Enhanced Stat3 and impaired Stat1 phosphorylation are also observed in tumor-exposed SIRPα-KD Mψ. Adoptive transfer with SIRPα-KD Mψ accelerates mouse

hepatoma cells growth in vivo by remolding the inflammatory microenvironment and promoting angiogenesis. SIRPα accomplishes this partly through its sequestration of the signal transducer Src homology 2-containing phosphotyrosine phosphatase (SHP2) from IκB kinase β (IKKβ) and PI3K regulatory subunit p85 (PI3Kp85). Conclusion: These findings suggest that SIRPα functions as an important modulator of tumor-polarized Mψ in hepatoma, and the reduction of SIRPα is a novel strategy used by tumor cells to benefit their behavior. Therefore, SIRPα could be utilized as a potential

target for HCC therapy. (Hepatology 2013;58:680–691) Hepatocellular carcinoma (HCC) is the fifth most common Selleckchem ICG-001 cancer worldwide, and the Small molecule library solubility dmso second leading cause of cancer death in China. HCC is usually present in inflamed fibrotic and/or cirrhotic liver with extensive leukocyte infiltration. Thus, the immune status at different tumor sites is tightly associated with the biological behavior of HCC.[1] Macrophages (Mψ) are the most prominent component of the infiltrated leukocytes in tumors. These cells are derived from circulating monocytes and recruited into tumor by cytokines and chemokines, such as CSF1 and MCP-1.[2, 3] Mψ have remarkable plasticity and can acquire special phenotypic characteristics with diverse functions in response to environmental signals.[4, 5] Tumor-associated Mψ (TAMs), closely associated with M2, can suppress antitumor immunity and promote tumor progression.[6] Evidence from clinical and epidemiological studies have shown a strong association between TAMs density and poor prognosis in several types of cancer, including medchemexpress HCC.[7] However, some studies demonstrated that Mψ in tumor stroma were activated

and displayed a human leukocyte antigen (HLA)-DRhigh phenotype. These cells can also facilitate tumor progression.[8-10] Taken together, these results indicate that tumors can take advantage of either immune suppression or activation status of Mψ at distinct tumor sites to promote tumor progression. Currently, the precise mechanism of how tumors educate Mψ to accomplish specific tasks has not been fully elucidated. Signal regulatory protein α (SIRPα) is a cell-surface protein mainly expressed on myeloid cells, including Mψ and dendritic cells.[11, 12] The extracellular region of SIRPα is heavily glycosylated and comprised of three immunoglobin superfamily (IgSF) domains, which are similar to TCR and BCR, suggesting that SIRPα may have a pivotal role in immune regulation.

Enhanced Stat3 and impaired Stat1 phosphorylation are also observed in tumor-exposed SIRPα-KD Mψ. Adoptive transfer with SIRPα-KD Mψ accelerates mouse

hepatoma cells growth in vivo by remolding the inflammatory microenvironment and promoting angiogenesis. SIRPα accomplishes this partly through its sequestration of the signal transducer Src homology 2-containing phosphotyrosine phosphatase (SHP2) from IκB kinase β (IKKβ) and PI3K regulatory subunit p85 (PI3Kp85). Conclusion: These findings suggest that SIRPα functions as an important modulator of tumor-polarized Mψ in hepatoma, and the reduction of SIRPα is a novel strategy used by tumor cells to benefit their behavior. Therefore, SIRPα could be utilized as a potential

target for HCC therapy. (Hepatology 2013;58:680–691) Hepatocellular carcinoma (HCC) is the fifth most common check details cancer worldwide, and the this website second leading cause of cancer death in China. HCC is usually present in inflamed fibrotic and/or cirrhotic liver with extensive leukocyte infiltration. Thus, the immune status at different tumor sites is tightly associated with the biological behavior of HCC.[1] Macrophages (Mψ) are the most prominent component of the infiltrated leukocytes in tumors. These cells are derived from circulating monocytes and recruited into tumor by cytokines and chemokines, such as CSF1 and MCP-1.[2, 3] Mψ have remarkable plasticity and can acquire special phenotypic characteristics with diverse functions in response to environmental signals.[4, 5] Tumor-associated Mψ (TAMs), closely associated with M2, can suppress antitumor immunity and promote tumor progression.[6] Evidence from clinical and epidemiological studies have shown a strong association between TAMs density and poor prognosis in several types of cancer, including MCE HCC.[7] However, some studies demonstrated that Mψ in tumor stroma were activated

