Die Huntington-Krankheit (HK) ist eine von George Huntington im Jahr 1872 zum ersten Mal beschriebene progressive neurodegenerative

Störung, die spät ausbricht, und zwar im Median im Alter von 39 Jahren. HK wird autosomal dominant vererbt und die Prävalenz liegt bei etwa 5 pro 100.000 Personen weltweit bzw. 1 pro 10.000 Personen in den USA [135]. HK ist gekennzeichnet durch motorische Beeinträchtigungen, Verschlechterung der kognitiven Funktionen, Gefühlsstörungen und psychiatrische Defizite. Die motorischen Symptome setzen ein mit Chorea, Alectinib purchase Gleichgewichtsstörungen, Dystonie, Koordinationsproblemen und Blickapraxie und schreiten fort zu Akinesie in späteren Stadien. HK-Patienten leiden außerdem an Gefühlsstörungen, wie z. B. Depressionen, Launenhaftigkeit, Apathie und Reizbarkeit, sowie buy CP-868596 kognitiven Defiziten in Bezug auf das Kurzzeitgedächtnis, die Aufmerksamkeit und die Lernfähigkeit. In der Tat können die kognitiven und emotionalen Symptome der HK den motorischen um mehrere Jahre vorausgehen [136] and [137]. HK wird durch die Expansion des glutamin-codierenden Triplett-Repeats (CAG) des normalen HTT-Gens verursacht [76], [135] and [138]; das Vorliegen von mehr als 36 Repeats ist krankhaft. Es ist wichtig anzumerken, dass zwischen dem Alter bei Ausbruch der Krankheit und der Zahl der Repeats eine umgekehrte Korrelation besteht [139]. Je länger der CAG-Repeat ist, desto

größer ist darüber hinaus der Einfluss, den

die Repeat-Länge auf das Alter bei Krankheitsausbruch hat. Bei Repeat-Längen von weniger als 50 gehen jedoch nur etwa 44 % der Varianz hinsichtlich des Ausbruchsalters auf die Repeat-Länge zurück [140]. Im Gegensatz dazu treten bei Personen mit 60 Repeats oder mehr Symptome ausnahmslos spätestens im Alter von 20 Jahren auf. Es wird angenommen, dass Umweltfaktoren (also nicht-familiäre Faktoren) einen erheblichen Anteil Fluorouracil clinical trial zur Restvarianz des Ausbruchsalters beitragen [140]. Nach Identifikation der Mutation, die die HK auslöst, gab es mehr als zehn Jahre lang widersprüchliche Berichte über den Zusammenhang zwischen vollständiger oder unvollständiger Penetranz der HK und der Länge der Triplett-Expansion. Es wurde vorgeschlagen, dass auch Umweltfaktoren einen Beitrag zur Restvarianz des Ausbruchsalters leisten könnten, möglicherweise sogar einen größeren als genetische Faktoren [140] and [141]. Gómez-Esteban und andere haben bei Zwillingsstudien Umweltfaktoren für Unterschiede beim Ausbruchsalter und beim klinischen Erscheinungsbild verantwortlich gemacht, da Zwillinge dieselbe Anzahl an Repeats aufweisen [142], [143], [144] and [145]. Bei diesen Zwillingsstudien wurde die Art der beteiligten Umweltfaktoren jedoch nicht aufgedeckt. Darüber hinaus ergaben sich auch aus Studien an Tiermodellen für HK weitere Belege für einen Einfluss von Umweltfaktoren auf den Ausbruch und das Fortschreiten der HK [141] and [146].

In the present study, we attempted to add cholesterol

to the oocyte plasma membrane using MβCD as a vehicle. We aimed to increase the cholesterol: phospholipid rate to improve oocyte vitrification results. For our approach, we loaded MβCD with cholesterol removed from FCS by incubating it overnight in a medium enriched with serum. After Linsitinib mouse incubation, MβCD loaded with cholesterol was added to medium containing the immature bovine oocytes, which were then exposed to cold treatments and assessed for cytoplasmic as well as nuclear viability. In the first experiment, different concentrations of MβCD were tested to determine if it could protect oocytes during their exposure to a 4 °C cold stress for 10 min. It was very clear that this duration of exposure was sufficient to affect oocyte viability and cause a subsequent decrease in nuclear and cytoplasmic maturation as well as an increase in degenerated oocytes. These results were similar to those observed by Wu et al. Wu et al. [39] who demonstrated

