In a number of EU countries, including Belgium, Germany, the Netherlands and the United Kingdom, the promotion of offshore wind energy has been a strong driving force behind the development of national MSP frameworks [25], [27] and [28]. The growing interest in offshore renewable energy represents a response to anticipated economic benefits in terms of job creation and stimulating growth, as well as concerns over energy security [29] and [30]. It is also a response to obligations under the EU Renewable Energy Directive (Directive 2009/28/EC), which is a key component of the EU Climate and Energy Pack adopted in 2008 to contribute to EU’s fulfilment of Kyoto Protocol objectives. The Pack

includes a legally binding obligation to increase the share of renewables to 20% of total energy consumption in the EU by 2020. The Renewable Energy Buparlisib mw Directive was adopted to address this obligation. Under this directive, Member States are required to meet its national overall target for the share of energy from renewable sources in 2020, which is set out in Annex I of the Directive. Each Member State is also required to adopt a national renewable energy action plan, providing projections for the share of renewable energy consumed in electricity, transport and heating/cooling sectors in 2020 (Table S1, Supplementary Material). According to the submitted

national renewable energy action plans, Selleck ABT-737 EU Member States are planning to install 44.2 GW of offshore wind energy and 2.3 GW of tidal, wave and ocean energy C1GALT1 in 2020 (increased from 2.6 and 0.2 GW in 2010), which accounts for 12.2% of total renewable electricity capacity, or 5.2% of total renewable energy (including

transport and heating/cooling) in 2020 [31]. As the offshore renewable industry grows, the spatial requirements are likely to have significant effects on other uses of the sea, such as fishing and navigation [32]. There are also potential tensions between offshore renewable developments and Natura 2000 sites [29]. How such conflicts are addressed will have major implications for MSP, which will be discussed in the next section. The reform of the CFP will have a significant effect on the implementation of other EU policies, particularly the Birds and Habitats Directives and the MSFD. A key difference between the CFP and other policy drivers discussed in this paper is that the European Commission has exclusive competence through the CFP for managing fisheries beyond 12 nautical miles in Member States’ EEZs. This is based on the recognition that fisheries in a given Member State’s waters have long been accessed by fishermen from other Member States, therefore fisheries regulation would benefit from an EU-wide approach, achieved through a number of regulations and Council Decisions adopted under the CFP. The CFP was officially established in 1983, and is currently undergoing a reform process. The revised CFP is expected to enter into force during 2013.

10 One of the major goals of the conference was to revisit the clinical diagnostic criteria published subsequent to the first International TSC Consensus Conference in 1998.11 Since 1998, one additional manuscript regarding the diagnostic criteria has been published that was designed to provide more guidance to practitioners by including pictures

of the major and minor findings.12 At the 2012 meeting, the most significant change recommended to the diagnostic criteria was the incorporation of genetic testing. Although the TSC1 and TSC2 genes were discovered before the 1998 conference, molecular testing was not widely available at that time. Molecular testing of the TSC1 and TSC2 genes yields a positive mutation result for 75-90% of TSC-affected individuals categorized as “definite” by the 1998 Consensus Conference Clinical Diagnostic Criteria. 2 The use of molecular testing in medicine has expanded CT99021 order greatly since the 1990s, becoming widely accepted as invaluable in the diagnosis of diseases with a genetic basis. Utilization of genetic testing for TSC was addressed along with refinement of clinical criteria. Comprehensive and reliable screens for TSC1 and TSC2

mutations are well-established, and many pathogenic mutations have been identified (www.lovd.nl/TSC1, www.lovd/TSC2). The recommendation of the Genetics Akt inhibitor Panel was to make identification of a pathogenic mutation in TSC1 or TSC2 an independent diagnostic criterion, sufficient

for the diagnosis or prediction of TSC regardless of the clinical findings ( Table part A). This will facilitate the diagnosis of TSC in some, particularly young individuals, allowing earlier implementation of surveillance and treatment with potential for better clinical outcomes. A “pathogenic” mutation was defined as a mutation that clearly prevents protein synthesis and/or inactivates the function of the TSC1 or TSC2 proteins (e.g., nonsense mutation or frameshift mutations, large genomic deletions) or is a missense mutation whose effect on protein function has been established by functional assessment. 13 and 14TSC1 and TSC2 genetic variants whose functional effect is less certain are not definitely pathogenic and would selleck products not be considered a major diagnostic criterion. A significant fraction (10-25%) of TSC patients have no mutation identified by conventional genetic testing. Therefore, a normal result does not exclude TSC. Nonetheless, if the mutation in an affected relative is known, testing for that mutation has very high predictive value for family members. Assembled experts at the Consensus Conference agreed with the recommendation that identification of a pathogenic mutation in TSC1 or TSC2 is an independent diagnostic criterion. In addition to diagnosis by genetic analysis, the clinical diagnostic criteria used to establish the diagnosis of TSC were also reviewed at the conference.

