PubMedCentralPubMedCrossRef 17. Sharp CP, Pearson DR: Amino acid supplements and recovery from high-intensity resistance training. J Strength Cond Res 2010, 24(4):1125–1130.PubMedCrossRef 18. da Luz CR, Nicastro H, Zanchi NE, Chaves DFS, Lancha AH: Potential therapeutic effects of branched-chain amino acids selleckchem supplementation on resistance exercise-based muscle damage in humans. J Int Soc Sports Nutr 2011, 8:23.PubMedCentralPubMedCrossRef 19. Graham TE: Caffeine and exercise: metabolism, endurance and PARP inhibitor performance.

Sports Med 2001, 31(11):785–807.PubMedCrossRef 20. Hackman RM, Havel PJ, Schwartz HJ, Rutledge JC, Watnik MR, Noceti EM, Stohs SJ, Stern JS, Keen CL: Multinutrient supplement containing ephedra LEE011 and caffeine causes weight loss and improves metabolic risk factors in obese women: a randomized controlled trial. Int J Obes 2006, 30:1545–1556.CrossRef 21. Molnar D, Torok K, Erhardt E, Jeges S: Safety and efficacy of treatment with an ephedrine/caffeine mixture. The first double-blind placebo-controlled pilot study in adolescents. Int J Obes Relat Metab

Disord 2000, 24(12):1573–1578.PubMedCrossRef 22. Greenway FL, De Jonge L, Blanchard D, Frisard M, Smith SR: Effect of a dietary herbal supplement containing caffeine and ephedra on weight, metabolic rate, and body composition. Obes Res 2004, 12(7):1152–1157.PubMedCrossRef 23. Goldstein ER, Ziegenfuss T, Kalman D, Kreider R, Campbell B, Wilborn C, Taylor L, Willoughby D, Stout J, Graves BS, Wildman R, Ivy JL, Spano M, Smith AE, Antonio J: International society of sports nutrition position stand: caffeine and performance. J Int Soc Sports Nutr 2010, 7:5.PubMedCentralPubMedCrossRef 24. Woolf K, Bidwell WK, Carlson AG: The effect of caffeine as an ergogenic aid in anaerobic exercise. Int J Sport Nutr Exerc Metab 2008, dipyridamole 18(4):412–429.PubMed 25. Kreider RB, Ferreira M, Wilson M, Grindstaff P, Plisk S, Reinardy J, Cantler E, Almada AL: Effects of

creatine supplementation on body composition, strength, and sprint performance. Med Sci Sports Exerc 1998, 30(1):73–82.PubMedCrossRef 26. Woolf K, Bidwell WK, Carlson AG: Effect of caffeine as an ergogenic aid during anaerobic exercise performance in caffeine naïve collegiate football players. J Strength Cond Res 2009, 23:1363–1369.PubMedCrossRef 27. Zoeller RF, Stout JR, O’Kroy JA, Torok DJ, Mielke M: Effects of 28 days of beta-alanine and creatine monohydrate supplementation on aerobic power, ventilator and lactate thresholds, and time to exhaustion. Amino Acids 2007, 33(3):505–510.PubMedCrossRef 28. Sale C, Saunders B, Harris RC: Effects of beta-alanine supplementation on muscle carnosine concentrations and exercise performance. Amino Acids 2010, 39(2):321–333.PubMedCrossRef 29. van Loon LJC, Oosterlaar AM, Hartgens F, Hesselink MKC, Snows RJ, Wagenmakers AJM: Effects of creatine loading and prolonged creatine supplementation on body composition, fuel selection, sprint and endurance performance in humans. Clin Sci 2003, 104:153–162.

