J Am Chem Soc1999,121(50):11912–11913.CrossRef selleck inhibitor 21. Wright SAI, Zumoff CH, Schneider L, Beer SV:Pantoea agglomerans strain EH318 produces two antibiotics that inhibit Erwinia amylovora in vitro. Applied and environmental microbiology2001,67(1):284–292.CrossRefPubMed 22. Giddens SR, Feng Y, Mahanty HK:Characterization of a novel phenazine antibiotic gene cluster in Erwinia herbicola Eh1087. Mol Microbiol2002,45(3):769–783.CrossRefPubMed 23. Van Rostenberghe H, Noraida

R, Wan Pauzi WI, Habsah H, Zeehaida M, Rosliza AR, Fatimah I, Nik Sharimah NY, Maimunah H:The clinical picture of neonatal infection with Pantoea species. Jpn J Infect Dis2006,59:120–121.PubMed 24. Cruz AT, Cazacu AC, Allen CH:Pantoea agglomerans , a plant pathogen causing human disease. J Clin Microbiol2007,45(6):1989–1992.CrossRefPubMed 25. Kratz A, Greenberg D, Barki Y, Cohen E, Lifshitz M:Pantoea agglomerans as a cause of septic arthritis after palm tree thorn injury; case report and literature review. Arch Dis Child2003,88:542–544.CrossRefPubMed 26. Geere JW:Enterobacter agglomerans : the clinically important plant pathogen. Palbociclib mw Can Med Assoc J1977,116:517–519.PubMed 27. Bergman KA, Arends JP, Schölvinck

EH:Pantoea agglomerans septicemia in three newborn infants. Pediatr Infect Dis J2007, (26):453–454. 28. Ruimy R, Genauzeau E, Barnabe C, Beaulieu A, Tibayrenc M, Andremont A:Genetic diversity of Pseudomonas aeruginosa strains isolated from LY294002 ventilated patients with nosocomial pneumonia, cancer patients with bacteremia, and environmental

water. Infect Immun2001,69:584–588.CrossRefPubMed 29. Lanotte P, Watt S, Mereghetti L, Dartiguelongue N, Rastegar-Lari A, Goudeau A, Quentin R:Genetic features of Pseudomonas aeruginosa isolates from cystic fibrosis patients compared with those of isolates from other origins. J Med Microbiol2004,53:73–81.CrossRefPubMed 30. Khan NH, Ishii Y, Kimata-Kino N, Esaki H, Nishino T, Nishimura M, Kogure K:Isolation of Pseudomonas aeruginosa from open ocean and comparison with freshwater, clinical, and animal isolates. Microbial Ecology2007,53:173–186.CrossRefPubMed 31. Kurz CL, Chauvet S, Andrès E, Aurouze M, Vallet I, Michel GP, Uh M, Celli J, Filloux A, De Bentzmann S,et al.:Virulence factors of the human opportunistic pathogen Serratia marcescens identified by in vivo screening. EMBO J2003,22:1451–1460.CrossRefPubMed 32. Coenye T, Vandamme P:Diversity and significance of Burkholderia species occupying diverse ecological niches. Environ Microbiol2003,5:719–729.CrossRefPubMed 33. Tabacchioni S, Ferri L, Manno G, Mentasti M, Cocchi P, Campana S, Ravenni N, Taccetti G, Dalmastri C, Chiarini L,et al.:Use of the gyrB gene to discriminate among species of the Burkholderia cepacia complex. FEMS Microbiol Lett2008,281:175–182.CrossRefPubMed 34.

In this study, chemo-sensitivity induced by CLU C59 wnt nmr gene silencing was directly correlated to the endogenous level of CLU protein expressed in a given cell line, being particularly enhanced in KF-TX, SKOV-3-TX, that express the highest levels of s-CLU. An experimental system in which OVK18 cells were genetically modified to specifically over-expression s-CLU rendered cells TX-resistant. Thus, in our system s-CLU seems essential for ovarian cancer cells to resist TX.

