BMC Cancer 2010, 10:281 PubMedCrossRef 7 Fuleihan Gel H, Salamou

BMC Cancer 2010, 10:281.PubMedCrossRef 7. Fuleihan Gel H, Salamoun M, Mourad YA, Chehal A, Salem Z, Mahfoud Z, Shamseddine A: Pamidronate in the prevention of chemotherapy-induced bone loss in premenopausal women with click here breast cancer:

a randomized KPT-8602 manufacturer controlled trial. J Clin Endocrinol Metab 2005, 90:3209–3214.CrossRef 8. Shapiro CL, Manola J, Leboff M: Ovarian failure after adjuvant chemotherapy is associated with rapid bone loss in women with early-stage breast cancer. J Clin Oncol 2001, 19:3306–3311.PubMed 9. Simpson ER, Dowsett M: Aromatase and its inhibitors: significance for breast cancer therapy. Recent Prog Horm Res 2002, 57:317–338.PubMedCrossRef 10. Jansen JP, Bergman GJ, Huels J, Olson M: The efficacy of bisphosphonates in the prevention of vertebral, hip, and nonvertebral-nonhip fractures in osteoporosis: a network meta-analysis. Semin Arthritis Rheum 2011, 40:275–284. e271–272PubMedCrossRef 11. Mauri D, Valachis A, Polyzos NP, Tsali L, Mavroudis D, Georgoulias V, Casazza G: Does adjuvant bisphosphonate in early breast cancer modify the natural course of the

disease? A meta-analysis of randomized controlled trials. J Natl Compr Canc Netw 2010, 8:279–286.PubMed 12. Hines SL, Mincey B, Dentchev T, Sloan JA, Perez EA, Johnson DB, Schaefer PL, Alberts S, Liu H, Kahanic S, Mazurczak MA, Nikcevich DA, Loprinzi CL: Immediate versus delayed zoledronic acid for prevention of bone loss in postmenopausal women with breast cancer starting letrozole after tamoxifen-N03CC. Breast Cancer Res Treat 2009, 117:603–609.PubMedCrossRef 13. Mauri D, Valachis A, Polyzos selleck chemicals llc IP, Polyzos NP, Kamposioras K, Pesce LL: Osteonecrosis of the jaw and use of bisphosphonates in adjuvant breast cancer treatment: a meta-analysis. Breast Cancer Res Treat Tryptophan synthase 2009, 116:433–439.PubMedCrossRef 14. Gnant M, Mlineritsch B, Schippinger W, Luschin-Ebengreuth G, Pöstlberger S, Menzel C, Jakesz R, Seifert M, Hubalek M, Bjelic-Radisic V, Samonigg H, Tausch C, Eidtmann H, Steger G, Kwasny W, Dubsky P, Fridrik M, Fitzal F, Stierer M, Rücklinger E, Greil R, ABCSG-12 Trial Investigators, Marth C: Endocrine

therapy plus zoledronic acid in premenopausal breast cancer. N Engl J Med 2009, 360:679–691.PubMedCrossRef 15. Shapiro CL, Halabi S, Hars V, Archer L, Weckstein D, Kirshner J, Sikov W, Winer E, Burstein HJ, Hudis C, Isaacs C, Schilsky R, Paskett E: Zoledronic acid preserves bone mineral density in premenopausal women who develop ovarian failure due to adjuvant chemotherapy: final results from CALGB trial 79809. Eur J Cancer 2011, 47:683–689.PubMedCrossRef 16. Hershman DL, McMahon DJ, Crew KD, Cremers S, Irani D, Cucchiara G, Brafman L, Shane E: Zoledronic acid prevents bone loss in premenopausal women undergoing adjuvant chemotherapy for early-stage breast cancer. J Clin Oncol 2008, 26:4739–4745.PubMedCrossRef 17.

