Overall MANOVA analysis revealed

a significant time effect (Wilks’ Lambda p = 0.02) with no significant overall interaction (Wilks’ Lambda p = 0.26). Univariate MANOVA analysis revealed some small time effects in chloride levels (p = 0.008) and a trend toward an interaction in potassium levels (p = 0.08) but the small changes observed would have no clinical significance. Finally, Table 12 shows whole blood markers assessed throughout the study. Overall MANOVA revealed no significant time (Wilks’ Lambda p = 0.25) or group x time effects (Wilks’ Lambda p = 0.78). Apoptosis inhibitor Likewise, no significant interactions were observed among groups in white blood cell count (WBC, p = 0.45), red blood cell count (RBC, p = 0.64), hematocrit (p = 0.65), hemoglobin (p = 0.59), mean corpuscular volume (MCV, p = 0.56), mean corpuscular hemoglobin this website (MCH, p = 0.44), mean corpuscular hemoglobin concentration (MCHC, p = 0.68), red blood cell distribution width (RBCDW, p = 0.92), or platelet count (p = 0.48). Table 12 Serum electrolyte status Marker N Group Day   p-level       0 7 28     Sodium (mmol/L) 11 KA-L 140.1 ± 2.3 139.9 ± 1.1 140.0 ± 1.3 Group 0.98   12 KA-H 139.9 ± 2.3 139.7 ± 2.4 140.3 ± 2.1 Time 0.28   12 CrM

140.8 ± 2.1 139.3 ± 1.4 139.7 ± 1.6 G x T 0.57 Potassium (mmol/L) 11 KA-L 4.54 ± 0.3 4.86 ± 0.4 4.82 ± 0.3 Group 0.65   12 KA-H 4.89 ± 0.5 4.71 ± 0.6 5.00 ± 0.3 Time 0.11   12 CrM 4.74 ± 0.4 Florfenicol 4.93 ± 0.4 4.81 ± 0.4 G x T 0.08 Chloride (mmol/L) 11 KA-L 103.3 ± 2.2 103.0 ± 2.4 103.8 ± 1.9 MRT67307 price Group 0.21   12 KA-H 102.4 ± 2.2 101.5 ± 2.2 102.6 ± 2.4 Time 0.008   12 CrM 104.3 ± 2.2 102.3 ± 1.7

103.1 ± 1.8 G x T 0.21 Values are means ± standard deviations. Data were analyzed by MANOVA with repeated measures. Greenhouse-Geisser time and group x time (G x T) interaction p-levels are reported with univariate group p-levels. Table 13 Whole blood markers Marker N Group Day   p-level       0 7 28     WBC (x103/ul) 9 KA-L 5.73 ± 0.6 6.13 ± 0.5 6.17 ± 1.5 Group 0.95   12 KA-H 5.83 ± 1.1 5.76 ± 0.9 6.36 ± 1.1 Time 0.16   12 CrM 5.97 ± 1.2 5.73 ± 1.0 5.98 ± 1.2 G x T 0.45 RBC (x106/ul) 9 KA-L 5.44 ± 0.4 5.38 ± 0.5 5.44 ± 0.3 Group 0.28   12 KA-H 5.10 ± 0.4 5.18 ± 0.3 5.23 ± 0.3 Time 0.91   12 CrM 5.42 ± 0.5 5.41 ± 0.5 5.35 ± 0.7 G x T 0.64 Hematocrit (%) 9 KA-L 48.4 ± 3.4 47.9 ± 4.3 48.1 ± 2.9 Group 0.17   12 KA-H 46.5 ± 3.2 47.0 ± 2.8 47.4 ± 1.8 Time 0.96   12 CrM 45.9 ± 2.3 46.1 ± 2.5 45.2 ± 5.4 G x T 0.65 Hemoglobin (g/dl) 9 KA-L 16.0 ± 1.6 16.0 ± 1.6 16.0 ± 1.2 Group 0.21   12 KA-H 15.2 ± 1.2 15.7 ± 1.0 15.6 ± 0.7 Time 0.60   12 CrM 15.1 ± 0.9 15.2 ± 1.1 14.9 ± 2.0 G x T 0.62 MCV (fL) 9 KA-L 89.0 ± 2.8 88.9 ± 2.9 88.3 ± 2.8 Group 0.10   12 KA-H 91.1 ± 3.5 90.8 ± 3.1 90.7 ± 3.6 Time 0.03   12 CrM 85.4 ± 9.2 85.7 ± 9.5 85.0 ± 9.1 G x T 0.56 MCH (pg/cell) 9 KA-L 29.4 ± 1.5 29.6 ± 1.2 29.3 ± 1.2 Group 0.

