Thus, measures of oxygen consumption (VO2, L/min), minute ventilation (VE, L/min), and heart rate (BPM) were incorporated into the protocol. Using standard indirect calorimetry procedures, a portable metabolic system (Oxycon Mobile, Viasys Healthcare, Yorba Linda, CA) was worn by each AZD9291 subject using a modified hydration backpack (Slipstream; Camelbak Products, LLC; Petaluma, CA). The oxygen and carbon dioxide analyzers were calibrated prior to each test using a certified

gas mixture. Both analyzers, as well as the ventilation meter, were calibrated prior to each test according to the manufacturer’s guidelines. The metabolic system collected breath-by-breath data which was then reported as 60-sec (for the Constant-Power Test) and 5-sec sample intervals (UBP10 and UBP60 tests) for both VO2 and VE. Using selleck chemicals llc a Polar Accurex Plus heart rate monitor strap (Polar Electro, Inc., Lake Success, NY), the metabolic system also collected and reported heart rate (BPM) data over the same 60- and 5-sec intervals. During JPH203 testing, the raw data signals from the metabolic system, including that for HR, were transmitted via telemetry to a computer base station within 20 meters of the UBP ergometer (telemetry

range is < 1000 meters). Blood lactate analyzer Using the handheld Lactate Pro analyzer (Arkray, Inc., Kyoto, Japan), whole blood lactate from a single fingertip

blood droplet is analyzed in 60 seconds. The reagent test strip for the meter requires 5 μl of whole blood, sampled by capillary action, to initiate an internal chemical reaction and subsequent electrical current proportional to the lactate concentration. Obatoclax Mesylate (GX15-070) Previous research has shown that while correlations between blood lactate values from different analyzers using the same blood sample can be high (r ≥ 0.97), the absolute difference between monitors can be practically meaningful (± 2-3 mM) over the physiological range of 1-18 mM). To help control for known confounders to the measurement of blood lactate for this study, several precautions were taken. First, the monitor’s Check Strip (allows a self-check by the monitor) and Calibration Strip (comes with each box of reagent strips) was utilized prior to each test session. Second, it is known that lactate concentrations can vary between boxes of test strips for the same blood sample. To help control for this variability, a single box of test strips was assigned to each subject for both pre- and post-testing lactate measures. Third, fingertip sampling for blood lactate can be highly variable due to inconsistent skin cleaning and sampling procedures. Lastly, it is possible for individual Lactate Pro meters to provide slightly variable lactate measures for the same blood sample.

While the various clustering methods resulted in slightly different final hierarchies, all were consistent in separating the unexposed control from the samples exposed to B. anthracis or to the Y. pestis and near neighbors. Agreement on this level among the various clustering procedures lends more confidence to the overall results. On a more detailed level, the methods grouped slightly differently the samples exposed to the Y. pestis and near neighbors, which indicates that these samples cannot be unequivocally

separated based on the current data and additional biomarkers or a larger sample set would be needed. The most advanced HOPACH method estimated the optimal number of clusters in the data as five, corresponding to the unexposed control, ARN-509 and the four species: B. anthracis, Y. pseudotuberculosis, Y. enterocolitica, and Y. pestis (avirulent and virulent) (Figure 3). Information gained from the targeted protein array data for host response complements genomic [52–56], and other proteomic studies [57–60] of host-pathogen interactions. The success of the WEEM and computational method to distinguish pathogen exposure, based on host response in this initial study, is encouraging and suggests a number of possibilities for future studies to refine the findings. Comparative analysis, such as the current work, can potentially reveal the critical pathogenic mechanism(s) and host innate immune responses

during infection as was previously shown for Y. pestis and Y. pseudotuberculosis[61]. Opportunities include using Rigosertib clinical trial statistical hypothesis tests based on analysis of variance to assess the significance of the observed differences among the host-pathogen cytokine concentration profiles, as well as performing follow-up studies to focus more on the Y. pestis and near neighbor cluster. In addition, the methods can be extended to investigate host responses to diverse pathogens in multiple host model

