The induction level of nanE in the presence of sialic acid and cAMP was similar to the expression observed when sialic acid alone was added. The 5 bp insertion eliminated the cAMP-dependent activation of nanE that was observed in the 2019ΔcyaA ΔnagB strain. In both the 2019ΔcyaA and 2019ΔcyaA ΔnagB backgrounds, altered helical phasing also resulted in the induction of siaP when cAMP was added (Figures 5A and 5C). In the 2019ΔcyaA+5 strain, the 5 bp insertion led to a 43-fold increase in siaP expression in the presence of cAMP (from 6-fold

in 2019ΔcyaA) and a 29-fold increase (from 2-fold in 2019ΔcyaA) when both cAMP and sialic acid were present. Taken together, these results indicate that altering the helical phasing succeeded in uncoupling SiaR- and CRP-mediated regulation of the nan and siaPT operons. It resulted in nanE expression becoming unresponsive Crenigacestat order to cAMP, much like it is in the 2019ΔcyaA ΔsiaR mutant. Altered helical phasing also prevented SiaR from exerting a negative influence on

the expression of siaP. We conclude that the insertion eliminated the ability of SiaR and CRP to interact to regulate both the nan and siaPT operons. SiaR and CRP bind to their respective operators simultaneously Mocetinostat chemical structure Binding of SiaR to an operator in the intergenic region between nanE and siaP was demonstrated previously [14]. The putative operator of CRP was identified in silico and was found to overlap the region protected by SiaR in a DNase I protection assay by three base pairs. The ability of both proteins to bind to their operators was examined using the electrophoretic mobility shift assay (EMSA). Both proteins were able to bind to a probe comprising the region between the G protein-coupled receptor kinase two operons and CRP binding was dependent on the addition of cAMP (Figure 6A). When both proteins were included in the binding reaction, the DNA probe was shifted slightly higher than the SiaR-bound probe. This indicates that both proteins bind to their operators simultaneously, further supporting the hypothesis that the two regulators interact to regulate the adjacent nan and siaPT operons. Figure 6 Electrophoretic mobility

shift assay. A. Binding of both SiaR and CRP to the nan-siaPT intergenic region. Both SiaR and CRP bind to the probe individually and CRP binding is dependent on the presence of cAMP. Both proteins bind the probe simultaneously as indicated by the higher shift of the probe when both proteins are added. B. GlcN-6P enhances binding of SiaR. Two-fold serial dilutions of SiaR were added to binding reactions in the absence and presence of 100 μM GlcN-6P. More probe was shifted when GlcN-6P was present. GlcN-6P alters binding of SiaR to its operator Many transcriptional regulators exhibit altered binding selleck inhibitor affinity for their operator sequences when a co-regulator is bound. To determine the effect of GlcN-6P on SiaR binding, EMSA was used.

O35 Colon Carcinoma Cell Interaction with Liver Sinusoidal Endothelium Inhibits Organ-Specific Anti-Tumor Immunity via Interleukin-1-Induced Mannose Selleckchem Evofosfamide Receptor Beatriz Arteta 1 , Nerea Lasuen1, Aritz Lopategi1, Baldur Sveinbjörnsson3, Bard Smedsrod2, Fernando Vidal-Vanaclocha1 1 Department of Cell Biology and Histology, Basque Country University School of Medicine, Leioa, Bizkaia, Spain, 2 Department

of Cell Biology and Histology, Tromso University, Tromso, Norway, 3 Childhood Cancer Research Unit, KarolinskaInstitutet, Stockholm, Sweden Mannose receptor (ManR)-mediated liver sinusoidal endothelial cell (LSEC) endocytosis plays a primary role in antigen presentation and innate immunity, but its role in hepatic metastasis is unknown. We studied ManR-mediated endocytosis during C26 colorectal cancer cell interaction with LSEC and its immunological implications in the hepatic metastasis microenvironment. CFTRinh-172 Labeled mannan or ovalbumin uptake and anti-mouse ManR immunohistochemistry were used to study Selleck SC79 ManR expression and endocytosis in vivo, in vitro, and by confocal microscopy. Several IL-1 inhibitors and cyclooxygenase

