Rapid Shutdown Research Articles

First demonstration of rapid shutdown using neon shattered pellet injection for thermal quench mitigation on DIII-D

Shattered pellet injection (SPI) is one of the prime candidates for the ITER disruption mitigation system because of its deeper penetration and larger particle flux than massive gas injection (MGI) (Taylor et al 1999 Phys. Plasmas 6 1872) using deuterium (Commaux et al 2010 Nucl. Fusion 50 112001, Combs et al 2010 IEEE Trans. Plasma Sci. 38 400, Baylor et al 2009 Nucl. Fusion 49 085013). The ITER disruption mitigation system will likely use mostly high Z species such as neon because of more effective thermal mitigation and pumping constraints on the maximum amount of deuterium or helium that could be injected. An upgrade of the SPI on DIII-D enables ITER relevant injection characteristics in terms of quantities and gas species. This upgraded SPI system was used on DIII-D for the first time in 2014 for a direct comparison with MGI using identical quantities of neon.This comparison enabled the measurements of density perturbations during the thermal quench (TQ) and radiated power and heat loads to the divertor. It showed that SPI using similar quantities of neon provided a faster and stronger density perturbation and neon assimilation, which resulted in a lower conducted energy to the divertor and a faster TQ onset. Radiated power data analysis shows that this was probably due to the much deeper penetration of the neon in the plasma inducing a higher core radiation than in the MGI case. This experiment shows also that the MHD activity during an SPI shutdown (especially during the TQ) is quite different compared to MGI. This favorable TQ energy dissipation was obtained while keeping the current quench (CQ) duration within acceptable limits when scaled to ITER.

Biphasic modulation of Wnt signaling supports efficient foregut endoderm formation from human pluripotent stem cells.

Pluripotent stem cells (embryonic stem cells and induced pluripotent stem cells) are of great promise in regenerative medicine, including molecular studies of disease mechanisms, if the affected cell type can be authentically generated during in vitro differentiation. Most existing protocols aim to mimic embryonic development steps by the supplementation of specific cytokines and small molecules, but the involved signaling pathways need further exploration. In this study, we investigated enhanced initial activation of Wnt signaling for definitive endoderm formation and subsequent rapid shutdown of Wnt signaling for proper foregut endoderm specification using 3 μM CHIR99021 and 0.5 μg/mL of secreted frizzled-related protein 5 (sFRP-5) for biphasic modulation of the Wnt pathway. The definitive endoderm and foregut endoderm differentiation capabilities of Wnt pathway-modulated cells were determined based on the expression levels of the endodermal transcription factors SOX17 and FOXA2 and those of the transcription activator GATA4 and the α-fetoprotein (AFP) gene, respectively. Furthermore, the resulting biphasic Wnt pathway modulation was investigated at the protein level by analyzing phosphorylation of glycogen synthase kinase 3 beta (GSK3β) and β-catenin. Finally, Wnt target gene expression was determined using an improved lentiviral reporter construct that enabled robust T-cell transcription factor 4 (TCF4)/lymphoid enhancer-binding factor 1 (LEF1)-mediated luciferase expression in differentiating pluripotent stem cells. In conclusion, we demonstrated robust, homogeneous, and efficient derivation of foregut endodermal cells by inducing a biphasic modulation of the Wnt signaling pathway.

Tumor resistance to vascular disrupting agents: mechanisms, imaging, and solutions.

The emergence of vascular disrupting agents (VDAs) is a significant advance in the treatment of solid tumors. VDAs induce rapid and selective shutdown of tumor blood flow resulting in massive necrosis. However, a viable marginal tumor rim always remains after VDA treatment and is a major cause of recurrence. In this review, we discuss the mechanisms involved in the resistance of solid tumors to VDAs. Hypoxia, tumor-associated macrophages, and bone marrow-derived circulating endothelial progenitor cells all may contribute to resistance. Resistance can be monitored using magnetic resonance imaging markers. The various solutions proposed to manage tumor resistance to VDAs emphasize combining these agents with other approaches including antiangiogenic agents, chemotherapy, radiotherapy, radioimmunotherapy, and sequential dual-targeting internal radiotherapy.

