Exclusion criteria included patients who were pronounced dead upon arrival and patients who were transferred from other acute care hospitals. All charts were retrospectively reviewed for demographics (age, gender, pre-existing co-morbidities, pre-existing anticoagulation medications, mechanism of injury, ISS, head abbreviated injury score [AIS], Cell Cycle inhibitor GCS at scene and upon presentation to the ED, intubation at scene or in

ED, injured body regions, admission serum creatinine and INR, intensive care unit length of stay (ICU LOS), hospital LOS, surgical interventions, complications (infectious and non-infectious), and in-hospital mortality. Any mortality within 30 days of injury was considered an in-hospital death regardless of patient location at the time of death. Time of death was extracted from the medical records which are updated regularly by the Israeli Governmental Ministry of Internal Affairs registry. Outcome variables were mortality and discharge placement. Discharge placement was defined as the patient destination after acute care in the trauma center, being home, rehabilitation center, assisted-living facility (ALF) (defined as lower level of dependence requiring professional

support), or transfer to another acute care hospital. PRI-724 mouse co-morbidities were defined as noted in Table 1. The absolute number of co-morbidities was calculated for patients with more than one listed illness. Table 1 Definition of co-morbidities identified in the study population Cardiac disease Known history of ischemic heart disease, previous cardiac interventions Malignancy Currently under oncological MRT67307 in vitro follow up or

treatment for active oncological disease Diabetes mellitus Patient requiring insulin or oral hypoglycemic therapy Neurological disease History of cerebro-vascular accident, severe parkinsonism and/ or antiepileptic therapy Dementia SPTBN5 Any case with established diagnosis of dementia Hypertension History of hypertension requiring medication Chronic anticoagulation Patients currently on anticoagulation (LMWH or Warfarin), and /or antiplatelet therapy (excluding aspirin) Chronic renal failure History of preexisting renal insufficiency on admission Chronic obstructive pulmonary disease Ongoing treatment for COPD Statistical analysis For quantitative variables, data is presented as mean and standard deviation (SD). The Chi-square test as well as the Fisher’s exact test was used to test the association between two qualitative variables. The Chi-square test for trends was used for qualitative ordinal variables. The Student’s T test was used to compare quantitative variables between the two groups. Univariate survival analysis was performed by Kaplan-Meier (K-M) methodology with significance of the difference between survival curves determined by the log-rank test. Variables which were significant in the K-M analysis, were entered into a stepwise, (forward, likelihood ratio) Cox regression model.

1998; Field et al. 1998). Calcifying phytoplankton species also contribute to the “”particulate inorganic carbon”" (PIC) pump and thereby play a dual role in regulating marine biogeochemical cycling of carbon through their effects on surface ocean alkalinity (Broecker and Peng 1982; Zeebe and Wolf-Gladrow 2007). One key species of calcifying phytoplankton is the cosmopolitan and bloom-forming coccolithophore Emiliania huxleyi, which has been established as a model organism over the recent decades (Paasche 2002; Raven and Crawfurd 2012; Read et al. 2013; Westbroek et al. 1993). While the calcifying diploid GDC 0449 life-cycle stage of this species has been selleck intensively studied

in field and laboratory experiments, the non-calcifying haploid stage has only recently gained attention due to its important ecological role. In blooms of diploid E. huxleyi, which are usually terminated by viruses, the haploid life-cycle stage functions as a virus-resistant backup population (Frada et al. 2012). Furthermore, the presence SAR302503 concentration and absence of calcification in the differing life-cycle stages of E. huxleyi make them ideal candidates to investigate the cellular mechanisms of calcification and their

interaction with photosynthesis under increasing oceanic CO2 concentrations (Mackinder et al. 2010; Rokitta and Rost 2012). Increasing pCO2 in oceanic surface water directly affects carbonate chemistry by elevating the concentration of dissolved inorganic carbon (DIC) and shifting the carbon speciation toward higher CO2 and H+ concentrations, a phenomenon often referred

