Infect Immun 1999,67(7):3518–3524 PubMed 99 Wang G, van Dam AP,

Infect Immun 1999,67(7):3518–3524.PubMed 99. Wang G, van Dam AP, Schwartz I, Dankert selleck chemicals llc J: Molecular typing of Borrelia burgdorferi sensu

lato: taxonomic, epidemiological, and clinical implications. Clin Microbiol Rev 1999,12(4):633–653.PubMed 100. Livey I, Gibbs CP, Schuster R, Dorner F: Evidence for lateral transfer and recombination in OspC variation in Lyme disease Borrelia. Mol Microbiol 1995,18(2):257–269.PubMedCrossRef 101. Fraser CM, Casjens S, Huang WM, Sutton GG, Clayton R, Lathigra R, White O, Ketchum KA, Dodson R, Hickey EK, et al.: Genomic sequence of a Lyme disease spirochaete, Borrelia burgdorferi. Nature 1997,390(6660):580–586.PubMedCrossRef 102. Hyde JA, Weening EH, Chang M, Trzeciakowski JP, Hook M, Cirillo JD, Skare JT: Bioluminescent imaging of Borrelia burgdorferi in vivo demonstrates that the fibronectin-binding protein BBK32 is required for optimal infectivity. Molecular microbiology 2011,82(1):99–113.PubMedCrossRef 103. Li X, Liu X, Beck DS, Kantor FS, Fikrig E: Borrelia selleckchem burgdorferi lacking BBK32, a fibronectin-binding protein, retains full pathogenicity. Infect Immun 2006,74(6):3305–3313.PubMedCrossRef 104. Zeidner NS, Schneider BS, Dolan MC, Piesman J: An analysis of spirochete

load, strain, and pathology in a model of tick-transmitted Lyme borreliosis. Vector Borne Zoonotic Dis 2001,1(1):35–44.PubMedCrossRef 105. de Souza M, Smith A, Beck D, Terwilliger G, Fikrig E, Barthold S: Long-term study of cell-mediated responses to Borrelia burgdorferi in the laboratory mouse. Infect Immun 1993, 61:1814–1822.PubMed 106. Yang L, Ma Y, Schoenfield R, Griffiths M, Eichwald E, Araneo B, Weis JJ: Evidence for B-lymphocyte mitogen activity in Borrelia burgdorferi-infected mice. Infect Immun 1992, 60:3033–3041.PubMed 107. Fraser CM, Norris SJ, Weinstock GM, White O, Sutton GG, Dodson R, Gwinn M, Hickey EK, Clayton aminophylline R, Ketchum KA, et al.: Complete genome sequence of Treponema pallidum, the syphilis spirochete. Science 1998,281(5375):375–388.PubMedCrossRef 108. Teh CS, Chua KH, Thong KL: Genetic variation

analysis of Vibrio cholerae using multilocus sequencing typing and multi-virulence locus sequencing typing. Infection, Selleck PD332991 genetics and evolution: journal of molecular epidemiology and evolutionary genetics in infectious diseases 2011,11(5):1121–1128.PubMed 109. Li X, Neelakanta G, Liu X, Beck DS, Kantor FS, Fish D, Anderson JF, Fikrig E: The role of outer surface protein D in the Borrelia burgdorferi life cycle. Infect Immun 2007,75(9):4237–4244.PubMedCrossRef 110. Stewart PE, Bestor A, Cullen JN, Rosa PA: A tightly regulated surface protein of Borrelia burgdorferi is not essential to the mouse-tick infectious cycle. Infect Immun 2008,76(5):1970–1978.PubMedCrossRef 111. Tilly K, Krum JG, Bestor A, Jewett MW, Grimm D, Bueschel D, Byram R, Dorward D, Vanraden MJ, Stewart P, et al.: Borrelia burgdorferi OspC protein required exclusively in a crucial early stage of mammalian infection.

