It is not likely that bias with respect to ascertainment and coding of the causes of death may have affected the study outcome. Information regarding the causes of death was collected from the CBS where the causes of death were coded at the time of death by trained nosologists who were unaware of our study Selleckchem C188-9 and were unaware of which persons were or were not a member of the cohort. Equally, information regarding exposure,

including the calculation of total intake, was performed without any knowledge of the vital status and cause of death if applicable. Also, the number of subjects lost to follow-up in this study is low when considering the long period of follow up. This follow up has even been able to trace

some of the respondents, which were lost-to-follow up in previous updates, due to remigration and improvements in the registries. A limitation of the study is its relatively small sample size. However, the power of a retrospective cohort study depends on the number of expected events of interest, in this case cancer deaths, in combination with the expected magnitude of the effect of the exposure. In fact, given an α level of 0.05 and 80% power, the sample size (i.e. person years) of this study is capable of detecting at least a 34% increase risk in cancer (Armstrong 1987), if such Selleckchem PARP inhibitor a risk did exist. However, as none of the cancers not revealed a significant excess mortality risk and no exposure response relationship was observed for any of the cancer sites, this follow up study supports the conclusion that aldrin/dieldrin exposure does not lead to an increased cancer risk in man. This cohort is one of two cohorts that have been involved in the production of dieldrin and aldrin in the world. Their exposure has been accurately documented and as such provides an excellent opportunity to learn more about the possible long-term effects of these pesticides. In addition, the time window of observation is 52 years, between 1 January 1954 and 30 April

2006, which is a sufficient latency period. In fact, all exposed workers were employed before 1 January 1970 and 52.3% before 1 January 1960. Our findings add to the growing body of evidence, provided by both epidemiological studies (Amoateng-Adjepong et al. 1995; Ward et al. 2000) and recent animal studies (Stevenson et al. 1999; Kamendulis et al. 2001), showing a lack of an association between aldrin/dieldrin exposure and cancer mortality. The overall mortality of this occupational cohort remains significantly lower than the general male population of the Netherlands, after 52 years of follow-up. This is commonly referred to as the healthy worker effect (Checkoway et al. 1989), which can be attributed to a number of factors (Li and Sung 1999).

S. Gov’t).PubMedCentralPubMedCrossRef 31. Sakoulas G, Eliopoulos GM, Moellering RC Jr, Wennersten C, Venkataraman L, Novick RP, et al. Accessory gene regulator (agr) locus in geographically diverse Staphylococcus aureus isolates with

reduced susceptibility to vancomycin. Antimicrob Agents Chemother. 2002;46(5):1492–502.PubMedCentralPubMedCrossRef 32. McDougal LK, Steward CD, Killgore GE, Chaitram JM, McAllister SK, Tenover FC. Pulsed-field ��-Nicotinamide ic50 gel electrophoresis typing of oxacillin-resistant Staphylococcus aureus isolates from the United States: establishing a national database. J Clin Microbiol. 2003;41(11):5113–20.PubMedCentralPubMedCrossRef 33. Tenover FC, Arbeit RD, Goering RV, Mickelsen PA, Murray BE, Persing DH, et al. Interpreting chromosomal

DNA restriction patterns produced by pulsed-field gel electrophoresis: criteria for bacterial strain typing. J Clin Microbiol. 1995;33(9):2233–9.PubMedCentralPubMed 34. Benvenuto M, Benziger DP, Yankelev S, Vigliani G. Pharmacokinetics and tolerability of daptomycin at doses up to 12 milligrams per kilogram of body weight once daily in healthy volunteers. Antimicrob Agents Chemother. 2006;50(10):3245–9.PubMedCentralPubMedCrossRef 35. Rose click here WE, Leonard SN, Sakoulas G, Kaatz GW, Zervos MJ, Sheth A, et al. Daptomycin activity against Staphylococcus aureus following vancomycin exposure in an in vitro pharmacodynamic model with simulated endocardial vegetations. Antimicrob Agents Isotretinoin Chemother. 2008;52(3):831–6.PubMedCentralPubMedCrossRef 36. Ludwig F, Edwards B, Lawes T, Gould IM. Effects of storage on vancomycin and daptomycin MIC in susceptible blood isolates of methicillin-resistant Staphylococcus aureus. J Clin Microbiol. 2012;50(10):3383–7.PubMedCentralPubMedCrossRef 37. Lee CH, Wang MC, Huang IW, Chen FJ, Lauderdale TL. Development of daptomycin nonsusceptibility with heterogeneous vancomycin-intermediate resistance and oxacillin susceptibility in methicillin-resistant

