7p/trial and CA|ER = .79. KD started on an increasing dose of ropinirole, an agonist acting largely D2 and D3 dopamine receptors. By contrast, l-dopa would have a balanced effect across all these receptors by increasing synaptic dopamine. On 4 mg ropinirole daily there was marked improvement in KD’s apathy. He was far more spontaneous in conversation, reported better social interactions and

was more interested in events around him. He managed to secure a job and now scored in the normal range (4/12) on the initiative and interest subscales of the Apathy Inventory (Robert et al., PARP inhibitor 2002). On the directional reward-sensitivity task, saccades were generally faster, but those to the RS were significantly faster (RS = 183 msec vs US = 208 msec; p < .001), far

larger than in controls ( Fig. 7). On the TLT by week four (on 4 mg ropinirole daily) KD demonstrated much greater early responding (45.2%). However, this was at the expense of greater numbers of errors (17.8% vs control mean = 24.2%) so the CA|ER (1.54) was not as high as on l-dopa. Despite this, mean reward (27.3p/trial) Selleckchem CX5461 exceeded that achieved on l-dopa, matching the highest performing individual healthy control. Thus KD showing increased willingness to anticipate frequently and take risks, an effect that persisted over 12 weeks on ropinirole ( Fig. 5D). We used novel probes of oculomotor decision-making to demonstrate relative insensitivity to reward in an individual with apathy following bilateral GPi lesions. Our TLT (Adam et al., 2012) requires reward sensitivity and motivation or effort to succeed, combined with fast reaction times and the ability to update behaviour in response to positive and negative feedback. A reactive response – simply waiting for the green light – is less well rewarded than an anticipatory response prepared in advance of the green signal. KD initially made very few anticipatory responses compared with age-matched controls. However, dopaminergic therapy, first with levodopa and then with ropinirole, increased anticipatory responses to within the normal range. The

directional saccade reward-sensitivity task, originally developed for the study of reward sensitivity in macaque monkeys (Hong Metformin clinical trial and Hikosaka, 2008), demonstrated that KD had SRTs within the normal range but showed no speeding to the rewarded side (RS), unlike healthy volunteers. Treatment with levodopa led to reward sensitivity, with speeding of responses to the RS and slowing to the unrewarded side (US) compared to baseline. Off medication, the difference in SRTs to rewarded and unrewarded targets became non-significant, while subsequently on ropinirole, a direct dopamine D2/D3 receptor agonist, KD again demonstrated reward sensitivity, as well as generalized speeding. These effects on dopaminergic medication were associated with clinical improvement – reduction of apathy and increased motivation to find work and in social interactions – most prominently while on the dopamine agonist.

A minimum of 6 images

per sample and 6 separate samples were used. To quantify the area of the growth plate composed of cartilage (which stains red after Safranin O/Fast Green staining), images were imported into Adobe PhotoShop. The area of the Safranin O stained cartilage growth plates was measured in a double-blinded manner by two independent investigators. To quantify the extent of cell proliferation selleck chemicals and cell death within the midpalatal suture complex, a standard process was employed [30], [31], [32] and [33] where regions of interest (ROI) were photographed using a minimum of 6 images per sample, and 6 separate samples. In the cases of TUNEL and Ki67, the number of positively stained cells was counted. The ROI used for Ki67 is outlined in Figs. 4I, J. The ROI used for TUNEL is outlined in Figs. 4L, M. Conclusions drawn from analyses of tissues at one time point were compared to analyses conducted at subsequent time points. Only data that showed a consistent, reproducible finding from one time point to the next were presented. The FE model was generated in COMSOL 4.4. The geometry of the palate and the resulting mucoperiosteal denudation wound was modeled based on measurements from histologic data. The assigned mechanical properties of the soft tissue, palatine bones, and midpalatal suture were based on published

reports (Table 2). The lateral edges of the palatine processes were constrained in their displacements in all directions. The values assigned to nursing [34] and tongue pressures [35] in the mouse were estimated using data obtained from human infants and then scaling according to the weight Apoptosis Compound Library of a mouse. The palatal structures were partitioned into > 30,000 volumetric elements that comprise the full 3D model and represent the model’s precision (Fig. 2B). In all quantitative analyses, results were presented as the mean ± SD. Differences between sets of data were determined by using the Mann–Whitney test in XLStat software version (Addinsoft, Paris, France). A p-value < 0.05 was Terminal deoxynucleotidyl transferase considered statistically significant.