Similar results have been obtained in cervical cancer [40]. Thus, up-regulation of s-CLU might be a candidate marker to predict ovarian cancer chemo-resistance, while its reduction after drug administration may predict chemo-response when tumor cells have high endogenous CLU. Importantly, our results support the idea that, s-CLU is a stress-associated cytoprotective protein that is up-regulated in an adaptive cell survival manner following various cell death trigger including chemotherapy in ovarian cancer cells as well as in most cancer cells [41, 35]. Therefore,

novel therapeutic strategy of silencing s-CLU expression to overcome chemoresistance were suggested when cancer cells over-express s-CLU as in lung [42], prostate [43], kidney [44] or breast [13]. In the current study, we firstly demonstrated that OGX-011, a second-generation antisense oligodeoxynuclotide targeting RAD001 cost the translation initiation site of human CLU gene exon II with a long tissue half-life, can modulate sensitivity

to TX in an acquired TX-resistant ovarian cancer cell line. OGX-011 improved the efficacy of chemotherapy, radiation, and hormone withdrawal by inhibiting expression of CLU and enhancing apoptotic rates in preclinical xenograft models of prostate, lung, renal cell, breast, and other cancers [44–46]. Interference with the innate apoptotic activity is a hallmark of neoplastic transformation and tumor formation. Modulation of the apoptotic cascade has been proposed as a new approach for the treatment of cancer. Phenoxodiol [47] and XIAP inhibitor [48] are currently tested in clinical trials as chemosensitizer for chemoresistant tumors [49]. recently reported the result of the phase II study of docetaxel and prednisone with or without OGX-011 in patients with metastatic castration-resistant prostate ASK1 cancer. They have shown that combination of OGX-011 with docetaxel significantly improved survival [49]. We do hope to test the efficacy of OGX-011 as a chemosensitizer to standard cytotoxic drugs for the patients with recurrent (resistant tumor) and refractory ovarian cancer. Conclusions In summary, present study demonstrated that alterations of s-CLU biogenesis are induced during development of TX-resistance. These changes include overexpression inside cells and subsequent secretion into media positively correlates to chemo-resistant phenotype.

2005). In a separate analysis, we examined the relationship between this website population density and likelihood of drastic population decline, among all species. We defined drastic population decline as possessing a sampled distribution in which at least 90% of individuals were captured in uninvaded plots (taking the average among sites for species that occurred at multiple sites). This level of inferred population reduction, while somewhat

arbitrary, identifies those species that are arguably the most likely to experience local extinction. We grouped species, both rare and non-rare, by successively larger population density categories, such that evenness was maximized among all but the lowest density category (in terms of number of species included) for both endemic and introduced species. We then calculated the percentage of species exhibiting click here patterns of drastic population decline in each density category. Because the likelihood of obtaining a highly skewed sampling distribution purely by chance is much higher among small populations, we also calculated the percentage of species expected to exhibit patterns consistent with drastic population decline, through random sampling alone, for each population density category. We did this by (1) calculating the probability of obtaining 90% or more of sampled

individuals in uninvaded plots for each observed population size, under the assumption that each individual had equal probability of existing in an invaded versus uninvaded plot, (2) multiplying these probabilities by the number of species that occurred at each population size, and (3) summing over population sizes and dividing by the total number of species, within each density category. Finally, we calculated a chance-corrected likelihood of drastic population decline for each density category by subtracting the percentage

of species expected to exhibit patterns of drastic decline due solely to chance from the observed percentage of species exhibiting this pattern. To examine variability in the inferred response to ant invasion, both Racecadotril within and among species, we tabulated species responses within each order, using the entire dataset including multiple incidences of species occurrence. Species were classified according to the identity and consistency of their responses. For non-rare species, we designated four categories: species whose responses were always strongly negative (impact scores ≤ −0.5 at all sites), always weakly interacting (between −0.5 and 0.5 at all sites), always strongly positive (≥0.5 at all sites), or variable (including scores in more than one of the categories at different sites). Rare species were classified into three categories: those that were absent in invaded plots at all sites, those that were present in invaded plots at all sites, and those that had variable responses among sites.