systems to cross validate the significance of the biomarkers to distinguish pathogen exposures. Conclusion Veliparib manufacturer results from this study suggest that cytokine arrays coupled with statistical clustering methods can distinguish exposures to pathogens, including multiple Histone demethylase strains of Y. pestis, Y. pseudotuberculosis, Y. enterocolitica, and B. anthracis. These methods differentiate both near neighbors and distant evolutionary microbes based on host response data. The distinct cytokine profiles also provide insight into both the host response and virulence mechanisms of diverse pathogens. In summary, characterization of host responses based on cytokine profiles has translational application, potentially providing the identification of infectious diseases and leading toward the ultimate goal of presymptomatic detection via sentinel surveillance of pathogen exposure and appropriate treatment. Acknowledgments We thank David Callender, Jonathan E. Forman, and Renee Tobias from Zyomyx for their assistance with the biochip analyses.

Isolates of the Bromosporine Iberian clone exhibited resistance against almost all antibiotics available for MRSA therapy including clindamycin, erythromycin, gentamicin, tobramycin, tetracycline, ciprofloxacin and rifampicin. From 1996 to 2003, the Iberian clone was gradually replaced by isolates of Clonal Complex 5 (ST125 and variants; selleck chemicals SCCmec type IV) related to the Paediatric clone (ST5; SCCmec type IV) [4]. Unlike the Iberian clone, these strains showed only consistent resistance to tobramycin and ciprofloxacin combined with variable resistance to clindamycin and/or erythromycin. Similar trends have been observed in other hospitals in Spain and in other countries such as

France, Germany, Belgium or Portugal, with involvement of different clonal lineages [5–10]. MRSA isolates resistant to clindamycin, erythromycin, gentamicin, tobramycin, and ciprofloxacin were detected in 2004. These isolates showed reduced susceptibility to rifampicin (RIF-R), according to the Clinical and Laboratory Standards Institute (CLSI) criteria [11]. This new phenotype Dehydrogenase inhibitor of multiresistance differed from that of the Iberian clone on the low level RIF-R and on the tetracycline susceptibility. The frequency of the RIF-R

MRSA isolates rapidly increased from 2004 to 2006: 25% (59/237) of all MRSA clinical isolates in 2004, 33% (67/206) in 2005, and 45% (116/256) in 2006. The percentage of RIF-R MRSA decreased to 30% (111/378) in 2007 and 25% in 2008 (75/300). Ibrutinib Rifampicin

cannot be used as a single agent to treat MRSA infections because of the rapid selection of resistant mutants [12, 13]. However, combinations of rifampicin with other anti-staphylococcal agents such as quinolones [14] or fusidic acid [15] could prevent the emergence of rifampicin resistance during therapy [16]. Rifampicin interacts specifically with the RNA polymerase beta-subunit encoded by the gene rpoB [12]. Rifampicin resistance in S. aureus, as in other bacteria, is associated with mutations in particular regions (cluster I and II) of the gene rpoB [13, 17]. The objectives of the present study were: i) to characterise a collection of MRSA isolates expressing this new multiresistant pattern, and to determine whether they represented a novel genotype or they were the current representatives of a previously detected clone, ii) to determine the different levels of the rifampicin resistance by disk diffusion, microdilution and E-test, and iii) to analyse mutations in the rpoB gene related to rifampicin resistance. Methods Hospital setting The Hospital Universitari de Bellvitge in Barcelona, Spain, is a nearly 900-bed tertiary care teaching centre. It is the reference hospital for a geographical area with a population of approximately 1 million inhabitants.

CX: literature search, serum collection and treatment, data analysis of mass-spectrum, draft of the manuscript. BBZ: data analysis of mass-spectrum, revise the article. ML: direct and help to the experiment. KFD: serum collection and treatment. MH: direct and help to the experiment. selleck All authors read and approved the final manuscript.”
“Background Gastric cancer is the fourth most common malignancy and the second cause of death [1]. Many studies indicated that gastric carcinoma is a polygenic disease with multistep processes for the abnormal development of many related genes [2]. However, the regulatory mechanism involved in the development of canceration is still not well understood.