(COX)-2 inhibitor Celecoxib were used to analyze the role of IL-1 and COX-2 in ManR regulation. Anti-mouse ManR antibodies and ManR knockout (ManR−/−) mice were used to identify ManR-dependent mechanisms during anti-tumor immune response of liver sinusoidal lymphocytes (LSL) interacting with tumor-activated LSEC. Both ManR expression and

endocytosis increased in tumor-activated LSEC through a two-step mechanism including: 1) Release of COX-2-dependent IL-1-stimulating factor(s) by LFA-1-expressing C26 cells in response to ICAM-1, which was over expressed and secreted Fossariinae by tumor-activated LSEC; and 2) widespread upregulation of ManR expression and endocytosis in LSEC by tumor-induced paracrine IL-1. In addition, LSL that had interacted with tumor-activated LSEC in vivo decreased their anti-tumor cytotoxicity and IFN-gamma secretion while increased IL-10 release to their supernatant ex vivo. IFN-gamma/IL-10 ratio also decreased in the hepatic blood from tumor-injected mice. Immune-suppressant effects of tumor-activated LSEC on LSL were abrogated in both LSEC from ManR−/− mice and tumor-activated LSEC given anti-mouse ManR antibodies. In summary, ICAM 1-induced tumor COX-2 led to regional anti-tumor immunity inhibition during hepatic colorectal metastasis via IL-1-induced ManR. ManR constituted a common mediator for prometastatic effects of IL-1, COX-2 and ICAM-1 in the liver. Rise of both hepatic IFNgamma:IL-10 ratio and anti-tumor cytotoxicity via ManR blockade is consistent with reported antimetastatic effects of IL-1, COX-2 and ICAM-1 inhibitors. These results support ManR as a molecular target for hepatic colorectal metastasis therapy.

02% Coomassie blue G-250, and the anode buffer contained 25 mM imidazole. Proteins were separated at 12 milli-amps for 2 hours in 4°C. Immunoblot analyses PAGE separated proteins were transferred to PVDF using tank transfer at 350 milliamps for 1 hour, blocked with 5% milk for one hour and probed with anti-Ago2 Ab diluted 1:100 [3]. ECL Plus chemiluminescence detection was used, and the blot was exposed to ECL film (Amersham). Acknowledgements We thank the Arthropod-borne RAD001 and Infectious

Diseases Lab Core Support for providing mosquitoes and viral titrations. We are also grateful to Richard Casey of the Bioinformatics Center of Colorado State University for providing support during preliminary investigations of analytical methods. This work

was funded by the SOLiD™ System $10 K Genome Grant Program sponsored by Life Technologies (CLC, AP), Gates Foundation/NIH Foundation grant (CLC, KEO), and by funds from the National Institute of Allergy and Infectious Disease, National Institutes of Health, under grant AI067380 (GDE, ANP). Electronic supplementary material Additional file 1: Additional viRNA profiles. A. sRNA reads from representative libraries of un-infected controls show non-specific alignment to the DENV2 genome. Panels from left to right indicate, 2, 4, and 9 dpi, respectively. Top panel shows count distribution along DENV2 genome for a representative library GKT137831 at each timepoint. Bottom panel shows mean sRNA distribution by size. Blue and red bars indicate sense and anti-sense sRNAs, respectively. B. viRNA WebLogos. viRNAs from a representative 9 dpi DENV2-infected cohort were separated by size group and subjected to WebLogo sequence alignment http://​weblogo.​berkeley.​edu/​ to identify the relative nucleotide frequency at each position. About Unoprostone 20,000 reads were analyzed for the combined categories. C. 24-30 nt piRNAs are more

