[15] Turkey, Ankara (40° N), at the end of summer Turkish M, mean 73 years, own home (n = 24) 158 ± 108 Female gender, living in old age home,

older age, lower benefit from ultraviolet index (ratio VX-689 in vitro of points for sunlight exposure and covering clothes) Turkish F, mean 72 years, own home (n = 171) 103 ± 98 Turkish M, mean 76 years, old age home (n = 87) 94 ± 72 Turkish F, mean 75 years, old age home (n = 138) 62 ± 74 Pregnant women Pehlivan et al. [14] Turkey, Last trimester Turkish, total group (n = 78) 18 ± 10, 80% < 25 Low educational level, insufficient intake of vitamin D within diet, “covered” dressing habits Turkish, with covered head and hands, not the face (n = 4) 10 ± 05 Turkish, with covered head, not the hands or face (n = 49) 17 ± 10 Turkish, with no cover on head, hands or face (n = 25) 20 ± 10 Children Olmez et al. [34] Turkey, Izmir, end of summer or end of winter Turkish

F, 14–18 years, low socioeconomic status, end of summer (n = 32) 52 ± 23 End of winter measurement, low socioeconomic status Turkish F, 14–18 years, high socioeconomic status, end of summer (n = 32) 65 ± 29   Turkish F, 14–18 years, low socioeconomic status, end of winter (n = 30) 34 ± 16   Turkish F, 14–18 years, high socioeconomic status, end of winter (n = 30) 59 ± 24   SD standard deviation a Unless mentioned otherwise Studies on Moroccan populations in Europe are presented in Table 3. Table 4 presents the only study found on the vitamin D status of a Moroccan population in Morocco. As was Selleck C59 wnt the result among Turkish Casein kinase 1 populations, the Moroccan populations in Europe had lower serum 25(OH)D concentrations than the indigenous European populations. The Moroccan adult women in Morocco, who were measured at the end of winter, had a mean serum 25(OH)D concentration of 45 nmol/l [17]. This was lower than the indigenous population in the Netherlands (selleckchem median 67 nmol/l) and in Belgium (mean 49 nmol/l) [1,

3]. The Dutch and Belgian populations consisted of both men and women, and these were measured year-round, which might explain the difference. Table 3 Studies among Moroccan populations in Europe Study Study characteristics Study population Serum 25(OH)D (nmol/l) Mean±SDa Determinants for lower serum 25(OH)D Adults Van der Meer et al. [1] The Netherlands, Amsterdam, The Hague, Amersfoort, and Haarlem (52° N) Dutch M (40%)+F, median 45 years (n = 102) Median 67, 06% < 25 Autumn or winter season, pregnant or breastfeeding, lower consumption of fatty fish, no use of vitamin D supplements, smaller area of uncovered skin, no use of tanning bed, lower consumption of margarine, no preference for sun Moroccan M (41%)+F, median 38 years (n = 96) Median 30, 37% < 25 Moreno-Reyes et al.

The data were expressed as mean ± SE from three independent experiments and analyzed by one-way ANOVA (*p < 0.05, **P < 0.01 and ***P < 0.001). EV71 infection activates and phosphorylates c-Fos and c-Jun The activator protein 1 (AP-1) is a heterodimeric transcription factor composed of proteins in the subfamilies of c-Jun, c-Fos, Maf, and activating transcription factor (ATF). It regulates gene CUDC-907 ic50 expression in response to a variety of stimuli, including cytokines, growth factors, stress, and bacterial and viral infections [28, 29]. The results of

RT-PCR showed that EV71 infection (MOI = 5) upregulated the expressions of c-Fos and c-Jun at mRNA level. To further investigate whether EV71 infection could activate and phosphorylate c-Fos and c-Jun, total and SGC-CBP30 research buy phosphorylated c-Fos

and c-Jun were detected by Western blot. The results showed that c-Fos was rapidly phosphorylated by EV71 infection, reaching its peak at 24 h p.i. (Figure  3A) and this effect was inhibited by pretreatment with SP600125 for 1 h (Figure  3B), but delayed by pretreatment with SB203580 (Figure  3C). Similarly, c-Jun was also rapidly phosphorylated by EV71 infection, reaching its peak within 2 h p.i. (Figure  3D). And this effect was significantly attenuated by pretreatment with SP600125 and SB203580 (Figure  3E and F). The data demonstrate that EV71 infection triggers JNK1/2 or p38 MAPK-mediated activation of c-Fos and c-Jun. Figure 3 Phosphorylation of c-Fos and c-Jun in EV71-infected iDCs. (A and D) Cilengitide supplier The western blot results of cell lysates collected at indicated times of iDCs infected with EV71 (MOI = 5) for 24 h using antibodies against total and phosphorylated c-Fos and c-Jun. (B and E) The western blot results of cell lysates collected at indicated times

