1%) and 526 (19.5%) [25]. Eight of the 14 different mutations observed in that study (57%) were present in our patient pool. The present study also emphasizes the frequency of codon changes at position 533. In clear contrast to previous reports [26] and [27], the majority of isolates in this study exhibited more

than one codon change (2–5). Many codon changes involved more than one base pair change. A significant portion appeared to involve a two-base pair inversion, while others were likely to involve multiple base pair substitutions through point mutations. The selleck inhibitor high GC/AT ratio may contribute mechanistically to the mutability of this hot spot region. Noticeably, codon changes at 533 were accompanied by other codon changes in almost all of the isolates (with one exception). Changes at this position are reported to result in variable resistance; therefore, additive resistance could be a significant resistance mechanism in these strains. Some rpoB codon changes have been shown to cause cross-resistance to antibiotics other than rifampicin in M. tuberculosis isolates. Codon changes at 513, 526, and 531 are associated with high-level resistance to rifampicin and rifabutin. Codon changes at 514, 515, 516, 522, and 533 have been reported

to cause rifampicin resistance concomitant with susceptibility CHIR-99021 mouse or low resistance to rifabutin [28]. Thus, depending on the genotype, the use and disuse of other antibiotics (e.g., in second-line Tb drug treatment) can be suggested

[28]. However, this conclusion depends on the assessment of the novel codon changes and the additive effects of multiple codon changes. Despite the dominance of isolates with the genotype S531 L, the diversity of the isolate PJ34 HCl genotypes is striking. With respect to the 18 isolates obtained from Aleppo, 6 had the S531 L genotype, while the rest (12) had 9 different genotypes. This diversity is consistent with the lower exogenous transmission of resistant strains in Syria, which was suggested by a previous strain genotyping study [21]. One drawback of this study is the small number of Lebanese samples, which cannot be considered representative of the rpo B pool of mutations in Lebanon. Future comparisons with other neighboring countries await more extensive local studies of the rpoB sequence. The authors have no competing interests to declare. This research was funded by the Lebanese University and the Syrian Ministry of Higher Education. “
“GAS TSS is an uncommon form of septicemia caused by Streptococcus pyogenes (Lancefield group A), which is also the pathogen responsible for scarlet fever and other Streptococcal soft tissue infections. As with Staphylococcal TSS, invasive Streptococcal diseases are also caused by biologically potent exotoxins that mediate fever, shock, and tissue injury [1].

Tabara et al. have shown that complete loss of the activating EGFR mutant gene results in the gain of a novel addiction to HER2/HER3 signaling and the acquisition of EGFR-TKI resistance in vitro [22]. In our resistant cells (4D8 and B10), cell proliferation was partially blocked buy Navitoclax by HER2 or HER3

knockdown (Supplementary Fig. 6). These findings indicate that the EGFR-unamplified resistant cells partially depend on not only EGFR but also HER2/HER3 signaling for survival. Compared with other solid tumors, NSCLC is well known for the heterogeneity of the cell populations in individual lesions [23]. Heterogeneous distribution of EGFR mutations in individual tumors has also been reported [24], [25] and [26]. In addition, loss of an EGFR mutation is reported in 3 out of 11 EGFR-mutated NSCLC patients with progressive disease after gefitinib treatment [22]. These findings indicate that some NSCLCs are genetically heterogeneous and concurrently have tumor cell populations

with either mutant or wild-type EGFR, and that the EGFR genetic heterogeneity might contribute to acquired resistance to EGFR-TKIs. Our results strongly support this mechanism of resistance, because we have clearly shown that the genetic heterogeneity of EGFR is constantly maintained by the loss of an EGFR-ampch7 in NSCLC cells with EGFR EX 527 cost mutations. In conclusion, we demonstrated that loss of amplified EGFR-mutated genes causes acquired resistance in HCC827 cells when the cells are exposed to a relatively low concentration of erlotinib, whereas high concentration of erlotinib

