[159, 161, 166] Reported factors related to HBeAg negative conver

[159, 161, 166] Reported factors related to HBeAg negative conversion were ALT level (high), and the history of IFN therapy in the past.[159, 166] If hepatitis associated with lamivudine-resistant HBV occurs, adefovir resistance develops if therapy is changed from lamivudine to adfovir, but if lamivudine+adefovir combination therapy is administered, Tyrosine Kinase Inhibitor Library in vivo the reported incidence of HBV resistant to both agents is low.[191] Entecavir therapy is also administered to patients with lamivudine-resistant HBV (including cases unresponsive to lamivudine). The short-term results for entecavir therapy are good, and in some USA studies reported an HBV DNA negative

conversion rate of 21% at 1 year, and 34–40% at 2 years, and an ALT normalization rate of 65% at 1 year, and 81% at 2 years.[192, 193] However, the appearance of entecavir-resistant HBV associated with long term administration of entecavir has been confirmed. The incidence of entecavir-resistant HBV was 6% at 1 year and 8–13% at 2 years, and rebound of the HBV DNA load due to entecavir-resistant

HBV was 1% at 1 year and 9% at 2 years. A Japanese study reported favorable results with a HBV DNA negative conversion rate of 16% at 6 months and 33% at 1 year, and ALT normalization rate of 78% at 6 months and 81% at 1 year,[194-196] although entecavir-resistant HBV was detected in 26% AZD4547 datasheet of cases up to year 3, in whom hepatitis rebounded in 40%.[196] In this way, entecavir therapy for lamivudine-resistant (or unresponsive) HBV may also produce viral strains resistant to entecavir. Recommendations Lamivudine+adefovir combination therapy is recommended for treatment of lamivudine-resistant HBV. Entecavir therapy of lamivudine-resistant HBV may also produce viral strains resistant to entecavir. Reported adefovir-resistant

mutations include rtA181V/T, rtI233V and rtN236T in the HBV polymerase reverse transcriptase (rt) region. Of these mutations, in vitro and in vivo testing has demonstrated sensitivity to both lamivudine and entecavir for the rtN236T mutation, but lamivudine resistance for the rtA181V mutation.[7, 197] selleck chemicals llc In 132 patients with lamivudine-resistant HBV treated with lamivudine+adefovir combination therapy, multiple resistant strains were seen in 3 cases before the commencement of adefovir therapy, and in 2 further cases after therapy commenced (overall incidence 4%).[168] Entecavir+adefovir combination therapy is administered to patients with HBV resistant to both lamivudine and adefovir, with undetermined results. On the other hand, in reports from Europe, in cases with resistance to lamivudine or adefovir monotherapy, or resistant/unresponsive to lamivudine+adefovir combination therapy, administration of the new agent tenofovir (median treatment period 23 months) yielded HBV DNA negative conversion in 79% of cases, HBeAg negative conversion in 24%, and HBsAg negative conversion in 3%.

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[159, 161, 166] Reported factors related to HBeAg negative conver

[159, 161, 166] Reported factors related to HBeAg negative conversion were ALT level (high), and the history of IFN therapy in the past.[159, 166] If hepatitis associated with lamivudine-resistant HBV occurs, adefovir resistance develops if therapy is changed from lamivudine to adfovir, but if lamivudine+adefovir combination therapy is administered, Dabrafenib mouse the reported incidence of HBV resistant to both agents is low.[191] Entecavir therapy is also administered to patients with lamivudine-resistant HBV (including cases unresponsive to lamivudine). The short-term results for entecavir therapy are good, and in some USA studies reported an HBV DNA negative

conversion rate of 21% at 1 year, and 34–40% at 2 years, and an ALT normalization rate of 65% at 1 year, and 81% at 2 years.[192, 193] However, the appearance of entecavir-resistant HBV associated with long term administration of entecavir has been confirmed. The incidence of entecavir-resistant HBV was 6% at 1 year and 8–13% at 2 years, and rebound of the HBV DNA load due to entecavir-resistant

