4). Fig. 4 Summary ROCs to explore heterogeneity based on overall study quality, type of health condition, and type of self-report measure In the sROC plot on the type of health condition, a comparison is made between the results of 8 symptom questionnaires on Alvocidib musculoskeletal disorders (MSD), 8 on skin disorders, and 2 on hearing loss. Although the outcomes were highly variable, the combined sensitivity and specificity of symptom questionnaires

on skin disorders was slightly better than for symptom questionnaires on musculoskeletal PCI-32765 molecular weight disorders and hearing loss. However, there were only a few self-report measures with a optimal balance between sensitivity and specificity. In the sROC plot on type of self-report measure, a comparison is made between the results for 15 symptom questionnaires (i.e., questionnaires reporting symptoms of illness such as aches, pain, cough, dyspnoea, or itch), eight self-diagnostic questionnaires, (i.e., usually a single question asking whether the respondent suffered from a specified illness or symptom in a certain time frame), and two measures rating the severity of a health problem (i.e., how do you rate your hearing loss on a scale from 1 to 5). Although again the outcomes were highly variable, the combined sensitivity and specificity click here of symptom-based questionnaires was slightly better than for self-diagnosis or

than for severity rating. In addition, symptom-based questionnaires tended to have better sensitivity, whereas self-diagnosis questionnaires tended to have better specificity. Another source of heterogeneity may come from the variety in case definitions used in the studies for both self-report and reference standard. In the large cohorts

of Descatha et al. (2007), the agreement differed substantially acetylcholine depending on the definition of a “positive” questionnaire result. If the definition was extensive (i.e., “at least one symptom in the past 12 months”), the agreement between the Nordic Musculoskeletal Questionnaire (NMQ) and clinical examination was low. With a more strict case definition (i.e., requiring the presence of symptoms at the time of the examination), the agreement with the outcomes of clinical examination was higher. Comparable results on the influence of case definition were reported by Perreault et al. (2008) and Vermeulen et al. (2000). Looking at the influence of heterogeneity in the reference standard, it showed that comparison of self-report with clinical examination seemed to result in mainly moderate agreement, whereas comparison of self-report with test results was low for exposure-related symptoms and tests (Lundström et al. 2008; Dasgupta et al. 2007) and moderate for hearing loss (Gomez et al. 2001) and self-rated pulmonary health change (Kauffmann et al. 1997).

Concerning animal experiments, a patent specification mentions “”moderate”" effects of mistletoe polysaccharides on tumour growth in uterusepithelioma. Ovarian cancer   Clinical studies: Two RCTs and two non-RCTs investigated the

influence of VAE on survival (Table 3) and reported a benefit, one of each with statistical significance. Tumour behaviour (Table 4) was investigated by two RCTs, each combining VAE and chemotherapy (plus radiotherapy in one study): these reported comparable outcomes. Eltanexor research buy The influence of VAE on QoL and tolerability of chemotherapy and radiation (Table 5) was investigated by three RCTs and one non-RCT; all of them reported a statistically significant positive effect. In one trial using an aggressive chemotherapy protocol, higher dosages of Cisplatin and Holoxan could be given in the VAE group as the side effects

were less intense [63]. One single-arm study applied recombinant lectins in ovarian cancer but found no remission. Regarding preclinical studies (Tables 7 and 9), VAE showed cytotoxic PD0332991 effects in various ovarian cancer cells. In SCID mice, rMLs led to increased survival and to more tumour-free animals at the highest and lowest dosage, while no effect was observed at the medium dosage. Genital cancer   Clinical studies: One non-RCT (published in 1963) reported partly improved disease-specific survival (Table 3). Regarding preclinical studies (Table 7), VAE showed cytotoxic effects in vulvar cancer cells. Malignant effusion   Clinical studies: One RCT and four single-arm studies investigated treatment of malignant pleural effusion and ascites (originating from breast or ovarian cancer, among other cancer sites), and all reported substantial remission rates (Tables 4 and 6). Safety Tolerability was generally good. One