prevents the emergence of resistance. In addition Fenbendazole to the major known mechanisms of acquired resistance to EGFR-TKIs, including secondary mutation of T790M, amplification of MET, mutations of PIK3CA, EMT, and transformation to SCLC [8], our findings propose a novel acquired resistant mechanism, namely, the selection of preexisting EGFR-unamplified cells, which are generated by the loss of an amplified EGFR-mutated gene, may contribute to the acquired resistance to EGFR-TKIs. Further studies are needed to identify alternative addictive signal pathway(s) after the loss of amplified EGFR with mutation and to lead to the development of a novel molecular targeted therapy against EGFR-TKI-refractory NSCLC. None. The authors thank Kumiko Kondoh, Hiromi Sawamura and Masako Takahashi for technical assistance in the experiments, and also thank Kazushige Mori, Naohito Inagaki, Masamichi Sugimoto and Keiji Kosaka for support and special advice in this study. “
“Lung cancer currently causes more deaths from cancer in the world than any other tumor type, and projections over the next 20 years indicate this is likely to continue unless substantial progress is made in areas such as screening, early detection, treatment and prevention.

120 However, the treatment duration employed in this study (5 days every 28 days for 9–12 cycles) may have been suboptimal in a population of patients with chronic infection. 121 Ongoing and future trials will inform us if inhaled antibiotics are a useful therapeutic option in the prevention of exacerbations

of COPD. Acute, efficacious antibiotic Raf inhibitor treatment is the mainstay in the management of patients with severe COPD and symptomatic exacerbations that include at least 2 of the 3 cardinal symptoms (increased sputum purulence, volume and increased dyspnoea; Anthonisen type I or II exacerbations). Although such treatment is associated with clinical benefit, treatment failure and relapse rates may Regorafenib solubility dmso be high in patients with the frequent exacerbator phenotype. Failure may be related to inadequate antibiotic efficacy through incomplete resolution of the initial exacerbation and persistent bacterial infection.23, 24, 25 and 26 These factors have led to recommendations for a stratified approach to antibiotic therapy based on patient risk factors.15 Patients at greatest risk for poorer outcome (i.e. those with complicated COPD) are likely to derive greatest benefit from early treatment with the most potent antibiotic therapy, such as amoxicillin/clavulanate and respiratory fluoroquinolones which

have a broad spectrum of activity against likely pathogens.28, 122, 123 and 124 The use of the most efficacious antibiotics in patients

with risk factors may be crucial in preventing relapses or delaying subsequent exacerbations which appear to cluster in time, and if the exacerbation Cell press is poorly controlled there is a high risk of the next episode occurring within a few weeks.30 A significant relationship exists between bacterial eradication at the end of antibiotic treatment and no relapse in the following eight weeks.28 Studies conducted in the last 20 years suggest that long-term or intermittent antibiotic therapy may have a beneficial effect on the outcome of COPD patients and may improve quality of life by reducing exacerbation frequency and hospitalisations for exacerbations, or by extending time to next exacerbation. The mechanisms underlying such improvements are unclear. It is possible that the benefit of long-term antibiotic treatment may be due to a reduction in the frequency of exacerbations due to eradication of colonising potentially pathogenic bacteria and/or reduction in chronic airway inflammation,37 though the evidence supporting such a hypothesis is limited. While macrolides are known to have both antibacterial and anti-inflammatory effects, it is unknown to what degree these actions are responsible for their efficacy when used for the treatment of chronic respiratory conditions.

Finally, changing the ratio at which ligands are released with respect to carbon (Fig. 6c) leads to a more uniform change in the average ligand profile. These characteristic

sensitivities of the ligand profile lead to corresponding sensitivities of the iron distributions. selleck kinase inhibitor Fig. 7 shows the covariation of globally averaged ligand and iron concentrations for the sensitivity runs. On the left we show the average over the whole water column, on the right the average over the top 50 m. The left plot in Fig. 7 shows that — independent of which parameter we change — the change in total iron content in the ocean is tightly coupled to the change in total ligand content, with all sensitivity experiments falling nearly on one line. It is interesting to note that in the global average, iron concentrations fall below the 1:1 line, i.e. Selleckchem BTK inhibitor the ligand excess L⁎ is always positive. A similar linear relation between dissolved iron and ligands has been also found in in-situ data from the Bering Sea ( Buck and Bruland, 2007). Of all the sensitivity experiment, changing the photochemical degradation rate (by a factor of 5) has the least