to as ocean acidification (OA; Caldeira and Wickett 2003; Wolf-Gladrow et al. 1999). Compared to preindustrial values, pH is expected to drop by 0.4–0.5 units until the end of this century. In several studies testing Astemizole the effects of OA on E. huxleyi, diploid strains were found to exhibit strong, yet opposing responses in terms of biomass and calcite production. While biomass production was either unaffected or stimulated by increased pCO2, calcification typically decreased and malformations of coccoliths increased (e.g., Hoppe et al. 2011; Langer et al. 2009; Riebesell et al. 2000). Bach et al. (2011) suggested that biomass production is stimulated by increasing CO2 concentration at sub-saturating conditions, whereas calcification is specifically responsive to the associated decrease in pH. Such differential CO2 and pH effects on biomass and calcite production are supported by the observation that OA distorts ion homeostasis and shifts the metabolism from oxidative to reductive pathways (Rokitta et al. 2012; Taylor et al. 2011). In a number of studies, the sensitivity of E. huxleyi toward OA has been attributed to its mode of inorganic carbon (Ci) acquisition, which is intrinsically responsive to changes in carbonate chemistry. Thus, for understanding the differential responses to OA, one needs to look at this crucial process of Ci assimilation.

Microbiology SGM 1998, 144:2803–2808.CrossRef 15. Wu M, Eisen JA: A simple, fast, and accurate method of phylogenomic inference. Genome Biol 2009, 9:R151.CrossRef 16. Zmase CM, Eddy SR: ATV: display and manipulation of annotated phylogenetic trees. Bioinformatics 2001, 17:383–384.CrossRef Authors’ contributions GEF conceived of the study and wrote the paper. MW constructed the tree. ID and GEF tabulated the genome sizes and operon copy number data. RR drew the trees, NF-��B inhibitor devised and implemented the coloring schemes.”
“Background Plague is an infectious disease caused by Yersinia pestis, a naturally

occurring bacterium found primarily in wild rodents. It is highly transmissible and brings a high mortality, leading to major public health disasters throughout the history of humanity [1]. In the early 1990s, the incidence of human

plague increased significantly [2], with outbreaks occurring in Africa [3] and India [4]. WHO has classified plague as a reemerging infectious disease for the past 20 years, and Y. pestis has been identified as a bioterrorism agent, posing as a significant threat to human health and safety [5]. In November 2005, a natural focus of human plague was discovered in Yulong, Yunnan province, China[6]. In this Compound C nmr study, we compared Y. pestis isolated from the Yulong focus to strains from other areas. Y. pestis couldn’t be separated by serotype and phage-type, but could be classified into three biovars: Antiqua, Mediaevalis and Orientalis, according to their ability to ferment glycerol and to reduce nitrate as described by Devignat in the 1950s [7]. Recently, a new biovar Microtus was proposed PRKACG based on whole genome sequencing and genetic analysis [8, 9]. Y. pestis has a broad host and vector range [10]. These hosts and vectors have their own natural environment, resulting in the diversity of micro-ecological environments for Y. pestis. During its expansion and adaption into new niches, Y. pestis undergoes considerable genome variability in response to natural selection.

This variability can partly explain the genomic diversity of strains from different plague foci [11]. At present, natural plague foci are widespread inChina. Through systematic analysis of Y. pestis in these areas, it is possible to understand the evolution of Y. pestis and investigate the source of new plague foci. Previous studies have revealed a large number of tandem repeat sequences (TRSs) in the Y. pestis genome, and these TRSs introduce diversity into various plague strains [12]. These loci are called variable-number tandem repeats (VNTRs). Multiple-locus VNTR analysis (MLVA) is an individual identification method that LY2606368 detects VNTR loci. MLVA is widely used in Y. pestis genotyping, and is useful for performing phylogenetic analysis [12–16]. In this study, 213 Y. pestis strains collected from different plague foci in China and a live attenuated vaccine strain of Y. pestis (EV76) were genotyped by MLVA using 14 loci.