Staphylococcus aureus during high-dose daptomycin treatment. Antimicrob Agents Chemother. 2010;54(9):4038–40.PubMedCentralPubMedCrossRef”
“Erratum to: Infect Dis Ther (2013) 2:27–36 DOI 10.1007/s40121-013-0006-6 The editors of Infectious Diseases and Therapy would like to make the following addition to the Acknowledgments section of the above-mentioned paper. This required wording was unintentionally missed off the original version of the manuscript. “Compliance with Ethics Guidelines: All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2000 and 2008. Informed consent was obtained from all patients for being included in the study.

Tabashnik BE, Liu YB, Dennehy TJ, Sims MA, Sisterson MS, Biggs RW, Carrière Y: Inheritance of resistance to Bt toxin CrylAc in a field-derived strain

of pink bollworm (Lepidoptera: Gelechiidae). J Econ Entomol 2002, 95:1018–1026.PubMedCrossRef 19. Sutherland PW, Harris MO, Markwick NP: Effects of starvation and the Bacillus thuringiensis endotoxin CrylAc on the midgut cells, feeding behavior, and growth of lightbrown apple moth larvae. Ann Entomol Soc Am 2003, 96:250–264.CrossRef 20. Johnson DE, BVD-523 Freedman B: Toxicity of Bacillus thuringiensis Spo – Cr + mutants for the European Corn Borer Ostrinia nubilalis . Appl Environ Microbiol 1981, 42:385–387.PubMed 21. Aronson AI, Beckman W, Dunn PE: Bacillus thuringiensis and related insect pathogens. Microbiol Rev 1986, 50:1–24.PubMed 22. Johnson DE, Oppert B, McGaughey WH: Spore coat protein synergizes Bacillus thuringiensis crystal toxicity for the indianmeal moth. Curr Microbiol 1998, 36:278–282.PubMedCrossRef 23. Toumanoff C, Vago C: Histopathological study of the silkworm with Bacillus cereus alesti . Ann Inst Pasteur 1953, 84:376–385. 24. Heimpel

AM: Investigations of the mode of action of strains of Bacillus cereus Fr. and Fr. pathogenic for the Larch sawfly, Pristiphora erichsonii (HTG). Can J Microbiol 1955, 33:311–326. 25. Nishitsutsuji-Uwo J, Endo Y: Mode of action of Bacillus thuringiensis δ-enodotoxn: this website Relative roles of spores and crystals in toxicity to Pieris , Lymantria , and Ephestia larvae. Appl

Entomol Zool 1980, 15:416–424. 26. Bizzarri MF, Bishop AH: The ecology of Bacillus thuringiensis on the phylloplane: Colonization from soil, plasmid transfer, and interaction with larvae of Pieris brassicae . Microb Ecol 2008, Leukocyte receptor tyrosine kinase 104:60–69. 27. Schnepf HE, Whiteley HR: Cloning and expression of the Bacillus thuringiensis crystal protein gene in Escherichia coli . Proc Natl Acad Sci USA 1981, 78:2893–2897.PubMedCrossRef 28. Cerstiaens A, Verleyen P, Van Rie J, Van Kerkhove E, Schwartz J-L, Laprade R, De Loof A, Schoofs L: Effect of Bacillus thuringiensis Cry1 toxins in tnsect hemolymph and their neurotoxicity in brain cells of Lymantria dispar . Appl Environ Microbiol 2001, 67:3923–3927.PubMedCrossRef 29. Shelton AM, Zhao JZ, Roush RT: Economic, ecological, food safety, and social consequences of the deployment of Bt transgenic plants. Annu Rev Entomol 2002, 47:845–881.PubMedCrossRef 30. Broderick NA, Raffa KF, Handelsman J: Midgut bacteria required for Bacillus thuringiensis insecticidal activity. Proc Natl Acad Sci USA 2006, 103:15196–15199.PubMedCrossRef 31. Broderick NA, Robinson CJ, McMahon MD, Holt J, Handelsman J, Raffa KF: Contributions of gut bacteria to Bacillus thuringiensis -induced mortality vary across a range of Lepidoptera. BMC Biology 2009, 7:11.PubMedCrossRef 32. Ryu JH, Kim SH, Lee HY, Bai JY, Nam YD, Bae JW, Lee DG, Shin SC, Ha EM, Lee WJ: Innate immune homeostasis by the homeobox gene caudal and commensal-gut mutualism in Drosophila . Science 2008, 319:777–782.