Disruption Mitigation System Developments and Design for ITER

A disruption mitigation system (DMS) is under design for ITER to inject sufficient material deeply into the plasma for rapid plasma thermal shutdown and collisional suppression of any resulting runaway electrons. Progress on the development and design of both a shattered pellet injector (SPI) that produces large solid cryogenic pellets to provide reliable deep penetration of material and a fast opening high flow rate gas valve for massive gas injection (MGI) is presented. Cryogenic pellets of deuterium and neon up to 25 mm in size have been formed and accelerated with a prototype injector and a full scale prototype MGI valve is now in testing. Implications of the design with respect to response time and reliability at the proposed injector locations on ITER are discussed.

Abstract 1812: Ultrasound-stimulated microbubble based biomechanical enhancement of radiation cell death: Role of acid sphingomyelinase and ceramide

Abstract We have recently demonstrated that mechanical perturbation of endothelial cells from ultrasound-stimulated microbubbles (USMB) results in enhanced tumour radiosensitivity. When exposed to high-power ultrasound, microbubbles release energy in the form of local mechanical forces on the membranes of surrounding endothelial cells. Upon irradiation, rapid vascular shutdown occurs followed by extensive secondary tumour cell death. Our hypothesis is that USMB-based endothelial membrane perturbations produce ceramide via a sphingomyelinase (ASMase) pathway, and act synergistically with radiation to enhance overall tumour response. Here we investigate the role of the SMase-ceramide pathway on USMB-based endothelial radiosensitization. Experiments were carried out in wild type (C57BL/6) and ASMase knockout mice, implanted with a fibrosarcoma line (MCA-129). Animals were treated with radiation doses varying from 0-8 Gy alone, or in combination with USMB. In addition, we pre-treated a subset of animals with sphingosine-1-phosphate (S1P). Treatments with USMB consisted of a 16-cycle tone burst at a 500 kHz center frequency and 570 kPa using a 2.86 cm element diameter ultrasound transducer. The total insonification time was 750 ms over 5 minutes. Microbubbles (Lantheus Medical) were injected through the tail-vein resulting in a blood volume concentration of 1% or 3% (v/v). Treatment response was assessed with Doppler ultrasound acquired at 3, 24 and 72 hrs using a VEVO770 preclinical ultrasound system. The vascularity index (VI) was used to quantify power Doppler data. Staining using ISEL, ceramide and CD31 immunohistochemistry of tumour sections was used to complement ultrasound images, and to confirm results. Results suggest a link between USMB-based radiosensitization and ASMase. We observed an average decrease of 30% in the VI by 3 hrs in wild type tumours receiving 8 Gy radiation alone. In contrast, those receiving 8 Gy and USMB resulted in a VI decrease of up to 50%. Similarly, while 2 Gy alone induced minimal effects on the tumour vasculature, combining it with USMB resulted in up to 40% decrease in the VI by 24 hrs. Vascular effects were significant (p < 0.05) and sustained for up to 72 hrs after combined treatments. These resulted in significant cell death. In contrast to wild type animals, ASMase knockout mice, or wild-type mice receiving S1P, were found to be generally resistant to the anti-vascular effects of radiation and USMB. We noted minimal cell death and no vascular shutdown following any of the treatments in those experimental groups. Overall conclusions drawn from this work point to a mechanotransduction-like effect that results in endothelial radiosensitization. Citation Format: Gregory Jan Czarnota, Ahmed El Kaffas, Anoja Giles, Azza Al Mahrouki, Amr Hashim. Ultrasound-stimulated microbubble based biomechanical enhancement of radiation cell death: Role of acid sphingomyelinase and ceramide. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1812. doi:10.1158/1538-7445.AM2015-1812

Abstract 1664: New moieties mimicking the trimethoxyphenyl (ring A) of combretastatin A-4: Synthesis and biological evaluation