09 0.0806 Change in cortical thickness vs. change in BMD total hip GH-treated 0.13 0.0005 Change in cortical thickness vs. change in BMD total hip Untreated 0.02 0.3824 Discussion The main finding of the present study was that GH substitution, after achievement of final height in young adults with CO

GHD, is associated with a significant increase in cortical bone thickness. The observed reduction in endosteal diameter in GH-treated patients in this study suggests that the increase results from endosteal bone growth rather from periosteal apposition. While there is no one single cause of bone fragility, fewer or thinner trabeculae and thin cortices, all play their part in low peak bone density [18]. In early click here adulthood, material and structural strength is maintained by remodelling, the focal replacement of old with new bone. During ageing, concurrent bone formation on the outer (periosteal) cortical bone surface partly compensates for bone loss. Although the GS-1101 in vitro structural basis of bone fragility is determined partly by genetic and environmental factors, growth during the pubertal and early adult years has a significant influence on bone strength in later years. Hence, a GH-induced reduction in endosteal diameter may, potentially, have beneficial effects on cortical bone strength [19, 20], thereby reducing the risk of bone fragility later in life [21]. Limited data are currently available on the growth

patterns of cortical bone during normal adolescence and in patients with CO GHD, and our findings therefore also contribute to the understanding of cortical bone development during growth. There are few data on changes in cortical bone density with GH therapy in patients with CO GHD. Using peripheral quantitative computed tomography, Schweizer et al. [22] reported that 12 months of GH therapy was associated with an increase in both outer and inner diameters of the radius, as well as decreased cortical thickness. The impact of GH on cortical bone might be different after epiphyseal closure and cessation of longitudinal bone growth. The findings of

this study are in agreement with the earlier reported densitometry findings of the same population [13], showing an increase in lumbar spine BMD of 3.5% and total hip BMD of 2.4% during GH therapy. Interestingly, some Benzatropine studies report a reduction in bone density during the first year of GH therapy, which is likely caused by an increase in remodelling space and a temporary reduction in bone mass and size [3, 23, 24]. Longer treatment periods show increased bone formation as the areal bone density tends to fall during the first 6 months of treatment and reaches baseline levels again between 6 and 12 months [13]. In the present study, in which only cortical bone is encountered, a linear increase in cortical area was observed from the very start of treatment. Despite only a marginal increase in bone width being observed in our study, there was a pronounced reduction in the inner bone diameter.

Although this study used a convenient rather than a random community sample and might have biased towards recruiting healthier subjects, the prevalence of osteoporosis at the femoral neck of 3.2% in this cohort was similar to the 2.0% reported in Caucasian White subjects in the population-based NHANES

2005–2006 survey in the US [13]. The prevalence of osteoporosis at the spine and hip were similar in this cohort. Similar to other populations, fractures of the hip, forearm, vertebrae, and humerus were among the most frequent sites of incident fractures in men. In comparison with postmenopausal women in the same population [5], the absolute fracture incidence was lower in men. The reason for this difference Z-VAD-FMK mw in the US population was postulated to be related to an increased frequency

of falls Ixazomib concentration in women [14, 15], and fracture risk after a fall was 2.2 times higher in women than men [16]. The relation of fracture risk after a fall in the two sexes was nonetheless reversed in Chinese. Although falls were recorded more often in women [5], the relative risk of fracture in subjects with one or more falls in 12 months was 14.5 for Chinese men and 4.0 for Chinese women. This study also identified the clinical risk factors for fracture in Chinese men and the interaction between risk factors and BMD. These risk factors partly overlap with those reported for Caucasian population of the MrOs study which are the use of tricyclic antidepressant, history of fracture, inability to complete a narrow walk trial, falls in previous year, age ≥ 80 years, depressed mood and decreased total hip BMD [12]. The risk factors for Chinese men are also slightly different from those identified by the Dubbo study which includes increasing age, decreased femoral neck BMD, quadriceps strength, body sway, previous falls,