that www.selleckchem.com/products/AG-014699.html storing bovine immature oocytes at 4 °C for 10 min substantially reduced their maturation and cleavage rates. Our results also showed that short MβCD exposure did not effectively protect oocytes against cold stress, as different concentrations did not increase the percentage of oocytes that reached MII by the end of the maturation period. However, it is worth mentioning that the MβCD-treated groups displayed a reduction in oocytes with degenerated chromatin. These results indicate that cyclodextrin might positively affect oocytes. Similar to nuclear maturation, the exposure to MβCD treatments PIK3C2G did not improve either the cleavage rate or blastocyst production. To analyze whether the time of exposure to cold stress in the first experiment was insufficient to detect the effect of MβCD, a second experiment was designed that increased the exposure time to cold stress from 10 to 30 min. Because no differences were observed with the different concentrations of MβCD, an intermediate concentration of 2 mg/mL was used. The amount of time of cold stress exposure in oocytes did not seem to

be the main cause of the cold-related damage, as increasing the time did not alter the rate of MII oocytes after IVM. Oocyte maturation was still significantly affected, regardless of the presence of MβCD, when the temperature was reduced to 4 °C even for a short period of time. Treatment with MβCD did not protect oocytes nor improve the maturation rates of the nucleus or cytoplasm. Finally, we tested the effect of MβCD on oocytes prior to vitrification. Oocytes incubated with or without cholesterol-loaded MβCD were vitrified and subsequently matured, fertilized and cultured in vitro. In this experiment, MβCD lowered the percentage of oocytes that underwent degeneration, while a higher percentage of oocytes reached MII stage. This beneficial effect was not observed in our previous experiment when oocytes were exposed to 4 °C temperature but not vitrification.

Along with the vertically binned ice shelf thickness distribution, Fig. 7(b) also shows the mean melt rates within each

depth bin (right axis) for nine different experiments, corresponding to the strongest (130), weakest (30), and intermediate wind forcing (100) for each of the three different hydrographic scenarios, temporally averaged over the respective last model year. The results generally reflect the spatial pattern of Fig. 7(a), with high melt rates above 10 m year−1 only occurring at deep ice below 400 m, and melt rates of less than 1 m year−1 at ice depths between 200 m and 400 m for all experiments. Somewhat higher melt rates of up to 3 m year−1 also occur at locations of very shallow ice above Belnacasan nmr 200 m depth, corresponding to enhanced melting Selleck GSK1120212 near the ice front. The contribution to the total basal mass balance within a given depth bin, obtained by multiplying the vertically binned mean melt rates by the ice shelf area distribution, is shown in Fig. 7(c), with three main features being evident

from the graph.3 Firstly, the deep and shallow melting respond in opposite ways to winds. Melting of shallow ice above 400 m increases with the strength of the wind forcing, whereas melt rates below 400 m are largest for the weakest winds for all hydrographic scenarios. Secondly, melting of both deep ice and shallow ice, are strongest in the constant summer scenario and weakest in the constant

winter scenario for equal wind forcings. Thirdly and perhaps most noticeably, the melting response is strongly modulated by the uneven distribution of ice shelf area. In most experiments, the basal mass loss is Baricitinib dominated by weak melting of large areas of shallow ice, while substantial changes of the mass loss at very deep ice only occur for the extremely large deep melt rates in the ANN-30 and SUM-30 experiments shown in Fig. 7(c). The characteristic depth-dependent melting response to varying forcing is summarized in Fig. 9(a) and (b). The colored curves are identical in both panels, showing the total amount of melting for the entire ice shelf as function of the wind forcing. The colored patches show the contribution of melting only from ice deeper than 300 m (Fig. 9(a)), or from melting at ice shallower than 300 m (Fig. 9(b)), respectively. For an applied surface stress above 60% of the climatological average (indicated by the vertical lines in Fig. 9), the melting response in all hydrographic scenarios is dominated by changes of the shallow melting contribution, which correlates roughly linearly with the applied surface stress (Fig. 9(b)).