At post-natal day 8 (P8) the midpalatal suture complex is made up of three elements: the bony palatine processes of the maxillae, the cartilage growth plates that cap the ends of the palatine processes (red arrows), and the fibrous interzone (asterisk) that separates the growth plates (Fig. 1A). The epithelia lining the sinus and roof of the mouth were intact (Fig. 1B). A few TUNEL+ ve cells were detected in the growth plates (red arrows), indicating that programmed cell death was restricted to dying chondrocytes at the chondro-osseous junction (asterisk, Fig. 1C). The intact bone of the palatine processes was undergoing active bone remodeling as indicated by the presence of TRAP+ ve osteoclasts (Fig. 1D). A procedure was performed in the palatal midline that mimicked elevation of the mucoperiosteum (Supplemental Fig. 1). Within 24 h (i.e.

When ‘ + 1′ score is assigned to the control tissue sections, ACB stained piroxicam treated animal tissue sections scored ‘ + 3′. Such observation revealed a pathological change in mucin secretion type on piroxicam treatment. The histopathological finding clearly indicates that piroxicam treatment increases acid mucin secretion in otherwise neutral mucin secreting normal gastric tissue. Reduction in

ACB staining intensity in tissue sections from only Cu LE treated group indicates that mucin secretion pattern did not alter significantly Selleck Palbociclib on pre-treatment with the extract. The free neutral mucin content depletes appreciably and the nature of secreted mucin turns acidic on ulcerated stomach. Figure 3D shows that piroxicam also mediates its ulcerative damage through reduction in mucin level by MDV3100 cell line 22.3% (*P≤ 0.001 Vs control). Cu LE pre-treated piroxicam fed animals had no such reduction in mucin content clearly indicating protection from ulcerative damage rendered

by the pre-feeding of the extract. Biomarkers of oxidative stress include lipid peroxidation level, protein carbonyl content, reduced glutathione (GSH), non enzymatic total sulfhydryl group content (TSH), oxidized glutathione (GSSG) content and GSH-GSSG ratio. Table 1 represents the changes in biomarkers of oxidative stress on piroxicam treatment and protection rendered on pre-treatment of rats with Cu LE at a dose of 200 mg/kg body weight. Lipid peroxidation level and protein carbonyl content increased in piroxicam treated rats by 2.16 folds and 5.57 folds respectively, compared to values obtained (P≤0.001Vs

control) in control rats. Levels of TSH and GSH decreased significantly in piroxicam fed rats by 59.17% and 59.63% respectively from control rats (*P ≤ 0.001 Vs control in each case). GSSG content increased by 51.16% and the ratio (GSSG: GSH) increased by 4.3 folds from control in piroxicam treated rats (*P≤0.001 Vs control in each case). Values in the table C-X-C chemokine receptor type 7 (CXCR-7) no.1 clearly indicate that no biomarkers altered on feeding rats with only aqueous extract of curry leaves at 200 mg/kg BW dose. Table 1 further indicate that altered biomarkers were restored to control values when rats were pre-treated with aqueous curry leaf extract at 200 mg/kg BW dose before feeding piroxicam at 30 mg/kg BW dose. Table 2 depicts the alterations in activities of different gastric antioxidant enzymes on piroxicam administration. Piroxicam feeding inhibits activities of key gastric antioxidant enzyme called gastric peroxidise and glutathione–S-transferase. Increased activities of gastric glutathione reductase, glutathione peroxidise, superoxide dismutases (Cu-Zn SOD and Mn SOD) and catalase are also observed on piroxicam feeding. Pre-treatment of piroxicam fed rats with Cu LE protected the activity of these antioxidant enzymes from being altered.