case of urticaria and angioedema [56] and one case of “”generalized Oxymatrine reaction”" [69] were described. Otherwise no major side effects or toxicity were reported. Frequent minor, dose-dependent and spontaneously subsiding symptoms included reactions at the injection site (swelling, induration, erythema, pruritus, local pain) and mild flu-like symptoms or fever. In one study, local reactions MK-4827 order intensified during concomitant chemotherapy [64]. A higher prevalence of depression was documented in the unadjusted data of a retrolective non-RCT [69] in VAE-treated patients; these patients also had a higher prevalence of other treatments such as hormones. After intrapleural instillation, VAE induced significantly fewer side effects than doxycycline [60]. No indication for an interaction of VAE and chemotherapy could be found (i.e. remission rate) and VAE had no influence on the plasma concentration of gemcitabine [44, 73]. No toxicity was observed in animal studies, except after application of high doses of an isolated protein complex with unknown constituents [132].

1 to 1 reduces the peak values of S abs and S sca by about a factor of 3.5 each. This indicates the need of a compromise between the performance of an HGN ensemble and the fabrication tolerance. Regardless of σ, the ensemble exhibiting the maximum absorption efficiency comprises of HGNs with core radii smaller than those required for maximizing the scattering efficiency. A similar trend exists for the optimal distribution f(h;μ H ,σ), with absorbing

nanoshells being much thinner than the scattering ones. Figure 2 Optimal lognormal distributions of core radius and shell thickness in an ensemble of hollow gold nanoshells exhibiting maximum average [(a) and (b)] absorption and [(c) and (d)] scattering efficiencies for σ =σ R = σ H =0.1 , 0.25, 0.5, and 1.0. The simulation parameters are the same as in Figures 1(a) and 1(b). The dependencies of the peak absorption ML323 datasheet and scattering efficiencies on the excitation wavelength are plotted in Figure 3(a) for n=1.55. The efficiencies are seen to monotonously decrease with λ, which makes shorter-wavelength near-infrared lasers preferable for both absorption- and scattering-based applications. Figures

3(b) and 3(c) show the ATM/ATR cancer dispersion HSP inhibitor of the geometric means for the optimal nanoshell distributions. One can see that the best performance is achieved for the nanoshells of smaller sizes, excited at shorter wavelengths. These results are summarized in the following polynomial fittings of the theoretical curves: Med[R]≈λ(21σ 2−61σ+106)−44σ 2+72σ−48 and Med[H]≈λ

2(−58σ 2+65σ+44)+λ(103σ 2−127σ−78)−56σ 2+77σ+39 for absorption, and Med[R]≈λ(281σ 2−409σ+225)−266σ 2+376σ−146 and Med[H]≈λ 2(−966σ 3+1921σ 2−1150σ+244)+λ(1731σ 3−3439σ 2+2046σ−430)−803σ 3+1607σ 2−967σ+231for scattering. Here λ is expressed in micrometers, 0.1≤σ≤1, and the accuracy of the geometric means is about ±1 nm. Figure 3 [(a) and (d)] Optimal average absorption (filled circles) and scattering (open circles) efficiencies, and parameters [(b) and (e)] Med [R] and [(c) and (f)] Med[H] of the corresponding optimal distributions as functions of excitation wavelength and tissue refractive index. Carnitine palmitoyltransferase II In (a)–(c), n=1.55; in (d)–(f), λ=850 nm. Solid, dashed, and dotted curves correspond to σ=0.25, 0.5, and 1.0, respectively. The parameters of the optimal lognormal distribution also vary with the type of human tissue. Figures 3(d)–3(f) show such variation for the entire span of refractive indices of human cancerous tissue [9, 19], λ=850 nm, and three typical shapes of the distribution. It is seen that the peak efficiencies of absorption and scattering by an HGN ensemble grow with n regardless of the shape parameter σ. The corresponding geometric mean of the core radii reduces with n and may be approximated as Med[R]≈n(−51σ 2+87σ−65)+72σ 2−136σ+147 for absorption, and as Med[R]≈n(−94σ 2+142σ−87)+114σ 2−179σ+178 for scattering.