Recently, researchers have found a new class of short, endogenously non-coding RNAs called microRNAs(miRNAs) in animals and plants [3–5]. They regulate the expression of protein-coding genes via degrading or inhibiting the translation of the targeted mRNAs[6]. Accumulated evidences demonstrated

miRNAs play important role in carcinogenesis. Xiao indicated miRNA-106a (miR-106a) had oncogenic activity in humans. The level of miR-106a in cancer tissues was significantly higher than that in non-tumor tissues expression [7]. Another paper showed that restoration of tumor suppressor miR-34 this website inhibits human p53-mutant gastric cancer tumorspheres [8]. Together, these observations suggest the possible existence of cancer-specific miRNAs. For this reason, miRNAs expression profiling has been investigated in different kinds of cancer to identify cancer-specific miRNAs [9–13]. In the present study, we detected the expression profiling of 328 miRNAs in 2 cell

lines, 24 gastric cancer samples and 3 normal gastric tissue samples, revealing the miRNA characteristics of gastric cancer. Furthermore, our data suggested significantly down-regulated A 1155463 miR-433 and miR-9, which were considered as the modulator of GRB2 and RAB34 respectively. GRB2 and RAB34 were involved in the molecular pathogenesis of gastric cancer. Methods Gastric tissues and cell lines culture All human gastric tissue samples including 3 normal gastric tissues and 24 malignant tissues (2 in early phase and 22 in late phase of gastric cancer) were obtained from General surgery dept. of the First and Second Sclareol Affiliated Hospital of Chongqing Medical University (Chongqing, China). All the patients signed the informed consent. The tissues were stored in liquid nitrogen after removing from patients. Gastric cancer cell SGC7901 was donated by Viral Hepatitis Research Institute of Chongqing Medical University (Chongqing, China). Gastric cell line GES-1 was purchased from Cancer Institute and Hospital of Chinese Academy of Medical Sciences (Beijing, China). Both cell lines were cultured in serum-free Roswell Park Memorial Institute (RPMI) 1640 medium supplemented with 10% low-endotoxin FCS.

Since Western blot was performed in denaturing conditions (after SDS-PAGE) the band depicted with asterisk might be observed due to the formation of a mixed disulfide bond between Pof1p and Ubc7p. Pof1p possesses six cysteine residues. Probably the concentrations of DTT (1 mM) employed were

too low to reduce the mixed disulfide between Pof1p and Ubc7p. Taking advantage of the anti-Pof1p antibody, the Pof1p sub-cellular distribution was studied. A punctuated Pof1p distribution in was observed in wild-type cells (Figure 6), which was more evident in Δpct1 cells. This is in agreement with higher protein expression of Pof1p in Δpct1 cells, which was also observed by Western blotting (data not shown), suggesting a compensatory response. Based on previous immunocytochemistry studies [30], we speculate that Pof1p localizes to the Golgi compartment. Figure 6 Immunocytochemistry assays to find more study Pof1 protein cell localization and distribution. The POF1 null cells were used as a negative control to establish antibody background levels. Discussion The first suggestion that the POF1 gene

was related to the protein quality control response arose from wide-scale studies about the relationship between MG 132 the ERAD and UPR systems [20]. Indeed, mRNA levels of POF1 gene were significantly increased in cells that were treated with ER stress agents (DTT and tunicamycin), and this induction was dependent on both Ire1p and Hac1p. In addition, a proteasome inhibitor (PS-341) provoked a four-fold induction of POF1 gene expression [31]. Furthermore, the expression of POF1 gene is repressed in the Δopi1 strain [20], suggesting an involvement of Pof1p with membrane and protein metabolism. The viability data presented here are in agreement with this idea, especially when considering the fact that all