It was also tested if the growth of LVS and ΔmglA on solid medium was affected by the oxygen concentration. Approximately 100 bacteria were spread onto agar plates that were incubated in an aerobic or a microaerobic milieu. LVS formed colonies > two mm in size in both environments within 6 days but with delayed kinetics aerobically (Table 1). ΔmglA formed only few and small colonies on plates incubated aerobically. In the microaerobic milieu, however, it formed colonies Akt inhibitor of the same size as LVS, but with slightly delayed kinetics. Thus, regardless of growth medium used, ΔmglA appeared to

exhibit markedly impaired growth under aerobic conditions. Table 1 Size of colonies formed by LVS and ΔmglA on agar plates under aerobic or microaerobic conditions   Colony sizea Incubation time (days) Aerobic Microaerobic   LVS Δ mglA LVS Δ mglA

see more 2 0 0 1 0 3 1 0 2 1 6 3 MCb 3 3 a Colony size was graded as follows: 0 = Not visible, 1 = colonies <1 mm in diameter, 2 = 1.0 -2.0 mm. 3 = >2 mm in diameter b Mixed colonies, a few large colonies growing in close proximity to each other but most colonies were hardly visible Oxidized proteins in LVS and ΔmglA cultivated under aerobic or microaerobic conditions We hypothesized that the aberrant oxidative stress response of ΔmglA reported previously [8, 10] may lead to suboptimal handling of the effects of oxidation. We therefore attempted to quantify such effects at a more general level. To this end, we analyzed the presence of oxidized proteins using the OxyBlot method. Preparations from

ΔmglA cultivated under the aerobic conditions contained significantly more oxidized proteins than did those prepared from LVS (Figure 2). In contrast, the amounts of oxidized proteins were similar after cultivation in the microaerobic milieu. We noted some inter-experimental variation, but there were markedly increased amounts of oxidized proteins in the ΔmglA preparations under aerobic conditions in a majority of the experiments performed. FUU301 contained similar amounts of oxidized proteins as LVS regardless of growth condition (Figure 2). Figure 2 Analysis RVX-208 of oxidized proteins by the Oxyblot assay. Relative amounts of oxidized proteins in LVS, ΔmglA, or FUU301 during growth in an aerobic or microaerobic environment. Similar results were seen in two additional experiments. The first well of each preparation contained 2.5 ng of protein and the following wells two-fold dilutions www.selleckchem.com/products/shp099-dihydrochloride.html thereof. Controls contain non-derivatized samples, and demonstrate the specificity of the antibodies used for detection of oxidative damage. In summary, the marked accumulation of oxidized proteins in ΔmglA during growth in the aerobic milieu strongly suggested that the mutant had an impaired response to oxidation. This may have been a reason for its delayed and lower maximal growth in the aerobic milieu.

Appl Environ Microbiol 1997, 63:3233–3241.PubMed 28. Smit E, Leeflang P, Glandorf B, Van Elsas JD, see more Wernars K: Analysis of fungal diversity in the wheat rhizosphere by sequencing of cloned PCR-amplified genes encoding 18S rRNA and temperature gradient gel electrophoresis. Appl Environ Microbiol 1999, 65:2614–2621.PubMed 29. Chelius MK, Triplett EW: The diversity of Archaea and Bacteria in association with the roots of Zea mays L. Microb Ecol 2001, 41:252–263.PubMed 30. Gomes NCM, Heuer H, Schönfeld J, Costa R, Mendonça-Hagler L, Smalla K: Bacterial diversity of the rhizosphere of maize ( Zea mays ) grown in tropical soil studied by temperature

gradient gel electrophoresis. Plant Soil 2001, 232:167–180.CrossRef 31. Dias ACF, Dini-Andreote F, Taketani RG, Tsai SM, Azevedo JL, Melo IS, Andreote FD: Archaeal communities in the sediments of the three contrasting mangroves. J Soils Sediments 2011, 8:1466–1476.CrossRef 32. McCune B, Mefford MJ: PC-ORD: Multivariate analysis of ecological data. Oregon, USA: version 6.0 MjM Software, Gleneden Beach; 2011. 33. Monteiro JM, Vollú RE, Coelho MR, Alviano CS, Blank