S5). CNTNAP2

hybridization signals were observed in layers II–VI in both V1 and V2 at P0 ( Fig. 5). CNTNAP2 hybridization signals in layers II, III, IVc, and VI in V1 were stronger than in other layers ( Fig. 5). In adulthood, CNTNAP2 hybridization signals were observed in layers II–VI in both V1 and V2, although signals in layer VI were higher in V1 than V2 ( Supplementary Fig. S5). CMIP hybridization signals were observed in layers II–VI in both V1 and V2 at P0 ( Fig. 5). CMIP hybridization signals at P0 were particularly strong in layers II, III, IVc, and VI in V1, and layers II, III, and VI in V2 ( Fig. 5). CMIP expression levels were lower in adulthood than P0, but detected in layers II, III, SB431542 chemical structure and VI in V2, and layers II and VI in V1 ( Supplementary Fig. S5). ROBO1 hybridization signals were observed in layers II, III, and VI in V1, and in layers II, III, V, and VI in V2 at P0 ( Fig. 5). ROBO1 hybridization signals in layers II and III were higher in V2 than in V1 ( Fig. 5). By contrast, ROBO1 hybridization signals were not observed in V1 or V2 in adulthood ( Supplementary Fig. S5). KIAA0319 hybridization signals were observed in layers II,

III, V, and VI in both V1 and V2 at P0 ( Fig. 5). KIAA0319 hybridization signals in layers II and III were higher in V2 than V1 ( Fig. 5). By contrast, KIAA0319 hybridization signals were not detected in adulthood ( Supplementary Fig. S5). DCDC2 hybridization signal second was not detected in V1 or V2 Epacadostat research buy at P0 or adulthood ( Fig. 5 and Supplementary Fig. S5). FoxP2 hybridization signals were observed in layers V and VI in the primary auditory cortex at P0 (Fig. 5), but signals were very weak in adulthood (Supplementary Fig. S5). FoxP1 was expressed in layers III–VI at P0 and adulthood (Fig. 5 and Supplementary Fig. S5). CNTNAP2 hybridization signals were observed

in all layers at P0 and adulthood (Fig. 5 and Supplementary Fig. S5). CNTNAP2 expression levels were higher in layers II and IV than the other layers at P0 (Fig. 5), and CNTNAP2 was broadly expressed throughout all layers in adulthood (Supplementary Fig. S5). CMIP hybridization signals were observed in all layers at P0, although the signal in layers II and IV were higher than other layers (Fig. 5). CMIP hybridization signals were observed in layers II–VI in adulthood, with higher signal in layer II than other layers (Supplementary Fig. S5). ROBO1 was expressed in layers II–VI at P0 (Fig. 5), with reduced expression levels in adulthood (Supplementary Fig. S5). ROBO1 was more highly expressed in layer II than the other layers at P0 (Fig. 5). KIAA0319 hybridization signals were observed in layers II–VI at P0 (Fig. 5), but not in adulthood (Supplementary Fig. S5). DCDC2 hybridization signal was not observed in the primary auditory cortex at P0 or adulthood (Fig. 5 and Supplementary Fig. S5).

05), except between dark and medium roasted filtered brews. Similar results were reported in a previous study by Tfouni et al. (2012) where no correlation was found between PAHs levels and the roasting degree of ground roasted coffee.

This is due to the high variability of the process, as shown by the results obtained within the same cultivar and roasting degree, submitted to the same brewing procedure. The coefficients of variation of the process replicates ranged from 12% (C. canephora cv. Apoatã, IDH tumor dark roasted, boiled) to 62% (C. canephora cv. Apoatã, medium roasted, filtered). This high variability is probably due to the roasting process since, although the temperature of the roaster was set at 200 °C, when green coffee beans are placed inside, the equipment suffers a temperature variation that is inherent to the roasting process. The internal temperature drops and then starts to increase again throughout the process. Although there was an effort to maintain the same roasting profile for replicates of all processes, some differences were observed, with some samples reaching higher temperatures

in a shorter/longer period of time than others ( Tfouni et al., 2012). Other authors presented results of PAHs levels in relation to coffee roasting process. Kayali-Sayadi, Rubio-Barroso, Cuesta-Jimenez, and Polo-Díez (1999) reported higher PAHs concentrations for brews made from commercial ground roasted coffees (2.87 ng/L) than the ones made from green or decaffeinated (1.99 and 1.65 ng/L, respectively),