Int J Hyperthermia 2006, 22:117–134 PubMedCrossRef 21 Kobelt D,

Int J Hyperthermia 2006, 22:117–134.PubMedCrossRef 21. Kobelt D, Aumann J, Fichtner I, Stein U, Schlag PM, Walther W: Activation of the CMV-IE promoter by hyperthermia in vitro and in vivo: biphasic heat induction of cytosine deaminase suicide gene expression. Mol Biotechnol 2010, 46:197–205.PubMedCrossRef 22. Pshenichkin S, Surin A, Surina E, Klauzińska

M, Grajkowska E, Luchenko V, Dolińska M, Wroblewska B, Wroblewski JT: Heat shock VS-4718 mouse enhances CMV-IE promoter-driven metabotropic glutamate receptor expression and toxicity in transfected cells. Neuropharmacology 2011, 60:1292–1300.PubMedCrossRef 23. Geelen JL, Boom R, buy Autophagy inhibitor Klaver GP, Minnaar RP, Feltkamp MC, van Milligen FJ, Sol CJ, van der Noordaa J: Transcriptional activation of the major immediate early transcription unit of human cytomegalovirus by heat-shock, arsenite and protein synthesis inhibitors. J Gen Virol 1987, 68:2925–2931.PubMedCrossRef Competing interests All authors declared no any conflict of interest. Authors’ contribution FW: Conduct experiments, prepare manuscript HW: perform experiment, data analysis JZ: perform experiments XC: cell culture

CL: experiment design, manuscript revision QH: experiment design, final approval of manuscript. All authors read and approved the final manuscript.”
“Background “”“If you have knowledge, let others light their candles with it””" “”Winston Churchill”" “”“The key question is whether there are new opportunities and new models OICR-9429 for scholarly publishing that would better serve researchers and better communicate and disseminate research findings” * “” “”*Digital broadband Content: Scientific Publishing, OECD, Paris. Available from: “” http://​www.​oecd.​org/​internet/​interneteconomy/​35393145.​pdf Open access (OA) paradigm has unquestionably reshaped the traditional

system of scholarly communication by closely linking the concepts of free access to research literature and its easy diffusion and re-use Oxymatrine through massive exploitation of Internet and related technologies and an innovative management of copyright rules. OA journals based on an “author-pays” business model are one of the two routes of the open access paradigm, the so called “gold” route. Golden OA is complementary to “green” OA, founded on depositing accepted manuscripts in institutional or discipline-based repositories. In offering a comprehensive overview of the OA movement, including its history and achievements, Peter Suber defines OA journals as: peer-reviewed journals available online to the reader “”without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself”" [1]. Recent studies of the economic implications of access to journal articles highlight the present and future scenarios of the scholarly publication system [2–5].

Tissues from the pancreas, liver, spleen, heart, lung, and kidney

Tissues from the pancreas, liver, spleen, heart, lung, and kidney were taken out and directly kept MK5108 clinical trial in liquid nitrogen. Then the mixed solution was kept static for 2 min and centrifuged at 5,000×g for 5 min at 4°C. After centrifugation at 5,000×g for 5 min at 4°C, the gemcitabine content in the supernatant was determined by high-performance liquid chromatography (HPLC), with a Diamond C18 chromatographic column (5 μm, ID 4.6 × 300 mm, Anoka, MN, USA) and at a flow rate of 1 mL/min. Toxic side effect OSI-027 in vitro assessment Both the high-dose (200 mg/kg) and low-dose (100 mg/kg) groups were constructed, as shown in Table 1. After administration for 3 weeks, each blood sample was collected from the arteriae femoralis. Different blood parameters, including white blood count (WBC), red blood cell count (RBC),

hemoglobin (Hb), alanine aminotransferase (ALT), BTSA1 datasheet aspartate aminotransferase (AST), creatinine (Cr), and urea (BUN), were measured using a biochemical autoanalyzer (Type 7170, Hitachi, Tokyo, Japan). The samples obtained from healthy

