Furthermore,

PbS has a SRT1720 cost large exciton Bohr radius of about 20 nm, which can lead to extensive quantum size effects. It has been reported that its absorption range can be tuned by adjusting the particle size of the quantum dots [16, 17]. Until now, as one of the most impressive alternative semiconductors, PbS-sensitized solar cells have been studied by many groups [18–22]. In most of the reported works, PbS quantum dots were grown on TiO2 nanotubes [20], ZnO nanorod arrays [21], and TiO2 photoanode with hierarchical pore distribution [22]. Little work has been carried out on large-area single-crystalline TiO2 nanorod array photoanode. Compared to the polycrystal TiO2 nanostructures such as nanotubes [23] and nanoparticles [24], single-crystalline TiO2 nanorods grown directly on transparent conductive oxide electrodes provide a perfect solution by avoiding the particle-to-particle hopping that occurs in polycrystalline films, thereby increasing the photocurrent efficiency. In addition to the potential Ferroptosis tumor of improving electron transport, they enhance light harvesting by

scattering the incident light. In this paper, narrow bandgap PbS nanoparticles and single-crystalline rutile TiO2 nanorod arrays were combined to produce a practical semiconductor-sensitized solar cell. Several sensitizing configurations have been studied, which include the deposition of ‘only PbS’ or ‘only CdS’ and the hybrid system PbS/CdS. Optimized PbS SILAR cycle was obtained, and the uniformly coated CdS layer can effectively minimize the chemical attack of polysulfide electrolytes on PbS layer. Therefore, the performance of sensitized solar cells was stabilized and long lasting. The power conversion efficiency of PbS/CdS co-sensitized solar cell showed an increase of approximately 500% compared with that Oxalosuccinic acid sensitized by only PbS nanoparticles. Methods Growth of TiO2 nanorod arrays by hydrothermal process The TiO2 nanorod arrays were grown directly on fluorine-doped tin oxide (FTO)-coated glass using the following hydrothermal methods: 50 mL of deionized

water was mixed with 40 mL of concentrated hydrochloric acid. After stirring at ambient temperature for 5 min, 400 μL of titanium tetrachloride was added to the mixture. The mixture was injected into a stainless steel autoclave with a Teflon container cartridge. The FTO substrates were ultrasonically cleaned for 10 min in a mixed solution of deionized water, acetone, and 2-propanol with volume ratios of 1:1:1 and were placed at an angle against the Teflon container wall with the conducting side facing down. The hydrothermal synthesis was conducted at 180°C for 2 h.After synthesis, the autoclave was cooled to room temperature under flowing water, and the FTO substrates were taken out, rinsed thoroughly with deionized water, and dried in the open air.

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Female employees with Ku-0059436 research buy neck pain have also shown to have less muscle rest during work (Hagg and Astrom 1997; Sandsjö

et al. 2000). Furthermore, prospective results have shown that perception of muscle tension is a strong risk factor to develop neck pain (Wahlström et al. 2004). Myofeedback of muscular tension may lead to decreased muscle activation and decreased pain. A method for myofeedback was developed within the “Neuromuscular Assessment in the Elderly Worker” (NEW) project (Hermens and Hutten 2002; Voerman et al. 2007). The myofeedback in this case indicates when the upper part of the trapezius has not had enough time for rest. There are studies that confirm that muscle activation patterns are of importance for developing neck pain. One prospective study found an association between pain in the neck area and a reduction in myoelectric rest periods in the trapezius muscle among female workers (Veiersted and Westgaard 1993). Whether work ability will increase due to myofeedback training is not known. An established treatment of non-specific pain in neck is strength training (Hartigan et al. 1996; Hurwitz et al. 2008). Composite observations and empirical findings guided our hypothesis of that intensive muscular strength training

could lead to decreased muscle activation (Sales 1987; Streepey et al. 2010). Earlier studies have reported associations between intensive muscular strength training and a prolonged relief Staurosporine solubility dmso from neck muscle pain (Andersen et al. 2008a). Moreover, that specific strength training was related to an increased activity level in the pain-inflicted muscle, leading to improved function and pain reduction (Andersen et al. 2008b). Intensive muscular strength training