HBV was 1% at 1 year and 9% at 2 years. A Japanese study reported favorable results with a HBV DNA negative conversion rate of 16% at 6 months and 33% at 1 year, and ALT normalization rate of 78% at 6 months and 81% at 1 year,[194-196] although entecavir-resistant HBV was detected in 26% see more of cases up to year 3, in whom hepatitis rebounded in 40%.[196] In this way, entecavir therapy for lamivudine-resistant (or unresponsive) HBV may also produce viral strains resistant to entecavir. Recommendations Lamivudine+adefovir combination therapy is recommended for treatment of lamivudine-resistant HBV. Entecavir therapy of lamivudine-resistant HBV may also produce viral strains resistant to entecavir. Reported adefovir-resistant

mutations include rtA181V/T, rtI233V and rtN236T in the HBV polymerase reverse transcriptase (rt) region. Of these mutations, in vitro and in vivo testing has demonstrated sensitivity to both lamivudine and entecavir for the rtN236T mutation, but lamivudine resistance for the rtA181V mutation.[7, 197] selleck chemicals In 132 patients with lamivudine-resistant HBV treated with lamivudine+adefovir combination therapy, multiple resistant strains were seen in 3 cases before the commencement of adefovir therapy, and in 2 further cases after therapy commenced (overall incidence 4%).[168] Entecavir+adefovir combination therapy is administered to patients with HBV resistant to both lamivudine and adefovir, with undetermined results. On the other hand, in reports from Europe, in cases with resistance to lamivudine or adefovir monotherapy, or resistant/unresponsive to lamivudine+adefovir combination therapy, administration of the new agent tenofovir (median treatment period 23 months) yielded HBV DNA negative conversion in 79% of cases, HBeAg negative conversion in 24%, and HBsAg negative conversion in 3%.

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12 They found that the proliferative activities in the two areas

12 They found that the proliferative activities in the two areas were similar and they speculated that the mechanism of intraepithelial spread was multicentric occurrence (concept of field Selleck MLN0128 carcinogenesis) rather than lateral cell proliferation. Our results also showed that lesions with m3 or deeper invasion contain a significantly narrower area of low-grade dysplasia component than do lesions of m2 cancer. These results suggest that a low-grade dysplasia component would transform to

carcinoma in situ and invasive carcinoma along with tumor progression. Although we cannot conclude from our results that low-grade dysplasia is a precancerous lesion, the possibility that some lesions categorized as low-grade dysplasia in the WHO criteria have malignant potential

has been confirmed. However, our results showed that the low-grade dysplasia BGB324 manufacturer component in early invasive carcinoma had a significantly higher grade of atypia in cytological abnormalities than did the small low-grade dysplasia control cases. Although both lesions are simply categorized as low-grade dysplasia regardless of degree of abnormalities in the current WHO classification, the possibility that these lesions originally have different biological characters should be considered. Further study using molecular technology is needed to clarify this. Our results also revealed the risk of early invasive SCC of the esophagus being histologically diagnosed as low-grade dysplasia by click here endoscopic biopsy and thus being followed up without treatment. As for the actual reliability of histological diagnosis for endoscopic biopsy specimens, we previously studied histological results of EMR for esophageal lesions diagnosed as high-grade intraepithelial squamous neoplasia by endoscopic biopsy.13 Examination

of totally resected specimens revealed that over 30% of such lesions are actually invasive carcinoma and we concluded that endoscopists and pathologists must accept the fact that discrepancies between diagnosis of a biopsy specimen and that of the final resection specimen cannot be avoided. However, performing EMR for all esophageal lesions diagnosed as low-grade dysplasia by endoscopic biopsy is not realistic. Most of the low-grade dysplasia components in early invasive carcinoma observed in our study showed degrees of cytological abnormalities similar to those in the tumor invasive front. We consider that another nomenclature for squamous cell lesions with a high degree of cytological abnormalities confined to the lower half of the epithelium is required. Only a half decade ago, most cases of intraepithelial squamous neoplasia of the esophagus were diagnosed on the basis of nuclear features and changes in the epithelial structure by Japanese pathologists.