mice were used as control. Table 1 Blood parameters of SD rats treated with the different formulations for 3 weeks Parameters Formulation (n = 6, p > 0.05)   110-nm GEM-ANPs 406-nm GEM-ANPs Gemcitabine ANPs Control   Normal dose High dose Normal dose High dose Normal dose High dose High dose – WBC (109/L) 7.3 ± 1.1 5.3 ± 2.0 6.1 ± 1.2 5.1 ± 2.2 6.1 ± 1.3 4.8 ± 2.8 8.2 ± 2.2 7.3 ± 1.9 RBC (1012/L) 5.6 ± 1.8 6.2 ± 1.6 6.2 ± 2.1 6.1 ± 1.1 6.5 ± 2.9 6.0 ± 2.0 6.6 ± 2.9 6.4 ± 1.2 Hb (g/L) 130.0 ± 23.0 134.0 ± 20.0 141.0 ± 14.0 138.0 ± 16.0 139.0 ± 20.0 132.0 ± 16.0 148.0 ± 23.0 143.0 ± 19.0 ALT (U/L) 44.8 ± 14.0 52.5 ± 12.9 46.0 ± 11.3 54.3 ± 12.8 51.8 ± 15.3 60.2 ± 21.9 44.7 ± 11.5 48.8 ± 13.2 AST (U/L) 109.1 ± 22.1 128.0 ± 31.8 115.5 ± 26.0 113.1 ± 26.9 129.4 ± 28.1 136.3 ± 33.4 Protein kinase N1 113.3 ± 28.4 109.5 ± 25.7 Cr (mM/L) 7.1 ± 2.4 8.7 ± 3.2 6.2 ± 1.5 7.8 ± 2.07 6.1 ± 1.9 7.4 ± 2.2 4.9 ± 1.5 6.1 ± 1.6 BUN (μM/L) 41.0 ± 15.1 45.5 ± 17.3 35.4 ± 16.0 40.9 ± 19.5 36.1 ± 18.2 45.0 ± 13.7 47.2 ± 16.2 41.3 ± 18.6 Antitumor activity in vivo Tumor induction and drug administration Each male nude mice (n = 30) was injected subcutaneously in the back skin with 0.2 mL PANC-1 cell line (1.0 × 108/mL). Those mice were randomly divided into five groups (n = 6): Group A: 110-nm GEM-ANPs Group B: 406-nm GEM-ANPs Group C: pure gemcitabine Group D: blank ANPs Group E: control (0.9% NS) One week later, a tumor about 5 mm in diameter could be observed in the mice.

2 Yes [14, 79, 88] No   bfd 5 9 Yes [12, 14, 15] No   feoB 11 8 Y

2 Yes [14, 79, 88] No   bfd 5.9 Yes [12, 14, 15] No   feoB 11.8 Yes[12, 14, 63, 134, 139, 140] No ArcA and Fnr Trichostatin A ic50 [141] STM3600 -6.8 No No Fnr [21] STM3690 -4.2 No No Fnr [21] rpoZ 3.9 No No   udp -5.4 No No IscS [142] sodA 9.1 Yes [14, 55, 82, 88, 143–148] Yes [85, 146, 148] Fnr, ArcA, IHF, SoxRS [53, 81] yjcD 2.8 No No   dcuA -5.8 No No   aspA -3.6 Yes

[13, 15] No NarL[149, 150] ArcA [151] ytfE 10.0 Yes [13] No NsrR [99] fhuF 8.5 Yes [12, 13, 15] Yes [11, 152, 153]   a Genes from the present study that are regulated by Fur and possess a putative Fur-binding motif bFold change of expression in Δfur relative to the wt 14028s c Evidence of direct Fur binding the regulatory region of the gene d Regulation by other transcription factors

besides Fur The appropriate metal cofactor was shown to be essential for detection of MnSOD activity, in spite of the 9-fold increase in sodA transcript for Δfur. Therefore, genetic backgrounds that alter the steady-state [Mn2+] or its competitor [Fe2+] may have dramatic effects on MnSOD activity. Indeed, we were only able to discern the role of Fur Selleck Ku 0059436 in sodA and MnSOD expression with the addition of excess MnCl2 to the growth media. These data are summarized in Figure 6, which depicts the transcriptional, translational, and post-translational role of Fur in sodA and sodB. This implies that disruption of iron homeostasis is likely to have a two-pronged effect, increase in Fenton Fedratinib order chemistry and a decrease in MnSOD activity due to iron overload. It appears that the inhibition of MnSOD by iron is evolutionarily conserved. Thus, the mitochondrial Mn2+-cofactored SOD2 has been shown to be inactivated in a similar manner when iron homeostasis was disrupted in yeast [106]. In addition, supplementation of the medium with Mn2+ reduced oxidative stress in a murine isometheptene model of hemochromatosis [107]. It is unknown if this is due to enhanced MnSOD or if Mn2+ supplementation reduces oxidative stress in other pathological states of altered iron

