoracetamide (BSTFA) containing 1 g/100 g trimethylchlorosilane (TMCS) (99:1) and 100 μL of pyridine, at 70 °C for 15 min. An aliquot of 1.0 μL of derivatized sample solution was injected into the column selleck at 250 °C with a split injector (split ratio 1:50). Sterols were separated at 300 °C and detected with flame ionization detector (FID) at 280 °C. The carrier gas was helium at flow rate of 1.0 mL/min. Reference standards were used to identify the peaks. Quantification was calculated based

on standard curve prepared with β-sitosterol/IS area ratio, as a linear function (r = 0.9983) of sterol concentration (0.5–5.0 mg). About 20 mg of the chocolate were placed in a tube glass with 19-hydroxycholesterol (0.58 mg in n-hexane:isopropanol (3:2, mL/mL)) used as internal standard for the quantification of POPs. The solvent was evaporated under nitrogen and 30 mL of 2 mol equiv/L KOH solution in methanol were added to perform a cold saponification at room temperature for 18 h in darkness and under continuous agitation ( Sander, Addis, Park, & Smith, 1989). The unsaponifiable material was extracted with diethyl ether. PD184352 (CI-1040) For determination of POPs, 70 g/100 g of the unsaponifiable matter was purified by silica solid-phase extraction (SPE) according to Guardiola, Codony, Rafecas, and Boatella (1995). After cartridge activation with hexane (5 mL), PS and impurities were removed with hexane (5 mL) and diverse solvent mixtures of n-hexane:diethyl ether (10, 30 and 10 mL of 95:5, 90:10, 80:20 (v/v), respectively). POPs were finally eluted with acetone (10 mL), then subjected to silylation, dried under nitrogen stream and dissolved in 40 μL of n-hexane. One μL of the TMSE derivatives was analyzed by GC–MS (GCMS-QP2010 Plus (Shimadzu, Kyoto, Japan)), using a Fast GC–MS method suggested by Cardenia, Rodriguez-Estrada, Baldacci, Savioli, and Lercker (2012), with minor modifications. The system was fitted with a capillary RTX-5 Restek column (10 m × 0.10 mm i.d. × 0.

However, given the wider dynamic range and greater sensitivity of

However, given the wider dynamic range and greater sensitivity of real-time PCR, the variation of differentially expressed genes from real-time PCR was more significant than that from the microarray analysis; we found that 22 DAP is an important turning point

in ear germination. MicroRNAs play integral roles in gene regulatory networks as one of the most abundant classes of gene regulators. The expression and activity of plant miRNAs can be regulated in many ways, including transcriptional control, as well as regulation imposed at the levels of miRNA processing and action. Moreover, changes in the expression of even a single miRNA could have a significant impact on the outcome of diverse cellular activities regulated by the product TGF-beta family of that mRNA. Repression of the target transcript by miRNAs may occur through translational inhibition, accelerated exonucleolytic mRNA decay, or slice ABT-199 datasheet within miRNA–mRNA base pairing [58]. Beyond the strict conservation of miRNAs across different species, some miRNAs appear to be species-specific. Compared with computational or heterologous approaches, direct miRNA cloning has the advantage of identifying non-conserved and new miRNAs. There are a number of highly conserved miRNA families in maize. In the present study, cloning and expression

analysis led to the identification of 26 miRNA variants belonging to 21 miRNA families, as well as 5 new miRNAs and 16 putatively new miRNAs. Non-conserved plant miRNAs presumably emerge and dissipate in short evolutionary time scales. Representation of many known and novel miRNAs in this single library indicates the presence of miRNAs that are

not yet discovered. The identification of a large number of miRNAs that are not previously reported in maize, at least 10 of which are conserved in monocots, suggests that many more monocot- or maize-specific miRNAs are yet to be identified. Certainly, additional tissues should be evaluated for further discovery of miRNAs in maize, coupled with similar studies in related monocots. This will help establish how many of the currently maize-specific miRNAs are conserved in other monocot species. Moreover, both in-depth analysis of the existing library Methamphetamine and organ-specific analysis of individual miRNAs will give insights into the functional mechanisms and pathways involved in particular in ear germination and ear development in general. Recent studies have demonstrated that miRNAs in Arabidopsis, rice, and other plant species target transcripts that encode proteins involved in diverse physiological processes by predominantly targeting transcription factors [25], [37], [44] and [59]. In this study, we predicted 90 unigenes as putative miRNA targets in maize ears, with one-third of the predicted targets of miRNAs being mRNAs of transcription factors, including AUX_IAA, MYB, ARF, bZIP, bHLH and MADS.

