05), we focused our attention on five spots (RplE, RplF, SodA, Dps and CpxR; Table 2) with pronounced overexpression in PA adapted gels and targeted them for identification. With respect to the overexpression of RplE and RplF in PA adapted gels, it should be noted that in general, the spot variances of basic proteins separated by 2 D gel electrophoresis have a low confidence level when a comprehensive analysis of total soluble proteins is intended. However, the results of 2 D gel experiments in this study were highly reproducible. Therefore, it is the opinion

of the authors that these proteins were truly overexpressed following long-term PA exposure. The data obtained and the reproducibility Selleckchem PD0332991 of the presented gels support this notion. Figure 2 2 D gel images of the soluble protein fractions from PA adapted and unadapted S. Enteritidis cultures. (a) Unadapted gel, (b) PA adapted gel. Proteins upregulated in PA gel selected for further examination are circled. Proteins restricted to PA adapted gels are designated with an asterisk (*) in gel (b). Labeled Proteins were identified as (1) CpxR, (2) RplE, (3) RplF, (4) SodA, (5) Dps. Table 2 Proteins identified in PA adapted gels by PMF, MS/MS Spot Number Protein Name Protein Description LY2835219 in vivo [Origin Species selected by MASCOT] Fold Change p value Mascot Score Peptides

Matched Molecular Weight (Da) 1 CpxR DNA-Binding transcriptional regulator [Shigella flexneri 5 str. 8401] +5.01 0.02136 185 11 26274 2

RplE 50 S ribosomal subunit protein L5 [Salmonella enterica serovar Typhi str. CT18] +5.84 0.03998 Glutathione peroxidase 85 8 20362 3 RplF 50 S ribosomal subunit protein L6 [Salmonella enterica serovar Typhi str. CT18] +6.09 0.04065 177 7 18905 4 SodA Manganese superoxide dismutase [Escherichia coli O157:H7] +7.51 0.01953 155 5 22886 5 Dps* starvation/stationary phase DNA protection protein [Salmonella enterica serovar Typhi str. CT18] – - 482 12 18706 Table 2. Proteins in Table 2 are those with the highest and most statistically significant changes in protein expression following exposure to PA. Fold change is the level of change of each protein following PA adaptation. A Student’s t test (performed by Melanie 5.0 gel analysis software) was used to determine the level of significance of expression values. *As Dps was not detected by Melanie 5.0 in the unadapted control gels (for unknown reasons), no fold change or p value for this protein can be reported. This protein was selected for further study because of its prominence in PA adapted gels. Mass Spectrometry Among the proteins identified were the 50 S rRNA-binding proteins RplE (an essential protein for cell viability in E. coli) and RplF (a protein associated with gentamycin and fusidic acid resistance) [19–21] (Additional Files 1 and 2, respectively).

The percentage of positive or negative IMP3 with the relationship to p53 staining results was calculated by the total IMP3 positive or negative cases. Roxadustat solubility dmso The p values listed in the table represented the comparisons within the same group of patients showing different status of IMP3 and/or p53. IMP3 and p53 Expression in HGSC We further examined the expression of IMP3 and

p53 in the invasive components of HGSC in both study groups (STIC group, n = 48, and HGSC without STIC, n = 62). Within the STIC group, the staining results for IMP3 and p53 in the invasive cancer areas were very similar to those found in the areas of STIC (Figure 3) with the exception of the two cases. These two cases showed positive IMP3 and negative p53 in STIC, but they were reversed (negative IMP3 and positive p53) in the invasive component.