homeostasis. Figure 6 Role of Fur in the transcriptional, translational and post-translational regulation of sodA and sodB. (A) Repression of sodA by Fur is depicted in addition to the role of Fur in iron homeostasis. Iron is known to bind to the active site of MnSODs that leads to inactivation of the enzyme [106, 124]. Increased expression of MnSOD was detected only when excess Mn2+ was added to the media in order to out compete the Fe2+. Deletion of fur under iron replete conditions results in increase transcription of sodA, but incorportation of Fe2+ into the active site of SodA resulting in SodA-Fe and an inactive enzyme. Addition of excess Mn2+ to the culture media can out compete Fe2+ for the active site of SodA resulting in SodA-Mn and an active enzyme. (B) Indirect regulation of SodB by Fur in S. Typhimurium. The small RNAs rfrA and rfrB of S. Typhimurium are likely to function as their homolog ryhB in E.

Some Pythium species appear to have evolved to colonize the roots

Some Pythium species appear to have evolved to colonize the roots

of mature trees MK-8776 purchase to prevent the establishment of young trees of the same species under the canopy. In such natural system, it would be beneficial to the well established trees to maintain a certain level of root colonization by rather weak root pathogen that are more aggressive on seedlings or young plants. However, in a horticulture or sylviculture situation where mature trees are removed or harvested to be replaced by young saplings, this could lead to a significant replant problem. Conclusion The oomycete community desperately needs an initiative such as the Assembling find more the Tree of Life (AFTOL) which served to really unify mycologists from a wide range of expertise. One of the unexpected side effects of the fact that many mycologists working on oomycetes are no longer interacting with mycological societies has been the deepening of the split between the marine/aquatic

and terrestrial scientific communities. The major oomycete symposia and workshops that are now found at phytopathological meetings such as the International Congress of Plant Pathology or the American Phytopathological Society do focus on terrestrial and plant pathogenic species. Saprophytic growth in oomycetes appears to have derived from simple holocarpic parasites living in the ocean (Beakes et al. 2011). In order to generate a complete phylogeny of oomycetes and truly understand their evolution, a better coverage of obligate parasites from less well known environments and hosts will be needed (e.g. Sekimoto et al. 2008b). Even for the obligate parasites of plants such as the downy mildews, advances are being made (e.g. Thines et al. 2008) but a major effort will be required to generate molecular data for many of the described species that are in herbaria. As we are working at building up a robust tree of life for oomycetes and as we are sequencing multiple markers for an increasing

number of taxa, it is becoming apparent that some well known and economically important genera are polyphyletic (e.g. Riethmüller et al. 2002). Bay 11-7085 We should refrain from sweeping reorganization of the oomycetes and their genera, particularly when many practitioners are routinely using the names for their work, until we have a more robust multigene phylogenetic framework. There is no doubt that molecular biology will continue to play a leading role with the advent of technologies like single DNA MG-132 molecule sequencing which should provide complete genome sequences at what used to be the cost to sequence a few genes. Single molecule DNA sequencing might help to solve the issue of obtaining sequence data from type specimens.