of iDCs pretreated with SP600125 (20 μM) for 1 h and infected with EV71 (MOI = 5) for 24 h using antibodies against total and phosphorylated c-Fos and c-Jun. (C and F) The western blot results of cell lysates collected at indicated times of iDCs pretreated with SB203580 (20 μM) for 1 h and infected with EV71 (MOI = 5) for 24 h using antibodies against total and phosphorylated c-Fos and c-Jun. The ROCK inhibitor intensities of phosphorylated c-Fos and c-Jun were quantitated and normalized as described. The data were expressed as mean ± SE from three independent experiments and analyzed by one-way ANOVA (*p < 0.05, **p < 0.01, ***p < 0.001). Secretions of IL-2, IL-6, IL-10, IL-12, TNF-α,IFN-α and IFN-β iDCs can secrete several cytokines once they are activated by viral infection. To examine the role of JNK1/2 or p38 MAPK pathways in cytokine secretion in iDC, the culture supernatants of control iDCs, EV71-infected iDCs and iDCs pretreated with inhibitor SP600125 or SB203580 (20 μM) prior to EV71 infection were collected at 24 h p.i. and used to detect the levels of IL-2, IL-6, IL-10, IL-12 p40, IL-12 p70, TNF-α, IFN-α and IFN-β using luminex fluorescent technique.

Nies further subdivided the HME-RND proteins into sub-groups, according to the substrate they transport: HME1 (Zn2+, Co2+, Cd2+), HME2 (Co2+, Ni2+), HME3a NVP-BSK805 mw (divalent cations), HME3b (monovalent cations), HME4 (Cu+ ou Ag+) and HME5 (Ni2+) [14]. The cytoplasmic membrane RND proteins have 12 transmembrane alpha helices (TMH), among which TMH IV contains amino acid residues that are conserved in most RND proteins [17]. The HME1-RND and HME2-RND have the same motifs, DFG-DGA-VEN, present in proteins CzcA (HME1) or CnrA

and NccA (HME2) [14, 23]. Both aspartate residues and the glutamate residue in TMH IV of CzcA are required for proton/substrate-antiport, suggesting that they are probably involved in proton translocation [14, 23, 24]. A model for cation transport by an HME-RND was recently proposed for the copper transporter CusA, in which the metal ion moves along a pathway of methionine find more residues, causing significant conformational changes

in both the periplasmic and transmembrane domains [25]. These systems are proposed to promote the efflux of both cytoplasmic and periplasmic substrates, CP-690550 chemical structure transporting of the substrate either via the RND protein or in some cases via the membrane fusion protein with the aid of periplasmic metal chaperones [14, 24]. The best characterized RND heavy metal efflux systems are mainly those from Cupriavidus (previously called Ralstonia and Alcaligenes): CzcCBA (Cd2+, Zn2+, and Co2+ resistance) from Ralstonia metallidurans CH34 [26–28]; CnrCBA (Ni2+ and Co2+) from Ralstonia eutropha[29, 30];

NccCBA (Ni2+, Co2+ and Cd2+) from Alcaligenes xylosoxidans 31A Reverse transcriptase [31]. However, other systems such as Pseudomonas aeruginosa Czr (Cd2+ and Zn2+ resistance) [32]; and Helicobacter pylori Czn (Cd2+, Zn2+ and Ni2+ resistance) were also studied [33]. In order to better understand the role of the RND efflux systems in the export of divalent cations in other Proteobacteria, we investigated the role of two HME-RND systems present in the Alphaproteobacterium Caulobacter crescentus. A previous bioinformatics analysis made by Nies (2003) through comparison of the genomes of 63 prokaryotes (Archaea and Bacteria) with the genome of C. metallidurans, identified seven ORFs encoding putative RND proteins in C. crescentus CB15 of which two, CC2724 (corresponding to CCNA_02809 in the derivative strain NA1000; here called CzrA) and CC2390 (CCNA_02473; here called NczA), belong to the HME subgroup. Previous works from our group [34] identified that the czrCBA locus is involved in resistance to cadmium and zinc and is induced by these cations, and other reports [35] confirmed that this operon is induced by cadmium.