: Study on the expression and clinical significances of Lewis y antigen and

BKM120 ic50 integrin αv, β3 in epithelial ovarian tumors. Int J Mol Sci 2011, 12:3409–3421.PubMedCrossRef 7. Taylor ST, Hickman JA, Dive C: Epigenetic determinants of resistance to etoposide regulation of Bcl-X(L) and Bax by tumor microenvironmental factors. J Natl Cancer Inst 2000, 92:18–23.PubMedCrossRef 8. Li J, Yen C, Liaw D, Podsypanina K, Bose S, Wang SI, et al.: PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer. Science 1997, 275:1943–1947.PubMedCrossRef 9. Steck PA, Perhouse MA, Jasser SA, Yung WK, Lin H, Ligon AH, et al.: Identification of a candidate ATM/ATR cancer tumour suppressor gene, MMAC1, at chromosome 10q23. 3 that is mutated in multiple advanced cancer. Nat Genet 1997, 15:356–362.PubMedCrossRef 10. Damiano JS, Cress AE, Hazlehurst LA, Shtil AA, Dalton WS: Cell adhesion mediated drug resistance (CAM-DR): role of integrins and resistance to apoptosis in human myeloma cell lines. Blood 1999, 93:1658–1667.PubMed 11. Zhang F, Liu J, Lin B, Liu Q, Zhao Y, Zhu L, et al.: Increase in docetaxel-resistance of ovarian carcinoma-derived RMG-1 cells with enhanced expression of Lewis Y antigen. Int J Mol Sci 2011, 12:7323–7334.PubMedCrossRef 12. Iwamori M, Tanaka K, Kubushiro K, Lin B, Kiquchi K, Ishiwata I, et al.: Alterations

in the glycolipid composition and cellular properties of ovarian carcinoma-derived RMG-1 cells on transfection of the α1,2-fucosyltransferase gene. Cancer Sci selleck inhibitor Thymidine kinase 2005,96(1):26–30.PubMedCrossRef 13. Easton EW, Bolsche JG, van den Eijnden DH: Enzymatic amplification involving glycosyltransferases forms the basis for the increased size of asparagine-linked glycans at the surface of NIH 3 T3 cells expressing the

N-ras proto-oncogene. J Boil Chem 1991, 266:21674–21680. 14. Zhao Y, Itoh S, Wang X, Miyoshi E, Kariya Y, Miyazaki K, et al.: Deletion of core fucosylation on α 3 β 1 integrin down-regulates its functions. J Boil Chem 2006,281(50):38343–38350.CrossRef 15. Yan LM, Lin B, Zhu LC, Hao YY, Qi Y, Wang CZ, et al.: Enhancement of the adhesive and spreading potentials of ovarian carcinoma RMG-1 cells due to increased expression of integrin a5β1with the LewisY-structure on transfection of the a1, 2-fucosyltransferase gene. Biochimie 2010, 92:852–857.PubMedCrossRef 16. Li Q, Liu S, Lin B, Yan L, Wang Y, Wang C, et al.: Expression and Correlation of Lewis y Antigen and Integrins a5 and β1 in Ovarian Serous and Mucinous Carcinoma. Int J Gynecol Cancer 2010, 20:1482–1489.PubMed 17. Wang C, Yan L, Wang Y, Lin B, Liu S, Li Q, et al.: Overexpression of Lewis (y) antigen protects ovarian cancer RMG-1 cells from carboplatin-induced apoptosis by the Upregulation of Topo-I and Topo-II b. The anatomical record 2011, 294:961–969.PubMedCrossRef 18. Maubant S, Cruet-Hennequart S, Poulain L, Carreiras F, Sichel F, Luis J, et al.

Table 18-1 Lifestyle modifications 1. Restriction of salt intake to less than 6 g/day 2. Increased intake of BKM120 vegetables and fruitsa Restriction of intake of cholesterol and saturated fatty acid 3. Maintenance of appropriate body weight:

not exceeding BMI ([body weight (kg)]/[height (m)]2) of 25 4. Exercise: indicated for hypertensive patients without cardiovascular disease Regular aerobic exercise for 30 min or longer every day 5. Restriction of alcohol intake: 20–30 g/day or less in terms of ethanol for men and 10–20 g/day or less for women 6. No smoking Comprehensive modification of one’s lifestyle is more effective Quoted from: Lifestyle Modifications in Japanese Society click here of Hypertension Guidelines for the Management of Hypertension (JSH 2004). Hypertens Res 2006;29(Suppl):S1–S105 aIncreased intake of vegetables and fruits is not recommended in patients with severe renal dysfunction, because it may induce hyperkalemia. Also, increased intake of fruits is not recommended in diabetic patients, because it may lead to an increase in calories Salt restriction is particularly essential. Physicians should advise patients to take less than 6 g/day salt. Salt restriction enhances

