These kinds of data will help us better understand who will most benefit from behavioral or pharmacological interventions to reduce adrenergic signaling or stress response states – for example, what levels of stress/distress are necessary at the outset for an intervention

to make a difference. Moreover, the use of discrete interventions is useful for mechanistic research purposes, but it is possible that multifaceted total lifestyle interventions that address stress factors, as well as nutritional and exercise lifestyle components, will be necessary to profoundly impact cancer growth. To date, research on multimodal selleck chemicals interventions remains quite limited. Additionally, the effects of biobehavioral pathways on recovery Bcl-2 cleavage from specific cancer treatments such as HSCT, adoptive immunotherapy, surgical recovery, are important frontiers for future work. Understanding tumor and treatment effects on the central nervous system are equally important.

As reported by some of the papers in this volume, we are just beginning to understand the relevant biology in post-chemotherapy fatigue and cognitive difficulties – this type of mechanistic understanding is critical before new treatments can be developed and tested. Future directions also include determination of what

are the most important intermediate outcome variables for biobehavioral cancer research. In addition to overall survival and progression-free survival, to what extent are gene signatures, metabolomics, and epigenetic changes important outcomes for this work? The research in this volume points to the dramatic discoveries that have been made in the last decade to define this field. Future research holds promise for discovery of novel biobehavioral signaling pathways that are relevant to cancer and a greater understanding of behavioral, pharmacologic, Cytidine deaminase and complementary interventions that target these mechanisms. In conclusion, we would be remiss if we did not thank lead authors and their authorship teams for contributing scientific advances relevant to this volume. These individuals and many others have worked quite tirelessly to improve methodological rigor, establish causation as appropriate, collaborate in the spirit of transdisciplinary team science, and move between different research designs to test and confirm experimental and clinical findings. We thank the many scholars who engaged in the peer review process to vet the invited mini-reviews and empirical papers that comprise this supplement.

, 2010 and Amunts et al., 1999). Areas 45a and 45p (Amunts et al., 2010) were included as the complete region has been reported to be activated during processing of semantic aspects at both the word (Fiez, 1997, Heim et al., 2009 and Thompson-Schill

et al., 1997) and the sentence level (Newman et al., 2010). Area 47 can be localized cytoarchitectonically (Brodmann, 1909) and by its position ventral to 45a and 45p, from which it is separated by the horizontal branch of the lateral fissure (Fig. 1A). Functional studies have demonstrated its involvement in language comprehension (Dronkers et al., Belnacasan in vivo 2004 and Turken and Dronkers, 2011). The temporal area Te2 was defined cyto- and receptor architectonically (Morosan, Schleicher, Amunts, & Zilles, 2005), and its function in speech stimuli and language processing was reported (Amunts et al., 2010, Kubanek et al., 2013 and Morosan et al., 2005). Eighteen cyto- and/or receptor architectonically localizable cortical areas, which are not associated with sentence comprehension, were included in order to compare the multireceptor expression of language-related versus that of non-language related areas (Fig. 1A and B): primary auditory cortex this website Te1 (Morosan et al., 2005), hand (4d) and mouth (4v) representation regions within the primary motor area 4 (Geyer

et al., 1996), primary visual area V1 (Amunts et al., 2000 and Eickhoff et al., 2007), extrastriate higher visual areas FG1 and FG2 on the fusiform gyrus (Caspers et al., 2013b and Caspers et al., 2013c), primary somatosensory area 3b (Geyer, Schleicher, & Zilles, 1997), prefrontal areas 9 and 46 (Brodmann, 1909), area 7 of the superior parietal lobule (Scheperjans, Palomero-Gallagher, Grefkes, Schleicher, & Zilles, 2005), areas PF, PFcm, PFm, PFop,

PFt, PGa, and PGp of the IPL(Caspers, Schleicher, et al., 2013), and cingulate area 32 (Palomero-Gallagher Baricitinib et al., 2009). These areas are mainly involved in motor control, visual and somatosensory perception, higher visual functions, and various cognitive or emotion-related functions (Caspers et al., 2013b, Caspers et al., 2013c, Caspers et al., 2010, Corbetta et al., 2008, Eickhoff et al., 2007, George et al., 1995, Jakobs et al., 2009, Keysers and Gazzola, 2009, Kross et al., 2009 and Smith et al., 2011). The regional distribution of 15 different neurotransmitter receptor binding sites (AMPA, kainate, NMDA, GABAA, GABAB, benzodiazepine binding sites of the GABAA receptor (BZ), M1, M2, M3, nicotinic α4/β2, α1, α2, 5-HT1A, 5-HT2, D1) for glutamate, γ-amino butyric acid (GABA), acetylcholine, noradrenaline, serotonin and dopamine were visualized, and their concentrations [fmol/mg protein] were measured in 26 brain regions of four left and four right human hemispheres by means of quantitative in vitro receptor autoradiography ( Zilles, Schleicher, Palomero-Gallagher, Amunts, 2002).