18 learn more Boceprevir and telaprevir also are associated with a high incidence of adverse events (AEs), including anemia, rash, and renal dysfunction.19, 20, 21 and 22 Recently, the nucleotide analog NS5B polymerase inhibitor sofosbuvir also was approved for the treatment of chronic HCV infection in the United States and Europe, representing an improvement on first-generation DAAs.23 and 24

Simeprevir (TMC435) is administered orally, once daily, as a single pill25; has been approved in Japan, Canada, the United States and Russia; and is under regulatory review in Europe for the treatment of chronic HCV infection. The median simeprevir EC50 and EC90 values against a HCV genotype 1b replicon were 9.4 and 19 nmol/L, respectively.26 Activity of simeprevir against a selection of genotype 1a (N = 78) and 1b (N = 59) chimeric replicons carrying NS3 sequences from HCV NS3/4A protease

inhibitor-naive subjects resulted in median fold change in EC50 of 1.4 (interquartile range [IQR], 0.8–11) and 0.4 (IQR, 0.3–0.7), compared selleck inhibitor with reference genotype 1b replicon. Genotype 1a (N = 33) and 1b (N = 2) isolates with a baseline Q80K polymorphism, a naturally occurring NS3 polymorphism that confers low-level resistance to simeprevir, resulted in a median fold change in simeprevir EC50 of 11 (IQR, 7.4–13) and 8.4, respectively. Simeprevir has antiviral activity in patients infected with HCV genotypes 1, 2, 4, 5, and 6,27, Apoptosis antagonist 28, 29 and 30 and is being evaluated in both PegIFNα/RBV and IFN-free combinations.27, 28, 31, 32, 33 and 34 Simeprevir in combination with PegIFNα/RBV showed SVR rates of approximately 80% in phase 3 trials in treatment-naive patients with HCV genotype 1 infection, with most patients (>84%) able to reduce their treatment duration to 24 weeks.33 and 34 In these studies, no additional AEs were observed with simeprevir compared with those seen with PegIFNα/RBV alone. Results of the PROtease inhibitor TMC435 In patientS who have previously

rElapsed on IFN/RBV (PROMISE) study, a randomized, double-blind, placebo-controlled, phase 3 trial undertaken to assess the efficacy, safety, and tolerability of simeprevir with PegIFNα-2a/RBV (PR) for the treatment of chronic HCV genotype 1 infection in patients who had relapsed after previous IFN-based therapy, are presented. Patients were enrolled at study sites in 14 countries across North America, Europe, and the Asia–Pacific region. Eligible patients were adults (≥18 y) with confirmed genotype 1 HCV infection and screening plasma HCV-RNA levels greater than 10,000 IU/mL, who had relapsed after 24 weeks or more of IFN-based therapy (undetectable HCV-RNA at end of treatment [EOT] or within 2 months after EOT, with documented relapse within 1 year after therapy).

No statistically significant mortality association was demonstrated for the CSF bacterial load or CSF white

cell count, HIV status, age or gender on model 1 (n = 102); seizures at any time in the illness, GCS or altered mental status and anaemia were associated with mortality ( Table 1). In model CHIR-99021 molecular weight 2 (n = 62) IL8 and IL10 were marginal predictors of non-survival; IL8 p = 0.036, OR 1.00 (95% CI 1.00: 1.00) and IL10 p = 0.029, OR 1.00 (95% CI 1.00 : 1.00); of the clinical parameters, only altered mental status or GCS retained significance in this model ( Supplementary Table 1). We have previously shown that coma, seizures and anaemia predict poor outcome from bacterial meningitis in Malawi,5 but the causes of the excess mortality compared to patients in more well-resourced settings remain unclear. In this study, there was no difference