Abstract Combretastatin A-4 (CA-4), its phosphate disodium (CA-4P) and serine hydrochloride salts (AVE8062) are part of a new class of anticancer agent named vascular disrupting agent (VDA). In addition to act as potent antimicrotubule agents in cancer cells, these drugs have the ability to target and disrupt the cytoskeleton of neo-endothelial vascular cells leading to selective and rapid shutdown of blood flow through tumors. The recent success of CA-4 salts in preclinical studies and its achievement in clinical studies prompted the comprehensive study of the structure-activity relationships related to CA-4. Several thousand derivatives and analogs were synthesised and biologically evaluated by modifying the ring B and the ethenyl bridge of CA-4; only few studies have been done on the trimethoxyphenyl (TMP) ring A since it had been previously found crucial for anticancer potency. In the course of our own structure-activity relationship studies, we recently reported two new families of antimicrotubule agents where the ethenyl bridge of CA-4 was substituted by a sulfonate group and the TMP was replaced either by a phenylimidazolidin-2-one (IMZ) or phenylchloroethylurea (CEU) moieties. IMZs are potent antiproliferative agents exhibiting IC50 in the nanomolar range while CEU are soft alkylating agent normally active in micromolar range. IMZ and CEU arrest the cell cycle in G2/M phase, bind to the colchicine-binding site (C-BS) on β-tubulin leading to the disruption of the cytoskeleton and apoptosis. Although the structure-activity relationship studies of IMZ and CEU derivatives suggest that they mimic the TMP moiety of CA-4, molecular modeling experiments show that IMZs replace the ring B of CA-4 instead of ring A. In this context, we synthesized 3 series of CEU and IMZ where the sulfonate bridge was replaced by an ethenyl bridge to confirm that IMZ and CEU mimic the TMP moiety of CA-4. First, IMZ and CEU analogs to CA-4 exhibited antiproliferative activities in nanomolar range and in micromolar range, respectively as their parent compounds. Moreover, the most potent compounds blocked the cell cycle progression in G2/M-phase, disrupted the cytoskeleton and bind also the C-BS. Our results strongly suggest that IMZ and CEU mimic the TMP (ring A) of CA-4. These two moieties could be used as bioisosteric equivalents to circumvent some problems that might be encountered during the clinical development of CA-4. In addition, they could be used also to replace the TMP moiety found in several other antimitotics such colchicine, podophyllotoxin and steganacin to design new potent antimicrotubule agents. Citation Format: Mathieu Gagné-Boulet, Sébastien Fortin, Jacques Lacroix, Carole-Anne Lefebvre, Marie-France Côté, René C-Gaudreault. New moieties mimicking the trimethoxyphenyl (ring A) of combretastatin A-4: Synthesis and biological evaluation. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1664. doi:10.1158/1538-7445.AM2015-1664

ChemInform Abstract: Ceramic Membranes for Intermediate Temperature Solid Oxide Fuel Cells (SOFCs): State of the Art and Perspectives

AbstractReview: 109 refs.

Biomechanical effects of microbubbles: from radiosensitization to cell death.

Ultrasound-stimulated microbubbles have been demonstrated to mechanically perturb cell membranes, resulting in the activation of biological signaling pathways that significantly enhance the effects of radiation. The underlying mechanism involves augmented ceramide production following both microbubble stimulation and irradiation, leading to rapid and extensive endothelial apoptosis and tumor cell death as a result of vascular collapse. Endothelial cells are particularly sensitive to ceramide-induced cell death due to an enriched presence of sphingomyelinase in their membranes. In tumors, this consequent rapid vascular shutdown translates to an overall increase in tumor responses to radiation treatments. This review summarizes the groundwork behind endothelial-based radiation enhancement with ultrasound-stimulated microbubbles, and presents ongoing research on the use of microbubbles as therapeutic agents in cancer therapy.

Status of research toward the ITER disruption mitigation system

An overview of the present status of research toward the final design of the ITER disruption mitigation system (DMS) is given. The ITER DMS is based on massive injection of impurities, in order to radiate the plasma stored energy and mitigate the potentially damaging effects of disruptions. The design of this system will be extremely challenging due to many physics and engineering constraints such as limitations on port access and the amount and species of injected impurities. Additionally, many physics questions relevant to the design of the ITER disruption mitigation system remain unsolved such as the mechanisms for mixing and assimilation of injected impurities during the rapid shutdown and the mechanisms for the subsequent formation and dissipation of runaway electron current.

Recent advances in vascular disrupting agents in cancer therapy.