and displayed a human leukocyte antigen (HLA)-DRhigh phenotype. These cells can also facilitate tumor progression.[8-10] Taken together, these results indicate that tumors can take advantage of either immune suppression or activation status of Mψ at distinct tumor sites to promote tumor progression. Currently, the precise mechanism of how tumors educate Mψ to accomplish specific tasks has not been fully elucidated. Signal regulatory protein α (SIRPα) is a cell-surface protein mainly expressed on myeloid cells, including Mψ and dendritic cells.[11, 12] The extracellular region of SIRPα is heavily glycosylated and comprised of three immunoglobin superfamily (IgSF) domains, which are similar to TCR and BCR, suggesting that SIRPα may have a pivotal role in immune regulation.

6–2.7% of IBD patients in some series1–3. Although the underlying

pathogenesis remains unclear, a possible hypothesis involves the uncontrolled production of interferon-alpha (IFNα) as a result of TNF blockade. IFNα is an important mediator produced by dermal plasmocytoid dendritic cells in the early phase of induction of psoriasis4. Aim: To review all cases of psoriatic and psoriatiform dermatological reactions induced by anti-TNF agents in patients with IBD at a tertiary center in Australia. Method: We retrospectively identified all cases Selleck Rucaparib of anti-TNF-induced psoriasis or psoriasiform manifestations in IBD patients receiving treatment at Canberra Hospital. Results: A total of 10 of 270 IBD patients treated with anti-TNF therapy developed drug-induced psoriatic or psoriasiform-like reactions: 6 female, 4 male; average age of IBD diagnosis was 21 (13–28) years; average age of skin reaction was 33.2 (23–48) years. Five patients were treated with infliximab and five with adalimumab; 9 had Crohn’s disease (CD) and 1 had ulcerative selleck chemical colitis (UC). Three were current smokers and 2 were ex-smokers. Three patients had concomitant therapy at time of the reaction: one on prednisolone, one on mesalazine and one subject on both mesalazine and azathioprine. The time from initiation of anti-TNF agent to onset of rash was on average 9.1 (2–25)

months. The most frequent distributions were the scalp (7) and extremities (6). Five patients had a personal history of atopy and 3 had a familial history of psoriasis. Three patients MCE discontinued anti-TNF treatment (2 because of the skin reaction and 1 due to autoimmune hepatitis), and the remaining

7 were maintained on anti-TNF therapy and managed with topical therapy. All 10 patients were reviewed by a dermatologist. Conclusions: Paradoxical psoriatic lesions induced by anti-TNF therapy in IBD is not uncommon. In this case series, there was no significant gender difference and the time to onset of rash was variable. The psoriatic manifestation was greater in CD than UC. The most frequent distributions were the scalp and extremities. Topical treatment of the lesions was effective in the majority of patients, allowing continued use of these biologicals and the withdrawal of these agents is seldom needed. 1. Afzali A, Wheat CL, Hu JK, Olerud JE, Lee SD. The association of psoriasiform rash with anti-tumor necrosis factor (anti-TNF) therapy in inflammatory bowel disease: A single academic center case series. J Crohns Colitis. 2014 Jun 1;8(6):480–488. 2. Rahier JF, Buche S, Peyrin-Biroulet L, Bouhnik Y, Duclos B, Louis E, et al. Severe skin lesions cause patients with inflammatory bowel disease to discontinue anti-tumor necrosis factor therapy. Clin Gastroenterol Hepatol. 2010 Dec;8(12):1048–1055. 3. Guerra I, Algaba A, Perez-Calle JL, Chaparro M, Marin-Jimenez I, Garcia-Castellanos R, et al.

6–2.7% of IBD patients in some series1–3. Although the underlying

pathogenesis remains unclear, a possible hypothesis involves the uncontrolled production of interferon-alpha (IFNα) as a result of TNF blockade. IFNα is an important mediator produced by dermal plasmocytoid dendritic cells in the early phase of induction of psoriasis4. Aim: To review all cases of psoriatic and psoriatiform dermatological reactions induced by anti-TNF agents in patients with IBD at a tertiary center in Australia. Method: We retrospectively identified all cases Kinase Inhibitor Library cost of anti-TNF-induced psoriasis or psoriasiform manifestations in IBD patients receiving treatment at Canberra Hospital. Results: A total of 10 of 270 IBD patients treated with anti-TNF therapy developed drug-induced psoriatic or psoriasiform-like reactions: 6 female, 4 male; average age of IBD diagnosis was 21 (13–28) years; average age of skin reaction was 33.2 (23–48) years. Five patients were treated with infliximab and five with adalimumab; 9 had Crohn’s disease (CD) and 1 had ulcerative CP-690550 cost colitis (UC). Three were current smokers and 2 were ex-smokers. Three patients had concomitant therapy at time of the reaction: one on prednisolone, one on mesalazine and one subject on both mesalazine and azathioprine. The time from initiation of anti-TNF agent to onset of rash was on average 9.1 (2–25)

