, 2008; Kabashi et al., 2008b; Sreedharan et al., 2008; Yokoseki et al., 2008). TDP-43 is a widely-expressed 414-amino-acid protein encoded by the TARDBP gene on chromosome 1 (Pesiridis et al., 2009; Geser et al., 2010). It has two RNA-binding domains and a glycine-rich domain in the C-terminal part, with which it binds

to various heterogenous nuclear nucleoproteins (hnRNPs). It is more abundantly present in the nucleus than in the cytoplasm. The exact role of TDP-43 is incompletely understood, but it is thought to play a role in a variety of processes such as processing, stabilisation and transport of RNA (Buratti & Baralle, 2009; Geser et al., 2010). A well known example is its role in the splicing of cystic fibrosis transmembranous conductance regulator mRNA (Buratti selleck chemicals et al., 2001). Of interest is the finding that another target for the find more action of TDP-43 in mRNA processing is the protein SMN, deficiency of which results in spinomuscular atrophy, an infantile or juvenile onset motor neuron disorder (Burghes & Beattie, 2009). Overexpression of TDP-43 enhances exon 7 inclusion during SMN splicing, a crucial event in yielding fully active SMN protein (Bose et al., 2008). SMN deficiency in its turn is thought to cause spinomuscular atrophy through defective RNA processing or

transport (Burghes & Beattie, 2009). The possible link between SMN and TDP-43 is of major interest when thinking of a common pathway for motor neuron degeneration. The more than 25 mutations found in the TARDBP gene are, primarily, missense mutations and are almost exclusively located in the C-terminal (glycine-rich) part of the protein (Lagier-Tourenne & Cleveland, 2009). There is also a truncating mutation in this gene (Daoud et al., 2009). TARDBP mutations are rare: they probably account for < 5% of familial ALS, i.e. < 1% Tyrosine-protein kinase BLK of all ALS (Ticozzi et al., 2009a). The major interest in them comes from the finding mentioned above, that wildtype TDP-43 containing inclusions are found in the majority of sporadic

ALS patients (Neumann et al., 2006; Fig. 3). Here, we will refer to this abnormal form of TDP-43 as TDP-43SALS/FTLD in contrast to ‘normal’ TDP-43, reminiscent of the naming in prion disease, where PrPC refers to the normal PrP and PrPSc refers to the pathogenic form of PrP in sporadic and infectious Creutzfeldt–Jakob disease; it does not differ from normal PrPC in its amino acid sequence. Mutant TDP-43 refers to the mutant proteins causing the hereditary forms of ALS, just as with mutant PrP and Creutzfeldt–Jakob disease, and will be referred to as TDP-43mutant. An overwhelming number of papers on the role of TDP-43 in neurodegeneration have been published over the last 2 years. A common finding seems to be that TDP-43mutant and TDP-43SALS/FTLD are mislocated, hyperphosphorylated, abnormally processed and ubiquitinated.

[8] In the last decade, simulated-patient methods have been used around the globe, as an assessment and educational tool, to identify issues in current pharmacy practice and inform interventions to

shape practice behaviour of pharmacists and their staff.[3,8–18] A simulated patient (also known as pseudo patron, pseudo patient, standardised patient, simulated patient, pseudo customer, covert participant, shopper patient, disguised shopper, surrogate shopper or mystery shopper) is an individual who is trained to go to a pharmacy and enact predetermined scenarios, KU-57788 order while being indistinguishable from genuine patients, to assess aspects of customer care provided by pharmacy staff.[3,8,13,19–23] Community pharmacy is an ideal setting for this type of real-time observation and research, as pharmacists and their staff can be accessed without appointment, unlike other healthcare professionals.[24] The simulated-patient method is an unobtrusive means of observing actual staff responses in a natural environment, under conditions uninfluenced by awareness that behaviour is being monitored.[25–27] It is thus an effective method of deriving

valid, true-to-life outcomes, which are otherwise challenging to achieve by any other method.[23] Although an effective assessment tool, using simulated-patient methods solely for assessment purposes has served as a basis for negative criticism of pharmacy staff skills and performance, and thus has attracted negative selleck compound attitudes from those who have been subject to this approach.[8,18] However, when used for educational purposes, simulated-patient methods are an effective training tool, rather than Liothyronine Sodium simply an observation.[18] A recent trend in simulated-patient methods has seen a shift of emphasis from merely assessing behaviour of pharmacists and their staff, to using the outcomes of these visits as formative feedback to enhance continuous professional development.[8,16] In well-designed