previous fractures, weight, height, alcohol use, physical activity index and thiazide use [6]. Similar to previous observations of other ethnic groups [17, 18], each SD reduction in BMD T-score is associated with a 1.8 to 2.6-fold increased risk of osteoporotic fractures PLEK2 in Chinese men. The relative risk prediction for osteoporotic fracture was better with BMD measurement at the hip than the spine: this concurs with the findings in Caucasian populations [6, 19]. However, subjects with a femoral neck BMD T-score < −2.5 had a 13.8-fold increased risk of fracture. The WHO FRAX model utilizes ten clinical risk factors with or without BMD for fracture risk prediction. In areas where BMD measurements are not available, WHO proposes to use BMI to replace BMD as it provides a similar risk profile for fracture prediction. Interestingly, our data revealed that addition of BMD information to clinical risk factors enhanced fracture prediction in this male cohort. This observation concurs with other US Caucasian male studies [20].

For device C, the situation is similar to device B, as indicated in Figure 3c. However, there is a 0.3-eV barrier at the [LUMO]EML/[LUMO]BCP interface, and electrons are confined in the LUMO energy level of BCP. Meanwhile, the larger barrier of 0.7 eV at the interface of [HOMO]EML/[HOMO]BCP results in holes confined in the HOMO energy level of EML. Since electrons and holes are confined in different organic layers, which

increase the probability of excitons disassociation and decrease the Tanespimycin cost recombination efficiency of carriers [23], device C presents inferior EL performances. Therefore, the different level alignments both for [LUMO]EML/[LUMO]PBL and [HOMO]EML/[HOMO]PBL for devices A, B, and C lead to the different distributions and recombination efficiencies of carriers. That is also proven by their different EL spectra as shown in Figure 4. From the emission

spectra, we note that device A with type-I MQW structure offers a larger blue emission than the reference device www.selleckchem.com/products/MS-275.html which makes better CIE coordinates (see Table 1). For devices B and C with type-II MQW structure, there is a low possibility of carrier recombination due to the fact that only a single carrier could be confined in the EML, while another carrier is confine in PBL, which results in poor EL performances. It is a fact that strong blue emission and week red emission present in device C resulted from the accumulation of holes at the interface of [HOMO]blue-EML/[HOMO]BCP and that there are less holes in potential wells of green EML and red EML, especially in potential wells of red EML. Conclusions In conclusion, WOLEDs with type-I MQW structure offer higher EL performances

in contrast with the reference device with traditional three-layer structure. WOLEDs with TPBi as PBL exhibits a peak current efficiency and a power efficiency of 16.4 cd/A and 8.3 lm/W at about 1,000 cd/m2, which increase by 53.3% and 50.9% over the reference device, GPX6 respectively; meanwhile, a maximum luminance of 17,700 cd/m2 is achieved, which keeps a similar luminance with the reference device. The achievement of high EL performance with type-I MQW structure WOLEDs would be attributed to the uniform distribution and rigorous confinement of carriers and excitons within EMLs. However, when Bphen or BCP acts as PBL instead of TPBi, low EL performances (especially for BCP) are obtained, which are attributed to poor level alignment at the interface of EML/PBL for type-II MQW structure; thus, incomplete confinement and low recombination efficiency of carriers occur. In terms of the results, we find that type-I MQW is a promising structure design for improving white EL performance by choosing the suitable PBL.

