Most PI cause the overconcentration of

CNI by inhibiting CYP3A4, while most NNRTI cause decreased levels of CNI by stimulating CYP3A4.[29, 42] As mentioned earlier, RAL is introduced as a key drug in LT in HIV positive patients, because the metabolism of this drug is not related to CYP450, so it does not affect the blood concentration of CNI. Several reports have demonstrated both the in vitro and in vivo effectiveness of rapamycin in reducing HIV replication,[43-45] and Di Benedetto et al. found that rapamycin monotherapy was significantly beneficial buy Talazoparib in long-term immunosuppression maintenance and HIV control after LT.[46] Mycophenolate mofetil is expected to be an effective immunosuppressive drug because of its efficacy in reducing HIV infection by both virological and immunological mechanisms.[47-49] Using these drugs, a more effective regimen of immunosuppression with ART may be established. In regard to the steroid, several studies proposed that a steroid-free regimen can be safely applied and effective in LT for HCV cirrhosis. Also, in HIV/HCV co-infected patients, steroid-free protocol may be beneficial to prevent both HIV and HCV recurrence after LT.[50, 51] LIVER TRANSPLANTATION FOR HIV/HCV co-infected patients remains challenging, but with recent http://www.selleckchem.com/products/BEZ235.html developments in perioperative management and novel drugs for both HIV and HCV,

the results are likely to be improved. ”
“It has been recently identified that hepatocytes can act as cytotoxic effectors and can kill contacted cells by way of CD95 ligand–CD95 and perforin-dependent pathways. However, it remained unknown whether hepatocyte-mediated cell killing is indiscriminant or is directed toward targets with particular cell surface characteristics, as well as whether hepatocytes have the capacity to directly eliminate contacted lymphocytes. In this study, we found that desialylation of surface glycoproteins significantly augments cell susceptibility to hepatocyte-mediated killing. Using asialofetuin

as a competitive ligand, and by silencing gene transcription with specific small interfering RNA, we found that the asialoglycoprotein receptor (ASGPR) is involved in hepatocyte recognition of cells predestined selleck compound for killing, including activated autologous T lymphocytes. Conclusion: Hepatocytes are constitutively equipped in the molecular machinery capable of eliminating cells brought into contact with their surface in a manner that is reliant, at least in part, upon the recognition of terminally desialylated glycoproteins by hepatocyte ASGPR. The study adds a new dimension to the physiological role of hepatic ASGPR and provides further evidence that hepatocytes can actively contribute to intrahepatic immune regulation and moderation of the local inflammatory response. (HEPATOLOGY 2011;) Hepatocytes constitute more than 80% of cells in liver parenchyma.

The important role of NK cells in the clearance of early hepatitis C virus (HCV) infection is suggested by the results of several genetic studies on the interaction between NK cell receptors and their ligands.4, 5 For instance, Khakoo et al.4 reported that patients with the inhibitory NK cell receptor (KIR2DL3) and its ligand (human leukocyte antigen C group1 [HLA-C1]) had a better chance of spontaneous recovery from acute Selleck Alvelestat HCV infection. This is likely due to weak inhibitory KIR2DL3–HLA-C1 interaction, which results in the lack of strong

NK cell inhibition and subsequent induction of strong NK cell functions that contribute to HCV clearance. However, the role of NK cell activating receptor NKG2D and its ligands in controlling HCV infection remains largely unknown. Recently, several studies have shown that NKG2D+NK cells are highly enriched in intrahepatic compartments in patients with chronic HCV infection, which correlates with hepatocellular damage.6 Although the expression of NKG2D

ligands on HCV-infected or HBV-infected hepatocytes in humans has not yet been explored, it is expected to be elevated because in several murine models of liver injury, up-regulated ligands have been detected on stressed hepatocytes (see below) (Fig. 1). The expression of RAE-1, MULT-1, and H60 is not detected on normal mouse hepatocytes; however, it is detected at this website high levels on hepatocytes from bile duct-ligated mice,7 hepatitis B virus (HBV) transgenic mice,8, 9 and mice with Selleck Ceritinib drug-induced liver injury.10 Elevated levels of these ligands trigger activation of NK cells, as well as natural killer T (NKT) cells, to kill hepatocytes, resulting

