Likewise, there is enough evidence on the role of mitochondrial d

Likewise, there is enough evidence on the role of mitochondrial dysfunction in pathophysiological features of diabetes, including insulin deficiency

and insulin resistance. Pancreatic beta cell failure has been reported to be associated with mitochondrial dysfunction and can be caused by exposure to pesticides (Jamshidi et al., 2009 and Pournourmohammadi et al., 2007). On the other hand, exposure to pesticides inhibiting complex I and III mitochondrial respiratory chain can lead to a diminished oxygen consumption and cellular energy supply which in turn can result in reduced insulin signaling cascade. In this way, organochlorines, atrazine, and some dioxin-like pesticides have been shown to decrease mitochondrial capacity in beta oxidation of fatty acids resulting in accumulation of intracellular fat, a situation considered to develop obesity and insulin resistance (Lee, 2011 and Lim et al., 2009). Increased production of click here ROS and/or decreased capacity of antioxidant selleck chemicals defense can disrupt oxidative balance and result in damaging all components of the cell, including lipids, proteins, and DNA. Further, oxidative stress can disrupt various parts of cellular signaling because ROS are considered as one of the main messengers in redox signaling. However, the role of oxidative stress has been uncovered

in induction and development of different kinds of human diseases, including cancer, diabetes, neurodegeneration, atherosclerosis, schizophrenia, chronic fatigue syndrome, and renal and respiratory disorders (Ahmad et al., 2010, Ciobica et al., 2011, Fendri et al., 2006, Lushchak and Gospodaryov, 2012 and Nathan et al., 2011). On the other hand, there is a huge body of literature on induction of oxidative stress by pesticides, and it has been implicated in development of health problems mediated by exposure to pesticides (Grosicka-Maciag, 2011, Olgun

and Misra, 2006, Slaninova et al., 2009 and Soltaninejad and Abdollahi, 2009). It has been revealed that pesticides can disturb oxidative homeostasis through direct or indirect pathways, including mitochondrial or extramitochondrial production of free radicals, thiol Phosphoglycerate kinase oxidation, and depletion of cellular antioxidant reservoirs (Abdollahi et al., 2004b, Abdollahi et al., 2004c, Braconi et al., 2010 and Mostafalou et al., 2012a). Considering the oxidative stress as a powerful promoter of other cellular pathways involved in disease process and as a unique attendant in inflammatory response, it has been put in the spotlight of the most mechanistic studies regarding the association of pesticide’s exposure with chronic disorders. Oxidative stress has been implicated in the onset and progression of pesticide induced Parkinson disease (Singh et al., 2007). In this regard, organochlorine pesticides have been reported to cause degeneration of dopaminergic neurons by an oxidative dependent pathway in Parkinson model (Kanthasamy et al., 2002 and Sharma et al., 2010).

The analytical procedure for the simultaneous determination of PB

The analytical procedure for the simultaneous determination of PBDEs and PCBs consisted basically of four steps: saponification, extraction and clean-up followed by chromatographic analysis. The methodology was based on an UltraTurrax (model T18 basic, IKA LTDA, Brazil) extraction described elsewhere (De Boer et al., 2001) with slight modifications. 1 g (dry wt) of homogenized sample was weighed and 10 μL of 3.5 ng μL−1 solution Pexidartinib solubility dmso of PCB 209 was added as surrogate standard to evaluate inherent loss along the analytical procedure. Saponification of the fat present in the biological tissues was performed by

adding 20 mL of 1 mol L−1 of KOH solution and allowing to rest for 30 min. The mixture was homogenized using Ultra

Turrax at 14000 rpm for 1 min. The solvent employed was a mixture of hexane/acetone 1:1. Then, 20 mL acetone was added and the mixture was again run in Ultra Turrax in the same initial conditions. Followed the addition of 20 mL hexane, the Ultra Turrax was run again for 1 min and this was repeated once more (at 22000 rpm for 1 min) after adding 20 mL Milli-Q water. After decantation, the organic layer was removed and transferred via a capillary pipette filled with 1 cm sodium sulphate to a beaker. The solvent was evaporated to dryness under a controlled water bath (40 °C) and under a gentle stream of high-purity nitrogen. SRT1720 molecular weight The extract was dissolved in 1 mL of hexane/acetone 1:1 for clean-up. The clean-up step was performed by an alumina column chromatography followed by a final treatment with sulphuric acid. The glass chromatography columns (internal diameter (id): 1.5 cm) were dry packed with 6 g of 5% deactivated alumina (Merck, 70–230 mesh,

