These nests are sometimes abandoned at an

early stage. On the one hand this may be caused by an accident or illness of the nest-founding queen. On the other hand, however, this may be caused by the increasingly higher temperatures in the course of the early breeding season. Temperatures at these locations may become as high as 45.8 °C when the this website sun shines on the tiles on warm days (our own unpublished observations). This is in the range of the wasps’ suggested upper thermal limit ( Käfer et al., 2011). Although wasps are known to cool their nests with water spread on the combs ( Klingner et al., 2005, Kovac et al., 2009 and Steiner, 1930), these nest temperatures may be higher than single insects or small colonies can survive. In this context the wasps’ critical thermal maximum (CTmax) is of special interest. Some vespine wasps are known to be more susceptible to high temperatures than honeybees ( Ono et al., 1987 and Ono et al., 1995). This allows honeybees to kill wasps by heat-balling

( Ono et al., 1987, Papachristoforou et al., 2007, Stabentheiner, 1996 and Tan et al., 2005). Stabentheiner (1996) and Stabentheiner et al. (2007) investigated this aggressive interaction between Apis mellifera carnica and Vespula sp. However, while the upper lethal temperature has been determined in Vespa mandarinia japonica (44–46 °C, selleck Ono et al., 1995), Vespa velutina (45.7 °C, Tan et al., 2005), and Vespa orientalis (50.6 °C, Papachristoforou et al., 2011) the upper thermal limit of Vespula has not yet been investigated. Because it is thought to be more relevant to natural conditions we choose the temperature ramping procedure ( Terblanche et al., 2011). We applied behavioral observations ( Klok et al., 2004) and thermolimit

respirometry ( Lighton and Turner, 2004) to determine the wasps’ upper critical thermal maximum (activity and respiratory CTmax). Experiments took place in late summer and autumn 2008 (September, October, November) and 2009 (October), and in summer 2010 (August). Foraging yellowjackets (V. vulgaris (Linnaeus 1758) and V. germanica (Fabricius 1793) – subsequently referred to as Vespula sp.) were caught at an artificial D-malate dehydrogenase feeding station provided with sucrose solution. Animals were collected for immediate analysis. In some cases (8 of 35 wasps) they were stored in cages overnight in a dark and cool area (12–15 °C, food provided) for use on the following day. Individuals were weighed before and after the experiments. Individuals were put into a flow-through respirometer measurement chamber made of brass and immersed into an electronically controlled water bath (Julabo F33 HT) regulated within ±0.1 °C of the set temperature. The chamber volume was 18 ml (3 × 3 × 2 cm). This allowed unrestricted movement of the wasps at a high measurement sensitivity. Because of the wasps’ long stay in the chamber (typically overnight, >6 h) they were also provided with a food source (1.

Ehrenstorfer (Augsburg, Germany). All solvents and reagents used were of analytical grade. The protocol used in this study was approved by the HSE Research Ethics Committee (ETHCOM/REG/06/03). After giving informed written consent, six volunteers were given a single oral dose (based on body weight) of methamidophos click here at the ADI (0.004 mg/kg) dissolved in ethanol and diluted with a soft drink. Volunteer details are shown in Table 1. Total

urine excreted was collected at timed intervals up to 24 h post-exposure. The volume of each sample was recorded and an aliquot retained for analysis (<−15 °C). Samples were also analyzed for creatinine concentration to account for dilution. Samples for five of Vemurafenib the six volunteers were stored frozen for five years prior to analysis. We investigated previously reported methods Montesano et al., 2007, Olsson et al., 2003, Jayatilaka et al., 2011 and Savieva et al., 2004) and found problems with recovery when freeze drying. Liquid/liquid extraction also gave some problems, but these were overcome with the use of a higher volume of solvent (10 mL). This was found to give fewer interferences in the chromatography and increased sensitivity, enabling a detection limit of 7 nmol/L,

although this is higher than reported for some other methods (Montesano et al., 2007 – 1.1 nmol/L; Centers for Disease Control and Prevention, National Biomonitoring Programme, 2013 – 0.7 and 2.6 nmol/L). All samples were analyzed in duplicate. Aliquots of urine (10 mL) were added to a sterilin tube and spiked with 50 μL internal standard (d6-methamidophos, 1 mg/L). Calibration standards (0–282 nmol/L were prepared in urine and quality control samples (prepared