stressful conditions tested (oxidative, heat shock, and ER stress in Figures 1, 2 and 4) Bcl-w are well known to provoke protein misfolding. Yet, oxidative stress and heat shock (Figures 1 and 2) caused the most severe phenotypes in Δpof1 cells, which is likely due to the fact that these stresses check details damage both membrane and protein homeostasis [32, 33]. The fact that POF1 overexpression was able to complement the function of PCT1 in Δpct1 cells during heat shock (Figure 2) and its expression levels by Opi1p [20] suggests the involvement of Pof1p in membrane lipid metabolism. In addition, the levels of Pof1p are augmented in Δpct1 cells (Figure 6 and western blot analyses – data not shown), which indicated that Pof1p might at least partially backing up Pct1p. However, the molecular function of Pof1p could not be directly related to membrane lipid synthesis although the protein displayed ATPase activity (Figure 3).

PubMedCrossRef 39. Bermudez LE, Goodman J: Mycobacterium tuberculosis invades and replicates within type II alveolar cells. Infection and immunity 1996,64(4):1400–1406.PubMed 40. El-Shazly S, Ahmad S, Mustafa AS, Al-Attiyah R, Krajci D: Internalization by HeLa cells of latex beads coated

with mammalian cell entry (Mce) proteins encoded by the mce3 selleck kinase inhibitor operon of Mycobacterium tuberculosis . Journal of medical microbiology 2007,56(Pt 9):1145–1151.PubMedCrossRef 41. Rezwan M, Grau T, Tschumi A, Sander MK-1775 clinical trial P: Lipoprotein synthesis in mycobacteria. Microbiology (Reading, England) 2007,153(Pt 3):652–658.CrossRef 42. Nguyen KT, Piastro K, Derbyshire KM: LpqM, a mycobacterial lipoprotein-metalloproteinase, is required for conjugal DNA transfer in Mycobacterium smegmatis . Journal of bacteriology 2009,191(8):2721–2727.PubMedCrossRef 43. Andersen P, Askgaard D, Ljungqvist L, Bennedsen J, Heron I: Proteins released from Mycobacterium tuberculosis during growth. Infect Immun 1991,59(6):1905–1910.PubMed 44. Andersen P, Askgaard D, Ljungqvist L, Bentzon MW, Heron I: T-cell proliferative response to antigens secreted by Mycobacterium tuberculosis . Infect Immun 1991,59(4):1558–1563.PubMed 45. Horwitz MA, Lee BW, Dillon BJ, Harth G:

Protective immunity against tuberculosis induced by vaccination with major extracellular proteins of Mycobacterium tuberculosis . Proceedings of the National Academy of Sciences of the United States of America 1995,92(5):1530–1534.PubMedCrossRef 46. Orme IM: Induction of nonspecific acquired resistance and delayed-type hypersensitivity, find more but not specific acquired resistance in mice inoculated with killed mycobacterial vaccines. Infect Immun 1988,56(12):3310–3312.PubMed 47.

Garcia-Perez BE, Mondragon-Flores R, Luna-Herrera J: Internalization of Mycobacterium tuberculosis by macropinocytosis in non-phagocytic cells. Microb Pathog 2003,35(2):49–55.PubMedCrossRef 48. Igietseme JU, Eko FO, He Q, Black CM: Antibody regulation of Tcell immunity: implications for Mannose-binding protein-associated serine protease vaccine strategies against intracellular pathogens. Expert review of vaccines 2004,3(1):23–34.PubMedCrossRef 49. Maglione PJ, Chan J: How B cells shape the immune response against Mycobacterium tuberculosis . Eur J Immunol 2009,39(3):676–686.PubMedCrossRef Authors’ contributions DPC carried out molecular assays and drafted the manuscript. MO participated in the experimental design, data analysis and interpretation, and critically revised the manuscript. MAP participated in the experimental design and coordinated the study. HC carried out ligand-receptor assays. MV participated in the peptide synthesis. MF carried out immunoassays. MEP conceived and supervised the study. All authors read and approved the final manuscript.”
“Background Ciliates are a diverse group of unicellular eukaryotes characterized by two kinds of nuclei in each cell: a germline micronucleus and a somatic macronucleus.