g. Phaeomoniella chlamydospora, Aureobasidium pullulans, Truncatella angustata, Botrytis cinerea or Phaeoacremonium viticola). Other species, especially closely related species within a single genus (e.g. Cladosporium, Phoma, Alternaria or the anamorphs

of Botryosphaeriaceae and Nectriaceae), JPH203 as well as some species exhibiting a variable morphology on Petri dishes (e.g. Epicoccum nigrum), could not be delimitated based on their vegetative morphology. We first amplified and sequenced the ITS region of a few fungal isolates for all morphotypes. For more plastic morphotypes, we sequenced more isolates. When the sequences obtained for the different isolates of plastic morphotypes were identical, we did not sequence the rest of the isolates grouped in this morphotype. When the sequences of the different isolates of a given morphotype were different we adopted two strategies depending on their similarity BLAST top score in GenBank: either the top score indicated that the isolates belong to the same species and we did not sequence the other isolates, or the BLAST top score indicated that they belonged to different species and we sequenced the ITS region for all isolates, except in the case of Alternaria for which we recovered ITS rDNA genotypes for 216 out of the 523 strains isolated (Online Resource 2) that differed only in the length of a T-repeat at the

end of the ITS2 (see the Discussion section). Having sequenced 907 out of a total of 2595 fungal isolates, we obtained 197 ITS genotypes. The GenBank VRT752271 cost accession numbers and the GenBank BLAST top score similarity of these YH25448 price ITS genotypes, excluding uncultured and environmental sequences, are listed in Online Ressource 2. We used a 99 % sequence BLAST similarity

threshold Tyrosine-protein kinase BLK for species delimitation (Gazis et al. 2011) even though previous fungal endophyte-related studies have used a lower threshold (≤98 %; Higgins et al. 2011; Neubert et al. 2006; O’Brien et al. 2005; Sánchez et al. 2007; Sánchez et al. 2008; U’Ren et al. 2010). The ITS sequence of the fungal isolate acwVHB69/4 (Online Resource 2) was 100 % similar with the ITS GenBank sequences of six different species of Cladosporium, including C. subtilissimum. In those cases where ITS rDNA sequences data discriminated more than one taxa, we used the prefix ‘cf’ in the fungal name (e.g. Cladosporium cf subtilissimum, Online Resource 2, Table 1). On the other hand, we also recovered variable ITS genotypes that corresponded to the same species under the blast results. In these cases we used the name derived from GenBank, accepting that this was not aligned with extype. For Alternaria, we recovered ITS rDNA genotypes for 216 isolates that differed only in the length of a T-repeat at the end of the ITS2. Sequences with 6, 7 or 8 T-repeats were respectively 100 % similar with GenBank sequences of Alternaria alternata, A. arborescens, and A. mali (Online resource 2).

Antagonism of TGF-β can lead to two opposite effects depending on the time. Early TGF-β inhibition, MAPK inhibitor within the first 24 h

after AMI, can increase levels of pro-inflammatory cytokines and infiltration of neutrophils, and consequently intensify the expression of MMPs which may result in aggravation of LV dysfunction and increase the rate of mortality [8]. Conversely, TGF-β antagonism after this time can have beneficial effects by reducing the extent of fibrotic and hypertrophic changes in the myocardium [9, 29, 30]. In the present study, we found that NAC did not have any significant effect on the level of TGF-β at 24 h, the time at which its inhibition can have a detrimental outcome. However, NAC administration could prevent TGF-β from increasing at 72 h as compared with patients receiving placebo, the time at which the proliferative

phase of remodeling will start, and therefore its suppression could have favorable therapeutic effects. Higher serum concentrations of TGF-β had strong positive correlations with LV systolic function and patients’ ejection fraction in the present study, which showed that a relationship existed between TGF-β and cardiac check details remodeling. This finding puts more emphasis on the necessity of TGF-β inhibition to prevent cardiac remodeling and its untoward consequences. As TGF-β was shown to promote extracellular matrix synthesis and collagen crosslink took place after MI, it could have an important role in the signaling AP26113 order pathway of LV remodeling [31]. An increased TGF-β level after MI was associated

