P. aeruginosa produces rhamnolipids, which are glycolipidic biosurfactants consisting of one or two hydrophilic l-rhamnose molecules (mono- and di-rhamnolipids, respectively) and of a hydrophobic fatty acid moiety, see [1] for review. Rhamnolipids are involved in a number of functions, such as the uptake of poorly soluble

substrates, AC220 molecular weight surface motility, biofilm development, or interaction with the immune system [2], and are considered as virulence factors. Most of the rhamnolipid biosynthetic pathway is clearly established [1, 3]: RmlA, RmlB, RmlC, and RmlD are responsible for dTDP-l-rhamnose synthesis from glucose-1-phosphate, while RhlA supplies the acyl moieties by converting two molecules of β-hydroxylacyl-Acyl Carrier Protein (ACP) in one BIX 1294 datasheet molecule of β-D-(β-D-hydroxyalkanoyloxy) alkanoic acid (HAA). Finally, the rhamnosyltransferase RhlB links one l-rhamnose molecule to one HAA to yield one mono-rhamnolipid, which either will be the final product or will be the substrate of the second rhamnosyltransferase RhlC to obtain one di-rhamnolipid. RhlG was described as an NADPH-dependent β-ketoacyl reductase specifically involved in rhamnolipid synthesis [4]. It was proposed to work just upstream

of RhlA, converting one β-ketoacyl-ACP molecule in one β-hydroxylacyl-ACP [5]. These conclusions were based on: i) the amino acid sequence similarities between RhlG and FabG, Selleck FHPI which is part of the general fatty acid synthetic pathway; ii) the absence of rhamnolipid production by an rhlG mutant of P. aeruginosa PAO1; and iii) similarities between the promoters of the rhlG gene and of the rhlAB operon, suggesting a coordinated expression of the genes involved in rhamnolipid synthesis [4]. However, two subsequent articles questioned the RhlG function. A structural and biochemical study of RhlG confirmed that Tolmetin it is an NADPH-dependent β-ketoacyl reductase, but indicated that the RhlG substrates are not carried by the ACP [6]. Zhu and Rock [3] then reported that RhlG was not required for rhamnolipid synthesis in the heterologous host

Escherichia coli and that rhlG mutants of P. aeruginosa PA14 and PAO1 were not affected in rhamnolipid production. These authors concluded that RhlG plays no role in rhamnolipid formation and that its physiological substrate remains to be identified [3]. The transcriptional regulation of the rhlG gene has not been so far studied in more details than in [4]. Among the rhamnolipid-related genes, the rhlAB operon was the first and most extensively studied at the transcription level. These works led to the discovery of the RhlRI quorum sensing (QS) system, which is encoded by genes lying just downstream of rhlAB and is required for rhlAB transcription [7–10]. RhlRI is a LuxRI-type QS system [11], RhlI synthesizing the communication molecule N-butyryl-l-homoserine lactone (C4-HSL) which binds to the transcription regulator RhlR.

01; Figure  4A) and FC-IBC-02 (P < 0.01; Figure  4C). However, the difference was not statistically significant compared with AZD8931 alone. Figure 4 AZD8931 inhibits the growth of SUM149 and FC-IBC-02 cells in vivo in SCID mice. SUM149 (A) and FC-IBC-02 (C) cells were orthotopically transplanted into the mammary fat

pads of SCID mice. Animals were randomized into groups (n = 5/group) when tumor volumes were approximately 50–80 mm3. AZD8931 was BGB324 concentration given by oral gavage at doses of 25 mg/kg per day, 5 days/week for 4 weeks. Paclitaxel was given twice weekly by subcutaneously injection at 10 mg/kg for 4 weeks. The mean tumor volumes were measured at the time points indicated. In SUM149 xenografts (A), *P < 0.01 (vs. control), **P = 0.01 (vs. paclitaxel + AZD8931). In FC-IBC-02 xenografts (C), *P < 0.001 (vs. control), **P < 0.01 (vs. paclitaxel + AZD8931). SUM149 (B) and FC-IBC-02 (D), the size of CHIR98014 order tumors was measured by weights (mg) after tumors were removed from Selleckchem Luminespib mice at the end of experiments. The data shown represent the mean of tumor weights with SD. *P < 0.05 (vs. control); **P < 0.01 compared to control. The combination of paclitaxel + AZD8931 compared with paclitaxel (P = 0.008, SUM149; P = 0.001, FC-IBC-02). In addition, we also examined the weight of xenografted tumors at the end of study. The inhibitory

pattern of tumor size following different treatments was very similar to that seen in tumor growth curves in both IBC models. The combination of paclitaxel + AZD8931 was more effective at RAS p21 protein activator 1 reducing tumor sizes than all of the other treatment groups. The difference was also significant for paclitaxel + AZD8931 versus paclitaxel alone in