We suggest that the presence of a circular array of 98 charges, with a net charge of −14, could restrict the possible pathways for association and find more dissociation between the cyt c 2 and the periplasmic surface of the RC. It seems likely that, when leaving the docking site on the RC, the cyt c 2 has to migrate out of plane (perpendicular to the membrane surface) in order to be able to evade the LH1-charged residues. This probable pathway coincides with the pulling trajectory

in our experiments (both PF-QNM and SMFS). The His-Ni2+-NTA coordination chemistry used in these experiments can achieve long-lasting attachment of proteins (several thousand force–distance cycles, up to several hours) to a functionalised AFM probe or surface, while sustaining significant force stresses (up to 500 pN) (Schmidt et al. 2002; Conti et al. 2000; Nevo et al. 2003; Berquand et al. 2005; Dupres et al. 2005) without the need of a covalent chemical linkage, thus preserving

the protein structure and functionality. The unbinding forces measured during the PF-QNM experiments, approximately 480 pN, are close to the estimated values in a theoretical study of the pathways for cyt c 2–RC-LH1-PufX interaction, with forces in the range 600–1,000 pN (Pogorelov et al. 2007). It is worth noting the fact that purified RC-LH1-PufX complexes were X-396 mouse found to retain 25–30 % of the endogenous quinone acceptor pool (Comayras et al. 2005). This quinone pool stores the electrons resulting from the photo-oxidation of the primary donor, thus maintaining the turnover of the electron transfer cycle during image acquisition. Cyt c 2 to RC electron transfer is in the low microsecond range (Overfield et al. 1979; Moser and Dutton 1988) so, having being brought into contact with a surface-bound RC, the cyt c 2 will be immediately oxidised, given the Tau-protein kinase dwell

time of ~160 μs (PF-QNM) or several milliseconds (SMFS). Thus, the interaction sampled by the unbinding events is likely to be between RC[red] and an oxidised cyt c 2 (cyt c 2[ox]). The negative control shows that a cyt c 2[red]–RC[red] interaction has a low probability. The more probable interaction arises when the initial states (prior to the tip-surface encounter) consist of reduced cyt c 2 and oxidised reaction centres. Therefore, it appears that the cyt c 2-RC association is maintained in the aftermath of the initial electron transfer event, although the oxidised cyt c 2—reduced RC control, which would have helped dissect the nature of the complex, was not performed. This study does, however, probe the long-lived forces that stabilise the cyt c 2–RC association, under controlled conditions of force and distance.

[42,43] The current paper presents an in-depth analysis of the safety profile of moxifloxacin, based on the manufacturer’s clinical trial database Angiogenesis inhibitor comprising

all actively controlled phase II–IV clinical trials. The objective of the analysis was to examine and compare the safety profile of moxifloxacin with those of the comparators that were all selected as reference therapies for the treatment of corresponding indications at the time the studies were designed. Methods Studies The analysis comprised all double-blind and open-label actively controlled clinical trials included in the clinical trial database of moxifloxacin 400 mg once daily and performed by the manufacturer as part of the phase II–IV programs that were initiated and completed between 1996 and 2010,

with the exception of one exploratory phase II study conducted in cirrhotic patients, most of them with Child–Pugh class C cirrhosis. All studies used the oral formulation (400 mg tablets), the 400 mg/250 mL solution for infusion formulation, or a sequence of intravenous and oral formulations. Forty-nine Hydroxychloroquine ic50 oral studies enrolled patients diagnosed with streptococcal pharyngitis (n = 1), ABS (n = 10), AECB (n = 17), CAP (n = 12), uSSSIs (n = 4), uncomplicated PID (uPID; n = 3), or uncomplicated (n = 3) or complicated (n = 1) urinary tract infection (UTI). Some patients could be enrolled in the same study looking at two different indications – for example, ABS and AECB, or AECB and CAP. Fifteen intravenous/oral studies enrolled patients with CAP (n = 7), cSSSIs (n = 3), cIAIs (n = 2), nosocomial pneumonia (n = 2), or lung abscess or aspiration pneumonia (n = 1). Four intravenous-only studies enrolled patients