001) difference in growth as compared to WT, which had survived better during this time period. The mutant MAV_5106

largely differed from other mutants and during four days of infection had shown constant survival (Figure  6 B). The capacity of mutant MAV_5106 to survive better in macrophages suggests that it may be characterised by a higher virulence as compared to the other mutants. Tateish et al.[70] compared the virulence of different M. avium isolates in humans, immuno-competent mice and THP-1 cells. They found that the strain causing the most serious disease in humans and the highest bacterial load in mouse lungs also grew better in THP-1 cells than the other strains tested. According to this, the mutants MAV_4334, MAV_1778 and MAV_3128 may display reduced virulence and the corresponding genes may represent virulence-associated genes. Figure 6 Intracellular https://www.selleckchem.com/products/cb-839.html survival of mutants compared to WT in human monocytes. Human blood monocytes (1.0×106) from healthy volunteers were infected (MOI 10) with mutants and WT. BVD-523 nmr Intracellular bacteria were quantified after 4 hour of infection, and after 1, 2, & 4 days. The monocytes were lysed in 1 ml of sterile water and 100 μl of 1:500 dilution in sterile water of sample were plated on Middlebrook agar plates supplemented with ADC for CFU counting. A: WT and mutant MAV_4334; B: WT and mutant MAV_5106; C: WT and mutant MAV_1778; D: WT and mutant MAV_3128. Statistical

analysis was done using a two tailed, paired Student’s t test. When compared to wild-type a P < 0.05 was considered significant (*) and a P < 0.01 very significant (**). Evaluation of the screening procedure We have employed five screening methods (colony morphology, pH stress resistance, amoeba resistance, cytokine induction, intracellular survival) to select mutants affected in virulence-related traits. Two mutants (MAV_4334 and MAV_3128) responded differently from the WT in four of these five screening tests and two mutants (MAV_5106 and MAV_1778) reacted differently in three screening tests. The most prominent differences

were exhibited by mutant MAV_3128. The other mutants either did not show any differences compared to the WT or reacted differently in only one or two tests. The insertions HSP90 in mutants MAV_4334, MAV_5106, MAV_1778 and MAV_3128 have been mapped and the structure of the mutated regions has been analyzed on nucleotide level. In all cases only one gene has been Z-VAD-FMK mw mutagenised. The insertions are located in the genes MAV_4334 (nitrogenase reductase family), MAV_5106 (phosphoenolpyruvate carboxykinase), MAV_1778 (GTP-binding protein LepA) and MAV_3128 (lysyl-tRNA synthestase LysS). Phosphoenolpyruvate carboxykinases (PEPCK) catalyse the reversible decarboxylation and phosphorylation of oxaloacetate to form phosphoenolpyruvate. Mutations of the PEPCK gene from M. bovis BCG are characterised by attenuated virulence and reduced survival in macrophages [72]. The PEPCK gene from M.

To understand the effects of https://www.selleckchem.com/products/3-methyladenine.html cobalt precursor on electrochemical performance of the corresponding AZD1152 in vitro Co-PPy-TsOH/C catalysts, many physicochemical techniques have been employed in this work. Figure 4 presents XRD patterns of the Co-PPy-TsOH/C catalysts prepared from various precursors, the standard data for CoO and α-Co are also shown for comparison. Four apparent characteristic peaks can be clearly observed at 2θ of 24.5°, 44.2°,

51.5°, and 75.8° in all of the synthesized catalysts, which could be assigned to C(002), Co(111), Co(200), and Co(220) plane. This suggests that cobalt in the Co-PPy-TsOH/C catalysts exists mainly as metallic α-Co with face-centered cubic (fcc) structure. The Co(111) and Co(200) peaks become sharper and sharper with the order of cobalt acetate, cobalt nitrate, cobalt chloride and cobalt oxalate, implying a growth in the crystallite size of metallic cobalt. Generally, an average crystallite size, d, can be estimated with the Shcherrer equation [27, 28]: (4) where λ is the wavelength of incident X-ray, θ is the incident angle of X-ray for a

specific mirror, and B is the half-peak width. In order to avoid the interference of CoO on the Co(111) plane, the Co(200) plane was adopted in this study to calculate the crystallite size of metallic cobalt. The calculated specific values are listed in Table 1. It can be inferred that the relativity of the crystallite size of metallic cobalt in the catalysts is exactly opposite to the trend of ORR performance. PS-341 supplier In addition, Baf-A1 two weak diffraction peaks observed at 2θ of 36.5° and 42.2° indicate the co-existence of a very small amount of CoO (PDF 43–1004) in the catalysts. Therefore, it could be figured out that the crystallite size of metallic cobalt in the catalysts has essential influence on the catalytic performance towards ORR, the smaller the crystallite size, the better the performance. A small-amount co-existence of CoO in the catalysts does not have an adverse effect on the performance. But on the contrary, it is probably that the synergetic effect between metallic cobalt and the oxide may effectively enhance