SUM149 (P = 0.008; Figure  4B) and FC-IBC-02 (P = 0.001; Figure  4D) models. Compared with AZD8931 alone, the difference was marginally significant for SUM149 tumors (P = 0.056) and FC-IBC-02 tumors (P = 0.07).Finally, we examined the expression of total EGFR, HER2, HER3, phosphorylated EGFR, phosphorylated HER2, and phosphorylated HER3 in SUM149 xenografted tumors by immunohistochemistry. As expected, high level expression of EGFR and low levels of HER2 and HER3 expression were observed in both AZD8931-treated and control tumors. The expression of phosphorylated EGFR, HER2, and HER3 was inhibited in AZD8931-treated tumors compared with control tumors (Figure  5A). The average of pathologist’s H-score for both membrane and cytoplasmic staining was shown in Figure  5B. Together, we conclude that AZD8931 significantly inhibits tumor growth in HER2 non-amplified IBC xenograft models by inhibiting EGFR, HER2 and HER3 phosphorylation. The combination of paclitaxel + AZD8931 was more effective than single agent paclitaxel or AZD8931 alone at delaying tumor growth. Figure 5 AZD8931 inhibits EGFR pathway protein expression in vivo . A.

IS629 prevalence in the A6 strains and the distribution amongst Sp, SpLE, backbone and the pO157 plasmids

did not show any specific pattern, however it appears that IS629 transposes actively in the A6 CC. Table 3 IS629 element presence/EPZ015666 research buy absence in CC strains from the O157:H7 stepwise evolutionary model           A6               A5         A4       A2   A1   A?   A6 NR Phage Or backbone 1 2 3 4 5 6 7 8 9 10 11 12 SBI-0206965 mw 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 IS.1 Sp 4 ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND IS.2 Sp 4 ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND IS. 3 Sp 5 stx2 + – - – - – - – - – - – - – - – - – - – - – - – - + – IS. 4 SpLE 1 – + – - – - + – - – - – - – - – - – - – - – - – - – - IS. 5 SpLE 1 + + + + + – + – - – - – - – - – - – - – - – - – - + + IS. 6 SpLE 1 – + – - – - + – - – - – - – - – - – - – - – - – - – - IS. 7 SpLE 1 + + + + + – + + – - – - – - – - – - – - – - – - – + + IS. 8 Sp 8 + – + – + – + – - – - – - – - – - – - – - – - – - + – IS. 9 Sp 8 – + – - – - – - – - – - -

– - – - – - – - – - – - – + IS. 10 back + + – - + – + + – - – - – - – - – - – - – - – - – + + IS. 11 back + + – - + – - – - – - – - – - – - – - – - – - – - + + IS. 12 Sp 12 + – - – - – - – - – - + + + – - – - – - – - – - – + – IS. 13 back + + + + + + + – - – - – - – - – - – - – - – - – - + + IS. 14 Sp 13 + + + + + + – + – - – - – - – - – - – - – - – - – + + IS. 15 Sp 14 + + + + + + + + – - – - – - – - – - – - – - – - – + – IS.16 SpLE 2 ND ND ND Ferrostatin-1 manufacturer ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND IS. 17 back + + – - – - – - this website – - – - – - – - – - – - – - – - – + + IS. 18 Sp 15 stx1 + + – - + – - – - – - – - – - – - – - – - – - – - + + IS. 19 back + – + + + – - + – - – - – - – - – - – - – - – - – + – IS. 20 Sp 17 + -

+ + + – + + – - – - – - – - – - – - – - – - – + – IS. 21 SpLE3 + + – + + + + + – - – - – - – - – - – - – - – - – + + IS.22 back ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND IS. 23 SpLE 5 + + – - + – + + – - – - – - – - – - – - – - – - – + + IS. 24 SpLE 1 – + – - – - – - – - – - – - – - – - – - – - – - – - + IS. 25 SpLE 1 – + – - – - – - – - – - – - – - – - – - – - – - – - + IS.26 933O ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND IS. 27 SpLE 2 – + – - – - – - – - – - – - – - – - – - – - – - – - + IS.28 933Y ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND ND IS. 29 Sp 1 – - + + – - – + – - – - – - – - – - – - – - – - – - – IS. 30 Sp 4 – - + – - – - – - – - – - – - – - – - – - – - – - – - IS. 31 Phage – - + + – - – - + + – + + + – - – - – - – - – - – - – IS. 32 back – - + + – - – + – - – - – - – - – - – - – - – - – - – IS. 33 Sp 13 – - + + – - – - – - – - – - – - – - – - – - – - – - – IS. 34 back – - + + – - – - – - – - – - – - – - – - – - – - – - – IS.

