During low tide, Corallina continued to out-perform Calliarthron when submerged in warming tidepools, but photosynthesis abruptly halted for both species when emerged in air. Surprisingly, pigment composition did not differ, suggesting that light harvesting does not account for this difference. Additionally, Corallina was more effective at resisting desiccation by retaining

water in its branches. When the tide returned, only Corallina PLX-4720 chemical structure recovered from combined temperature and desiccation stresses associated with emergence. This study broadens our understanding of intertidal algal physiology and provides a new perspective on the physiological and morphological underpinnings of habitat partitioning. “
“Coccolithophores, especially the PF-562271 manufacturer abundant, cosmopolitan species Emiliania huxleyi (Lohmann) W. W. Hay et H. P. Mohler, are one of the main driving forces of the oceanic carbonate pump and contribute significantly to global carbon cycling, due to their ability to calcify. A recent study indicates that termination of diploid blooms by viral infection induces life-cycle transition, and speculation has arisen about the role of the haploid, noncalcifying stage in coccolithophore ecology. To explore gene expression patterns in both life-cycle stages, haploid and diploid

cells of E. huxleyi (RCC 1217 and RCC 1216) were acclimated to limiting and saturating photon flux densities. Transcriptome analyses were performed to assess differential genomic expression related to different ploidy levels and acclimation light intensities. Analyses indicated that life-cycle stages exhibit different properties of regulating

genome expression (e.g., pronounced gene activation and gene silencing in the diploid stage), proteome maintenance (e.g., increased turnover of proteins in the haploid stage), 上海皓元医药股份有限公司 as well as metabolic processing (e.g., pronounced primary metabolism and motility in the haploid stage and calcification in the diploid stage). Furthermore, higher abundances of transcripts related to endocytotic and digestive machinery were observed in the diploid stage. A qualitative feeding experiment indicated that both life-cycle stages are capable of particle uptake (0.5 μm diameter) in late-stationary growth phase. Results showed that the two life-cycle stages represent functionally distinct entities that are evolutionarily shaped to thrive in the environment they typically inhabit. “
“Australia Rivers Institute, Griffith University, Nathan, Queensland, Australia Department of Environment and Primary Industries, AgriBiosciences Centre, Biosciences Research Division, La Trobe University, Bundoora, Victoria, USA The extracellular matrix of the ovoid and fusiform morphotypes of Phaeodactylum tricornutum (Bohlin) was characterized in detail. The structural and nanophysical properties were analyzed by microscopy.

CagZ seems to stabilize Cagβ, and interactions between Cagβ and CagA and between CagZ and Cagβ were also described, thus giving fresh insights into T4SS assembly see more [21]. Further studies demonstrated that purified HP0539/CagL mimics the host extracellular matrix protein fibronectin in vitro [22]. Upon contact with integrin α5β1 receptor of various human and mouse cell lines, purified CagL (like fibronectin) triggers cell spreading, focal adhesion formation, and activation

of several tyrosine kinases including focal adhesion kinase (FAK), Src, and epidermal growth factor receptors EGFR and Her3/ErbB3. These findings suggest that CagL exhibits functional mimicry with fibronectin [22]. Investigation of how CagL activates EGFR revealed that docking dissociates metalloprotease ADAM17 from integrin α5β1, which

activated HB-EGF production, and also repressed HKα promoter activity important in hypochlorhydria [23,24] Interestingly, CagL polymorphisms (Y58/E59) were described in gastric cancer patients from Taiwan to correlate with a corpus shift of integrin α5β1 leading to severe corpus gastritis and carcinogenesis [25]. Thus, CagL is a profound T4SS-factor with important roles in pathogenesis. Furthermore, new studies investigated the effects of Metformin solubility dmso H. pylori infection on histone modifications in AGS cells. Infection induced the dephosphorylation of histone H3 at serine residue 10 and other modifications [26]. The results demonstrate that histone alterations occur via cagPAI-dependent but cagA-independent mechanisms, which may contribute to transcriptional changes and pathogenesis [26]. Studies reporting the effects of injected CagA on gp130-receptor-mediated signaling were evaluated. CagA, phosphatase SHP2, and gp130 were in complex, and phospho-CagA showed enhanced SHP2-binding activity and ERK1/2 phosphorylation, whereas nonphospho-CagA showed preferential STAT3 activation. These