Interestingly, eight (20%) cases with negative expression for both IMP3 and p53 in STIC were also negative in the corresponding invasive areas (Table 3). In the patients of HGSC without STIC group, the overall staining results for these two markers were also similar to those cancer cells in the STIC group (Figure 4). The click here detailed results are presented in Table 3. Figure 4 IMP3 and p53 overexpression in invasive component of high-grade serous carcinoma (HGSC). Example of invasive HGSC (top panel) showed positive for both p53 (mid panel) and IMP3 (low panel). Original magnifications: left panel, 40x; right panel, 200x. Discussion Although IMP3 expression, which is associated with tumor growth, progression, and unfavorable prognosis, has been explored in a number of human malignancies, only two studies on immunohistochemical analysis for IMP3 in ovarian cancers have been published. Kobel et al. demonstrated IMP3 expression in 86% of mucinous tumors, in about half of clear-cell and high-grade serous carcinomas, and in 27%

of endometrioid cancers [19]. Noske et al. detected expression of IMP3 in 32 (47%) of 68 ovarian carcinomas but did not report their findings according to various histologic types [33]. However, no studies have been addressed regarding the IMP3 expression in precursor or early lesions of HGSC of either tubal or “ovarian” origins. In this study, we have shown that IMP3 signatures, Benzatropine defined as strong positive cytoplasmic staining in more than 10 benign appearing consecutive tubal epithelia, were found in 15 (31%) of the 48 cases with STIC. This is in contrast to the benign control group, which showed no single IMP3 signature, found in 60 studied cases (p < 0.0001). Interestingly, the tubal IMP3 signature rate was also significantly higher than those in 10 (16%) of the 62 cancer cases without STIC (p < 0.05). Additionally, concordance expression of IMP3 and p53 signatures in the STIC group was found in up to one-third of the cases, while the remaining was either discordant or independent (Table 2).

Analysis was performed, using the delta-delta Ct method. The gene expression levels obtained by QRT-PCR were normalized, using the 16S ribosomal gene, which showed similar expression levels at different time points after infection. The gene expression level was compared between microarray and QRT-PCR. Similarly, the microarray ratio for each gene analysed was normalised against the microarray ratio obtained for 16S ribosomal gene. This allowed direct comparison between the 16S ribosomal gene-normalized QRT-PCR ratio and the 16S ribosomal gene microarray ratio for each transcript investigated.

Acknowledgements The authors thank J.Leach Gefitinib chemical structure (CSU) and CM.Vera Cruz (IRRI) for providing us with DNA of Xoo strains. We thank B.Piégu for his help with sequence analyses. We thank Thierry Mathieu for his help during greenhouse experiments. We are very grateful to Michèle Laudié for her help in preparing the materials for sequencing and Richard Cooke for access to the Montpellier Languedoc-Roussillon Génopole sequencing facilities. The authors thank Ralf Koebnik for his critical reading on the first draft of the manuscript and his helpful suggestions. We thank anonymous reviewers for their valuable suggestions to improve the manuscript. We thank Elizabeth McAdam for editing.

MS was supported by a doctoral fellowship awarded by Programme Alβan of the European Commission (grant E05D057941CO). Electronic supplementary material Additional file 1: Xoo strain MAI1 RANTES genes identified as differentially expressed in planta by microarray analysis. The non-redundant Lapatinib set of sequences, composed of 147 Xoo strain MAI1 genes differentially expressed during infection, was searched against the genomes of all available sequenced strains of X. oryzae (Xoo strains KACC10331, MAFF311018, and PXO99A, and Xoc strain BLS256), and against the draft genome of the African Xoo strain BAI3. Changes in gene expression across different

time points during infection are also presented. (DOC 489 KB) References 1. Nino-Liu D, Ronald P, Bogdanove A: Xanthomonas oryzae pathovars: model pathogens of a model crop. Mol Plant Pathol 2006, 7:303–324.PubMedCrossRef 2. Séré Y, Onasanya A, Verdier V, Akator K, Ouédraogo L, Segda Z, Coulibaly M, Sido A, Basso A: Rice Bacterial Leaf Blight in West Africa: Preliminary Studies on Disease in Farmers’ Fields and Screening Released Varieties for Resistance to the Bacteria. Asian Journal of Plant Sciences 2005, 4:577–579.CrossRef 3. Leach J, Rhoads M, Vera Cruz C, White F, Mew T, Leung H: Assessment of genetic diversity and population structure of Xanthomonas oryzae pv. oryzae with a repetitive DNA element. Appl Environ Microbiol 1992, 58:2188–2195.PubMed 4. Nelson R, Baraoidan M, Vera Cruz C, Yap I, Leach J, Mew T, Leung H: Relationship between phylogeny and pathotype for the bacterial blight pathogen of rice. Appl Environ Microbiol 1994, 60:3275–3283.PubMed 5.