the catalytic performance as presented by previous researches [29, 30]. Figure 4 XRD patterns of Co-PPy-TsOH/C catalysts prepared from various cobalt precursors. Table 1 Crystallite size of metallic cobalt in Co-PPy-TsOH/C catalysts prepared from various cobalt precursors Cobalt precursor Crystallite size of metallic co/nm Cobalt acetate 0.4253 Cobalt nitrate 0.4947 Cobalt oxalate 0.6432 Cobalt chloride 0.6099 Figure 5 displays TEM images of the Co-PPy-TsOH/C catalysts prepared from various precursors. Small and uniformly distributed metallic cobalt particles can be clearly seen in the catalyst with cobalt acetate as precursor. Yet, when cobalt nitrate is used as the precursor, serious agglomeration of the catalyst particles can be found, the particle size even reaches as large as 50 nm.

In the case of tetracycline-resistant isolates, all were SmaI-restricted, generating 30 pulsotypes with a similarity range of 42.16 to 100.0% (Figure 1). The Sma10a emm77T28 and Sma64 emm11T11 pulsotypes may be associated with tetracycline resistance since 100% of these isolates were resistant to

this antibiotic. All co-resistant (erythromycin #learn more randurls[1|1|,|CHEM1|]# and tetracycline) isolates were SmaI-restricted. Discussion Several reports show that GAS resistance to macrolides and tetracyclines are high some countries such Spain and continue to increase; indeed, they have become clinically problematic. In Europe, the most northerly countries (with the exception of Finland) have reported low levels of resistance (<4%) [5] while strong resistance has been reported from Mediterranean countries such as Italy (22,6%), France (22.4%), Greece (24.0%),

Spain (21.3%) and Portugal (26.6%) [6–10]. This values contrast with those of Israel (1.8%) and Iran (0.2%) [11, 12]. In our study, 32.8% of isolates showed resistance to macrolides. Efflux pumps (M phenotype) are one of the major mechanisms conferring resistance to macrolide antibiotics, and streptococci making use of this system have been commonly reported from European countries, Argentina, the USA and Canada [5, 13–15]. The M phenotype has been identified as predominant in several Spanish studies, reaching a rate of 95.6% in a multicentre study undertaken in 1998 or 64.5% in an extensive national GSK621 in vivo multicenter surveillance study in 2006–2007 [16, 17]. In the present population, the efflux system was also the main macrolide resistance mechanism seen, being manifested by 76.9% of isolates. cMLSB phenotype, another common phenotype reported in Europe [18], was displaced Selleckchem Depsipeptide by the M phenotype in several European countries from 1990 [10, 19]. In our study, cMLSB phenotype was the second most commonly encountered (20.3%) like SAUCE project carried out in 2006–2007 [17]. In this last

report, flutuations in the rates of resistance to macrolides are observed (1996–1997: 26.7%; 1998–1999: 20.4%; 2001–2002: 24.3; 2006–2007: 19%) meanwhile there is an increasing trend in the prevalence of MLSB phenotype from 14% in 2001–2002 to 35.5% in 2006–2007 [17]. Among Spanish isolates of this work, iMLSB phenotype was minority (2.7%) in contrast to Norway (75%) (1993–2002) or Bulgaria (57.7%) (1993 – 2002) where it was reported the most prevalent phenotype [5]. A gene-phenotype correlation previously described was also noticed [3, 9]. mef(A) and erm(B) were predominant in isolates with the M and cMLSB phenotype respectively, whereas all isolates with the iMLSB phenotype harboured the erm(A) gene. The mef(A) gene responsible for the M phenotype was detected in all but three of the present Spanish isolates with that phenotype.