Third, the logit transformations of the ratios were fitted by simple linear regression up to the end of the follow-up period. The estimated regression line, together with survival function of the reference population beyond the follow-up limit, was used to extrapolate the lifetime survival function of the NSCLC cohort. The life expectancy of the NSCLC cohort (up to 600 months) after diagnosis

was thus CX-5461 concentration estimated. The expected years of life lost of the NSCLC cohort was defined as the survival difference between the cohort and the reference population. The method described above has been demonstrated by computer simulation [13] and proven mathematically [14]. It has also been corroborated by several examples of cancer cohorts [15] and [16]. An open access software, the iSQoL statistical package,

was used for the computation [17]. From May 2011 to April 2012, all consecutive patients with NSCLC from PR-171 supplier the outpatient oncology, chest surgery, and chest medicine departments of NCKUH were invited to participate in this study. To minimize any magnitude of overestimation of the QoL, we also consecutively screened patients admitted to the wards between November 2011 and January 2012. The inclusion criteria were realization of a lung cancer diagnosis by each participant, the absence of malignancy at another site, and each subject’s ability to understand and answer the questionnaire. In some individuals, measurements were performed repeatedly; however, each measurement was taken at least 3 months after the previous one. The 5-dimension EuroQol questionnaire (EQ-5D) [18], the Taiwanese version of which has been validated in a previous work [19], was used with face-to-face interviews to estimate the utility values of QoL. The Fludarabine nmr five dimensions assessed by the EQ-5D are mobility, self-care,

usual activities, pain/discomfort, and anxiety/depression, each of which has three levels of severity. Using the scoring function from Taiwan, these health state parameters were transformed into a utility value ranging from 0 to 1, in which 0 represented death and 1 indicated full health. The duration-to-date for each measurement was defined as the period between the date of NSCLC diagnosis and the date of interview. A kernel-smoothing (i.e., the moving average of the nearby 10%) method was used to estimate the mean QoL function [6] and [7]. The utility values of QoL beyond the follow-up period were assumed to be the same as the average of the last 10% of patients near the end of follow-up. The lifetime survival function of the NSCLC cohort was adjusted by the corresponding mean QoL function to obtain a quality-adjusted survival curve, in which the sum of the area under this curve was the QALE of NSCLC patients [6]. We borrowed the EQ-5D utility values of the age- and sex-matched general population from the 2009 National Health Interview Survey in Taiwan.

There was no DNA amplification in the negative controls in which the chromosomal DNA of the wild type CHO cell line was used as template. Due to the clone CHO-HAH5 78 exhibited the highest levels of the HAH5 protein measured by ELISA, it was selected for being adapted to suspension culture. The gradual medium change from DMEM plus FCS to SFM4CHO made the cells to detach of the polystyrene surface and successfully adapted

to suspended culture with stirring (Fig. 3A and B). The initial inoculum for scaling up the suspension culture to the volume of 1 l in spinners was 2,5 × 104 cells/mL (Fig. 3C). Two days later, cells increased twofold their concentration and Caspase inhibitor began to grow until reaching more than 3 × 105 cells/mL at day 7. The next day of culture cells decreased their concentration to around 2,5 × 105 cells/mL and became stable until day 10. By day 11, the cell concentration abruptly dropped to almost 1 × 105 cells/mL. Cell viability ranged between 100% and 80% from days 1 to 8. At day 9, cell viability

began to decrease and by the last day of the experiment there was a 40% of cell viability. The results obtained above led us to maintain the suspension culture until day 10, where cell concentration and viability met acceptable values, hence the production of the HAH5 protein could be favored. In this sense, the concentration of the HAH5 protein was measured by ELISA (Fig. 4). The average production of the HAH5 protein by different batches of the clone GSK J4 manufacturer CHO-HAH5 78 in suspension culture was approximately 5,1 μg/mL. There were no significant differences among the individual batches analyzed. The purification process of the HAH5 protein obtained in the culture supernatant was carried out by immunoaffinity chromatography (IC) using a monoclonal Oxalosuccinic acid antibody against the HAH5 protein (Fig. 5). The graphic of absorbance versus time showed a well-defined peak when the elution buffer was applied to the matrix ( Fig. 5A) which could correspond

to the elution of the HAH5 protein. SDS-PAGE and western blot assays revealed that the peak observed after elution in the graphic of absorbance versus time was indeed the elution of the HAH5 protein ( Fig. 5B and C). The immunoreactive band pattern was the same compared to the observed during the transient transfection of HEK-293 cells. The bands corresponding to the precursor protein HAH50 and the subunits HAH51 and HAH52 were detected. A portion of the HAH5 protein was lost in the material not retained to the matrix, which was not observed during the wash of the matrix. The HAH5 protein purified by IC was obtained with more than 95% of purity as estimated by a SDS-PAGE densitometric analysis. The production of the HAH5 protein in a suspension culture system allowed to obtain enough protein to perform immunodetection assays type ELISA with the aim of detecting antibodies against this protein.