Such an interaction prevents the Subunit C from participating in the assembly of the Vacuolar Subcomplex (V0 Subcomplex) that is required for the formation of the mature V-ATPase on the vacuolar membranes [19]. This significantly delays the proteolytic endosomal degradation of the internalized EGFr that eventually recycles to the

plasma membrane. This extend the EGFr lifespan and increases the EGF dependent/EGFr signalling [20, 21] suggesting that the interaction with the subunit C selleck chemical represent an elective function of E5. Conversely, other authors believe that the impairment of V-ATPase and consequent delayed degradation of internalized EGFr is an indirect result of trafficking disruption selleck and impaired fusion of early endosomes with late acidic endosomes [22, 23]. The pH modulation is very important in the regulation of cell organellar trafficking and function in many cellular strains. In particular intra-melanosomal pH has been indicated as an essential factor for the control of melanin deposition in melanocytes [24]. Melanogenesis is regulated through the modulation of tyrosinase, the rate-limiting enzyme of the melanogenic pathway. Differences in tyrosinase activity of melanocytes from different

skin photo types (Caucasian or Black skin) have been reported [25]. It has also been shown that these differences were not due to variations in tyrosinase abundance or gene activity, but to the regulation of catalytic activity Protein Tyrosine Kinase inhibitor of the enzyme [25]. In fact, near neutral melanosomal pH is optimal for human tyrosinase activity and melanogenesis while melanin production is suppressed in Caucasian melanocytes by low melanosomal pH [24]. Accordingly, tyrosinase mRNA and tyrosinase protein are actually present also in amelanotic melanomas, where no tyrosinase activity and no melanin deposition can be detected [26, 27]. The probable reason of the declined catalytic activity in these cells, where tyrosinase is present in a inactive state, is the low internal pH due to elevated V-ATPase activity consequent to elevated glycolysis and extra-cellular

acidification occurring during the metastatic spread. Accordingly, it has been demonstrated that substances that act as selective inhibitors of V-ATPase [28, 29] are able to determine the re-activation of tyrosinase and melanogenesis and melanotic reversion of amelanotic melanomas [26]. In the present work we expressed the HPV 16 E5 protein in two lines of human, tyrosinase-positive, amelanotic melanomas with the aim to examine whether the E5 expression could modulate the melanosomal pH and tyrosinase activity. Here we provide evidence that HPV-16 E5 protein inhibits proton pump, causing alkalinisation of endocellular pH, tyrosinase activation, melanin deposition and modulation of sensitivity to dopamine mimetic drugs.

(DOCX 17 KB) Additional file 3: Primers for loss of heterozygosity analysis by single nucleotide polymorphism genotyping. Sequences of the primers used for SNP

LOH PF-01367338 concentration evaluation are shown. All primers designed for use on the Sequenom MassARRAY platform. The percentage of heterozygosity among informative SNPs within two populations from the International HapMap Project are listed. (CEU = Utah residents with Northern and Western European Ancestry; YRI = Samples from Yoruba descent Ibadan, Nigeria; UEP = unextended primer). (DOCX 20 KB) Additional file 4: Characterization of SOSTDC1-specific antiserum. A) A renal cell carcinoma sample with LOH at the SOSTDC1 locus was treated with and without SOSTDC1 antiserum as an internal control to demonstrate effective SOSTDC1 detection. B) Increasing amounts of recombinant SOSTDC1 protein were gel-resolved and immunoblotted with SOSTDC1 antiserum. C) Proteins from the breast carcinoma KU-57788 cell line cell line MDA-MB-231 and those from the breast epithelial cell line MCF10A were resolved and immunoblotted with SOSTDC1-specific antiserum in the presence or absence of competing peptide. The lack of banding in the presence of the immunizing peptide demonstrates

antibody specificity. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein levels were used to verify loading. D) SOSTDC1 was purified from HEK-293 cells transiently transfected to express FLAG epitope-tagged SOSTDC1 protein. The coincident banding when membranes were probed with FLAG-specific antibody and SOSTDC1-directed antiserum verifies the specificity of the antiserum. (TIFF 493 KB) References 1. Aune GJ: Wilms tumor. Pediatr Rev 2008, 29: 142–143. discussion