effect on global ligand and iron concentrations, which is mostly because changes are limited to the upper ocean only. Changes in average ligand and iron concentration near the surface (right plot in Fig. 7) are less universally coupled: While an increase in ligand always leads to an increase in iron and vice versa, the slopes of the relations are significantly different. A decrease in ligands through an increase in photochemical degradation affects ligand concentrations most strongly in the subtropical Pacific, with high mixed-layer irradiances and low production. Here iron concentrations are low anyway and decreasing ligands does not lead to further decreases. Paclitaxel Decreasing ligand to carbon ratios, on the other hand affects ligand production everywhere, also in regions where they affect iron residence time strongly, and hence lead to a stronger iron reduction. The number of open-ocean observations of iron-binding ligands has steadily increased

over the last decade or so, and will further do so as the international GEOTRACES program continues. One clear result of these in-situ measurements is that iron-binding ligands show substantial spatial variability in ligand concentrations between different oceanic regions (1 to 10 nM, Gledhill and Buck (2012)). In contrast, ocean biogeochemical models mostly still assume a uniform and comparatively low ligand concentration (typically between 0.6 and 1 nM). There are some exceptions to this (Tagliabue and Völker, 2011 and Misumi et al., 2013), but even these newer studies rely on empirical relationships and do not attempt to describe the sources and sinks of ligands prognostically, despite the existence of a conceptual model for their dynamics (Hunter and Boyd, 2007 and Ye et al., 2009).

Tollefsen et al. (2008) studied the cytotoxicity

of a range of APs in cultures of primary hepatocytes from rainbow trout. Toxicity measured as metabolic inhibition and loss of membrane integrity increased with the hydrophobicity of the APs for compounds with logKOW < 4.9, but deviated from this for more hydrophobic compounds (logKOW > 4.9). Metabolic inhibition occurred at lower concentrations than loss of membrane integrity for most of the APs, which suggests that effects on cellular metabolic functions were the main causes of the cytotoxicity. The study gives insight into the structure–toxicity relationship of important PW components, but it is difficult to extrapolate to real PW exposure. Still, for chemicals with logKOW < 2–3 www.selleckchem.com/products/atezolizumab.html the metabolic high throughput screening inhibition and to a lesser degree also loss of membrane integrity was claimed to correspond to reported in vivo acute toxicity in fathead minnow (Pimpehales promelas) ( Schultz et al., 1986). The in vitro toxicity of the more hydrophobic compounds underestimated the in vivo toxicity in this fish. Meier et al. (2010) found that exposure of Atlantic cod to PW during the embryonic and early larval stages (up to 3 months of age) and during the early juvenile stage (from 3 to 6 months of age) had no effect on embryo survival or hatching success, but 1% PW interfered with the development of normal

larval pigmentation. After hatching most of the larvae exposed to 1% PW failed to begin feeding and died of starvation. This inability to feed may be linked to an increased frequency of jaw deformities in the exposed larvae. No similar effects were seen at exposure to 0.1% and 0.01% PW. Analysis

of DNA adducts in fish tissue has been recommended for assessment of genotoxic effects of contaminants in PW (Balk et al., 2011 and Hylland et al., 2006). Similarly, the micronuclei frequency method has been found sensitive and feasible for use as a biomarker of genotoxicity in blue mussel exposed to PW contaminants (Brooks et al., 2009). Holth et al. (2009) found time and dose dependent formation of DNA adducts in Atlantic cod exposed for 44 weeks to APs and a WSF of oil. Elevated DNA adduct values have been measured Montelukast Sodium in wild haddock in the Tampen region in 2002, 2005 and 2008 (Balk et al., 2011, Grøsvik et al., 2010 and Hylland et al., 2006). The cause of the effect was unclear, as the DNA adduct signal could possibly stem from recent PW discharges or from fish being in contact with PAHs or other contaminants in deposits of drill cuttings. Monitoring surveys at the Ekofisk field have detected elevated micronuclei frequencies in blue mussel caged up to 1.6 km from the discharge point (Sundt et al., 2008). After implementation of a new PW treatment system elevated micronuclei frequencies were only detected in cages at 500 m distance (Brooks et al., 2009). Brooks et al. (2011a) studied the biological impact of treated PW under laboratory conditions in the blue mussel.