findings indicate that the phosphorylation status of CagA affects a switch between the SHP2/ERK and JAK/STAT3 pathways through gp130 [27]. In nonpolarized epithelial cells, ERK activation results in oncogenic stress, up-regulation of the p21 (Waf1/Cip1) cyclin-dependent kinase (Cdk) inhibitor, and induction MCE of senescence [28]. In polarized epithelial cells, CagA-driven ERK signals prevent p21 (Waf1/Cip1) expression by activating a guanine nucleotide exchange factor-H1-RhoA-RhoA-associated kinase-c-Myc pathway. The microRNAs miR-17 and miR-20a, induced by c-Myc, are needed to suppress p21 (Waf1/Cip1) expression. CagA also drives an epithelial-mesenchymal transition in polarized epithelial cells which may be important in oncogenesis [28]. Another study identified the actin-binding protein cortactin as a novel downstream target of H. pylori-activated ERK kinase [29]. Upon infection, serine-phosphorylated cortactin was found to interact with and stimulate the kinase activity of FAK, suggesting that H.

CagZ seems to stabilize Cagβ, and interactions between Cagβ and CagA and between CagZ and Cagβ were also described, thus giving fresh insights into T4SS assembly www.selleckchem.com/products/ABT-888.html [21]. Further studies demonstrated that purified HP0539/CagL mimics the host extracellular matrix protein fibronectin in vitro [22]. Upon contact with integrin α5β1 receptor of various human and mouse cell lines, purified CagL (like fibronectin) triggers cell spreading, focal adhesion formation, and activation

of several tyrosine kinases including focal adhesion kinase (FAK), Src, and epidermal growth factor receptors EGFR and Her3/ErbB3. These findings suggest that CagL exhibits functional mimicry with fibronectin [22]. Investigation of how CagL activates EGFR revealed that docking dissociates metalloprotease ADAM17 from integrin α5β1, which

activated HB-EGF production, and also repressed HKα promoter activity important in hypochlorhydria [23,24] Interestingly, CagL polymorphisms (Y58/E59) were described in gastric cancer patients from Taiwan to correlate with a corpus shift of integrin α5β1 leading to severe corpus gastritis and carcinogenesis [25]. Thus, CagL is a profound T4SS-factor with important roles in pathogenesis. Furthermore, new studies investigated the effects of Selleckchem R788 H. pylori infection on histone modifications in AGS cells. Infection induced the dephosphorylation of histone H3 at serine residue 10 and other modifications [26]. The results demonstrate that histone alterations occur via cagPAI-dependent but cagA-independent mechanisms, which may contribute to transcriptional changes and pathogenesis [26]. Studies reporting the effects of injected CagA on gp130-receptor-mediated signaling were evaluated. CagA, phosphatase SHP2, and gp130 were in complex, and phospho-CagA showed enhanced SHP2-binding activity and ERK1/2 phosphorylation, whereas nonphospho-CagA showed preferential STAT3 activation. These