Medium with 10% FBS was added to the lower chambers as a chemoattractant. After 24 h of incubation, cells that invaded through the membrane

filter were fixed and stained with H&E. The number of invading cells was counted under fluorescence microscope in five random high power fields. Statistical analysis All experiments were repeated independently a minimum of three times, and the results were expressed as the mean values ± standard deviation. The differences between groups were analyzed by two-tailed unpaired Student’s t test. A value of p < 0.05 was considered to indicate statistical significance. AZD1390 clinical trial Results MTA1 knockdown leads to the upregulation of miR-125b level in NSCLC cells First we established 95D and SPC-A-1 cell lines with stable knockdown of MTA1 by transfecting the cells with MTA1 shRNA. The knockdown efficiency was confirmed by qRT-PCR and Western blot analysis. Compared to the control cell lines, the expression of MTA1 mRNA and protein was significantly reduced in 95D and SPC-A-1 cells transfected with pLVTHM-MTA1-si plasmid (Figure  1A, B). Figure 1 MTA1 knockdown

leads to the upregulation of miR-125b level in NSCLC cells. A. Quantification of MTA1 mRNA level by quantitative RT-PCR in 95D and SPC-A-1 cells untransfected, transfected with MTA1 shRNA or control shRNA. B. Western blot analysis of MTA1 protein level in 95D and SPC-A-1 Selleckchem BLZ945 cells untransfected, transfected with MTA1 shRNA or control shRNA. B-actin was loading control. C. Quantification of miR-125b level by quantitative RT-PCR in 95D and SPC-A-1 cells transfected with MTA1 shRNA or control shRNA. D. Quantification of miR-125b level by quantitative RT-PCR in 95D and SPC-A-1 cells transfected with MTA1 shRNA or control shRNA, together with miR-125b inhibitor or control. *P < 0.05, **P < 0.01

compared to the controls. Next we detected miR-125b level in the established cell lines. The results showed that miR-125b level was 2.75 and 1.67-fold higher in 95D/MTA1-si and SPC-A-1/MTA1-si cells, compared to the control 95D and SPC-A-1 cells, respectively (Figure  1C). To confirm the negative correlation between MTA1 and miR-125b in NSCLC cells, we transfected miR-125b-inhibitor or nonspecific control miRNA (NC) RANTES into 95D and SPC-A-1 cells. qRT-PCR analysis showed that miR-125b-inhibitor decreased the expression of miR-125b in 95D/CTL-si and SPC-A-1/CTL-si cells only by 30 percent, but it significantly reduced miR-125b expression in 95D/MTA1-si and SPC-A-1/MTA1-si cells (Figure  1D). These data suggest that MTA1 knockdown leads to the upregulation of miR-125b level in NSCLC cells. MTA1 and miR-125b have antagonistic effects on the migration and invasion of NSCLC cells Next we investigated the antagonistic effects of MTA1 and MiR-125b on the migration and invasion of NSCLC cells. Wound healing assay showed that in 95D cells, knockdown of MTA1 led to reduced cell migration.

Figure 2 Schematic diagram of the n-type GAA Si NW MOSFET. Discrete distributions of the active As atoms are introduced into the S/D extensions. To mimic metal electrodes, the S/D regions are heavily doped with N d = 5 × 1020 cm−3 (continuously KU55933 doping). The channel region is intrinsic. We simulated 100 samples using 200 different random seeds (each sample needs two random seeds for S/D extensions). Results and discussion As distribution by KMC simulation Figure