References 1 McCord N, Owen P, Powls A, Lunan B: A complete audi

References 1. McCord N, Owen P, Powls A, Lunan B: A complete audit cycle of intrapartum group B streptococcus prophylaxis. Health Bull (Edinb) 2001, 59:263–267. 2. Krohn MA, Hillier SL, Baker CJ: Maternal peripartum complications associated with vaginal group B streptococci colonization. J GW-572016 in vitro Infect Dis 1999, 179:1410–1415.PubMedCrossRef 3. Phares CR, Lynfield R, Farley MM, Mohle-Boetani J, Harrison LH, Petit S, Craig AS, Schaffner W, Zansky SM, Gershman K, et al.: Epidemiology of invasive find more group B

streptococcal disease in the United States, 1999–2005. JAMA 2008, 299:2056–2065.PubMedCrossRef 4. Schuchat A: Group B streptococcal disease in newborns: A global perspective on prevention. Biomed Pharmacother 1995, 49:19–25.PubMedCrossRef 5. Verani JR, Schrag SJ: Group B streptococcal disease in infants: Progress in prevention and continued challenges. Clin Perinatol 2010, 37:375–392.PubMedCrossRef 6. Verani JR, McGee L, Schrag SJ: Prevention of perinatal group B streptococcal disease-revised guidelines from CDC, 2010. MMWR Recomm Rep 2010, 59:1–36.PubMed

7. Edmond KM, Kortsalioudaki C, Scott S, Schrag SJ, Zaidi AK, Cousens S, Heath PT: Group B streptococcal disease in infants aged younger than 3 months: Systematic review and meta-analysis. Lancet 2012, 379:547–556.PubMedCrossRef PCI-34051 manufacturer 8. Edwards MS, Baker CJ: Group B streptococcal infections in elderly adults. Clin Infect Dis 2005, 41:839–847.PubMedCrossRef 9. Skoff TH, Farley MM, Petit S, Craig AS, Schaffner W, Gershman K, Harrison LH, Lynfield R, Mohle-Boetani J, Zansky S, et al.: Increasing burden of invasive group B streptococcal disease in nonpregnant adults, 1990–2007.

Clin Infect Dis 2009, 49:85–92.PubMedCrossRef 10. Duarte RS, Bellei BC, Miranda OP, Brito MA, Teixeira LM: Distribution of antimicrobial resistance and virulence-related genes among Brazilian group B streptococci recovered from bovine and human sources. Antimicrob Agents Chemother 2005, 49:97–103.PubMedCentralPubMedCrossRef 11. Palmeiro JK, Dalla-Costa LM, Fracalanzza Montelukast Sodium SE, Botelho AC, da Silva Nogueira K, Scheffer MC, de Almeida Torres RS, de Carvalho NS, Cogo LL, Madeira HM: Phenotypic and genotypic characterization of group B streptococcal isolates in southern Brazil. J Clin Microbiol 2010, 48:4397–4403.PubMedCentralPubMedCrossRef 12. Correa AB, Silva LG, Pinto Tde C, Oliveira IC, Fernandes FG, Costa NS, Mattos MC, Fracalanzza SE, Benchetrit LC: The genetic diversity and phenotypic characterisation of Streptococcus agalactiae isolates from Rio de Janeiro, Brazil. Mem Inst Oswaldo Cruz 2011, 106:1002–1006.PubMedCrossRef 13. Nakamura PA, Schuab RBB, Neves FP, Pereira CF, Paula GR, Barros RR: Antimicrobial resistance profiles and genetic characterisation of macrolide resistant isolates of Streptococcus agalactiae . Mem Inst Oswaldo Cruz 2011, 106:119–122.PubMedCrossRef 14.

As these putative GPCRs represented a separate clade in the phylo

As these putative GPCRs represented a separate clade in the phylogenetic analysis (Figure 1), they were assigned to a new class (class XIII, Table 1) thereby extending the classification system of fungal GPCRs to 14 classes. Conclusions A thorough examination of the genomes of the two mycoparasites T. atroviride and T. virens and the saprophyte T. reesei for putative GPCRs revealed for most classes a high conservation of their number and structure within this genus. On the other hand, remarkable differences in individual classes were found among the three Trichoderma species and among Trichoderma and other filamentous fungi.