Figure 7 Transcriptional expression patterns of the three Bdellovibrio chaperonin genes during axenic Host-Independent growth. RT-PCR with transcript specific

primers was carried out on matched concentrations of RNA (matched by Nanodrop spectrophotometer readings) from axenically grown Host-Independent Bdellovibrio. Three independently isolated strains of each sigma factor mutant and each host-independent (HI) wild-type were used to account for HI strain-to strain variation. L- NEB 100 bp ladder –ve – no template negative control + ve- HD100 genomic DNA positive control. Conclusions We have shown that of three B. bacteriovorus HD100 sigma factor genes with at least partial rpoE homology, one- bd3314, Crenigacestat concentration is likely essential for Bdellovibrio cell life and cannot be deleted. bd0881 and bd0743 can be deleted with the Bdellovibrio retaining the ability to grow predatorily or prey-independently. In the case of ΔBd0881 the AZD1480 cost predatory efficiency was reduced,

despite the flagellar motility of the mutant being slightly increased, (despite a slight but statistically significant shortening of Nutlin 3a flagellar filament length) thus the change in predation efficiency may not be due to motility changes but regulation of other predatory genes. The bd0881 gene has an expression pattern across the predatory cycle that is similar to that of the flagellin genes whose expression is required for Bdellovibrio

motility. That bd0881 expression is turned off and then resumes at a similar time to flagellin gene expression, during the predatory cycle, implies http://www.selleck.co.jp/products/abt-199.html that Bd0881 may have a role associated with pre-septation developmental maturation of Bdellovibrio around the time that flagella are being built in newly dividing cells. However the Bd0881 sigma factor does not directly regulate the expression of fliC flagellin or mot flagellar motor genes themselves. Surprisingly, predatory efficiency was not affected in our cultures by the slower swimming speed of the ΔBd0743 sigma factor mutant; this is probably indicative of sufficient mixing of predator and prey at close quarters in lab conditions. The slight increase in flagellar length in ΔBd0743 mutants is likely to have come with the incorporation of a higher percentage of a less rigid flagellin in the flagella causing a less efficient “bow wave” and this may account for the slower swimming. In both the ΔBd0743 and ΔBd0881 mutants, small but significant changes in swimming speed were paradoxically associated with changes apparently in the wrong direction in flagellar length. This shows that it is not simply flagellar length that governs the thrust produced by flagellar propellers.

Tumor Biol 2013,34(3):1337–1347.CrossRef 23. Delgado PO, Alves BC, Gehrke Fde S, Kuniyoshi RK, Wroclavski ML, Del Giglio A, Fonseca FL: Characterization of cell-free circulating DNA in plasma in patients with prostate cancer. Tumor Biol 2013,34(2):983–986.CrossRef 24. Diamandis EP: Prostate cancer screening with prostate-specific antigen testing: more answers or more confusion? Clin Chem 2010,56(3):345–351.PubMedCrossRef 25. Shariat SF, Karakiewicz PI, Suardi N, Kattan MW: Comparison of nomograms with other methods for predicting outcomes in prostate cancer: a critical analysis of the literature. Clin Cancer GSK621 nmr Res 2008,14(14):4400–4407.PubMedCrossRef

Competing interests The authors declare that they have no competing interests. Authors’ contributions ZH, QC and XY conceived and designed the study, performed the experiments and wrote the paper. ZH and XY contributed to the writing and to the

critical reading of the paper. ZH, QC, LL performed patient collection and clinical data interpretation. ZH and LL participated performed the statistical analysis. All authors read and approved the final manuscript.”
“Introduction Nasopharyngeal carcinoma (NPC) is an epithelial malignant tumor with a high incidence in southern China and Southeast Asia. Radiotherapy is a dominant treatment approach for NPC. Primary tumor volume (GTV-P) is known to be positively correlated with the prognosis of NPC [1, 2]. Despite recently increased use of intensity-modulated radiation therapy (IMRT), GTV-P is still an mTOR inhibitor independent Z-IETD-FMK solubility dmso prognostic indicator for treatment outcome of NPC, and has correlations with T classification, cervical lymph node metastasis as well Ureohydrolase as post-treatment distant metastasis [3, 4]. Tumor volume is known to be positively correlated with the proliferation ability of tumor cells. Thus further understanding of molecular mechanisms underlying abnormal proliferation of NPC cells will help develop novel options for the diagnosis, therapy and prognosis of NPC. Metastasis-associated gene 1 (MTA1) has been implicated in the carcinogenesis and metastasis of