Oncogene 2004, 23:2838–49.PubMedCrossRef 27. de Melo M, Gerbase MW, Curran J, Pache JC: Phosphorylated Extracellular Signal-regulated Kinases are Significantly Increased in Malignant Mesothelioma. J SU5402 cell line Histochem Cytochem 2006, 54:855–861.PubMedCrossRef 28. Udayakumar ST, Stratton MS: Fibroblast

HSP inhibitor Growth Factor-1 Induced Promatrilysin Expression Through the Activation of Extracellular-regulated Kinases and STAT3. Neoplasia 2002, 4:60–67.PubMedCrossRef 29. Decker T, Kovarik P: Serine phosphorylation of STATs. Oncogene 2000, 19:2628–2637.PubMedCrossRef 30. Pahl HL: Activators and target genes of Rel/NF-kB transcription factors. Oncogene 1999, 18:6853–6866.PubMedCrossRef 31. Tchirkov A, Khalil T, Chautard EE: Interleukin-6 gene amplification and shortened survival in glioblastoma

patients. Br J Cancer 2007, 96:474–476.PubMedCrossRef 32. Weissenberger J, Loeffler S, Kappeler A: IL-6 is required for glioma development in a mouse model. Oncogene 2004, 23:3308–3316.PubMedCrossRef KU-57788 33. Lee H, Herrmann A, Deng JH: Persistently activated STAT3 maintains constitutive NF-kB activity in tumors. Cancer Cell 2009, 15:283–293.PubMedCrossRef 34. Brantley EC, Benveniste EN: Signal Transducer and Activator of Transcription-3: A Molecular Hub for Signaling Pathways in Gliomas. Mol Cancer Res 2008, 6:675–684.PubMedCrossRef 35. Haura EB: SRC and STAT pathways. J Thorac Oncol 2006, 1:403–405.PubMedCrossRef 36. Wheeler DL, lida M, Dunn EF: The Role of Src in Solid Tumors. The Oncologist 2009, 14:667–678.PubMedCrossRef 37. Deo DD, Axelrad TW, Robert EG, Marcheselli V, Bazan NG, Hunt JD: Phosphorylation

of STAT-3 in Response to Basic Fibroblast Growth Factor Occurs through a Mechanism Involving Platelet-activating Factor, JAK-2, and Src in Human Umbilical Vein Endothelial Cells. JBC 2002, 277:21237–21245.CrossRef 38. Chan SL, Yu VC: Proteins of the bcl-2 family in apoptosis signaling: from mechanistic insights to therapeutic opportunities. Clin Exp Pharmacol Physiol 2004, 31:119–128.PubMedCrossRef Competing interests The authors declare that Fenbendazole they have no competing interests. Authors’ contributions JL carried out experiments and drafted the manuscript. XX participated in study design and helped to draft the manuscript. XF and BZ participated in study design, performed experiments and JW participated in study design and revised manuscript. All authors approved the final manuscript.”
“Background Ubiquitination is a highly diverse and complex post-translational modification responsible for controlling protein expression and activity in a vast array of cellular processes such as proteasomal degradation, cell cycle regulation, protein trafficking, inflammation and DNA repair [1, 2]. Removal of ubiquitin via the action of deubiquitinating enzymes (DUBs) is integral to the regulation of the ubiquitin system, hence the importance of these enzymes in the maintenance of protein expression and function.