with the development of heart failure secondary to cardiac remodeling [31]. In the present study, a significant association was found between serum concentrations of TGF-β and the presence of diabetes. This finding is in line with a previous study, which showed a relationship between elevated serum concentrations of TGF-β and diabetes after considering demographic, Gefitinib mw anthropometric, metabolic, and lifestyle factors [32]. This could be explained by the mechanism of insulin resistance as inflammation can be an important factor in its development and thus the incidence of diabetes [33]. Another association was between a history of statin use and the level of TGF-β. TGF-β is one of the most important mediators of cardiomyocyte fibrosis and hypertrophic growth through the action of Smad proteins as an essential component of the intracellular signaling pathway [34]. Statins can suppress the up-regulation of TGF-β induced by angiotensin and the resultant cardiac remodeling and systolic dysfunction [35, 36]. This suppression can be attributed to the inhibition of superoxide production favored by angiotensin [36]. Thus, the low level of TGF-β in patients receiving statins as observed in the present study is a reasonable finding. The other finding of this study was the relationship between the coronary angiography finding, in particular stenosis of the LMCA, and TGF-β levels.

It is possible that senescence-associated modifications of the leaf tissue enabled the penetration of the mycelium inside the host cells and the saprotrophic development of these strains. It should be noted that some mycelium development could be detected by real-time RT-PCR prior to any visible necrotic

symptom, as early as 1 dpi in case of E139, E70 and CCP. We suspect that these isolates may have a phase of epiphytic development before the mycelium penetrates through the cells upon toxin action (necrotrophy) or senescence-induced alteration of the tissues (saprotrophy). In the case of the isolate E78, which remained avirulent even at 9 dpi, check details we cannot rule out all saprobic activity but the very low amount of mycelium detected at 5 and 9 dpi demonstrated that it is clearly less competitive than the other isolates in senescing tissue. Discovery of new cassiicolin gene homologues New cassiicolin gene homologues potentially encoding two new cassiicolin precursor protein isoforms (Cas3 and Cas4) were found in the endophytic C. cassiicola isolates. Their predicted amino acid sequence is similar to that of the Cas1 reference isoform. In particular, the

Copanlisib supplier mature cassiicolin domain is highly conserved, with only one amino acid substitution (S instead of T) at position 2. This amino acid is especially important because it carries the sugar moiety (0-methyl-mannose) of the active cassiicolin (Barthe et al. 2007; de Lamotte et al. 2007). Thiamine-diphosphate kinase Although the role played by this sugar in toxicity is still unknown, it should be noted that Serine (S), like Threonine (T), can be 0-glycosylated. Therefore, the glycosylation of the toxin is not jeopardized by the T to S substitution. The cassiicolin gene may be under BIBW2992 purifying selection pressure, as indicated by the low (<1) d N /d S ratios. This suggests that this gene is playing and important functional role in C. cassiicola. However, this will have to be confirmed when a higher number of Cas gene sequences reflecting C. cassiicola

evolution history will be available. Although the genes encoding Cas3 and Cas4 appear structurally functional, no Cas3 and Cas4 transcripts could be detected post-inoculation. Therefore, if Cas3 and Cas4 genes are functional, it seems that their transcription is negatively controlled under the conditions used in this experiment. We have previously shown (Déon et al. 2012) that Cas1 is transiently expressed, with a sharp peak of expression at 1 or 2 dpi depending on the cultivar. This was confirmed in this work for RRIM 600 inoculated with CCP. In the cultivar FDR 5788 inoculated with CCP, Cas1 was expressed, but no peak of expression was observed. We suggest that the peak may have occurred at a different time-point not tested in this experiment. Whether Cas3 and 4 can be switched on and under which conditions is unknown.

The solution was composed of 5 ml H2O and 0.1 mM NaOH. The films both had an area of 1 cm2. Figure 4 enables DAPT chemical structure the calculation of the dye loadings and the light absorptions at 370 and 530 nm (the dye’s absorption maximum) for both NRs and tree-like films. Compared

to the upstanding ZnO NRs film, the tree-like film shows an improvement in both light harvesting and dye loading. The Nyquist plots of the impedance spectra are shown in Figure 5. To characterize the ZnO/dye/electrolyte interface characteristics, the DSSCs were at V oc under AM 1.5 illumination by EIS measurement. The Nyquist plots (Figure 5) show a large semicircle at low frequencies and a small semicircle at high frequencies. As shown in Figure 5, they were fitted with an equivalent circuit alike to those reported in the literature. The equivalent circuit comprises R s (ohmic resistance), R ct1 (the Pt counter electrode), PRIMA-1MET manufacturer and R ct2 (ZnO/dye/electrolyte interfaces): (1) where τeff is the electron efficacious lifetime and f min is the frequency corresponding to the imaginary part minimum. R ct and τ eff are reported in Table 1. Here, it is shown that the interface area increases and R ct2 decreases for tree-like nanostructures. The electrochemical parameters were evaluated by fitting the EX 527 manufacturer experimental data with the equivalent circuit, as summarized in Table 1. The R CT2 value