a variety of human cancers [5–7]. In particular, recent studies suggest the prognostic value of MTA1 in NPC because MTA1 overexpression was an independent prognostic factor for poor overall survival of NPC patients [8, 9]. Our recent study provided direct evidence that MTA1 regulated actin cytoskeleton reorganization to promote NPC metastasis [7]. However, the role of MTA1 in NPC cell proliferation is not clear. In the present study, we employed both gain and loss of function approaches to investigate the role of MTA1 in NPC growth. We examined the effects of MTA1 overexpression or knockdown on NPC cell proliferation, cell-cycle distribution, and colony formation in vitro. In addition, we evaluated the effects of MTA1 knockdown on NPC xenograft growth in nude mice.

The suspensions obtained from each soil samples were seeded onto nutritive plates, and incubated in triplicate over a range of temperatures (4, 10, 15 and 22°C). After 30–90 days of incubation, approximately 30 to 60 yeast-like colonies developed on each plate. In contrast, no colonies or low colony numbers (4 to 8) appeared on plates from water samples. Because large numbers of

isolates were obtained, isolates were grouped according to their isolation growth temperature and colony characteristics such as pigmentation, texture, elevation and size. Among the 64 groups, several differed only by isolation growth temperature. These isolates were buy I-BET-762 grown at different temperatures and re-grouped according to macromorphological characteristics at their optimal growth temperature. In this way, 35 groups were ultimately generated. Several isolates from each group (at least one isolate per sampling site; a total of 78 isolates) were selected for molecular and biochemical analyses. Molecular identification of yeasts The chromosomal DNA was purified from cultures of each yeast isolate and the D1/D2 region of 26S rDNA and the ITS1-5.8S- ITS2 (hereafter designated the ITS region for simplicity) regions of the rDNA were amplified OSI-027 chemical structure by PCR. The amplicons obtained were purified from gels and sequenced on both strands. Isolates showing 100% identity in both rDNA sequences

were grouped and their DNA sequences were submitted to GenBank under the accession numbers Anlotinib ic50 listed in Table 1. Species identification was performed

by comparison with the GenBank references, using as criterion the Blast-hits with ≤ 0.5% difference with the query [14]. In 84% of the isolates the closest Blast-hits obtained for both rDNA sequences were coincident. When this NADPH-cytochrome-c2 reductase was not the case, the D1/D2 results were used for identification because they yielded higher identity percentages than did the ITS (see Additional file 1). 76% of the isolates could be identified to species level by this molecular analysis. 22 species belonging to12 genera were identified, of which 80 and 20% were Basidiomycetes and Ascomycetes, respectively. The genera containing the highest number of species were Mrakia (5 species) and Cryptococcus (4 species). However, the species Sporidiobolus salmonicolor was the most abundant, being identified in 24 isolates from 13 different sampling sites. Mrakia gelida was the only yeast species present in both water and soil samples. Of the three isolates identified as Leuconeurospora sp., two of them (T11Cd2 and T27Cd2) possessed identical D1/D2 and ITS sequences, both of which differed from the third (T17Cd1) by 0.7%. However, the macromorphological characteristics of the three isolates, including pigmentation, differed markedly under identical culture conditions (see Additional file 2). Because of these discrepancies, the molecular and morphological analyses were repeated several times, but the results were highly consistent.