studies, when simulated patients are used for educational purposes in the pharmacy setting, educators have entered the pharmacy immediately after the simulated-patient visit, to discuss the observations with pharmacists and/or their staff.[8,26] These methods not only provide an accurate assessment of practice behaviour, but also use performance feedback as a basis for further skills acquisition.[8] The simulated-patient method is negotiated with pharmacists and their staff beforehand, being fully integrated into an educational programme. This is otherwise known as ‘in principle’ consent, when participants give prior consent without knowing the exact timing of the simulated-patient visit.[16] Research has shown that the awareness of an impending simulated-patient visit serves as a powerful motivator to continue applying acquired skills, as participants cannot predict when another assessment will take place.

[21] Nonetheless, of particular interest in regards to autoimmune diseases, is evidence for the contribution of the microbiome to the development of Th17 T helper beta-catenin assay cells.[22] These cells are shown to be important for the pathogenesis of several autoimmune diseases[23] and the induction of these cells is dependent upon the microbiome. That immune system development depends on the microbiome has been amply demonstrated by germ-free conditions. Germ-free

individuals show reduced peripheral CD4+ T cells, reduced immunoglobulin levels, immune deviation toward a Th2 phenotype, among other defects. A paper in Cell by Ivanov and colleagues showed that mono-association of segmented filamentous bacteria with germ-free animals was sufficient to induce fully functional Th17 T helper cells.[6] These provocative data suggest that manipulation click here of the microbiome to alter the immune phenotype might be possible. Another recent paper shows that this same bacteria can drive experimental autoimmune disease.[24] Under germ-free conditions the K/BxN mouse, which under specific pathogen-free conditions develops inflammatory arthritis, has greatly attenuated disease. Mono-association with segmented

filamentous bacteria restores gut-associated Th17 cells, autoantibody production and arthritis in this arthritis model.[24] Other animal models of autoimmunity also depend on gut-derived Th17 cells.[25] Investigation of the role of a particular member of the mouth microbiome, namely, P. gingivalis, in the

pathogenesis of rheumatoid arthritis has been ongoing for several years. The accumulated data demonstrate a strong association Etomidate as well as a plausible biological mechanism. Involvement of the microbiome in other rheumatic diseases has not been extensively studied. However, gut-associated organisms are critical to the development and activation of the immune system, especially with regard to cell types intimately associated with autoimmunity. These data indicate that the relationship of the microbiome to autoimmune rheumatic disease is an area of high interest. “
“Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by periods of flares and remission, resulting in organ damage over time caused by persistent disease activity and treatment-related complications. Conventional therapies are not ideal in terms of efficacy and safety. Novel biological therapies are being developed to enhance therapeutic efficacy, minimize disease exacerbation and reduce toxicities. As dysregulation of B cells is the hallmark of SLE, B-cell targeted therapies are the focus of recent clinical research. Rituximab, a chimeric anti-CD20 monoclonal antibody, has been used with success in recalcitrant lupus manifestations. However, randomized controlled trials have failed to reveal its benefit in renal and non-renal SLE when combined with conventional immunosuppressive protocols.

These responses were initially predicted by clustering analysis, as these mutants fall into clusters being predicted involvements in blue light signalling (clusters I, II, IV and V) and those predictions involving blue, red and far-red light signalling (clusters III). These putative components of light signalling in Xcc included three HKs, four GGDEF-characterized

proteins and buy GS-1101 four hybrid HKs. Motility is an important characteristic for infection in a number of plant pathogenic species (Swings et al., 1993); thus, we tested whether PAS proteins participate in the development of motility in the Xcc in response to variable light conditions. Five of 33 mutants showed significantly modified motility responses to light (Fig. 3). Among them, DLT4313 was increased, and DLT0728, DLT0818 and DLT1965 were decreased in blue light. DLT1036 exhibited decreased motility in blue, red, far-red or white light. These results partially agreed with the results of clustering analysis (Fig. 1c), in which the protein altered in DLT0728 was associated with cluster IV and was a putative blue light–signalling component. see more We cultured cabbage infected with Xcc strains under two levels of light intensity. The light intensity reaching into