3 shows random discrete active As distribution in the Si NW calculated by the KMC simulation. The histogram shows the normal distribution curve, and therefore, 200 seeds are large enough to represent the randomness. The average number of active As atoms in the NW is 27 with the standard deviation of 5. Out of 300 As atoms implanted into the selleck screening library 3-nm-wide Si region, only approximately 10% of As atoms are active in the Si NW. Most of the As atoms are in the oxide (approximately 40 atoms), at the oxide/Si interface (approximately 50),

in As-vacancy (As-V) clusters (approximately 90), and As precipitates (approximately 90) (see Figure 1). As-V clusters and As precipitates are inactive and immobile. They are formed when As concentration exceeds approximately 1020 cm−3 (for As-V clusters) and the solubility limit (for As precipitates) [14, 15]. In Sentaurus, not only As-V clusters but also As-Si interstitial (I) clusters (inactive and immobile) are taken into account, but As precipitates are not. In the present study, therefore, As-Si interstitial clusters in Sentaurus are interpreted as As precipitates. The calculation results show that the As activation ratio decreases with higher As dose because inactive As species (As-V clusters Calpain and As precipitates) are more likely to be formed. In NWs with smaller widths and heights, the As activation is found to be lower because more As atoms are closer to the oxide/Si interface and hence are piled up at the interface. Figure 3 Histogram of the number of active As atoms in the Si NWs. Si NWs (3

nm wide, 3 nm high, and 10 nm long) with 1-nm-thick oxide are implanted with As (0.5 keV, 1 × 1015 cm−2) and annealed at 1,000°C with a hold time of 0 s. Two hundred different random seeds were calculated. NEGF simulation Figure 4 shows the I d-V g characteristics at V d = 0.5 V of 100 devices with different discrete As distributions (gray lines). In the figure, their average value 〈I d〉 (open circles) and the I d of a continuously doping case in the S/D extensions (solid circles) are also shown for comparison. For the continuously doping case, the S/D extensions are uniformly n-doped with a concentration of 3 × 1020 cm−3, which corresponds to the average active As concentration in the Si NWs (see Figure 3). The I-V characteristics of devices uniformly n-doped with 2 × 1020, 2.5× 1020, and 3.

All of these strains were intimin-β; two were O33:H6, and the others were O139:H14 and Ont:H6. Two aEPEC strains, both O2:H4, intimin-κ, Screening high throughput screening belonged to the EPEC-3 clade, which also included tEPEC strain O86:H34, intimin-κ. Overall, three of 75 Australian and New Zealand isolates from humans reported here belonged to EHEC clades, 11 fell within EPEC clades, 38 belonged to clades distinct for aEPEC, and 23 could not be classified. Of the eight Australian calf isolates examined, three were not assigned

to a particular clade, and four belonged to the EHEC-2 clade (intimin-β and H11), but were of different serotypes from each other (O111:H-, O111:H11, O177:H11 and Ont:H-). This clade also included archetypal aEPEC strains E65/56 (O26:H-) and F41 (Ont:H-),

which were isolated in Europe more than 50 years ago, and a well-studied, REPEC strain, 83/39 (O15:H-), BGB324 datasheet in which Ral, a K88-like adhesin, was first identified [21]. None of the Australian or New Zealand strains of human origin investigated in this study belonged to this clade, suggesting that there was no major exchange of aEPEC strains between the cattle and humans from whom these bacteria were obtained. One calf isolate (O103:H2) was assigned to the EPEC-2 clade, which also contained REPEC strains E22 and 84/110-1 (also O103:H2), tEPEC strain, Stoke W (O111:H2),

and the prototypical aEPEC strain, E128012 (O114:H2). No aEPEC strains carrying intimin-β2, Rho -ξ, -o, -ρ or -σ were identified in the entire collection of 87 test and 8 reference strains reported here. Frequency of adhesins and other virulence determinants of pathogenic E. coli in aEPEC strains None of the 67 Australian aEPEC strains of human origin investigated in this study was positive in the PCR for genes encoding the following adhesins of pathogenic E. coli: BFP, Lda, Pap, Saa, Afa, Sfa/Foc, K88, K99, Af/R2 or RalG (Table 1). On the other hand, all strains were positive in the PCR for FimH of Type 1 pili. Moreover, all isolates exhibited mannose-sensitive haemagglutination, indicating that they produced functional Type 1 pili. Table 1 Characteristics of atypical EPEC strains that were positive in one or more PCR or DNA hybridization assays for virulence-associated determinants of E.