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12 They found that the proliferative activities in the two areas

12 They found that the proliferative activities in the two areas were similar and they speculated that the mechanism of intraepithelial spread was multicentric occurrence (concept of field MLN0128 carcinogenesis) rather than lateral cell proliferation. Our results also showed that lesions with m3 or deeper invasion contain a significantly narrower area of low-grade dysplasia component than do lesions of m2 cancer. These results suggest that a low-grade dysplasia component would transform to

carcinoma in situ and invasive carcinoma along with tumor progression. Although we cannot conclude from our results that low-grade dysplasia is a precancerous lesion, the possibility that some lesions categorized as low-grade dysplasia in the WHO criteria have malignant potential

has been confirmed. However, our results showed that the low-grade dysplasia PCI-32765 order component in early invasive carcinoma had a significantly higher grade of atypia in cytological abnormalities than did the small low-grade dysplasia control cases. Although both lesions are simply categorized as low-grade dysplasia regardless of degree of abnormalities in the current WHO classification, the possibility that these lesions originally have different biological characters should be considered. Further study using molecular technology is needed to clarify this. Our results also revealed the risk of early invasive SCC of the esophagus being histologically diagnosed as low-grade dysplasia by click here endoscopic biopsy and thus being followed up without treatment. As for the actual reliability of histological diagnosis for endoscopic biopsy specimens, we previously studied histological results of EMR for esophageal lesions diagnosed as high-grade intraepithelial squamous neoplasia by endoscopic biopsy.13 Examination

of totally resected specimens revealed that over 30% of such lesions are actually invasive carcinoma and we concluded that endoscopists and pathologists must accept the fact that discrepancies between diagnosis of a biopsy specimen and that of the final resection specimen cannot be avoided. However, performing EMR for all esophageal lesions diagnosed as low-grade dysplasia by endoscopic biopsy is not realistic. Most of the low-grade dysplasia components in early invasive carcinoma observed in our study showed degrees of cytological abnormalities similar to those in the tumor invasive front. We consider that another nomenclature for squamous cell lesions with a high degree of cytological abnormalities confined to the lower half of the epithelium is required. Only a half decade ago, most cases of intraepithelial squamous neoplasia of the esophagus were diagnosed on the basis of nuclear features and changes in the epithelial structure by Japanese pathologists.

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Separate regression models were also tested with the individual c

Separate regression models were also tested with the individual components of MS (considered as continuous or categorical measures) simultaneously included in the same equation. We took the maximum value of cIMT as the dependent variable in the regression models because the strongest association between the different measurements of IMT and coronary risk factors in otherwise healthy individuals

is achieved by applying the maximum value of IMT and not the mean value of IMT.17 A P value of less than check details 0.05 was considered statistically significant. A total of 250 obese children and adolescents, 100 with ultrasound-diagnosed NAFLD (and elevated ALT) and 150 without liver involvement, as well as 150 healthy normal-weight subjects were included in the study analysis (Fig. 1). None of the 250 obese children had type 2 diabetes mellitus. Baseline clinical and laboratory characteristics of the study population are presented in Table 1. MS, as well as MS components, were significantly more prevalent in obese children with NAFLD than in those without NAFLD (Table 2). At baseline, no differences were observed in the diameter of the brachial artery among the study groups (Table 1). In response to ischemia, obese children with NAFLD had significantly reduced

FMD compared to those without NAFLD and CP-690550 in vitro to healthy controls. In addition, percent FMD was remarkably larger in obese children without MS compared to obese children with MS (12.8% [95% CI, 11.0 to 14.5] versus 7.78% [5.30 to 10.2]; P < 0.01). When subdividing the obese population into subjects with and without MS, and with and without NAFLD, the FMD response was lower in children with MS and NAFLD than in those without MS and NAFLD (Fig. 2A). In

the entire study population, low percent FMD was significantly associated selleck with BMI-SDS, WC, high arterial BP, high triglycerides, high glucose, IR, CRPHS levels, and low HDL cholesterol after adjustment for age, gender, and Tanner stage (Table 3). Moreover, low percent FMD was associated with MS and NAFLD (Table 3). When the obese group was analyzed separately, low percent FMD was significantly associated with BMI-SDS, WC, high glucose, IR, CRPHS levels, and low HDL cholesterol, as well as with MS and NAFLD (Table 3). None of the variables were associated with FMD in the healthy group after correction for age, gender, and Tanner stage. When multiple logistic regression analysis was performed after adjusting for age, gender, Tanner stage, and MS (considered as a single clinical entity), NAFLD was significantly associated with low percent FMD (Table 4). Even after adjustment for age, gender, Tanner stage, and the individual components of MS, NAFLD remained significantly associated with low percent FMD. In this model, other covariates independently associated with low percent FMD were high glucose or IR (Table 4). Similar results were found when we considered FMD as a continuous measure and performed multivariate linear regression analyses.