antihypertensive effects of ACE inhibitors and ARBs. In the elderly, excessive salt restriction may disturb appetite, resulting in dehydration, leading to reduced kidney function. When salt restriction is difficult, a small dose of diuretics may be useful in combination. BIIB057 Concurrent use of thiazide diuretics (CKD stages 1–3) or loop diuretics (CKD stages 3–5) can accelerate salt excretion. However, physicians are to be aware of possible complications of diuretics such as hypokalemia, hyperuricemia, and dehydration. Kidney protection by ACE inhibitors or ARBs Kidney protection by ACE inhibitors and Thymidine kinase ARBs has been demonstrated. These agents are recommended for diabetic nephropathy with hypertension and even without hypertension. Nondiabetic CKD patients are expected to benefit from ACE inhibitors and ARBs. These agents, therefore, are prescribed

if blood pressure is high. Caution for administration of ACE inhibitors or ARBs Administration of ACE inhibitors or ARBs may increase serum creatinine level. Despite this, these agents are allowed to be continued, placing priority on pharmacological effects unless an increment of serum creatinine exceeds 30% of previous level or 1 mg/dL. For example, these agents may be continued if serum creatinine is elevated from 1.34 to 1.74 mg/dL after starting treatment. Serum creatinine and potassium are measured at 2 weeks or 1 month after starting ACE inhibitors or ARBs, and if continued, they are constantly monitored thereafter. If serum creatinine is elevated to the above-mentioned degree, these agents should be reduced in dosage or discontinued, and consultation to nephrologists is required.

pestis isolated from fleas [9]. However, actual levels of the Y. pestis Tc proteins in the flea or Entospletinib molecular weight during growth in liquid culture, or a potential role in survival within or transmission from the flea have not yet been determined. In this study, we show that the Tc proteins YitA and YipA are highly produced by Y. pestis in the flea but not during growth in culture at the same temperature (22°C) and that over-production of YitR increases YitA and YipA synthesis

in vitro. YitA and YipA production was greatest during growth at lower temperatures (less than 22°C) and minimally produced at 37°C, although the proteins persisted for more than 9 hours after a transition from 22°C to 37°C. YipA appears to be processed near the C-terminus between the click here RhsA and PTP domains. Furthermore, YitA and YipA are localized to the outer membrane, and YitA is surface-exposed. We also show that the Y. pestis Tc proteins do not play a detectable role in X. cheopis infection or the ability to produce a transmissible infection. Results YitA and YipA are synthesized in the flea P5091 but not in vitro unless the YitR regulator is over-produced A diagram of the Y. pestis Tc locus is shown in Figure 1a. X. cheopis fleas were infected with KIM6+ or KIM6+ΔyitA-yipB (Figure 1A) to compare YitA and YipA (Figure 1B) protein levels following

growth in the flea to growth in BHI culture. YitA and YipA were both highly produced by Y. pestis in the flea (Figure 2, lane 2) compared to stationary phase BHI cultures (Figure 2, lane 4) incubated at 22°C, the same temperature at which the fleas were maintained. YitA was detected as a prominent band around 95 kDa, which corresponded to the expected size based on the YitA amino acid sequence. YipA was selleck chemicals llc detected as two major bands. The smaller band at ~73 kDa was the most prominent. The larger band at ~106 kDa corresponds to the full length YipA predicted by its amino acid sequence and with recombinant YipA synthesized in and purified from E. coli (Figure 2, lane 9). Figure 2 YitA and YipA are only detectable in Y. pestis isolated from fleas

but over-production of YitR increases their synthesis in vitro . Lane 1, molecular weight ladder. Lane 2, Y. pestis KIM6+ isolated from infected fleas. Lane 3, KIM6+ΔyitA-yipB isolated from infected fleas. Lane 4, KIM6+ grown at 22°C in BHI. Lane 5, KIM6+ (pWKS130::yitR) grown at 22°C in BHI. Lane 6, KIM6+ (pCR-XL-TOPO::yitR) grown at 22°C in BHI. Lane 7, KIM6+ΔyitA-yipB (pCR-XL-TOPO::yitR) grown at 22°C in BHI. Lanes 8–9, recombinant YitA and YipA purified from E. coli. Panels show Western blots probed with anti-YitA, anti-YipA, or anti-Ail (sample loading control) antiserum. To determine if over-production of YitR would result in increased levels of YitA and YipA proteins during growth in vitro, the regulator yitR was cloned with its native promoter into the low-copy plasmid pWKS130 and the high-copy plasmid pCR-XL-TOPO. Y.