Vascular disrupting agents (VDAs) are an important class of compounds that exhibit selective activity against pre-existing tumor vasculature, causing rapid shutdown of the tumor blood flow and consequent necrosis of the tumor mass. The VDAs can be divided into flavonoid compounds, which are related to flavone acetic acid, and tubulin-binding agents. Tubulin-binding agents represent the largest group of VDAs and are characterized by different chemical structures, although most of them are derivatives of the lead compound combretastatin (CA-4). They demonstrated clinical activity, although recent findings have established that they have insufficient activity as single agents. Several resistance mechanisms occur, such as the resistance of the tumor rim cells, while promising results have been described in combination with other chemotherapeutics.

Analytical model for performance verification of liquid poison injection system of a nuclear reactor

Shut down system-2 (SDS-2) in advanced vertical pressure tube type reactor, provides rapid reactor shutdown by high pressure injection of a neutron absorbing liquid called poison, into the moderator in the calandria. Poison inside the calandria is distributed by poison jets issued from holes provided in the injection tubes. Effectiveness of the system depends on the rate and spread of the poison in the moderator.In this study, a transient one-dimensional (1D) hydraulic code, COPJET is developed, to predict the performance of system by predicting progression of poison jet with time. Validation of the COPJET is done with the data available in literature. Thereafter, it is applied for advanced vertical pressure type reactor.

Experimental investigations of transient pressure variations in a high head model Francis turbine during start-up and shutdown

Penetration of the power generated using wind and solar energy to electrical grid network causing several incidents of the grid tripping, power outage, and frequency drooping. This has increased restart (star-stop) cycles of the hydroelectric turbines significantly since grid connected hydroelectric turbines are widely used to manage critical conditions of the grid. Each cycle induces significant stresses due to unsteady pressure loading on the runner blades. The presented work investigates the pressure loading to a high head (Hp = 377 m, Dp = 1.78 m) Francis turbine during start-stop. The measurements were carried out on a scaled model turbine (HM = 12.5 m, DM = 0.349 m). Total four operating points were considered. At each operating point, three schemes of guide vanes opening and three schemes of guide vanes closing were investigated. The results show that total head variation is up to 9% during start-stop of the turbine. On the runner blade, the maximum pressure amplitudes are about 14 kPa and 16 kPa from the instantaneous mean value of 121 kPa during rapid start-up and shutdown, respectively, which are about 1.5 times larger than that of the slow start-up and shutdown. Moreover, the maximum pressure fluctuations are given at the blade trailing edge.

New Vascular Disrupting Agents in Upper Gastrointestinal Malignancies

Antivascular approaches aim to cause rapid and catastrophic shutdown in the vascular function of the tumour, leading to extensive tumour cell death. Tumour vascular disrupting agents (VDAs) are a new class of cancer therapies that target the existing vasculature of tumours, taking advantage of the relative instability of tumour vasculature and its supporting structures. Treatment with VDAs induces a rapid collapse and regression of tumour vessels, with a consequent deprivation of blood and oxygen which leads to ischemic or hemorrhagic necrosis of the tumour. In this review, an overview of the most recently developed vascular disrupting agents is reported, focusing on the biological effects exerted by these compounds on endothelial cells and tumour vasculature, potentially effective in the treatment of several malignancies including upper gastrointestinal tumours. In particular, we have focused on the antimitotic agent combretastatin and its numerous synthetic analogues such as combretastatin A-4-phosphate, OXI4503, and AVE8062, and on the colchicine analogue ZD6126.

Response to Metronidazole and Oxidative Stress Is Mediated through Homeostatic Regulator HsrA (HP1043) in Helicobacter pylori

Metronidazole (MTZ) is often used in combination therapies to treat infections caused by the gastric pathogen Helicobacter pylori. Resistance to MTZ results from loss-of-function mutations in genes encoding RdxA and FrxA nitroreductases. MTZ-resistant strains, when cultured at sub-MICs of MTZ (5 to 20 μg/ml), show dose-dependent defects in bacterial growth; depressed activities of many Krebs cycle enzymes, including pyruvate:ferredoxin oxidoreductase (PFOR); and low transcript levels of porGDAB (primer extension), phenotypes consistent with an involvement of a transcriptional regulator. Using a combination of protein purification steps, electrophoretic mobility shift assays (EMSAs), and mass spectrometry analyses of proteins bound to porG promoter sequences, we identified HP1043, an essential homeostatic global regulator (HsrA [for homeostatic stress regulator]). Competition EMSAs and supershift analyses with HsrA-enriched protein fractions confirmed specific binding to porGDAB and hsrA promoter sequences. Exposure to MTZ resulted in >10-fold decreases in levels of HsrA and in levels of the HsrA-regulated gene products PFOR and TlpB. Exposure to paraquat (PQ), hydrogen peroxide, or organic peroxides showed near equivalence with MTZ, revealing a common oxidative stress response pathway. Finally, direct superoxide dismutase (SOD) assays showed an inverse relationship between HsrA levels and SOD activity, suggesting that HsrA may serve as a repressor of sodB. As a homeostatic sentinel, HsrA appears to be ideally positioned to enable rapid shutdown of genes associated with metabolism and growth while activating (directly or indirectly) oxidative defense genes in response to low levels of toxic metabolites (MTZ or oxygen) before they reach DNA-damaging levels.