Bacteria were grown to mid-log phase at 37°C (controlled by the evaluation of optical density at 600 nm) and resuspended in PBS buffer (pH = 7.4). The bacteria suspensions were then diluted 10 times in 100 μl of solutions containing antibacterial agents by themselves or with mucin (1000 μg/ml), or bile (the final 1:10 bile dilution mimics the environment of the upper small intestine into which bile is secreted [36] (pH = 7.4)). In another set of experiments antibacterial activity of these components was determined following their preincubation in simulated gastric juice [36, 37] at pH ~1.5 with and without pepsin (0.5 mg/ml). After

incubating bacteria with antibacterial molecules find more for one-hour at 37°C, the bacterial suspensions were placed on ice and diluted 10- to 1000- fold. CDK inhibitor Aliquots of each dilution (10 μl) were spotted on LB Agar plates for overnight culture at 37°C. The number of colonies at each dilution was counted the following morning. The colony forming units (CFU/ml) of the individual samples were determined from the dilution factor. Mass spectrometry Analytical characterization was Tubastatin A cell line performed

on the CSA-13 and LL-37 suspensions after 3H incubation with pepsin (0.5 mg/ml) at low pH (~1,5) at 37°C, using the Shimadzu (Columbia, MD) instrument (the LC-MS system consisted of a LC-20AB solvent delivery system and SIL-20A auto-sampler coupled to dual wavelength UV-Vis detector and a LCMS 2010EV single quadrupole mass spectrometer), coupled to a Shimadzu Premier C18 column (150 mm × 4.6 mm i.d., 5 μm particle size). The mobile phase flow rate was 1 ml/min with a starting ratio of 90% mobile phase A (water) and 10% mobile Orotidine 5′-phosphate decarboxylase phase B (acetonitrile) both with 0.1% (v/v) formic acid. The analytical method consisted of the following steps: (i) sample injection and holding at 10% B for 5 min, (ii) linear gradient from 10% to 90% B over 15 minutes, (iii) holding at 90% B for 5 minutes, (iv) isocratic step to 10% B and holding for 5 minutes prior to the next sample injection. Mass spectrometry was performed on the eluent using electrospray ionization (ESI) in positive ion mode with a scanned m/z range from 160-2000. Red blood cell lysis

The hemolytic activity of LL-37, WLBU-2 and CSA-13 (0-200 μg/ml), against human red blood cells (RBC) was tested using erythrocytes suspended in PBS. RBC prepared from fresh blood (Hematocrit ~5%) were incubated for 1 h at 37°C after addition of test molecules. Relative hemoglobin concentration in supernatants after centrifugation at 2000 × g was monitored by measuring the absorbance at 540 nm. 100% hemolysis was taken from samples in which 2% Triton X-100 was added. Cell culture Human gastric adenocarcinoma cells (ATCC; CRL-1739) were maintained in DMEM (BioWhittaker) culture supplemented with 10% heat-inactivated fetal bovine serum (Hyclone) at 37°C and 5% CO2. For LDH release assay and microscope evaluation cells were plated in 24 well plates and grown to confluence.

43 (P = 0.018) NS NS OHCLI 0.61 (P < 0.001)   0.42 (P = 0.002) OHREF   0.61 (P < 0.001) 0.50 (P = 0.005) OHBIA NS NS 0.50 (P = 0.005) Height NS NS 0.43 (P = 0.018) Pre-HD weight 0.43 (P = 0.017) 0.55 (P = 0.002) 0.62 (P < 0.001) Pre-HD SBP NS NS NS Pre-HD DBP 0.54 (P = 0.002) selleck NS 0.51 (P = 0.004) Pre-HD MAP 0.38 (P = 0.042) NS 0.48 (P = 0.008) NT-proANP NS NS NS LAD, LVEDD NS NS NS VCCI −0.45 (P = 0.013) NS −0.36 (P = 0.048) Cardiothoracic index

NS NS NS Vital capacity NS NS NS Pre-HD calf circumference 0.37 (P = 0.041) 0.47 (P = 0.009) 0.56 (P = 0.001) ECW 0.52 (P = 0.003) 0.50 (P = 0.005) 0.94 (P < 0.001) OH REF reference overhydration, OH CLI clinically assessed overhydration, OH BIA bioimpedance calculated overhydration, HD hemodialysis, SBP systolic blood pressure, DBP diastolic blood pressure, MAP mean arterial blood pressure,