This decline in expression was also detected for apical aquaporin-2 in CCRCC tumor cells (Figure 3B). Galectin-3, on the other hand, could be well detected in the cytosol as well as in nuclei of most of the non-polar tumor cells. Figure 3 Confocal fluorescence images showing the distribution of galectin-3 and different polarity markers in normal kidney and tissue from clear cell renal cell carcinoma. All sections were immunostained against apical aquaporin-2 (AQP-2)

and www.selleckchem.com/products/anlotinib-al3818.html villin or basolateral E-cadherin. In all fluorescence images the polarity markers are indicated in green, galectin-3 is depicted in red and the nuclei are stained click here with Hoechst 33342 (blue). In normal kidney sections aquaporin-2 is concentrated on the apical domain of epithelial

cells of the collecting duct, whereas villin is part of the brush border of the proximal tubule. E-cadherin can be detected in cells of the distal tubule and the collecting duct. Arrows mark the apical localization of AQP-2 and villin (A, C) or the basolateral localization of E-cadherin (E). In all tissue sections of the tumor the expression of the polarity markers is reduced or completely lost. In normal kidney areas, galectin-3 is found in the collecting duct as well as in the distal tubule, but not in the proximal tubule. Stars depict single cells, in which galectin-3 is expressed. Scale bars: 25 μm. 3.4 Nuclear accumulation of galectin-3 in CCRCC tumor cells To determine if galectin-3 was enriched in the nuclei ��-Nicotinamide of tumor cells, we recorded the fluorescence of galectin-3 staining in image stacks of whole cells in normal as well as in CCRCC tumor tissues. This approach verifies that the whole fluorescence

of a cell is registered and excludes misinterpretations due to fluorescence detection Smoothened restricted to a single focal plane. The 3D-reconstructions depicted in Figure 4A show a concentration of galectin-3 in the Hoechst-stained cell nuclei of tumor cells, whereas the lectin was mainly distributed in the cytosol of normal renal epithelial cells. Figure 4 Nuclear localization of galectin-3 in normal and tumor tissue samples. A. Immunofluorescence of galectin-3 and nuclear Hoechst was recorded in different layers of normal and CCRCC tissues. The recorded image stacks were processed by deconvolution and background elimination. Dual colors are depicted in the 3D-reconstructed images. On the left galectin-3 (red) is shown; nuclei are depicted in blue. Images without nuclear staining are depicted on the right. Scale bars: 15 μm. B. Immunoblots of nuclear lamin and LDH in isolated nuclei or cytosolic fractions. C. Imunoblots of galectin-3 or lamin in nuclear or cytosolic fractions from normal or tumor tissue. D. Relative changes in nuclear versus cytosolic localization as quantified from 9 immunoblots from normal or CCRCC tissues are depicted.

In general, MAPK inhibition resulted in a greater reduction of cytokine production in PCM treated HKs compared to BCM treated HKs. Results represented as mean ± SD, n = 3, *p < 0.05, **p < 0.01. We have previously described characteristic morphology changes in BCM treated HKs [20]. The effects of MAPK inhibitors on BCM induced cell morphology were investigated here. Inhibition of JNK, p38, or ERK did not

prevent the biofilm-induced formation of filopodial structures in HKs (data not shown). Overall, this indicates that cytoskeletal rearrangements buy NVP-BGJ398 induced by BCM act through MAPK-independent mechanisms. Discussion S. aureus biofilm and planktonic-conditioned medium induced distinct responses in HKs in vitro. The adverse effects of planktonic bacterial cultures on mammalian cells have been well documented in vitro. Bacterial cells grown in broth