by spiking urine with methamidophos at a concentration of 70 nmol/L) were also analyzed throughout the analytical run. Liquid/liquid extraction was carried out by adding 10 mL of dichloromethane to all tubes and rolling for 20 min. The samples were then centrifuged and the solvent layer was removed and evaporated to dryness Rolziracetam under nitrogen. Samples were reconstituted in 50 μL methanol and transferred to vials for analysis. LC–MS/MS analysis was performed on a Shimadzu SPD-M20A HPLC coupled to a 3200 Q-Trap AB Sciex tandem mass spectrometer with compounds optimised in positive ion electrospray MRM (Table 2 and Table 3). An isocratic HPLC method (70% A:30% B) was set up using a ZORBAX SB-C3 Agilent column (4.6 × 150 mm – 5 μm), with mobile phase A (0.1% formic acid in water) and B (0.1% formic acid in methanol) run at a total flow rate of 0.2 mL/min with an overall run time of 15 min. The injection volume was 2 μL. Selected transitions monitored were m/z 142/94 (methamidophos) and 148/97 (d6-methamidophos), see Table 2. The assay was linear up to at least 282 nmol/L (least squares regression coefficient of >0.99).

This in turn predominantly activates subcortical and cortical structures in the hemisphere contralateral to the stimulation. CVS was performed positioning the participant’s head 30° backward from the horizontal plane, so as to place the lateral semicircular canal in the vertical plane (Coats and Smith, 1967), and 30° towards the right. 30 ml of cold (iced) water was slowly introduced using a syringe (Schmal et al., 2005) for 30 sec with a short piece of tubing attached and placed in the external auditory canal, close to the tympanic membrane but

without touching it, allowing any additional iced water to run out (Fig. 1A). 3-MA purchase Participants were asked to close their eyes during the stimulation to reduce discomfort. After CVS, the participant’s head was positioned in the upright position to check the effectiveness of the vestibular stimulation and to perform the somatosensory detection tasks. Effectiveness of the vestibular stimulation was confirmed by three established measures (Table 1). First, straight-ahead pointing showed significant leftward

displacement immediately after CVS compared to before (p < .001). Second, electrooculogram (EOG) during eccentric fixation to the right was recorded in all experimental conditions, and the presence of oculomotor nystagmus characterized by leftward slow-phase and rightward fast-phase www.selleckchem.com/products/ldk378.html was confirmed immediately after the irrigation. Specifically,

each value obtained was based on an average of five 3 sec epochs. We then measured the velocity in degrees/second from the peak of the saccade to its end and the number of microsaccades occurring in the slow-phase. We found both increased slow-phase eye velocity (p < .001) and increased frequency of fast-phase saccades (p < .02) immediately after CVS compared to before. The time taken for irrigation, reported Liothyronine Sodium cessation of vertigo, pointing and oculomotor recording was up to 3 min. At this point, Post-CVS somatosensory testing was begun. Because CVS effects have limited duration, care was taken to ensure the Post-CVS condition was completed within 15 min following CVS, which corresponds to the window of maximal effect (Bottini et al., 1995; Ngo et al., 2007). Six subjects received tactile (electrocutaneous) stimuli to the left and right index fingers, and contact heat-pain stimuli to the tips of the left and right middle fingers (see Fig. 1B). In the remaining subjects, the assignment of stimuli to fingers was reversed. Data from one participant were discarded due to an inability to measure stable cutaneous thresholds prior to CVS. Participants were blindfolded during somatosensory testing to avoid the influence of confounding visual inputs or tonic gaze deviation (Figliozzi et al., 2005).

The seawater was added to 500 mL Erlenmeyer flasks to a final volume of 300 mL

and sample treatments were spiked with a final concentration of 10 μg L−1 glyphosate. The same volume of carrier was added to control sample flasks and was 0.0004% (v/v). Each flask was stoppered with autoclaved silicone bungs to allow for aerobic conditions. The physical/chemical characteristics of the filtered seawater were measured for: pH, DIC, DOC, DIN, DON, TSS, bacterial counts (see below) see more and particle size distribution. Flow cytometry was used to quantify the microbial populations in the seawater used in the experiment. Samples were fixed with 5% formaldehyde and stored at 4 °C. Sub-samples were stained using Sybr Green, diluted to 1:10,000, and allowed to develop in the dark for 30 min. Samples were run using a BD Accuri C6 cytometer (BD Biosciences, CA, USA) equipped with a red and blue laser (488 nm, 50 mW maximum solid state; 640 nm, 30 mW diode) and standard filter setup. Flow rate was 14 μL min−1, 10-μm core. The natural microbial