AF, Seldin L: Comparison of the bacterial community and characterization of plant growth-promoting rhizobacteria from different genotypes of Chrysopogon zizanioides (L.) Roberty (vetiver) rhizospheres. J Microbiol 2009, Ipatasertib concentration 47:363–370.PubMedCrossRef 34. Tiwari R, Kalra A, Darokar MP, Quizartinib order Chandra M, Aggarwal N, Singh AK, Khanuja SP: Endophytic bacteria from Ocimum sanctum and their yield enhancing capabilities. Curr Microbiol 2010, 60:167–171.PubMedCrossRef 35. Franke IH, Fegan M, Hayward C, Leonard G, Sly LI: Molecular detection of Gluconacetobacter

sacchari associated with the pink sugarcane mealybug Saccharicoccus sacchari (Cockerell) and the sugarcane leaf sheath microenvironment by FISH and PCR. FEMS Microbiol Ecol 2000, 131:61–71.CrossRef 36. James EK, Gyaneshwar P, Mathan N, Barraquio WL, Reddy PM, Iannetta PP, Olivares FL, Ladha JK: Infection and colonization of rice seedlings by the plant growth-promoting RVX-208 bacterium Herbaspirillum seropedicae Z67. Mol Plant Microbe Interact 2002, 15:894–906.PubMedCrossRef 37. Sun L, Qiu F, Zhang X, Dai X, Dong X, Song W: Endophytic bacterial diversity in rice ( Oryza sativa L.) roots estimated by 16S rDNA sequence analysis. Microb Ecol 2008, 55:415–424.PubMedCrossRef 38. Marquez-Santacruz HA, Hernandez-Leon R, Orozco-Mosqueda MC, Velazquez-Sepulveda L, Santoyo G: Diversity of bacterial endophytes in roots of Mexican husk tomato plants ( Physalis ixocarpa ) and their detection in the rhizosphere. Genet Mol Res 2010, 9:2372–2380.PubMedCrossRef 39. Asis CA Jr, Adachi K: Isolation of endophytic diazotroph Pantoea agglomerans and nondiazotroph Enterobacter asburiae from sweetpotato stem in Japan. Lett Appl Microbiol 2003, 38:19–23.CrossRef 40.

(DOC 58 KB) References 1. Bleul CC, Wu L, Hoxie JA, Springer TA, Mackay CR: The HIV coreceptors CXCR4 and CCR5 are differentially expressed and regulated on human T lymphocytes. Proc Natl Acad Sci USA 1997, 94: 1925–1930.PubMedCrossRef 2. Zou YR, Kottmann AH, Kuroda M, Taniuchi I, Littman DR: Function of the chemokine receptor CXCR4 in haematopoiesis and in cerebellar development. Nature 1998, 393: 595–599.PubMedCrossRef 3. Busillo JM, Benovic JL: Regulation of CXCR4 signaling. Biochim Biophys Acta 2007, 1768: 952–963.PubMedCrossRef 4. Parkin DM, Bray F, Ferlay J, Pisani P: Global cancer statistics, 2002. CA

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Figure 3 Neutrophil recruitment inhibits the conidial germination in alveolar macrophages-depleted mice one day after infection. (A): Alveolar macrophage and neutrophil populations were counted in BAL fluids one day after infection of mice treated with the liposome control and clodrolip. N = 5 mice per group. One of three independent experiments is shown. * denotes a p-value < 0.05. (B): Light emission in BAL-fluids one day after infection of mice treated

with liposome control (upper cell well), clodrolip (middle cell well) and LCZ696 in vivo Cortisone acetate (lower cell well). BAL cells were collected by cytospin centrifugation using labtek chamber slides. D-luciferin was incorporated to the medium and luminescence acquired after 10 min with the IVIS 100 system. The graph shows the total luminescence evaluated JNK-IN-8 price by using the living image software 3.1. Furthermore, we performed an evaluation eFT508 price of the luminescence in the BAL one day after infection, comparing clodrolip versus liposomes (control) or cortisone acetate treated mice. Cortisone acetate was used as a positive control for fungal germination within the lung tissue, because we previously showed that cortisone acetate