cultures have long been assumed to retain the same pathogenic properties as bacteria in natural settings. While important discoveries have been realized based on planktonic studies, data presented here provide evidence that bacterial biofilms differentially induce pathogenesis in cultured HKs. Host-pathogen interactions were investigated between a clinical isolate of S. aureus and HKs. A preliminary analysis of the extracellular proteome of S. LY2874455 aureus biofilm and planktonic cultures was performed by 1D gel electrophoresis and mass spectrometry. Several differences were observed in the 1D gel band patterns of BCM and PCM (Figure 1). The total protein concentrations of BCM and PCM were found to be similar, but BCM clearly contained more features. Smearing of BCM in 1D gels was observed indicating possible bacterial protease activity, although such a protease was not identified by mass spectrometry (Table 1). S. aureus secretes Aurora Kinase a variety of proteases which are important in pathogenesis [24]. The presence of such a protease could explain some of the observed effects in HKs after

treatment with BCM or PCM. Several 1D gel bands visible in PCM and not BCM contained glycolytic enzymes (Figure 1, Table 1). The presence of intracellular glycolytic enzymes in the extracellular proteome of S. aureus may be due to cell lysis, but cell wall Quisinostat in vivo associated glycolytic enzymes have been described for numerous pathogens, including S. aureus [25, 26]. Links between central metabolism and virulence in S. aureus have been described. In S. aureus, when carbon sources are plentiful, glycolysis is active while the tricarboxcylic acid (TCA) cycle is largely repressed [27]. The TCA cycle has been described as a signal transduction pathway capable of regulating toxin production [28], adhesion synthesis and biofilm formation [29, 30], and antibiotic susceptibility [31]. Additionally, S.

MnATP (but not MgATP) induces a conformational change in GlnJ We hypothesized that, in the case of GlnJ, only the binding of MnATP would stabilize a protein conformation that allows the correct positioning of the T-loop for interaction Temsirolimus mw with GlnD, resulting in uridylylation. To analyze this possbility we used circular dichroism (CD) spectroscopy to evaluate changes in the secondary structure of GlnJ/GlnB upon incubation with either MgATP or MnATP. It is visible from our results that only MnATP induced a conformational

change in GlnJ, translated as a significant change in the CD spectrum (Figure 5A), while both Mg2+ and Mn2+ elicited a similar conformational change in GlnB (Figure 5B). These observations of divalent cation-induced conformational changes in the PII proteins correlate well with the conditions required for efficient uridylylation by GlnD. Figure 5 CD spectra for GlnJ

(A) and GlnB (B); protein only (dashed), protein + MnATP (solid) and protein + MgATP (dotted). Proteins were at 100 μM trimer concentration, ATP at 10 mM and MgCl2/MnCl2 at 10 mM. Spectra were recorded at 24°C. The GlnJ and GlnB variants retain functionality To determine if the substitutions affected protein LY2603618 function we analyzed the functionality of the GlnJ and GlnB variants using an assay based on one of the cellular targets of PII proteins, the adenylyltransferase MK-0457 GlnE. We have previously used this assay as means to determine whether PII variants are still able to perform a PII dependent function [13]. GlnE is responsible for the regulation of GS activity by post-translational adenylylation [5]. PII proteins (in the unmodified form) interact with GlnE promoting adenylylation of GS, leading to lower GS activity (Figure 6A). Figure 6 Analysis of PII protein function in

the activation of GlnE.(A) Model representing the role of PII proteins in the regulation of GS activity, through GlnE in R. rubrum . (B) Glutamine synthetase activity after 30 minutes of incubation with GlnE and PII proteins (as indicated). Results are the average of three experiments and are shown as mean ± SD. To analyze the functionality of all variants constructed, we tested the ability to activate GS adenylylation DCLK1 by GlnE, resulting in reduced GS activity. As shown in Figure 6B, all variants tested were able to activate the adenylylation activity of GlnE. Conclusions The two PII proteins GlnJ and GlnB from R. rubrum show different requirements in terms of divalent cations (Mg2+/Mn2+) for efficient uridylylation by GlnD. Specifically, the uridylylation of GlnJ requires the presence of Mn2+, with Mg2+ not being able to support this modification. Most likely this is due to the fact that only Mn2+ (or MnATP) is able to bind and induce a conformational change in GlnJ, as demonstrated here with CD spectroscopy.

International Book Distributing Company, Lucknow, pp 457–479 Ranghoo VM, Hyde KD (1999) Ascomauritiana lignicola gen. et. sp. nov., an ascomycete from submerged wood in Mauritius.

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