TNF-α can trigger iNOS expression in macrophages and cardiac myocytes. The overproduction of NO by proinflammatory cytokines may depress myocyte contractility [48]. Excessive production of ROS and RNS in myocardial cells leads to the exhaustion of cellular GSH stores and dysregulation of antioxidant enzymes as GSH-Px, thereby leading to the impairment of antioxidant defences (Solaini et al., 2005). These effects were reflected in our results in the form of decreases in the GSH level and GSH-Px activity in cardiac tissues in clozapine–treated animals. Clinical and

experimental investigations suggested that increased oxidative stress associated with an impaired antioxidant defence status initiates a cascade of reactions responsible for clozapine-induced cardiotoxicity [49]. The increase in free radical formation and the attenuation check details of antioxidant defences by clozapine,

can lead to oxidative damage to cellular lipids, proteins and DNA [44]. This can explain the observed increase in both serum and cardiac levels of 8-OHdG the biomarker of DNA damage and the increase in the expression of NF-κB p65, the nuclear factor that contributes in inflammatory response and cell apoptosis. Moreover, the results showed selleck chemicals llc increased expression of caspase-3 in cardiac tissues of clozapine-treated animals. Caspase-3 is an important marker of apoptosis, and this finding indicates that the clozapine-induced cardiotoxicity can lead to apoptosis of cardiac cells. This can be attributed to the observed increase

in oxidative stress with attenuation of antioxidant defences and the consequent cellular and DNA damage. Over the long term, these changes can lead to the development of myocarditis and cell apoptosis in cardiac muscle and to profound cardiac injury and cardiomyopathy [14]. In conclusion, clozapine-induced cardiotoxicity is a serious and potentially lethal complication during the course of clozapine therapy for schizophrenia. Increased myocardial 4��8C oxidative stress, inflammatory cytokines, cellular and DNA damage and apoptosis with attenuation in antioxidant defences are all contributing factors. This necessitates a high degree of clinical care through the course of clozapine therapy. The use of echocardiographic monitoring as a routine periodical check during the course of clozapine therapy, and biohumoral investigation if any signs of cardiotoxicity starts to appear is recommended. Interruption of the clozapine treatment or combination with other drugs that can modulate the above-mentioned pathogenesis in susceptible patients requires further studies. [50] This work was financially supported by Najran University Program for Health and Medical Research Grants, Grant No. (NU 3/10). This study was carried out in the College of Medicine, Najran University, Najran, Saudi Arabia. “
“Antiepileptic drugs, which are also referred to as anticonvulsants, are used in the treatment and prophylaxis of epileptic seizures.

, 1998). This effect co-exists with highly irregular firing on a single-cell level. Our findings allow for making testable predictions and can

be linked to cortical substrates of memory ABT-199 clinical trial function. We examined oscillatory and spiking phenomena emerging during simulated memory retrieval in two different paradigms using a layer 2/3 attractor network. The network had a hypercolumnar structure (Fig. 1) spanning some 1.5×1.5 mm2 of a subsampled cortical sheet and comprising ~15,000 Hodgkin–Huxley-type multi-compartmental neurons and ~2,000,000 synapses. The model was constituted by 9 hypercolumns each containing 49 minicolumns. Pyramidal cells within the same functional minicolumn had dense recurrent connections and common inputs from layer 4 (Yoshimura et al., 2005). Each hypercolumn was defined by the minicolumns

sharing non-specific feedback inhibition (Yoshimura et al., 2005) from the same basket cell pool, and thus extending ~500 μm (Yuan et al., 2011). The model operated Akt targets in a bistable regime (Amit and Brunel, 1997, Djurfeldt et al., 2008 and Lundqvist et al., 2010) with two distinct network states. During a so-called non-coding ground state all pyramidal cells exhibited low-level irregular activity (~0.2 s−1, Cv2=0.97±0.20), whereas in the coding attractor state each hypercolumn acted as a winner-take-all module with cells in only one minicolumn active at an elevated rate (~3–10 s−1, Cv2=0.98±0.25). There were 49 distinct, globally distributed patterns of network activity, or cell assemblies, acting as attractor memories. Although these patterns ( Fig. 1) were set up manually (see Experimental procedures), they could be assumed to have been formed by prior learning. They consisted of subsets of minicolumns, one from every hypercolumn, connected by structured horizontal