143PubMedCrossRef 2. Varan A: Wilms’ tumor in children: an overview. Nephron Clin Pract 2008, 108: c83–90.PubMedCrossRef 3. Linehan WM, Zbar B: Focus on kidney cancer. Cancer Cell 2004, 6: 223–228.PubMedCrossRef 4. Sossey-Alaoui K, Vieira L, David D, Boavida MG, Cowell JK: Molecular characterization of a 7p15–21 homozygous deletion in a Wilms tumor. Genes Chromosomes Cancer 2003, 36: 1–6.PubMedCrossRef 5. Rubin BP, Pins MR, Nielsen GP, Rosen S, Hsi BL, Fletcher JA, Renshaw AA: Isochromosome 7q in adult Wilms’ tumors: diagnostic and pathogenetic implications. second Am J Surg Pathol 2000, 24: 1663–1669.PubMedCrossRef 6. Pavlovich CP, Padilla-Nash H, Wangsa D, Nickerson ML, Matrosova V, Linehan WM, Ried T, Phillips JL: Patterns of aneuploidy in stage IV clear cell renal cell carcinoma revealed by comparative genomic hybridization and spectral karyotyping. Genes Chromosomes Cancer 2003, 37: 252–260.PubMedCrossRef 7. Jiang F, Richter J, Schraml P, Bubendorf L, Gasser T, Sauter G, Mihatsch MJ, Moch H: Chromosomal imbalances in papillary renal cell carcinoma: genetic differences between histological subtypes. Am J Pathol 1998, 153: 1467–1473.PubMedCrossRef 8.

0–6.3 W m−2

UV-A; PAB: 55 μmol photons m−2 s−1 PAR + 7.3–9.2 W m−2 UV-A + 0.4–0.5 W m−2 UV-B), according to the methodology described by Karsten et al. (2007). The data clearly indicated that growth, photosynthesis and respiration were not affected by both UV-A and UV-B, and were even slightly stimulated (Fig. 1), indicating a high UVR tolerance. Fig. 1 The effect of PAR+UV-A and PAR+UV-A/B on growth, photosynthesis, respiration, and the capability to synthesize and accumulate UV-sunscreen Cell Cycle inhibitor compounds in the alpine biological soil crust green alga Klebsormidium dissectum strain ASIB V103. This species was isolated at 2,363 m a.s.l. (Pitschberg, St. Ulrich RNA Synthesis inhibitor in Gröden, South Tyrol, Italy). The physiological responses are expressed as relative percentages in relation to the control (PAR, 100 %) If BSC algae are confronted with UVR in their natural habitats, they rely on several different strategies to mitigate or even prevent biologically harmful UV-effects and assure long-term survival. These include avoidance, numerous protective mechanisms, and repair of DNA, which is demonstrated in a summary scheme (Fig. 2). BSC algae typically

occur in a matrix of polymeric organic and inorganic substances, and in association with other organism groups. In BSC of North American deserts, green algae occupy microenvironments within the crust matrix, where they are protected from damaging radiation levels and exposure to drying atmosphere (Gray et al. 2007). DOK2 These data clearly show that self-shading

by surrounding cells or filamentous algae inside BSCs is an important protective mechanism. Under natural conditions the filamentous BSC green alga Klebsormidium often forms multi-layered mat-like structures on top of or interwoven with the upper millimeters of soil, which contribute to a high degree of self-shading as a passive photoprotective mechanism (“umbrella”) for individual filaments inside such a population (Karsten et al. 2010). Similarly, in the semi-terrestrial green algal genus Zygnema, thick mat-like layers survive experimentally generated high UVR to PAR ratios by self-shading (Holzinger et al. 2009; Pichrtová et al. 2013). In addition, the formation of spores and other permanent stages (such as akinetes) may contribute to coping with enhanced UVR (for summary see Holzinger and Lütz 2006). Fig. 2 Strategies of alpine biological soil crust algae to counteract biologically harmful UV radiation and dehydration The response of any alga to UV-B exposure is determined by the interplay of genetically fixed adaptation and physiological acclimation (Bischof et al. 2006). While the UVR-tolerance mechanisms of marine algae are very well studied, adequate data on alpine BSC algae are still missing.