abundant in DENV2-infected samples. Total mean transcriptome-mapped reads of un-infected and DENV2-infected libraries categorized by sRNA size group. Blue and red bars indicate sense and anti-sense viRNAs, respectively. (PDF 108 KB) Additional file 2: Host sRNA Profile Summary Tables. Summary data categorized by mapped read orientation and sRNA size group. ‘Summary’ page shows total sRNA reads in pooled libraries for each selleck inhibitor condition tested. ”Transcripts’ shows the number of targets remaining after removing low-abundance (<10 reads) and flagged candidates. “”Flagged”" segments are those for which a replicate accounted for 70% or more of the total reads; these were deleted from the final analysis. ‘Enriched’ and ‘Depleted’ indicate the number of targets showing significant changes in DENV2-infected pools over controls. Significance was determined using the edgeR exact test, and a Benjamini-Hochberg cut-off of 0.05 was used to adjust for multiple testing and control the false discovery rate. The following pages list raw sRNA count data for each target transcript at 2, 4, or 9 dpi.

CrossRef 2. Grayfer ED, Makotchenko VG, Nazarov AS, Kim S-J, Fedorov VE: Graphene: chemical approaches to the synthesis and modification. Russ Chem Rev 2011,80(8):751–770.CrossRef 3. Bonaccorso F, Lombardo A, Hasan T, Sun Z, Colombo L, Ferrari AC: Production and processing of graphene and 2d crystals. Mater Today 2012,15(12):564–589.CrossRef 4. Rao CNR, Sood AK, Voggu R, Subrahmanyam KS: Some novel attributes of graphene. J Phys Chem Lett

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laser deposition. AIP Adv 2011,1(2):022141–1-022141–9.CrossRef 12. Wang YY, Ni ZH, Yu T, Shen ZX, Wang HM, Wu YH, Chen W, Wee ATS: Raman studies of monolayer graphene: the substrate effect. J Phys Chem C 2008,112(29):10637–10640.CrossRef Idelalisib datasheet 13. Ren PG, Yan DX, Ji X, Chen T, Li ZM: Temperature dependence of graphene oxide reduced by hydrazine hydrate. Nanotechnology 2011, 22:055705–1-055705–8. 14. Werner H, Schedel-Niedrig T, Wohlers M, Herein D, Herzog B, Schlögl R, Keil M, Bradshaw AM, Kirschner J: Reaction of molecular oxygen with C 60 : spectroscopic studies. J Chem Soc Faraday Trans 1994,90(3):403–409.CrossRef 15. Kalita G, Adhikari S, Aryal HR, Umeno M, Afre R, Soga T, Sharon M: Fullerene (C 60 ) decoration in oxygen plasma treated multiwalled carbon nanotubes for photovoltaic application. Appl Phys Lett 2008,92(6):063508–1-063508–3.CrossRef 16. Borghesi A, Guizzetti G: Graphite (C). In Handbook of Optical Constants of Solids, vol. II. Edited by: Palik ED. San Diego: Academic; 1991:449–460. 17. Albrektsen O, Eriksen RL, Novikov SM, Schall D, Karl M, Bozhevolnyi SI, Simonsen AC: High resolution imaging of few-layer graphene. J Appl Phys 2012,111(6):064305–1-064305–8.CrossRef 18.

Significantly, the modified Cobimetinib nano-TiO2 is grafted with hydroxyl functional groups on the surface [44], which was also proved by the FT-IR spectra in Figure 1. Accordingly, the effect of BIBF 1120 modified nano-TiO2 on the crosslinking of polyester with TGIC was investigated by real-time FT-IR.