long-range axons ( Muir et al., 2010). The cell assemblies had finite life-time Glutathione peroxidase due to the mechanism of cellular adaptation (see Experimental procedures), which forced them to terminate after ~300 ms and caused the network to return to the ground state, i.e. its default operational mode. In this work we considered two alternative approaches to disrupting this default state dynamics and forcing the network’s transition to the coding attractor state. They relate to two separate memory phenomena but result in similar retrieval dynamics once a cell assembly activation is initiated. The first approach, functionally corresponding to pattern completion from a fragmentary input, consisted in partial stimulation of one of the stored memory patterns (stimulation of 5 out of 9 minicolumns participating in a unique distributed pattern, see Experimental procedures) leading to a short-lasting activation of the cell assembly (Fig. 2A). In every 20-s simulation, 20 different patterns were stimulated (partially cued) at a rate of 1 s−1.

Niemowlę 4,5-miesięczne, płci żeńskiej, z obciążonym wywiadem rodzinnym alergią u obojga rodziców i brata, urodzone z ciąży II, obciążonej cukrzycą ciężarnych, porodu II, o czasie, cięciem cesarskim z powodu dyskopatii matki,

z masą ciała 3480 g, ocenione na 10 punktów w skali Apgar, było karmione naturalnie przez 1. miesiąc życia, następnie hydrolizatem kazeiny z powodu oddawania przez dziecko wodnistych stolców. Dotychczas było raz hospitalizowane w 5. tygodniu życia z powodu niedokrwistości i ostrego nieżytu żołądkowo-jelitowego. W tym czasie dziecko otrzymywało cefuroksym dożylnie, w trakcie antybiotykoterapii nie stosowano probiotyków. Niemowlę zostało przyjęte do kliniki z powodu przewlekłej biegunki. Z wywiadu wynikało, że dziewczynka od około miesiąca oddawała liczne wodniste stolce, około 7 na dobę, z obfitym śluzem, z nasileniem dolegliwości od kilku find more dni. Ponadto występowały u niemowlęcia ulewania oraz wzdęcia, którym towarzyszył niepokój sugerujący ból brzucha. Przy przyjęciu stan ogólny dziecka był średni, w badaniu przedmiotowym z nieprawidłowości stwierdzono cechy miernego odwodnienia, ciemieniuchę, odparzenia skóry okolicy krocza. W badaniach laboratoryjnych

z odchyleń od normy wykazano leukocytozę (WBC 19,77 tys./μl, CRP 1,45 mg/l). Wykluczono badaniami kału zakażenie adenowirusem CB-839 supplier i rotawirusem jako przyczynę biegunki oraz nie stwierdzono obecności nearly Salmonella spp., Shigella spp., Yersinia spp. i Enterococcus. Z uwagi na obraz kliniczny, obecność obfitego śluzu w kale oraz dane z wywiadu dotyczące wcześniejszej antybiotykoterapii podjęto diagnostykę w kierunku zakażenia Clostridium difficile i wykazano obecność toksyny A i B tej bakterii w kale. Do leczenia włączono doustny preparat wankomycyny, dzięki czemu uzyskano szybką poprawę kliniczną z normalizacją stolców. Po 7 dobach antybiotykoterapii dziecko w stanie ogólnym dobrym wypisano do domu z zaleceniem stosowania probiotyku (Lactobacillus rhamnosus GG). Po 10 dniach od wcześniejszej hospitalizacji i zakończeniu antybiotykoterapii dziecko ponownie zostało hospitalizowane z powodu nawrotu luźnych

stolców z domieszką śluzu. W wykonanym ambulatoryjnie badaniu kału wykazano obecność toksyny A i B Clostridium difficile. W badaniach laboratoryjnych stwierdzono leukocytozę (WBC 13,81 tys./μl, CRP < 0,20 mg/l). Przy nawrocie choroby zastosowano ponownie wankomycynę doustnie przez 10 dób, następnie kontynuowano leczenie metronidazolem doustnym w warunkach ambulatoryjnych przez 7 dni, nie obserwowano nawrotu biegunki. Dziewczynka 2-letnia, urodzona z ciąży II, powikłanej cukrzycą ciężarnych leczoną insuliną, porodu II, o czasie, siłami natury, z masą ciała 3820 g, oceniona na 8 punktów w skali Apgar, karmiona była mlekiem modyfikowanym od urodzenia, następnie od 8. miesiąca życia hydrolizatem serwatki z powodu alergii na białka mleka krowiego.