community populations and their abundances were measured for the initial seawater as well as treatments for the experiment using the Accuri CFlow plus software. For each sampling period, 5 mL control and glyphosate samples were collected and stored at 4 °C. The glyphosate selleck compound samples were then sent to Queensland Health Forensic and Scientific Services (Coopers Plains, Australia) for analysis. Standards and blanks were derivatised with fluorenylmethylchloroformate. The derivatisation procedure follows a published method with minor adjustments for volume of sample available (Hanke et al., 2008). The sample was then concentrated on a SPE cartridge (Phenomenex Strata X 200 mg 3 m L−1) prior to analysis by HPLC-MS/MS. The glyphosate and degradation product concentrations were determined by HPLC-MS/MS using an ABSciex 4000Q Trap mass spectrometer (ABSciex, Concord, Ontario, Canada) equipped with an electrospray (TurboV) interface and coupled to a Shimadzu Prominence HPLC system (Shimadzu Corp., Kyoto, Japan). Column conditions

were as follows: Phenomenex Gemini-NX C18 column aminophylline (Phenomenex, Torrance, CA) 3 μm 30 × 2.0 mm, 40 °C, with a flow rate of 0.35 mL min−1. The column was conditioned prior to use and for analyte separation required a linear gradient starting at 0% B for 1.0 min, ramped to 100% B in 8 min then held at 100% for 2 min followed by equilibration at 0% B for 7 min (A = HPLC grade water, B = 95% methanol in HPLC grade water, both containing 5 mM ammonium acetate and 0.008% (v/v) 32% ammonia solution). The mass spectrometer was operated in the negative ion, multiple reaction-monitoring mode (MRM) using nitrogen as the collision gas. The transition ions monitored after sample derivatisation were 390/168, 390/150 for glyphosate and 332/110, 332/136 for AMPA.

At greater depths hard substrates become more common; they are occupied by red algal communities: at 3–4 m depth by Polysiphonia fucoides and from 4 to 16 m by Furcellaria lumbricalis ( Bučas 2009). The most conspicuous macrozoobenthos species on the hard substrates are blue mussels Mytilus trossulus and bay barnacles Balanus improvisus ( Olenin & Daunys 2004). The Baltic herring spawning grounds were mapped in 2009–2010 during the spawning period (March–May). In the 2009 season the sampling points were evenly

distributed (the average distance between the sampling points was approximately 800 m) over the F. lumbricalis biotopes, reported to be the most important for Baltic herring spawning in Lithuanian coastal waters ( BaltNIIRH 1989, Olenin learn more & Labanauskas 1995, Maksimov et al. 1996, Fedotova 2010) ( Figure 1). In the 2010 season sampling efforts were concentrated in the central part of the study area, where high resolution (1.9 × 1.9 m per pixel) multibeam bathymetry (KU MARSTEC, unpublished data) opportunistically became available. This data allowed the small geomorphological bottom features to be derived for the assessment of their role in the

distribution of Baltic herring spawning beds. Baltic herring eggs are relatively small (<2 mm) and semi-transparent, therefore hardly detectable by remote methods (e.g. underwater video), especially in FK866 cell line low visibility conditions. Field data were collected by SCUBA divers. At each sampling point the diver recorded the presence/absence of Baltic herring eggs and spawning substrate. Additionally, a benthic sample was collected from the substrate using a 0.04 m2 frame (Kautsky 1993). The benthic samples were analysed using a Nikon Eclipse E200 microscope to confirm the presence/absence of eggs, and developmental stages (from a to q) were distinguished according to Veersalu & Saat (2003). In 2009–2010 93 points were sampled by SCUBA divers. Opportunistic

data from five occasional findings Selleck Paclitaxel of Baltic herring eggs in 2006–2008 (KU MARSTEC unpublished data) were added (Table 1, Figure 1). The total data consisted of 98 sampling points, 56 of which were in the multibeam area (Figure 1). The samples were collected at depths from 3 to 14 m, whereas most of them within the 5–10 m depth interval (Figure 2). Weather conditions were very calm during the 2009 season, allowing us to perform an additional detailed survey of a single spawning bed: five transects, the lengths of which ranged from 46 to 149 m (Figure 3). The presence/absence of Baltic herring eggs was recorded by divers who used a floating buoy to signal their findings and position to the crew on the boat. During the same season the sampling window was relatively wide (22 days) with more or less evenly distributed sampling dates, which allowed egg development to be monitored.