Purified hsAtg7 (1 µM), hsAtg3 (2 µM), and LC3 (5 µM) were incubated at 37 °C with liposomes (350 µM) composed of 55 mol% PE, 35 mol% POPC, 10 mol% yeast PI or 10 mol% PE, 80 mol% POPC, 10 mol% yeast PI in the presence of 1 mM ATP for the indicated

time periods, followed by SDS-PAGE and CBB-staining. Peritoneal cells from naïve mice were analyzed using transmission EM. Representative macrophages from three separate pooled isolates is shown in Fig. 1A. Healthy-looking mitochondria (small, compact, and with well-defined cristae) are seen in wild type drug discovery cells. In contrast, 12/15-LOX−/− macrophages are swollen and granular. 12/15-LOX−/− macrophages also demonstrate a large number of vacuoles (yellow arrows) and potential lysosomal storage bodies, visible as dark inclusions (red arrows). Some have double membranes, suggestive of autophagosomes (blue arrows). Far lower numbers of vacuoles and suspected lysosomal storage bodies are seen in wild type macrophages. Macrophages from both WT and 12/15-LOX−/− mice show low levels of LC3-I and II by western blot. To inhibit the turnover of autophagosomes, cells were incubated with chloroquine, which raises the lysosomal pH, and leads to inhibition of both fusion of autophagosome with lysosome and lysosomal protein degradation. As a result, we see an accumulation of LC3-II which is the membrane associated lipidated form. Macrophages

from 12/15-LOX−/− mice contained similar amounts of LC3-I and LC3-II to wild type controls,

although there was a high degree of variability between Selleckchem Sirolimus mice (Fig. 1B). To examine whether Atg8 is conjugated to HETE-PE or SAPE, in vitro conjugation reactions using liposomes composed of mixed PE/PC and yeast PI, where the PE consisted of DOPE, SAPE or 15-HETE-PE, were undertaken. DOPE is shown for comparison, as this is the usual lipid used for Atg8 conjugation reactions, rather than SAPE [18]. As shown in Fig. 2A, Atg8 was conjugated to HETE-PE more efficiently than SAPE. In addition, the mobility of Atg8-HETE-PE/SAPE and Atg8-DOPE was different, specifically the mobility of Atg8-HETE-PE/SAPE Bacterial neuraminidase was slightly lower than that of Atg8-DOPE. This is likely due to the longer fatty acid chain length at the sn2 position of SAPE/HETE-PE. A comparison of SAPE-PE versus HETE-PE was conducted three times, and densitometry scanning averaged, clearly showing HETE-PE as a preferred substrate at all time points tested versus SAPE ( Fig. 2A, right panel). This indicates that oxidized phospholipids can be conjugated to Atg8, and that introduction of the -OH at C15 leads to a more effective substrate. Next, the ability of HETE-PE to act as a substrate for the mammalian LC3 was tested using recombinant proteins. In these experiments, it was initially seen that 55 mol% SAPE and HETE-PE were similarly conjugated over 30 minutes (Fig. 2B, left panel).

The authors

suggest early life stress as a plausible risk factor for inflammation that undergirds cancer-related fatigue. The empirical paper by Witek-Jansek et al. in this volume explores whether childhood adversity is associated with vulnerability for intense sustained behavioral symptoms, including fatigue and depressive symptoms, and quality of life and immune dysregulation (Witek Janusek et al., 2012). Irwin and colleagues describe the common presentation of sleep disturbance and depression in cancer survivors (Irwin et al., 2012). The authors outline a model in which sleep disturbance drives alterations in inflammatory biology, which result in of depressive symptoms and in clinical depression for some. The model acknowledges depression history and other psychosocial, biobehavioral, and medical factors that might act as moderators. The Lutgendorf selleckchem laboratory contributes an analysis of associations between cortisol, interleukin-6, http://www.selleckchem.com/products/dabrafenib-gsk2118436.html depression, fatigue, and disability in ovarian cancer patients followed prospectively from pre-surgical baseline to one-year post surgery, and illustrates how chemotherapy acts to normalize these biological markers (Schrepf et al., 2012). Although challenges exist, the review by Costanzo et al. identifies opportunities to explore clinically significant PNI relationships