has also been found to be related to an increased function through better nerve muscle coupling and reduced pain through activation of stretch receptors and the release of endorphins (Thoren et Adenosine triphosphate al. 1990; Kannus et al. 1992; Hagberg et al. 2000). Based on these results, it is also plausible that strength training may increase work ability by reducing persistent pain and increasing functional capacity among subjects with work-related neck pain. Whether the muscle activation pattern will change due to strength training has not been investigated in earlier studies, but our hypothesis is that changes in activation patterns of the muscles could be one of the mechanisms involved in the self-rated as well as observed increased muscle function. The overall aim of this randomized controlled trial (RCT) study was to investigate whether rehabilitation of female HSOs on long-term sick leave with chronic neck pain may be facilitated using interventions aimed at changing the activity in the trapezius muscle. A primary aim was to test whether the interventions changed the activity in the trapezius muscle (reported elsewhere).

Given HMB’s capacity to subsequently enhance and depress anabolic and catabolic pathways [16,

22], HMB would be a good candidate as a dietary supplement to partially reverse deficits in net anabolism in sarcopenic muscle following RET. To our knowledge, no research has investigated the effects of HMB on age-related changes in muscle cell (myofiber) size. Moreover, no study to date has compared and contrasted if differential responses AZD1208 nmr exist between young and older individuals to HMB consumption. Therefore, the primary aim of this study was to determine the effects of 16 wk. of HMB administration in young and old rats on age-related changes in body composition, functionality, and myofiber dimensions using advanced ex vivo magnetic resonance (MR) imaging techniques and the potential molecular mechanisms mediating these effects. Methods Animals and overview of experiment All procedures in this study were approved by our institutions Animal Care and Use Committee. Fourteen young (44 wk.), 7 middle aged (60 wk.), 14 old (86

wk.), and 7 very old (102 wk.) male Fisher 344 rats were used in the study. However, death due to the aging process as well as general anesthesia during various imaging processes resulted in a remainder of 12 young (44 wks.), 6 middle aged, which served as the control (60 wk.), 10 old (86 wk.), and 5 very old, which served Tanespimycin order as the control (102 wk.) animals that completed the study (see Figure 1 for timeline), which still met the criteria for our original sample size determination (see power analysis below). Each animal was assessed for functionality (grip strength and motor performance using

incline plane) as well as lean, fat, and total body mass using dual-energy X-ray absorptiometry (DXA) pre- and post-treatment (see Figure 1 for experimental design). After baseline measures, 6 young, 6 middle aged control, 5 old, and 5 very old control rats were anesthetized 17-DMAG (Alvespimycin) HCl and their right gastrocnemius (GAS) and soleus (SOL) muscles were isolated, blotted, and quickly frozen in liquid nitrogen for later in vitro molecular analysis. After isolating muscles from the right hind limb, a cardiac perfusion protocol was implemented to drain blood from the rat’s body. Following, the left GAS and SOL muscles of the rats were harvested and directly immersed in 4% paraformaldehyde for an ex vivo analysis of myofiber dimensions. Remaining young (44 wk.) and old (86 wk.) rats were given HMB (0.46 g/kg/d) for 16 wk. After the supplementation period, the remaining rats were assessed for post-treatment measures in body composition and functionality and then sacrificed for in vitro molecular and ex vivo MR analyses. Figure 1 Schematic of experimental timeline for the experiment. HMB administration All animals were raised in our laboratory prior to experimentation, therefore giving us a strong basis for how much HMB should be added to their food.

Loss of heterozygosity at 7p21 in adult renal tumors Three of the 36 adult patients samples analyzed showed LOH in the 2.4 Mb region of interest (Figure 2). Two of these patients had clear cell renal carcinoma (RCC-1 and RCC-614); while one had a less common oncocytoma (RCC-635). Patient RCC-614 showed LOH

over much of the area, while RCC-1 and RCC-635 showed LOH at approximately 15-20% of informative SNPs. Direct sequencing of SOSTDC1 exons in adult tumors also showed LOH in patients RCC-614 and RCC-635 in several locations of exon 1 (Table 1). Additionally, patients RCC-129 and RCC-737 also showed LOH in one SNP each. The adult tumors displaying LOH did so at some but not all loci, HM781-36B even within the SOSTDC1 gene itself. This is in contrast to what was observed within the Wilms tumors, where the samples with LOH displayed complete LOH at every heterozygous allele. Among all samples (adult and pediatric), LOH within SOSTDC1 was

