Demographic and clinical characteristics of the subjects are summarized in Table 1. We performed brain MRI in 32 patients who met the International Panel criteria for either MS or a clinically isolated syndrome (CIS),20 and 17 normal controls. Among patients with MRI and neurologic examination, we were also able to obtain cognitive testing in 24 within 2 weeks of MRI. All 17 normal controls underwent Maraviroc cost cognitive testing and MRI. MS patients were enrolled consecutively from a community-based, university-affiliated MS clinic. Controls were recruited by using an Institutional Review Board (IRB)-approved

advertisement that was posted in a local newspaper and our hospital website. Telephone interview was conducted by using a questionnaire. Control subjects did not differ demographically from the MS group [control mean ± standard deviation age = 45.5 ± 7

years, education = 16.5 ± 1.9 years (P= .74), 71% female (P= .79)]. Our IRB approved this study and informed consent was obtained on all subjects. Within 1 month of MRI, MS disease course21 and clinical measures including HIF cancer Expanded Disability Status Scale (EDSS) score22 and timed 25-foot walk (T25FW)23 (Table 1) were assigned by a treating neurologist. This study was part of a larger ongoing study in which patients are being recruited to assess the relationship between MRI findings and the development of sustained disability 3 years later. For this reason, patients were included only if they had “active click here disease.” This was defined as a clinical relapse, new or enlarging MRI-defined central nervous system lesion, or an increase in EDSS score of at least .5 in the year prior to recruitment. Only patients aged 18-55 years were included to minimize confounding

effects from age-related phenomena. To avoid confounding neuropsychological testing, we excluded any potential participants (both MS patients and controls) with a history of major medical, neurologic, or neuropsychiatric disorders or a history of substance abuse or motor/sensory deficits that may impact cognitive testing. Whole brain axial 2-dimensional fast FLAIR was performed in all subjects at 1.5T and 3T using the scan protocols shown in Table 2. The primary goal of this study was to determine correlation between 3T lesion burden and clinical measures rather than to directly compare 1.5T and 3T platforms. Attention was paid to achieving feasible scan time with optimized image quality on both platforms. Because of the potential at 3T to exceed specific absorption rate (SAR) patient safety limitations24 and scanning time considerations, repetition time (TR), echo time (TE), and echo train length varied between the 2 platforms, although voxel size was nearly equivalent. Image analysis was performed using the software package Jim (Version 3.0, Xinapse Systems Ltd.

Inhibition of PI3K/AKT and JNK attenuated

the induction of IL-23 by TCA; whereas, p38 inhibition enhanced TCA-induced IL-23 production. Overall, these studies identified the key signal transduction ZD1839 molecular weight pathways that mediate the interaction between bile acids and the IL-23/IL-17A axis. Pharmacological targeting of these pathways could alleviate hepatic inflammation and injury in patients with cholestatic liver disease. Disclosures: The following people have nothing to disclose: Kate M. O’Brien, Kara Kelly, Bryan Copple Introduction: It is unclear whether liver injury in acute hepatitis E is due to virus-induced cytolysis or the host immune response. We therefore studied host gene expression and enumerated immune cells in liver tissues from fulminant hepatitis E (FHF-E) patients, in comparison with healthy livers and those from fulminant hepatitis B (FHF-B) patients. Methods: Microarray-based expression profiling was done on post-mortem liver tissue this website from 5 FHF-E and 6 FHF-B patients, and normal liver tissue from 6 persons. Differential expression was defined as ≥2.0-fold change with Benjamini-Hochberg corrected p-value below 0.05. CD4+, CD8+ and CD56+ cells were counted using immunohistochemistry.

Results: Compared to normal, the livers from FHF-E and FHF-B showed differential expression of 3377 (up-regulated 1703, down-regulated 1674) and 2572 (up 1164, down 1408) entities, respectively. This included 2142 (up 896, down 1246) entities that were common between the two sets; most of these belonged to metabolic, hemostatic (intrinsic and extrinsic prothrombin activation), and complement (classical, alternative and lectin-induced) pathways. Analysis of 1235 (up 807, down 428) entities with differential expression in FHF-E but not in FHF-B showed activation of several immune response pathways, particularly those involving cytotoxic T cells (Table). CD8+ T cells were increased in both FHF-E (median 53.4 [range 31.2-99.9]) and FHF-B (49.3 [19.3-51]; p=0.005) compared to controls (6.9 [3.1-14.9]). Conclusion: Liver tissue from FHF-E patients