in a hematopoietic stem cell transplantation context (HSCT) (Costanzo et al., 2012). Improved understanding of the factors that moderate timely immune recovery and optimal immune

regulation might confer improved short- and long-term Fossariinae outcomes for HSCT recipients. Noted as challenges for PNI researchers working in a HSCT context are the pace of change and evolution in HSCT medicine and associated technical innovations. The secondary data analysis by McGregor et al. investigating the effect of pre-transplantation distress on white blood cell count among autologous hematopoietic cell transplantation patients, highlights these challenges (McGregor et al., 2012). Within the last decade, exercise has been established as an effective adjuvant therapy to control adverse consequences associated with cancer treatment. Jones et al. comprehensively reviews extant evidence linking exercise behavior, functional capacity/exercise capacity, disease recurrence, and cancer-specific and all-cause mortality (Betof et al., 2012). Further, the authors outline host and tumor-related mechanisms underlying the exercise/fitness and prognosis relationship and review evidence from pre-clinical animal models of cancer. This exciting work highlights exercise as one critical component of energy balance influences on cancer etiology, progression, and outcome (Hursting et al., 2012).

Of the 95 patients

HSP inhibitor identified as IHC 2+, 61 were classified as HER2-non-amplified and 34 were HER2-amplified according to the 2007 guideline. Of 63 IHC 3+ patients, 56 were HER2-amplified, and seven were HER2-negative by FISH. In the IHC 2+ cases, FISH determined that a much larger proportion was HER2-negative than HER2-positive (64.8% vs. 35.2%). We obtained different results when we reevaluated HER2 status using the 2013 ASCO/CAP scoring criteria. As shown in Table 1, there were significantly more HER2-positive cases, which were, in order of case increases: IHC 2+ (from 34 to 43 cases, p < 0.05), IHC 3+ (from 56 to 60, p > 0.05), IHC 1+ (increase from 0 to 3, p < 0.05). There was also a significant increase in HER2-equivocal cases, Bioactive Compound Library solubility dmso where IHC 2+ cases increased from 0 to 5, followed by IHC 1+ cases. Correspondingly, there were fewer HER2-non-amplified cases ( Table 1). According to the 2007 ASCO/CAP guideline, HER2-positive status by FISH was defined as HER2/CEP17 ratio > 2.2, but based on the 2013 ASCO/CAP guideline, many HER2-non-amplified cases with polysomy 17 should be redefined, given that previously defined HER2-negative cases may be defined as HER2-amplified according to the 2013 guideline. There was

polysomy 17 in 100 (57.1%) of the 175 patients, of which 48 were defined as HER2-non-amplified based on the 2007 criteria. Using the criterion of ≥6 HER2 signals per nucleus to denote positive amplification, 16 cases (33.3%) were categorized as HER2-amplified. Of these, three, nine, and four were IHC 0/1+, IHC 2+, and IHC 3+, respectively. We observed >4 HER2 copies but <6 HER2 copies per nucleus in another six cases (12.5% of 48 polysomy 17 cases) categorized as HER2-equivocal, where one and five cases were IHC 0/1+ and IHC 2+, respectively. Of the 48 HER2-non-amplified cases, 26 Carbohydrate were persistently HER2-non-amplified despite the CEP17 status ( Table 2). Therefore, these findings demonstrate that there was discrepant interpretation of gene amplification

status in 22 (12.6%) cases when the number of CEP17 copies was taken into account, and illustrates how breast cancer with polysomy 17 can be interpreted as HER2-positive, -equivocal, or -negative partly depending on which scoring method is applied to interpret the HER2 FISH results. Using FISH, we investigated the frequency of polysomy 17 and its association with HER2 alteration in patients with invasive breast cancer. As polysomy 17 is relatively common in breast carcinoma, it is possible that HER2 FISH results can be misinterpreted. In a recently published series, Vanden Bempt et al. reported that >40% of breast carcinomas harbor increased CEP17 copy numbers [32]. In our study, there was polysomy 17 in 57.1% (100/175) of primary invasive breast carcinoma cases.