months. The most frequent distributions were the scalp (7) and extremities (6). Five patients had a personal history of atopy and 3 had a familial history of psoriasis. Three patients 上海皓元医药股份有限公司 discontinued anti-TNF treatment (2 because of the skin reaction and 1 due to autoimmune hepatitis), and the remaining

7 were maintained on anti-TNF therapy and managed with topical therapy. All 10 patients were reviewed by a dermatologist. Conclusions: Paradoxical psoriatic lesions induced by anti-TNF therapy in IBD is not uncommon. In this case series, there was no significant gender difference and the time to onset of rash was variable. The psoriatic manifestation was greater in CD than UC. The most frequent distributions were the scalp and extremities. Topical treatment of the lesions was effective in the majority of patients, allowing continued use of these biologicals and the withdrawal of these agents is seldom needed. 1. Afzali A, Wheat CL, Hu JK, Olerud JE, Lee SD. The association of psoriasiform rash with anti-tumor necrosis factor (anti-TNF) therapy in inflammatory bowel disease: A single academic center case series. J Crohns Colitis. 2014 Jun 1;8(6):480–488. 2. Rahier JF, Buche S, Peyrin-Biroulet L, Bouhnik Y, Duclos B, Louis E, et al. Severe skin lesions cause patients with inflammatory bowel disease to discontinue anti-tumor necrosis factor therapy. Clin Gastroenterol Hepatol. 2010 Dec;8(12):1048–1055. 3. Guerra I, Algaba A, Perez-Calle JL, Chaparro M, Marin-Jimenez I, Garcia-Castellanos R, et al.

6–2.7% of IBD patients in some series1–3. Although the underlying

pathogenesis remains unclear, a possible hypothesis involves the uncontrolled production of interferon-alpha (IFNα) as a result of TNF blockade. IFNα is an important mediator produced by dermal plasmocytoid dendritic cells in the early phase of induction of psoriasis4. Aim: To review all cases of psoriatic and psoriatiform dermatological reactions induced by anti-TNF agents in patients with IBD at a tertiary center in Australia. Method: We retrospectively identified all cases selleck inhibitor of anti-TNF-induced psoriasis or psoriasiform manifestations in IBD patients receiving treatment at Canberra Hospital. Results: A total of 10 of 270 IBD patients treated with anti-TNF therapy developed drug-induced psoriatic or psoriasiform-like reactions: 6 female, 4 male; average age of IBD diagnosis was 21 (13–28) years; average age of skin reaction was 33.2 (23–48) years. Five patients were treated with infliximab and five with adalimumab; 9 had Crohn’s disease (CD) and 1 had ulcerative PD98059 cell line colitis (UC). Three were current smokers and 2 were ex-smokers. Three patients had concomitant therapy at time of the reaction: one on prednisolone, one on mesalazine and one subject on both mesalazine and azathioprine. The time from initiation of anti-TNF agent to onset of rash was on average 9.1 (2–25)

months. The most frequent distributions were the scalp (7) and extremities (6). Five patients had a personal history of atopy and 3 had a familial history of psoriasis. Three patients 上海皓元 discontinued anti-TNF treatment (2 because of the skin reaction and 1 due to autoimmune hepatitis), and the remaining

7 were maintained on anti-TNF therapy and managed with topical therapy. All 10 patients were reviewed by a dermatologist. Conclusions: Paradoxical psoriatic lesions induced by anti-TNF therapy in IBD is not uncommon. In this case series, there was no significant gender difference and the time to onset of rash was variable. The psoriatic manifestation was greater in CD than UC. The most frequent distributions were the scalp and extremities. Topical treatment of the lesions was effective in the majority of patients, allowing continued use of these biologicals and the withdrawal of these agents is seldom needed. 1. Afzali A, Wheat CL, Hu JK, Olerud JE, Lee SD. The association of psoriasiform rash with anti-tumor necrosis factor (anti-TNF) therapy in inflammatory bowel disease: A single academic center case series. J Crohns Colitis. 2014 Jun 1;8(6):480–488. 2. Rahier JF, Buche S, Peyrin-Biroulet L, Bouhnik Y, Duclos B, Louis E, et al. Severe skin lesions cause patients with inflammatory bowel disease to discontinue anti-tumor necrosis factor therapy. Clin Gastroenterol Hepatol. 2010 Dec;8(12):1048–1055. 3. Guerra I, Algaba A, Perez-Calle JL, Chaparro M, Marin-Jimenez I, Garcia-Castellanos R, et al.