Tumor-associated macrophages (TAMs) represent a substantial fraction of the growing tumor mass and are associated with poor prognosis in several human cancers [8]. TAMs exist in two different polarizations www.selleckchem.com/products/epz-6438.html state classified as M1 and M2. M1 macrophages show a protective

role in tumor-genesis activating tumor-killing mechanisms and antagonizing the activities of M2. M2 macrophages are clearly involved in learn more suppression of adaptive tumour-specific immune responses and in promotion of tumour growth, invasion, stroma remodelling and angiogenesis [9–13]. Considering the rationale of BCG use, we hypothesized that endovescical instillation efficacy could be modulated according to TAM polarization and conversely macrophage could be influenced by BCG itself. Material and methods A total of 40 patients (36 males and 4 females), mean age 69 years (40-83 years), diagnosed with non-muscle invasive bladder cancer (NMIBC) at our institution

(Campus Bio-Medico, Eltanexor price University of Rome) from 1999 to 2011 were selected randomly for study. Between them, 23 patients had not recurrence at follow-up versus 17 patients with bladder cancer recurrence. Diagnosis of bladder cancer was made by histological examination of specimens obtained by transurethral bladder biopsy. Histological specimens were fixed in 10% neutral buffered formalin and routinely processed for paraffin Phospholipase D1 embedding. Serial 5 μm sections were cut, stained with hematoxylin and reviewed by a pathologist. All patients underwent same intravescical BCG regimens (80 mg Immucyst/80 ml Salin solution 0.9%). After initial therapy, patients were followed with periodic

cystoscopy, urine cytology and Uro-TC. We evaluated two consecutive histological sections (before and after intravescical BCG instillations) by Immunoflorescence. Histologic reviewers were blinded to recurrence outcomes. TAMs were labeled using CD68 monoclonal antibody (monoclonal mouse clone PG-M1), Ab anti-iNOS (Rabbit mAb) and Ab anti-CD163 (Rabbit mAb; 1:200). DAPI was used for detection of nucleate cells. Cells positive for CD68 were considered whole macrophage population (Mtot); cells positive for CD68 and CD163 were considered M2 population and those positive for CD68 and iNOS were considered M1 population (Figures 1 and 2). Figure 1 CD68/CD163 expression in M2 macrophage in bladder cancer. A) CD68 (green), shows nucleated cells positive staining for CD68; B) CD163 (red 2), shows CD163 staining in macrophage phenotype; C) DAPI, shows the cell nuclei marked with DAPI; D) merged image of DAPI, CD68 and CD163 showing a number of macrophages with positive staining for the phenotype marker M2. Original magnification × 400. Figure 2 CD68/iNOS expression in M1 macrophage in bladder cancer.

Manufacturer’s manuals were

followed for BioPlex (Bio-Rad, Inc) and human IL-8 ELISA assay (BD OptEIATM, BD Bioscience). For Bio-Plex analysis, 2 μl of anti-cytokine conjugated beads were added to each well, followed by diluted culture supernatants. After 30 min incubation, samples were washed three times with Bio-Plex wash buffer, and then 25 μl of detection antibody solution was added and incubated for another 30 min. Streptavidin-phycoerythrin (1X; 50 μl) was added to each well and then washed. For hIL-8 ELISA, duplicate measurements were done for four separate experiments. Samples check details were read at 450 nm on an ELISA reader (Bio-Rad), of which lowest detection limit was 0.8 pg/ml (BD OptEIATM, BD Bioscience). Functional analysis and network generation Online