in hepatocellular damage.7–10 Induction of RAE-1 expression has also been reported on Kupffer cells in mice treated with polyinosinic:polycytidylic acid (poly I:C) plus D-galactosamine (D-GalN).11 The interaction between NKG2D and RAE-1 stimulates NK cells to produce interferon-gamma (IFN-γ), which then acts together with Kupffer cell-derived tumor necrosis factor-α to synergistically induce fulminant hepatitis.11 In addition to triggering hepatocyte damage, the interaction between NKG2D and corresponding ligands is also involved in NK cell-mediated cholangiocyte injury in a murine model of biliary atresia induced by rotavirus infection.12 In this model, NK cells accumulate in extrahepatic bile ducts and hepatic expression of RAE1, H60, MULT-1 messenger RNAs is markedly up-regulated. Blockade of NKGD2 prevents both epithelial cell injury and the development of the atresia phenotype. In vitro, NK cells lyse cholangiocytes in a contact-dependent and NKG2D-dependent manner.

1 The potential of human hepatic stem cells (hHpSCs) and other stem/progenitors for pharmaceutical research, cell-based therapies, and tissue engineering relies on being able to isolate them, propagate them in culture and differentiate them to a functional mature cell fate(s).2 Current methods for differentiation of stem cells

involve subjecting cells to a mix of soluble signals and/or extracellular matrix components, and the stem cells must be treated with multiple sets of such signals over weeks of time. The Everolimus adult fate achieved is typical of only partially differentiated cells with over- or underexpression of specific adult genes.3 Here we demonstrate strategies for rapidly differentiating stem cells using matrix scaffolds that elicit more efficient and reproducible responses. Extracellular matrix is an extraordinarily complex mixture of molecules that are highly regulated, secreted by, and adjacent to cells on one or more of their surfaces, and long understood to be critical for determining GSK458 the morphology,

growth, and differentiation of attached cells.4, 5 Tissue-specific gene expression in cultured cells is improved by culturing the cells on or embedded in matrix extracts or purified matrix components.6, 7 However, individual matrix components, alone or in combination, are unable to recapitulate a tissue’s complex matrix chemistry and architecture. This is related to the fact that the matrix components are in patterns associated with natural tissue zones and with histological structures such as blood vessels. This complexity of the tissue matrix is more readily achieved by matrix extracts of decellularized

tissue.8-10 Matrix extracts selleck screening library found useful for ex vivo maintenance of cells include amniotic membrane extracts11; Matrigel, an urea extract of a murine embryonal carcinoma12; extracellular matrix (ECM), a detergent- or NaOH-extract of monolayer cell cultures13,14; and biomatrices, an extract of homogenized tissues.10, 15 More recently, decellularized tissues, prepared by collagenase digestion of a tissue16 or by delipidation followed by distilled water washes,8 have been used to mimic the matrix environment in vivo.17 Even though these protocols result in major losses of some matrix components, the decellularized scaffolds from different tissues or organs, such as small intestinal submucosa (SIS), bladder submucosa matrix (BSM),17, 18 vascular tissue,19 heart,20 airway,21 and liver22 have been used successfully in both preclinical and clinical applications.23 Here we describe a strategy, focused on collagen chemistry, that is ideal for preparing substrata of tissue extracts comprised of tissue-specific matrix components and factors bound to the matrix.

[37] This was associated with elevated levels of TLR4 ligands in the portal blood, supporting a PAMP-driven inflammatory response in NASH. There is therefore very strong evidence for a TLR4/TLR9-initiated and inflammasome/IL-1β-mediated pathway of steatosis, hepatitis, and fibrosis in NASH. PAMPs and DAMPs are likely both contributing to the TLR ligand pool. After acetaminophen toxicity, the release of a number of DAMPs can be detected in the serum in rodents

and humans. These include HMGB1, hyaluronic acid, DNA, keratin, and cyclophilin A, and the neutralization of individual DAMPs has reduced injury.[2, 49-55] Antibody-mediated neutralization of HMGB1 was shown to result in less inflammation after acetaminophen (APAP) toxicity, and liver perfusate from mice treated with high doses of APAP contained HMGB1 and HSP-70,