We prepared the polyester/nano-TiO2 composites with unmodified and modified nano-TiO2 (the amount is 2.0 wt.%), and their FT-IR spectra were recorded from 130°C to 205°C. Figure 5 Crosslinking through the reaction between the COOH of polyester and epoxy group of TGIC. (a) Schematic mechanism for the crosslinking reaction between the polyester and TGIC; FT-IR spectra of the polyester/nano-TiO2 composites with 2.0 wt.% nano-TiO2 from 130°C to 205°C. (b) The nano-TiO2 was not modified. (c) The nano-TiO2 was modified with aluminate coupling agent. (d) The absorbance at 908 cm-1 as a function of temperature for the two systems. Generally, the absorption band

around 910 cm-1 was assigned to monitor the epoxy equivalent conversion (the C-O-C bond of epoxy groups) [45, 46]. Figure 5b,c selleck inhibitor shows the FT-IR spectrum of the composites with unmodified and modified nano-TiO2, respectively. The decreased intensity of the absorption band could be attributed to the ring-opening of epoxy groups induced by the reaction between hydroxyl of COOH and epoxy groups during the crosslinking. In contrast to the sample with unmodified nano-TiO2, the sample with modified nano-TiO2 exhibits larger decreasing amplitude of the absorbance. Particularly, the absorbance at

908 cm-1 Megestrol Acetate as a function of temperature for the two systems were plotted in Figure 5d, demonstrating a faster decreasing tendency of the absorbance at this band for the polyester/modified nano-TiO2 composite. It suggests a promoting effect of modified nano-TiO2 on the crosslinking reaction. For the ageing resistance of the polyester/nano-TiO2 composites, gloss and colour aberration measurements were done during the exposure in the UV accelerated ageing chamber for 1500 h. In particular, the gloss changes and aberration are strongly correlated with the degradation level of the polymer composites. Figure 6a illustrates the gloss retention of the samples with different concentrations of modified nano-TiO2, as a function of exposure times. Compared with the sample without nano-TiO2, the gloss retention of the samples with nano-TiO2 improves significantly. In particular, the sample without nano-TiO2 exhibits gloss retention of 43.3%. By contrast, the gloss retention of the sample modified with 2.0 wt.% nano-TiO2 is 61.7%. So a 42.5% improvement was deduced. Furthermore, we noticed that the gloss retention of sample improves with the concentration of nano-TiO2 in the range 0.5 to 2.0 wt.%. Figure 6 Gloss retention (a) and colour aberration of the composites with different concentration of modified nano-TiO 2 (b). As a function of exposure times.

Given the

interdependence of STAT1 and STAT3 activation following IL-27 stimulation, STAT3 inhibition was evaluated by adding Stattic, a nonpeptidic small molecule that inhibits the function of the SH2 https://www.selleckchem.com/products/jph203.html domain required for tyrosine phosphorylation, dimerization and subsequent nuclear translocation of STAT3 [33]. The STAT3 inhibitor was added to A549 cells for 1 hour prior to IL-27 exposure for 15 or 30 minutes and the expression of activated and total amounts of STAT1 and STAT3 proteins were analyzed by Western blot. As expected, the expression of P-STAT3 was markedly reduced by pretreatment of STAT3 inhibitor at both time points of IL-27 treatment without affecting T-STAT3 (Figure 3B). However, activated or total amount of STAT1 protein MK5108 concentration was not significantly changed in the pre-treated cells with Stattic when compared with untreated cells, indicating that inhibition of STAT3 alone does not have a considerable impact on STAT1 activation. These results suggest that although IL-27 activates both STAT1 and STAT3, the regulation and prevention of over-expressing phosphorylated STAT3 requires the presence of

activated STAT1 in NSCLC cells. IL-27 see more induces an epithelial phenotype in lung cancer cells through STAT1 activation A fundamental event during EMT is the loss of cell polarity, resulting in transition of polarized epithelial cells into mobile mesenchymal cells [34]. To evaluate the phenotypic changes of NSCLC cells in response to differential STAT1 and STAT3 activation following IL-27 treatment, changes in morphologic features of lung cancer cells were assessed. In comparison to untreated cells (upper left, Figure 3C), IL-27-treated cells exhibited a more epithelial phenotype characterized by a markedly more cohesive and organized appearance of the cells in a cobblestone monolayer formation (lower left, Figure 3C). Suppression of STAT1 expression by siRNA prior to IL-27 treatment resulted in a phenotype characterized