05) after the exposure of bacteria on different concentration of pilicides. Only the result for the lowest concentration of pilicide 2 was statistically not significant relatively to the positive control (p = 0.068). The increasing concentration of pilicides also had the influence on adhesion level (p < 0.05). For further

evaluation of the activity of compounds 1 and 2 as inhibitors of Dr fimbriae biogenesis, we used a haemagglutination test (HA) conducted in a manner similar to the case of published data describing the activity of Tanespimycin ic50 pilicides 1 and 2 as P and type 1 pili biogenesis inhibitors [34]. The assay is based on an analysis of human erythrocyte agglutination mediated by the bacterial cells. The reaction is dependent on the specific interaction between Dr fimbriae and DAF receptor located on the erythrocyte surfaces. The interaction between DAF receptor

and Dr fimbriae is inhibited by the addition of chloramphenicol at a concentration of 2 μM [37]. The specificity of the haemagglutination observed was confirmed by an analysis of its reversibility as a consequence of the addition of chloramphenicol. The observed haemagglutinating ability of the bacteria reflects the amount of Dr fimbriae produced in the presence of the pilicide. The HA-titer, the highest bacterial dilution, in duplicates, which still provides erythrocyte agglutination selleck compound is determined in the experiment (Figure 2). A low HA-titer indicates that a higher concentration of bacteria, with low amount of fimbriae, is required for agglutination to occur. In our assay, the bacteria of E. coli BL21DE3/pBJN406 were grown analogically to the CHO cells adherence experiments, on agar plates containing 3.5 mM pilicide. The fully-fimbriated bacteria grown in the absence of pilicide (positive control) resulted in an HA-titer of 128. The non-fimbriated bacteria E. coli BL21DE3/pACYC184 (negative control) gave an HA-titer of 1. GPX6 The bacteria cultivated in the presence of pilicides 1 and 2 in media had a reduced HA-titer of 16/32 (Figure 2). The HA-titers were determined as an average from duplicate runs in three independent experiments These results clearly

show that bacteria grown in the presence of these pilicides possess a reduced amount of Dr fimbriae as an effect of blocking the chaperone-usher pathway. Figure 2 Blocking of Dr fimbriae-dependent agglutination of human erythrocytes by pilicides. The following bacterial preparations, normalized to OD600, were used in the hemagglutination assays: negative control – E. coli BL21DE3/pACYC184, grown on TSA plates with 5% DMSO, non-fimbriated strain; positive control – E. coli BL21DE3/pBJN406, grown on TSA plates without pilicide, fully-fimbriated strain; chloramphenicol –E. coli BL21DE3/pBJN406, grown on TSA plates without pilicide, the agglutination experiment was performed in the presence of 2 μM of chloramphenicol; pilicide 1 and pilicide 2 – the E. coli BL21DE3/pBJN406 grown on the TSA plates in the presence of 3.

Scientists from different organizations throughout the world accomplished a benchmark research on the thermal conductivity of nanofluids, and the results indicated that the experimental data were in

good agreement when Nan’s model is used. According to Nan’s model, the thermal conductivity of the nanofluid can be calculated as follows: (2) where L ii and ϕ are the geometrical factor and the volume fraction of particles, respectively. β ii is defined as (3) where k p is the thermal conductivity of the particles. For GNPs, the aspect ratio is very high, so L 11 = 0 and L 33 = 1. It should be mentioned that the thermal conductivity determined here by Nan’s model has taken the matrix additive interface contact resistance into consideration. In Equation 2, the predicted thermal conductivity of composite is sensitive to the small change Ceritinib of the nanoparticles’ Apoptosis inhibitor thermal conductivity. Additionally, the theoretical calculation established that the thermal conductivity of graphene can be influenced by the dimensions, edge roughness, and defect density. Figure 11 shows the thermal conductivity enhancement of GNP nanofluids as a function of loading at a constant temperature of 30°C. From the results, it can be clearly seen that experimental results