for the photoelectrode containing a tree-like structure (95.8 Ω) is lower than that of the photoelectrode containing a nanorod structure (109.2 Ω), whereas the R CT1 value is almost the same. One possible cause for low-load transport resistance might be that axial charge transport in tree-like ZnO structures effectively obstructs the recombination progress with iodine

redox carriers [8]. Figure 3 Scanning electron microscopy images. SEM images of different ZnO nanostructures on FTO substrates. Side-view (a,c) and top-view (b,d) of vertically grown tree-like structures. Figure 4 Absorption spectra of DSSCs with ZnO nanostructures. Optical absorption spectra of D-719 dye-sensitized ZnO nanostructured electrodes. Figure 5 Analysis of electrochemical impedance spectroscopy. EIS of different ZnO nanostructure electrodes. Nyquist plots are used to measure under illumination (100 mA cm−2). Table 1 Electrochemical out and photovoltaic parameters of DSSCs Sample V oc (V) J sc (mA/cm2) FF R ct2 (Ω) τ eff (ms) Eff (%) NRs 0.661 0.699 0.397 109.2 3.23 0.203 Tree-like 0.680 0.784 0.413 95.8 3.91 0.231 Regarding branch-free rods, less accumulation on the electrode layer leads to poor electrolyte filling, improving the recombination pathway and raising the charge transport resistance. The surface charge density and trap level of the ZnO layer also play an important role in deciding the charge transport resistance by depleting the space charge layer.

One hundred parameter initiation values ranging from 5 to 105 were tested and the best converging model with the smallest Sum Square of Error (SSE) was chosen for estimation of doubling time. Acknowledgements We thank Dr. C. Szekeres and Dr. R. Chen at USF Health core facilities for help with flow cytometry and statistical analyses, respectively. We thank B. White, B. Wisler and Y. Xi at the University of Notre Dame for their technical

assistance. This work was supported by grants from the National Institute of Allergy and Infectious Diseases to J.H.A. Electronic supplementary material Additional file 1:List of piggyBac insertion loci in the P. falciparum genome. Complete 17DMAG list ofpiggyBacinsertion loci identified thus far is provided along with the mutant name and insertion position relative to the coding sequences of the genome. (XLS 33 KB) Additional file 2:Best-fit growth curve models for doubling time estimation of mutant clones. The predicted best-fit and observed growth curves for each parasite clone is shown. (PDF 201 KB) Additional file 3:Lack of gene expression in mutant P. falciparum clones with insertions in the coding sequences. RT-PCR analysis confirms the knockout of gene

expression in mutant clones, selected for growth assays, with insertions in coding sequences. (PDF 157 KB) Selleckchem C188-9 References 1. Snow RW, Guerra CA, Noor AM, Myint HY, Hay SI:The global distribution of clinical episodes of Plasmodium falciparum malaria. Nature2005,434(7030):214–217.CrossRefPubMed 2. Yamey G:Roll Back Malaria: www.selleckchem.com/products/sch772984.html a failing global health campaign. Bmj2004,328(7448):1086–1087.CrossRefPubMed 3. Le Roch KG, Zhou Y, Blair PL, Grainger M, Moch JK, Haynes JD, De La Vega P, Holder Enzalutamide order AA, Batalov S, Carucci DJ,et al.:Discovery of gene function by expression profiling of the malaria parasite life cycle. Science2003,301(5639):1503–1508.CrossRefPubMed 4. Bozdech