in the bacterial load and only marginal difference in the cytokine response between survivors and non-survivors despite lower CSF white cell counts in non-survivors. Our findings are markedly different to data in children with pneumococcal meningitis in Malawi and Europe, and adults with pneumococcal bacteraemia in Europe or meningococcal meningitis in the UK.6, 7, 8 and 14 No published data has quantified CSF pneumococcal load in adults Alectinib with meningitis in either setting. The lack of association between outcome and pneumococcal load, in contrast to these other studies was unexpected. HIV uninfected adults with pneumococcal meningitis in Europe have a 10 fold higher CSF WCC click here than our patients, a CSF WCC of <1000 cells/mm3 has been shown to be significantly associated

with mortality in Europe.4 In our study, the median CSF WCC was substantially below this threshold, and low CSF WCCs were associated with poor outcome. We hypothesise that in adults with pneumococcal meningitis in Malawi, rapid bacterial growth occurs within the CSF with relatively little restriction by the host immune response, leading to high bacterial loads in both outcome groups. In addition, delays from symptom onset to admission in the community and to lumbar puncture within the hospital system may have resulted in the bacterial growth reaching the plateau, as opposed to the exponential growth phase in the CSF by the time of lumbar puncture, and hence any differences between outcome groups may have equalised by the time of examination. Time from symptom onset to lumbar puncture in the included studies was 3–5 days, compared to <48–72 h for most European studies.11, 12, 15, 16 and 17 Adults with pneumococcal meningitis in Malawi have different baseline characteristics compared to those studied in other settings outside of sub-Saharan Africa,4 and 5 and disease is caused disproportionately by serotype one.18 Data from studies of pneumococcal meningitis in this region may not be directly comparable to data from other regions.

The average wave height reaches 1.01 m at one location of relatively shallow depth in the Arkona Basin. This maximum is not represented in some other wave hindcasts (M. Meier, personal communication) and may be caused by certain local effects; however, it may also stem from the overestimation of geostrophic wind speeds in this part of the basin because of the low spatial resolution of the relevant information (cf. Pryor & Barthelmie

2003). The highest wave activity in the northern Baltic Proper occurs along the PLX3397 research buy coasts of Estonia and Latvia. The wave heights are relatively low in the south-eastern part of the sea, although this area has a relatively long fetch. The average wave heights reach 0.7 m at the entrance to the Gulf of Finland and in its central part (Soomere et al. 2010). The Gulf of Riga is even calmer, with the average wave height slightly exceeding 0.6 m in the open sea (Räämet & Soomere 2010a). The hindcast average wave heights underestimate the reliably measured buy Carfilzomib ones by about 18% at Almagrundet (Räämet et al. 2009, Räämet & Soomere 2010a) and almost exactly coincide with the observed ones at Pakri and Vilsandi (Räämet & Soomere 2010a). This suggests that the model underestimates the average wave heights in the open Baltic Sea by about 15–20%. The modelled values for the Gulf of Finland, however, match well a similar estimate for the vicinity of Tallinn

Bay (0.56 m) based on one-point forcing of the WAM model with high-quality marine wind data (Soomere 2005) and considerably (by 21%) exceed the observed wave heights at Narva-Jõesuu. This suggests that, despite the relatively low resolution of the wave calculations, the

modelled results may be a good representation of the long-term wave properties in semi-enclosed sub-basins of the Baltic Sea. Changes to average and extreme wave heights. The modelled trends in wave activity over the 38 years of simulations in the Baltic Sea have an even more complicated spatial pattern (Soomere & Räämet 2011). The largest changes have occurred in the southern Baltic Proper. The increase in wave heights in the Arkona basin is consistent Farnesyltransferase with the reported gradual increase in the modelled wind speed over this sea area (Pryor & Barthelmie 2003, 2010). The decrease in wave intensity has been the greatest between Öland and Gotland, and to the south of these islands down to the Polish coast. A considerable increase in wave activity is indicated by the model from the coast of Latvia to the sea area between the Åland archipelago and Sweden. A large part of these changes represent statistically significant trends. The significance is the highest, about 99%, for the area to the south of Bornholm. The spatial pattern of changes is largely uncorrelated with the areas of high and low wave intensity. The already large wave heights in the Arkona basin increase, while the wave activity in the neighbouring area of large waves decreases at almost the same rate (by about 15% in 40 years).