and was pro-inflammatory to Kupffer cells, resulting in up-regulation of IL-1β and MCP-1.[54, 2] Mice www.selleckchem.com/products/PLX-4720.html with deficiency in TLR4 or TLR9 signaling have reduced histological injury and serum transaminases after APAP challenge.[7, 56] All of these DAMPs provide signal 1, and cytokines that use MyD88 associated receptors and activate an NFκβ pathway (IL-1α and IL-1β) can further amplify this. Recently, the importance of ATP and its receptor (P2X7) in providing PF-562271 signal 2 in APAP hepatotoxicity was demonstrated.[57] There was less injury in P2X7 deficient mice and in wild-type mice after depletion of ATP by apyrase. The requirement for ATP and P2X7 points to a direct involvement of the NLRP3 inflammasome, and this was demonstrated in mice lacking NLRP3, ASC, and caspase-1, but this was not reproduced in a second study.[7, 58] Mice lacking IL-1R, or neutralization click here of IL-1β and IL-1α in wild-type mice, resulted in significantly less APAP toxicity, but this was also not reproduced in a second

study.[59, 60] Collectively, there is a large body of evidence for a role of DAMPs and SI in APAP-induced hepatotoxicity. This has added to the known toxic metabolic pathways of APAP hepatotoxicity, and this has suggested DAMP receptors and signaling pathways as new targets for therapy. Acute pancreatitis is predominantly a sterile inflammatory condition, whether induced by alcohol, pancreatic duct obstruction by biliary stones, hypercalcemia, hypertriglyceridemia, or medication toxicities. Evidence from randomized controlled trials has established that broad-spectrum antibiotic therapy does not alter the natural history of severe acute pancreatitis early in the course of disease, providing strong evidence that infectious etiology is unlikely a significant contributor to the evolving pancreatic inflammation and necrosis. Chronic pancreatitis is similarly thought to be a sterile inflammatory process, induced by chronic alcohol ingestion or recurrent acute pancreatitis, yet conspicuously persistent in the absence of ongoing noxious stimuli.

6 In this study, CL58 retained its inhibitory activity when added at even later time points than anti-CD81 antibody. Interestingly, Flag-tagged CL58 immunoprecipitated with HCV E1E2. Therefore, it is possible that CL58 readily penetrates lipid membrane owing to its small size and hence becomes capable of interacting with HCV E1E2. However, what this interaction means to CL58-mediated inhibition remains unclear. It will be interesting if such

interaction disrupts the yet-to-be confirmed interactions between HCV glycoproteins and endogenous CLDN1 or the CLDN1-CD81 complex.24, 25 Although we are unable to nail down either possibility (data not shown), the observation that CL58 also inhibited cell-cell fusion mediated by HCV glycoprotein and CLDN1 warrants further investigation in its ability to inhibit intracellular PLX4032 solubility dmso fusion between HCV and cellular membranes. It is noteworthy that TJ was first depicted as a Maraviroc clinical trial fusion of the outer lipid leaflets of adjacent cell membrane bilayers (hemifusion).26 Regardless of its direct target, the anti-HCV activity is unique to CL58, but not those peptides derived from the respective region of CLDN6, CLDN7, and CLDN9. In conclusion, the identification of CL58 now adds new tools in developing novel antiviral drugs that target HCV entry. This reagent will also aid to dissect the molecular mechanisms of HCV entry. Although most small molecule

inhibitors that have advanced to the clinic target viral components, the peptide inhibitor described here may offer advantages, because it targets cellular selleck compound proteins that are required for HCV infection

and hence reduce the likelihood of developing resistance. By virtue of its distinct mechanisms of inhibition, CL58 may be used in combination with other anti-HCV drugs for potential synergistic effects in treating HCV infections. We thank T. Wakita, H. Greenberg, C. Rice, F. Chisari, F. Cosset, G. Luo, Y. Chen, R. Bartenschlager, G. Gao, J. Dubuisson, C. Coyne, and J. McKeating for providing cell lines, reagents, and technical assistance. Additional Supporting Information may be found in the online version of this article. ”
“Altered expression and activity of immunomodulatory cytokines plays a major role in the pathogenesis of alcoholic liver disease. Chronic ethanol feeding increases the sensitivity of Kupffer cells, the resident hepatic macrophage, to lipopolysaccharide (LPS), leading to increased tumor necrosis factor alpha (TNF-α) expression. This sensitization is normalized by treatment of primary cultures of Kupffer cells with adiponectin, an anti-inflammatory adipokine. Here we tested the hypothesis that adiponectin-mediated suppression of LPS signaling in Kupffer cells is mediated via an interleukin-10 (IL-10)/heme oxygenase-1 (HO-1) pathway after chronic ethanol feeding.