An attraction of the approach is that efficient use is made of BM

An attraction of the approach is that efficient use is made of BMD testing. Application

of probability thresholds The application of these assessment thresholds depends critically on the availability (and reimbursement) of densitometry which varies from country to country. It has been estimated that the requirements to service osteoporosis amount to approximately 11 DXA units/million selleck compound of the general population [100], though this estimate probably requires updating to take account of population demography. The availability of DXA falls above this estimate in a minority of European selleck products countries (Fig. 6). The large variation in resources for BMD testing demands the consideration of three assessment scenarios that depend on the access to central densitometry. Fig. 6 The density of central DXA equipment (units per million of the general population in the EU countries in 2010 [Kanis JA, data on file]) Unrestricted

access to densitometry Where resources for BMD testing are adequate, BMD tests can be undertaken in women with any clinical risk factors as shown in Fig. 7. Treatment is recommended where fracture probability exceeds the intervention threshold. Note that the lower assessment threshold is set as equivalent to women without clinical risk factors (see above). In those countries where screening of women without risk factors is recommended, selleck inhibitor there would be no lower assessment threshold. An additional option is to recommend treatment in women with a prior fragility fracture without recourse to BMD (though BMD might be undertaken to monitor treatment). Fig. 7 Assessment of fracture risk in countries with high access to DXA. DXA is undertaken in women with a clinical risk factor. Assessment with DXA and/or treatment is not recommended where the FRAX probability is lower than the lower assessment

threshold (green area). BMD is recommended in other women and treatment recommended where the fracture probability exceeds the intervention threshold (dotted line). The intervention threshold used is that derived from Table 7 The assessment algorithm is summarised in Box 1. BMD tests are recommended in all postmenopausal women with a clinical risk factor. BOX 1 Assessment of fracture risk with HAS1 FRAX with unlimited access to BMD Limited access to densitometry Several countries must take a parsimonious approach to the use of BMD, and this is reflected in the NOGG guidelines used in the UK. The guidance recommends that postmenopausal women with a prior fragility fracture may be considered for intervention without the necessity for a BMD test. In women without a fragility fracture but with one or more other clinical risk factors (CRF), the intervention threshold set by NOGG is at the age-specific fracture probability equivalent to women with a prior fragility fracture and BMD testing is recommended in those in whom fracture probability lies between the upper and lower assessment threshold as described above [89].

The Co layer, E A is set at θ = 0°, 30°, 60°, and 90° in the simu

The Co layer, E A is set at θ = 0°, 30°, 60°, and 90° in the simulations, respectively. Compared with the single-layer dots, the stray fields from the uncompensated magnetic poles in the Co layer influence the magnetization reversal of the Fe layer drastically. A strong E A direction dependence of the Fe layer hysteresis loops for the circle trilayer dot is illustrated in Figure 3. see more As is shown, H c, M r/M s, H n, and H a are all affected. When θ = 0°, 30°, and 60°, a shift of the loop center along the field axis is obvious, which reflects the interlayer selleck chemicals llc interaction directly [18–20]. The bias field H B of the Fe layer is defined from the two H n here, i.e.,

H B = (H n1 + H n2)/2, to evaluate the interaction strength, where H n1 and H n2 are XMU-MP-1 research buy the nucleation field of the descending and ascending branches of the loop. The bias field depending on θ is displayed in Figure 4 for different asymmetric dots. It is clearly seen that with θ increasing, H B decreases monotonically, which can be interpreted intuitively from the viewpoint of magnetic poles on the Co layer edge. However, a simple fitting with the relationship of

H B(θ) = H B(0)cosθ failed quantitatively, as also shown in the Figure. A detailed inspection in the magnetization reversal elucidates that a new S-state is formed before it evolves to a vortex in the

circle dot. This S-state is the straight result in the Fe layer to respond the Co magnetic poles. A magnetization reversal process through the S-state of a circle dot with θ at 30° is depicted in Figure 5, in which the S-state is indicated in Figure 5c. For the semicircle dots, the shape anisotropy is sufficiently strong to dominate their nearly magnetization process in spite of the Co poles, leading to undetected bias effect. Figure 3 Fe layer minor loops of circle trilayer dots on easy axis direction of Co layer. The Co layer easy axis deviates from the applied field direction by the angle of 0°, 30°, 60°, 90°. The loop of a single Fe layer dot is also presented. Figure 4 The Fe layer bias field as a function of the easy axis direction of Co layer. The Co layer easy axis deviates from the applied field direction by the angle of 0°, 30°, 60°, 90°. The asymmetric dots are characterized by α = 0, 0.25, 0.5, 0.75, 1. The dash line denotes a cosine function fitting for the circle dots. Figure 5 Snapshots of magnetization reversal process through S-state of a circle dot with θ at 30°. The applied field is (a) 2,500, (b) 560, (c) 180, (d) 160, (e) - 2,320, and (f) - 2,500 Oe. The dot shows saturation, S-, vortex, and reverse saturation states in sequence. The interlayer dipolar interaction influences the stabilizing range of the Fe vortex as well.