a leaf was initially estimated in a light transmission assay, which indicated that a light intensity of 4512 and 593 lux reached the middle of a leaf exposed to light sources of 12 000 and 2000 lux, respectively (Fig. S2). The results of Xcc strains are shown in Fig. S3. We also tested rescue strains of three mutants, DLT1036, DLT 2324 and DLT3829. In assays of Xcc strains infecting cabbage, four mutants (DLT3829, DLT1036, DLT2324 and DLT1476) had an effect on light-condition-dependent shifts in bacterial virulence. Leaf-lesion photographs of the four mutants are shown in Fig. 4a (strong light) and 4b (weak light), and the mutants showed different changes in lesion length

(LL) in strong/weak light or between the two light intensities, as shown in Fig. 4c. The relative lesion rate (RLR) values of the four mutants were significantly different from Telomerase wild-type Xcc 8004 (Fig. 4d). The tests of complementary strains are shown in Fig. S4, in which the virulence of pLC1036, pLC2324 and pLC3829 were partially rescued in comparison with either LL or RLR. In addition, three of the four mutants have been shown to be GGDEF-characterized proteins involved in virulence under natural light (Ryan et al., 2007). These data strongly suggest that these PAS proteins are light-signalling components that are vital for Xcc pathogenesis. Some of the PAS proteins in Xcc may have roles as intermediates in photo-signalling pathways other than light sensing, and some of those involved in light signalling may not have phenotypes that could be observed in our screen. Previous studies have suggested that PAS domains sense light, and the subsequent functions result in various responses, for example, a PAS domain can be activated in blue light to regulate B.

These responses were initially predicted by clustering analysis, as these mutants fall into clusters being predicted involvements in blue light signalling (clusters I, II, IV and V) and those predictions involving blue, red and far-red light signalling (clusters III). These putative components of light signalling in Xcc included three HKs, four GGDEF-characterized

proteins and EGFR assay four hybrid HKs. Motility is an important characteristic for infection in a number of plant pathogenic species (Swings et al., 1993); thus, we tested whether PAS proteins participate in the development of motility in the Xcc in response to variable light conditions. Five of 33 mutants showed significantly modified motility responses to light (Fig. 3). Among them, DLT4313 was increased, and DLT0728, DLT0818 and DLT1965 were decreased in blue light. DLT1036 exhibited decreased motility in blue, red, far-red or white light. These results partially agreed with the results of clustering analysis (Fig. 1c), in which the protein altered in DLT0728 was associated with cluster IV and was a putative blue light–signalling component. PI3K inhibitor We cultured cabbage infected with Xcc strains under two levels of light intensity. The light intensity reaching into

a leaf was initially estimated in a light transmission assay, which indicated that a light intensity of 4512 and 593 lux reached the middle of a leaf exposed to light sources of 12 000 and 2000 lux, respectively (Fig. S2). The results of Xcc strains are shown in Fig. S3. We also tested rescue strains of three mutants, DLT1036, DLT 2324 and DLT3829. In assays of Xcc strains infecting cabbage, four mutants (DLT3829, DLT1036, DLT2324 and DLT1476) had an effect on light-condition-dependent shifts in bacterial virulence. Leaf-lesion photographs of the four mutants are shown in Fig. 4a (strong light) and 4b (weak light), and the mutants showed different changes in lesion length

(LL) in strong/weak light or between the two light intensities, as shown in Fig. 4c. The relative lesion rate (RLR) values of the four mutants were significantly different from CYTH4 wild-type Xcc 8004 (Fig. 4d). The tests of complementary strains are shown in Fig. S4, in which the virulence of pLC1036, pLC2324 and pLC3829 were partially rescued in comparison with either LL or RLR. In addition, three of the four mutants have been shown to be GGDEF-characterized proteins involved in virulence under natural light (Ryan et al., 2007). These data strongly suggest that these PAS proteins are light-signalling components that are vital for Xcc pathogenesis. Some of the PAS proteins in Xcc may have roles as intermediates in photo-signalling pathways other than light sensing, and some of those involved in light signalling may not have phenotypes that could be observed in our screen. Previous studies have suggested that PAS domains sense light, and the subsequent functions result in various responses, for example, a PAS domain can be activated in blue light to regulate B.