However, nothing is known about metabolites of the tryptophan catabolism on DC function. CD14+ cells were isolated from periperal blood and activated to fully mature DC in vitro. In parallel cultures, DCs were generated in the presence of different concentrations of LY2109761 nmr kynurenine and quinolinic acid. These mature DC were used to analyse expression of differentiation markers by FACS, to stimmulate naïve T-cells to proliferation, and to induce Th-1 T-cell Selleckchem MK-4827 response. Kynurenine, but not quinolinic acid, had a dramatic effect on the expression of the DC maturation marker CD83, suggesting that kynurenine has an impact on DC maturation.

The expression of MHC-class I molecules, the co-stimulatory receptors CD80/CD86 and CCR7 on DC was not affected by kynurenine or quinolinic acid. In further analysis we found that kynurenine treated DC dramatically decrease the ability of T-cells to produce INF-gamma a key cytokine indicating a Th-1 immune response. Subsequently T-cell subpopulations were analysed and found that the portion of CD4+CD25+ T-cells was significantly increased in the T-cell population generated by kynurenine treated DC, which indicate an increase in a suppressor see more T-cell population. In summary, these data suggest that kynurenine “primed” mDC induce generation of suppressor T-cells. Based on the data

presented above we hypothesize that metabolites of the kynurenine pathway are important determinants in turning the immune system especially DC to a tolerogenic phenotype. Poster No. 54 Impact of Hypoxia on Furin Trafficking and the Formation of Invadopodia Dominique Arsenault 1 , Sébastien GrandMont1, Martine Charbonneau1, Kelly Harper1, Claire M. Dubois1 1 Department of Pediatric, Immunology Division, Université de Sherbrooke, Sherbrooke,

QC, Canada Recent studies indicate that tumoral invasion and metastasis, triggered by the hypoxic microenvironment, involves strategic relocalization of convertases, adhesion molecules, and metalloproteases. We used the highly invasive human new fibrosarcoma cells HT-1080, stably transfected with eGFP-tagged-furin in order to study the impact of hypoxia on the cellular localization of the convertase furin. Our results indicate that in hypoxic cells, furin is relocalized at the plasma membrane and is internalized via both clathrin- and caveolin/raft dependent endocytosis. Using furin trafficking mutants, we demonstrate that filamin-A, a cytoskeletal tethering protein, is essential for the membrane localization of furin under hypoxia. We further demonstrate that in hypoxic cells, furin and its substrate MT1-MMP relocalize to specific pericellular compartments and this relocalisation is associated with an increased cell ability to convert pro-MT1-MMP into its active form.

This supports the notion that TIP60 might play an important role during Salmonella infection. This increase is SseF-independent, as similar increase was also observed when infected with an sseF mutant Salmonella strain and TIP60 was not concentrated at the vacuoles (data not shown). SseF was not detected in infected cells possibly due to the low amounts translocated during Salmonella infections. GSK2118436 order Figure 3 TIP60 is up regulated upon Salmonella infection. HeLa cells were infected with wild-type Salmonella for the indicated time intervals. Infected cell lysates were PI3K inhibitor subjected

to SDS-PAGE followed by Western blot using anti-TIP60 antibody (upper panel). Actin levels in the same samples were also determined as a control (lower panel). TIP60 is required for efficient intracellular Salmonella replication Previous studies have shown that SseF is required for efficient intracellular