Associations between the memory and language variables were exami

Associations between the memory and language variables were examined with correlations (Pearson’s r) computed separately for each pair of memory (central executive, phonological loop, visuo-spatial sketchpad, verbal declarative memory, visual declarative memory, procedural memory) and language (lexical abilities, grammatical abilities) measure

being examined, selleck screening library separately for the TD and SLI groups. None of the three working memory measures (for the central executive, phonological loop, visuo-spatial sketchpad) correlated significantly with either lexical or grammatical abilities in either the TD or SLI groups (Table 6). In contrast, lexical abilities correlated with verbal declarative memory, with large effect sizes (i.e., Pearson’s r ≥ .371, Cohen, 1988), in both the TD and SLI groups ( Table 6). Lexical abilities were not correlated Ivacaftor molecular weight with visual declarative memory, which yielded small to medium effect sizes. However, a direct comparison of the r-values for the correlations of lexical abilities with verbal and visual declarative memory revealed no significant differences

between them, either for the TD group [t(48) = 1.51, p = .139] or the SLI group [t(48) = 1.05, p = .298]. Grammatical abilities showed a different pattern. These were correlated with procedural memory for the TD group and verbal declarative memory for the SLI group ( Table 6). A direct comparison of the r-values for the correlations of grammatical abilities with verbal and visual declarative memory in SLI yielded a borderline significant difference between the two [t(48) = 1.61, p = .057]. Finally, we examined whether the observed

pattern of correlations could be explained by working memory. First, we tested whether any of the three working memory almost composites (for the central executive, phonological loop, and visuo-spatial sketchpad) correlated with either any of the declarative memory, procedural memory, lexical, or grammatical measures. Only the central executive composite correlated with visual declarative memory for the TD children and with verbal declarative memory for the SLI children. However, even after controlling for the influence of the central executive on visual declarative memory in the TD children, and on verbal declarative memory in the SLI children, the correlations showed the same pattern as described above. Therefore working memory did not explain the pattern of correlations between language and declarative or procedural memory. This study examined multiple measures of working, declarative, and procedural memory in native English-speaking children with and without SLI of about 10 years of age. The children with SLI were impaired at a visuo-spatial procedural memory task, even when controlling for working memory.

Thus, the amaranth flour film should meet some requirements, rega

Thus, the amaranth flour film should meet some requirements, regarding mechanical strength, flexibility, and permeability to water vapor and gases, in order to ensure food preservation during storage. Therefore, the aim of this work was to examine the effect of the drying conditions on the mechanical, solubility, barrier properties, and drying time of amaranth flour films plasticized with glycerol or sorbitol and optimize the drying process by using a response surface methodology and multi-response analyses, targeting the production

of films with low solubility and good mechanical properties. The Amaranthus cruentus BRS Alegria seeds were grown in the state of Santa Catarina (Brazil) at 18.8–22 °C, soil pH of 5.5. The seeds were harvested in early October, transported to Campinas (Brazil), cleaned, and stored at 10 °C. The amaranth flour was obtained by using a modification to the alkaline wet milling method of Perez, Bahnassey, and Breene (1993), as proposed by Tapia-Blácido et al. (2005a). The composition of amaranth flour is: moisture content 8.3 ± 0.4 g/100 g, ashes 2.1 ± 0.0 g/100 g, lipids 7.9 ± 0.2 g/100 g,

protein 14.1 ± 0.3 g/100 g, and starch 75.7 ± 0.3 g/100 g (11.9 ± 0.3 g amylose/100 g flour) (db). All the reagents were analytical compound screening assay grade. Sorbitol and NaOH were purchased from Synth (São Paulo, Brazil). All the solutions were prepared with deionized water. The films were produced by the casting method. Amaranth flour films were prepared by using the methodology proposed by Tapia-Blácido et al. (2005a). A suspension Dimethyl sulfoxide of flour in water (4 g/100 g) was homogenized in a mixer for 25 min, and the pH was regulated to 10.7 with 0.1 mol equi/L NaOH, to dissolve the protein. This suspension was then heated at 75 °C for 15 min, followed by addition of the plasticizer (29.6 g sorbitol/100 g flour or 20.02 g glycerol/100 g flour). For each film, 85 ± 3 g of the film-forming solution was poured onto acrylic plates (18 × 21 cm), in order to obtain a constant thickness

of 80 ± 5 μm. The films were dried under different drying conditions by using an oven with air circulation and controlled temperature (model MA 415UR, Marconi, Piracicaba, Brazil). The studied drying conditions were 30 °C, 40% RH; 30 °C, 70% RH; 50 °C, 40% RH; 50 °C, 70% RH; 25.9 °C, 55% RH; 54.1 °C, 55% RH; 40 °C, 33.8% RH; 40 °C, 76.2% RH; and 40 °C, 55% RH, defined according to the experimental design that was being used (Tables 1 and 2). The drying kinetics curves of the amaranth flour films were determined for all the studied conditions. Prior to characterization, all the films were preconditioned for at least 48 h in desiccators containing a saturated NaBr solution (25 ± 3 °C, 58 ± 2% RH). The thickness of the films was measured with a digital micrometer Fowler (average of 8 measurements).