NT-proANP N-terminal atrial natriuretic peptide, LAD left atrial diameter, LVEDD left ventricular end diastolic diameter, VCCI vena cava collapsibility index, ECW extracellular water, NS not significant Pre-HD calf circumference was positively correlated with OHREF (R = 0.37; P = 0.041), OHCLI (R = 0.47; P = 0.009), ECW/BSA (R = 0.56; P = 0.001) and pre-HD weight (R = 0.68; P < 0.001), Omipalisib mouse indicating a strong association of this simple anthropometric measure with fluid overload. VCCI was negatively correlated with OHREF (R = −0.45; P = 0.013), concordant with decreasing collapsibility of the vena cava with increasing OH. In terms of fluid overload, N-terminal

atrial natriuretic this website peptide (NT-proANP) levels did not correlate with OH or left atrial diameter (LAD) (although positively with CTI, R = 0.67; P < 0.001), parameters with known association in the normal population. The significant influence of impaired renal function on NT-proANP levels is evident by its positive correlation with serum creatinine levels (R = 0.57; P = 0.001). Blood pressure The average pre-HD BP was 125/71 mmHg, post-HD BP 110/62 mmHg, and the average BP reduction was 6/3 mmHg per one liter of OH removed. The mean 24-h ambulatory BP on a HD-free day was 116/68 mmHg. Pre-HD diastolic blood pressure (DBP) (R = 0.54; P = 0.002), mean arterial blood pressure (MAP) (R = 0.38; P = 0.04), but not systolic blood pressure (SBP) (R = 0.09; P = 0.64) correlated DOK2 with OHREF. Interestingly, after HD, SBP (R = 0.43; P = 0.02), DBP (R = 0.37; P = 0.04) and MAP (R = 0.43; P = 0.02) were positively correlated with the number of antihypertensive drugs (no correlation was seen before HD). Prognostic data are presented in the Electronic Supplementary Material. Multiple regression models Parameters significant in the univariate analyses (Table 2) were combined in multiple regression models (Table 3). Calf circumference was considered as a part of the clinical examination and not explored separately.

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65. Rambaut A: Molecular evolution, phylogenetics and epidemiology: Tracer. 2009. [http://​tree.​bio.​ed.​ac.​uk/​software/​tracer/​] Competing interests The authors declare no competing interests; financial or otherwise. Authors’ contributions Conceived the study: RMW. Designed and performed the practical experimental work: SM, MY, DCLB, YBH, WKL, RMW. Designed and performed the computational analyses: SM, MY, YCFS, DCLB, GJDS, RMW. Wrote the manuscript: SM, MY, YCFS, DCLB, GJDS, WKL, RMW. All authors have read and approved the final manuscript.”
“Background Lantibiotics are ribosomally synthesized peptides produced by Gram-positive bacteria that frequently exhibit potent antimicrobial activities against other bacteria. Nisin A (nisin) is the most intensively investigated lantibiotic, and was first discovered in 1928 [1]. It has a long history of safe use in the food industry and is approved by the US Food and Drug Administration, by WHO and by the EU (as natural food preservative E234) [2–4].

modesticaldum. The growth on D-ribose

confirms the proposed function of a putative ribose ABC transporter (rbsDACB, Selleck Stattic HM1_2417 – HM1_2420) and ribokinase (rbsK, HM1_2416) through genome annotation, and growth supported by D-ribose, D-glucose and D-fructose suggests that annotated EMP and non-oxidative pentose phosphate pathways in H. AZD1390 nmr modesticaldum are active in carbohydrate metabolism. As D-fructose and D-glucose are polar molecules, glucose, fructose or hexose transporter proteins are required to move those molecules across the cell membrane into the cells. No known hexose transporter has been reported for H. modesticaldum, which may partially explain slower growth on D-hexose than on D-ribose. It remains to be determined if the putative ribose transporter of H. modesticaldum functions as a

hexose transporter, since no ribose transporter has been reported previously to accommodate a hexose. Metabolism of carbohydrate through the EMP pathway supplies 2 ATP and 2 NADH to the cells, which are significant for the energy metabolism of H. modesticaldum, because essential genes in the oxidative pentose phosphate and ED pathways, which provide reducing equivalents during carbohydrate metabolism, are absent in the genome. Moreover, utilization of glucose can provide an additional path for H2 production in H. modesticaldum as reported in some non-phototrophic bacteria [28]. The biological significance of the alternative CO2-assimilation pathways Selleckchem BLZ945 The CO2-anaplerotic pathways are known to replenish the intermediates of TCA cycle, so that removal of the intermediates for synthesizing cell materials will not significantly slow down the metabolic flux through the TCA cycle. Our recent studies showed that the photoheterotrophic bacterium R. denitrificans uses the anaplerotic pathways to assimilate CO2. All of the genes encoding the enzymes for CO2-anaplerotic pathways, PEP carboxylase, PEP carboxykinase, pyruvate carboxylase and malic enzyme, have been annotated in the R. denitrificans genome, and activities of these enzymes have been detected.