This concept will offer novel perspectives in designing new pharmacological agents for therapeutic interventions in cancer, inflammatory and autoimmune diseases. “
“Current Opinion in Genetics & Development 2012, 22:533–541 This review comes from a themed issue on Genetics of system biology Edited by James Briscoe and James Sharpe For a complete overview see the Issue and the Editorial Available online 4th January 2013 0959-437X/$ – see front matter, © 2012 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.gde.2012.10.005 The blastoderm TGF-beta assay embryo of Drosophila melanogaster

is one of the most thoroughly and intensively studied morphogenetic fields. In the blastoderm, most of the nuclei are arranged as a monolayer at the cortex (or periplasm) of the embryo. This stage starts 1 min after completion of the ninth cleavage division when the nuclei have arrived at the cortex, lasts approximately 1.5 hours until the onset of gastrulation, and includes cleavage cycles 10–14A ( Figure 1a) [ 1]. The VX-809 research buy basic body plan of Drosophila is determined during the blastoderm stage. Four systems of maternal protein gradients specify polarity along the main embryonic axes ( Figure 1b) [ 2, 3 and 4]. The anterior system, centered around the Bicoid (Bcd) gradient,

the posterior system, including the maternal Hunchback (Hb) gradient, and the terminal system, consisting of graded

signals of the Torso (Tor) MAP-kinase pathway, specify the antero-posterior (A–P) axis of the embryo. Graded nuclear localization of the Dorsal (Dl) morphogen specifies the dorso-ventral (D–V) axis. All of these maternal gradients act by regulating zygotic downstream gene expression ( Figure 1b). The A–P systems activate gap, pair-rule, and segment-polarity genes, which constitute the segmentation gene network, as well as homeotic genes that specify segment identity [ 5, 6 and 7]. The D–V system interacts with the Decapentaplegic (Dpp) morphogen, an ortholog of BMP signaling ligands, and activates targets that are involved in specification of the mesoderm, as well as the neural and dorsal ectoderm [ 8, 9 and 10]. All of these systems use graded signals to subdivide the embryo Vildagliptin into discrete territories along the main embryonic axes. This agrees with a classic paradigm of pattern formation first described by the French Flag model [11 and 12]. Since then, the blastoderm embryo has been used by many pioneering modeling studies, which have established that the situation is a lot more complex than initially thought. Complex regulatory interactions among target genes lead to a dynamic view of positional information, encoded by expression domain boundaries that change location over time [13 and 14].

The DU-induced shift of

Th cells (towards Th2) may lead to increased susceptibility to autoimmune disease, cancer, and infectious diseases. The mechanism for Th1/Th2 imbalance was complex, and the transcription factors (GATA3, STAT1, STAT4, STAT6, T-bet, c-Maf, and so on) might play a relevant role in this process. Further study is necessary to elucidate the mechanism of DU exposure on Th1/Th2 balance. In addition, our results suggest that the immune system is one of the systems most sensitive to damage induced by chronic uranium poisoning. Therefore, selleck chemical the present study indicates that in-depth investigations examining the immune function of the population that is chronically exposed to uranium should be performed, mTOR inhibitor which may lead to the discovery of valuable biomarkers. The authors declare no conflict of interest. This work was supported by the National Natural Science Fund of China (no. 30970678) and State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Combined Injury, China (no. SKLZZ200809). We thank Ying Wan as well as members of Institute of Immunology, Third Military Medical University for technical assistance and helpful discussion in some aspects of these studies. “
“Vitamin A (retinol) and its derivatives

control diverse cellular processes by modulating gene transcription through the activation of the so-called retinoid receptors. These receptors belong to the superfamily Fossariinae of steroid/thyroid hormones nuclear receptors and are subclassified into RAR (retinoic acid receptors) and RXR (retinoid X receptors) (Krinsky and Johnson, 2005). Furthermore, retinol also exerts an important function in the maintenance of the cellular redox homeostasis, protecting biomolecules from