27. Jones JC, Rogers TJ, Brookmeyer P, Dunne WM Jr, Storch GA, Coopersmith CM, Fraser VJ, Warren DK: Mupirocin resistance in patients colonized with methicillin-resistant Staphylococcus aureus in a surgical intensive care unit. Clin Infect Dis 2007, 45:541–547. 28. Simor AE, Tammy L, Stuart TL, Louie L, Watt C, Marianne Ofner-Agostini M, Denise Gravel D, Michael Mulvey M, Loeb M, McGeer A, Bryce E, Matlow A: Mupirocin-resistant, methicillin-resistant Staphylococcus aureus

strains in Canadian hospitals. Antimicrob Agents Chemother 2007, 51:3880–3886. 29. Aly R, Shinefield HR, Litz C, Maibach HI: Role of teichoic acid in Adavosertib order the binding of Staphylococcus aureus to nasal epithelial cells. J Infect Dis 1980, 141:463–465. 30. Patti JM, Allen BL, McGavin MJ, Hook M: MSCRAMM-mediated adherence of microorganisms to host tissues. Annu Rev Microbiol 1994, 48:585–617.PubMedCrossRef 31. O’Brien LM, Walsh EJ, Massey RC, Peacock SJ, Foster TJ: Staphylococcus aureus clumping factor B (ClfB) promotes adherence to human type I cytokeratin 10: implications for nasal colonization. Cell Microbiol 2002, 4:759–770. 32. Roche FM, Meehan M, Foster TJ: The Staphylococcus aureus

surface protein SasG and its homologues promote bacterial adherence to human desquamated GDC-0068 ic50 nasal epithelial cells. Microbiology 2003, 149:2759–2767. 33. Weidenmaier C, Kokai-Kun JF, Kristian SA, Chanturiya T, Kalbacher H, Gross M, Nicholson G, Neumeister B, Mond JJ, Peschel A: Role of techoic acids

in Staphylococcus aureus nasal colonization, a major risk factor in nosocomial infections. Nat Med 2004, 10:243–245. 34. Wertheim HF, Vos MC, Boelens HA, Voss A, Vandenbroucke-Grauls CM, Meester MH, Kluytmans JA, van Keulen PH, Verbrugh HA: Low prevalence of methicillin-resistant Staphylococcus aureus (MRSA) at hospital admission in the Netherlands: the value of search and destroy and restrictive antibiotic use. J Hosp Infect 2004, 56:321–325. ID-8 35. Coates T, Bax R, Coates A: Nasal decolonization of Staphylococcus aureus with mupirocin: strengths, weaknesses and future prospects. J Antimicrob Chemother 2009, 64:9–15. 36. Dziewanowska K, Patti JM, Deobald CF, Bayles KW, Trumble WR, Bohach GA: Fibronectin binding protein and host cell tyrosine kinase are required for internalization of Staphylococcus aureus by epithelial cells. Infect Immun 1999, 67:4673–4678. 37. Jevon M, Guo C, Ma B, Mordan N, Nair SP, Harris M, Henderson B, Bentley G, Meghji S: Mechanisms of internalization of Staphylococcus aureus by cultured human osteoblasts. Infect Immun 1999, 67:2677–2681. 38. Lammers A, Nuijten PJM, Smith HE: The fibronectin binding proteins of Staphylococcus aureus are required for adhesion to and invasion of bovine mammary gland cells. FEMS Microbiol Lett 1999, 180:103–109. 39.

Measurements are made at 540 nm, and require a non-specific intercalating dye [12]. Real-time PCR detection can be performed by using free dyes or labelled sequence-specific probes. One combination of the two techniques uses unlabelled probes for the amplicon detection and Tm determination [13]. Another parallel application was the combination of TaqMan chemistry and the very new, aspecific dye, Apoptosis inhibitor BOXTO, as a multiplex PCR [14]. The novelty of our prototype

system lies in the use of non-specific SYBR Green dye as a donor molecule, instead of a labelled primer or other specific anchor probe. With this technique, it is possible to examine pathogenic fungi, G + and G- bacteria in a single tube multiplex PCR reaction. Results and discussion Discrimination of the fungal, G + and G- bacterial pathogens DNA samples from all species studied were prepared and amplified successfully with the SYBR Green dye-based method in the LightCycler instrument. Species-specific Tm-s were obtained by melting-point analysis on three detection channels and all pathogens were identified correctly as fungi or G- or G + bacteria (Table 1). On the F1 channel (540 nm), the melting points of all the amplicons (Tm A) were visible, due to the fluorescent signal of the SYBR Green non-specific intercalating dye. On the F2 (640 nm) and F3 (705 nm) channels, XAV 939 the G- and the G + probes (Tm P), respectively, gave fluorescence

signals. After the discrimination of the G- and G + strains, the fungal pathogens could be screened, because the fungal strains gave no signal on the F2; F3 channels. Table 1 Melting points of bacterial and fungal amplicons and probes Microbial strains Tm P (°C) Tm A (°C) Gram positive (G+) Mean SD Mean SD Enterococcus faecalis 67.94 0.07 84.14 0.36 Enterococcus faecium 67.84 0.21 84.59 0.78 Listeria monocytogenes 67.80