showed increased expression of genes belonging to cytotoxic T cell effector pathways, accompanied by CD8+ T cell Oxymatrine infiltration. This suggests a role for CD8+ T cells in the pathogenesis of hepatitis E. Pathways whose genes were over-represented among entities differentially expressed in fulminant hepatitis E (FHF-E), and in FHF-E but not in fulminant hepatitis B (FHF-B) Disclosures: The following people have nothing to disclose: Anshu Naik, Amit Goel, Vinita Agrawal, Aditya N. Sarangi, Nanda Chhavi, Vineeta Singh, Shahid Jameel, Rakesh Aggarwal 501 CEACAM1 (Carcinoembryonic antigen-related cell adhesion molecule 1) protects from acute immune-mediated liver injury The T cell mitogenic plant lectin concanavalin A (ConA) induces acute immune-mediated liver injury. Hallmarks of liver injury are increased plasma transaminase activities and the release of pro-inflammatory cytokines.

“
“The distribution of suitable rest sites is considered to be a key determinant of spatial patterns in animal activity. However, it is not immediately evident which landscape features satisfy rest site requirements or how these sites are configured within the Metformin solubility dmso home range. We used Global Positioning System (GPS)/accelerometer telemetry to investigate rest site selection at the home-range scale for northern tamanduas Tamandua mexicana on Barro Colorado Island (BCI), Panama.

We developed models specifying each tamandua as the individual experimental unit and averaged coefficients to produce population-level estimates. Tamanduas had on average 17.8 (± 8.1) rest sites within their home range and used 1.36 (± 0.51) on any given day. These rest sites

tended to be located in the core of tamandua home ranges, with active locations associated with the periphery of the home range. Rest sites were positively associated with (1) a high density of Attalea butyracea palm trees; (2) elevation; (3) tall vegetation. There was a slight negative relationship between the distribution of rest sites and slope, and no apparent relationship between rest site selection and relative distance to forest canopy gaps. From focal animal observations, we identified that tamandua rest sites were typically located Napabucasin in trees (90%), with 25% (12 of 49) occurring in palms. We contend that northern tamanduas on BCI selected vegetated arboreal rest sites because of reduced likelihood of detection from terrestrial predators in these sites. Our

models identified considerable individual variation in rest site selection, which suggests that the practice of pooling individuals and fitting models at an aggregate level may be inappropriate for certain types of habitat selection research. “
“We use the term ‘aggressive mimic’ for Olopatadine predators that communicate with their prey by making signals to indirectly manipulate prey behaviour. For understanding why the aggressive mimic’s signals work, it is important to appreciate that these signals interface with the prey’s perceptual system, and that the aggressive mimic can be envisaged as playing mind games with its prey. Examples of aggressive mimicry vary from instances in which specifying a model is straight forward to instances where a concise characterization of the model is difficult. However, the less straightforward examples of aggressive mimicry may be the more interesting examples in the context of animal cognition. In particular, there are spiders that prey on other spiders by entering their prey’s web and making signals. Web invasion brings about especially intimate contact with their prey’s perceptual system because the prey spider’s web is an important component of the prey spider’s sensory apparatus. For the web-invading spider, often there is also a large element of risk when practising aggressive mimicry because the intended prey is also a potential predator.

01). Post-LT AKI by AKIN criteria was numerically higher in the CKD group (48% v 28%, p=0.07), though similar by RIFLE-R (41% v 38%, p=0.76) and RIFLE-I (16% v 14%, p=0.80)

criteria. The 4 year cumulative incidences of CKD and death were 68.5% and 24.9%, respectively. uNGAL 24 hours post-LT was the most predictive time point for CKD (AUC 0.65), with uNGAL>93 ng/ml being highly predictive of CKD (log rank p=0.002, PPV 100%, NPV 36%). The final multivariable model for the prediction of time to CKD included uNGAL at 24 hours (HR1.09 per 100 ng/ml, p=0.03), age at LT (HR 1.41 per decade, p=0.048), HCV (HR 1.86, p=0.04), and BMI (<30 ref, 30≤BMI>35 HR 1.04, p=0.92, 35≤BMI>40 HR 4.76, p=0.007, BMI≥40 HR 1.86, p=0.27). All patients who died post-LT developed EPZ6438 CKD prior to death (p<0.001). 24 hour post-LT uNGAL>30 ng/ml was predictive of death (log rank p=0.05, PPV 32%, NPV 87%). Additional predictors of time to death in multivariable modeling included age at LT (HR 3.02 per decade, p=0.002), HCV (HR 3.0, p=0.048), BMI (<30 ref,