Salmonella replication in macrophages [10]. Since TIP60 acetyltransferase interacts with SseF, TIP60 might be required for efficient intracellular Salmonella replication. To test this, we used siRNA to down-regulate the endogenous level of TIP60. Macrophages were transfected with a plasmid expressing TIP60 siRNA or a control vector expressing the PF 2341066 scrambled siRNA. As shown in Fig. 4, TIP60 siRNA effectively suppressed the endogenous TIP60 expression, while the control siRNA did not. Transfected macrophages were infected with wild-type S. typhimurium or the sseF mutant strains. As shown in Fig. 4, down-regulation of TIP60 leads to less efficient Resveratrol Salmonella replication comparable to the level of sseF mutant strain [10]. There was not significant replication change in cells expressing the scrambled siRNA. These data support our notion that TIP60 is required for efficient intracellular Salmonella replication in macrophages. Figure 4 TIP60 is required for efficient Salmonella replication. Transfected macrophages

were infected with wild-type S. typhimurium or the sseF mutant strains at an MOI of 10. Extracellular bacteria were removed by washing and gentamicin treatment. At 2 and 24 h after bacterial invasion, cells were lysed, and the number of intracellular bacteria was enumerated. The data shown were obtained from three independent experiments with standard errors. The effect of TIP60 knockdown is verified by Western blot using the anti-TIP60 antibodies. Actin was used a control. Discussion We do not know yet the molecular mechanism of how SseF and TIP60 interaction affects the SCV and intracellular Salmonella replication. Ideally, a mutant SseF lacking the TIP60-binding domain can be used to assess the requirement for SseF-TIP60 interaction for its function, however such a mutant is defective in secretion and thus not translocated, making it impossible to assess its effect during infection.

LPS mutants in wbtN, wbtE, wbtQ, and wbtA loci were tested. RND efflux mutants in dsbB, acrA, acrB, tolC, and ftlC were also tested (Table 7). F. tularensis Schu S4 (CDC, Fort Collins, CO) and F. tularensis Schu S4 deletion mutants ΔdsbB, ΔacrA, and ΔacrB (21) were tested in an approved biosafety level 3 laboratory by trained personnel at the University of Virginia, Charlottesville, selleck products VA (Table 7). Table 7 F. novicida and F. tularensis subsp. tularensis

Schu S4 mutants used. Mutant abbreviation Mutant name Gene wbtN tnfn1_pw060420p04q142 wbtN FTN_1422 wbtE tnfn1_pw060328p03q164 wbtE FTN_1426 wbtQ tnfn1_pw060419p04q158 wbtQ FTN_1430 wbtA tnfn1_pw060419p03q166 wbtA FTN_1431 tolC tnfn1_pw060419p03q111 tolC FTN_1703 tolC* tnfn1_pw060328p03q137 tolC FTN_1703 ftlC tnfn1_pw060418p04q166 Hypothetical protein FTN_0779 dsbB tnfn1_pw060323p05q173 dsbB FTN_1608 acrA tnfn1_pw060328p06q117 Membrane fusion protein FTN_1609 acrA* tnfn1_pw060419p03q103 Membrane fusion protein FTN_1609 acrB tnfn1_pw060323p02q131 RND efflux transporter, AcrB/AcrD/AcrF family FTN_1610 acrB* tnfn1_pw060418p04q118 RND efflux transporter, AcrB/AcrD/AcrF family FTN_1610 ΔacrB BJM1032 Schu S4 ΔacrB [16] (FTT0105c) ΔacrA

BJM1040 Schu S4 ΔacrA [16] (FTT0106c) (*= these mutants were tested, but data is not AZD3965 manufacturer shown as it was the same as the first mutant). Cell culture Mouse macrophage cells J774A.1 (ATCC #TIB-67) and human lung epithelial cells A549 (ATCC #CCL-185) were obtained from ATCC, Manassas, VA. J774A.1 cells were grown in Dulbecco’s Modified Eagle Medium (DMEM) with 10% fetal bovine serum and passed every 3 days in a 1:3 dilution following manufacturers’ instructions. A549 cells were grown in Ham’s F-12 with 10% fetal bovine serum and passed every 3 days in a 1:3 dilution. Disc inhibition assay Selleckchem SC75741 Kirby-Bauer disc inhibition assay protocol was followed [57]. 100 μl of overnight bacterial cultures were spread on Chocolate II agar and Schu S4 strains were spread on Mueller-Hinton agar plate with for three discs each containing 15 μg Az placed in a triangle and incubated based on length of time for bacterial