In another application of this line, BRAF expression was associated with a distinct gene signature that resembled expression profiles of embryonic neural crest stem/progenitor cells, thereby motivating White

et al. [ 30••] to screen for suppressors of this embryonic phenotype. A class of compounds, called inhibitors of dihydroorotate dehydrogenase (DHODH), was found to selectively abrogate neural crest development in zebrafish as well as melanoma growth in mouse xenografts and human cell lines. Currently being followed in Phase I/II clinical trials, the DHODH inhibitor leflunomide is a pivotal demonstration of how an embryonic phenotype can be translated to findings about Trametinib in vitro the human disease and lead molecules from zebrafish research into clinical investigation. Detailed live imaging of melanocytes in a temperature sensitive mitfa (mitfavc7) mutant has provided novel insights into the direct consequences of mitfa activity on tumorigenesis. Reduced mitfa activity caused a dramatic increase in melanocyte ERK high throughput screening cell division [ 31] and was found to directly affect tumor morphology and formation in the BRAF model [ 32•]. As these findings could be reversed with the restoration of mitfa’s

activity, this work substantiates the notion that mitfa is a modifier of BRAF-driven melanoma and provides a functional link between low MITF expression in patients with their poor melanoma prognosis. Recent studies using a KRASG12D-driven model of embryonal rhabdomyosarcoma (ERMS) [ 11] have highlighted the importance of the cell of origin as a determinant of ERMS. For example, Ignatius et al. [ 33] used dynamic cellular imaging of a mosaic transgenic rag2-KRASG12D model to track the movement and evolution of ERMS cell subpopulations in embryonic and adult zebrafish. Their findings revealed new roles for differentiated ERMS cells in tumor growth and suggest that mechanisms governing their homeostatic maintenance in regulating growth could be relevant considerations

in developing Avelestat (AZD9668) potential therapeutic treatment. In a similar approach, using promoters representing various stages of muscle development (cdh15, rag2, mylz2), Storer et al. [ 34] drove expression of KRASG12D and observed that tumors that originated from the more progenitor like cells were more invasive and undifferentiated. These tumors were found to closely recapitulate subgroups of human ERMS based on differentiation status and harbor unique signaling pathways in each subgroup. Confirmation of these pathways as therapeutic targets awaits further study but demonstrates how cross-species oncogenomics can be used to guide therapeutic targeting strategies. Important insights have also been described in other zebrafish models that cannot be described here [35, 36, 37, 38 and 39] (reviewed in [40••, 41••, 42 and 43]). It is apparent though that some tumor types are better modeled in zebrafish than others.

The lack of stringent criteria to select differential proteins together with the absence of further result validation, an almost impossible task given the usually large differential protein datasets, may lead

to the identification of false positives and false negative candidates. Consequently, only a small percentage of proteins were found similarly differential across the few proteomic studies analyzing SN for instance, although a high proportion of non-differential proteins were concordant between them. The fact that differential proteins are sometimes found inversely expressed across studies may indicate the presence of different protein isoforms that may still participate in the same pathogenic mechanism. Indeed, PD is known to be SGI-1776 mouse a heterogeneous disease and distinct alterations in common pathways may induce a common phenotype. For example, different point mutations and multiplications

of α-SYN all result in familial PD. Similarly to what is generally thought for transcriptomic data, the absence of concordance between proteomic studies could be due to the utilization of protein list for comparisons, EPZ015666 rather than standardized pathways, which could indicate the involvement of common pathogenic mechanisms. To conclude, instead of being taken as conflictual, results obtained in proteomics may rather be seen globally, each proteomic study identifying a fraction of the changes occurring L-NAME HCl in the SN and contributing step-by- step to a better knowledge of the extraordinarily complex molecular jigsaw puzzle at the basis of PD. Some work reported in this article has been made possible through the generosity of the Memorial A. de Rothschild Foundation and Swiss Parkinson. “
“Cardiovascular disease (CVD) is the leading cause of mortality in the U.S, and diabetes is an important risk factor [1]. Recent trials examining

the impact of intensive glycemic control on the reduction of CVD endpoints [2], [3] and [4] highlight the challenges for reducing the increased CVD risk, and the need for new biomarkers of diabetic complications. Several studies suggest that the function of HDL is defective in diabetes [5]. Shao et al. demonstrated that the ability of apolipoprotein A-I (ApoA-I) to activate LCAT is impaired by methionine oxidation of residue 148, M148(O) [6]. LCAT esterifies cholesterol on HDL and is an important component for reverse cholesterol transport [7]. Thus, ApoA-I methionine oxidations are potential markers of diabetic complications. Mass spectrometry (MS)-based applications are particularly well-suited to measure post-translational modifications of proteins [8]. Conventional MS-based quantitation workflows using spectral counting or extracted ion chromatograms involve lengthy MS data acquisition and analysis times and are often limited to quantifying differences between small sample sets.