observed mostly in the putative exon 1, with no observed heterozygosity loss in the regions of the gene that are known to be transcribed. Whether adult or Wilms, for each SNP that showed LOH in more than one sample, the same allele was lost. For example, at the beginning of exon 1 (position 16,536,641) the G is absent from the C/G in RCC-614 and RCC-635 (Table 1). Impact of SOSTDC1 LOH on protein expression We hypothesized that SOSTDC1 LOH might lead to decreased protein expression in the RCC and Wilms tumor samples. To RNA Synthesis inhibitor address this possibility, the SOSTDC1 protein expression of tumor samples with and without LOH at SOSTDC1 was analyzed by immunohistochemistry. Antiserum from rabbits immunized with a peptide corresponding to the 18 C-terminal amino

acids of the SOSTDC1 protein was used for this analysis. The antiserum has much been used previously in an immunohistochemical application and additional characterization is included ([16]; see Additional file 4). When tumor samples were stained for SOSTDC1, the protein showed defined perinuclear and diffuse cytosolic localization in both adult and pediatric renal tumors. Representative images are shown in Figure 3. SOSTDC1 expression was not markedly reduced within tumor samples with SOSTDC1 LOH in either Wilms tumors or RCC [compare Wilms -LOH (W-8178) to Wilms +LOH (W-733) in Figure 3A and adult renal tumors -LOH (RCC-347) to +LOH (RCC-614) in Figure 3B]. Other samples with SOSTDC1 LOH similarly exhibited no observable variations in SOSTDC1 protein expression or localization. As the SOSTDC1 -specific LOH in these samples was largely in the putative or regulatory exon 1 (Table 1), this observation is not necessarily unexpected. Figure 3 Immunohistochemical analyses of SOSTDC1 and β-catenin protein levels and localization. A) Pediatric Wilms tumor samples and B) adult renal cell carcinoma samples with and without SOSTDC1 LOH were stained with antibodies directed against SOSTDC1 and β-catenin.

In the dairy lactic bacterium S. thermophilus, the PrtS subtilisin-like proteinase degrades casein into peptides, which are required for efficient growth [27, 28]. S. agalactiae is a major causal agent of mastitis in cattle [29] and is the principal cause of neonatal meningitis [30]. The CspA subtilisin-like proteinase of this pathogenic streptococcus is considered to be a critical selleck compound virulence factor [22]. This proteinase has been shown to be involved in bacterial virulence in a neonatal rat sepsis model and in resistance to opsonophagocytic killing by human neutrophils in vitro

[22]. More recently, the CspA of S. agalactiae has been shown to hydrolyze and inactivate CXC chemokines, many of which can recruit neutrophils to sites of infection [31]. Bacterial pathogenicity is a complex process that depends on the ability of the pathogen to multiply. The S. suis subtilisin-like proteinase appears to contribute to nutrient acquisition given that proteinase-deficient mutants had longer generation times than the parent strain in vitro. This is consistent with the study of Courtin et al. [28], who reported that the PrtS subtilisin-like proteinase of S. thermophilus is involved in nitrogen supply through casein hydrolysis. The mutants and the wild

type strain were also compared for their ability to survive in human whole blood. We found that the parent strain was much more resistant to killing than the mutants. This suggests that the proteinase may degrade human serum proteins with bactericidal activity or opsonins involved in phagocytosis by immune cells. This is in agreement with

the study of Harris et al. [22], who Selleckchem SB203580 reported that the CspA subtilisin-like proteinase of S. agalactiae, which shares a high degree of identity with S. suis, contributes to the resistance to phagocytosis by neutrophils. Given its cell surface localization, the subtilisin-like proteinase of S. suis may interact with host cells and induce an inflammatory response which is a feature of meningitis. Indeed, Morin Hydrate the S. suis proteinase may activate protease-activated receptors (PAR), which are members of the G protein-coupled receptors also known as seven-transmembrane domain receptors [32]. These receptors are found on several cell types and play an important role in inflammatory processes. More specifically, PAR-2 is known to be activated by serine proteases and bacterial proteinases [33]. Since S. suis cells are known to induce the production of pro-inflammatory cytokines by endothelial cells [34] and macrophages [35], part of this activation may be caused by the cell surface subtilisin-like proteinase identified in this study. Studies are currently in progress in our laboratory to verify this hypothesis. In a previous study, we reported that the presence of fibrinogen during growth of S. suis modulates its capacity to form a biofilm [36]. Given the ability of bacterial subtilisin-like proteinases to degrade fibrinogen [22, 37, 38], it may be hypothesized that the proteinase of S.