computational tools of Metacore (Thomson Reuters, Philadelphia, PA) were used to identify annotated networks of interacting genes, pathways and associated biological functions among genes profiled Evofosfamide supplier from the microarray analysis, using more than 700 canonical maps and pathways which are continuously being updated (http://​www.​genego.​com). The networks generated were ranked and built according to G-scores and p values. Statistical analysis All data in each experiment of ELISA and real time PCR are presented as mean ± SEM of three or four different experiments. To check for any difference between the several treatments we did a one-way ANOVA analysis. To determine differences between specific treatments we did a two-tailed unpaired t-test. Acknowledgements This work was supported many in part by a grant of the Translational Research Initiative of the Louisiana State University Health Sciences Center and by the Louisiana Cancer Research Consortium (LCRC) and COBRE Grant number 149740220B (to JZ) and Public Health Service Grant RO1 CA101931 (to DJM from the National Institutes of Health). References 1. Blaser MJ: Helicobacter pylori and gastric diseases. BMJ 1998, 316:1507–1510.PubMedCrossRef 2. Day AS, Jones NL, Policova Z, Jennings HA,

Yau EK, Shannon P, et al.: Characterization of find more virulence factors of mouse-adapted Helicobacter pylori strain SS1 and effects on gastric hydrophobicity. Dig Dis Sci 2001, 46:1943–1951.PubMedCrossRef 3. Backert S, Ziska E, Brinkmann V, Zimny-Arndt U, Fauconnier A, Jungblut PR, et al.: Translocation of the Helicobacter pylori CagA protein in gastric epithelial cells by a type IV secretion apparatus. Cell Microbiol 2000, 2:155–164.PubMedCrossRef 4. Gebert B, Fischer W, Weiss E, Hoffmann R, Haas R: Helicobacter pylori vacuolating cytotoxin inhibits T lymphocyte activation. Science 2003, 301:1099–1102.PubMedCrossRef 5. Mobley HL, Island MD, Hausinger RP: Molecular biology of microbial ureases. Microbiol Rev 1995, 59:451–480.PubMed 6.

The presence of metal nanoparticles in CNT array, as it was shown in [20–23], plays the important role in the energy absorption by the array. The importance of the present investigation is defined by the possible

applications of the obtained CH5183284 results. The arrays of CNTs with the intercalated ferromagnetic nanoparticles, so called magnetically functionalized CNTs (MFCNTs) [31, 32], may be considered as an ideal medium for different magnetic applications. They can be used as sensors, sensitive elements of magnetometers, magnetic filters, ferrofluids, xerography, magneto-resonance imaging, magnetic hypothermia, and biomedical applications. The superior application of oriented MFCNT arrays can be in a sphere of magnetic write/read heads and high-density data storage devices [33–36]. The FSL irradiation may become an instrument for the machining of the mentioned devices based on the arrays of MFCNTs. In particular, in the present work, we investigate the surface morphology

modification of the vertically aligned MFCNTs upon FSL irradiation and Ivacaftor in vitro properties of the products obtained after irradiation and develop the mechanism of the interaction of FSL with such complicated media as the arrays of MFCNTs. Methods CNT arrays were synthesized on Si substrates by the floating catalyst CVD via a high-temperature pyrolysis of the xylene/ferrocene learn more solution injected into the reaction zone of quartz reactor. In our particular case, the concentration of ferrocene in the solution was 10%; the temperature in the reaction zone was 875°C, and the process duration was 30 s. Obtained as a result of ferrocene decomposition, Fe phase nanoparticles serve as catalyst for CNTs growth. During the growth process, these nanoparticles are intercalating into CNT arrays and are considered as fillers of CNTs. The morphology of the CNT arrays before and after the FSL irradiation was investigated by scanning electron microscopy (SEM) (Hitachi

S-4800 FE-SEM, Chiyoda-ku, Japan). For Raman measurements, Renishaw micro-Raman Spectrometer (Series1000, Renishaw, Wotton-under-Edge, UK) with much laser beam of 1.5 mW incident power and 514 nm wavelength was used. The structure of CNTs was characterized by transmission electron microscopy (TEM, JEM 100-CX, JEOL) and a high-resolution TEM (JEM-2010, JEOL Ltd., Akishima-shi, Japan). For X-ray diffraction analysis (XRD), DRON-3 diffractometer (Bourevestnik, Inc., Maloochtinskiy, Russia) was used; the local configurations of iron ions of CNTs fillers were examined with Mössbauer spectroscopy (spectrometer MS2000 with Fe/Rh source, 40 mCu). Elemental analysis was made by energy-dispersive X-ray spectroscopy (EDX) (SUPRA-55WDS with the EDX prefix, Carl Zeiss, Inc., Oberkochen, Germany).