oxidative damage caused by reactive oxygen species (ROS) produced from endogenous metabolism or xenobiotic compounds (Halliwell and Gutteridge, 2007). Recently, retinol and some derivatives, such as retinoic acid, have been also demonstrated to promote the activation of signaling pathways and modulation of transcription factors by mechanisms not related to the RAR/RXR-mediated gene transcription (Masia et al., 2007). Among the processes triggered by a non-genomic fashion by retinoids are included the activation of mitogen-activated protein kinases (MAPK) (Canon et al., 2004), phosphatidylinositol-3-kinase (PI3 K) and Akt (Canon et al., 2004 and Masia et al., 2007), Src non-receptor tyrosine kinase (Gelain et al., 2006), and modulation of protein kinase C (PKC) activity (Miloso et al., 2004). Due to its ability to scavenge free radicals and related species, retinol was considered an important antioxidant component of diet.

A.R.) sought in 1995, histologic guidance and training on sporadic flat colonic adenomas by Dr Tetsuichiro Muto, Tokyo University, Japan. Subsequently, one of the authors reviewed all sporadic flat adenomas filed at Muto’s Department8 and later examined all sporadic flat adenomas filed at other hospitals in the Tokyo area.9, 10 and 11 A total of 1014 flat colorectal lesions were reviewed in Tokyo, which GSI-IX were compared with 600 lesions in Sweden. Those studies

revealed that sporadic flat (nonpolypoid) adenomas were more advanced (in terms of high-grade dysplasia [HGD]) and more aggressive (in terms of intramucosal and submucosal invasion) in Japan than in Sweden. Although the causes for the difference in those disparate geographic regions remains debatable, the findings helped us to understand some of the unclear

points and discussions that appeared in the literature on this subject. In 1996, Jaramillo and colleagues3 detected at endoscopy 104 small polyps in 38 of 85 Swedish patients with UC: 74% were endoscopically flat, 23% polypoid (20% sessile and 3% pedunculated), and in 3% the endoscopic appearance was not recorded. The pathologic examination revealed nonpolypoid (flat) adenomas in 14%, tubular or villous structures with dysplastic cells in the lower part of the crypts in 5%, nonpolypoid hyperplastic polyps in 34%, mucosa with inflammation in 7%, and mucosa in remission in 40%. Data show that nonpolypoid adenomatous lesions are commonly found in IBD colectomy specimens with carcinoma. One of the authors has previously reviewed 96 colectomy specimens with Epigenetics inhibitor UC and carcinoma filed at the Department of Pathology, St Mark’s Hospital, London, UK (Fig. 1). A total of 3049 sections were available in the 96 colectomy specimens; the mean number of sections/colectomy studied was 31.8 (range 7–97 sections).1 In addition to carcinomas, several circumscribed adenomatous

lesions were found elsewhere in the colon or rectum; they will be referred over to as synchronous adenomatous lesions (SALs). Using a low-power examination (4x), the histologic profile of these circumscribed lesions was classified into polypoid and nonpolypoid, both in areas with UC and in areas without inflammation. A total of 104 SALs were found in the 96 colectomies: 73 SALs, which occurred in areas with inflammation, and 31 SALs, in areas without inflammation. Polypoid SALs were recorded in 35% (n = 34) of the 96 colectomies. Polypoid SALs in areas with inflammation exhibited irregular dysplastic glands with a jigsaw pattern having irregular bands in the interspersed lamina propria. The mucosa adjacent to these adenomatous lesions showed irregular, dysplastic crypts. Polypoid SALs were found in 47% (n = 34) of the 73 SALs occurring in areas with inflammation. Polypoid SALs in areas without inflammation had a more regular glandular pattern and the interspersed lamina propria was more regularly distributed, and the adjacent mucosa showed no dysplasia.

Moreover, these exposure agents are not fully representative of human exposure as cells are not fully exposed to both the particulate and vapour phase components of the cigarette smoke. A number of whole smoke exposure systems are being developed to address these problems, but have only recently entered a phase where dosimetric comparisons can be made and have not yet been validated. Whole smoke exerts significant cytotoxicity and therefore precise exposure conditions need to be defined in order to detect specific genotoxic effects. Of course the real key to definition of appropriate smoke exposure systems for toxicity testing is to understand the contribution buy RAD001 of individual tobacco