activated at 450 °C for 6 h and allowed to rest for 24 h before use) and topped with a 1 cm layer of anhydrous sodium sulphate. The sample aliquot was placed on top of the column and eluted with n-hexane, and two fractions of 4 mL were collected. As tested previously, PAK6 only the second fraction contained the target analytes, which was evaporated until 1 mL followed by sulphuric acid treatment. 2 mL of sulphuric acid was added to the 1 mL n-hexane extract and this mixture was homogenised for 30 s using a vortex. The resulting emulsion was centrifuged for 1–2 h until the separation of phases. The organic phase was transferred via a capillary pipette and washed twice with Milli-Q water (extracted 5 times with 20 mL of n-hexane to each 1 L of water). After clean-up, the final extract (in hexane) was evaporated in the same conditions as described previously. At the end of the procedure, 10 μL of 3.5 ng μL−1 of PCB-53 solution were added as internal standard for gas chromatographic analysis to a final volume of 100 μL isooctane.

The images

The images Dinaciclib clinical trial are reconstructed on a 128 × 128 pixel grid corresponding to a resolution of 0.2 mm × 0.2 mm × 1 mm with

a 25 mm FOV. The sequence is run with a two-step phase cycle to eliminate the DC offset and the total acquisition time for the image was 2 min. The second UTE sequence is run using the same parameters, however, only one average with 32 spokes of data is acquired and a 10° tip angle is used to further reduce the acquisition time. The total acquisition time for this sequence was 500 ms. Slice selection was validated using a uniform sample of doped water and the pulse sequence shown in Fig. 3. The slice select gradient was set to 5.1 G cm−1 and the acquisition gradient was set to 11.7 G cm−1. The homospoil pulses were set to 22.0 G cm−1 and had a duration of 1 ms with a 5 ms delay before and after the 180° hard pulse. The SW was set to 106 and 512 complex points were collected. As a comparison for the UTE image, a spin echo image was run for each sample. The spin echo used a TE of CDK inhibitor drugs 3 ms with a resolution of 0.2 mm × 0.2 mm × 1 mm. A 512 μs Gaussian pulse was used for slice selection and the SW was set to 105. The total acquisition time for the image was 4 min. In the following, UTE is first simulated using the Bloch equations to demonstrate

the concept and illustrate the artifacts that commonly arise during slice selection. The gradient optimization and slice selection are then explored. The accuracy of UTE image reconstruction is demonstrated using a challenging sample with a complex three dimensional structure. The benefits of UTE are then shown by imaging two samples, one of cork and one of rubber. Finally, the potential for dynamic imaging is explored using CS. Fig. 4 shows a simulation of the Bloch equations for a typical Gaussian slice selection. A Gaussian r.f. excitation pulse is used with a gradient on for the duration of the r.f. pulse. The gradient is then applied in a negative direction for half of the time of the r.f. pulse with the same magnitude as during the r.f. pulse. The negative gradient acts to rephase the spins that have been dephased during

the second half of the r.f. pulse. The slice selected by this sequence is a Gaussian shape as expected. The slice selection for UTE attempts unless to emulate the shape of the slice selected using this traditional method of slice selection, but using a half Gaussian pulse to reduce TE. Fig. 5 shows the equivalent slice selection performed using UTE. UTE uses a half Gaussian pulse for soft pulse excitation, which eliminates the need for a negative refocusing gradient. However, the half-Gaussian pulse results in the formation of a complex dispersion mode excitation profile. To select a Gaussian slice, the acquisition must be run twice, once with a positive slice select gradient and once with a negative slice select gradient. The imaginary slice profile for these two acquisitions will be in anti-phase, as shown in Fig.

Hence, in the last few decades, considerable attention has been d

Hence, in the last few decades, considerable attention has been drawn to functional teratology, an extension beyond the investigation of morphological examinations to include the evaluations of

functional integrity of organ systems. In this work we have proposed an evaluation of the functional integrity in organs system of mothers and their offspring by redox evaluation of several enzymatic and non-enzymatic parameters. The redox profile is important because ROS are generated in cells by several pathways and there has been much speculation regarding the role of free radicals during development (Allen and Balin, 1989 and Hitchler and Domann, 2007). According to the free radical theory of development, it is the influence of the balance between the production and removal BYL719 mw of ROS/RNS (Hitchler and Domann, 2007). We show in the present work, for the first time, vitamin A supplementation at 2500, 12,500 and 25,000 IU/kg/day during pregnancy and nursing to rats inducing a prooxidant state in maternal and offspring hippocampus and striatum. In addition, SGI-1776 behavioral alterations were also observed in the homing and open field tests.