findings indicate that the phosphorylation status of CagA affects a switch between the SHP2/ERK and JAK/STAT3 pathways through gp130 [27]. In nonpolarized epithelial cells, ERK activation results in oncogenic stress, up-regulation of the p21 (Waf1/Cip1) cyclin-dependent kinase (Cdk) inhibitor, and induction MCE公司 of senescence [28]. In polarized epithelial cells, CagA-driven ERK signals prevent p21 (Waf1/Cip1) expression by activating a guanine nucleotide exchange factor-H1-RhoA-RhoA-associated kinase-c-Myc pathway. The microRNAs miR-17 and miR-20a, induced by c-Myc, are needed to suppress p21 (Waf1/Cip1) expression. CagA also drives an epithelial-mesenchymal transition in polarized epithelial cells which may be important in oncogenesis [28]. Another study identified the actin-binding protein cortactin as a novel downstream target of H. pylori-activated ERK kinase [29]. Upon infection, serine-phosphorylated cortactin was found to interact with and stimulate the kinase activity of FAK, suggesting that H.

2 NKT cells are abundant in the liver. They recognize lipid antigens presented by CD1d and had different roles in liver diseases. NKT cells produce a wide range of cytokines promptly after activation.23 It is well accepted that Th1 cytokines suppress fibrosis, whereas Th2 cytokines promote fibrosis.24 In wildtype (WT) mice, it was reported that NKT cells can suppress the activation of HSC.22 But in different animal models and in human patients the conclusions were controversial.25, 26 Although the acceleration of HBV infection to liver fibrosis Selleckchem Epigenetics Compound Library have been extensively observed in clinical settings,

the immune response during this process is not clear, especially in the condition of the HBV carriers with no obvious symptoms. In this study, by using HBV transgenic mice (HBV-tg) that mimic human HBV healthy carriers,27 we found liver fibrosis spontaneously occurred in old age of HBV-tg mice, and, importantly, learn more HBV-tg mice were much more sensitive to the hepatotoxin CCl4-induced liver injury and liver fibrosis with the accompanied overactivation of HSCs. Further study demonstrated

that hepatic NKT cells from HBV-tg mice could directly activate HSCs and thereafter induce liver fibrosis in the experiments of cellular depletion and adoptive transfer, and IL-4 and IL-13 secreted by NKT cells were considered a crucial step for the activation of HSCs. α-SMA: α smooth muscle actin; CCl4: carbon tetrachloride; ECM: extracellular matrix; HBV: hepatitis B virus; HBV-tg: HBV transgenic mice; HSC: hepatic stellate cells; IFN-γ, interferon gamma; IL: interleukin; MMP: matrix metalloproteinase; MNC: mononuclear cell; mRNA: messenger RNA; NKT, natural killer T; qPCR: quantitative polymerase chain reaction; TIMP: tissue inhibitor of metalloproteinase. MCE公司 HBV transgenic mice C57BL/6J-TgN (AlblHBV) 44Bri, which contains HBV genome S, pre-S, and X domains, were purchased from VITALRIVER experiment animal company (Beijing, China), who obtained the animals from Jackson Laboratory

(Bar Harbor, ME). C57BL/6 mice were also purchased from VITALRIVER experiment animal company. Rag1−/− mice were purchased from Model Animal Research Center (Nanjing, China), who obtained the mice from Jackson Laboratory. Mice were housed in a specific pathogen-free facility and used according to the regulations of animal care of University of Science and Technology of China. For chronic liver injury and fibrosis, male 7 to 10-week-old C57BL/6 and HBV-tg mice (weighing about 20-25 g) were injected (intraperitoneally, i.p., 2 times a week) with 0.5 μL per gram of body weight of pure CCl4 diluted with olive oil (Sigma). After several weeks’ injections (2, 4, 10, and 14 weeks, respectively), mice were sacrificed 72 hours following the last CCl4 injection, and liver tissues and serum were collected. For acute liver injury, both mice were injected CCl4 once and then killed and analyzed at different timepoints.