with CAP (n = 2), cIAIs (n = 2), or AECB (n = 1; this study also enrolled patients with CAP). Patients The studies were conducted in Europe, the Americas, the Middle East, Africa, and the Asia/Pacific region. Safety-valid Immune system patients were defined as those randomized within an actively controlled clinical trial, having received at least one dose of the study drug and having had at least one observation after initial drug intake. The following subgroups of patients with pre-existing risk factors were evaluated: elderly (age ≥65 years); diabetes mellitus (blood glucose level >200 mg/dL at baseline or at least one medical history finding coded to a preferred term [PT] with a primary path in the high-level term [HLT] diabetes [including subtypes]); renal impairment (serum creatinine ≥1.5 mg/dL for women and ≥1.

PubMedCrossRef 48. Hongoh Y, Deevong P, Inoue T, Moriya S, Trakulnaleamsai S, Ohkuma M, Vongkaluang C, Noparatnaraporn N, Kudo T: Intra- and interspecific comparsions of bacterial diversity and community structure support coevolution of gut microbiota and termite host. Appl Environ Microb 2005, 71: 6590–6599.CrossRef 49. Dethlefsen L, McFall-Ngai M, Relman Selleckchem GS 1101 DA: An ecological and evolutionary perspective on human-microbe mutualism and disease. Nature 2007, 449: 811–818.PubMedCrossRef 50. Klyachko

O, Stein BD, Grindle N, Clay K, Fuqua C: Localization and visualization of a Coxiella -type symbiont within the lone star tick, Amblyomma americanum . Appl Environ Microb 2007, 73: 6584–6594.CrossRef 51. Jasinskas A, Zhong J, Barbour AG: Highly prevalent Selleck Ferrostatin-1 Coxiella sp. bacterium in the tick vector Amblyomma americanum . Appl Environ Microb 73: 334–336. 52. Padbidri VS, Rodrigues JJ, Shetty PS, Joshi MV, Rao BL, Shukla RN: Tick-borne rickettsioses in Pune district, Maharashtra, India. Int J Zoonoses 1984, 11: 45–52.PubMed 53. Wen B, Cao W, Pan H: Ehrlichiae and ehrlichial diseases in China. Ann NY Acad Sci 2003, 990: 45–53.PubMedCrossRef 54. Ghosh S, Azhahianambi P, Yadav MP: Upcoming and future strategies

of tick control: a review. J Vect Borne Dis 2007, 44: 79–89. 55. Zhong J, Jasinskas A, Barbour AG: Antibotic treatment of the tick vector Amblyomma americanum reduced reproductive fitness. PLoS ONE 2007, 2: e405.PubMedCrossRef 56. Mediannikov O, Sekeyová Z, Birg ML, Raoult D: A novel obligate intracellular gamma-proteobacterium associated with Ixodid ticks, Diplorickettsia massiliensis , gen. nov., sp. nov. PLoS ONE 2010, 5: e11478.PubMedCrossRef 57. Matton P, Van Melckebeke H: Bovine borreliosis: comparison of simple methods for detection of the spirochaete in the blood. Trop Anim Hlth Prod 1990, 22: 147–152.CrossRef 58. Wen B, Jian R, Zhang Y, Chen R: Simultaneous detection of