vulgare . Gene transcripts were quantified by RT-qPCR and normalized with the expression of the ribosomal protein (RbL8) and the Elongation Factor 2 (EF2). Each bar represents the mean of three independent measurements with standard error. (PDF 132 KB) References 1. Werren JH, Baldo L, Clark ME: Wolbachia : master manipulators

of invertebrate biology. Nat Rev Microbiol 2008, 6:741–751.PubMedCrossRef 2. Bouchon D, Cordaux R, Grève P: Feminizing Wolbachia and the evolution of sex determination in isopods. In Insect symbiosis. selleck chemicals llc Volume 3. Edited by: Bourtzis K, Miller TA. Boca Raton, FL: Taylor & Francis Group; 2008:273–294.CrossRef 3. Cordaux R, Bouchon D, Grève P: The HM781-36B nmr impact of endosymbionts on the evolution of host sex-determination mechanisms. Trends Genet 2011, 27:332–341.PubMedCrossRef 4. Negri I, Pellecchia M, Grève P, Daffonchio D, Bandi C, Alma A: Sex and stripping: the key to the intimate relationship between Wolbachia and host? Commun Integr Biol 2010, 3:110–115.PubMedCrossRef 5. Cordaux R, Michel-Salzat A, Frelon-Raimond M, Rigaud T, Bouchon D: Evidence for a new feminizing Wolbachia strain in the isopod Armadillidium

vulgare : evolutionary implications. Heredity 2004, 93:78–84.PubMedCrossRef 6. Lachat M: Impact de deux souches de Wolbachia sur les traits d’histoire de vie de leurs hôtes Armadillidium vulgare . PhD thesis. Université de Poitiers, Ecole doctorale ICBG; 2009. 7. Moreau J, Bertin A, Caubet Y, Rigaud T: Sexual selection in an isopod with Wolbachia -induced sex reversal: males prefer real females. J Evol Biol 2001, Selleckchem AICAR 14:388–394.CrossRef 8. Rigaud T, Moreau J: A cost of Wolbachia -induced sex reversal and female-biased sex ratios: decrease in female fertility after sperm depletion in a terrestrial isopod. Proc Biol Sci 2004, 271:1941–1946.PubMedCrossRef 9. Lachat M, Caubet Y, Bouchon Depsipeptide order D: Does Wolbachia influence survival in starved Armadillidium vulgare ? In Proceedings of the International Symposium of Terrestrial

Isopod Biology ISTIB 07; Tunis. Edited by: Zimmer M, Charfi-Cheikhrouha F, Taiti S. Shaker Verlag; 2008:125–130. 10. Braquart-Varnier C, Lachat M, Herbinière J, Johnson M, Caubet Y, Bouchon D, Sicard M: Wolbachia mediate variation of host immunocompetence. PLoS ONE 2008, 3:e3286.PubMedCrossRef 11. Sicard M, Chevalier F, De Vlechouver M, Bouchon D, Grève P, Braquart-Varnier C: Variations of immune parameters in terrestrial isopods: a matter of gender, aging and Wolbachia . Naturwissenschaften 2010, 97:819–826.PubMedCrossRef 12. Cook PE, McGraw EA: Wolbachia pipientis : an expanding bag of tricks to explore for disease control. Trends Parasitol 2010, 26:373–375.PubMedCrossRef 13. Fytrou A, Schofield PG, Kraaijeveld AR, Hubbard SF: Wolbachia infection suppresses both host defence and parasitoid counter-defence. Proc Biol Sci 2006, 273:791–796.PubMedCrossRef 14.