inhibits the killing capacity of AM and resulted in the germination of conidia even one day after infection [20, 21]. Mice treated with clodrolip had a fourfold lower BAL luminescence signal than cortisone actetate-treated mice (102000 ± 37000 versus 394000 ± 19500 photons flux) (Figure 3B), consistent with the finding that preserved airway neutrophil recruitment under these conditions can inhibit the conidial germination. However, although not significantly different, the signal in the BAL from clodrolip treated mice was higher than that of liposome treated control mice (102000 ± 37000 versus 66300 ± 19500). Nevertheless, germination and

mycelium formation was inhibited in AM-depleted mice as confirmed by lung histopathology analyses performed one and eight days post infection (see below). Neutrophils may act as the first line of defense against conidia One day post-infection, the lungs of clodrolip-treated mice contained multifocal lesions (Figure 4A) characterised by scattered hemorrhagic foci associated with small (surface < 200 μm2) perivascular, Org 27569 peribronchiolar, or intra-bronchiolar/alveolar inflammatory infiltrates (Figure 4B). At this stage, few macrophages were detected, which implies that alveolar macrophage depletion was not compensated by massive monocyte recruitment at day one after infection. The cellular infiltrates contained mostly karyorrhectic (i.e. fragmented) neutrophils (Figure 4C, E), embedded in a necrotic material associated with extravasated erythrocytes. Clusters of non-germinated conidia were observed in the neutrophilic infiltrates (Figure 4D, F). Figure 4 At the early stage of pulmonary colonisation, neutrophil influx limits fungal germination after clodrolip treatment.

Furthermore, several studies have shown an increased incidence of p53 nuclear accumulation

in liver metastases in comparison to the primary tumor, hypothesizing a role for p53 in CRC liver metastatization. In particular, the presence of ≥ 3 liver metastases identified a subset of patients with a very poor prognosis mainly when associated to p53 mutations [17]. A number of studies have also shown that tumors that do not express detectable levels of Bcl-2, but which exhibited nuclear accumulation of p53, were associated with the shortest patient survival, while Bcl-2-positive and p53-negative tumors had the best prognosis [12, 17]. Studies conducted at our Institute

showed that p53 positivity combined with Bcl-2 negativity and elevated Ki-67 score correlated with advanced tumor stage, poorly differentiated Cyclosporin A ic50 tumors and increased probability of selleck chemicals relapse. Also elevated survivin expression levels in primary CRC are related to decreased survival [14, 15]. In resected liver tumors, altered expression of survivin, p53, Ki-67 and, more recently, KRAS mutations, have been shown to be independently predictive of hepatic recurrence and poor survival [13, 16, 18]. It is recently reported that defective mismatch repair predicts resistance to 5-fluorouracil (5FU) and KRAS mutation resistance to anti-EGFR antibody therapy [19]. Nevertheless, no predictive markers of RE efficacy in mCRC have been identified Selleckchem NSC 683864 Suplatast tosilate up to now. In terms of the predictive response to radiotherapy, several studies have linked epidermal growth factor receptor (EGFR) and vascular endothelial

growth factor (VEGF) expression to a lack of response to pre-operative radiotherapy in locally advanced rectal cancer [19–21]. Neither p53, Ki-67 and survivin expression appear to be correlated to pre-operative chemo-radiotherapy response and prognosis in locally advanced rectal cancer [22, 23]. To date, however, no study has evaluated the predictive value of molecular markers on radiosensitivity of CRC liver metastasis. In this context, our findings, although in a very limited number of patients, may be clinically relevant. The rapid changes of biomarkers observed in our series post-90Y-RE may be due to clonal selection or to epigenetic changes, not previously recorded in this context. Such mechanisms are usually discussed in the context of cell adaption to chemotherapy and evolving resistance. Radio-sensitivity of colorectal cancer cells may be determined by p53 mutation [23, 24], whereas there is no evidence that chemotherapy per se cause changes in the cellular expression of p53 [25]. This is the first time that we have recorded a down-staging in p53 protein expression after 90Y-RE.