As shown in Fig. 11A, the mushroom bodies are divided in the peduncle and calyx, which consists of the lip, collar, and basal rings, and in the non-compact and inner compact Kenyon cells. A myosin-Va antibody recognized proteins in the peduncle and calyx (Fig. 11C and D), which also contain high zinc concentrations (Fig. 11B), whereas synaptophysin

localization learn more was restricted to the Kenyon cells (Fig. 11E and F), visualized in blue by cresyl violet (Fig. 11A). An affinity-purified polyclonal antibody against chicken myosin-Va, an ancient myosin conserved from yeast to mammals (Berg et al., 2001), was successfully used to identify its heavy chain in the honey bee brain and to immunolocalize this myosin in brain sections. Myosins -IIb, -VI and -IXb, cytoplasmic dynein intermediary chain (DIC74), light chain DYNLL1/LC8, CaMKII and SNARE proteins were also immunodetected in the honey bee brain. The DNA sequences of these immunodetected myosins and cytoplasmic dynein in the honey bee brain were found in the A. mellifera genome and in the genomes of other species ( Odronitz et al., 2009). Bioinformatic analyses using the Blastp tool showed a high level of sequence similarity for these proteins in the honey bee and vertebrates (e-value 0.0). In regards to myosin-Va, there is a UniGene record for an A. mellifera nucleotide sequence Depsipeptide ic50 (Ame.1621, similar

to myosin VA, heavy polypeptide 12, myoxin, LOC726456), the transcribed sequence of which matches the head domain of D. melanogaster myosin-V. Our results indicated myosin-Va was present in the honey bee nervous system in larvae and adult castes and subcastes using an antibody

that also cross-reacts with myosin-V from the extruded axoplasm of the squid optical lobe ( Tabb et al., 1998). To examine the potential for cross-reactions between honey bee brain proteins and antibodies generated against vertebrate proteins, we probed Western blot of brain samples from rabbit, rat and honey bee with chicken brain myosin-Va and bovine brain CaMKII antibodies. The expression CaMKII gene has been previously reported in the honey bee brain by (Kamikouchi et al., 2000). Moreover, microtubule- and actin-based motors, such as dynein and myosins (classes II, V, VI and IX), were immunodetected in MycoClean Mycoplasma Removal Kit the honey bee brain, which indicates that molecular motors and SNARE proteins could potentially be studied as neuronal targets in the honey bee nervous and visual systems. As recently reviewed by Hirokawa et al. (2010), the kinesin, dynein, and myosin superfamilies of molecular motors play fundamental roles in neuronal function. In addition to our findings that report dyneins and myosin-IIb and -IXb for the first time in the honey bee brain, other studies have shown that myosin-IXb is expressed in the rat brain (Chieregatti et al., 1998) and myosin-IIb is associated with synaptic function (Rex et al., 2010 and Ryu et al., 2006).

The biological significance of repetitive RNA editing is largely unknown, but examples have shown involvement in RNA induced gene silencing (RNAi) and microRNA (miRNA) modulation, stabilization of mRNA and nuclear retention (Figure 4) [38]. Viral RNA is also often deaminated by host ADARs which has pro- or antiviral effects depending on the specific type of virus (Figure 4) [39]. Since the identification of ADAR and ADAT enzymes in the early

90s, the presence and importance of inosine in RNA have been well recognised [31]. A-to-I editing of RNA substrates are rarely complete and it appears that ADAR activity is dynamically regulated through yet poorly I-BET-762 nmr understood mechanisms [34]. In addition to tight regulation of ADAR activity, specific destruction of A-to-I edited transcripts could be a way to control the level of editing. ZD1839 supplier Until very recently, no such activity was proven. Last year, Morita et al. [ 40••] and Vik et al. [ 41••] both demonstrated efficient cleavage of inosine-containing RNA by human EndoV suggesting that EndoV could fulfill such a role ( Figure 2b). The cytosolic localization of hEndoV supports this notion [ 42]. Another protein, the Tudor staphylococcal nuclease 1 (Tudor-SN) has also been linked to processing of inosine-containing RNA [ 43 and 44] ( Figure 2b). Tudor-SN was initially identified in extracts from Xenopus laevis by its ability to bind inosine-containing RNA [ 43]. Tudor-SN has five staphylococcal

nuclease-like domains (SN1–5) in addition to one tudor domain and is a multifunctional protein participating in diverse processes including RNAi, transcriptional coactivation and mRNA splicing [ 45]. The specific activity for Tudor-SN for inosine-containing RNA has not been