Whereas for class Ralimetinib molecular weight I to VII members, orthologous triplets with similar length and sequence are present in the genomes of the three Trichoderma species and their number is also similar to other fungi, the PAQR family has expanded especially in T. atroviride. Considering the identification of members of classes X, XI, and XII and proteins similar to the P. sojae GPR11 receptor in Trichoderma, the presented 14 classes now define the most comprehensive classification system for GPCR-like proteins of fungi. The huge diversity of GPCRs in Trichoderma spp. and especially in the mycoparasites is likely to reflect the capability of these fungi to establish various ecological niches and interactions with other organisms. It is worth mentioning that Vactosertib clinical trial with the exception

of few members, the proteins identified as putative GPCRs in this study have only been characterized in silico. Taking into account that only three α, one β and one γ subunit of heterotrimeric

G proteins are encoded in the Trichoderma genomes which face more than 55 GPCRs, studying the signaling output and identifying the respective intracellular until interaction partners of those receptors will provide interesting insights on how these fungi adapt to their different lifestyles. Methods Identification of GPCR-encoding genes of Trichoderma atroviride and Trichoderma virens Version 2 of the T. atroviride genome database [57] comprises 11,863 gene models on 29 scaffolds; version 2 of the T. virens genomic sequence [58] comprises 12,427 gene models on 93 scaffolds. For the homology-based PI3K inhibitor search of GPCR-like proteins from T. atroviride and T. virens, the genomic sequences and deduced proteomes of the following fungi were used: Trichoderma reesei[59]Aspergillus nidulans, Aspergillus fumigatus, Aspergillus oryzae[62], Neurospora crassa[63], Magnaporthe grisea[64], Podospora anserine[65], Chaetomium globosum[66], Fusarium graminearum[67], and Nectria haematococca[68]. An e-value limit of 1e-09 was applied. To identify putative GPCRs within the T. atroviride and T. virens proteomes that lack significant sequence similarity to known GPCR-like proteins and therefore may escape detection by homology search, a more sensitive database searching using hidden Markov models (HMM) was performed using the program HMMER (http://​hmmer.​janelia.

In Figure 1b, the bulk and surface XPS spectra of the HfO2 film i

8 eV without any shifts. In Figure 1b, the bulk and surface XPS spectra of the HfO2 film illustrate that the binding energies of the Hf 4f5/2 and 4f7/2 are at the EPZ5676 molecular weight positions of about 18.4 and 16.7 eV, respectively, with a 1.7-eV spin-orbit splitting. From the O 1s spectrum in Figure 1b, the

Hf-O bond is at 530 eV in the interior and at the surface of the HfO2 film [24]. However, from the surface XPS of O 1s in both Al2O3 and HfO2, the existence of -OH is observed with a peak at around 532 eV. This is either incorporated by residue water precursors during the process because of the high desorption energy of water at low temperatures or exposing the film check details to the atmosphere (CO2 and moisture) before XPS measurement [23]. The XPS qualification report shows that the ratios of the O/Al in the bulk of the Al2O3 film and the O/Hf in the bulk of the HfO2 are about 1.7 and 2, respectively, which means that our films obtained at low temperature are almost stoichiometric. Figure

1 The XPS spectra. (a) Al 2p and O 1s peaks at the surface and in the bulk of the Al2O3 film. (b) Hf 4f and O 1s peaks at the surface and in the bulk of HfO2 film. Typical I-V characteristics of the device are shown in Figure 2, which indicates a bipolar resistive switching. The initial resistance state of the TiN/HfO2/Al2O3/ITO flexible RRAM (schematically shown in the inset of Figure 2) device was found (curve 1) to be even lower than the low resistance state (LRS) of the device, and an excess negative voltage was applied to reset the device to high resistance state

(HRS). The initial reset voltage and current were −3 V and 10 mA, Everolimus purchase respectively. This phenomenon was not observed in RRAMs C1GALT1 grown at high temperatures, except in some cases after high-temperature annealing [25–27]. We attribute this phenomenon to the high density of defects in the film grown at low temperature. As with our low-temperature ALD processing using H2O as oxidant, it is inevitable that there will be some incomplete reactions during the process, such as residual -OH groups, fixed positive charges, and oxygen vacancies. It is considered that when the density of defects exceeds the percolation theory threshold value, the resistance of the insulating layer will be lower than the typical value [26, 28]. This large density of defects may be very suitable for RRAM applications which work dependently on the defects. After the initial reset operation, the set operation was achieved by sweeping a positive voltage from 0 to 1.5 V with 1 mA of current compliance to protect the device from a hard breakdown (curve 3). An abrupt increase of current was observed at 1 V, and the device was set to LRS (approximately 650 Ω). A negative bias was then applied to the device by a sweep from 0 to −1 V, and a sudden descent of current occurred at −0.6 V, indicating that the device was reset to HRS with a reset current in the same magnitude as the set current.