These doses were used in order to evaluate the effects of equivalent doses to those stated as safe for humans during pregnancy and breastfeeding upon dams and their offspring. Additionally, the doses investigated Clomifene in this work are all lower than 163,000 IU/kg/day, the lowest observed adverse effect level (LOAEL) of retinyl palmitate in rats, established in segment II developmental toxicity testing (Ritchie et al., 1998). The brain

is sensitive to oxidative stress due to its high content of peroxidizable fatty acids and relative decreased antioxidant defenses (Halliwell and Gutteridge, 1999). Clearly, in maternal striatum and hippocampus, lipid peroxidation occurred when dams received retinyl palmitate supplementation. In addition, protein carbonylation also increased in these maternal tissues and was present at lower doses then lipid peroxidation, as did decreased protein thiol content in the hippocampus. These molecular changes could indicate an increased vulnerability of nigral proteins to the oxidative insult induced in this experimental model. In offspring striatum and hippocampus, retinyl palmitate supplementation also increased lipid peroxidation and protein carbonylation; however, reduced thiol content was found only in male offspring striatum. Increased lipoperoxidation, protein carbonylation levels, and decreased total thiol content make it easier for intra- and inter-molecular cross-links of proteins, which in turn induce conformational changes leading to increased hydrophobicity and aggregation (Goetz and Gerlach, 2004).

Some systematic reviews have identified capacity of preferences t

Some systematic reviews have identified capacity of preferences to impact on trial outcomes

[7] whereas others have not [8]. Zelen designs have also been developed for situations where seeking consent to be randomized may be problematic [9]. Systematic reviews provide evidence of the use of Zelen and patient preference designs in many areas [8] and [10], which might suggest that the underlying problems associated with disappointment, and their implications, are well understood. There have been valuable studies of public understanding of various aspects of randomization [11] and [12]. Qualitative studies have identified preferences to be potentially complex and dynamic, as well as being amenable to dedicated interventions [13]. How information about Selleck VE 821 randomization is presented in seeking informed consent has received scrutiny [14] TSA HDAC and dedicated interventions have successfully enhanced informed consent and

recruitment to trials [15]. There are also qualitative studies investigating whether and how trial participants react to being randomized [16], though most such studies have been undertaken in clinical contexts where contextual effects may be pronounced, such as neo-natal intensive care units [17]. Cook and Campbell [3] have suggested possible responses to disappointment, ranging from control group participants trying harder by accessing interventions outside trials (termed

“compensatory rivalry”) to participants giving up as a result of disappointment (“resentful demoralization”). Without control of such reactions, trials may be vulnerable to performance bias (1). One leading trialist [18] has gone as far as to suggest that “the next substantive milestone in the history of efforts to create unbiased comparison groups may be erected when someone solves the interesting methodological conundrum presented by biases resulting from patient preferences”. Randomized controlled trials, like other research studies, involve interactions between participants and researchers. Patient preferences may have PD184352 (CI-1040) implications for the actual conduct of these studies, although trial design seeks to preclude this possibility, along with any impact on trial outcomes. This preliminary investigation explores how patient preferences may be associated with performance bias in one trial by examining reasons for participation and participant engagement with the research study. In so doing, it seeks to offer a participant-centered view of what it is like to become involved in a trial, in order to better appreciate the potential for biases that stem from research participation itself, which may not be well understood [19]. Case studies are investigations which pay particular attention to the contexts in which data are produced [20].