Indeed ultrasound techniques have a high dynamicity, and therefore a good temporal resolution and neuroradiological techniques have a high anatomic definition, and therefore a good spatial resolution. The possibility of combining

the ultrasound examination with a reference modality in real time allows confirming the anatomical assumption of a new approach. Moreover the identification of vessel segments (TS in this case) is faster and more reliable. This system is a Virtual Navigator software, already used in other body districts. Therefore, after the identification and the proposal of an extended ipsilateral insonation for the TS an imaging fusion system was implemented and tested validating it. Forty consecutive subjects (28 men and 12 women, mean drug discovery age 55.63 ± 7.61 years) were chosen among patients who underwent standard TCCS examinations at our lab and had – age >18 years; All subjects have not a disease of the venous system and the reasons why they underwent brain MR were migraine or dizziness or a control examination of a previously known nonspecific lesion pattern in the white matter or previous ischemic stroke in the arterial circulation.

The basal TCCS examination was performed by using a MyLab 60 equipment and both the contralateral and the ipsilateral approach were Ivacaftor purchase used for the insonation of the TS. The Ureohydrolase first 20 subjects underwent a further study with the Virtual Navigator software in order to validate the ipsilateral approach. Fig. 1 shows an example of the contralateral and ipsilateral approach to the TS. It is notable that the proposed insonation plane for the ipsilateral TS, with a more anterior positioning of the probe and an opposite tilting, as compared to the contralateral approach, allows a larger field of view,

and therefore an examination of a greater extent of TS. The increased field of view led us to distinguish three segments of the TS through an ipsilateral approach, as shown in Fig. 2, because of the visualization of the entire course of the TS in the correspondent bone groove. All segments were looked for during the basal TCCS and during the Virtual Navigator examination, and separated insonation rates were calculated. Therefore, the global insonation rate of the TS is composed: – for the contralateral approach by the insonation of the proximal segment; so potentially increasing the rate of success in the TCCS insonation of the TS. Considering both sides, 80 TS were insonated with both contralateral and ipsilateral approach. Insontation rates were compared by using the Fisher exact test.

e., 2 h after treatment, the animals were sedated with diazepam (1 mg i.p.), anesthetized with pentobarbital sodium (20 mg kg body weight−1 i.p.), tracheotomized, and a snugly fitting cannula (0.8 mm id) was introduced into the trachea. The adequate anesthetic level was assessed by the absence of the palpebral, toe pinching, and corneal reflexes before animal paralysis. Thereafter, animals were paralyzed with pancuronium bromide (0.1 mg/kg i.v.) and mechanically KU-60019 mouse ventilated with a constant-flow ventilator (Samay VR15, Universidad de la Republica, Montevideo, Uruguay) with a respiratory frequency of 100 breaths/min, a tidal volume of 0.2 ml,

flow of 1 ml/s, and positive end-expiratory pressure of 2 cm H2O. The anterior chest wall was then surgically removed. Since all measurements took no longer than 30 min and the combination of pentobarbital sodium and diazepam yields a depth and stable anesthetic level for at least 1 h (Fieldi et al., 1993 and Green, 1975), the animals were bound to remain under deep anesthesia throughout the experiment. A pneumotachograph (1.5 mm ID, length = 4.2 cm, distance between side ports = 2.1 cm) (Mortola and Noworaj, 1983) was connected to the tracheal cannula for the measurements of airflow (V′). Lung volume (VT)

was determined by digital integration of the flow signal. Tracheal pressure was measured with a Validyne MP-45 differential pressure transducer (Engineering Corp, Northridge, CA, USA). The flow resistance of the equipment (Req), tracheal cannula included, was constant up this website to flow rates of 26 mL s−1 and amounted to 0.12 cm H2O mL−1 s. Equipment resistive pressure (=Req.V′) was subtracted from pulmonary resistive pressure so that the present results represent intrinsic values. All signals were conditioned and amplified in a Beckman type R Dynograph (Schiller Park, IL, USA). Flow and pressure signals were then passed through 8-pole Bessel low-pass filters (902LPF, Frequency Devices, Haverhill, MA, USA) with the corner frequency set at 100 Hz, sampled at 200 Hz with a 12-bit analog-to-digital converter Florfenicol (DT2801A, Data Translation, Marlboro, MA, USA), and stored on a microcomputer. All data were collected using