2 NKT cells are abundant in the liver. They recognize lipid antigens presented by CD1d and had different roles in liver diseases. NKT cells produce a wide range of cytokines promptly after activation.23 It is well accepted that Th1 cytokines suppress fibrosis, whereas Th2 cytokines promote fibrosis.24 In wildtype (WT) mice, it was reported that NKT cells can suppress the activation of HSC.22 But in different animal models and in human patients the conclusions were controversial.25, 26 Although the acceleration of HBV infection to liver fibrosis Selleckchem KPT-330 have been extensively observed in clinical settings,

the immune response during this process is not clear, especially in the condition of the HBV carriers with no obvious symptoms. In this study, by using HBV transgenic mice (HBV-tg) that mimic human HBV healthy carriers,27 we found liver fibrosis spontaneously occurred in old age of HBV-tg mice, and, importantly, R428 molecular weight HBV-tg mice were much more sensitive to the hepatotoxin CCl4-induced liver injury and liver fibrosis with the accompanied overactivation of HSCs. Further study demonstrated

that hepatic NKT cells from HBV-tg mice could directly activate HSCs and thereafter induce liver fibrosis in the experiments of cellular depletion and adoptive transfer, and IL-4 and IL-13 secreted by NKT cells were considered a crucial step for the activation of HSCs. α-SMA: α smooth muscle actin; CCl4: carbon tetrachloride; ECM: extracellular matrix; HBV: hepatitis B virus; HBV-tg: HBV transgenic mice; HSC: hepatic stellate cells; IFN-γ, interferon gamma; IL: interleukin; MMP: matrix metalloproteinase; MNC: mononuclear cell; mRNA: messenger RNA; NKT, natural killer T; qPCR: quantitative polymerase chain reaction; TIMP: tissue inhibitor of metalloproteinase. MCE公司 HBV transgenic mice C57BL/6J-TgN (AlblHBV) 44Bri, which contains HBV genome S, pre-S, and X domains, were purchased from VITALRIVER experiment animal company (Beijing, China), who obtained the animals from Jackson Laboratory

(Bar Harbor, ME). C57BL/6 mice were also purchased from VITALRIVER experiment animal company. Rag1−/− mice were purchased from Model Animal Research Center (Nanjing, China), who obtained the mice from Jackson Laboratory. Mice were housed in a specific pathogen-free facility and used according to the regulations of animal care of University of Science and Technology of China. For chronic liver injury and fibrosis, male 7 to 10-week-old C57BL/6 and HBV-tg mice (weighing about 20-25 g) were injected (intraperitoneally, i.p., 2 times a week) with 0.5 μL per gram of body weight of pure CCl4 diluted with olive oil (Sigma). After several weeks’ injections (2, 4, 10, and 14 weeks, respectively), mice were sacrificed 72 hours following the last CCl4 injection, and liver tissues and serum were collected. For acute liver injury, both mice were injected CCl4 once and then killed and analyzed at different timepoints.

2 NKT cells are abundant in the liver. They recognize lipid antigens presented by CD1d and had different roles in liver diseases. NKT cells produce a wide range of cytokines promptly after activation.23 It is well accepted that Th1 cytokines suppress fibrosis, whereas Th2 cytokines promote fibrosis.24 In wildtype (WT) mice, it was reported that NKT cells can suppress the activation of HSC.22 But in different animal models and in human patients the conclusions were controversial.25, 26 Although the acceleration of HBV infection to liver fibrosis Smoothened Agonist supplier have been extensively observed in clinical settings,

the immune response during this process is not clear, especially in the condition of the HBV carriers with no obvious symptoms. In this study, by using HBV transgenic mice (HBV-tg) that mimic human HBV healthy carriers,27 we found liver fibrosis spontaneously occurred in old age of HBV-tg mice, and, importantly, click here HBV-tg mice were much more sensitive to the hepatotoxin CCl4-induced liver injury and liver fibrosis with the accompanied overactivation of HSCs. Further study demonstrated