Thus, the best results were obtained when the final concentration

Thus, the best results were obtained when the final concentration of the three primer sets, MgCl2, and Taq polymerase was increased respectively to 0.8 μM, 3 mM and to 1.5 U and the m-PCR was check details carried

out in a final volume of 50 μl. The thermal cycler parameters of the m-PCR were similar to those of the individual PCR using 61°C as an optimal annealing temperature. Positive and negative control DNA samples were run in each experiment. PCR products were analyzed in 1.2% agarose gel electrophoresis, stained with ethidium bromide and visualised with ultraviolet transillumination. All PCR reactions assessing limits of detection or specifiCity were performed in duplicate. Sensitivity and specifiCity of the m-PCR Sensitivity of the PCR assay was checked using serial fold dilutions of bacterial suspension Akt inhibitor of references strains AB7, iB1 and Nine-Miles at 107 bacteria per ml. Simulated positive samples were also obtained by adding

50 μl of bacterial suspension dilution to 50 μl of bacteria-free vaginal swab extract or milk sample. These preparations were then submitted to extraction procedures and to simplex and m-PCR as described above. The specifiCity of the PCR was assessed on 20 strains of Cp. abortus, 5 strains of Cp. pecorum and, 4 strains of C. burnetii VEGFR inhibitor from our laboratory bacteria collection and on some isolates suspected to be present into tested clinical samples: Brucella melitensis, Brucella abortus, Brucella suis, Escherichia coli, Bacillus cereus, Listeria monocytogenese, Salmonella abortus ovis, Salmonella Typhimurium, Staphylococcus aureus, Staphylococcus chromogenese, Staphylococcus hominis, Streptococcus dysgalactiae and Streptococcus ogalactiae, Mycobacterium avium, Legionella pneumophila. In addition, RFLP-PCR analysis was carried

out as a confirmatory test for the PCR reaction specifiCity. Thus, 10 μl of amplification products obtained from naturally infected clinical samples and those obtained from 102 genomic DNA templates of the reference strains AB7, IB 1, Nine Miles were subjected to 5 units DOCK10 of AluI restriction enzyme (Promega, Charbonnières-Les-Bains, France) in a 20 μl final volume for 3 hours at 37°C. The digested products were examined by using 2% agarose gel stained with ethidium bromide and viewed under UV illumination. In addition, PCR products amplified from clinical samples were purified with a QIAquick PCR purification Kit (Qiagen, Courtaboeuf, France) and directly sequenced with an ABI PRISM 310 genetic analyzer (Applied Biosystems). Isolation of Chlamydophila and Coxiella strains Pathogen isolation was performed to confirm the presence of the involved bacteria, on 20-different PCR positive samples showing high ethidium bromide intensity on agarose gel. Chlamydophila strains isolation were performed using both plaque assays and blind passages on McCoy monolayer cell cultures [27].

The enrollment period was from

The enrollment period was from see more July 2003 to June 2006, and the study finished in June 2009. All patients who underwent hip fracture surgery at the participating institutions and were discharged during the enrollment period were tentatively enrolled by uploading data to a web page. The enrollment items were sex, age, height, body weight, body mass index (BMI), presence/absence of osteoporosis, presence/absence of vertebral fracture, site of hip fracture surgery, date of injury, date of hospitalization, treatment of the fracture, address at the time of injury, postoperative period, independence rating before injury, independence rating at discharge, drug

treatment for osteoporosis at discharge, past history at discharge, complications at discharge, BMD, and possibility/impossibility of outpatient follow-up. The attending physician explained the purpose and methods of this study to each patient. We specified Japanese criteria for the diagnosis of osteoporosis according to the diagnostic standard for primary osteoporosis (2000 revised edition) of the Japanese Society for Bone and Mineral Research [19]. The exclusion

criteria were as follows: (1) no diagnosis of primary osteoporosis according to the above criteria, (2) bilateral hip fracture, (3) prior history of hip fracture, (4) patients CA4P ic50 discharged death, and (5) patients who could not be followed-up after discharge. Out of the preliminary enrolled patients, those treated with risedronate at the approved Japanese dose of 2.5 mg/day (Benet® 2.5 mg; Takeda Pharmaceutical Co., Ltd, Osaka, Japan) at the initial visit after 4SC-202 discharge on the judgment of the physician