by elongated spindle-shaped, 17-DMAG (Alvespimycin) HCl fibroblast-like cells that were morphologically similar to untreated cells (lower middle, Figure 3C), while STAT1 siRNA single treatment did not significantly affect the phenotype of untreated cells (upper middle, Figure 3C). The addition of the STAT3 inhibitor (Stattic) did not demonstrate marked morphologic changes in A549 cells when compared to IL-27- treated or -untreated cells (lower right and upper right, Figure 3C). These findings suggest that STAT1 activation is the dominant pathway by which IL-27 mediates polarization of NSCLC cells towards an epithelial phenotype. IL-27 promotes expression of epithelial markers through a STAT1 dominant pathway EMT results in cellular changes associated with alterations in expression of EMT markers [35].

Pneumonia, of which the pneumococcus is the leading cause, still accounts worldwide for over 150 million clinical episodes yearly, which contribute to approximately 1.9 million deaths [1]. Even more frequent are non-invasive pneumococcal acute conjunctivitis and otitis media. Pneumococci are also part of the normal flora of humans, as they colonise the nasopharynx soon after birth and carriage Sapanisertib ic50 is reported

to be self limited to periods from few days to few months [2, 3]. Successive carriage episodes are generally due to strains of different capsular types. Progression to invasive disease occurs within the first weeks of carriage [2]. Recently, interest has been raised on physiology of bacteria in different niches of their natural environment: the human host. Direct microscopy analysis, carried out on human biopsy specimens of the sinus and the middle ear mucosa and the adenoids showed the presence of pneumococcal cells embedded in extracellular matrix indicative of microbial biofilms [4–6]. Recently, the presence of biofilm-like structures in the lungs of animals infected with S. pneumoniae was also documented [7]. These studies provided important evidence that pneumococci in different diseases are not behaving as planktonic cells, but predominantly show characteristics of a biofilm like state. Pneumococcal

animal models of disease as well as models of carriage have been associated to biofilm-like infections PD173074 clinical trial [8–13]. It has been shown that gene expression of pneumococci during infection of lungs and meninges in mice was comparable to that of pneumococcal biofilms [8]. In this model the development of biofilm depended on the competence system, and the addition of the competence stimulating peptide Branched chain aminotransferase (CSP) to the medium was necessary for biofilm formation. The direct association of the competence system to pneumococcal disease was demonstrated by the fact that virulence in sepsis and pneumonia could be modulated by CSP and by showing increase of disease severity in mice directly challenged with biofilm

cells [8, 14]. The correlation of biofilm to carriage was confirmed by mutants that produced less biofilm in an in vitro model and also showed reduction in their colonisation capacity [9]. Recent data from our group showed that free sialic acid in culture medium represents the signal necessary for biofilm formation. Furthermore, this signal increases pneumococcal colonisation and translocation to the lung in mouse models of carriage [10]. It is of interest to underline that despite existence of pneumococcal biofilms in humans and correlation between virulence in experimental infection models and aspects of biofilm, so far no important correlation of pneumococcal clinical isolates, RG7112 order clones, serotypes, or MLST types to their capacity to form in vitro a biofilm was shown [15, 16]. Biofilm models are less standardised than the classical mid log growth phase, in which most microbiological research has been done.

To determine more precisely the ranges of immunity in the vaccinated mice, the titer of anti-exotoxin A was measured by enzyme-linked immunosorbent assay (ELISA) as previously described [14]. Rabbits hyperimmunization with toxoid A group of 4 rabbits were immunized with the toxoid. Each rabbit received weekly subcutaneous injections for 6 weeks. Each injection contained 200 μg of semi-purified toxoid in 4 mL of PBS. 1 week after the last injection, the animals were bled from the ear. Sera were pooled and the presence of antitoxin againstP.