robusta homologues (i.e. ORF249) appear to be poorly

conserved, and are likely not functional. Fragments of the plasmid ORFs are also found in the gene-poor regions. Eight incomplete ORFs with similarity to C. fusiformis ORF482/ORF484, sometimes without start codon, are interspersed throughout region III and IV. One of the contigs with high read depth could not be assembled into the chloroplast genome. Upon closer analysis, this contig was found to constitute a separate circular molecule with a size of 3813 bp with significant similarity to C. fusiformis pCf2, which we designated as http://www.selleckchem.com/products/XL184.html pSr1 ( Fig. 3C). A previous survey did not identify any plasmids in two other members of the Naviculaceae, Fistulifera pelliculosa and Navicula incerta ( Hildebrand et al., 1991), and no plasmid was reported in Fistulifera sp. JPCC DA0580 ( Tanaka et al., 2011). Thus, the pSr1 plasmid is the first to be identified in a diatom belonging to Naviculales. Plasmids may not be a common feature in diatoms belonging to this order. Alternatively, plasmids have not been detected in previous studies due to technical limitations. Purification of chloroplast DNA by cesium chloride or sucrose gradient centrifugation may result in the loss of any associated plasmid DNA. pSr1 contains three ORFs encoding putative proteins of 494, 317

and 121 AAs, which show significant similarity to pCf2 ORF484, ORF246 and ORF125, respectively (NCBI BlastP expect value < 1e-36). The C-terminal part of pSr1 ORF317 also shows similarity to a small click here Loperamide ORF in pCf2 (ORF64) that overlaps with pCf2 ORF246 (Fig. 3B). Introducing a deletion at position 732 of pCf2 ORF246 and an insertion in position 191

of ORF64 results in a continuous ORF encoding a putative protein of 311 AAs (ORF311) showing high similarity to pSr1 ORF317 and S. robusta chloroplast ORF292 ( Fig. 3B; Fig. A.3). The two frameshifts in pCf2 may be the result of sequencing errors. Alternatively, they have occurred as part of an inactivation of the ORF311 locus. The only C. fusiformis plasmid ORFs with a putative function are ORF217/ORF218, which show similarity to serine recombinases. Homologues of these ORFs are not found in pSr1; however, gene-poor region III in the chloroplast genome encodes a serine recombinase, termed SerC2, with similarity to CfORF217 and CfORF218 as well as K. foliaceum SerC1 and SerC2 and Fistulifera sp. SerC2. Residues found to be critical for the active site of serine recombinases (Arg-8, Ser-10, Asp-67, Arg-68 and Arg-71 in the Escherichia coli γδ resolvase ( Grindley et al., 2006)) are conserved in all diatom chloroplast serine recombinases. They also show a similar size and domain structure as γδ resolvase, suggesting that they may act through a similar mechanism. Although the intracellular localisation of pSr1 is not known, it appears to be closely associated with the chloroplast genome. Cloned pCf2 hybridised to both chloroplast and nuclear DNA from C. fusiformis ( Jacobs et al., 1992).

Most patients can be treated effectively by following simple and logical practices, as we have emphasized in this article. We note that most hospital patients would benefit from simple nutrition interventions: food enrichment and ONS. The feedM.E. Study Group thanks Cecilia Hofmann, PhD, for her valuable assistance with efficient compilation of the medical literature and with editing

this English-language review article. “
“Globally, concern for marine conservation grows rapidly because virtually no marine area remains unaffected by human influence and, indeed, a very large fraction of the seas (41%) is strongly affected MG-132 price by multiple anthropic drivers (Halpern et al., 2008 and Pennisi, 2010). This growing interest in marine conservation is triggering a worldwide rush to establish Marine Protected Areas (MPAs), a tool intended to ensure the persistence of the full range of marine biodiversity, thus preserving the full functioning of the ecosystem in providing goods and services for present and future generations (Lubchenco et al., 2003). Simple stated, “No one should doubt that our seas need protection” (Anonymous, 2011). Yet, while simply stated and a fundamentally necessary objective, conserving biodiversity is in

fact a complex process that requires much more attention. Thus, a key question is to what extent we are in fact conserving a broad and representative array of marine areas that ensure the conservation of biodiversity and associated processes (Fox et al., 2012a). While this question is fundamental and of extreme importance to scientists, it is not clear that the question is understood, check much less taken Alectinib nmr seriously, by politicians and MPA planners. This is