14 and 25, para calcular o número total de mortes associadas ao VHC. De acordo com o painel de peritos, atualmente serão atribuíveis ao VHC 20% do número total de mortes devidas a cirrose hepática e 50% do número total de mortes devidas ao CHC em Portugal. Recorrendo

ao método de cálculo de Muhlberger et al. e utilizando os dados de mortalidade da OMS de 2008 e as frações atribuíveis para Portugal supramencionadas, a estimativa para Portugal é de 984 mortes/ano devidas ao VHC, correspondente a uma taxa de mortalidade de 9,21 mortes/100.000 habitantes (tabela 1). Por outro lado, BMS-907351 in vivo se o cálculo relativo à mortalidade for efetuado com base numa taxa de mortalidade de 4% em doentes cirróticos devido ao VHC e na distribuição atual dos doentes pelos diferentes estádios de progressão da doença em Portugal, ambas obtidas através do painel de

peritos, estima‐se que ocorram 600 mortes/ano em doentes com cirrose hepática (incluindo descompensação hepática e CHC). O número estimado de mortes devidas ao VHC em Portugal poderá assim oscilar entre as 600‐984 mortes/ano. Durante a fase aguda da infeção, a maioria dos doentes mantém‐se assintomática, pelo que é frequente a ausência de diagnóstico26 and 27. Em alguns doentes a infeção é autolimitada, com erradicação espontânea do vírus. No entanto, em 54‐86% dos doentes adultos há evolução para cronicidade26 (fig. 1). Uma vez estabelecida a hepatite C crónica, find more a erradicação espontânea do VHC raramente ocorre e a doença poderá progredir, causando lesão celular do fígado e cirrose hepática. Estima‐se que 15‐51% dos doentes com hepatite C crónica desenvolvam cirrose

hepática num determinado momento da sua vida (fig. 1). A progressão para este estádio decorre durante várias décadas, sendo influenciada por diversos cofatores, como consumo de álcool, diabetes, idade avançada, coinfeção pelo VIH ou outros vírus hepatotrópicos26. Numa meta‐análise de 111 estudos realizados em doentes com hepatite C crónica, Docetaxel supplier Thein et al. estimaram que a probabilidade cumulativa da progressão para cirrose 20 e 30 anos após a infeção é de 16% (IC 95%: 14‐19%) e 41% (IC 95%: 36‐45%), respetivamente28. A cirrose hepática tem uma fase de doença compensada e outra, mais tardia, de descompensação, quando surgem complicações da doença associadas à hipertensão portal e/ou insuficiência hepática (por exemplo, ascite, icterícia, encefalopatia hepática, rotura de varizes esofágicas, peritonite bacteriana espontânea, sépsis)2, 26 and 27. Estima‐se que anualmente 3‐6% dos doentes com cirrose hepática compensada sofram uma descompensação clínica grave26 (fig. 1). Após a primeira descompensação, a mortalidade aumenta para 18% no ano seguinte26. A taxa de sobrevivência a 5 anos é de 50%2.

A usual intake of 20 g protein at least, probably just after physical exercise, is recommended as muscle sensitivity to amino acids may be increased after exercise.24 Another aspect is the amino acid content of the protein source, as leucine has been reported as an interesting stimulating factor for muscle protein synthesis. From the available studies, it is accepted that 2.0 to 2.5 g of leucine intake should be contained in the amino acid mixture.24 and 25 Some individuals may not be able to tolerate

exercise (eg, those with acute myocardial infarction, unstable angina, uncontrolled arrhythmia) or very high protein/amino acid supplementation (eg, nondialyzed late-stage kidney patients). As always, all treatment decisions are guided by clinical judgment see more and a full perspective of the patient’s health condition. In these situations, muscle electrical stimulation may be

an effective therapy to help alleviate muscle loss.186, 187 and 188 PROT-AGE recommendations on dietary protein and amino acid quality for older people • The list of indispensable amino acids is qualitatively identical for young and old adults. For older people, a high-quality protein is one that has a high likelihood of promoting healthy aging or improving age-related problems and diseases. Protein quality was traditionally defined by amino acid composition,