Z, Llinas M, Pulliam BL, Wong ED, Zhu J, DeRisi JL:The Transcriptome of the Intraerythrocytic Developmental Cycle of Plasmodium falciparum.PLoS Biol2003,1(1):5.CrossRef 5. Florens L, Washburn MP, Raine JD, Anthony RM, Grainger M, Haynes JD, Moch JK, Muster N, Sacci JB, Tabb DL,et al.:A proteomic view of the Plasmodium falciparum life cycle. Nature2002,419(6906):520–526.CrossRefPubMed 6. Lasonder E, Ishihama Y, Andersen JS, Vermunt AM, Pain A, Sauerwein RW, Eling WM, Hall N, Waters AP, Stunnenberg HG,et al.:Analysis of the Plasmodium falciparum proteome by high-accuracy mass spectrometry. Nature2002,419(6906):537–542.CrossRefPubMed 7. LaCount DJ, Vignali M, Chettier R, Phansalkar A, Bell R, Hesselberth JR, Schoenfeld LW, Ota I, Sahasrabudhe S, Kurschner C,et al.:A protein interaction network of the malaria parasite Plasmodium falciparum.Nature2005,438(7064):103–107.CrossRefPubMed 8. Date SV, Stoeckert CJ Jr:Computational modeling of the Plasmodium falciparum interactome reveals protein function on a genome-wide scale. Genome Res2006,16(4):542–549.CrossRefPubMed 9.

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0–)3.3–4.0(–4.8) × (2.8–)3.0–3.6(–4.0) μm, l/w (0.9–)1–1.2(–1.3); proximal cell oblong or wedge-shaped, (3.2–)4.0–5.0(–6.0) × (2.3–)2.7–3.1(–3.5) μm, l/w (1.1–)1.3–1.8(–2.2) (n = 120). Cultures and anamorph: ascospore germination and growth slow, optimal growth at 25°C on all media; no growth at 30 and 35°C. On CMD after 72 h 1–2 mm at 15°C and 5–7 mm at 25°C; mycelium covering the plate after 3–4 weeks at 25°C. Colony hyaline, thin, radial, shiny, indistinctly zonate; little mycelium on the agar surface, dense mycelium within the agar. Aerial hyphae inconspicuous, Ilomastat price becoming fertile. No autolytic excretions nor coilings seen. Colour none to pale Talazoparib solubility dmso yellowish in aged cultures; odour indistinct

or mushroomy, aromatic, reminiscent of Sarcodon imbricatus, vanishing with age. Chlamydospores (examined after 46 days) noted after 3–7 weeks in surface

and aerial hyphae, (10–)11–18(–22) × (9–)10–16(–19) μm, l/w (0.9–)1.0–1.3(–1.6) (n = 21), globose or oblong, smooth, intercalary, less commonly terminal. Conidiation noted after 4–5 days, green after (7–)14–25 days, effuse, on simple, erect conidiophores around the plug and on aerial hyphae (0.1–1 mm long), and in loosely disposed loose shrubs and denser granules to 0.5 mm diam, aggregations to 2 mm, mainly concentrated along the colony margin; white, turning green, 28D5–6 to 27E4–6, finally degenerating and conidia Selleck VS-4718 often adhering in chains. Conidiophores (CBS 332.69, CBS 120535) short, simple, of a stipe with thick wavy (verrucose when old) outer wall to 6–11 Chlormezanone μm wide, with asymmetric branches, or broad shrubs or small pustules with sparse asymmetric branches, without clearly discernable main axes. Branches mostly 4–6 μm wide,

attenuated terminally to 2.5–3.5 μm. Branches and phialides typically divergent but steeply inclined upward. Phialides and conidial heads concentrated in the upper, terminal levels of the conidiophores, in verticillium-like or irregular arrangements on short, 1–3 celled, broad (e.g. fan-shaped, 200 μm diam, 80–100 μm long) terminal branches. Terminal branches and phialides often paired, straight, sometimes sinuous. Phialides arising solitarily or in whorls of 2–4(–5) on cells 2.5–4.5 μm wide. Conidia formed in mostly dry minute heads <30 μm diam. Phialides (5–)8–13(–19) × (2.5–)3.0–3.8(–4.8) μm, l/w (1.7–)2.3–3.8(–5.4), (1.5–)2.0–2.8(–4.0) μm wide at the base (n = 91), lageniform or subulate, straight, curved or sinuous, mostly inaequilateral, not or slightly widened in or above the middle. Conidia (3.0–)3.5–5.5(–8.5) × (2.0–)2.5–3.0(–3.8) μm, l/w (1.1–)1.3–1.9(–3.0) (n = 97), light (yellowish) green, oblong or cylindrical, more ellipsoidal in lower size range, smooth, finely multiguttulate or with 1–2 larger guttules, scar indistinct. On MEA structure of conidiophores and sizes identical to those on CMD (measurements here united).