Benefits of diagnosing and treating this problem far outweigh the costs and toxicities of this fairly safe agent in the light of a strong biological basis. Whether or not to test for vitamin D in diffuse musculoskeletal pain needs to be weighed against the prevalence of low vitamin D state in the population under study. “
“Vasculitis is relatively uncommon in Selleckchem AZD1208 lymphoproliferative disease and may predate the diagnosis of lymphoproliferative disease. Many vasculitides have been associated with hairy cell leukemia

(HCL), including polyarteritis nodosa (PAN) and leukocytoclastic vasculitis. We herein report a case whose initial presentation was like Behçet’s disease (BD) (arthritis, oral and genital ulcerations, papulopustular skin lesions) BMN 673 cost in addition to pancytopenia, but turned out to have HCL. Because of the overlap between their symptoms, like oral ulcerations, skin lesions, arthritis and constitutional findings, HCL and BD may mimic each other. We should keep in mind other reasons for vasculitis such as lymphoproliferative disease, especially whose who have hematological abnormalities such as pancytopenia. “
“Tumour necrosis factor inhibitors have demonstrated significant clinical

and radiological benefits in rheumatoid arthritis (RA). However, they have important adverse effects including an association with infection. Results from current studies, including meta-analyses of randomized controlled trials and observational studies, are conflicting regarding the risk of serious infection in RA patients treated with TNF inhibitors. The majority of data suggest an increased risk, in particular of respiratory, skin and soft tissue infections, including tuberculosis. This increased risk of tuberculosis is of particular concern in the APLAR region. However, adverse event analysis remains a difficult area to Tacrolimus (FK506) study and decisions regarding

initiation of TNF inhibitors must be made on a case-by-case basis after carefully considering the risks and benefits. “
“Reports of hospitalized systemic connective tissue disorders (SCNTD) are mostly disease-specific reports from institutional databases. To clarify the admission rate, disease determination, hospital mortality rate, length of stay and hospital charges among hospitalized patients diagnosed with SCNTD. The data were extracted from the 2010 national database of hospitalized patients provided by the Thai Health Coding Center, Bureau of Policy and Strategy, Ministry of Public Health, Thailand. Patients over 18 years having International Classification of Diseases (ICD)-10 codes for a primary diagnosis related to SCNTD were included. There were 6861 admissions coded as disorders related to SCNTD during the fiscal year 2010. The admission rate was 141 per 100 000 admissions.

Levels of interleukin-17 and vitamin-D binding protein (VDBP) by enzyme-linked immunosorbent assay could distinctly demarcate active disease Dasatinib ic50 versus remission. Our study provides potential protein markers of active disease versus remission in GPA. “
“Consideration of the safety of liver transaminases monitoring every 12 weeks in patients with inflammatory connective tissue disorders who are treated with methotrexate (MTX). In a retrospective study, the data from rheumatic patients receiving MTX were analyzed. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured every 12 weeks. Based

on the physician’s final decision about the continuation of MTX, the patients were classified into one of the following groups: continuation of MTX without MTX dose reduction, MTX dose reduction, MTX discontinuation PLX4032 research buy due to liver complication and MTX discontinuation due to other reasons. A total of 809 patients who

were on MTX were included in the study. The mean follow-up duration and the mean duration of treatment with MTX were 31.22 and 19.76 months, respectively. The mean accumulation dose of MTX was 865.85 mg. Due to the increase in the level of transaminases in 3.2% of the patients, MTX dose was reduced; and in 1.1% of the cases it was temporarily discontinued. In the follow-up of the patients with elevated transaminases, they returned to normal limits in 99.5% of patients; and only in four cases (0.5%) they remained elevated and MTX was discontinued. The probability of the patients remaining on MTX for 5 years without discontinuation for liver complications was 98.5% Liver transaminase monitoring every 12 weeks for MTX-treated patients is safe. “
“To evaluates the pregnancy outcomes in systemic lupus erythematosus (SLE) patients in South Korea and determine the predictive factors for adverse fetal and

maternal outcomes. All pregnancies in SLE patients who were seen at the Samsung Medical Center between November 1994 and December 2010 were included and retrospectively analyzed. Arachidonate 15-lipoxygenase SLE flares were determined by the Lupus Activity Index-Pregnancy (LAI-P) score. Sixty-two pregnancies were observed in 50 patients. Fifty-one (82.3%) live births and 11 (17.7%) fetal losses were observed. Thirty-eight of the live births (74.5%) were full-term and 13 (25.5%) were preterm births. Fetal losses included three spontaneous abortions, two stillbirths and six therapeutic abortions. Proteinuria during pregnancy was a predictive factor for adverse fetal outcomes (adjusted odds ratio [OR] 12.50; P = 0.032). An LAI-P score was obtained in 36 pregnancies, and SLE flares occurred in 12 pregnancies (33.3%), primarily during the second trimester (46.2%). Renal involvement (69.2%) was the most common SLE flare during pregnancy.