aeruginosa confirmed by CIEP. The sera were used as an antitoxin when necessary, to evaluate the presence of the toxin in the sera of the experimental and control mice. Counterimmunoelectrophoresis KU55933 clinical trial CIEP was carried out for qualitative detection of toxin and antitoxin in the sera of the immunized mice [12]. This technique was applied on 13 × 18 cm glass slides which were covered by 1% melted agarose selleck kinase inhibitor in acetate buffer (pH 7.6). 2 rows of wells with a diameter of 6 × 6 mm were punched in each glass slide and 0.4 mL of semi-purified exotoxin A or serum containing the exotoxin A (antigen) and 0.4 mL of immunized mice or rabbit serum (antibody) were placed in

the anodal and cathodal wells, respectively. The slide was subjected to electrophoresis using an acetate buffer (pH 7.6 at 40 mA for 30 min). Production of a precipitation line between the two wells indicated the presence of antitoxin or toxin A in the sera. The Amidoblack staining method was used to reveal the precipitation lines more clearly. Determining the efficacy Prostatic acid phosphatase of the candidate vaccine 73 mice (48 immunized = experimental group, 25 non-immunized = control group) were anesthetized and burns (grade 3) were C646 cost induced on the thigh using a 1 × 2 cm piece of hot metal, producing

a burn of up to 10% of the total body surface and extending to all layers of skin but not involving the muscular tissue. After 24 h, 108 colony forming units (CFU) of toxigenic strains ofP. aeruginosa (PA 103) were inoculated subcutaneously into the burned area. Both groups were supervised in their cages for 70 days. Samples were obtained from the infected areas using sterile swabs and saline and checked for the presence ofP. aeruginosa at different time intervals. Blood samples and the tissue samples of spleens and livers of dead mice were also examined for presence ofP. aeruginosa. The presence ofP. aeruginosa was determined as CFU/mL of the blood samples. The quantity ofP. aeruginosa in the spleens and livers was measured as the number of CFU per 1 g of homogenized tissue. The survival rate in both groups was compared. The efficacy of vaccine was calculated as the percentage survival during the 70-day observation period following inoculation with toxogenicP. aeruginosa (PA 103).

There were no significant differences (ANOVA, p > 0.05). C) pH of bile measured at 37°C as a function of state. Values represent means ± SE from T (n = 4), IBA (n =

4), SA (n = 10), and AB squirrels (n = 4). All values are significantly different except between T and IBA (ANOVA, p > 0.05). D) Total protein concentration in bile as a function of state. Values represent means ± SE from T (n = 3), IBA (n = 3), SA (n = 5), and AB squirrels (n = 4). There were no significant differences between T and Panobinostat molecular weight IBA or between SA and AB. All other values are significantly different (ANOVA, p < 0.05). Discussion The winter season for a hibernator is marked by extended anorexia [2]. Given the liver's role in fueling metabolism, we hypothesized that there might be changes in liver function as a function of hibernation and associated anorexia.

We present here the first data on the effects of hibernation on gallbladder bile constituents. Although there were no significant differences in bile constituents between torpid and aroused winter squirrels, a few differences were found between the winter squirrels and summer squirrels. Except for [GW4869 in vitro bilirubin], these differences did not involve critical indicators of metabolic function. Finally, we examined bile in winter animals that failed to enter torpor and found that they had significantly lower [bile acids] and [lecithin] as compared to all other groups. We discuss below the implications of these findings. To satisfy its energetic demands during Angiogenesis inhibitor winter, a hibernator relies on stored lipids. Changes in lipid pools have dramatic effects on the ability of a hibernator to successfully employ torpor; increased dietary poly-unsaturated fatty acids increase torpor bout usage, length, and depth [15]. A major function of the liver, and more specifically Glycogen branching enzyme bile, is to facilitate digestion and absorption of lipids from the intestine. However, what happens to hepatobiliary function when there are no foodstuffs in the gut? The anorexia of hibernation allows for an examination of an extended (months long) anorexia not available

with almost any other mammalian system except denning bears. In our study, we were surprised by the few changes in the bile constituents between summer and normal winter squirrels (both IBA and T); important indicators of metabolic function such as biliary [bile acids], [cholesterol], [free fatty acids], and [lecithin] were unchanged despite the months long anorexia experienced by winter squirrels (Figs. 2, 3). Although biliary changes as a function of season were found for [bilirubin], spectral characteristics, pH, and [total protein], the roles that most of these other factors have as indicators of hepatobiliary function seems less robust (Figs. 1, 2, 3). For instance, biliary pH is known to be quite variable [e.g., [16]].