growth to be seen on the plate: 24 (for F. novicida, F. philomiragia, and F. tularensis Schu S4), 48 (for F. tularensis LVS), and 72 hours (for F. tularensis NIH B38) at 37°C in 5% CO2. The diameter of the zone of inhibition including the 6 mm disc was measured (in mm) with three independent measurements for each zone (n = 9). Inhibition was defined as the area of no bacterial growth around the discs. A reading of 6 mm indicates no inhibition [57]. Minimal inhibitory concentration (MIC) Assays were performed with small modification following published protocols [58]. The MIC for F. novicida, F. philomiragia, F. tularensis LVS, related F. novicida mutants, F. tularensis Schu S4, and related F. tularensis Schu S4 mutants were determined in TSB-C media by antibiotic dilution in triplicates. The broth was then inoculated with 105 CFU/ml per strain.

Jae-Gyu Jeon and Pedro L. Rosalen were supported by Chonbuk National University (Republic of

Korea) funds for overseas research (2006) and CAPES/MEC (BEX 2827/07-7) and CNPq/MCT (302222/2008-1) from Brazilian government, respectively. References 1. Marsh PD: Are www.selleckchem.com/products/cbl0137-cbl-0137.html dental diseases examples of ecological catastrophes? Microbiology 2003, 149:279–94.CrossRefPubMed 2. Quivey RG, Kuhnert WL, Hahn K: Adaptation of oral streptococci to low pH. Adv Microb Physiol 2000, 42:239–274.CrossRefPubMed 3. Schilling KM, Bowen WH: Glucans synthesized in situ in experimental salivary pellicle function as specific binding sites for Streptococcus mutans. Infect Immun 1992, 60:284–295.PubMed 4. Hayacibara MF, Koo H, Vacca-Smith AM, Kopec LK, Scott-Anne K, Cury JA, Bowen WH: The influence of mutanase and dextranase on the production and structure of glucans synthesized by streptococcal glucosyltransferases. Carbohydr Res 2004, 339:2127–2137.CrossRefPubMed 5. Kopec LK, Vacca-Smith AM, Bowen WH: Structural aspects of glucans formed in solution and

on the surface of hydroxyapatite. Glycobiology 1997, 7:929–934.CrossRefPubMed 6. Rölla G, Ciardi JE, Eggen K, Bowen WH, Afseth J: Free Glucosyl- and Fructosyltransferase in Human Saliva and Adsorption of these P5091 order Enzymes to Teeth In Vivo. Glucosyltransferases, Glucans Sucrose, and Dental Caries (Edited by: Doyle RJ, Ciardi JE). Washington, DC: Clemical Senses IRL 1983, 21–30. 7. Schilling KM, Bowen WH: The activity of glucosyltransferase adsorbed onto saliva-coated hydroxyapatite. J Dent Res 1988, 67:2–8.CrossRefPubMed 8. Vacca-Smith AM, Bowen WH: Binding properties of streptococcal glucosyltransferases for hydroxyapatite, saliva-coated hydroxyapatite, and bacterial surfaces. Arch Oral Biol 1998, 3:103–110.CrossRef 9. Li Y, Burne RA: Regulation of the gtfBC and ftf genes of Streptococcus mutans in biofilms in response to pH and carbohydrate.