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(2010), we found a strong correlation between past and future int

(2010), we found a strong correlation between past and future internal details (r = .63, p < .01) and past and future external details (r = .73, p < .001). In contrast, past internal and external details were uncorrelated (r = .30, p = .23) as were future internal and external details (r = .06, p = .82). The positive correlations between internal and external

details for past and future events AZD4547 nmr have been accounted for as evidence for the close overlap between the specificity of past and future events (Addis et al., 2008). However, it should be kept in mind that these correlations are boosted by the large differences between the TBI and control group, and therefore should be interpreted with caution. To take into account the fact that patients produced fewer details overall and to examine the effect of temporal distance to the remembered/imagined event together with the other factors, we looked at the ratio of internal-to-total details. The ratios were

analysed by means of a 2 (Group: TBI vs. controls) × 2 (Temporal Direction: past vs. future) × 3 (Temporal Distance: 1 month, 5 years, or 10 years) mixed-factor analyses of variance (ANOVA) with Group as a between-subject factor, and Temporal Direction and Temporal Distance as within-subjects factors. As illustrated by Figure 2, a significant main effect of Group was found, F(1, 16) = 58.18, η2p = .78, p < .0001, together with a significant Epacadostat effect of Temporal Direction, F(1, 16) = 15.34, η2p = .49, p < .001, and Temporal Distance F(1, 16) = 12.18, η2p = .43, p < .0001.

The main effect of Group reflected, that the TBI participants proportionally reported fewer episodic event-specific details for both past and future events compared with healthy controls across all time periods. The main effect of Temporal Direction indicated that proportionally more episodic event-specific details were produced for past events than for future events. The main effect of Temporal Distance reflected that events closer in time contained a greater proportion of episodic event-specific details than distant events. Importantly, the Temporal Distance × Group interaction was significant. The results of a repeated measures ANOVA performed on each group separately showed that the Temporal Distance effect was significant only for the TBI participants, F(2, 16) = 10.66, η2p = .57, find more p < .001, but not for the controls F(2, 16) = 2.00, p = .17, reflecting that TBI patients produced proportionally fewer episodic, event-specific details for past and future events the further the events were located away from the present. In sum, this series of analyses showed that TBI patients’ representations contained relatively fewer episodic, event-specific details than the ones of the controls, even when controlling for the total number of details. Moreover, while the TBI patients reported proportionally fewer internal details than did the healthy controls, this trend was not symmetrical.

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Although the miRNA family constitutes only a minor fraction of th

Although the miRNA family constitutes only a minor fraction of the human

genome, they hold fundamental importance in diverse physiological and developmental processes due to their pleiotropic effects on the post-transcriptional regulation of many vital genes. This class of regulatory RNAs has also emerged as important players in carcinogenesis; most, if not all, cancer types have abnormal miRNA expression patterns. In hepatocellular carcinoma (HCC), miRNA dysregulation plays a key role in mediating the pathogenicity of several etiologic risk factors and, more importantly, they promote a number of cancer-inducing signaling pathways. Recent studies have also demonstrated their potential values in the clinical management of HCC patients as some miRNAs may be used as prognostic GSK-3 inhibitor or diagnostic markers. The significance of miRNAs in liver carcinogenesis emphasizes their values as therapeutic targets, while technological advances in the delivery of miRNA has shed new possibilities for their use as novel therapeutic agents against HCC. In the past few decades, genome

research has established the fundamental importance of genetic and epigenetic alterations of oncogenes and tumor suppressor genes (TSGs) in the initiation and progression of human neoplasms. The recent discovery of microRNA (miRNA) put forward an alternate regulatory element, in which the check details actions of miRNAs regulate cancer-inducing cellular genes post-transcriptionally. The founding member of miRNA, lin-4, was discovered in the larval development of Caenorhabditis selleck elegans in 1993.1 Nevertheless, the role of small RNA in gene expression regulation had to await the discovery of a second miRNA member, let-7, 7 years later.2 Pioneering studies further revealed let-7 as a negative regulator of the RAS oncogene in human tumor cells.3 This discovery soon aroused tremendous efforts into the research of cancer-related miRNAs. By now,