Levels of interleukin-17 and vitamin-D binding protein (VDBP) by enzyme-linked immunosorbent assay could distinctly demarcate active disease Palbociclib ic50 versus remission. Our study provides potential protein markers of active disease versus remission in GPA. “
“Consideration of the safety of liver transaminases monitoring every 12 weeks in patients with inflammatory connective tissue disorders who are treated with methotrexate (MTX). In a retrospective study, the data from rheumatic patients receiving MTX were analyzed. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured every 12 weeks. Based

on the physician’s final decision about the continuation of MTX, the patients were classified into one of the following groups: continuation of MTX without MTX dose reduction, MTX dose reduction, MTX discontinuation Cytoskeletal Signaling inhibitor due to liver complication and MTX discontinuation due to other reasons. A total of 809 patients who

were on MTX were included in the study. The mean follow-up duration and the mean duration of treatment with MTX were 31.22 and 19.76 months, respectively. The mean accumulation dose of MTX was 865.85 mg. Due to the increase in the level of transaminases in 3.2% of the patients, MTX dose was reduced; and in 1.1% of the cases it was temporarily discontinued. In the follow-up of the patients with elevated transaminases, they returned to normal limits in 99.5% of patients; and only in four cases (0.5%) they remained elevated and MTX was discontinued. The probability of the patients remaining on MTX for 5 years without discontinuation for liver complications was 98.5% Liver transaminase monitoring every 12 weeks for MTX-treated patients is safe. “
“To evaluates the pregnancy outcomes in systemic lupus erythematosus (SLE) patients in South Korea and determine the predictive factors for adverse fetal and

maternal outcomes. All pregnancies in SLE patients who were seen at the Samsung Medical Center between November 1994 and December 2010 were included and retrospectively analyzed. Methisazone SLE flares were determined by the Lupus Activity Index-Pregnancy (LAI-P) score. Sixty-two pregnancies were observed in 50 patients. Fifty-one (82.3%) live births and 11 (17.7%) fetal losses were observed. Thirty-eight of the live births (74.5%) were full-term and 13 (25.5%) were preterm births. Fetal losses included three spontaneous abortions, two stillbirths and six therapeutic abortions. Proteinuria during pregnancy was a predictive factor for adverse fetal outcomes (adjusted odds ratio [OR] 12.50; P = 0.032). An LAI-P score was obtained in 36 pregnancies, and SLE flares occurred in 12 pregnancies (33.3%), primarily during the second trimester (46.2%). Renal involvement (69.2%) was the most common SLE flare during pregnancy.

The characteristic features of TA loci are that they comprise a VX-809 mouse TA gene pair in a bicistronic operon, consisting of an upstream antitoxin and a downstream toxin gene. Normally, two small proteins, a stable toxin and a labile antitoxin, associate tightly so as to keep the toxin component inert (Kwong et al., 2010). The putative role of the antitoxin gene product has been widely discussed, suggesting that there are at least two types of antitoxin. In Type I systems, the antitoxin is an RNA molecule

that neutralized the toxin translation and in Type II systems the antitoxin is a small labile protein that binds avidly to the toxin, inhibiting its activity or by downregulating its expression (Hayes, 2003). On the other hand, the toxins of Type I systems are small, hydrophobic proteins that confer their toxicity by damaging cell membranes, while Type II toxins damage particularly either DNA or RNA molecules (Van Melderen & Saavedra de Bast, 2009). In short, whatever their real function is, TA modules

can attack cells from within (Engelberg-Kulka et al., 2005) and a number of different intracellular targets have already been identified (Hayes, 2003). In recent years, the TA system has been consistently associated with a crucial regulatory process in living organisms better known as PCD. PCD is an active process that results in cell suicide and is an essential mechanism in multicellular organisms, required for Tyrosine Kinase Inhibitor Library manufacturer the elimination of superfluous or potentially harmful cells (Engelberg-Kulka & Glaser, 1999). PCD is currently used to refer