PubMedCrossRef 6. Wang W, Yu L: Effects of oxygen supply on growth and carotenoids accumulation by Xanthophyllomyces dendrorhous . Z Naturforsch C 2009, 64:853–858.PubMed 7. Cifuentes V, Hermosilla G, Martinez C,

Leon R, Pincheira G, Jimenez A: Genetics and electrophoretic karyotyping of wild-type and astaxanthin mutant strains of Phaffia rhodozyma selleck chemicals llc . Antonie Van Leeuwenhoek 1997, 72:111–117.PubMedCrossRef 8. Liu ZQ, Zhang JF, Zheng YG, Shen YC: Improvement of astaxanthin production by a newly isolated Phaffia rhodozyma mutant with low-energy ion beam implantation. J Appl Microbiol 2008, 104:861–872.PubMedCrossRef 9. Calo P, De Miguel T, Jorge B, Vila TG: Mevalonic acid increases trans-astaxanthin and carotenoid biosynthesis

in Phaffia rhodozyma . Biotech Lett 1995, 17:575–578.CrossRef 10. Gu WL, An GH, Johnson EA: Ethanol increases carotenoid production in Phaffia rhodozyma . J Ind Microbiol Biotechnol 1997, 19:114–117.PubMedCrossRef 11. Niklitschek M, Alcaino J, Barahona S, Sepulveda D, Lozano C, Carmona M, Marcoleta A, Martinez C, Lodato P, Baeza M, Cifuentes V: Genomic organization of the structural genes controlling the astaxanthin biosynthesis pathway of Xanthophyllomyces dendrorhous . Biol Res 2008, 41:93–108.PubMedCrossRef 12. Visser H, van Ooyen AJ, Verdoes JC: Metabolic engineering of the astaxanthin-biosynthetic pathway of Xanthophyllomyces dendrorhous . FEMS Yeast Res 2003, 4:221–231.PubMedCrossRef 13. Breitenbach J, Visser H, Verdoes JC, van Ooyen AJ, Sandmann G: Engineering of geranylgeranyl pyrophosphate PD173074 purchase synthase selleck levels and physiological conditions for enhanced carotenoid and astaxanthin synthesis in Xanthophyllomyces dendrorhous . Biotechnol Lett 2010, in press. 14. Ogura K, Koyama T: Enzymatic Aspects of Isoprenoid Bcl-w Chain Elongation. Chem Rev 1998, 98:1263–1276.PubMedCrossRef 15. Lee PC, Schmidt-Dannert C: Metabolic engineering towards biotechnological production of carotenoids in microorganisms.

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Specific antigen detection by immunofluorescence Detection of 20-kDaPS and PIA by immunofluorescence was performed, as previously described [7, 70]. Briefly, overnight cultures of S. epidermidis strains in TSB were diluted 1:100 in 2 mL fresh medium and incubated for Selleckchem Luminespib 18 h at 37°C with shaking. After brief vortex, bacterial suspensions were adjusted to approximate absorbance578 0.2 (Spectrophotometer, Novaspec Plus) and aliquots (10 μL per well) were applied to immunofluorescence slides (CA Hendley Essex Ltd, Essex, United Kingdom). Slide preparations were air-dried, fixed

with cold acetone and stored at 4°C until use. Aliquots (20 μL per field) PIA or 20-kDaPS antisera diluted 1:50 in PBS were applied

to slides which were incubated for 30 min at 37°C. After washing three times with PBS, 10 μL of fluorescein-conjugated anti-rabbit immunoglobulin G (Sigma, UK) diluted 1:80 in phosphate buffered saline were applied, and slides were incubated for 30 min at 37°C. After washing, they were mounted using Vectashield and viewed with a Zeiss AxioImager fluorescence microscope fitted with an AxioCam MR3 camera. Specific antigen detection by ELISA ELISA for polysaccharide detection Selleck EGFR inhibitor was performed as previously described [17]. Briefly, antigens, bacterial cells or polysaccharide, were applied on a 96-well flat bottom high binding ELISA plate (Greiner) and incubated overnight at 4°C. Afterwards, plates were blocked by BSA and incubated with 20-kDaPS or PIA antisera for 1 h at 37°C. Peroxidase H-conjugated goat anti-rabbit IgG (Sigma Chemical Company, St