Anaplasma marginale and however a new Ehrlichia species closely related to Ehrlichia chaffeensis by sequences analyses of 16S ribosomal DNA in Boophilus microplus ticks from Tibet. J Clin Microbiol 2002, 40: 3286–3290.PubMedCrossRef 59. Smith RD, Miranpuri GS, Adams JH, Ahrens EH: Borrelia theileri : isolation from ticks ( Boophilus microplus ) and tick-borne transmission between splenectomized calves. Am J Vet Res 1985, 46: 1396–1398.PubMed 60. Callow LL, Hoyte HMD: Transmission experiments using Babesia bigemina , Theileria mutans , Borrelia sp. and the cattle tick, Boophilus microplus . Aust Vet J 1961, 73: 381–390.CrossRef 61. Rodríguez Vivas RI, Cen Aguilar F, Domínguez Alpízar JL, Cob Galera LA, Solís Calderon JJ: Detección de espiroquetas del género Borrelia en hemolinfas de teleoginas de Boophilus microplus en el estado de Yucatán, México. Vet Mex 1996, 27: 187–188. 62. Rezende J, Kessler RH, Soares CO, Martins OP: Ocorrência de Borrelia spp. em cultura de células embrionárias do carrapato Boophilus microplus (Acari: Ixodidae) no estado do Mato Grosso do Sul, Brasil.

Colony similar to that on CMD, with wavy margin, mycelium denser and faster on the agar surface, after a week degenerating, many hyphae appearing empty. Aerial hyphae inconspicuous, more frequent and long along the colony margin. Autolytic

activity and coilings absent Talazoparib molecular weight or inconspicuous, more frequent at higher temperatures. No diffusing pigment, no distinct odour produced. Chlamydospores seen after 3–6 days at 25°C, frequent, terminal and intercalary, (5–)6–10(–13) × (3.5–)5–8(–12) μm, l/w (0.9–)1.0–1.4(–1.9) (n = 40), globose, ellipsoidal or fusoid. Conidiation noted after 3–4 days at 25°C, earlier at higher temperatures, in many amorphous, loose white cottony tufts mostly median from the plug outwards, confluent to masses up to 17 mm long; white, turning green, 27CD3–4, 27E5–6, 28CE5–8, from inside after 4–5 days; conidiation becoming dense within the tufts, loose at their white margins first with long, straight or slightly sinuous, sterile ends in the periphery, projecting 50–150(–300) μm from the tuft margins when young, sterile and beset with minute droplets along their length, mostly becoming fertile and incorporated into the tufts. Tufts consisting of a loose reticulum

with mostly unpaired branches often in right angles, giving rise to several main axes. Main axes up to 0.6 mm long, regularly https://www.selleckchem.com/products/abt-199.html tree-like, with few or many paired or unpaired side branches often in right angles, mostly (30–)40–110(–150) Histidine ammonia-lyase μm long, progressively longer from the top down, regularly tree-like at lower levels. Branches (1.5–)2.0–4.0(–5) mm wide, flexuous; apparent paired branches or phialides often not strictly opposite but slightly shifted on the axis. Branching points often thickened to 4.5–7(–9) μm, particularly in older tufts. Phialides generally solitary along main axes

and side branches, also often on cells that resemble phialides, sometimes paired, in terminal position of the main axes sometimes in whorls of 2–3, often cruciform, or up to four in pseudo-whorls, i.e. including unicellular branches, each of which produces a phialide. Phialides (3.7–)4.7–7.8(–10.5) × (2.3–)2.5–3.0(–3.4) μm, l/w (1.3–)1.6–3.0(–4.4), (0.9–)1.2–2.0(–2.2) μm wide at the base (n = 70), lageniform or ampulliform, symmetric, straight or slightly curved, often distinctly widened in the middle, base often constricted, neck short, less commonly long. Conidia produced in minute heads <20 μm diam, (2.7–)3.0–3.7(–5.2) × (1.8–)2.0–2.5(–2.7) μm, l/w (1.1–)1.3–1.7(–2.1) (n = 90), at first hyaline, turning yellow-green, oblong or ellipsoidal, rarely cylindrical with constricted sides, smooth, eguttulate or with minute guttules, scar indistinct, size uniform. At 15°C colony irregular in shape, loose; conidiation in green 26–27DE4–5, confluent tufts similar to those at 25°C; chlamydospores numerous in narrow hyphae.