Guidelines on how to assay new factor concentrates, and which PK parameters should be measured, are needed. Concerns were raised regarding the possibility of breakthrough bleeding, and current thinking on how to prevent breakthrough bleeding may no longer be appropriate. Finally, as treatment adherence may be more important to ensure that a therapeutic level of a new coagulation factor concentrate is maintained, behavioural techniques could be implemented to help to improve treatment adherence. “
“Summary.  Imaging

is an essential tool for evaluation Lenvatinib purchase and monitoring of haemophilic arthropathy. Ultrasonography is increasingly used for joint assessment, due to its great sensitivity for soft tissue and relatively low cost. To assess the joint status and the role of ultrasonography in routine diagnosis and monitoring of joint disease in cohort haemophilic patients. Findings of patients with haemophilia, selleckchem who routinely underwent ultrasonography were retrospectively evaluated to assess their joint status and the role of ultrasonography in routine diagnosis and monitoring of joint disease. Out of 325 joints examined (115 ankles,

210 knees), ultrasonography identified damages in 50% of ankles and 33% of knees in overall 111 patients, aged 7–80 years (median = 29 years). Synovial hypertrophy and cartilage abnormalities were the most frequent observations (88% and 76% in affected knees, respectively). Pristine joints were more frequently found in patients on primary prophylaxis, young age or no bleeding in the year prior to examination. Furthermore, no concordance was found between presence of joint changes at

ultrasonography, and clinical joint status. Ultrasonography was shown to be able to detect joint damage involving soft tissues and bone surface. Its use might allow frequent monitoring of patients with haemophilia and early detection of arthropathy. For 上海皓元 these reasons it might represent a valid tool in the routine management of haemophilia. “
“Summary.  ‘History can change blood. And blood can change the course of history’. Haemophilia is an illustration of this, as this congenital hereditary coagulation disorder, passed through the majority of royal European families at the beginning of the 20th century by Queen Victoria of England and Empress of the Indies, had indisputable political consequences, which led to one of the most defining moments of contemporary history: the Bolshevik Revolution. Today, none of Queen Victoria’s living descendents carry haemophilia. Because of this, the characterization of haemophilia (deficit of either factor VIII or XI) and the identification of the causal mutation are rendered impossible. In 1991, a tomb containing the remains of Czar Nicolas II’s entire family was discovered. A second tomb was discovered in 2007, allowing Russian and American scientists to fill in this gap in medical history.

Guidelines on how to assay new factor concentrates, and which PK parameters should be measured, are needed. Concerns were raised regarding the possibility of breakthrough bleeding, and current thinking on how to prevent breakthrough bleeding may no longer be appropriate. Finally, as treatment adherence may be more important to ensure that a therapeutic level of a new coagulation factor concentrate is maintained, behavioural techniques could be implemented to help to improve treatment adherence. “
“Summary.  Imaging

is an essential tool for evaluation ABT-263 clinical trial and monitoring of haemophilic arthropathy. Ultrasonography is increasingly used for joint assessment, due to its great sensitivity for soft tissue and relatively low cost. To assess the joint status and the role of ultrasonography in routine diagnosis and monitoring of joint disease in cohort haemophilic patients. Findings of patients with haemophilia, Selleck Caspase inhibitor who routinely underwent ultrasonography were retrospectively evaluated to assess their joint status and the role of ultrasonography in routine diagnosis and monitoring of joint disease. Out of 325 joints examined (115 ankles,