LABDAT software (RHT-InfoData Inc., Montreal, QC, Canada). Lung resistive (ΔP1) and viscoelastic/inhomogeneous (ΔP2) pressures, total pressure drop (ΔPtot = ΔP1 + ΔP2), static elastance (Est), and elastic component of viscoelasticity (ΔE) were computed by the end-inflation occlusion method (Bates et al., 1985 and Bates et al., 1988). Briefly, ΔP1 selectively reflects airway resistance in normal animals and humans and ΔP2 reflects stress relaxation, or viscoelastic properties of the lung, together with a tiny contribution of time constant inequalities (Bates et al., 1988 and Saldiva et al., 1992). Lung static (Est) elastance was calculated by dividing Pel by VT. ΔE was calculated as the difference between static and dynamic elastances (Bates et al., 1985 and Bates et al., 1988).

Participants listened passively to stimuli in the Reversed Speech condition. The Dabrafenib clinical trial task was explained verbally by the experimenter before the start of the functional data acquisition

to ensure participants understood it and could overtly produce a small set of target stimuli. A short practice was given to the participants inside the scanner immediately before the start of data acquisition. During this practice they heard five stimuli for the Speech condition followed by five stimuli for the Reversed Speech condition. Participants were instructed not to overtly produce the target word because speaking produced head movements during scanning. They were asked instead to “think of the word inside their heads” and keep as still as possible. The practice stimuli were not used again during the functional data acquisition. If the participants were happy to proceed with the task, functional data were acquired. The Speech and Reversed Speech conditions and a

baseline condition during which learn more no stimuli occurred were presented in 30-s blocks and repeated four times each in a fixed pseudorandom order so that no condition was presented consecutively. Each 30-s block of the Speech and Reversed Speech conditions comprised six stimuli presented one every 5 s. The T1-weighted structural brain images were analysed with an ‘optimised’ ADAMTS5 voxel-based morphometry (VBM)-style protocol (Good et al., 2001) within FMRIB’s Software Library (FSL v4.1, www.fmrib.ox.ac.uk/fsl). The skull was stripped from this image using the Brain Extraction Tool (Smith, 2002) and the brain images were segmented to form images representing partial volume estimates of each tissue class (i.e. how much of the signal in each voxel was grey or white matter or cerebrospinal fluid) (Zhang, Brady, & Smith, 2001). The total volume of grey matter was calculated from these images (by multiplying

the average voxel value by the total number of voxels). These images were also used in the functional analyses below as voxel-dependent covariates. For the VBM-style analyses of structure, the 32 images of grey matter were non-linearly registered to the MNI-152 grey matter template using FMRIB’s Nonlinear Registration Tool (FNIRT) (Andersson et al., 2007a and Andersson et al., 2007b). Each image was flipped across the midline to create a mirror image and the 64 images were averaged to create a left–right symmetric study-specific grey matter template. The 32 original images of grey matter were then non-linearly transformed to this new template.

Collectively, these findings indicate that additional benefits of vedolizumab treatment may accrue between weeks 6 and 10, regardless of previous TNF antagonist response, and could be associated with effects of an additional vedolizumab dose at week 6 or with the incremental effect of time on the drug’s ability to exert a therapeutic benefit. Similar findings have been observed with natalizumab induction check details therapy, 6 which suggests that a gradual onset

of efficacy may be an attribute of drugs that modulate lymphocyte trafficking. This observation may help with the optimization of vedolizumab induction therapy in real-world settings. The lack of statistical significance of primary outcome results contrasts with the GEMINI 2 induction study results in patients with previous TNF antagonist failure.24 However, several patient characteristics and design parameters differed between these 2 studies (eg, differences in upper CDAI score cut-off values, defined by entry criteria,

and in mean CDAI scores, and re-randomization selleck chemicals llc at week 6 in GEMINI 2). In a prespecified subgroup analysis of patients from GEMINI 2 with previous TNF antagonist failure, the proportion of patients with week 6 clinical remission was similar between vedolizumab-treated (10.5%) and placebo-treated groups (4.3%; treatment difference, 6.2%; 95% CI, -9.1% to 21.3%). In a prespecified subgroup analysis of TNF antagonist–naive patients from GEMINI 2, the week 6 remission rate was higher with vedolizumab (17.4%) than with placebo (9.2%; treatment difference, 8.2%; 95% CI, -1.4% to 17.9%). The week 6 treatment difference in patients with previous TNF antagonist failure was similar in GEMINI 3 (3.0%) and GEMINI 2 (6.2%), whereas the week 6 treatment difference in TNF antagonist–naive patients was larger in GEMINI 3 (19.2%) than in GEMINI 2 (8.2%). Observed differences in week 6 remission rates between overall populations of the