as measured by Compound C an essential amino acid score or by the ratio of essential to nonessential nitrogen. It was believed that a high-quality protein supplied all needed amino acids in quantities sufficient to satisfy demands for ongoing protein synthesis in the human body; however, the definition of protein quality has evolved in recent years. Protein quality still considers amino acid content but also includes new concepts: digestibility and absorption of the protein, as well as newly recognized roles of specific amino acids in regulation of cellular processes.147 and 189 The following section reviews state-of-the-art understanding Roflumilast of protein quality and relates these concepts to practical aspects of protein intake by older adults. Nutritive amino acids were originally classified as essential (no endogenous synthesis pathway in humans possible) or non-essential (endogenous enzymatic synthesis possible). This simple classification did not take all physiological situations into account, so the classification was revised.190 and 191 Dispensable amino acids can be synthesized by the human body in sufficient amounts for all physiological situations. Indispensable amino acids are never synthesized in humans because enzymatic pathways are lacking; supplies must be provided from dietary sources.

, 2009). From occupational exposure studies, there is no evidence of adverse pulmonary effects from SAS exposure (ECETOC, 2006). Workers in SAS manufacturing industries did not exhibit fibrosis of the lungs (silicosis) or any other permanent respiratory ailments.

SAS, including surface-treated Angiogenesis inhibitor SAS, were not mutagenic in standard bacterial test systems with and without metabolic activation (Ames-test) and did not induce chromosomal aberrations in mammalian cells (ECETOC, 2006, EPA, 2011 and OECD, 2004). At highly cytotoxic doses of silica gel (Spherisorb® suspensions at concentrations of 80 and 160 μg/cm2), a weak induction of micronuclei was found in V79 cells in vitro. At doses lower than 40 μg/cm2, the test material failed to significantly increase

the frequency of micronuclei ( Liu et al., 1996), suggesting that micronucleus induction was a secondary or indirect result of other cytotoxic processes. Incubation of A549 lung carcinoma cells for 40 h with non-cytotoxic doses of amorphous silica particles synthesised according to the Stöber method (16, 60 and 104 nm) resulted in an increased number of micronuclei which was statistically not significant. In addition, other weak chromosomal effects were observed, but again without reaching statistical significance ( Gonzalez et al., 2010). The potential of four differently sized SAS particles (nominal sizes: 10, 30, 80 and 400 nm; actual sizes: 11, 34, 34 and 248 nm) to induce chromosomal Avelestat (AZD9668) aberrations and

gene mutations was studied using two in vitro genotoxicity assays ( Park et al., 2010a and Park Akt inhibitor et al., 2010b). The particles had been synthesised with the Stöber-method without stabiliser and were endotoxin-, bacteria- and fungi-free. Only the 80 (34) nm silica nanoparticles induced a weak, but statistically significant increase in the number of chromosomal aberrations in a micronucleus assay using 3T3-L1 mouse fibroblasts (quantitative data not shown in the original publication; test concentrations were 4, 40 or 400 mg/L). The 30 (34) and 80 (34) nm silica nanoparticles induced gene mutations in mouse embryonic fibroblasts carrying the lacZ reporter gene (quantitative data not shown in the original publication, but it is mentioned that the increases were at most three-fold and only for the 80 nm particles statistically significant). TEM imaging demonstrated that the majority of nanoparticles were localized in vacuoles and not in the nucleus of 3T3-L1 cells, indicating that the observed DNA damage was most likely a result of indirect mechanisms. DNA damage (most probably as a result of cytotoxicity or indirect mechanisms) was found in Comet assays performed on hamster and human embryonic lung fibroblasts, in a neuronal cell line (without dose-response) and with alumina coated SAS particles in a human breast cell line ( Kim et al., 2010, Pacheco et al., 2007 and Zhong et al., 1997). Yang et al.

Thus, it seems reasonable to think that Selleckchem Enzalutamide any additional anabolic effect of Cr supplementation on muscle hypertrophy can be attributed to an enhanced ability to train under high intensity and not to a direct effect on muscle. Previous studies have used the synergist ablation model to investigate the additional hypertrophy effect of Cr on skeletal muscle, independently of a higher workload in Cr-supplemented muscles. Moreover, these studies used indirect methods (muscle dry and wet weight) and small muscle biopsies to measure the increase in muscle mass. The advantages of our study

compared with previous studies in this area include full control over the environmental conditions of the subjects (temperature, food and Cr intake, and subjects’ motivation during training and lifestyle) and the direct analysis of muscle hypertrophy by measurement of the muscle fibers CSA. To our knowledge, we are showing, for the first time, that muscle Cr loading does not promote any additional hypertrophic effect on the oxidative slow-twitch soleus muscle fiber CSA when Cr-supplemented muscles are subjected to the same workload than Cr-nonsupplemented muscles. This rejects the hypothesis of this study that the beneficial effect of muscle GSI-IX in vitro Cr loading on muscle hypertrophy