smoke constituents to the genotoxic effects (both singly and in combination) and to estimate their concentration in tobacco smoke particulate and vapour phase fractions. This understanding then facilitates the design of appropriate tobacco smoke exposure systems, focusing on key drivers of genotoxicity, facilitating product comparisons and providing a scientific rationale for any observed differences in genotoxic potential. To date, there are a limited number of studies using whole mainstream cigarette smoke (WMCS) in in vitro genotoxicity assays. WMCS was first used as a smoke exposure system in the in vitro micronucleus assay ( Massey et al., 1998 and Okuwa

et al., 2010). In addition, Aufderheide et al. developed a WMCS method to evaluate the mutagenicity of cigarette smoke in various bacterial strains in the Ames test ( Aufderheide

and Gressmann, 2007 and Aufderheide and Histone demethylase Gressmann, Staurosporine concentration 2008). To date, there is no published information of this exposure system in the MLA assay. In the field of non-regulatory assays, WMCS was used by Thorne et al. to measure oxidative DNA damage in the in vitro comet assay ( Thorne et al., 2009). Studies to measure the activation of H2AX in response to DNA damage in vitro after cigarette smoke exposure have also used CSC, TPM or cigarette smoke extract (CSE) as a smoke exposure system ( Albino et al., 2004, Albino et al., 2006, Albino et al., 2009, Tanaka et al., 2007a, Tanaka et al., 2007b, Luo et al., 2004, Zhao et al., 2009, Jorgensen et al., 2010 and Darzynkiewicz et al., 2011). The in vitro γH2AX assay was originally used to measure DSBs following cigarette smoke exposure ( Albino et al., 2004). Human A549 pulmonary adenocarcinoma cells were exposed to cigarette smoke and normal human bronchial epithelial (NHBE) cells to CSC. Both cell systems showed a dose-related response in γH2AX activation. Once the relationship between smoke exposure and γH2AX activation was confirmed, Albino et al. used the assay to evaluate cigarettes with different tar deliveries. The results indicated that the increment in γH2AX intensity was proportional to the estimated tar delivery rather than the cigarette type or smoking behaviour ( Albino et al., 2009). Interestingly, when Kato et al.

These model descriptions enable the above quantum yields Φfl(z) and Φph(z) to be estimated Epacadostat from the three main environmental parameters governing phytoplankton growth in the sea: basin trophicity, assumed to be

the surface concentration of chlorophyll a, Ca(0); the light conditions in the sea, the index of which are values of the irradiance PAR(z) at various depths; and the temperature temp(z) at different depths. These models are based on empirical material collected in the surface layer of waters, i.e. from the surface down to a depth of ca 60 m. This is equivalent to the water masses in roughly half the euphotic zone in basins with Ca(0) < 1 mg m−3, and almost the whole of the euphotic zone or even transgressing it in other basins. The measurements were carried out in basins of different trophicity and at temperatures ranging from ca 5°C to ca 30°C. We can therefore assume that the relationships are practically universal: to a good approximation they quantitatively describe the processes of photosynthesis and the natural fluorescence

of phytoplankton in any ocean or sea basin. The modelling of the yields of heat processes presented in this work is based on the same principles as the above models of fluorescence and photosynthesis. The appropriately modified assumptions of this modelling are as follows: • Assumption 1: The model quantum yields of the heat production ΦH(z) at particular

see more depths in the sea are complementary to the unity of the sum of the quantum yields of photosynthesis Φph(z) and fluorescence Φfl(z), as emerges from equation (1). The set of equations, derived from assumptions 1–4, describing the models of the dependences of the quantum yield of heat production in the sea on environmental factors, is given in Table 1. where Ca(0) – total chlorophyll a concentration in the surface water layer [mg m− 3], The mathematical description of the relationship between the quantum yields of processes of the deactivation of phytoplankton pigment excitation energy Thymidine kinase and environmental factors, presented in this paper (see (2), (3) and (4) and Table 1), enables their variability under different conditions in the water column to be tracked down to a depth of ca 60 m. On this basis Figure 1 illustrates the dependences of the quantum yields of all three sets of processes by which excited states in the molecules of all phytoplankton pigments are dissipated on the PAR irradiance in different trophic types of water. Apart from the dependence of the yield ΦH ( Figure 1b), the figure also shows the dependence of the quantum yield of fluorescence Φfl ( Figure 1a) and the quantum yield of photosynthesis Φph ( Figure 1c). In order to compare the strongly differentiated ranges of variability of these three yields, their values are presented on a logarithmic scale.