Epigenetic inhibitor concentration there was no mention on the samples roasting degree. Houessou et al. (2007) did not detect or detected only traces of BbF, BkF and BaP in coffee brews prepared from ground coffees roasted for 5 min under different temperatures. BaA was detected in the range of traces to 0.15 μg/L (260 °C/5 min). The PAHs transfer to the coffee brew could be related to the known formation of a caffeine-PAHs complex (Kolarovic and Traitler, 1982, Moret and Conte, 2000 and Navarro et al., 2009). As C. canephora presents higher caffeine content than C. arabica, one should expect that the levels of PAHs in C. canephora brews would be higher due to the formation of the complex, which would facilitate the transfer of these lipophilic compounds to the brew. Nevertheless, in the Phospholipase D1 present study, coffee brews prepared with C. arabica cv. Catuaí Amarelo ground roasted beans presented mean summed PAHs levels higher than the ones prepared with C. canephora cv. Apoatã, independently of the brewing procedure used ( Fig. 1). C. arabica was contaminated with mean summed PAHs concentrations of 0.052 and 0.034 μg/L (filtered and boiled brews, respectively), while C. canephora presented 0.034 and 0.030 μg/L. This might be explained by the fact that the caffeine levels are much higher than the PAHs in both coffees (1195 mg/100 g, arabica; 1729 mg/100 g, canephora ( Tfouni et al.

In Table 2b, univariate analysis shows that the odds of being bedfast or chairfast are significantly higher in the malnourished group compared to no risk find more of malnutrition. This means that malnourished LTC residents

are significant less active than residents in the no risk of malnutrition group. In Table 2c, univariate analysis shows that the odds of being a faller are significantly higher in the group that walks occasionally and in the group that walks frequently compared to bedfast. This means that LTC residents who walk occasionally or frequently are significantly more often a faller, and most in the group that walks occasionally. Significant differences in resident’s characteristics, i.c. gender, number of diseases, care dependency, physical activity, and BMI were checked for confounding by adding them sequentially into the multi varied model but none of them appeared to be an effect modificator. In Table 3, multivariate logistic regression analyses confirmed the relation between nutritional status and fallers but no effect-modification for activity was found (p = 0.222) indicating that the level of activity does not interfere with the relation between nutritional status

and fallers. Looking specifically CT99021 supplier at the active group, i.c. those LTC residents who walk occasionally or frequently, the relation between nutritional status and fallers was also not interfered by activity (no effect modification; p = 0.272). Multivariate logistic regression analysis shows no effect-modification of nutritional intervention on the relation between nutritional status and fallers in LTC residents at risk of malnutrition or malnourished (p = 0.277). This indicates that the relation between nutritional status and fallers is similar for those residents who received nutritional intervention and those who did not receive any nutritional intervention. However, looking at this relation in the group at risk of malnutrition and the malnourished group separately, Fig. 2 shows a lower rate of fallers, specifically in the malnourished group PFKL (OR 0.738, 95% CI: 0.541–1.007, p = 0.056). Although various

risk factors for falls have been identified, including muscle weakness and physical activity (AGS et al., 2001), an impaired nutritional status is seldom indicated as a risk factor. The present study therefore explored the relationship between nutritional status and fallers in elderly LTC residents. The secondary data analysis confirms that a relationship exists: the risk of being a faller is higher when there is an impaired nutritional status, and malnutrition can be considered as a determinant for being a faller in this population. Therefore our study provides further evidence for the increased propensity to fall with malnutrition, which was hypothesized in sparse previous publications (Daniels, 2002, Vellas et al., 1990 and Vellas et al., 1992).

The differing statistical

significance of the results between the two studies may be explained by the very low numbers in our study hampering our ability see more to detect a significant difference in 6MWT results. Alternative possibilities include the differing study populations (unexplained anemia vs. congestive heart failure), dose and formulation of intravenous iron given, and baseline 6MWT results, which were higher in our study. The study intervention was well tolerated, and there were no serious adverse events considered to be related to the study drug. With regard to secondary outcomes, a modest increase in hemoglobin was seen in the immediate intervention group compared to the wait list control group at 12 weeks. In addition, one patient in each group had an increase of at least 1 g/dL in hemoglobin at 12 weeks following initiation of IVIS. This suggests the possibility that a subgroup of subjects

with UAE may respond to parenteral iron therapy. Interestingly, the increase in hemoglobin was not correlated with iron indices, although again, small numbers preclude making more definitive observations about these findings. One of the lessons learned was the great difficulty in recruiting subjects to this type of study. All of the participating institutions were well-established clinical trial sites with histories of robust accrual to clinical trials. Subjects were vigorously recruited through multiple mechanisms, including specialty clinic and primary care referrals, the placement of study flyers at hospital and clinic Akt inhibitor sites, newspaper advertisements, the mailing of thousands of flyers to targeted population areas, electronic check medical record searching, chart reviews, and investigator-led anemia lectures at local community and senior centers. Approximately 1000 subjects were voluntarily reported by the sites to have been prescreened for the study. Nonetheless, despite intense recruitment efforts, including targeted mailing, which in some studies of the elderly has been shown to be the most effective

recruitment maneuver [20] and [21], enrollment remained poor and the study was terminated early. Poor recruitment was likely driven by multiple factors, including the general clinician tendency to ignore typically mild anemia in older adults in the face of more prominent medical issues, the complex requirements for this study, including extensive functional testing, and the logistical difficulties for older adults in participating in interventional studies with involved follow-up. One of the most important barriers to recruitment was the overly restrictive eligibility criteria, which led to the exclusion of many subjects. In addition, the negative results from studies using erythropoietic agents may have blunted enthusiasm for anemia trials in general [22], [23] and [24].