of outmost importance, since decision making in conservation relies in the political system and planners determine how and where MPAs are implemented. Although total ocean area protected by MPAs can be estimated at approximately 4.2 million km2 of ocean, this represents only 1.17% of the marine area of the world. Further, the focus remains mainly on Exclusive Economic Zones (EEZs) of the continental shelf areas, where MPA coverage is ca. 4.32%. EEZs claimed by most nations cover roughly 40% of the world’s ocean surface, and thus there is a large fraction of ocean surface in off-shelf, international waters, where MPAs extents stands at 0.91%. Ecologically, MPA coverage is very uneven and does not adequately represent all ecoregions and habitats important for conservation (Toropova et al., 2010). Among nations, the distribution of MPAs varies from zero to over 30% of a country’s EEZ, and currently only 12 of 151 coastal countries exceed the 10% MPA target. Thus, we are still far from reaching the CBD target for achieving effective conservation of 10% of marine ecological regions. It is clear that despite the lack of a strong scientific foundation for such fixed percentage targets, they are politically appealing.

Thus, although melittin presents antinociceptive activity, it is not the only component that contributes to the antinociceptive

activity of AMV. The demonstration that melittin induces two contrasting effects, nociception (present study, Chen et al., 2006, Li and Chen, 2004, Mackler and Kreil, 1977 and Sumikura et al., 2006) and antinociception (present study), adds to the results showing that AMV Tanespimycin price also presents such profile. Convincing evidence that AMV presents such profile was obtained in the protocol in which AMV, administered into the dorsum (s.c. injection) of the animals, inhibited the nociceptive response induced by the same AMV injected into the dorsum of the paw. As the s.c. injection of AVM into the dorsum of the animals probably induces a discomfort, it is possible that its antinociceptive activity results from a non-specific

activation of endogenous antinociceptive mechanisms associated with the previous exposure to a noxious stimulus. Antinociception associated with exposure to stimuli that induce discomfort and pain is widely known and multiple mechanisms have been proposed to explain such phenomenon (Gebhart, 2004). To explore this possibility, we evaluated the effects induced by venoms obtained from other species, T. serrulatus and B. jararaca. These venoms induced a nociceptive response, as already reported ( Carneiro et al., 2002 and Olivo et al., 2007). However, these venoms did not inhibit the nociceptive response induced by formaldehyde. These results clearly learn more indicate that the antinociceptive

activity of AMV, F<10 and melittin does not result from a non-specific activation of endogenous antinociceptive mechanisms, but from the action of different components that specifically inhibit the nociceptive processing, both in the periphery and in the central nervous system. Concluding, the present study demonstrated that AMV, F<10 and melittin induce two contrasting effects: nociception and antinociception. Although melittin exhibits an antinociceptive activity, it is not the Thalidomide only component that contributes to the antinociceptive activity of AMV. The antinociceptive activity of the AMV does not result from a non-specific activation of endogenous antinociceptive mechanisms associated with the exposure to noxious stimuli. Different components of the AMV contribute to the inhibition of the nociceptive response and oedema. The knowledge of the pharmacological properties of the AMV and its components may allow the development of more effective treatment of inflammatory and painful disorders, as well as the discovery of new pharmacological tools. We thank Fundação de Amparo à Pesquisa de Minas Gerais (FAPEMIG), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) and Coordenação de Aperfeiçoamento de Pessoal de Ensino Superior (CAPES) for financial support. Cristália Produtos Químicos e Farmacêuticos Ltda.

Na altura terá feito estudo para doença celíaca que foi negativa. Por análise retrospetiva dos exames de imagem realizados atualmente, pode constatar-se que a suposta invaginação descrita na TC abdominal nada mais era do que a presença do DDI, verificando-se a imagem característica do sinal em «halo». O trânsito duodenal foi de grande importância no diagnóstico do DDI, mostrando o tão característico sinal de «windsock». No estudo com EDA observou-se um esófago com aspeto traqueiforme, duodeno

com pregas espessadas condicionando estenose relativa com restos alimentares impactados e mucosa erosionada e friável. Embora http://www.selleckchem.com/products/PLX-4032.html essas alterações macroscópicas sejam incaracterísticas, tem-se constatado a sua presença em doentes com GEE mucosa. Foi a histologia que ditou o diagnóstico de GEE mucosa. Ao contrário de alguns casos publicados, neste doente não se visualizou o orifício de entrada do DDI via EDA10. learn more No caso clínico exposto, a sintomatologia apresentada era escassa e não é a típica de