To further investigate if the capsular polysaccharide accumulated in the cell, as would be anticipated if the exportation of capsule were interrupted, immunoblots and stains-all/silver stain with different cell fractions were performed (Figure 6). There was no difference in K-antigen present outside or inside the cells between the Δwzabc mutant and the wild type. Therefore, our results suggested that the wza, wzb and wzc exportation system was not required by either K6-antigen or O3-antigen production in V. parahaemolyticus O3:K6. Figure

6 Immuno blot and stains-all/silver-stain of cell fractions. Outer membrane (OM) and cytoplasmic (CP) fractions were separated on polyacrylamide gel, then were either transferred to PVDF membrane and probed with K6 specific antiserum (A), or stained with stains-all/silver KU-57788 mouse stain (B). Lane1, wild type CP; lane 2, ∆wzabc CP; lane 3, ∆EPS CP; lane 4, wild type OM; lane 5, ∆wzabc OM; lane 6, ∆EPS OM. However, a K-antigen processing system similar to the O-antigen/capsule

polysaccharide genes in V. cholerae O139 [13, 20, 21] is present in V. parahaemolyticus. VP0219-0221 are homologous to wbfE, wbfF and wzz genes in V. cholerae O139, sharing 49%, 69% and 54% amino acid identities. Therefore a similar capsule processing mechanism may exist for both taxa. We generated an in frame deletion of VP0220, the wbfF homolog. Mutant ∆0220 displayed an intermediate level of translucence. Immunoblots indicated that deletion of VP0220 did not affect O3 antigen synthesis (Figure 4). However, the midpoint of the K-antigen band shifted selleckchem in this mutant, suggesting a role of VP0220 in the later Abiraterone datasheet stage of the K-antigen processing. Complementation of ∆0220 with over expressed wild type VP0220 gene restored mostly the pattern of the wild type K antigen (Figure 4). However, there was more reactive material away from the midpoint of the K-antigen band in the complemented mutant than the wild type (Figure 4), possibly due to the over expression of VP0220 or other reasons that remain unclear. Other K-antigen region features

A complete set of genes of the rhamnose pathway rmlBADC are present in the K-antigen genes of V. parahaemolyticus. However, four open reading frames, VP0225-0228, are inserted between the rmlD and rmlC genes. Analysis of the GC percentage revealed that the average GC percentage in VP0225-0228 is lower than the rest of the genes in this operon (Figure 2). The unusual arrangement of the rhamnose gene order and the mosaic GC percentage pattern indicated that there was a recent recombination event in the K antigen genes. Between gmhD and the K-antigen operon like genes, there are four genes (VP0215-0218) transcribed to the opposite direction (Figure 2). In frame deletion of these four genes led to the over expression of K-antigen polysaccharides (Figure 4), suggesting these genes may have a regulatory role in capsule expression.

All sequences were analyzed with RDP3 and GARD software to detect the recombinants. The analysis in silico displayed the recombinants and one parental

strain. B) The E protein gene from MEX_OAX_1656_05 was cloned in TOPO TAV4 to detect possible recombinants and/or the parental sequences. One parental sequence was detected in addition to one recombinant. The first task in this phylogenetic analysis was to determine the best model of nucleotide substitution for DENV-2 virus sequence evolution. This assignment was undertaken using the Model LY294002 mouse Selection test from DataMonkey online server [28, 29], which compares 201 models of DNA substitution. Our results demonstrated that the best model was TrN93 [30]. Accordingly, the most complex general time-reversible value was the best fit to the data (relative substitution rates of A↔C = 0.057, A↔G = 1, A↔T = 0.057, C↔G = 0.057, C↔T = 1, and G↔T = 0.057); the Ln likelihood = -4550.59; parameter count = 38;