that hepatic NKT cells from HBV-tg mice could directly activate HSCs and thereafter induce liver fibrosis in the experiments of cellular depletion and adoptive transfer, and IL-4 and IL-13 secreted by NKT cells were considered a crucial step for the activation of HSCs. α-SMA: α smooth muscle actin; CCl4: carbon tetrachloride; ECM: extracellular matrix; HBV: hepatitis B virus; HBV-tg: HBV transgenic mice; HSC: hepatic stellate cells; IFN-γ, interferon gamma; IL: interleukin; MMP: matrix metalloproteinase; MNC: mononuclear cell; mRNA: messenger RNA; NKT, natural killer T; qPCR: quantitative polymerase chain reaction; TIMP: tissue inhibitor of metalloproteinase. 上海皓元 HBV transgenic mice C57BL/6J-TgN (AlblHBV) 44Bri, which contains HBV genome S, pre-S, and X domains, were purchased from VITALRIVER experiment animal company (Beijing, China), who obtained the animals from Jackson Laboratory

(Bar Harbor, ME). C57BL/6 mice were also purchased from VITALRIVER experiment animal company. Rag1−/− mice were purchased from Model Animal Research Center (Nanjing, China), who obtained the mice from Jackson Laboratory. Mice were housed in a specific pathogen-free facility and used according to the regulations of animal care of University of Science and Technology of China. For chronic liver injury and fibrosis, male 7 to 10-week-old C57BL/6 and HBV-tg mice (weighing about 20-25 g) were injected (intraperitoneally, i.p., 2 times a week) with 0.5 μL per gram of body weight of pure CCl4 diluted with olive oil (Sigma). After several weeks’ injections (2, 4, 10, and 14 weeks, respectively), mice were sacrificed 72 hours following the last CCl4 injection, and liver tissues and serum were collected. For acute liver injury, both mice were injected CCl4 once and then killed and analyzed at different timepoints.

8 However, almost all RCTs comparing propranolol or nadolol to placebo or to other pharmacotherapy excluded patients with advanced cirrhosis, especially patients with refractory ascites. Therefore, there is insufficient evidence on the relative risks and benefits of NSBB use in this subgroup of ill patients. The question of whether

the risk/benefit ratio favors the use of NSBB in patients with advanced cirrhosis remains unresolved. In this issue of HEPATOLOGY, Didier Lebrec, who originally described the effectiveness of propranolol in reducing the risk of variceal bleeding, and his colleagues from Clichy Adriamycin attempt to answer this crucial question. They report the results of an observational study on the survival of 151 patients with cirrhosis with refractory ascites,9 as defined by the International Ascites Club.10 Of the 151 patients enrolled, 77 (51%) had esophageal varices and were taking propranolol, whereas the remaining 74 patients without varices (except four cases) were not. It is unclear whether propranolol was given as primary or secondary prophylaxis against variceal bleeding. Patients treated with propranolol had a significantly lower median survival of 5 months versus 20 months in patients not taking propranolol. Multivariable analysis showed that treatment with NSBB was one of the four

X-396 price predictors of mortality in this population of patients with cirrhosis. The authors concluded that propranolol was potentially harmful in patients with cirrhosis with refractory ascites, and therefore should be contraindicated. Before accepting the conclusion of this study, which involves a strong clinical recommendation, we believe that the characteristics

of the study and the quality of the results should be scrupulously evaluated. First, the study was not an RCT, which is the best way to evaluate the effects of specific medications. This is because the allocation of treatment by randomization is the only way to prevent selection bias. When treatment allocation is not randomized, unrecognized but often substantial differences between patient groups may alter the interpretation of results. For example, the group not receiving propranolol did not 上海皓元 have varices, and this difference immediately separates the two groups of patients into different risk categories for mortality.1 However, the HVPG before the initiation of treatment was similar in both groups. It is important to emphasize that the HVPG was measured only in selected patients in both groups. It is possible that the HVPG may have been higher in the NSBB group if measurements were carried out in all patients; this possible difference could then explain the higher mortality in the patients treated with propranolol. Second, the causes of death in two-thirds of cases were either progression of HCC or sepsis, 25 patients died from unknown causes, and nine patients were unaccounted for.