210 knees), ultrasonography identified damages in 50% of ankles and 33% of knees in overall 111 patients, aged 7–80 years (median = 29 years). Synovial hypertrophy and cartilage abnormalities were the most frequent observations (88% and 76% in affected knees, respectively). Pristine joints were more frequently found in patients on primary prophylaxis, young age or no bleeding in the year prior to examination. Furthermore, no concordance was found between presence of joint changes at

ultrasonography, and clinical joint status. Ultrasonography was shown to be able to detect joint damage involving soft tissues and bone surface. Its use might allow frequent monitoring of patients with haemophilia and early detection of arthropathy. For MCE these reasons it might represent a valid tool in the routine management of haemophilia. “
“Summary.  ‘History can change blood. And blood can change the course of history’. Haemophilia is an illustration of this, as this congenital hereditary coagulation disorder, passed through the majority of royal European families at the beginning of the 20th century by Queen Victoria of England and Empress of the Indies, had indisputable political consequences, which led to one of the most defining moments of contemporary history: the Bolshevik Revolution. Today, none of Queen Victoria’s living descendents carry haemophilia. Because of this, the characterization of haemophilia (deficit of either factor VIII or XI) and the identification of the causal mutation are rendered impossible. In 1991, a tomb containing the remains of Czar Nicolas II’s entire family was discovered. A second tomb was discovered in 2007, allowing Russian and American scientists to fill in this gap in medical history.

Because of the large proportion of Medicare patients that enter the program in advanced stages of disease, treatment prior to Medicare entry is likely to be more effective in mitigating the health consequences of HCV. Disclosures: David B. Rein – Grant/Research Support: Gilead GSK-3 beta pathway Sciences, Inc. The following people have nothing to disclose: John S. Wittenborn, Danielle Liffmann, Joshua M. Borton Background: Several combinations of Direct Acting Antivirals (DAAs) can cure Hepatitis C (HCV) in the majority of treat-ment-naïve patients, in a range of genotypes. Mass treatment programmes to cure HCV in developing countries are only feasible if the costs of treatment and monitoring are very low.

This analysis aimed to estimate minimum costs of DAA treatment and associated diagnostic monitoring. Methods: Clinical trials of HCV DAAs were reviewed to identify combinations with consistently high rates of Sustained Virological Response (SVR) in different genotypes. For each DAA, molecular structures, doses, treatment duration and components of retro-synthesis were used to estimate costs of mass production. Manufacturing

costs per gram of DAA were projected as formulated product cost, based upon treating at least 5 million patients/year (to arrive at volume demand) and a 40% margin for formulation. Costs of diagnostic support were estimated based on published developing country prices of genotyping, HCV antigen tests (to confirm infection pre-treatment and identify relapse/re-infection post-treatment), BYL719 solubility dmso plus full blood count/clinical chemistry.

上海皓元 Results: Predicted minimum costs for 12-week courses of HCV DAAs (patent expiry dates) were: US$50 for ribavirin 1200mg/day (generic), US$20 for daclatasvir 60mg/day (2027), US$102 for sofosbuvir 400mg/day (2029), US$90 for ledipasvir 90mg/day (2030), US$44 for MK-8742 (2028), and US$71 for MK-5172 (2030). Predicted minimum costs for 12 week courses of combination DAAs with the most consistent efficacy results were: US$122 per person for sofosbuvir+da-clatasvir, US$152 for sofosbuvir+ribavirin (US$304 for 24 weeks), US$192 for sofosbuvir+ledipasvir and US$115 for MK-8742+MK-5172. Diagnostic testing costs were estimated at US$90 for genotyping (if treatment not pan-genotypic), US$34 for two HCV antigen tests (lower detection limit 2000 IU/mL) and US$22 for two full blood count, ALT and creati-nine tests (before and during treatment). Conclusions: Minimum costs of treatment and diagnostics to cure HCV were estimated at US$171-360 per-person, without genotyping or US$261-450 per-person with genotyping. These cost estimates assume that similar large-scale treatment programmes for HIV/AIDS can be established for HCV. Treatments with proven pan-ge-notypic activity will be required to avoid expensive pre-treat-ment genotyping. Further reductions in price could be achieved through shorter durations of treatment, if efficacy is shown in future trials. Disclosures: Andrew M.

Because of the large proportion of Medicare patients that enter the program in advanced stages of disease, treatment prior to Medicare entry is likely to be more effective in mitigating the health consequences of HCV. Disclosures: David B. Rein – Grant/Research Support: Gilead click here Sciences, Inc. The following people have nothing to disclose: John S. Wittenborn, Danielle Liffmann, Joshua M. Borton Background: Several combinations of Direct Acting Antivirals (DAAs) can cure Hepatitis C (HCV) in the majority of treat-ment-naïve patients, in a range of genotypes. Mass treatment programmes to cure HCV in developing countries are only feasible if the costs of treatment and monitoring are very low.