Louis, MO, USA), diluted 1:2,000 was added for 1 h. Color was developed by adding 100 μL/well SureBlue TMB Microwell Peroxidase Substrate (KPL). After incubation for 15 min at room temperature in the absence of light, the reaction was terminated with 100 μL/well of 1 M H2SO4 and measured at absorbance450. ELISA was also performed, as previously described, on 96-well tissue culture plates (Nunc) with similar Parvulin results. PIA isolation Isolation of PIA antigen was performed, as previously described [6], with slight modification. Briefly, S. epidermidis 1457 was grown for 22 h at 37°C with shaking at 100 rpm/min in 900 mL of TSBdia, prepared by dialysis of 100 mL of 10-fold-concentrated TSB against 900 mL of water. Bacterial cells were collected by centrifugation and were suspended in 20 mL of PBS. The antigen was extracted by learn more sonicating cells four times for 30 sec on ice (Branson Digital Sonifier). Cells were removed by centrifugation at 6,000 rpm for 30 min at 4°C, and extracts were clarified by centrifugation for 60 min at 12,000 rpm. The extracts (20 mL) were filter sterilized, dialyzed against 50 mM Tris–HCl, pH 7.

Note that only the UV radiation curve is shown in graph B since the visible light curve is the same as in graph A. Black arrows indicate the time point of the shift. White and black bars indicate light and dark periods. The dashed line indicates the growth irradiance curve (right axis). Abbreviations as in Fig. 1. Table 2 Growth parameters of PCC9511 batch cultures shifted from LL to HL during 12 h/12 h L/D cycles. Growth Parameters* Cycle 1 (LL) Cycle 2 (HL) Cycle 3 (HL) μcc (d-1) 0.43 ± 0.03 0.67 ± 0.01

0.62 ± 0.01 μnb (d-1) 0.37 ± 0.04 0.59 ± 0.09 0.58 ± 0.05 TG1 (h) 30.8 ± 3.1 16.7 ± 0.3 18.8 ± 0.2 TS (h) 4.12 ± 0.01 5.15 ± 0.14 5.53 ± 0.12 TG2 (h) 3.89 ± 0.01 2.85 ± 0.14 selleck chemicals 2.47 ± 0.12 Sr 20.8 ± 1.7 32.4 ± 0.4 29.8 ± 0.3 Values shown are averages (± mean deviation) of two biological replicates * Growth rates per day calculated from: cell cycle data (μcc) or cell numbers (μnb); TG1, TS, TG2: cell cycle phase duration in hours; Sr: rate of synchronization estimated from the ratio

(TS+TG2)/(TG1+TS+TG2) In the second shift experiment, HL Doramapimod acclimated PCC9511 cultures were sampled during one complete L/D cycle, then on the following two days were subjected to a modulated L/D cycle TH-302 ic50 of HL+UV radiations. As for the HL+UV acclimated cells, UV exposure seemed to cause a delay in the initiation of DNA replication, but with the peak of S cells occurring 3 to 4 h after the LDT (Fig. 2B), instead of 2 h. Furthermore, although the UV dose received by the cells was the same in the UV acclimation and UV shift experiments, UV irradiation was clearly much more stressful for the cells in the second case, as they reacted by dramatically decreasing their growth rate (Table 3), an effect which was even more marked on the second day after switching the UV lamps on. Table 3 Growth parameters of PCC9511 batch cultures shifted from HL to HL+UV during 12 h/12

h L/D cycles. Growth Parameters* Cycle 4��8C 1 (HL) Cycle 2 (HL+UV) Cycle 3 (HL+UV) μcc (d-1) 0.69 ± 0.02 0.61 ± 0.01 0.45 ± 0.00 μnb (d-1) 0.64 ± 0.05 0.45 ± 0.02 0.1 ± 0.02 TG1 (h) 18.0 ± 0.6 21.4 ± 0.3 29.3 ± 0.2 TS (h) 3.67 ± 0.14 3.72 ± 0.09 6.25 ± 0.03 TG2 (h) 2.33 ± 0.14 2.28 ± 0.09 1.75 ± 0.03 Sr 25.0 ± 0.7 21.9 ± 0.2 21.5 ± 0.1 Values shown are averages (± mean deviation) of two biological replicates *Growth rates per day calculated from: cell cycle data (μcc) or cell numbers (μnb); TG1, TS, TG2: cell cycle phase duration in hours; Sr: rate of synchronization estimated from the ratio (TS+TG2)/(TG1+TS+TG2) Comparative cell cycle dynamics of acclimated P. marinus PCC9511 cells grown in continuous cultures with and without UV radiation Large volume, continuous cultures of P.

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