in charge were included in the administration group. Following the initial outpatient visit after discharge from hospital, patients were enrolled by uploading the required data to the web page. After enrollment of patients in the group receiving BCKDHA risedronate, the patient enrollment center selected all of the matching patients as candidates for the control group. The demographic data and other items used for matching the groups are listed in Appendix 1. Patients in the control group were not being treated with any bisphosphonate preparation and the required data was uploaded as the control group to the web page (Fig. 1). Fig. 1 Disposition of the patients. Of the 2,051 patients who underwent preliminary enrollment, 1,142 patients were ineligible, and 280 patients were excluded from enrollment for several reasons. Among the rest, 184 patients were taking risedronate at the initial outpatient visit after discharge. Four hundred forty-five patients were matched with patients with taking risedronate.

The correct spelling is Rossbeevera T Lebel

& Orihara ge

The correct spelling is Rossbeevera T. Lebel

& Orihara gen. nov. A list of the species names follows. Rossbeevera bispora (B.C.Zhang & Y.N.Yu) T.Lebel & Orihara comb. nov. Rossbeevera eucyanea Orihara sp. nov. Rossbeevera griseovelutina Orihara sp. nov. Rossbeevera mucosa (Petri) T.Lebel comb. nov. Rossbeevera vittatispora (G.W.Beaton, Pegler & T.W.K.Young) T.Lebel comb. nov. Rossbeevera westraliensis T. Lebel sp. nov.”
“Introduction Graphidaceae (including Thelotremataceae; Mangold et al. 2008) is the second largest family Selleckchem MEK162 of lichenized fungi, next to Parmeliaceae, and the most important element of lichen communities in tropical regions, with over 1500 species (Staiger 2002; Frisch et al. 2006; Archer 2006, 2007, 2009; Lücking and Rivas Plata 2008; Rivas Plata et al. 2008; Lücking et al. 2008, 2009; PS-341 ic50 Mangold et al. 2009). For a long time, family and generic concepts in this group were based on apothecia and ascospore types, separating the bulk of taxa into four genera with rounded (Thelotremataceae: Ocellularia, Thelotrema, Phaeotrema, Leptotrema), four genera with lirellate (Graphidaceae: Graphis, Graphina, Phaeographis, Phaeographina), and four genera with stromatic ascomata (Graphidaceae: Glyphis, Medusulina, Sarcographa, Sarcographina). Genera within each morphotype were separated based on whether

ascospores were transversely septate or muriform and hyaline or pigmented (Müller Argoviensis 1887; Hale 1974, 1978; Wirth and Hale 1963; 1978; Staiger 2002; Frisch et al. 2006). Salisbury (1971, 1972, 1978) and Hale (1980) challenged this schematic genus concept in the former Thelotremataceae, but rather than splitting the artificial ascospore genera into smaller units, Hale (1980) proposed

a more inclusive concept, with only three genera based on excipular structures: carbonized lacking periphysoids (Ocellularia), non-carbonized lacking periphysoids (Myriotrema), and non-carbonized with periphysoids (Thelotrema). This concept was subsequently applied to the treatment of Thelotremataceae for Montelukast Sodium Sri Lanka (Hale 1981). While Hale’s classification delimited two largely natural groups later recognized as supported clades in phylogenetic studies, the Ocellularia clade (including Ocellularia sensu Hale p.p. and Myriotrema sensu Hale p.p.) and the Protein Tyrosine Kinase inhibitor Thelotrema clade (including Thelotrema sensu Hale and some species of Myriotrema sensu Hale), the delimitation of large genera with well over 300 species each and the problems with generic assignment of aberrant taxa made this concept unsatisfactory. In addition, no comparable solution was proposed for lirellate and stromatic species classified in the supposed sister family Graphidaceae, which was treated until most recently using concepts established in the 19th century (Archer 1999; 2000; 2001a; b; c; d; 2002).