This analysis aimed to estimate minimum costs of DAA treatment and associated diagnostic monitoring. Methods: Clinical trials of HCV DAAs were reviewed to identify combinations with consistently high rates of Sustained Virological Response (SVR) in different genotypes. For each DAA, molecular structures, doses, treatment duration and components of retro-synthesis were used to estimate costs of mass production. Manufacturing

costs per gram of DAA were projected as formulated product cost, based upon treating at least 5 million patients/year (to arrive at volume demand) and a 40% margin for formulation. Costs of diagnostic support were estimated based on published developing country prices of genotyping, HCV antigen tests (to confirm infection pre-treatment and identify relapse/re-infection post-treatment), Rucaparib clinical trial plus full blood count/clinical chemistry.

上海皓元 Results: Predicted minimum costs for 12-week courses of HCV DAAs (patent expiry dates) were: US$50 for ribavirin 1200mg/day (generic), US$20 for daclatasvir 60mg/day (2027), US$102 for sofosbuvir 400mg/day (2029), US$90 for ledipasvir 90mg/day (2030), US$44 for MK-8742 (2028), and US$71 for MK-5172 (2030). Predicted minimum costs for 12 week courses of combination DAAs with the most consistent efficacy results were: US$122 per person for sofosbuvir+da-clatasvir, US$152 for sofosbuvir+ribavirin (US$304 for 24 weeks), US$192 for sofosbuvir+ledipasvir and US$115 for MK-8742+MK-5172. Diagnostic testing costs were estimated at US$90 for genotyping (if treatment not pan-genotypic), US$34 for two HCV antigen tests (lower detection limit 2000 IU/mL) and US$22 for two full blood count, ALT and creati-nine tests (before and during treatment). Conclusions: Minimum costs of treatment and diagnostics to cure HCV were estimated at US$171-360 per-person, without genotyping or US$261-450 per-person with genotyping. These cost estimates assume that similar large-scale treatment programmes for HIV/AIDS can be established for HCV. Treatments with proven pan-ge-notypic activity will be required to avoid expensive pre-treat-ment genotyping. Further reductions in price could be achieved through shorter durations of treatment, if efficacy is shown in future trials. Disclosures: Andrew M.

Flasks were then separated and one of each acclimated as above to high light and low light for 3 d before exposure to the light and dark treatments, respectively. Esoptrodinium and C. ovata prey cells were dispensed into triplicate 25 cm2 flasks at a 1:200 predator:prey ratio with each replicate receiving 20 mL of early stationary phase C. ovata culture (~150,000 cells · mL−1) INCB024360 cell line and 5 mL of fresh modified Bold basal medium. Control replicate flasks contained 20 mL of C. ovata, a treatment-equivalent volume of sterile-filtered

Esoptrodinium culture, and 5 mL of modified Bold basal medium. Light treatment replicates were incubated at 45 μmol photons · m−2 · s−1 illumination, and dark treatment replicates were Selleckchem MG132 incubated in a light-proof box in the same location. Treatments were sampled initially and daily thereafter until Esoptrodinium growth ceased (dark treatments were sampled in a darkened room to minimize light exposure). Sampling, fixation, and analysis of experimental

replicates were conducted as above. To minimize potentially confounding effects of dark treatment on microalgal prey vitality/survival in batch culture, and determine if Esoptrodinium could grow in the absence of light when provided fresh prey cells daily, a semicontinuous culture experiment was conducted following methods modified from Kim et al. (2008). Isolates UNCCP, RP, and HP were grown as above, then inoculated into triplicate light versus darkness treatment flasks at an initial cell density of ~1.0 × 103 cells · mL−1 in 6 mL of fresh, early stationary phase C. ovata prey culture (ca. 1:200 predator:prey ratio).

Light and dark treatments were conducted under conditions identical to the batch culture experiment (above). Treatments were sampled and fixed for Esoptrodinium cell enumeration as above initially and then once per day for 10 d. Cell abundances estimated daily from light treatment replicates of each strain were referenced to dilute all treatments each day back to the initial (time 0) Esoptrodinium cell densities by discarding culture MCE volume and replacing it with an equivalent volume of fresh C. ovata culture grown in light. In this fashion, Esoptrodinium cells in both treatments (light and darkness) were exposed over the course of the experiment to “saturating” prey abundances (Li et al. 1999) consisting of fresh prey cells taken daily from the same stock culture grown in light. To determine if feeding by Esoptrodinium was affected by darkness, ≥50 randomly selected fixed cells from each treatment replicate were examined on days 2, 5, and 8 by LM (400×) for possession of one or more prey-replete food vacuole(s).