30≤BMI>35 selleck inhibitor HR 6.01, p=0.005, 35≤BMI>40 HR 1.12, p=0.85, BMI≥40 HR 3.18, p=0.33), CIT (HR 1.21 per hour, p=0.002) and EBL (HR 1.15 per liter, p=0.02). Conclusions: uNGAL predicts not only early post-LT AKI, but also the development of long-term CKD, in this cohort with preserved pre-LT kidney function. Given the significant correlation between CKD and death, such early predictors could be used to guide preventative interventions. Disclosures: Elizabeth C. Verna – Advisory Committees or Review Panels: Gilead; Grant/ Research Support: Salix, Merck Robert S. Brown – Advisory Committees or Review Panels: Vital Therapies; Consulting: Genentech, Gilead, Merck, Abbvie, Janssen; Grant/Research

Support: Gilead, Merck, Vertex, AbbVie, Salix, Janssen, Vital Therapies The following people have nothing to disclose: Giuseppe Cullaro, Joseph F. Pisa, Gebhard Wagener BACKGROUND. Declining physical capacity, deconditioning, is thought to cause poor outcomes among patients awaiting liver transplantation. Very little is known about the ability of tests of deconditioning to predict adverse pre-transplant end-points, or whether measured deconditioning has predictive value independent of MELD and Child scores. We hypothesized that measured deconditioning would predict deaths and morbidity expressed as inpatient hospital days Cytidine deaminase caused by the complications of cirrhosis. METHODS. We measured deconditioning in 218 patients evaluated or listed for transplantation using a simple test, dominant hand grip strength, known to predict outcomes in large chronic disease populations. We used Poisson regression stratified by gender to determine whether grip testing was associated with the number of inpatient days between the test date and the end of a 6 month observation period. A multivariable Poisson model was used to test grip strength, MELD and Child scores as covariates against the outcome of inpatient days.

1% in. ≤20 age stage, 61.5% in 20–39 age stage, 40.4% in ≥40 age stage. There were increase about the percentage

of patients with cHBcAg c-nHBcAg expression following the age increase. (4.6%/4.6%; 19.3%/7.7%; 26.9%/20.4%), but there was no significant difference (X2 = 8.94, P > 0.05). Conclusion: The expression of HBcAg for the patients with chronic hepatitis B virus infection was related to the serum HBeAg expression. The histologic grade of hepatitis were Erlotinib in vivo significantly correlated with the subcellular localization of intrahepatic HBcAg. There were different characteristic for the expression of HBcAg in the different age stage, perhaps due to the different natural history stage. Key Word(s): 1. chronic hepatitis B; 2. HBeAg; 3. HBcAg; Presenting Author: NINGNING ZHANG Additional Authors: WEI LU Corresponding Author: NINGNING ZHANG Affiliations:

Tianjin Second People’s Hospital Objective: Introduction: Hepatocellular carcinoma (HCC) is the third most common cause of death worldwide. The risk of developing HCC in patients suffering from cirrhosis is increased in the setting of chronic HCV. Objective: To determine the tumor recurrence, safety, and survival outcomes of HCC patients with chronic hepatitis C (genotype 1) infection after receiving radiofrequency ablation (RFA) and antiviral therapy using peg-alfa interferon and weight based ribavirin. Methods: Using our institution’s database, we identified all patients with chronic Hepatitis C (HCV) genotype 1 and small HCC (less EX 527 price than 3.0 cm) between December 2007 – December 2010. The following data was from extracted; sustained virological rate (SVR), tumor necrosis rate and tumor recurrent rate, and 1-year survival rate. HCC recurrence and monitoring was done using serum a-fetoprotein (AFP) test and radiological findings. Results: During the study period, there were 75 patients (42 males, 33 females, age 43 years (32–54) with HCC (≤3 cm) and HCV (genotype 1). We divided the patients into two

groups: control group (n = 33) received RFA only and treatment group (n = 42) received RFA and peg-alfa interferon with weight based ribavirin. The tumor complete necrosis rate at three months in the control group was 24.24% versus Rx group was 50% (P < 0.05). The one-year viral suppression in the control group was 30.3% versus Rx group 64.28% (P < 0.05). The HCC recurrence rate in the control group was 38.39% versus Rx group 7.1% (P < 0.05). The one-year survival rate was 30.3% in control group versus Rx group 61.9% (P < 0.05). Conclusion: The above results demonstrate potential benefits of adding antiviral therapy and suppressing HCV virus in patients with compensated cirrhosis and small HCC undergoing RFA. Further trials involving larger number of patients are needed to delineate the overall impact of HCV eradication in the patient with compensated cirrhosis and HCC.