CO2 emission was always cyclic, sometimes on the verge of continuous respiration ( Fig. 2D). Fig. 3 shows the duration Ribociclib ic50 of cycles, and of open, closed and flutter phases (where present)

as a function of experimental ambient temperature. The course of all components of DGC follows exponential curves. With rising ambient temperature the open phase decreased slower in duration than the flutter and the closed phases at low to medium Ta. Closed phases were only detectable up to Ta ⩽ 26.3 °C. Fig. 4 shows the duration of the respiration cycles and cycle phases in dependence on resting metabolic rate (RMR). However, the courses of data points indicate a higher order of dependence than a simple exponential decrease. Good linear regression in a double logarithmic graph (inset) strengthens this finding. With rising Ta the cycle frequency (f) increased ( Fig. 1, Fig. 2) following an exponential curve ( Fig. 5). Data fitted best with an exponential function of the type f = y0 + A1Ta/t1, with y0 = 0.12716, A1 = 2.18932, t1 = 11.2997 (R2 = 0.51337, P < 0.0001, N = 37). Respiration cycle frequency was 2.55 ± 3.58 mHz at 4.7 °C, 9.33 ± 13.2 mHz at 9.8 °C, 13.0 ± 24.66 mHz at 19.8 °C, 39.92 ± 25.35 mHz at 31.1 °C selleck screening library and 73.97 ± 28.85 mHz at 39.7 °C. Data at 42.4 °C were not included in the fitting curve because single CO2 “peaks”

merged to “plateaus”. Comparison of variances of cycle frequency at the same Ta revealed significant differences between individuals (P < 0.05, N = 2–10, ANOVA). Over the entire temperature range these tests indicated significant differences in 69.5% of comparisons. An ANOVA with the means per animal and Ta (of both species) indicated a slight negative temperature dependence of CO2 release per cycle (P < 0.05; R2 = 0.06685, N = 62, F = 5.36977, DF = 60). The correlation was more pronounced in an analysis with all cycles of all animals, which includes the intra-individual variation ( Fig. 6). CO2 release per cycle as estimated from

the regression line changed from 39.51 μl g−1 cycle−1 at 2.9 °C to 25.4 μl g−1 cycle−1 at 42.4 °C, Single individuals compared at the same temperature showed significant differences these in the variances of mean CO2 emission per cycle and animal (P < 0.05, N = 2–8, ANOVA; see large circles in Fig. 6). Over the entire temperature range these within-Ta comparisons showed inter-individual differences in 56.8% of cases. This implies that the other 43.2% of cases indicated no difference. However, measurements where data of only one individual could be evaluated indicate also considerable intra-individual variance ( Fig. 6, Ta = 22.5 and 42.4 °C). In direct comparison, wasps differed from honeybees significantly in slope and intercept (P < 0.0001 in both cases, ANOVA; see Fig. 6). Cycle frequency (f) increased linearly with the mass specific RMR ( Fig. 7, f (mHz) = −2.54647 + 0.65394 * RMR CO2 (μl g−1 min−1), R2 = 0.976, P < 0.0001, N = 37, means per animal).

He began his study of medicine at the University of Wilno in Eastern Poland (now part of Lithuania) under Soviet occupation where he completed the first trimester, and joined the Polish Army and spent World War II from 1940 to 1945 as a prisoner of war in Germany and France, an experience he speak sparingly of except about when he escaped from his imprisonment in Hamburg, Germany and recaptured in Strasbourg, France. He resumed his medical education at the University of Brussels, Belgium after the GSK J4 in vitro war and graduated with a M.D. degree in 1949. As a student, he listed

seven papers, wherein he is a co-author or author, pertaining to the effects of hormone on vaginal cytology from the Research Laboratory of the Department of Obstetrics and Cytology. He Pirfenidone emigrated to Canada in 1951 where he was