A template search was

performed through the PDB database,

A template search was

performed through the PDB database, using the BLAST algorithm (Altschul et al., 1990) for the TsNP sequence, with the structure of lebetin 2 isoform alpha from Macrovipera lebetina (PDB code: 1Q01) selected. The following alignment properties check details with TsNP were found: E-value: 0.0181276; Score: 35.039 bits (79); Identities: 14/19 (74%); Positives: 17/19 (89%); Gaps: 0/19 (0%). The PDB 1Q01 structure was used as the template for the homology modeling. Multiple sequence alignments among the target (TsNP) and reference sequences were performed using the ClustalX program ( Thompson et al., 1997) with its default parameters. Adult male Wistar rats (weighing 260–320 g) click here from the Animal Facility of Universidade Federal do Ceará were used in the renal function experiments. The rats were kept in a housing room with controlled ambient humidity, room temperature maintained at 22 ± 2 °C, laminar air flux and 12 h light/dark

circles. All animal studies were performed according to Brazilian laws for animal experimentation and were approved by the Ethical Committee of Animal Experimentation of Universidade Federal do Ceará under the number 107/07. The rats (n = 6) were fasted for 24 h with free access to water before the experiment. The rats were anesthetized with sodium pentobarbital (50 mg/kg, i.p.). After careful dissection of the right kidney, the right renal artery was cannulated via the mesenteric artery without interruption of blood flow, as described by Bowman (1970) and modified by Fonteles et al. (1983). A modified Krebs-Henseleit Phosphoprotein phosphatase solution (MKHS, composition in mmol/L: 118.0 NaCl, 1.2 KCl, 1.18 KH2PO4, 1.18 MgSO4.7H2O, 2.50 CaCl2 and 25.0 NaHCO3) was used for the perfusion. Bovine serum albumin (BSA) fraction V (6 g) was added to 100 mL of MKHS, and this solution was dialyzed for 48 h at 4 °C against 10 volumes of MKHS. Immediately before the beginning of each perfusion

protocol, 100 mg of urea, 50 mg of inulin and 50 mg of glucose were added to the dialyzed solution (100 mL), and the pH was adjusted to 7.4. In each experiment 100 mL of MKHS were recirculated for 120 min. The perfusion pressure (PP) was measured at the tip of the stainless steel cannula in the renal artery. Samples of urine and perfusate were collected at 10 min intervals for the determination of sodium, chloride and potassium levels using ion-selective electrodes (Electrolyte Analyzer 9180, Roche™). Inulin levels were determined as described by Walser et al. (1955). Osmolality was measured with a vapor pressure osmometer (VAPRO® 5520,Wescor™). TsNP (0.1 μg/mL or 0.03 μg/mL) was added to the system 30 min after the beginning of each perfusion.

2B) above vehicle-treated animals Food intake Food intake was n

2B) above vehicle-treated animals. Food intake. Food intake was not stimulated above vehicle at any time interval examined (0–1, 1–2, 2–4, 4–24 h) by Arc injection of BIIE0246 for all three foraging treatments

(10REV, FW, and BW; Fig. 3A–C). Food PARP inhibitor hoarding. BIIE0246 injection into the Arc did not stimulate food hoarding compared to vehicle injection at any time point examined for each foraging treatment (10REV, FW, and BW; Fig. 4A–C). During the 2–4 h interval after the 5.0 nmol BIIE0246 injection, hoarding in the 10REV group approached significance (P = 0.059) when compared with vehicle injection. Wheel running. PYY(3-36) treatment inhibited the food deprivation-induced increases in wheel running during the 0–1 h interval ( Fig. 5A). The inhibition of wheel running is not indicative of malaise caused by PYY(3-36), because the inhibition also was not seen in the 10REV group (see below). Food foraging. Arc injection of PYY(3-36) did not result in a significant inhibition of food foraging compared to saline injection at any time point measured (0–1, 1–2, 2–4, 4–24 h as well as during the next 6 d; Fig. 5B). Food intake. Arc injection of PYY(3-36) attenuated food intake after food deprivation compared with Arc saline injection at 0–1 and 1–2 h for the 10REV foraging treatment ( Fig. 6C), but not in

the BW or FW group ( Fig. 6A and B); no significant differences were present after the first two hours of refeeding for any group. Food hoarding. In the 10REV group, agonism of the NPY-Y2R in the Arc using PYY(3-36) inhibited food hoarding upon refeeding compared with saline injection at 1–2 h and approached significance at 0–1 h (P = 0.07; Fig. 7C). Significant ADP ribosylation factor differences were not seen at any other time point or foraging treatment ( Fig. 7A and B). Controlling ingestive behavior is a vital aspect of preventing/treating