Vascular disrupting effect of CKD-516: preclinical study using DCE-MRI

Vascular disrupting agents (VDAs) are new class of anti-cancer drugs targeting pre-existing tumor vasculature which lead to tumor ischemia and necrosis. An innovative tubulin polymerization inhibitor, CKD-516, was recently developed as a VDA. We attempted to evaluate its tubulin destabilizing effect using immunofluorescence staining on human endothelial cells (HUVECs) and to ascertain its antivascular effect in a rabbit VX2 tumor model using dynamic contrast-enhanced (DCE) MRI by measuring the changes in kinetic parameters such as K-trans and IAUGC. Immunofluorescence staining using anti-tubulin and anti-actin antibodies on HUVECs showed that CKD-516 selectively disrupted tubulin component of the endothelial cytoskeleton. Serial DCE-MRI showed a significant decrease in K-trans and IAUGC parameters from baseline at 4 h (39.9 % in K-trans; -45.0 % in IAUGC) and at 24 h (-32.2 % in K-trans; -36.5 % in IAUGC), and a significant recovery at 48 h (22.9 % in K-trans; 34.8 % in IAUGC) following administration of CKD-516 at a 0.7-mg/kg dose. When the tumors were stratified according to the initial K-trans value of 0.1, tumors with a high K-trans > 0.1 which was indicative of having well-developed pre-existing vessels, showed greater reduction in K-trans and IAUGC values. On histologic examination, the degree of necrosis of treated tumors was significantly greater than that of untreated tumors. In summary, CKD-516 is an effective VDA which results in rapid vascular shutdown by targeting the tubulin component of tumor vessels and thus leads to necrosis.

Inactivation of Intergenic Enhancers by EBNA3A Initiates and Maintains Polycomb Signatures across a Chromatin Domain Encoding CXCL10 and CXCL9

Epstein-Barr virus (EBV) causes a persistent infection in human B cells by establishing specific transcription programs to control B cell activation and differentiation. Transcriptional reprogramming of EBV infected B cells is predominantly driven by the action of EBV nuclear antigens, among them the transcriptional repressor EBNA3A. By comparing gene expression profiles of wt and EBNA3A negative EBV infected B cells, we have previously identified a broad array of cellular genes controlled by EBNA3A. We now find that genes repressed by EBNA3A in these cells are significantly enriched for the repressive histone mark H3K27me3, which is installed by Polycomb group (PcG) proteins. This PcG-controlled subset of genes also carries H3K27me3 marks in a variety of other tissues, suggesting that the commitment to PcG silencing is an intrinsic feature of these gene loci that can be used by EBNA3A. In addition, EBNA3A targets frequently reside in co-regulated gene clusters. To study the mechanism of gene repression by EBNA3A and to evaluate the relative contribution of PcG proteins during this process, we have selected the genomic neighbors CXCL10 and CXCL9 as a model for co-repressed and PcG-controlled genes. We show that EBNA3A binds to CBF1 occupied intergenic enhancers located between CXCL10 and CXCL9 and displaces the transactivator EBNA2. This impairs enhancer activity, resulting in a rapid transcriptional shut-down of both genes in a CBF1-dependent manner and initiation of a delayed gain of H3K27me3 marks covering an extended chromatin domain. H3K27me3 marks increase gradually and are maintained by EBNA3A. Our study provides direct evidence that repression by EBNA3A requires CBF1 and that EBNA3A and EBNA2 compete for access to CBF1 at identical genomic sites. Most importantly, our results demonstrate that transcriptional silencing by EBNA3A precedes the appearance of repressive PcG marks and indicate that both events are triggered by loss of enhancer activity.