in private practice, served a year residency in medicine at the University Hospital in Saskatoon, and joined its faculty where he obtained a research fellowship in the laboratory of Dr. E.R. Yendt in the Department of Medicine, University of Toronto to study metabolic bone disease, parathyroid, kidney stones and renal hypertension. Dr. Yendt spent time with Dr. John E. Howard at John Hopkins University, a former member of Fuller Albright’s team in Massachusetts General Hospital. George moved to the University of Ottawa in 1963 from Saskatoon where he was involved in the first hospital to introduce maintenance hemodialysis and kidney transplantation in Canada. In late 1960, George decided to spend his sabbatical years working in calcified tissue laboratories. He wrote about his sabbatical in the Medical Research Council of Canada short summary of research accomplishment and personalized biography of their most

talented senior award winner in Canada as follows: “Subsequently the work of two investigators influenced my research. First, that of Dr. Harold Frost, head of Orthopedics at Henry Ford Hospital in Detroit, originator of a method of studying lamellar bone turnover system by means of bones labeled in vivo with tetracycline. Second that of Dr. Webster S.S. Jee, Anatomy professor at the University of Utah in Salt Farnesyltransferase Lake City in whose laboratory I familiar myself with the study of cell kinetics by means of tritiated thymidine”. Originally he was to stay 3 months in Frost’s laboratory but he extended it to 9 months where he came in contact with other “Frostians” which included Pierre Meunier, Eimei Takahashi, Bruce Epker, Bob Hattner and others. George spent a short 3 months in my laboratory in which he enhanced my research by critiquing our manuscripts and mentoring my postdoctoral trainees and summer dental student investigators.

This provides a preliminary indication that this specialized program can effect change more quickly than demonstrated by Lam et al. (2012), thus providing the impetus for a larger-scale study to determine the trajectory of change in the longer term. Finally, unlike Lam et al. (2012), our study involved participants who did not have a cultural background related to Tai Chi (i.e., Americans rather than Chinese) and showed that the potential effects are not culture specific. The precise mechanism(s) underlying the improvement Dabrafenib cost in the global cognitive measure in this study is unclear. Potentially, given the deliberate multi-tasking

nature of its movements, the Tai Ji Quan program is expected to engage significant spatial-temporal orientation, memory, and executive control resources as well as attention devoted to specific multi-segmental bodily movements and postural demands. The combined physical and mental challenges then tax the physiological and neurophysiological processes that drive positive adaptations in the brain. Future studies with neuroimaging may shed light on this explanation. Additionally, based on previous research (Curlik & Shors, 2013) that indicates that the combined effects of physical and mental training on cognition are greater than either independently because each affects Veliparib ic50 different pathways,

the integrated motor-cognitive training characteristics of this program may have driven the changes in cognitive function in the study population. Other possibilities include gains in physical function as a result of training leading to enhanced cognitive functioning. Currently these explanations are speculative and check need further investigation. With improved design and methodologies for defining cognitive impairment and using multiple domains of cognitive outcome measures, future studies should continue to focus on examining the potential of the program by incorporating incremental attention-demanding Tai Ji Quan-based

motor tasks that tax the ability of older adults to perform exercises that involve quick recall of forms/movements, movement recognition, spatial orientation, movement switching/ordering, and movement retrieval. Implementation, however, should emphasize a slow progression and repetitive training approach in order to minimize negative learning and frustration that may arise among older adults due to the complex, multi-tasking training paradigm. These training features, when appropriately implemented, represent an improved approach that actively and concurrently engages cognitive and motor tasks that enhance cognitive functioning through dynamic Tai Ji Quan movements. Given the preliminary nature of this study, several limitations should be noted.

By means of the first generated pattern no novel sequences were retrieved by regular expression search. This first attempt failed due to the high pattern specificity, since it was constructed based on only eight sequences. Therefore, a more generalized pattern was needed, in order to find the

uncharacterized hevein-like peptides precursors in NR. Among the five originally identified precursors, three of them (CBI18789 from V. vinifera, EEE61250 from O. sativa and XP_002962191 from S. moellendorffii) have sequences larger than the hevein domain. This feature had already been observed for the Screening Library in vitro hevein-like precursors of Ac-AMP2 [9], Ar-AMP [37] and WAMP-1 [3]. In fact, these sequences after the hevein domain are propeptides and are posteriorly cleaved, leaving the mature peptide. In the case of hevein-like peptides,