to any form of cell death mediated by an intracellular program, no matter what triggers it and whether or not it displays the characteristics of apoptosis (Hengartner & Bryant, 2000). The recent discovery of TA modules in many bacteria suggests that PCD may be a general phenomenon in bacteria (Picardeau et al., 2001). In this study, we report the presence of a TA locus in the genome of Piscirickettsia salmonis, a Gram-negative fish bacterial pathogen that has affected the salmonid industry since 1989 (Bravo & Campos, 1989). Piscirickettsia salmonis, the aetiological agent of the Salmonid Rickettsial www.selleck.co.jp/products/Pomalidomide(CC-4047).html Septicaemia (SRS) or Piscirickettsiosis, belongs to the Gammaproteobacteria group (Fryer & Hedrick, 2003) and was recently reclassified as a facultative intracellular organism (Mauel et al., 2008; Mikalsen et al., 2008; Gómez et al., 2009). Piscirickettsiosis was first reported in coho salmon (Oncorhynchus kisutch) (Bravo & Campos, 1989), but infectivity has also been demonstrated in cultured salmonid species such as the Atlantic salmon (Salmo salar), Chinook salmon (Oncorhynchus tshawytscha), and rainbow trout (Oncorhynchus mykiss) from the south of Chile to the northern hemisphere (Rojas et al., 2009).

, 2001). This appearance has been well studied in higher organisms particularly in Insecta (Ghiradella, 1991; Vukusic et al., 2004;

Seago et al., 2009), Aves (Greenewalt et al., 1960; Prum & Torres, 2003; Doucet et al., 2006), and in fishes (Land, 1972; Lythgoe & Shand, 1989). Iridescence is also encountered in viruses (Williams & Smith, 1958) and in marine organisms such as ctenophore (Welch et al., 2006) and diatoms (Noyes et al., 2008). Iridescence High Content Screening has been poorly studied in the prokaryote kingdom. Both direct illumination and trans-illumination have been used to observe colonies’ iridescence on solid media (Pijper, 1923; Nogrady & Guérault, 1964; Zierdt, 1971). Recently (Kientz et al., 2012), a comparison of a wide range of bacterial strains

permitted to defined four classes of iridescence: rainbow-diffuse and rainbow-edge iridescences under trans-illumination and, metallic appearance and intense glitter-like iridescence under direct illumination. Cellulophaga lytica was the unique bacterium belonging to the latter class. As this type of iridescence occurred under direct natural light exposure, it was described Epigenetics inhibitor as a more natural coloration effect. The visual appearance corresponds to sub-millimeter-sized centers of color of varying brightness distributed across the biofilm giving a glitter-like character. Iridescent green is the dominant color, but red and blue-violet are also observed at the colonies’ edges on classical marine

media. Though the physiology of C. lytica has never been thoroughly characterized, some microbiological features (Johansen et al., 1999) and genomic data (Pati et al., 2011) suggest that the bacterium is well adapted to extreme conditions. Moreover, C. lytica is frequently isolated from coastal shore. In this biotope, high variations of temperature, salinity, or light exposure are common. It is still unknown whether C. lytica’s iridescence can occur under such conditions, in vitro or in natural habitats. In the present work, we examine the effect of key abiotic factors on C. lytica’s iridescence. Several stress conditions that mimic the natural ADAMTS5 biotope of the bacterium were preferentially employed. Unless otherwise specified, agar concentration was 1.5%. Ready-to-use media marine agar (MA), nutrient agar (NA), tryptic soy agar (TSA), and Luria–Bertani (LB) were purchased from Dutscher (France). Cytophaga agar (CYT ASW) and low nutrient (LN ASW) media were made with artificial seawater (ASW) Instant Ocean© (30 g L−1 in pure water). CYT ASW medium contained 1 g tryptone, 0.5 g yeast extract, 0.5 g CaCl2·2H2O, 0.5 g MgSO4·7H2O, and 15 g agar in 1 L of ASW (Johansen et al., 1999). Casein was replaced by tryptone because C. lytica does not degrade casein (Kientz et al., 2012). LN ASW medium only contained agar (15 g) in 1 L of ASW (Jensen et al., 1996).