thoroughly addressed and the individual contribution of EndoV and Tudor-SN remains to be elucidated. The concentrations of cellular nucleotides are highly controlled [46 and 47]. Defects in genes involved in the nucleotide metabolism and imbalance in the nucleotide pools are found in several human diseases such as immunodeficiency, hyperuricemia with neurological filipin symptoms (Lech-Nyman syndrome) and several types of cancer [48 and 49]. One possible mechanism underlying these pathologies involves the formation of non-canonical NTPs with subsequent incorporation into DNA and RNA contributing to mutagenesis and carcinogenesis. Cells express enzymes counteracting such threats, for example inosine triphosphate pyrophosphatase (ITPA in mammalian cells, RdgB in E. coli) that hydrolyses dITP to its monophosphate form. Mutations in the ITPA orthologs in model organisms lead to genetic instability and, in mice, to severe developmental abnormalities [ 50]. It has been shown that Itpa−/− mice accumulates inosine in DNA and RNA [ 51• and 52]. In contrast, ITPA deficiency in human is seemingly innocuous, but has been linked to psychological disorders [ 53] and overexpression of ITPA is seen in several cancers [ 54].

Details on all patients find more were captured on a prospective database, BrachyNet. No patients were lost to followup. At each review, patients completed standard survey forms, including International

Prostate Symptom Score (IPSS), rectal toxicity, and erectile dysfunction. Urethral stricture events were collected prospectively. A stricture was documented if a patient underwent a surgical procedure for a stricture (dilation or urethrotomy). This definition is equivalent to Grade 2 or higher Common Terminology Criteria for Adverse Events version 3 toxicity (9). The medical records and surgical report, when available, were used to identify the site of the stricture. The risk of stricture was compared among the various dose groups (the dose fractionation schedule 18 Gy/3, 20 Gy/4, 19 Gy/2, or 16 Gy/2). Potential confounding factors were identified: urinary retention (defined as requiring an in-dwelling catheter within 2 weeks following the removal of the HDRB needles), previous transurethral resection of prostate (TURP), order of the treatment (HDRB before or after EBRT), the IPSS, the radiation oncologist, and the urologist. The managing urologist was included because the definition of stricture relies on a surgical procedure.

This makes the definition of stricture subjective, and potentially the urologist’s intervention “threshold” may influence Selleck GSK126 the stricture rate. The end point was date of first stricture. Time to stricture formation was calculated from the date of HDRB implantation. Otherwise, the date for analysis was date of last followup or date of death. Analysis was done using

STATA version 8. Nelson–Aalen cumulative hazard modeling was used to estimate risk over time. Thiamine-diphosphate kinase The statistical significant of difference between hazard curves was calculated using the log-rank test. Univariate and multivariate analysis was performed using a Cox proportional regression model. A two-sided p-value of less than 0.05 was considered significant. Interactions between variables were tested by separately adding factors into the model. All variables in the univariate model were used for the multivariate analysis. A biologic model was also used to evaluate the total dose received by the urethra. Three hundred fifty-four patients were treated with an HDRB at William Buckland Radiotherapy Center (Table 1). The median age was 65 years. Low-, intermediate-, or high-risk nonmetastatic prostate adenocarcinoma made up respectively 2.5%, 65%, and 19.5% of patients. Forty-three patients received 20 Gy/4, 214 patients received 18 Gy/3, and 95 patients received 19 Gy/2. Two patients received 16 Gy/2 fractions as described above. In total, 45 patients had one or more strictures: 5 in the 20 Gy/4 group (11.6%), 20 in the 18 Gy/3 group (9.3%), and 20 in the 19 Gy/2 group (21%). Neither of the two patients who received 16 Gy developed a stricture. Thirteen patients had a dilatation, whereas 32 had an urethrotomy as initial management.