Microbiology 2001,147(Pt 10):2841–8.PubMed 10. Marquis RE, Clock SA, Mota-Meira M: Fluoride and organic weak acids as modulators of microbial physiology. FEMS Microbiol Rev 2003, 760:1–18. 11. Cegelski L, Marshall GR, Eldridge GR, Hultgren SJ: The biology and future prospects of antivirulence therapies. Nat Rev Microbiol 2008, 6:17–27.CrossRefPubMed Amino acid 12. Koo H: Strategies to enhance the biological effects of fluoride on dental biofilms. Adv Dent Res 2008, 20:17–21.CrossRefPubMed 13. Koo H, Schobel B, Scott-Anne K, Watson G, Bowen WH, Cury JA, Rosalen PL, Park YK: Apigenin and tt -farnesol with fluoride effects on S. mutans biofilms and dental caries. J Dent Res 2005, 84:1016–1020.CrossRefPubMed 14. Koo H, Seils J, Abranches J, Burne RA, Bowen WH, Quivey RG: Influence of apigenin on gtf gene expression in Streptococcus mutans UA159. Antimicrob Agents SAR302503 Chemother 2006, 50:542–546.CrossRefPubMed 15. Bowen WH, Hewitt MJ: Effect of fluoride on extracellular polysaccharide production by Streptococcus mutans. J Dent Res 1974, 53:627–629.CrossRef 16.

Results and discussion Figure 2 shows LSM images of an as-deposited Al film

and samples annealed for different durations at 550°C. The surface of as-deposited Al film is smooth, as seen in Figure 2a. When the 40-nm-thick Al film on Si substrate is annealed for 3 h, particles with a size distribution of 0.3 to 7 μm start to form on the surface. This indicates that Al atomic flow is activated at this condition and forms randomly distributed AZD8931 nmr seeds of Al particles. Prolonging the annealing time to 6 h, small particles disappear and large particles with more size uniformity are left behind, which may result from the agglomeration of small particles. The particle size is in general larger than 5 μm. At GW3965 a longer annealing time of 9 h, the particle size distribution is similar

to the case of 6 h annealing, but small pit-like nonuniform structures are observed in the film, presumably originating from local Al deficiency and Si inflow from the substrate. It is inferred that Si’s outward diffusion and its mixing with Al atoms are the reasons why the color of the particles in Figure 2d is dissimilar to that in Figure 2c. If it is the real case, the microparticles should not be pure Al, but Al-Si alloys. The density and the average size of particles are apparently found to increase as the Al film thickness increases, as demonstrated in Figure 2e. This is because the Al film plays as a major source material nourishing the microparticles and the particles become bigger and denser at the expense of the film. For the 90-nm-thick Al film,

the density of the particles is calculated to be 2,500 to 5,560 mm−2 and the particle size reaches up to 13 μm. This spontaneous granulation was rarely observed when an Al film on mafosfamide Si substrate was annealed at 400°C, justifying that the microparticle formation is a process caused by atomic diffusion. Figure 2 LSM images of an as-deposited and annealed Al films on Si substrate. (a) As-deposited film. Samples annealed at 550°C: (b) 3 h, (c) 6 h, (d and e) 9 h. (a to d) 40-nm-thick Al films and (e) 90-nm-thick Al film. Scale bars 20 μm. The detailed structure and the composition of microparticles were analyzed using SEM. Figure 2 exhibits top view SEM images of three samples corresponding to Figure 2c,d,e, learn more respectively. The general shape of the microparticles looks like a distorted hemispheroid with rough surface. It was observed from tilted views that the out-of-plane height relative to in-plane diameter becomes larger with an increase in the average particle size (not shown). From the point of composition, the microparticles are not pure Si, but Al-Si alloys, as deduced from the previous LSM images, with some amount of oxygen. The observed oxygen content is considered to stem from the surface oxidation of the microparticles during cooling and in storage [21].