obesity and accordingly a concerted effort has been made to describe the mechanisms involved in food intake. NPY is the most potent central orexigenic neurochemical in laboratory rats [13], [33] and [43] with marked increases in food hoarding and intake occurring with stimulation of Y1-R and Y5-R, respectively in Siberian hamsters [20]. The NPY-Y2R agonism/antagonism had not been tested for its role in the appetitive ingestive behaviors of food hoarding or foraging [14] in any species before the present study. Here we found for the first time that agonism of the Y2-R by PYY(3-36) inhibited food intake and hoarding early (first few hours) after refeeding following food deprivation and that antagonism of the Y2-R by BIIE0246 did not affect appetitive or consummatory ingestive behaviors in fed hamsters. These results suggest a possible inhibitory role of PYY(3-36) in food hoarding. Antagonism of the Y2-R in the Arc using BIIE0246 causes short term increases in food intake by laboratory rats [1], effects similar to those of NPY Y1-R and Y5-R agonism [e.g., [24] and [45]].

Diese Symptome treten nicht auf bei therapeutischen oder prophyla

Diese Symptome treten nicht auf bei therapeutischen oder prophylaktischen Dosen, da der NOAEL für akute Eisenintoxikation bei 10 bis 20 mg Fe/kg Körpergewicht liegt [127] and [154]. Die möglichen Einflüsse des Eisens auf das kardiovaskuläre Risiko werden höchst kontrovers diskutiert [136] and [155], was zum Teil an der Schwierigkeit liegt, bei den zu Grunde liegenden pathogenen Feedback-Mechanismen zwischen Ursache und Wirkung zu unterscheiden. Selbst eine signifikante Korrelation zwischen Atherosklerose und Serumferritin [156] lässt offen, ob das Ferritin in diesem Fall

gut gefüllte Eisenspeicher repräsentiert oder ob es als Antwort auf die entzündungsauslösende LDK378 cell line Wirkung der Atherosklerose erhöht

wurde. So Sorafenib kann eine Ursache-Wirkungs-Beziehung weder bewiesen noch widerlegt werden. Die Diskussion begann mit der Beobachtung eines 2,2-fach höheren relativen Risikos für akuten Myokardinfarkt (= AMI) in Ostfinnland bei Ferritinkonzentrationen im Serum von mehr als 200 mg/L. Solche Ferritinkonzentrationen werden bei etwa 18% der Männer in den USA und in Europa gefunden [8] and [73]. Follow-up-Studien ergaben widersprüchliche Resultate. In den meisten Folgestudien korrelierte das kardiovaskuläre Risiko mit dem Füllstand der Eisenspeicher, obwohl oft keine Signifikanz erreicht wurde [73], nicht einmal dann, wenn die entsprechenden Daten einer Metaanalyse unterworfen wurden [159]. Die Transferrinsättigung und die Eisenkonzentration im Serum als Maß für die Eisenspeicher reagieren weniger auf Veränderungen der Eisenbeladung als vielmehr auf den Turnover

des erythrozytären Eisenpools; alle diese Faktoren korrelieren kaum mit dem kardiovaskulären Risiko [160]. Dagegen spiegelt die Ferritinkonzentration im Serum die Eisenspeicher direkt wider, wenn sie nicht durch Entzündungsprozesse beeinflusst wird. Deshalb wurden bei den besser kontrollierten Studien die Eisenspeicher anhand des Serumferritins zusammen mit Entzündungsparametern wie CRP, Blutbild (WBC), Blutsenkungsgeschwindigkeit und Leberenzymen bestimmt [160]. Der Serum-Transferrinrezeptor 3-mercaptopyruvate sulfurtransferase (= TfR) wird weniger stark von Entzündungen beeinflusst als das Serumferritin. Dieser Parameter reagiert eher auf Eisenmangel anstatt auf Eisenüberladung und kann deshalb verwendet werden, um nachzuprüfen, ob erhöhte Serumferritinspiegel aufgrund einer Entzündung oder infolge gut gefüllter Eisenspeicher vorliegen [161]. Serumferritin und TfR wurden zusammen mit CRP und der Blutsenkungsgeschwindigkeit in zwei Studien gemessen, bei denen eine signifikante Korrelation zwischen hohen Eisenspeichern und dem kardiovaskulären Risiko gezeigt wurde [160] and [162].