Costs of diagnostic support were estimated based on published minimum prices of genotyping, hepatitis C virus antigen tests plus full blood count/clinical chemistry. Results:

Angiogenesis inhibitor Predicted minimum costs for 12-week courses of combination direct-acting antivirals with the most consistent efficacy results were: US$122 per person for sofosbuvir+daclatasvir, US$152 for sofosbuvir+ribavirin, US$192 for sofosbuvir+ledipasvir and US$115 for MK-8742+MK-5172. Diagnostic testing costs were estimated at US$90 for genotyping US$34 for two hepatitis C virus antigen tests and US$22 for two full blood count/clinical chemistry. Conclusions: Minimum costs of treatment and diagnostics to cure hepatitis C virus infection were estimated at US$171-360 per-person without genotyping or US$261-450 per-person with genotyping. These cost estimates assume that existing large-scale treatment programmes can be established. This article is protected by copyright. All rights reserved. “
“Childhood food allergy appears to be on the rise in ‘Westernized’

countries although little is known about whether this phenomenon is also occurring in developing countries.1 The potential allergenicity of cow’s milk protein was first convincingly demonstrated in the 1950s.2 Since then there has been a growing awareness that cow’s milk protein allergy (CMPA) can present in diverse ways. Immunoglobulin E (IgE)-mediated cow’s milk protein allergy is characterized by immediate-onset symptoms (within 1 hour of ingestion) to small volumes (usually less than 10 mL) of cow’s milk that include urticaria, facial angioedema, vomiting or even life-threatening anaphylaxis, whereas mTOR inhibitor non-IgE mediated syndromes are usually characterized by late-onset symptoms (hours to

days after ingestion) to larger volumes of cow’s milk that include vomiting, diarrhea, hematochezia, failure to thrive and iron deficiency anemia. Non-IgE mediated syndromes include cow’s milk protein-induced Metalloexopeptidase enteropathy, proctocolitis and enterocolitis as well as cow’s milk induced gastro-esophageal reflux. Eosinophilic esophagitis may also respond to cow’s milk elimination although a more extensive six-food elimination regime is usually initiated for diet-responsive cases.3 Food-protein induced enterocolitis (FPIES) is most commonly caused by cow’s milk4 and is a curious, recently described syndrome where infants less than 12 months of age typically present with severe but self-limiting vomiting and diarrhea (although 15% present with hypovolemic shock) that occurs almost pathognomically 2–4 h after ingestion of an intermediate volume of milk (for example 20–40 mL). Table 1 outlines recommended formula feeding for the management of CMPA syndromes in infants. As many as 2% of children are believed to develop cow’s milk protein allergy in the first 3 years of life6 of which approximately 75% is attributed to non-IgE mediated allergy. The vast majority of CMPA resolves by age 5 years.

Methods:  Patients aged 18 to 65 years were included in this observational, prospective study if they had evidence of a HCV genotype 1 infection. The serum HCV RNA concentration was determined at baseline and week 12. A

qualitative HCV RNA test was performed at baseline and at weeks 48 and 72. Liver function tests were performed at each study visit. The primary efficacy measure was the sustained virological response in the intention-to-treat population. Logistic regression analyses were also performed to explore predictors of virological response. Results:  A sustained virological response was observed in 100 of the 175 patients (57%). An early virological response and end-of-treatment response were seen in 159 patients Selleckchem Nutlin 3a (91%) Selleckchem JNK inhibitor and 133 patients (76%), respectively. Thirty-seven of the 122 evaluable patients for this outcome (30%) showed

a rapid virological response. A higher viral load was a significant predictor for a lack of rapid virological response and lack of sustained virological response. There were not any unexpected safety or tolerability findings. Conclusions:  Our study suggests that the efficacy of the combination of peginterferon α-2a and ribavirin in patients with HCV genotype 1 infection and normal ALT levels is at least similar to that reported in patients with elevated ALT levels. “
“High levels of dietary saturated fat have been closely associated with the development of hepatic steatosis, but the factors that mediate this process remain elusive. Here, we observed that the level of cell death-inducing DNA fragmentation factor-alpha-like effector a (Cidea) expression was highly correlated with the severity of hepatic steatosis in humans. Overexpression of Cidea in mouse liver resulted in increased hepatic lipid accumulation and the formation of large lipid droplets (LDs). In contrast, mice with a Cidea deficiency had decreased lipid accumulation and alleviated hepatic steatosis when