Rapid shutdown experiments with one and two gas jets on Alcator C-Mod

Massive gas injection rapid shutdown experiments have been conducted on the Alcator C-Mod tokamak using two toroidally separated gas injectors, in order to investigate the effect of multiple gas injection locations on the toroidal asymmetry in the radiated power. Toroidal radiation asymmetry is diagnosed by an array of six single-channel photodiodes mounted on the vessel wall. The presence of magnetohydrodynamic (MHD) activity is diagnosed using an array of magnetic pickup (Mirnov) coils, mounted on stalks on the vessel wall. Scans were conducted of the relative timing between the two jets, of the 95th percentile safety factor, and of the plasma elongation. It is observed that firing the two gas jets so that the injected impurities arrive at the plasma at nearly the same time produced an increase in the toroidal radiation asymmetry. In addition, the radiation asymmetry in the thermal quench phase correlates with the growth rate of low toroidal mode number MHD modes, indicating that these mode(s) are playing a role in setting the radiation asymmetry.

The Analytical Research and Development of On-Line Monitoring Models of Thermal State for Turbine Rotor

Steam turbine units are required to start up and shut down as fast as possible to improve economy and load-response ability of the units under the qualification of safety. it is important to monitor and control thermal state in turbine during operation, especially during the process of start-up and shutdown. Thermal stresses in turbine rotor in thermal power plants are the limiting factors for rapid startup, shutdown or load change. In this paper the online calculation models of temperature and thermal stress for a two-dimensional axis-symmetric object are obtained after disposing of the nonlinear factor such as temperature-dependent properties by a transformation. The model gained can be used to analyze thermal states in thick-walled components, monitoring and control online.

Control and dissipation of runaway electron beams created during rapid shutdown experiments in DIII-D

DIII-D experiments on rapid shutdown runaway electron (RE) beams have improved the understanding of the processes involved in RE beam control and dissipation. Improvements in RE beam feedback control have enabled stable confinement of RE beams out to the volt-second limit of the ohmic coil, as well as enabling a ramp down to zero current. Spectroscopic studies of the RE beam have shown that neutrals tend to be excluded from the RE beam centre. Measurements of the RE energy distribution function indicate a broad distribution with mean energy of order several MeV and peak energies of order 30–40 MeV. The distribution function appears more skewed towards low energies than expected from avalanche theory. The RE pitch angle appears fairly directed (θ ∼ 0.2) at high energies and more isotropic at lower energies (ε < 100 keV). Collisional dissipation of RE beam current has been studied by massive gas injection of different impurities into RE beams; the equilibrium assimilation of these injected impurities appears to be reasonably well described by radial pressure balance between neutrals and ions. RE current dissipation following massive impurity injection is shown to be more rapid than expected from avalanche theory—this anomalous dissipation may be linked to enhanced radial diffusion caused by the significant quantity of high-Z impurities (typically argon) in the plasma. The final loss of RE beams to the wall has been studied: it was found that conversion of magnetic to kinetic energy is small for RE loss times smaller than the background plasma ohmic decay time of order 1–2 ms.

High-CO2 tolerance in microalgae: possible mechanisms and implications for biotechnology and bioremediation

Recent developments in the field of microalgal biotechnology, including CO2 biomitigation and the discovery of new species of microalgae that are tolerant to extremely high CO2 levels (40-100 vol%), have renewed interest in the physiological effects and mechanisms of high-CO2 tolerance in photoautotrophs. Photosynthetic apparatus state transitions that increase ATP generation, upregulation of H(+)-ATPases pumping protons out of the cell, rapid shutdown of CO2-concentrating mechanisms, and adjustment of membranes' fatty acid composition are currently believed to be the key mechanisms governing cellular pH homeostasis and hence microalgae's tolerance to high CO2 levels, which is especially characteristic of extremophile and symbiotic species. The mechanisms governing acclimation to high CO2 comprise the subject of this review and are discussed in view of the use of CO2 enrichment to increase the productivity of microalgal cultures, as well as the practice of carbon capture from flue gases.