This assumption also yields marginally conservative values of the

This assumption also yields marginally conservative values of the deficit-volume which is a desirable feature in the design of water resources systems towards ameliorating the drought conditions. It is worthy to mention that Millan and Yevjevich (1971) developed the regression equations for predicting E(LT) and E(MT) which were also tested for the annual and monthly hydrological droughts using Canadian

river flows. These relationships were found reasonably JQ1 reliable although at times they tended to under predict in the range of 3–10%. As a note in the context of analysis of monthly droughts, it is prudent to mention that the values of ρ1 in the SHI sequences were low suggesting a weak dependence structure. Therefore, the first order Markov chain model (Markov chain-1, Eq. (8)) was tried to estimate E(LT). It was noted that the predictions of LT tended to be almost the same as predicted by the extreme number theorem. However, at times the predictions by the extreme

number theorem tended to be marginally higher than the Markov chain-1 model and also be nearer to the observed counterparts. This observation vindicates the applicability of the extreme number theorem on monthly as well as annual basis. In fact as the name reads “theorem of extremes of random numbers of random variables” essentially is meant for random sequences, which is evidenced by the results in the present case (annual flows). It has the capability to perform reasonably well in the presence of weak dependence structure and for this reason Alectinib order it performed satisfactorily even in monthly streamflow series. It was also observed that when the degree of the first order dependence is remarkable (i.e. ρ1 being above 0.5) then the extreme number theorem breaks down and recourse to the Markov chain models,

among others becomes a necessity. The weekly SHI sequences of rivers with negligible lake effects such as those in Atlantic Canada tended to follow AR-1 process, therefore the extreme number theorem based relationships (Eqs. (1), (2), (3), (4) and (5)) were attempted to model E(LT). In general, such a model resulted in consistent under prediction. As noted earlier, the weekly SHI sequences Plasmin of rivers riddled with significant lake storages tend to obey AR-2 process or even higher order dependence processes ( Table 2). For such rivers, the extreme number theorem does not hold because of a lack of accountability for the second order dependence. Therefore, a second order Markov chain model (Eq. (7)) was envisaged in which the parameters were computed using the counting method ( Sen, 1990 and Sharma and Panu, 2010). The best estimates of the first order probabilities were obtained using the non-standardized weekly flow series ( Table 2).

The reason for this is that it is practically impossible to make

The reason for this is that it is practically impossible to make direct measurements of the heat production. The most one can do is to take simultaneously defined empirical quantum yields of fluorescence Φfl and of photosynthesis Φph and use them to calculate the yields of the heat production as values complementary to the unity of the sum of the quantum yields of fluorescence and photosynthesis, that is, on the basis of relationships that are rearrangements of equation (1). Etoposide ic50 Unfortunately, I neither possess nor have been unable to find in the available

literature such data containing yield ΦH indirectly determined empirically for different environmental conditions in the sea in quantities sufficient to make statistical generalizations. In this situation, to derive the model of the dependence of the heat production in the sea on environmental selleck chemicals llc factors I have used two models that I developed

independently or in cooperation with others, the successively updated versions of which were published in the reports mentioned below. These are models of two complementary means by which the excitation energies of pigment molecules in the photosynthetic apparatus are dissipated, namely, photosynthesis in the sea and the Sun-Induced Chlorophyll a Fluorescence (SICF) in the sea. These models and the results of the subsequent modelling performed on their basis will now be described. As already mentioned, the model description of the dependence of the heat production in the sea on environmental factors, presented in this work, is a kind of synthesis of two models that I developed earlier

independently or with the cooperation of other scientists. The first is the model of photosynthesis in the sea and, in particular, its quantum yield Φph. It was developed successively, starting in 1992 (Woźniak et al., 1992a, Woźniak et al., 1992b, Woźniak et al., 1995, Woźniak et al., 2002, Woźniak et al., 2003, Woźniak et al., 2007, Dera, 1995 and Ficek et ID-8 al., 2000), and the latest synthetic version can be found in Ostrowska (2012). This model is founded on the results of statistical analyses of primary production measured in situ, and the basic environmental parameters governing this production (temperature, irradiance, chlorophyll concentration) in different trophic types of basins of the World Ocean, though mainly in the Black and Baltic Seas. The other model I am going to use in this work is the model of the quantum yield of the natural fluorescence of chlorophyll a in the sea Φfl, which I have been working on since 2009 ( Ostrowska, 2010 and Ostrowska, 2011); the latest updated version will be found in Ostrowska (2012).