2 studies may be attributable to variations between 2 otherwise similar patient populations, including proportions of patients with previous exposure to 1, 2, or 3 TNF antagonists (GEMINI 2, 47.6%; GEMINI 3, 75.7%). The upper bound of patients’ CDAI scores (GEMINI 2, 450; GEMINI 3, 400) or random variation could have accounted for the observed differences in subgroup 5-Fluoracil datasheet analyses of week 6 remission rates among TNF antagonist–naive patients. Effects of vedolizumab induction therapy were modest overall, and maintenance effects were not evaluated in this short-term study; however, the modest efficacy of vedolizumab induction therapy in GEMINI 2 was contrasted by the pronounced benefit of vedolizumab maintenance therapy over the course of 52 weeks. Among vedolizumab induction responders in GEMINI 2, week 52 clinical remission occurred in 39.0% (P < .001) and 36.4% (P = .004) of patients who continued vedolizumab every 8 and 4 weeks, respectively, and in 21.6% of patients who were assigned randomly to switch to placebo during maintenance.

Coefficient bbpis computed by using the MODIS

Cabozantinib standard products of Rrs(531), Rrs(547) and Kd(490) (http://oceancolor.gsfc.nasa.gov); a brief description of the algorithm is given at (http://optics.ocean.ru) and in more detail by Burenkov et al. (2001). The regression equation TSM vs. bbp was derived from our field data of 2012 and 2013; the combined data set included 39 stations (15 in 2012, 24 in 2013). The TSM concentration varied from 1.0 mg 1−1 (St. 19F) to 5.5 mg 1−1 (St. 3L) in 2012 and from 1.7 mg 1−1 (St. 10F and 33F) to 4.4 mg 1−1 (St. 3FG) in 2013. The regression equation was derived in logarithmic form: equation(3) logTSM=0.79logbbp+1.95,where TSM is expressed in mg 1−1, bbp in m−1.

Figure 8 shows the regression line TSM vs. bbp on a logarithmic scale; Figure 9 is a scatterplot showing TSMcalc vs. TSMmeas. As seen from the figure, the agreement is rather good: the coefficient of determination r2 = 0.61, the standard error of the regression is equal to 0.62 mg 1−1; the averages of TSMcalc and TSMmeas are close to each other at 2.56 and 2.62 mg 1−1 respectively; the averaged ratio of TSMcalc/TSMmeas is equal to 1.03, and the ratio range is 0.72-1.5. Figure 10 shows the spatial distributions of TSM concentration calculated from MODIS-Aqua data selleck on 22 July 2012 and 27 July 2013 using (3). One can see a general similarity of these distributions with the distributions of chlorophyll concentration in Figure 7. Such a similarity is to be expected, because MTMR9 there is a common factor determining the distribution of both TSM and chlorophyll: the River

Neva carries suspended particles and phytoplankton with chlorophyll and nutrients for primary bioproduction. We evaluated the applicability of the regional Baltic algorithms by Darecki & Stramski (2004) and Woźniak et al. (2008) for determining chlorophyll concentrations in the Gulf of Finland by using our data set of 2012–2013. The input parameter of the second of them (the DESAMBEM algorithm – Development of a Satellite Method for Baltic Ecosystem Monitoring) is the ratio XR = [Rrs(490) —Rrs(665)]/[Rrs(550) —Rrs(665)], which is completely unsuitable for the Gulf of Finland because of the abnormally high values of Rrs(665). The regional parameterisation of MODIS algorithms for chlorophyll retrieval in the Baltic was presented by Darecki & Stramski (2004) in two versions: #9 Baltic_chlor_MODIS: Chl = 100.4692–20.6802X, where X = log[Lwn(443) + Lwn(488)/Lwn(551)], The values of Lwn are related to Rrs by a simple formula: Lwn(λ) = F0(λ) Rrs(λ), where F0(λ) is the mean extra-terrestrial solar irradiance (http://oceancolor.gsfc.nasa.gov). The results of the evaluation of these algorithms are presented in Table 2 and can be compared with the results for algorithms #4 and #8 from Table 1.