Main axes broad, forming conidiophores to ca 0.6 mm long or bearing shorter lateral trees. Trees mostly wider downwards; branches right-angled or slightly inclined upwards, usually paired, unpaired in lower regions, 1-celled at the top, 2- to several-celled downwards, with 1–2 further 1-celled branches bearing terminal whorls of phialides. Phialides mostly in whorls of 3–4(–5), divergent, but often strongly curved upward and nearly Milciclib parallel, gliocladium-like. Conidia formed in small numbers. Stipe and primary branches thick-walled and to 8–9 μm wide, conidiophores 3–5 μm wide for the most part; phialide Pifithrin-�� ic50 origins 3–4 μm wide. Phialides

6–10(–13) × (2.5–)2.8–3.5(–4.0) μm, l/w (1.7–)2.0–3.1(–4), (1.5–)1.9–2.6(–3) μm (n = 40) wide at the base, lageniform, or beak-like with a pointed apex, widest in or below the middle, sometimes strongly curved to sinuous. Conidia (2.8–)3.5–4.5(–5.7) × (2.0–)2.2–2.6(–3.0) μm, l/w (1.3–)1.5–1.8(–2.1) (n = 46), hyaline, smooth, narrowly ellipsoidal or oblong, with numerous minute guttules or 1 to few larger guttules, scar indistinct

or narrowly truncate. Habitat: on stalks of Calamagrostis epigejos. Distribution: Denmark, known only from the type location. Holotype and only known specimen: Denmark, Nordjylland, Tranum, meadow at Vestkystvejen, close to crossing with Strandvejen, 57°08′32″ N, 09°26′28″ E, elev. 10 m, on stalks of Calamagrostis epigejos, 25 Aug. 2006, W. Jaklitsch & H. Oligomycin A mouse Voglmayr, W.J. 2944 (WU 29198, culture CBS 121133 = C.P.K. 2447). Holotype of Trichoderma calamagrostidis isolated from WU 29198 and deposited as a dry culture with the holotype of H. calamagrostidis as WU 29198a. Notes: Hypocrea calamagrostidis differs from H. junci, found on for Juncus in a comparable habitat, in distinct ostiolar dots, lighter and more rosy stroma colour, and a white-conidial anamorph. The pachybasium- to gliocladium-like conidiation on stout conidiophores in white pustules is in good agreement with other species of the Psychrophila clade like H. crystalligena and H. psychrophila. Hypocrea crystalligena

Jaklitsch, Mycologia 98: 502 (2006a). Fig. 83 Fig. 83 Teleomorph of Hypocrea crystalligena. a, b, d, f. Fresh stromata (a. young, velutinous, b. with visible ostioles, f. (over-)mature). e, h, i. Dry stromata (e. fraction of d; i. showing white powder on surface). c. Surface of rehydrated wet stroma showing hyaline ostioles. g. Ostiole in section showing periphyses and apical cells. j. Perithecium in section. k. Ostiole in face view. l. Stroma surface in face view. m. Subperithecial tissue in section. n, o, p. Asci with ascospores (n, o. in cotton blue/lactic acid). a, c, d, e. WU 24050. b. WU 24059. f. WU 24060. g, h, j–o. holotype WU 24041. i: WU 24053. p: WU 24052. Scale bars: a, e, f, h, i = 1.5 mm. b = 0.3 mm. c = 0.2 mm. d = 2 mm. g, l, p = 10 μm. j, m = 25 μm. k, n, o = 5 μm Anamorph: Trichoderma crystalligenum Jaklitsch, Mycologia 98: 502 (2006a). Fig. 84 Fig.