Second, trans-translation

functions to direct incomplete

Second, trans-translation

functions to direct incomplete peptides to degradation by the addition of a specific tag [4]. Trans-translation is generally non-essential and requires two factors: SsrA, a small stable structured RNA (also called tmRNA) that acts both as a tRNA by its alanylated AZD6738 molecular weight tRNA-like domain (TLD) and as a mRNA-like domain (MLD) [4] and its protein cofactor, SmpB. The length and sequence of the trans-translation appended peptide tag varies with the bacterial species (between 8 and 35 amino acids) [5]. Mostly studied in E. coli, the tag encoded by SsrA is sufficiently informative to target any trans-translated proteins to degradation pathways [4]. The phenotypes of mutants deficient in this process depend on the species examined and are related to environmental adaptation, differentiation, stress response or virulence (for a review see [6]). Growing evidence indicates that trans-translation tagging targets specific substrates and therefore plays a regulatory role in organisms such as Caulobacter crescentus

[7, 8]Yersinia pseudotuberculosis [9], Helicobacter pylori [10] or Streptomyces coelicolor [11]. In E. coli, numerous Selleck MCC-950 phenotypes were associated with the deficiency of trans-translation, among which a slight enhancement of the doubling time that was observed even under normal growth conditions [12]. One of the tools used to characterize the SsrA determinants in vivo was the dependence Tyrosine-protein kinase BLK on trans-translation of the growth of the hybrid bacteriophage λimm P22 in E. coli [13–15]. This phage is a hybrid between

the E. coli lambda phage and the selleck inhibitor Salmonella P22 phage and is specific for E. coli. E. coli strains defective in trans-translation display a characteristic phenotype termed “”Sip”" (for selectively inhibits of λimm P22) [13]. Indeed, the frequency of infection by λimm P22 is 10,000-fold lower in ΔsmpB or ΔssrA E. coli mutants as compared to that in the corresponding parental strain [13, 16]. The precise molecular basis of the phage plating defect in trans-translation-deficient cells is not yet understood. The impact of SsrA point mutations on λimm P22 growth in E. coli was first analyzed by Withey and Friedman [14] who showed (i) that charging of tmRNA with Ala was essential and, (ii) that degradation of proteins tagged by tmRNA was only required to achieve optimal levels of phage growth. A more recent study challenged these conclusions and demonstrated that λimm P22 propagation in E. coli is exclusively dependent on ribosome recycling functions of trans-translation and not on its proteolysis targeting activity [15]. We have recently investigated the role of trans-translation in Helicobacter pylori [10]. H. pylori is a bacterial pathogen that colonizes the stomach of half of the human population and is strongly adapted to persist and multiply under stressful conditions such as low pH. Colonization of the stomach by H.

Radiologic stigmata of SBO are the presence/coincidence of multip

Radiologic stigmata of SBO are the presence/coincidence of multiple air-fluid levels, dilatation/distension of small bowel loops and the absence of gas in the colonic section. Plain film has sensitivity

and specificity ranging from 65% to 80% [28]. Ultrasound can be useful only in expert hands; US is usually of limited value in bowel obstruction and/or in P005091 datasheet patients with distended bowel buy CAL-101 because the air, limiting ultrasound transmission, may obscure the underlying findings. The scan should be performed through flanks to avoid distended SB [29]. Usual US findings are: distention, peristalsis (differential diagnosis of ileus vs. mechanical SBO), differences in mucosal folds I-BET-762 around transition point, free fluid