the propeptides could be related to the evolution process which originated this class. Andreev et al. [3] have proposed that the WAMP-1 peptide emerges from a deletion of the catalytic domain of a chimerolectin (class I chitinase from plants). These three peptides with sequences after the hevein domain also show similarities to chimerolectins (data not shown), indicating that these sequences may be originated from a similar evolutionary process of WAMP-1. There are two other hypotheses involving the evolution of lectins with the hevein domain, which propose duplication Smad inhibitor or transposition of hevein domains, contrasting with Andreev et al. [3]. Wright et al. [62] have proposed that the consecutive duplication of hevein domains in the same gene generated the hololectins, and Shinshi et al. [50] have suggested that the transposition of an hevein domain into the gene of a chitinase generated the chimerolectins. Presumably, these sequences

after the hevein domain are remnants of the evolutionary process. In CBI18789 (V. vinifera), this sequence corresponds to a short hydrophobic tail. This tail does not generate great changes in structure and, probably, neither in protein function. In fact a transition PAK6 of coil-to-β-sheet was observed in MD, however, without influences in the binding to (GlcNAc)3 (data not shown). In addition, there is no clear evidence that this tail is cleaved. Similarly, XP_002962191 from S. moellendorffii also shows an additional sequence after the hevein domain. Nonetheless, it is longer than CBI18789′s tail and, in this case, there may be a structural or functional change if it is not cleaved. Hence, it was removed from the analysis, since clear evidence of cleavage was not observed. In contrast, EEE61250 (O. sativa) has a similar cleavage site to Ac-AMP2 and Ar-AMP, indicating that the additional sequence may be a propeptide. In this last case, besides the cleavage site, these sequences also share the same number of cysteine residues. The other two retrieved sequences have only the signal peptide and the hevein domain, without additional sequences after the hevein domain.

The calculations also show that the differences in Tmax between scenarios 1, 2 and 3 for the first 20 years are insignificant and that the distributions of Tmax are very similar in each scenario. In the first scenario, there is a small average increase (ca 0.8°C) of Tmax in the whole Baltic Sea for the period

investigated. Case 2 predicts an increase in Tmax from 22.08°C (in the first year) to 24.12°C (after 45 years), whereas case 3 envisages a decrease of Tmax to 19.91°C (after 45 years). The difference in Tmax between these cases is ca 2°C. Compared to case 1, the respective increase and decrease in Tmax is ca 1.3°C and 3°C in cases 2 and 3. This is due to the influence of short-wave radiation, which compensates for changes in temperature. Moreover, the increasing wind speed and westerly component of the wind speed mean that the drop buy ZD1839 in Tmax in case 3 is greater than the rise forecast by case 2 (a respective 20% decrease and increase in short-wave radiation). Time series of the one-year averaged Phytave and annual maximum Phytmax of the phytoplankton biomass at the nine stations are shown in Figures 7 and 8. Comparison of Phytave and Phytmax of the phytoplankton biomass in the subsurface layer shows that there are only slight differences between these parameters foreseen by scenarios 2 and 3. This implies

that short-wave radiation has a negligible influence on the distribution of phytoplankton biomass. In addition, the results indicate that the distributions of Phytave and Phytmax for the selleck compound three scenarios differ little in the gulfs (Gdańsk, Finland, Riga and Bothnia). In the other regions investigated (Gdańsk Deep, Gotland Deep, Bornholm Deep, Bothnia

Sea and Danish Straits), however, there are evident differences in Phytave and Phytmax between scenarios 1 and 2/3: they are higher in cases 2 and 3 than in case 1, i.e. Phytave is ca 10 mgC m−3, Phytmax from 100 to 250 mgC CYTH4 m−3. This corresponds to the depths of these regions: Phytmax increases by 20% (ca 100 mgC m−3) in the Bornholm Deep and by 50% (ca 250 mgC m−3) in the Gotland Deep. The results show significant changes in the distributions of phytoplankton biomass Phyt in open sea areas, where there is a considerable increase in current velocities. Scenarios 2 and 3 predict increased turbulence (mixing) (30% faster wind speed and westerly wind speed component), and hence an increase in phytoplankton biomass distributions. This is the result of the rise in nutrient concentration Nutr in the upper layer caused by the higher wind speed, i.e. by deep mixing. The phytoplankton biomass reflects the availability of nutrients, showing a strong increase with rising total inorganic nitrogen concentration. It shows that increasing wind speed causes currents to exert a greater influence on Nutr, which in turn influences Phyt distributions.