This suggests that a) the SSTRs

This suggests that a) the SSTRs expression is found along the B cell differentiation stages b) SSTRs expression is not modulated during this process b) SSTRs expression pattern

is not a marker for B cell differentiation. Sst and its analogs have been demonstrated to negatively regulate tumor cell proliferation (see for review [42]) and have been used in inoperable patients where neuroendocrine tumours stabilization or shrinkage can be obtained Staurosporine solubility dmso [43]. However, in other cancers such as hepatocellular carcinoma, the SIS3 molecular weight clinical benefit of Oct is not evidenced even in positive Oct scintigraphy patients [44]. To our knowledge, only one study examined the effects of Sst and Oct in MM cell lines and showed a strong decrease of viable cells after 48 h Oct exposure [41]. This is in marked contrast with our data since either Sst or Oct were unable to affect

cell proliferation of the U266 cell line. Such discrepancies should be explained by the use of different clones of the U266. We can also hypothesize that our U266 cells would express SSTRs with opposite effects on proliferation. SSTR2 and 5 were reported to inhibit cell proliferation by phosphotyrosine phosphatase (PTP) activation and inhibition of calcium channels, respectively [42, 45]. In contrast, SSTR4 were shown to activate the MAPK cascade and promoting proliferation [46]. So, no effect on proliferation would be observed upon co-activation of those SSTRs. Discrepancies between our study and the one of Georgii-Hemming and collaborators [41] about Bortezomib manufacturer Chlormezanone cellular viability should also be due to the presence or the absence of serum in the culture medium. However, we can rule out such explanation since we observed no effect upon SSTR agonists when experiments were conducted in serum-free culture medium (data not shown). Anti-tumoral activity of Sst or its analogs are also due to pro-apoptotic effects (see for review [47]). In two MM cell lines U266 (current study) and LP-1 (data not shown), we observed that neither Sst nor Oct promote apoptosis in our experimental

conditions. This was illustrated by the lack of sub-G1 peak in cell cycle assay and the absence of labelling in annexin V/PI experiments. In contrast, Georgii-Hemming et al. showed that in three MM cells (HL-407L, HL-407E and U-1958) Oct induced a weak increase in annexin V/PI staining suggesting that SSTRs could promote apoptosis [41] but the U266 cell line was not investigated. Sharma et al. first described the role of SSTR3 in apoptosis when expressed in Chinese hamster ovary cells and demonstrated that Oct promotes dephosphorylation of wild-type p53 which leads to DNA fragmentation [35]. Even in the absence of apoptosis, we can not rule out that SSTRs are not coupled to apoptotic pathways since U266 was shown to express the anti-apoptotic protein Bcl-2 [48].

For the two

For the two training sessions with 1000 m interval runs × 15 that were performed

on the first and the last days of the training camp on February 15 (the temperature and humidity were 2°C and EPZ004777 price 38%, respectively) and 22 (the temperature and humidity were 3°C and 35%, respectively) of 2008, 16 subjects were assigned to 3 teams (A-C) according to ability. The number of the subjects was 4 in team A, 6 in team B, and 6 in team C and each team included the same number of CT or P group. Each 1000 m interval run was followed by a 200 m jog. Team A ran 1000 m in 3 min 15 s × 5, 3 min 10 s × 5, 3 min 5 s × 4, and then ran the last 1000 m interval at full speed (average run time: 3 min 5 s). Team B ran 1000 m in 3 min 20 s × 5, 3 min

15 s × 5, 3 min 10 s × 4, and then ran the last one at full speed (average run time: 3 min 9 s). Team C ran 1000 m in 3 min 25 s × 5, 3 min 20 s × 5, 3 min 15 s × 4, and then ran the last one at full speed (average run time: 3 min 16 s). The interval runs were performed so that the load of exercise was comparable regardless of the runners’ abilities. Test schedule and analysis items Blood and saliva samples were collected before and after the 1000-m interval runs × 15 performed in the early morning on 15 and 22 February 2008 on the first and last day of the training camp, respectively. The CRT0066101 cell line above samples were collected immediately after the subjects woke up in the early morning at 6 AM, before breakfast and before they engaged in any Momelotinib physical activities. After blood and saliva samples were collected, 1000-m interval runs × 15 training

was performed from 7 AM, and blood and saliva samples were collected Amylase again after the training without any massage or pressure to the skeletal muscle. Nineteen ml of blood was collected from the antecubital vein by the standard procedure using a blood collection tube. White blood cell (WBC), neutrophil, and lymphocyte counts were measured using blood samples as part of a general peripheral blood test. In addition, blood levels of creatine phosphokinase (CPK), myoglobin (Mb) and IL-6 were included in the general biochemical examination and cortisol was measured in a saliva test. All analyses were performed in a biomedical clinical laboratory (Health Sciences Research Institute, Inc., Japan). Statistical analysis Data are shown as the means ± SEM.

5 million species estimate revisited Mycol Res 105:422–1432Cross

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