Methods: A 55 year old female patient was diagnosed

with early Roxadustat chemical structure gastric cancer on screening endoscopy. Abdominal computed tomography showed incidental right renal cell carcinoma. Results: Robot assisted distal gastrectomy was performed followed by partial nephrectomy. Conclusion: Robot assisted combined operation could be a treatment option for early stage of synchronous malignancies. Key Word(s): 1. gastric cancer; 2. robot assisted gastrectomy; 3. robot assisted nephrectomy Presenting Author: DEWI NORWANI BASIR Additional Authors: WAI LEONG QUAN Corresponding Author: DEWI NORWANI BASIR Affiliations: Tan Tock Seng Hospital Objective: Buried Bumper Syndrome is a known but uncommon complication in patients with Percutaneous Endoscopic Gastrostomy (PEG) tubes. We describe an elderly man with a background of laryngeal cancer with post radiotherapy swallowing impairment. He also had stomach cancer with Billroth II gastrectomy performed previously. A Percutaneous Endoscopic Jejunostomy (PEJ) tube was recently inserted because of a persistently misplaced nasogastric tube.

It was placed through the jejunal wall due to altered anatomy with no other suitable sites found. Patient presented with a blocked tube and was referred for endoscopic re-evaluation and change of PEJ tube. Methods: On endoscopy, a small punctum located at the site where the internal bumper was expected to be was identified. This finding is diagnostic of a complete buried bumper syndrome. We proceeded Seliciclib mouse with the one step pull through method to remove and replace the PEJ tube at the same time. The PEJ tube was cut approximately 2 to 3 cm from the skin and an ordinary PEG trocar was inserted through the cut end of the PEJ tube into the stomach under endoscopic view. The trocar was removed leaving the white sheath in place. We then inserted the

blue nylon string through the white sheath into the stomach in the usual manner. The string was then captured with a snare and pulled out through check details patient’s mouth. Results: Once outside the body, a new PEG tube was attached to the nylon string the usual manner and gently pulled back into the stomach. The tapering plastic end of the new tube was made to push against the buried bumper which forced it to exit through the skin while the new tube was pulled into position. This one step pull through method not only removed the buried bumper syndrome but also replaced the PEJ tube at the same time thereby minimising the risk of peritoneal leak. The final position of the new PEJ tube appeared satisfactory endoscopically. Conclusion: The 1 step pull through method is simple and safe to perform. No new incision is needed and the removal and reinsertion of PEG/PEJ tube can be performed at the same setting. Key Word(s): 1. buried bumper syndrome; 2.

13, 26, 27 These histological and clinical features are distinct from classical descriptions of acute allograft rejection.28 Hepatotoxicity due to certain drugs can also target the centrilobular

region; halothane hepatitis, the best defined, results from metabolic idiosyncrasy and autoantibody formation toward antigens located within pericentral hepatocytes.30 Therefore, it seems plausible that specific antigens, whether environmental, drug-derived, or expressed on non-self hepatocytes, may trigger an immune-mediated injury to the centrilobular region by targeting SB203580 antigens preferentially expressed by zone three hepatocytes. The fact that no true gold standard exists for the diagnosis of AIH represents a limitation of our observations. Accordingly, we reasoned that patients with bona fide AI-ALF would more often develop chronic hepatitis in their native livers (in spontaneous

survivors) or allografts (in transplant recipients) than those with indeterminate ALF. After Selumetinib nmr 1-4 years follow-up, we found a high (44%) incidence of hepatitis in the study population, and those with histologically proven hepatitis were more frequently those with positive ANA ± ASMA who were given a final histological diagnosis of probable AI-ALF. These data seem further supported by the fact that none of these markers of autoimmunity before transplant were associated with allograft rejection (data not shown). The clinical relevance of non–organ specific autoantibodies in ALF remains uncertain. A recent screen of ANA, ASMA, AMA, and LKM autoantibodies in patients with ALF revealed a prevalence of 25% in patients with non-acetaminophen drug reactions and hepatotrophic viral infections, but in none of patients with