For the study of electrical transport in amorphous semiconductors,

especially chalcogenide glasses, dc conductivity is one of the important parameters. The dc conductivity of chalcogenide glasses depends on the combination of starting components, synthesis conditions, rate of melt annealing, purity of starting components, thermal treatment, and on some other important factors. The electrical conduction process in amorphous semiconductors is generally governed by the three mechanisms namely (1) the transfer of charge carriers between delocalized states in the conduction band (E > E c) and valence band (E < E v), (2) transitions of charge carriers in the band tails, and (3) the hopping of charge carriers between delocalized states in bands near the Fermi find more level (E F). To explain the conduction mechanism in amorphous semiconductors, studies on check details temperature dependence

of conductivity is reported by various workers [54–57]. It is understood that conduction in chalcogenide glasses is intrinsic [58, 59] and that the Fermi level is close to the midway of the energy gap. Intrinsic conduction of amorphous semiconductors is determined by carrier hopping from the states close to the edge of the valence band to localized CB-839 in vivo states near the Fermi level or from the state near the Fermi level to the conduction band. The suitable conduction mechanism is decided depending on the predominant process. In the case of chalcogenide glasses, the Fermi level is somewhat

shifted from the middle of the energy gap toward the valence band [60]. In the present work, we have also studied the temperature dependence of dc conductivity of thin films of a-(PbSe)100−x Cd x nanoparticles over the temperature range of 297 to 400 K. From the variations of dc conductivity with temperature, it is found that the experimental data for the entire temperature range is fitted well with the thermally activated process model. To elucidate the conduction mechanism in the present sample of a-(PbSe)100−x Cd x nanoparticles, we have applied the thermally activated process for the temperature over region of 297 to 400 K. The plot of ln σdc versus 1000/T for the temperature range of 297 to 400 K is presented in Figure 8. The graph is a straight line, indicating that the conduction in this system is through a thermally activated process. The conductivity is, therefore, expressed by the usual relation given as follows [4]: (7) where σ0 represents the pre-exponential factor, and ΔE c is the dc activation energy which is calculated from the slope of ln σdc versus 1000/T plot. Figure 8 Variation of refractive index ( n ) with incident photon energy (h ν ) in thin films of a-(PbSe) 100−x Cd x nanoparticles. Using the slope and intercept of Figure 8, we have calculated the value of ΔE c and σ0, respectively. The calculated values of ΔE c and σ0 for different compositions of cadmium in a-(PbSe)100−x Cd x nanoparticle thin films are shown in Table 1.

B. mallei are also highly infectious organisms by aerosol and it is widely believed that it harbors the potential for use as a biological weapon [2]. In fact, the bacterium was one of the first agents used in biologic warfare during the American Civil War, World Wars I and II, and Russian invasion of Afghanistan. Consequently, it has been placed on the CDC category B agent list [3]. Inhalation of aerosol or dust containing B. mallei can lead

to septicemia, pulmonary or chronic infections of the muscle, liver and spleen. The disease has a 95% case fatality rate for untreated septicemia infections and a 50% case fatality rate in antibiotic-treated individuals [4]. The ability of B. mallei to cause severe, rapidly fatal invasive infection initiated via aerosol in animals and humans, coupled with intrinsic resistance to antibiotics and diagnostic difficulty at early stage BAY 11-7082 mw of disease

make the bacterium a good candidate as a possible biological threat agent [5, 6]. Our knowledge of pathogenesis of disease due to B. mallei is minimal. The disease was eliminated from domestic animals in the United States during the 1940s and the last reported naturally acquired human case in the United States occurred in 1945. There is little data available on antibiotic treatment of glanders and human cases are treated with the same regimens used for melioidosis, an endemic disease in Southeast of Asia and Northern Australia, caused by Burkholderia pseudomallei. Selleck OTX015 Only one case of laboratory-acquired human glanders was reported to CDC recently [7]. This single Farnesyltransferase human case of glanders corroborated in vitro data with in vivo efficacy for the B. mallei ATCC 23344 strain when a combination of intravenous doxycycline plus imipenem followed by oral doxycycline plus azithromycin successfully controlled a

disseminated infection [7]. However, at present, the treatment of B. mallei with antibiotic therapy is still not well established and no effective vaccines are available. Few in vitro antibiotic susceptibility studies for B. mallei have been performed. The antibiotic susceptibility of B. mallei is similar to that of B. pseudomallei, with resistance to a number of antibiotics [8]. Both organisms appear to be sensitive to imipenem and doxycycline, while most strains are susceptible to ceftazidime, ciprofloxacin, and piperacilin [9]. Unfortunately clinical experience with B. pseudomallei infections has shown that despite good in vitro activity, an antibiotic may be ineffective in vivo [10, 11]. We chose ceftazidime, highly recommended drug for treatment of melioidosis. Ceftazidime belongs to the beta-lactam group, a broad spectrum antibiotic, structurally and pharmacologically related to penicillins, which work by inhibiting the bacterial cell wall synthesis. This third Vorinostat research buy generation cephalosporin is effective against Pseudomonas and other Gram-negative bacteria.