they received Bupivacaine a high-fat-diet feeding or in ob/ob mice. Furthermore, the knockdown of Cidea in livers of ob/ob mice resulted in significantly reduced hepatic lipid accumulation and smaller LDs. Importantly, we observed that Cidea expression in hepatocytes was specifically induced by saturated fatty acids (FAs), and such induction was reduced when sterol response element-binding protein (SREBP)1c was knocked down. In contrast, the overexpression of SREBP1c restored the saturated FA-induced expression of Cidea. In addition, we observed that the stability of Cidea protein in hepatocytes increased significantly in response to treatment with FAs. Conclusion: Cidea plays critical roles in promoting hepatic lipid accumulation and in the development of hepatic steatosis by acting as a sensor that responds to diets that contain FAs.

Almost all patients with the same mutation had the same response to Pifithrin-�� molecular weight DDAVP or only a minor discordance

in response. Patient’s age, disease severity and genotype all are predictors of response to DDAVP. “
“Congenital factor V (FV) deficiency is an autosomal recessive bleeding disorder associated with mild to severe hemorrhagic symptoms and a prevalence in the general population of 1/1000 000 in the homozygous form. Frequent symptoms are epistaxis and menorrhagia, and postoperative and oral cavity hemorrhages; other less common symptoms include hemarthroses and hematomas. Aside from mutations in the F5 gene, a reduction of the circulating level of FV can also be observed in combined FV and FVIII deficiency (F5F8D), an autosomal recessive bleeding disorder as well. This deficiency, characterized by concomitantly low levels of both FV and FVIII, is associated with a mild to moderate bleeding tendency and it is also estimated to be extremely rare (1/1000 000) in the general population. F5F8D-causing mutations are located in genes encoding proteins involved in the FV and FVIII intracellular transport (MCFD2 and LMAN1). Replacement LY2157299 cell line therapy for FV-deficient patients can only rely on administration of fresh frozen plasma because specific FV concentrates are unavailable and FV is not present in cryoprecipitate

or prothrombin complex concentrates. F5F8D treatment of bleeding episodes requires replacement of FVIII, in addition to that for FV, by FFP and desmopressin or specific FVIII concentrates other than

FFP. “
“Summary.  Treatment studies in haemophilia focus on joint bleeds; however, some 10–25% of bleeds occur in muscles. This review addresses management of muscle haematoma in severe haemophilia, defines gaps in the published evidence, and presents a combined clinician and physiotherapist perspective of treatment modalities. The following grade 2C recommendations were synthesized: (i) Sport and activity should be based on individual factor levels, bleeding history and physical PDK4 characteristics, (ii) Musculoskeletal review aids the management of children and adults, (iii) ‘Time to full recovery’ should be realistic and based on known timelines from the healthy population, (iv) Diagnosis should be carried out by both a clinician and physiotherapist, (v) Severe muscle bleeds should be treated similarly to surgical patients: a 50% trough for 10–14 days followed by high-level prophylaxis, (vi) Protection, rest, ice, compression and elevation should be implemented in the acute stage, and (vii) Physiotherapy and rehabilitation should be divided into: control of haemorrhage (phase 1); restoration of Range of Movement (ROM) and strength (phase 2); functional rehabilitation and return to normal living (phase 3).

Furthermore, ribosomal protein S5 (RPS5) was identified as a direct target of MASM, which stabilized RPS5 in cultured HSCs and in the liver of experimental animals after dimethylnitrosamine (DMN) or bile duct ligation (BDL). Functional studies revealed that RPS5 could prevent HSC activation. RPS5 overexpression in HSCs resulted in Akt dephosphorylation at both Ser473 and

Thr308, and led to subsequent dephosphorylation of GSK3β or P70S6K. Progression of DMN- and BDL-induced hepatic fibrosis was aggravated by Rps5 knockdown and alleviated by RPS5 overexpression, which correlated with the modulation of Akt phosphorylation and HSC number in the fibrotic livers. Moreover, RPS5 was substantially reduced in the transdifferentiated