(sign of ischemia) [30]. CT scan is highly diagnostic in SBO and has a great value in all patients with inconclusive plain films for complete or high grade SBO [31]. However CT-scans should not be routinely performed in the decision-making process except when clinical history, physical examination, and plain film are not conclusive for small bowel obstruction diagnosis [32]. CT can confirm the presence of complete obstruction and allow the diagnosis of the cause of SBO, it can also exclude a non-adhesional pathology and assess the occurrence of strangulation with a sensitivity and specificity higher than 90% and a NPV of nearly 100% [33]. IV contrast is necessary. Oral is not Water-soluble contrast follow-through is valuable in patients undergoing initial non operative conservative management in order to rule out complete ASBO and predict the need for surgery [34]. This investigation Niclosamide is safer than barium in cases of perforation and peritoneal spread

and has possible therapeutic value in the case of adhesive small intestine obstruction [35]. MRI use should be restricted to those patients having CT or iodine contrast contraindications. – Conservative treatment and timing for surgery The management of small bowel obstruction caused by adhesions is controversial because surgery can induce new adhesions, whereas conservative treatment does not remove the cause of the obstruction [36]. Conservative treatment involves nasogastric intubation, intravenous fluid administration, and clinical observation. Strangulation of the bowel requires immediate surgery, but intestinal ischemia can be difficult to determine clinically. Several issues are raised when managing patients with ASBO.

If these cultures are not considered, the R 2 value for cyanobact

If these cultures are not considered, the R 2 value for cyanobacteria improved from 0.45 to 0.76. These results suggest a tight coupling between the F v/F m from PBS pigments and PSII Chla, which is further explored in the next section. The high amount of scatter in the results comparing community F v/F m(590,650) against the algae fraction provides further indication that Adriamycin mw the variable fluorescence of cyanobacteria cultures can be observed from community F v/F m without interference from the presence of algae. The nature of cyanobacterial fluorescence in the Chla emission

band The emission spectra of algal cultures at room temperature have a predictable shape because their main PU-H71 source of fluorescence is Chla located in PSII and to a much smaller extent

in PSI. In cyanobacteria, we observe fluorescence in the red spectral domain from (1) PSII Chla (variable), (2) PBS fluorescence (weakly variable) and (3) PSI (non-variable), where the contribution of the latter is relatively strong in cyanobacteria compared to algae. The role of PSI fluorescence in the red spectral domain is likely to be important in fluorometers that record fluorescence >700 nm (discussed below). The role of accessory PSII pigment composition VX-680 datasheet on fluorescence in the PSII Chla emission band and towards shorter wavelengths has received very little attention altogether and is explored here. It has been suggested that phycobilipigments have a significant effect on the F 0 signal that is otherwise attributed to Chla (e.g. Campbell et al. 1996, 1998). A non-variable fluorescence

source elevates F 0 and F m check equally, which leads to dampening of F v/F m. We observed in the previous exercise that the PBS fluorescence does have a (weakly) variable component, which in turn should alleviate this dampening. To quantify the influence of PBS fluorescence on the variable fluorescence from PSII it is necessary to isolate F 0 and F m of the individual pigments. We decomposed F 0 and F m emission spectra of our cyanobacteria cultures into Gaussian band contributions of phycobilipigments and Chla. The Gaussian decomposition allows us to express F v/F m of each pigment component. Emission spectra were taken from the excitation–emission matrices of all cultures used in the simulations described in the previous section. We restrict ourselves to fluorescence emission between 625 and 690 nm, assuming that components of PSI and PSII that fluoresce at longer wavelengths (PSII Chla at 730–740 nm, PSI Chla >700 nm, c.f. Ley 1980) have minimal influence in the area around 680 nm. The emission band corresponding to excitation at 590 nm (10-nm bandwidth) was selected as it yields high fluorescence in all cyanobacteria cultures. The choice or width of the excitation band does not influence the shape of the emission spectrum, as long as the excitation band overlaps with the absorption domain of the PBS pigments that fuel PSII.