miRNAs have been reported in a variety of organisms, ranging from viruses to mammals. To facilitate miRNA research, a miRNA registry (miRBase) has been established and is currently maintained by the University of Manchester.4 So far, 940 human miRNAs have been reported (miRBase release 15) and the list is still expanding. The family of miRNA constitutes about 1–3% of the human genome. Most miRNA genes are situated within the intergenic regions and have their own transcription units. About a quarter are located within exons or introns of other coding genes where their transcription is controlled by the host genes. MiRNAs can be transcribed as monocistronic transcripts or in polycistronic clusters; the latter involves several miRNAs situated on a single transcript being controlled by the same promoter (Fig. 1). In the nucleus, miRNA genes are transcribed as primary-miRNAs (pri-miRNAs) by RNA polymerase II (PolII).

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Although the miRNA family constitutes only a minor fraction of th

Although the miRNA family constitutes only a minor fraction of the human

genome, they hold fundamental importance in diverse physiological and developmental processes due to their pleiotropic effects on the post-transcriptional regulation of many vital genes. This class of regulatory RNAs has also emerged as important players in carcinogenesis; most, if not all, cancer types have abnormal miRNA expression patterns. In hepatocellular carcinoma (HCC), miRNA dysregulation plays a key role in mediating the pathogenicity of several etiologic risk factors and, more importantly, they promote a number of cancer-inducing signaling pathways. Recent studies have also demonstrated their potential values in the clinical management of HCC patients as some miRNAs may be used as prognostic selleck chemicals or diagnostic markers. The significance of miRNAs in liver carcinogenesis emphasizes their values as therapeutic targets, while technological advances in the delivery of miRNA has shed new possibilities for their use as novel therapeutic agents against HCC. In the past few decades, genome

research has established the fundamental importance of genetic and epigenetic alterations of oncogenes and tumor suppressor genes (TSGs) in the initiation and progression of human neoplasms. The recent discovery of microRNA (miRNA) put forward an alternate regulatory element, in which the www.selleckchem.com/products/FK-506-(Tacrolimus).html actions of miRNAs regulate cancer-inducing cellular genes post-transcriptionally. The founding member of miRNA, lin-4, was discovered in the larval development of Caenorhabditis this website elegans in 1993.1 Nevertheless, the role of small RNA in gene expression regulation had to await the discovery of a second miRNA member, let-7, 7 years later.2 Pioneering studies further revealed let-7 as a negative regulator of the RAS oncogene in human tumor cells.3 This discovery soon aroused tremendous efforts into the research of cancer-related miRNAs. By now,

miRNAs have been reported in a variety of organisms, ranging from viruses to mammals. To facilitate miRNA research, a miRNA registry (miRBase) has been established and is currently maintained by the University of Manchester.4 So far, 940 human miRNAs have been reported (miRBase release 15) and the list is still expanding. The family of miRNA constitutes about 1–3% of the human genome. Most miRNA genes are situated within the intergenic regions and have their own transcription units. About a quarter are located within exons or introns of other coding genes where their transcription is controlled by the host genes. MiRNAs can be transcribed as monocistronic transcripts or in polycistronic clusters; the latter involves several miRNAs situated on a single transcript being controlled by the same promoter (Fig. 1). In the nucleus, miRNA genes are transcribed as primary-miRNAs (pri-miRNAs) by RNA polymerase II (PolII).

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Moreover, N2 fixation by cyanobacteria

Moreover, N2 fixation by cyanobacteria PARP inhibitor is much more likely in freshwater ecosystems than in marine ecosystems (Conley et al. 2009; but Elser et al. 2007). These findings mentioned above may lead to a more often P-deficient than N-deficient

condition and thus a good correlation between PUFAs and POP for primary producers in a lake. The correlation between FAs and QN shows that elemental and biochemical properties of phytoplankton covaried in the three species under N deficiency in our study. The incorporation of two properties is important for studying the limitation of food quality on zooplankton via bottom-up processes. On the other hand, the lack of common correlation between FAs and QP in this study might