Adicionalmente, a dose de corticoterapia utilizada neste caso parece ser a ideal tendo em conta a relação Venetoclax risco/benefício: doses mais elevadas não parecem trazer maior benefício clínico e relacionam-se com mais efeitos adversos7. Tão importante como o início precoce da terapêutica dirigida é a monitorização apertada da resposta à mesma, com avaliação clínica, analítica e radiológica diária. Doentes sem resolução do megacólon tóxico após 48-72 horas de terapêutica intensiva ou com evidência de complicações como perfuração, hemorragia maciça ou falência multiorgânica têm indicação para colectomia de urgência7 and 8. No caso clínico apresentado

observou-se rápida resolução do megacólon com corticoterapia; contudo, a resposta aos corticoides manteve-se insatisfatória. De facto, um dos maiores desafios nestas situações é a identificação precoce dos doentes com resposta insatisfatória à corticoterapia. A sua identificação permite o início precoce de terapêutica médica de 2.ª linha e, desta forma, diminui a necessidade de colectomia e, caso esta seja necessária, reduz o seu atraso inapropriado6, E7080 research buy 7 and 9. Várias têm sido as abordagens criadas com este objetivo7, 9 and 10. Um dos algoritmos mais simples e úteis é a avaliação ao 3.ª dia após início de terapêutica intensiva, do número de dejeções

diárias e do valor da PCR. A persistência de mais de 8 dejeções ou mais de 3 dejeções associadas a um valor de PCR superior a 4,5 mg/dl (índice

de Oxford) predizem a necessidade de colectomia em 85% dos casos 11. Por outro lado, a ausência de resposta evidente aos corticoides ao fim de 7 dias torna muito improvável uma resposta posterior Fenbendazole 5. Desta forma, ao 3.° dia de corticoterapia deve tentar-se a identificação dos doentes refratários, avaliando-se a eventual necessidade de terapêutica médica de 2.ª linha ou colectomia. Esta decisão deve ser tomada até ao 5.°-7.° dia 6 and 8. Quer os inibidores da calcineurina (ciclosporina e tacrolimus) quer o infliximab têm-se revelado 2 opções válidas nos casos de colite ulcerosa grave corticorefratária2, 6, 7 and 12. Porém, a ausência de estudos comparativos dificulta a opção terapêutica6, 7 and 12. A decisão deverá então ser individualizada, tendo em conta eventuais contraindicações, terapêuticas prévias do doente e experiência clínica local6. Apesar de a eficácia da ciclosporina na capacidade de indução da remissão ter sido demonstrada na ordem dos 50-80% dos casos, não parece ser eficaz na manutenção da mesma, reservando-se, na maioria das vezes, como «ponte» para outra terapêutica imunosupressora6 and 7. Assim, caso o doente apresente uma agudização já sob tratamento imunosupressor (p. ex. azatioprina) ou intolerância a essa medicação, o papel da ciclosporina é reduzido a médio/longo prazo. Neste contexto, o infliximab revela-se uma melhor opção, visto que se encontra indicado tanto para a indução da remissão como para a sua manutenção.

Pulmonary function was assessed by the ratio of the forced expiratory volume in 1

second (FEV1) to the forced vital capacity (FVC). Values of FEV1/FVC below 0.7 indicate chronic airflow obstruction. Visual impairment was defined as having corrected binocular vision worse than 20/40, as used in other studies. 35Hearing impairment was assessed using self-report and the standard whisper test. Functional dependency was assessed by self-reported difficulty and requiring help on 1 or more IADL or basic ADL activities, previously validated for use in the local population. 36 and 37Hospitalization was determined by the participants’ self-reports of new hospitalizations for any chronic medical conditions over the previous year. Quality of life was measured using the Medical Outcomes Study SF12-PCS of quality of life. 28 All social-demographic, health, biochemical, and other characteristics