HSCs, experimental fibrotic livers, and human cirrhosis samples. selleck compound Conclusion: These results demonstrate that RPS5 is implicated in hepatic fibrogenesis and may represent a promising target for potential therapeutic intervention in liver fibrotic diseases. (Hepatology 2014;60:648–660) “
“Biliary strictures can be categorized according to technical factor as anastomotic or nonanastomotic strictures. Biliary anastomotic stricture is a common complication after living-donor liver transplantation, occasionally causing deaths. The two most commonly used methods for biliary anastomosis are duct-to-duct anastomosis and hepaticojejunostomy. Before presenting a description of the latest techniques of duct-to-duct anastomosis and hepaticojejunostomy, this review first relates

the technique of donor right hepatectomy, as click here most biliary complications suffered by recipients of living-donor liver transplantation originate from donor operations. Clomifene Three possible causes of biliary anastomotic stricture, namely impaired blood supply, biliary anomaly, and technical flaw, are then discussed. Lastly, the review focuses on the latest management of biliary anastomotic stricture. Treatment modalities include endoscopic retrograde cholangiography with dilatation, percutaneous transhepatic biliary drainage with dilatation, conversion of duct-to-duct anastomosis to hepaticojejunostomy, and revision hepaticojejunostomy. End-to-side versus side-to-side hepaticojejunostomy is also discussed. Liver transplantation is a life-saving procedure for patients with end-stage liver diseases. As the supply of liver grafts from deceased donors always fall shorts, living-donor liver transplantation (LDLT) has been developed as the alternative to deceased-donor liver transplantation. LDLT was initially limited to pediatric recipients because of restriction of graft size. Later when it was extended to adult patients, still only the left lobe of the liver was used. In order to extend the benefit of LDLT to as many patients as possible, transplantation of the right liver lobe, which is a bigger graft, to an adult was initiated in 1996.

M. Drew et R. Ross, it was possible to identify a 2,3-dimethoxy-5-methyl-6-decaprenyl-1,4-benzoquinone (CoQ10) within these extracts using a matrix-assisted laser desorption ionization (MALDI) curved field reflectron (CFR) mass spectrometer. Detected mass fragments showed a high significance and could be structurally interpreted for both commercialized standard and CoQ10 isolated from P. purpureum. “
“Knowledge concerning the ability of microalgae to produce metabolites of interest such as toxins or high-value secondary metabolites requires exhaustive details to be supplied on how the research was conducted. These should include the microalgal species and strain characterization, the culture conditions, the cell density, and

physiological state at the time of harvesting, the harvesting method, the sample pre-treatment protocol, and the subsequent instrumental analytical separation/detection system. In this comment, we discuss issues that affect algal research from an BI6727 analytical chemistry perspective, particularly (i) the need to specify detection capabilities

of the entire method (i.e., limits of detection or threshold detection levels), which we illustrate in relation to classification of a species or strain as being “toxin producing” or “non-toxin producing”; and (ii) the requirements that have to be satisfied to confirm a microalgal species (new or not) as a producer of a particular chemical of interest for phycologists, which again we illustrate in relation to toxins. A successful collaboration among phycologists and analytical chemists will only be achieved as a result of a synergistic collaboration between the two disciplines, with a reciprocal https://www.selleckchem.com/products/gdc-0068.html understanding at least at a background level. “
“Increasing anthropogenic carbon dioxide Monoiodotyrosine is causing changes to ocean chemistry, which will continue in a predictable manner. Dissolution of additional atmospheric carbon dioxide leads to increased concentrations of dissolved carbon dioxide and bicarbonate and decreased pH in ocean water. The concomitant effects on phytoplankton

ecophysiology, leading potentially to changes in community structure, are now a focus of concern. Therefore, we grew the coccolithophore Emiliania huxleyi (Lohmann) W. W. Hay et H. Mohler and the diatom strains Thalassiosira pseudonana (Hust.) Hasle et Heimdal CCMP 1014 and T. pseudonana CCMP 1335 under low light in turbidostat photobioreactors bubbled with air containing 390 ppmv or 750 ppmv CO2. Increased pCO2 led to increased growth rates in all three strains. In addition, protein levels of RUBISCO increased in the coastal strains of both species, showing a larger capacity for CO2 assimilation at 750 ppmv CO2. With increased pCO2, both T. pseudonana strains displayed an increased susceptibility to PSII photoinactivation and, to compensate, an augmented capacity for PSII repair. Consequently, the cost of maintaining PSII function for the diatoms increased at increased pCO2. In E.