and AIC = 9177.19. Finally, the estimated base composition was A = 0.340, C = 0.278, G = 0.225, and T = 0.157. Our analysis with RDP3 showed that the sequences of isolate MEX_OAX_1038_05 and MEX_OAX_1656_05 present statistical evidence of recombinants for GENECOV (P-Val = 2.467 × 10-2), BOOTSCAN (P-Val = 4.289 × 10-5), MAXCHI (P-Val = 1.438 × 10-5), CHIMERA (P-Val = 3.790 × 10-3), SISCAN (P-Val = 1.108 × 10-9), and DNA ligase 3SEQ (P-Val = 4.478 × 10-4), in two regions (Figure 2): the first breakpoints were located in 499nt and 512nt respectively; the second breakpoints were located in BGB324 concentration 868nt and 826nt respectively, and the third breakpoint was located in 2239nt in both recombinants (Figure 2A, 2B respectively). In addition, the analysis with GARD confirmed the breakpoints and recombination data for maximum likelihood. This analysis

displayed the same site for the three breakpoints in both isolates: the first, second and third breakpoints were located in the nucleotides 498, 828 and 2226, respectively (Figure 2C). The recombinant regions were the intersection of prM-M structural gene to intersection of M-E structural genes and the second recombinant region started in the intersection of E-NS1 genes (Figure 2D). Interestingly, we found that the parental major strain was the non-recombinant clone MEX_OAX_1656_05_ C241 (obtained from the MEX_OAX_1656_05 isolate) and the minor parental strain was the Cosmopolitan genotype strain INDI_GWL_102_01 (accession number DQ448235). Figure 2 Recombination plots of structural gene regions from MEX_OAX_1038_05 and MEX_OAX_1656_05 sequences. A) BOOTSCAN plot analysis of the C(91)-prM-E-NS1(2400) gene sequences from the MEX_OAX_1038_05 isolate and the parental strains INDI_GWL102_01 and MEX_OAX_1656_05_C241.

36 respectively. Table 2 Semi-quantitative analysis of mdr1 and MRP in A549 cells, A549 MTS after irradiation, and MCF7/VCR cells Type of cells Mdr1/β2-MG MRP/β2-MG A549 parent cells in single-layer 0 0.76 A549 MTS 0 0.62

A549 MTS, d-9 after 15 Gy32P irradiation [11] 0 0.54 A549 MTS, d-9 after 15 Gy X-ray irradiation [11] 0 0.34 A549 MTS, d-4 after 30 Gy X-ray irradiation[6] 0 0.70 A549 re-proliferated radioresistant cells 0 0.78 MCF7/VCR resistant cells 35 4.36 Discussion In this study, re-proliferated cells derived from post-irradiated A549 lung adenocarcinoma MTS were used for an investigation of the disparity of drug Selleck Raf inhibitor sensitivity between the radioresistant cells and their parent cells. It is of great significance for the rational option of chemotherapeutic programs for relapsed cancer after HM781-36B order radiotherapy. The living cell number of A549 MTS became decreased after a medium dose of irradiation, and their mdrl and MRP gene expression levels examined by RT-PCR became temporarily reduced, subsequently showed little variation with their parent

cells after re-proliferated. In mono-layer culture, A549 re-proliferated radioresistant cell was resistant to DDP, but sensitive to VDS, 5-Fu, HCP, MMC and ADM. The sensitivity to the 6 kinds of chemotherapeutic drugs between the radioresistant cells and their parent cells were almost the same, but the radioresistant cells was resistant to high concentration of VPL, however their parent cells were sensitive to it. The mdrl and MRP multi-drug resistant gene expression in MCF7/VCR cells showed a very high level. Moreover, the cells which were resistant or had low sensitivity to a variety of chemotherapeutic agents showed a higher sensitivity to high concentration of VPL than A549 re-proliferated