buy Trametinib of the participants were dichotomized and described using proportions. Bivariate associations of potential risk indicator variables with frailty defined by the CHS Frailty scale were analyzed based on the Cochran-Mantel-Haenszel test. ADL disability, IADL disability, falls, and hospitalization were not included as candidate risk predictor variables in the selection models. Stepwise buy EPZ015666 logistic regression (P < .05 for entry and P < .05 for retention in the model) was performed to select significant independent predictors of frailty. All variables were entered as candidate predictor variables in the initial regression model. The strengths of associations were estimated by odds ratio (OR) and 95% confidence interval (CI). A summary risk score for frailty was derived from the β coefficients

associated with the significant predictor variables RAS p21 protein activator 1 in the final selection model for frailty. We assigned a risk score for each variable based on its coefficient value, standardized with the lowest value, which was assigned a value of 1, and rounded to the nearest integer. The summary risk score for an individual was obtained by summing the weighted scores of each of the risk factors. Validation of the FRI on the external validation sample was performed by analyzing the association of the FRI score as a continuous variable with the observed proportions of prefrailty and frailty in multinomial logistic regression models, and estimating the OR (95% CI) of prefrailty and frailty associated with each unit of FRI score in the baseline sample, together with receiver operating characteristics (ROC) analyses. In the prospective follow-up data, longitudinal associations of the FRI with adverse health outcomes (IADL-ADL disability, hospitalization, lowest quintile of SF12-PCS) at the 2-year follow-up were analyzed. The ability of the FRI to predict adverse health outcomes was compared with the CHS Frailty scale and the FRAIL scale.

isnff.org International Conference on Food Factors – “Food for Wellbeing-from Function to Processing” 20-23 November 2011 Taipei, Taiwan Internet: twww.icoff2011.org/download/Invitationlette.pdf EuroCereal 2011 6-7 December 2011 Chipping Campden, UK Internet:http://www.eurocerealconference.com/ Food Colloids 2012 15-18 April 2012 Copenhagen, Denmark E-mail: Richard Ipsen: [email protected] 8th International Conference on Diet and Activity Methods 8-10 May 2012 Rome, Italy Internet:http://www.icdam.org 11th International Hydrocolloids Conference 14-17 May 2012 Purdue University, USA Internet:http://www.international-hydrocolloids-conference.com/ IDF International Symposium on Cheese

Ripening 20-24 May 2012 Madison, Wisconsin, USA Internet:www.fil-idf.org this website 50th CIFST Conference 27-30 May 2012 Niagara Falls, Canada Internet:http://cifst.ca/default.asp?ID=1250 IDF/INRA International Symposium on Spray-Dried Dairy Products 19-21 June 2012 St Malo, France Email: [email protected] IFT Annual Meeting and Food Expo 25-29 June 2012

Las Vegas, USA Internet:www.ift.org 2nd International Conference on Food Oral Processing – Physics, Physiology, and Psychology of Eating 1-5 July 2012 Beaune, France Internet:https://colloque.inra.fr/fop XVI IUFoST World Congress of Food Science and Technology 7-11 August 2012 Salvador, Brazil Internet:www.iufost2012.org.br ICoMST 2012 – 58th International Congress of Meat Science and Technology 12-17

August 2012 mafosfamide Calgary, Canada Internet: TBA XVI IUFoST World Congress of Food Science and Technology 19-24 August 2012 Salvador, Brazil Internet:www.iufost2012.org.br Romidepsin supplier Foodmicro 2012 3-7 September 2012 Istanbul, Turkey Internet:www.foodmicro.org Eurosense 2012 - European Conference on Sensory and Consumer Research 9-12 September 2012 Bern, Switzerland Internet: TBA Full-size table Table options View in workspace Download as CSV “
“Amino acids are biomolecules of great relevance in many fields, widely used in the food, pharmaceutical, and agrochemical industries. Amongst the 20 common amino acids used to biochemically build proteins and perform other functions in the human body, nine are classified as essential, due to the inability of the human body to synthesize them. Phenylalanine (Phe) is a non-polar aromatic amino acid, classified as essential, and extensively used as ingredient in the food, pharmaceutical and nutrition industries, with a large demand for its free form for the synthesis of the artificial sweetener aspartame, used as ingredient in diet-labeled drinks and food (Sprenger, 2007). Regardless of the production process of phenylalanine (extraction from natural products, chemical synthesis or microbiological fermentation), product separation, recovery and purification steps are required. The commonly employed processes for these purposes are based on selective adsorption of Phe on solid matrices, e.g.