The most common complications after 7 days were redness and pain. These complications occurred most commonly in the suturing group (34.55% and 21.87%, respectively) followed by stapling technique (26.42% and 13.21%, respectively), and hair SN-38 apposition Lazertinib technique (16.22% and 13.51%, respectively). The distribution of

the complications 7 days after the procedure by the technique used is summarized on Table 4. Table 4 Distribution of the complications on 7th day by the techniques used   Hair apposition Suturing Stapling p value Complications n % n % n %   Pain 5 13.51 12 21.87 7 13.21 X2 = 2.56, p > 0.05 Serous wound drainage 1 2.7 0 0 0 0 X2 = 2.61, p > 0.05 Infection 0 0.0 3 5.45 1 1.89 X2 = 3.05, p > 0.05 Redness 6 16.22 19 34.55 14 26.42 X2 = 5.54, p > 0.05 Hair loss 0 0 5 9.093 2 3.77 X2 = 4.78, p > 0.05 Wound dehiscence 1 2.7 0 0 3 5.66 X2 = 3.15, p > 0.05 There was a significant relationship between the technique and the satisfaction level after 15 days (X2 = 6.75, p < 0.05). According to this,

satisfaction after 15 days depends on the technique used. The crosstabulation between the techniques used and satisfaction level after 15 days revealed that a stapling and suturing techniques were association with dissatisfaction whereas hair apposition technique was associated Rigosertib concentration with much lower dissatisfaction rate (Figure 2). Figure 2 The graph of the relationship between the techniques and satisfaction level after 15 days. The crosstabulation between the techniques used and the rate of cosmetic problems after 15 days revealed a higher rate of cosmetic problems in the suturing group than

other groups (X2 = 8.81, p < 0.05) (Figure 3). Figure 3 The graph of the relationship between the techniques and cosmetic problems. Discussion Emergency physicians can also employ hair apposition technique in addition to suturing and stapling in the treatment of scalp lacerations. In our study, hair apposition technique was associated with a higher rate of satisfaction than other techniques 7 days and 15 days after the procedure. however Hock et al., in a study where they used techniques of suturing and hair apposition in patients with scalp laceration, included lacerations up to 10 cm but did not mentioned about any relationship between the technique used and laceration length [7]. Both our study and previous studies suggested that a hair length of at least 1 cm is essential for application of hair apposition technique in scalp lacerations [7, 8]. In our study there was no significant difference between the technique used and hair length. Hock et al. compared complication and healing rates 7 days after treatment of scalp lacerations with suturing or hair apposition techniques and reported that wound healing and scar formation occurred more commonly in suturing whereas rates of infection or bleeding were not different in both groups [7]. Karaduman et al. used all three techniques in scalp lacerations and reported no cases of infection 7 days after the procedure.

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variation of photoinhibition using chlorophyll fluorescence imaging of a chilled, variegated leaf. J Exp Bot 58:453–463 Hogewoning SW, Wientjes E, Douwstra P, Trouwborst G, van Ieperen W, Croce R, Harbinson J (2012) Photosynthetic quantum yield dynamics: from photosystems to leaves. Plant Cell 24:1921–1935PubMedCentralPubMed Holzwarth AR (1996) Data analysis of time-resolved measurements. In: Amesz J, Hoff AJ (eds) Biophysical heptaminol techniques in photosynthesis. Kluwer, The Netherlands, pp 75–92 Holzwarth AR (2008) Ultrafast primary reactions in the photosystems of oxygen-evolving organisms. In: Braun M, Gilch P, Zinth W (eds) Ultrafast laser pulses in biology and medicine. Springer, Berlin, pp 141–164 Holzwarth AR, Lenk D, Jahns P (2013) On the analysis of non-photochemical chlorophyll fluorescence quenching curves: I. Theorethical considerations. Biochim Biophys Acta 1827:786–792PubMed Horton P, Hague A (1988) Studies on the induction of chlorophyll fluorescence in isolated barley protoplasts: IV. Resolution of nonphotochemical quenching. Biochim Biophys Acta 932:107–115 Horton P, Ruban AV, Walters RG (1996) Regulation of light harvesting in green https://www.selleckchem.com/products/BIRB-796-(Doramapimod).html plants. Annu Rev Plant Physiol Plant Mol Biol 47:655–684PubMed Hsu B-D, Leu K-L (2003) A possible origin of the middle phase of polyphasic chloropyll fluorescence transient.