can be validate using Nan’s model. Furthermore, the comparison between carbon-based nanofluids in most recent works is shown in Table 2. Figure 11 Thermal conductivity enhancement based on Nan’s model and experimental results at 30°C. Table 2 Thermal conductivity enhancement of recent nanofluids in literature Base fluid Concentration (wt.%) Dispersant + base fluid Maximum enhancement (%) Reference MWNTs 0.60 DW 34 [34] Graphite 0.5 DW + PVP 23 [35] GO 12 EG 61 [11] GNP 300 0.1 DW 14.8 Present study GNP 500 0.1 DW 25 Present study GNP 750

0.1 DW 27.6 Present study MWNTs, multiwall carbon nanotubes; GO, graphene oxide; DW, distilled water; EG, ethylene glycol; PVP, polyvinylpyrrolidone. Based on the results in Table 2, it is outstandingly evident that GNP nanofluids provide a significant thermal conductivity enhancement compared to those of other works when they have higher concentrations of nanoparticles. From these results, it can be seen that the use of low concentration of GNPs can achieve acceptable thermal conductivity enhancement for medium-temperature applications including solar collectors CYTH4 and heat exchanger systems. Electrical conductivity analysis Though important, the electrical conductivity of nanofluids has not yet been widely studied as compared to thermal conductivity. The electrical conductivity of a suspension can either increase or decrease depending on the background electrolyte, particle size, particle loading, and charge of the particle. The electrical conductivity (σ) of water is related to the temperature and increases by 2% to 3% for each 1°C increase (typical electrical conductivity of distilled water at 25°C is about 5.5 × 10−6 S/m).

Genome integrity is maintained by an intricate network of DNA repair proteins [33, 34]. Organisms have developed several DNA-repair pathways as well as DNA-damage checkpoints. Defects in this complex machinery are associated with genotoxic susceptibility and familial predispositions VEGFR inhibitor to cancer [35]. Increasing evidence links environmental exposures, subtle modification in DNA repair efficiency, and cancer risk [36]. XRCC1 participates in DNA single strand break and base excision repair to protect genome stability in mammalian cells. One of the common polymorphisms of XRCC1

the Arg399Gln is located in the BRCT1 domain responsible for interacting with other repair components of BER. It was reported that Arg→Gln substitution produces significant conformational changes at BRCT1 domain that may be critical for DNA repair protein-protein interactions [37], thus absence or impairment repair

may cause genome instability and cancer occurrence. It is also important to Buparlisib integrate DNA-repair process with DNA-damage checkpoints and cell survival, to evaluate the role of DNA repair at both cellular and organismic levels. Therefore, protective effects of XRCC1 polymorphisms in cancer may also be observed by the enhanced efficiency of apoptosis at a cellular level as a result of diminished DNA repair capacity secondary to the genetic polymorphisms [38, Branched chain aminotransferase 39]. In our study, neither of these SNPs was found to individually contribute to head and neck cancer risk. There were no differences between the distribution of the genotypes or alleles frequences in patients and controls. However, we found statistically non-significant increase of Arg194Trp genotype frequency (OR, 1.37; 95% CI, 0.70–2.68) and Trp194 allele (OR, 1.32; 95% CI, 0.70–2.49) according to wild-type of Arg194Arg

reference genotype and Arg194 allele frequency (table 2). Non-statistical increase of Arg399Gln (OR, 1.10; 95% CI, 0.61–1.97) according to reference genotype of Arg399Arg was also found. (table 3). While, no altered risk has been found individually for the XRCC1 Arg194Trp or Arg399Gln polymorphisms, the halophyte analysis according to wild-type of Arg194Arg-Arg399Arg showed high association with head and neck cancer (table 4). The findings indicated that a statistically non-significantly increased risk of HNSCC was associated with the combined Arg194Arg-Arg399Gln genotype (OR, 1.33; 95% CI, 0.70–2.56). The higher risk of head and neck cancer occurrence was associated with the combined Arg194Trp-Arg399Arg genotype (OR, 2.96; 95% CI, 1.01–8.80) but no altered risk was associated with others haplotypes. For Tyr165Tyr genotype we also observed positive correlation with cancer progression assessed by tumor size (OR 4.56; 95% CI 1.60–12.95).