0.19 86.01 0.36 Staphyloccus aureus 64.85 0.21 83.91 0.54 Staphyloccus epidermidis 64.50 0.30 83.60 0.36 Streptococcus pyogenes 46.54 0.56 84.38 0.78 Gram negative (G-)         Acinetobacter baumannii 66.09 0.15 82.90 0.16 Bacteroides fragilis 48.65 0.18 84.47 0.84 Enterobacter aerogenes 63.95 0.34 83.47 0.48 Enterobacter cloacae 64.98 0.09 84.38 0.24 Escherichia coli 64.69 0.44 84.74 0.54 Thalidomide Haemophilus influenzae 61.99 0.35 84.28 0.30 Klebsiella pneumoniae 65.13 0.23 84.57 0.20 Proteus vulgaris 64.58 0.18 82.87 0.24 Pseudomonas aeruginosa 53.32 0.33 83.00 0.34 Serratia marcescens 64.01 0.30 84.17 0.30 Stenotrophomonas maltophilia 58.10 0.07 84.42 0.15 Fungi         Candida albicans – - 87.1 0.33 Candida dubliniensis – - 85.5 0.50 Candida quillermondii – - 85.1 0.70 Candida krusei – - 89.8 0.02 Candida parapsilosis – - 85.4 0.88 Candida tropicalis – - 84.5 0.75 Aspergillus fumigatus – - 91.0 0.38 All the amplicons Tm were measured at the F1 channel (540 nm). The signal was generated by aspecific SybrGreen dye.

Experimental procedures In order to evaluate the blood leukocyte and glucose levels of C. callosus infected with P. brasiliensis, the animals Vistusertib clinical trial were i.p. injected followed by macroscopic and microscopic evaluations done at days 7, 15, 30, 45, 60, and 75 post infection (three to four animals were analyzed

per group at each time point of infection). The organs showing macroscopic lesions were selected for further analysis. Control groups consisted of three animals per time point inoculated with sterile saline. To determine the role of estrogen during P. brasiliensis infection, an additional C. callosus group (seventy animals) was subdivided into two sets: one being bilaterally see more ovarectomized (31 animals) and the other sham-operated (39 animals). Forty days after surgery, all animals were inoculated in the peritoneum with 1 × 106 viable infective forms of P. brasiliensis. An additional control group consisting of non-operated and non-infected animals (5 animals per

time point) received only saline injection. Histology On days 15, 45, 60, and 75 of infection, two to three animals from each group were sacrificed, grossly inspected, and fragments of mesentery, liver, spleen, pancreas, and lungs were collected and fixed in 10% formaldehyde. Representative sections from each organ were embedded in paraffin, processed and stained with haematoxilin-eosin (HE). Quantification of the lesion extensions was determined using a computer-aided densitometric software (OPTIMAS Bioscan Inc. WA, Sitaxentan USA). For each organ, five slides with tissue sections were entirely evaluated. The number and area of the granulomas were determined, and the extent of tissue section occupied by the lesion was calculated by dividing the area occupied with lesions by the total area of the organ. Leukocyte counts and glucose levels Blood samples for leukocyte counts or glucose determinations were withdrawn from the retro-orbital plexus. Leucocytes were counted in a haemocytometer and the results were reported

as number of leukocytes per mL of blood. Serum glucose levels were determined by the method of Trinder [18] and reported as mg/dL. Results PB01 infection in Calomys callosus Gross inspection of C. callosus i.p. infected with 106 yeast forms of PB01 revealed peritonitis characterized by the presence of exudates containing a large number of yeast cells. Adherence involving several parts of mesentery and spleen was also observed. These signs increased in intensity with time from injection of the fungus until the infection turned to the chronic phase (sixty days post infection). Following the acute phase of the inflammatory reaction, the infection became circumscribed due to granuloma formation in the peritoneal cavity as well as in several distant organs such as the liver, spleen, lungs, and pancreas.

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