acetaminophen-induced click here ALF,31 suggesting that their presence may nonspecifically accompany overwhelming immune activation. Our observations suggest that the presence of autoantibodies correlate with histological diagnosis of AI-ALF. Specifically, patients with AI-ALF more frequently had ANA and/or ASMA, and anti-LKM, anti-SLA, and anti-tTG were exclusively detected in patients with histological AI-ALF (data not shown). Moreover, the addition of ANA ± ASMA to a histological diagnosis of AI-ALF appeared to improve the detection of histology alone to identify an autoimmune phenotype. In conclusion, we propose that four histological features of autoimmune liver disease can be interpreted as probable AI-ALF. Patients with probable AI-ALF on histology have a distinctly autoimmune clinical phenotype, and the presence of ANA and/or ASMA may improve the distinction of AI-ALF from other cases of indeterminate ALF. Similar to aggressive, refractory cases of acute cellular allograft rejection, centrilobular necroinflammatory features appear to be a hallmark of AI-ALF.

Furthermore, the well-demonstrated increased bicarbonate and mucus secretion by PG and numerous other

gastroprotective drugs could also result in luminal dilution of damaging agents whose access to subepithelial blood vessels may be further delayed by the perivascular edema created in this mild hyperacute inflammation that Andre Robert called “gastric cytoprotection.” It may well be that gastric motility stimulants which also prevent the ethanol-induced hemorrhagic mucosal erosions also contribute to this pre-epithelial mucosal defense mechanism.[39] The new multicomponent physiologic defense mechanism is also consistent with previous vascular studies, that is, although markedly increased vascular permeability selleck chemical is pathologic, slight increase in this permeability seems to be protective, that is, a key element in the complex pathophysiologic response during acute gastroprotection. Although “gastric cytoprotection,” as originally Wnt inhibition described,[1, 2] is strictly an acute phenomenon which is

related to the prevention of mucosal lesions. Over the years, more and more investigators used “gastroprotection” for the accelerated healing, that is, treatment of chronic gastric ulcers without the involvement of reduced gastric acidity. Actually, the clinically proven ulcer healing effects (without reducing gastric acidity) of sofalcone and sucralfate[3-5] suggested this possibility in the very early stages of gastroprotection research. In parallel studies, to search the mechanism(s) of acute gastroprotection, 上海皓元医药股份有限公司 these drugs were also found

to increase mainly gastric mucus secretion and to strengthen the poorly defined “mucosal barrier.” Yet, for accelerated healing of existing gastroduodenal ulcers, strengthening the already broken mucosal barrier is probably not of much value—or just another example of “true-true but unrelated” fallacy. Because of mechanistic uncertainties, and from pathologist’s point of view, gastroduodenal ulcers are internal wounds. In the late 1980s and early 1990s, we (Judah Folkman and my lab) proposed the possibility of treating ulcers with angiogenic growth factors (e.g. basic fibroblast growth factor [bFGF], platelet-derived growth factor [PDGF]), which stimulate the formation of granulation tissue that consists of angiogenesis-dependent proliferation of fibroblasts depositing collagen over which surviving and proliferating epithelial cells from the edge of the ulcer migrate and cover the large mucosal defect. Unlike Epidermal growth factor (EGF) which stimulates only the proliferation of epithelial cells—but these cells cannot grow over necrotic debris that is usually on the top of both external and internal wounds. In this respect, bFGF is misnomer, yet probably is the best candidate since it stimulates the division of not only fibroblasts and epithelial cells, but it turned out to be the first angiogenic peptide.

Aims: To study these parameters in patients with LC in Tajikistan. Methods: There were diagnosed 1374 patients with LC. Survival was assessed according to the Kaplan-Meier method. The mortality risk of cirrhosis complications was analyzed by a time-dependent Cox regression model. Results: The main etiological factors of development of LC were: HBV (49%), HCV (36%) and alcohol (4%). The incidence of viral LC was 23.2, of alcohol-induced LC (ALC) – 1.4 and primary biliary cirrhosis (PBC) – 0.3 per 100 000 of adult populations. Lifetime and 3-year survival rate of patients depend on a phase of

cirrhotic process compensation. The highest 3-years survival rate of patients from the producing NVP-AUY922 research buy moment of this diagnosis was 79% at Child–Pugh grade A vs. 28% at grade C. The cause of death of 89% of patients has been directly related to