GEE ou DDI. Provavelmente, a febre inexplicada, com cedência aos antibióticos, poderia estar associada a síndrome de hiperproliferação bacteriana, tanto pela presença do DDI como pelas erosões da mucosa que permitiriam que agentes microbianos atravessassem a barreira intestinal. O tratamento da GEE baseia-se fundamentalmente na corticoterapia (prednisolona 20-40 mg/dia) durante 8 semanas4, com redução progressiva, e visa a resolução dos sintomas14. Em casos graves, corticodependentes ou corticorresistentes, os imunossupressores (azatioprina ou 6-mercaptopurina) constituem uma alternativa1 and 4. Atendendo a que o doente se encontrava sintomático, mas sem gravidade, e que a maioria dos casos de GEE responde aos corticosteróides com uma

taxa de sucesso de 90%, optou-se por instituir corticoterapia. No nosso doente, a resposta terapêutica foi imediata. Contudo, em virtude do caráter crónico da doença, com remissões e recaídas frequentes, apesar do seu caráter benigno, estes doentes devem ser mantidos em consultas de seguimento. Embora, o tratamento tradicional dos pacientes com DDI sintomáticos e de grandes dimensões seja a resseção cirúrgica, atualmente preconiza-se incisão endoscópica13. No caso clínico apresentado, tendo em conta as dimensões do Resveratrol DDI (quase 4 cm) e o caráter progressivo desta entidade, colocou-se a hipótese de resseção do DDI. Assim, poder-se-iam evitar possíveis complicações futuras. Apesar da unanimidade em considerar a etiologia da GEE desconhecida, pensamos que o raciocínio fisiopatológico apresentado para explicar a relação causal entre o DDI e a GEE é plausível e, de todo, não desprezável. A grande limitação neste caso é demonstrar a veracidade deste raciocínio fisiopatológico, porque poderemos apenas estar perante um caso clínico com 2 diagnósticos independentes e raros.

This work was supported by the Engineering and Physical Sciences Research Council Extending Quality of Life Grant [GR/R2 6856/01], Nintedanib United Kingdom. “
“Falls are a major threat to the health of elderly. Approximately one in three community dwelling elderly over 65 years, and even one in two over 85 years experience at least one fall every year (Cameron et al., 2010, CBO, 2004, Neyens, 2007 and Tinetti, 2003). In institutionalized elderly, the incidence rates of falls are even higher: 1.5–2 falls per bed annually

(Dijcks et al., 2005). One out of ten falls results in a serious injury (CBO, 2004, Dijcks et al., 2005, Neyens, 2007 and Rubenstein et al., 1994). The consequences of falls are therefore considerable. Besides a physical and economical impact, such as fractures and health care costs, falls also have a psychological impact, for example by increasing the fear of falling (Zijlstra, 2008). Few falls have a single click here cause; the majority occurs by interactions between long-term predisposing factors, mainly intrinsic risk factors, and short-term

factors, mainly extrinsic risk factors (Nevitt, Cummings, & Hudes, 1991). Therefore, all strategies that can help to reduce the risk of falling are important. With aging, major risk factors for falls are related to physical activity and muscle strength impairment. Muscle weakness and gait and balance deficits increase the risk of falling about Selleckchem Rucaparib 3- to 4-fold (AGS, BGS, & American Academy of Orthopedic Surgeons Panel on Falls Prevention, 2001). The underlying decline in muscle mass and muscle function that occurs with aging is also known as sarcopenia

(Boirie, 2009). This condition has a multi-factorial etiology in which senescent changes in neuromuscular tissue (Tomonaga, 1977), chronic diseases and medications (Tinetti, 2003), atrophy of disuse (Bortz, 2009), an imbalance in protein metabolism, inadequate nutritional intake and malnutrition (Jeejeebhoy, 1994 and Kinney, 2004) play a role. Several nutrients and nutritional indicators have been associated with impaired muscle mass and function, e.g. protein under nutrition, protein-energy malnutrition, and low dietary intake of vitamins and minerals (Brown, 1995 and Coleman et al., 2000). Inadequate nutritional intake is common in elderly and indicative of the anorexia of aging. Swallowing disorders, bad oral health, lack of taste and smell, eating dependency and chewing problems are often part of the multi-morbidity, especially in frail and disabled elderly in residential LTC. The prevalence of malnutrition in these care facilities is about 25% (Halfens et al., 2008 and Meijers, 2009). Yet, malnutrition is often unrecognized despite being associated with (a) an increased chance of institutionalization, i.c.