radioresistant cells. VPL had not significant cell toxicity in a concentration of 10 μg/ml. It was found that a high concentration of VPL was needed for the in vitro reversion experiment of drug-resistance. In this article, the concentration of 200× PPC of VPL was used for in vitro experiment. If intra-arterial infusion or chemotherapeutic embolism were used for solid tumor, such a high local concentration can be achieved in the tumor without affecting the general dose and PPC in the body. According to Non-specific serine/threonine protein kinase comparative analysis, the reduction of sensitivity of A549 re-proliferated radioresistant cells to VPL was not due to the levels of mdrl and MRP multidrug resistant genes. It has been reported in literature that the over-expression of GSH transferase (GST) pi protein in the MCF-7 cells after irradiation leads to an increase of VCR-resistance by 5-times, and the resistance to VP-16 increased by 3-times. In MCF-7 drug resistant sub-line, the selective resistance to some drugs may be related to an increase of the intracellular GST activity [15].

“Fulvoincarnati” A.H. Sm. & Hesler, Lloydia 2: 36 (1939), invalid, Art. 36.1]. Pileus glutinous to viscid, pallid, tinted yellow, salmon-buff, fulvous, reddish brown in center; lamellae subdecurrent, subdistant, white or pallid; stipe glutinous or viscid, pallid, apex dry floccose-fibrillose. Phylogenetic support GS 1101 We included only H. arbustivus in our ITS analysis. In the four-gene analysis presented

by Larsson (2010; unpublished data), subsect. Fulventes (H. arbustivus, H. carpini, H. leucophaeo-ilicis, H. lindtneri, H. roseodiscoideus, and H. unicolor) appears as a paraphyletic grade basal to subsect. Hygrophorus (54 % MPBS support for basal branch). Species included Type species H. arbustivus. Hygrophorus GSK-3 signaling pathway carpini Gröger, H. leucophaeo-ilicis Bon & Chevassut, H. lindtneri M.M. Moser, H. roseodiscoideus Bon & Chevassut and H. unicolor Gröger are included based on morphological and phylogenetic data. Comments Singer (1986) and Kovalenko (1989, 1999, 2012) placed the type of

subsect. Fulventes together with species from sect. Pudorini in subsect. Fulvoincarnati A.H. Sm. & Hesler (1939)[invalid] making it polyphyletic. Bon (1990) and Candusso (1997) placed a similar mixture of species in sect. Fulventes (Fr.) Bon. [invalid] Series Fulventes (Hesler and Smith 1963, invalid because basionym was three words) and is consequently also polyphyletic. Hygrophorus [subgen. Hygrophorus ] sect. Discoidei (Bataille) Konrad & Maubl., Icon. Sel. Fung. 6: 428 (1937). Type species: Hygrophorus discoideus (Pers. : Fr.) Fr., Epicr. syst. mycol. (Upsaliae): 323 (1838) [1836–1838] ≡ Agaricus discoideus

Pers., Syn. meth. fung. (Göttingen) 2: 365 (1801) : Fr. Basionym: Hygrophorus [unranked] Discoidei Bataille, Mém. Soc. émul. Doubs, sér. 8 4: 162 (1910). Pileus viscid when moist, pale yellowish brown, fulvous, sometimes with a gray tone, or disc reddish brown; lamellae, concolorous, sometimes with a violaceous gray tone; stipe viscid, pale or fulvous, sometimes with a gray tinge, apex floccose-fibrillose. until Phylogenetic support Sect. Discoidei is only represented by the type species in our Supermatrix and LSU analyses, and H. subviscifer in our ITS analysis. In the analysis presented by Larsson (2010; unpublished data), sect. Discoidei is a monophyletic clade with 100 % MPBS. Species included Type species: H. discoideus. Hygrophorus subviscifer (P. Karst.) Harmaja is included based on morphology and phylogeny. Comments Bataille (1910) included H. arbustivus (the type of subsect. Fulventes) and H. mesotephrus (sect. Olivaceoumbrini) along with the type in Discoidei. Series Discoidei (Hesler and Smith 1963) and sect. Discoidei (in Singer 1986; Kovalenko 1989, 1999, 2012; Arnolds 1990) are also polyphyletic. Bon (1990) only included H. roseodiscoideus (from the adjacent sect. Fulventes) in subsect. Discoideini Bataille [invalid]. Similarly, Candusso (1997) included H. roseodiscoideus and H. lindtnerii from the adjacent sect. Fulventes, (listing H.