complications of cirrhosis. The main reasons of patients death were: hepatic encephalopathy (46.7%), bleeding serve (18.3%), hepatorenal syndrome (12.5%), spontaneous bacterial peritonitis (9.2%) and portal vein thrombosis Y 27632 (2.5%). The prognosis of survival is most unfavorable at hepatic encephalopathy in comparison with other complications of the LC. Presence more than one complication increases probability of death of patients more than 2.5 times. The higher relative risk of death has patients with grade B and C with comparison to grade A. Conclusion: The main etiological factors of LC are HBV and HCV in Tajikistan. The incidence of viral LC does not differ from that in other countries. ALC

and PBC are over 10 and 5 times less frequent that in Russia. Key Word(s): 1. liver cirrhosis; 2. etiological factor; 3. prevalence; 4. survival rate; Presenting Author: DONGYE YANG Additional Authors: TAOFIC MOUNAJJED, SAMARH IBRAHIM, DEBORAHK FREESE, LIZHI ZHANG Corresponding Author: LIZHI ZHANG Affiliations: Central South University; Mayo Clinic Objective: Autoimmune sclerosing cholangitis (ASC) is a poorly understood autoimmune liver disease in MCE公司 childhood which is referred as an overlap syndrome of autoimmune hepatitis (AIH) associated with bile duct disease typical of primary sclerosing cholangitis (PSC). Recently, IgG4-related sclerosing cholangitis (ISC) is recognized in adult population as biliary manifestation of a steroid-responsive multisystem fibroinflammatory disorder in which affected organs are infiltrated with IgG4+ plasma cells. In this study, we sought to evaluate clinicopathological features of ASC and its correlation with IgG4+ plasma cells infiltration.

A similar result was also found in the cyanobacterium Synechococcus sp. at certain growth rates (Ahlgren and Hyenstrand 2003). The results in this study are consistent with those mentioned above, showing significantly higher contents of SFAs and MUFAs in all three algal species under the lowest N:P supply

ratio (N deficiency) at lower growth rates. This indicates that the observed increase in SFAs and MUFAs and the potential increase in TAGs could be triggered by the extremely N-deficient condition at lower growth Small molecule library rates in the three species, which can be used to store carbon and energy to support growth when conditions improve (Dunstan et al. 1993). The responses of PUFAs to N deficiency revealed no consistent pattern in the three species in this study, showing significantly higher PUFA, ALA, and EPA contents in Rhodomonas sp., relatively lower PUFA and EPA contents in P. tricornutum, and no clear response of PUFAs in I. galbana at lower see more growth rates. Similar to Rhodomonas sp. in this study, R. salina in Malzahn et al. (2010)

also had higher PUFA contents under the N-depleted condition. In general, PUFAs are important components of cellular membrane lipids (Guschina and Harwood 2009). However, TAGs in some microalgae have been found to be a depot of PUFAs under stressful conditions (e.g., N starvation and the stationary growth phase), which can be mobilized for growth at favorable conditions (Cohen et al. 2000, Khozin-Goldberg et al. 2002). The capacity of marine phytoplankton to incorporate n-3 PUFAs into TAGs has shown interspecific differences (Tonon et al. 2002). This may contribute to variation in PUFA responses to N deficiency between the three species in this study. Based on our results, the effect of nutrient supply on PUFAs associated with TAGs is suggested to be addressed in future studies. The responses of PUFAs to P deficiency also showed interspecific differences in this study, with markedly lower PUFA, ALA, and EPA contents in Rhodomonas sp., relatively higher PUFA and EPA contents in P. tricornutum, and no clear response of PUFAs in I. galbana at lower growth rates. Harrison et al.

(1990) reported species-specific responses of PUFAs to P starvation, showing a reduced amount of MCE DHA in both Chaeotoceros calcitrans and Thalassiosira pseudonana and a reduced EPA only in T. pseudonana. In contrast, a higher EPA content was observed in the marine flagellate Pavlova lutheri under higher N:P supply ratios (P deficiency; Carvalho et al. 2006). These findings further reveal highly variable responses of PUFAs in phytoplankton under P deficiency. As mentioned above, PUFAs are important membrane lipid components (Guschina and Harwood 2009). Phospholipids as a main group of membrane lipids are major biochemical reservoirs of P in marine plankton (Van Mooy et al. 2009). Thus, the inhibition of phospholipid synthesis under P deficiency might explain the reduced PUFA content in phytoplankton, e.g.