, 2012). Certain organophosphate methyl esters in organophosphate compounds allow promutagenic alkylation damage to DNA, which in turn can produce methylation of DNA (Ray and Richards, 2001). In addition, pesticides exposure can also interact with other methylation-related factors, for example, methyl-donor-related dietary factors and genetic predispositions, to confer increased NHL risk. Epigenetic modifications are relative stable over time and may be influenced by the environment. Exposure to pesticides may lead to epigenome modifications. Experimental, clinical, and epidemiological studies of epigenetic changes caused by pesticides exposure have increased our understanding of the

mechanisms of action by which they can modify gene expression. Most of the studies conducted so far click here have been centered on DNA methylation, whereas only a few recent investigations have studied the effects on histone modifications and miRNAs. Many questions remain open, for example if the learn more observed effects may be the result of the exposure either to a single pesticide compound or to a complex mixture of different chemicals. Far from being conclusive, the reported evidences suggest

that epigenetic modifications may be one of the mechanism by which pesticides can have noxious effects on human health. Further studies are warranted to evaluate if epigenetic modifications may act as a causal link between pesticide exposure and health effects,

or rather be a sensitive marker of exposure. The authors state that they have no conflict of interest. This work was support by INAIL Foundation and Lombardy Region Research Contracts UniMi 8614/2006 and UniMi 9167/2007. Dr. Bollati received support from the EU Programme “Ideas” (ERC-2011-StG 28413). “
“This article has been removed: please Depsipeptide mouse see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been removed at the request of the author. This abstract was inadvertently published in the journal when the authors had requested that it should not. “
“This article has been removed: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been removed at the request of the author. This abstract was inadvertently published in the journal when the authors had requested that it should not. “
“This article has been removed: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been removed at the request of the author. This abstract was inadvertently published in the journal when the authors had requested that it should not. “
“This article has been removed: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been removed at the request of the author.

Blocking lymphocyte localization to the gastrointestinal mucosa as a therapeutic strategy for inflammatory bowel diseases. Gastroenterology RO4929097 in vivo 2011;140:1776–1784. In the above article it should be noted that Drs Eduardo J. Villablanca and

Barbara Cassani contributed equally to this work. Also, Drs Ulrich H. Von Andrian and J. Rodrigo Mora contributed equally to this work. “
“Hsu P–I, Lai K–H, Liu C–P. Esomeprazole with clopidogrel reduces peptic ulcer recurrence, compared with clopidogrel alone, in patients with atherosclerosis. Gastroenterology 2011;140:791–798.e2. Dr Ping–I Hsu, first author in the above article, is affiliated with Kaohsiung Veterans General Hospital and National Yang-Ming University. “
“Pawlotsky J–M. The results of phase III clinical trials with telaprevir and boceprevir presented at the liver meeting 2010: a new standard of care for hepatitis C virus genotype 1 infection, but with issues still pending. Gastroenterology 2011;140:746–754. On page 751 in the above article, below the paragraph JAK assay heading, “What Is the Importance of Adherence to Treatment?” The sentence: “Full adherence to the protease inhibitor may be easier with telaprevir for 12 months than with boceprevir for 24 or 44 months.” should be corrected to read: Full adherence to the protease inhibitor may be easier with telaprevir for 12 weeks than

with boceprevir for 24 or 44 weeks. “
“Hoechst B, Ormandy LA, Ballmaier M, et al. A new population of myeloid-derived

suppressor cells in hepatocellular carcinoma patients induces CD4+CD25+Foxp3+ T cells. Gastroenterology 2008;135: 234–243. In figure 1C of this article, the y-axis was originally labeled as % CD14-HLA-DR-/low. The authors would like to clarify that figure 1C shows the frequency of HLA DR-/low population in CD14+CD19- PBMC. The y-axis of figure 1C has been modified accordingly as %HLA DR-/low cells in CD14+CD19- PBMC in the figure below and in the online version of Gastroenterology. “
“Common beans (Phaseolus vulgaris L.) are susceptible to the hardening (hard-to-cook) phenomenon during their shelf life, which has directly affected the consumption of this food. Although bean present many nutrients that make their consumption Sinomenine advantageous ( Cardador-Martínez, Loarca-Piña, & Oomah, 2002; Leterme, 2002; Oomah, Corbe, & Balasubramanian, 2010), they have been passed over because of less nutritious foods, or foods with faster cooking time and also precooked foods. This fact is a reflection of changing dietary habits of the population, and especially to the time required for cooking common beans ( Leterme & Muñoz, 2002). Breeding programs aim to develop new cultivars that meet consumer preference for appearance and textural characteristics, so this food of high nutritional value is not completely replaced by poor nutritional foods.