be evidence of dominant nonphosphorus lipids in response to P deficiency in some species of marine phytoplankton. Although these two aspects are out of the scope of this study, our results can be very useful for further research on lipid biosynthetic mechanisms, as well as the energy and matter transfer in food webs. In this study, the effects of N:P supply ratios and growth rates on phytoplankton FA composition were studied in laboratory conditions. This approach this website focuses on the evaluation of these two factors in regulating biochemical quality of phytoplankton. However, phytoplankton in natural conditions faces interactive effects of multiple abiotic factors and resources, e.g., temperature, light, nutrient supply, and CO2. For example, light supply is identified as a dominant trigger of the phytoplankton spring bloom, and nutrients is suggested to define the carrying capacity of phytoplankton in the plankton ecology group model (Sommer et al. 2012). Recent studies have simultaneously considered the effects of nutrient

supply and other abiotic factors (or resources) on phytoplankton FA (or lipid) composition, e.g., the combined effect of nutrient supply and temperature (e.g., Piepho et al. 2012, Roleda et al. 2013), light intensity (e.g., Piepho et al. 2012), light:dark cycles (e.g., Lacour et al. 2012), check details or CO2 (e.g., Spijkerman and Wacker 2011). Thus, other ambient factors may influence the effects of N:P supply ratios and growth rates on phytoplankton FA composition, on which further studies are recommended for better understanding responses of chemical composition of phytoplankton in more realistic scenarios. This study examined the influence of highly variable chemical conditions (N:P supply ratios) and biological conditions (growth rates) on biochemical outcome (FA composition) in three species of marine phytoplankton (representing particular algal classes). It scaled intraspecific variation in FA profiles (simultaneously affected by nutrient supply and growth rates) against variation between phytoplankton classes, and thus provides important empirical data for further studies on phytoplankton lipid biosynthesis in changing oceans.

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Moreover, N2 fixation by cyanobacteria

Moreover, N2 fixation by cyanobacteria www.selleckchem.com/products/CP-690550.html is much more likely in freshwater ecosystems than in marine ecosystems (Conley et al. 2009; but Elser et al. 2007). These findings mentioned above may lead to a more often P-deficient than N-deficient

condition and thus a good correlation between PUFAs and POP for primary producers in a lake. The correlation between FAs and QN shows that elemental and biochemical properties of phytoplankton covaried in the three species under N deficiency in our study. The incorporation of two properties is important for studying the limitation of food quality on zooplankton via bottom-up processes. On the other hand, the lack of common correlation between FAs and QP in this study might

be evidence of dominant nonphosphorus lipids in response to P deficiency in some species of marine phytoplankton. Although these two aspects are out of the scope of this study, our results can be very useful for further research on lipid biosynthetic mechanisms, as well as the energy and matter transfer in food webs. In this study, the effects of N:P supply ratios and growth rates on phytoplankton FA composition were studied in laboratory conditions. This approach Buparlisib focuses on the evaluation of these two factors in regulating biochemical quality of phytoplankton. However, phytoplankton in natural conditions faces interactive effects of multiple abiotic factors and resources, e.g., temperature, light, nutrient supply, and CO2. For example, light supply is identified as a dominant trigger of the phytoplankton spring bloom, and nutrients is suggested to define the carrying capacity of phytoplankton in the plankton ecology group model (Sommer et al. 2012). Recent studies have simultaneously considered the effects of nutrient

supply and other abiotic factors (or resources) on phytoplankton FA (or lipid) composition, e.g., the combined effect of nutrient supply and temperature (e.g., Piepho et al. 2012, Roleda et al. 2013), light intensity (e.g., Piepho et al. 2012), light:dark cycles (e.g., Lacour et al. 2012), selleck kinase inhibitor or CO2 (e.g., Spijkerman and Wacker 2011). Thus, other ambient factors may influence the effects of N:P supply ratios and growth rates on phytoplankton FA composition, on which further studies are recommended for better understanding responses of chemical composition of phytoplankton in more realistic scenarios. This study examined the influence of highly variable chemical conditions (N:P supply ratios) and biological conditions (growth rates) on biochemical outcome (FA composition) in three species of marine phytoplankton (representing particular algal classes). It scaled intraspecific variation in FA profiles (simultaneously affected by nutrient supply and growth rates) against variation between phytoplankton classes, and thus provides important empirical data for further studies on phytoplankton lipid biosynthesis in changing oceans.

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