The alternative CO2-fixation pathways account for making up 10-15% cellular proteins of R. denitrificans [9]. Our studies presented here also suggest that H. modesticaldum uses two anaplerotic RANTES pathway, PEP carboxykinase (PEPCK) and pyruvate:ferredoxin oxidoreductase (PFOR), for assimilating CO2. What is the biological importance of PEPCK and PFOR in H. modesticaldum? Although the anaplerotic CO2-assimilation cannot support (photo)heterotrophic growth in the way that the autotrophic CO2-fixation supports (photo)autotrophs, these two CO2-anaplerotic pathways are critical for the carbon metabolism of H. modesticaldum (see Figure 5). First, the CO2-assimilation by PFOR catalyzes the formation of pyruvate from acetyl-CoA, a reaction that cannot be catalyzed by pyruvate dehydrogenase.

No diffusing pigment, no distinct odour noted. Chlamydospores (5–)7–13(–19) × (6–)7–12(–15) μm, l/w 0.9–1.3(–1.6) (n = 32), noted after 4 days at 25°C, becoming extremely abundant (also

at 15°C) on the entire plate, globose, oval or ellipsoidal to angular in thick hyphae, terminal and intercalary. MEK activity conidiation unreliable, noted after 2–4 weeks. Effuse conidiation seen as scant minute heads on aerial hyphae, appearing warted under low magnification, in distal areas of the colony. Conidiation dense in few irregularly disposed, compact, white pustules 1–4 mm diam; with short straight to slightly sinuous elongations bearing minute droplets. Conidia formed in minute dry heads of 10–15 μm. Sometimes few light brownish stromata 0.4–1.3 mm diam appearing close to

the distal margin, surrounded by moniliform hyphae. Habitat: on well-rotted, soft wood of deciduous trees and shrubs, often emerging from underneath loosely ICG-001 supplier attached bark R788 manufacturer or from cracks in the wood. Distribution: Europe (Austria, Germany). Holotype: Germany, Baden-Württemberg, Freiburg, Landkreis Breisgau-Hochschwarzwald, shortly before Breisach heading north, in the riverine forest at the river Rhine, MTB 7911/4, 48°00′10″ N, 07°36′55″ E, elev. 190 m, on 2 partly decorticated branches of Fraxinus excelsior 3–4 cm thick, on wood, soc. Gliocladium sp. and Chaetosphaeria pulviscula, 3 Sep. 2004, H. Voglmayr & W. Jaklitsch W.J. 2671 (WU 29173, culture CBS 119286 = C.P.K. 2017). Holotype of Trichoderma albolutescens isolated from WU 29173 and deposited as a dry culture with the holotype of H. albolutescens as WU 29173a. Other specimens examined: Austria, Kärnten, Klagenfurt Land, St. Margareten im Rosental, Tumpfi, MTB 9452/4, 46°32′35″ N, 14°25′32″ E, elev. 565 m, on decorticated branch of Alnus glutinosa second 1.5 cm thick, on wood, 25 Sep. 2006, H. Voglmayr & W. Jaklitsch, W.J. 2986 (WU 29174). Niederösterreich, Scheibbs, Lunz am See, forest

path from Schloß Seehof in direction Mittersee, MTB 8156/3, 47°50′40″ N, 15°04′25″ E, elev. 630 m, on decorticated branches of Corylus avellana and Fraxinus excelsior, on wood, soc. Nemania chestersii, 16 Oct. 2003, H. Voglmayr & W. Jaklitsch, W.J. 2459 + 2460, WU 29171. Tirol, Innsbruck-Land, Ampass, Ampasser Hügel, MTB 8734/2, 47°15′31″ N, 11°27′13″ E, elev. 700 m, on decorticated branches of Corylus avellana, Quercus robur and Alnus incana, on wood, soc. rhizomorphs, 2 Sep. 2003, W. Jaklitsch & U. Peintner, W.J. 2352 + 2356 (WU 29170). Vienna, 10th district, recreation park Wienerberg, MTB 7864/1, 48°09′56″ N, 16°20′56″ E, elev. 220 m, on thin decorticated branches of well-rotted ?Populus tremula, 1–3 cm thick, on wood, erumpent from holes, between thick fibres, soc. Eutypa sp., Lycogala epidendron, 13 Jun. 2004, W. Jaklitsch, W.J. 2509 (WU 29172). 22nd district, Lobau, at Panozzalacke, MTB 7865/1, 48°11′06″ N, 16°29′20″ E, elev. 150 m, on branches of Prunus padus, 18 Nov. 2006, W. Jaklitsch, W.J.