Photosynth Res 76(1–3):371–377PubMedCrossRef Sundqvist C, Björn LO (2007) A tribute to Hemming Virgin (1918–2005), a Swedish pioneer in Crizotinib mouse plant photobiology. Photosynth Res 92(1):13–16PubMedCrossRef Sweeney BM (1987) Living in the golden age of biology. Annu Rev Plant Physiol 38:1–9CrossRef Tabita FR (2004) Research on carbon dioxide

fixation in photosynthetic microorganisms (1971–present). Photosynth Res 80(1–3):315–332CrossRef Tamiya H (1966) Synchronous cultures of algae. Annu Rev Plant Physiol 17:1–21CrossRef Tandeau de Marsac N (2003) Phycobiliproteins and phycobilisomes: the early observations. Photosynth Res 76(1–3):197–205 Thake B (2006) Gordon Elliott (Tony) Fogg (1919–2005): pioneering plant physiologist and gifted writer. Photosynth Res 90(1):1–4PubMedCrossRef Thornber JP (1995) Thirty years of fun with antenna pigment-proteins and photochemical reaction centers: a tribute to the people who have influenced my career. Photosynth

Res 44(1–2):3–22CrossRef Tobin E (2006) Samuel Goodnow Wildman (1912–2004): discoverer of fraction I protein, later named Rubisco, who worked till he was 92. Photosynth Res 88(2):105–108PubMedCrossRef Tolbert NE (1997) The C2 oxidative photosynthetic cycle. Annu Rev Plant Physiol Plant Mol Biol 48:1–25PubMedCrossRef Trebst A (2007) Inhibitors in the functional dissection of the photosynthetic electron transport system. Photosynth Res 92(2):217–224PubMedCrossRef Trebst A, Depka B (1995) Polyphenol oxidase and photosynthesis research. Photosynth Res 46(1–2):41–44CrossRef selleck compound van Ginkel G, Goedheer J (1991) Jan Bartholomeus Thomas (1907–1991). Photosynth Res 30(2–3):65–69 Van Niel CB (1967) The education of a microbiologist:

some reflections. Annu Rev Microbiol 21:1–30CrossRef Van Rensen JJS (2002) Role of bicarbonate at the acceptor side of photosystem II. Photosynth Res 73(1–3):185–192PubMedCrossRef Vass Tyrosine-protein kinase BLK I (2003) The history of photosynthetic thermoluminescence. Photosynth Res 76(1–3):303–318PubMedCrossRef Vennesland B (1981) Recollections and small confessions. Annu Rev Plant Physiol 32:1–48CrossRef Verméglio A (2002) The two-electron gate in photosynthetic bacteria. Photosynth Res 73(1–3):83–86PubMedCrossRef Vernon LP (2003) Photosynthesis and the Charles F Kettering research laboratory. Photosynth Res 76(1–3):379–388PubMedCrossRef Virgin H, Volotovskii (1993) Tikhon N Godnev (1892–1982). Photosynthetica 29:163–165 Vredenberg WJ (1981) Professor Dr. E.C. Wassink (1904–1981). Photosynthetica 15:315–316 Wada H, Murata N (2007) The essential role of phosphatidylglycerol in photosynthesis. Photosynth Res 92(2):205–215PubMedCrossRef Walker DA (1992) Robert Hill. Photosynth Res 34(3):337–338CrossRef Walker DA (1995) One thing leading to another. Photosynth Res 46(1–2):45–46CrossRef Walker DA (1997) Tell me where all the past years are. Photosynth Res 51:1–26CrossRef Walker DA (2002) ‘And whose bring presence’—an appreciation of Robert Hill and his reaction.