Mycol Res 111:748–757CrossRefPubMed Price MJ, Worth GK (1974) The occurrence of ergosta-4, 6, 8(14), 22-tetraen-3-one in several fungi. Aust J Chem 27:2505–2507CrossRef Raistrick H, Smith G (1941) Antibacterial substances from mould. I. Citrinin, a metabolic product of Penicillium citrinum Thom. Chem Ind 6:828–830

Ramirez C (1982) Manual and atlas of the Penicillia. Elsevier Biomedical, New York Raper KB, Thom C (1949) Manual of the Penicillia. Williams & Wilkins, Baltimore Reynolds DR, Taylor JW (1991) Nucleic acids and nomenclature: name stability under Article 59, 171–177. In: Hawksworth DL (ed) Improving the stability of names: needs and options. Regnum Veg. 123. Koelte Scientific Books, Köningstein, Germany Sakai K, Kinoshita H, Shimizu T, Nihira T (2008) Construction of a citrinin gene cluster expression

system in heterologous Aspergillus PF2341066 oryzae. J Biosci Bioeng 106:466–472CrossRefPubMed Samson RA, Frisvad JC (2004) Penicillium subgenus Penicillium: new taxonomic schemes and mycotoxins and other extrolites. Stud Mycol 49:1–266CrossRef Samson RA, Hoekstra ES, Frisvad JC (2004) Introduction to food- and airborne fungi, 7th edn. Centraalbureau voor Schimmelcultures, Utrecht Samson RA, Houbraken J, Varga J, Frisvad JC (2009) Polyphasic taxonomy of the heat resistant ascomycete genus Byssochlamys and its Paecilomyces anamorphs. Persoonia 22:14–27PubMed Sasaki M, Tsuda M, Sekiguchi M, Mikami Y, Kobayashi J (2005) Perinadine

A, a Metalloexopeptidase novel tetracyclic alkaloid JPH203 from marine-derived fungus Penicillium citrinum. Org Lett 7:4261–4264CrossRefPubMed Smedsgaard J (1997) Micro-scale extraction procedure for standardized screening of fungal metabolite production in cultures. J Chromatogr A 760:264–270CrossRefPubMed Smith G (1963) Some new species of Penicillium, and some observations on the taxonomy of the genus. Trans Br Mycol Soc 46:331–337CrossRef Stolk AC, Samson RA (1983) The ascomycete genus Eupenicillium and related Penicillium anamorphs. Stud Mycol 23:1–149 Størmer FC, ABT-888 chemical structure Sandven P, Huitfeldt HS, Eduard W, Skogstad A (1998) Does the mycotoxin citrinin function as a sun protectant in conidia from Penicillium verrucosum. Mycopathologia 142:43–47CrossRefPubMed Taira T, Yamatodani S (1947) Biochemistry of Penicillium group. II. Determination of citrinin. J Penicillin 1:275 Takahashi S, Kakinuma N, Iwai H, Yanagisawa T, Nagai K, Suzuki K, Tokunaga T, Nakagawa A (2000) Quinolactacins A, B and C: novel quinoline compounds from Penicillium sp. EPF-6. II. Physico-chemical properties and structure elucidation. J Antibiot 53:1252–1256PubMed Tejesvi MV, Kini KR, Prakash HS, Subbiah V, Shetty HS (2007) Genetic diversity and antifungal activity of species of Pestalotiopsis isolated as endophytes from medicinal plants. Fungal Divers 24:37–54 Thom C (1910) Cultural studies of species of Penicillium.