is independent of a greater training intensity for Cr-supplemented muscle in relation to Cr-nonsupplemented muscles. Our findings indicate that any benefits of Cr supplementation on hypertrophy gains during resistance training might not be related to a direct anabolic effect on the

skeletal muscle. A limitation of this study was the absence of a Cr-supplemented trained group that performed the training with an overload higher than Cr-nonsupplemented trained group. This group could support the idea that Cr-supplemented muscles can train at a higher intensity than Cr-nonsupplemented muscles and, consequently, exhibit a greater hypertrophic response. Another limitation was the lack of Erythromycin tissue analysis to determine the levels of muscle Cr. Moreover, other analyses (eg, molecular and functional analyses) could be undertaken to support the morphometrical data. Future studies will be conducted to investigate the exact mechanisms by which Cr can promote an increase in muscle mass in different skeletal muscles as well as the possible relationship between the increased amount of Cr loading in muscles and the stimulation of hypertrophy-related myogenic pathways. In conclusion, we reject the hypothesis that Cr supplementation promotes an additional hypertrophic effect on the skeletal muscle independent of a greater training intensity on Cr-supplemented muscle in relation to Cr-nonsupplemented muscles.

, Ferraz de Vanconcelos, SP, Brazil) until the dough reached complete gluten development. Mixing times and speeds of hook and bowl (clockwise Galunisertib and anti-clockwise movements, respectively) were: 2 min in slow speed (190 rpm hook and 50 rpm bowl) and 4 min in fast speed (380 rpm hook and 100 rpm bowl). Refrigerated water was used and final dough temperature was monitored so as not to exceed 30 °C. Immediately after mixing, doughs were divided into pieces of 450 ± 1 g and rounded. Then, they were left to rest for 15 min in a Climática Evolution proofer (Super Freezer, Pouso Alegre, MG, Brazil) at 30 ± 1 °C and 80 ± 1% RH. After this time, the pieces were molded in a Perfecta molder (Perfecta, Curitiba, PR, Brazil), put

into pans and taken selleck products to the proofer

at 37 ± 1 °C and 80 ± 1% RH for 120 min. After proofing, breads were baked in a Prática oven (Prática Technipan, Pouso Alegre, MG, Brazil) at a temperature of 190 ± 1 °C for 20 min. After baking, breads were depanned, cooled (for approximately 1 h), sliced (1.25 cm thick) in a Maquipão electric slicer (Maquipão, São Paulo, SP, Brazil), packaged in low-density polyethylene plastic bags, closed with twisted ties and stored at room temperature (approximately 26 °C) until analyses. Pan bread apparent volume (V) was determined in mL by seed displacement, and mass (m), in grams, using a semi-analytic scale. Specific volume (SV) was calculated as the ratio (V/m). Specific volume determination was carried out 1 h after leaving the oven, in triplicate. Bread firmness was determined on Days 1, 6 and 10 after baking, according to AACC Method 74-09.01 (AACC, 2010). Bread firmness is defined as the force required in grams-force for a compression of 25% of a sample of bread of 25 mm thickness. The values of bread firmness were obtained using a

TA-XT2 texture analyzer (Stable Micro Systems, Haslemere, UK). Ten determinations (in 3 breads) of each assay were carried out. Four formulations, apart from the Control, were selected for sensory evaluation on Day 6 of storage. The evaluation was carried out using as basis the scoring system reported by El-Dash PRKACG (1978). Scores were given for the following attributes: external characteristics (volume, crust color, shred and symmetry), internal characteristics (crust characteristics, crumb color, crumb structure and crumb texture), aroma and taste; totalizing a maximum of 100 points. This score was converted into a global concept determined as: very good (>90), good (80–90), regular (70–80) and detestable (<70) (Camargo & Camargo, 1987). The breads were evaluated by a team of 5 specialists in bakery products. To evaluate the effect of the addition of different levels of SSL and of maltogenic amylase on pan bread quality during storage, an experimental design that permitted the analysis of the results through the Response Surface Methodology was used. The Statistica Software, version 7.0 (Statsoft Inc.