8 However, almost all RCTs comparing propranolol or nadolol to placebo or to other pharmacotherapy excluded patients with advanced cirrhosis, especially patients with refractory ascites. Therefore, there is insufficient evidence on the relative risks and benefits of NSBB use in this subgroup of ill patients. The question of whether

the risk/benefit ratio favors the use of NSBB in patients with advanced cirrhosis remains unresolved. In this issue of HEPATOLOGY, Didier Lebrec, who originally described the effectiveness of propranolol in reducing the risk of variceal bleeding, and his colleagues from Clichy PF2341066 attempt to answer this crucial question. They report the results of an observational study on the survival of 151 patients with cirrhosis with refractory ascites,9 as defined by the International Ascites Club.10 Of the 151 patients enrolled, 77 (51%) had esophageal varices and were taking propranolol, whereas the remaining 74 patients without varices (except four cases) were not. It is unclear whether propranolol was given as primary or secondary prophylaxis against variceal bleeding. Patients treated with propranolol had a significantly lower median survival of 5 months versus 20 months in patients not taking propranolol. Multivariable analysis showed that treatment with NSBB was one of the four

EPZ015666 datasheet predictors of mortality in this population of patients with cirrhosis. The authors concluded that propranolol was potentially harmful in patients with cirrhosis with refractory ascites, and therefore should be contraindicated. Before accepting the conclusion of this study, which involves a strong clinical recommendation, we believe that the characteristics

of the study and the quality of the results should be scrupulously evaluated. First, the study was not an RCT, which is the best way to evaluate the effects of specific medications. This is because the allocation of treatment by randomization is the only way to prevent selection bias. When treatment allocation is not randomized, unrecognized but often substantial differences between patient groups may alter the interpretation of results. For example, the group not receiving propranolol did not 上海皓元医药股份有限公司 have varices, and this difference immediately separates the two groups of patients into different risk categories for mortality.1 However, the HVPG before the initiation of treatment was similar in both groups. It is important to emphasize that the HVPG was measured only in selected patients in both groups. It is possible that the HVPG may have been higher in the NSBB group if measurements were carried out in all patients; this possible difference could then explain the higher mortality in the patients treated with propranolol. Second, the causes of death in two-thirds of cases were either progression of HCC or sepsis, 25 patients died from unknown causes, and nine patients were unaccounted for.

huxleyi virus 1 (EhV1). Resistant E. huxleyi strains were consistently characterized by low caspase specific activity and a relatively simple metacaspase expression profile. In contrast, sensitive E. huxleyi strains had markedly elevated caspase specific activity and consistently expressed more diverse metacaspase proteins. Using pooled data sets from triplicate experiments, we observed statistically significant linear correlations between infectivity, caspase activity, and metacaspase expression, with each strain forming distinct clusters, within a gradient in viral susceptibility. At the same time, we observed positive

correlations between the expression of a subset of metacaspase proteins and lower susceptibility, suggestive of potential protective roles. Our findings implicate the importance of see more subtle differences in the basal physiological regulation of the PCD machinery to viral resistance or sensitivity and cell fate. “
“The responses of respiration and photosynthesis to temperature fluctuations in marine macroalgae have the potential to significantly affect coastal carbon fluxes mTOR inhibitor and sequestration. In this study, the marine red macroalga Gracilaria lemaneiformis was cultured at three different temperatures (12, 19, and 26°C) and at high- and low-nitrogen (N) availability, to investigate the

acclimation potential of respiration and photosynthesis to temperature change. Measurements of respiratory and photosynthetic rates

were made at five temperatures (7°C–33°C). An instantaneous change in temperature resulted in a change in the rates of respiration and MCE公司 photosynthesis, and the temperature sensitivities (i.e., the Q10 value) for both the metabolic processes were lower in 26°C-grown algae than 12°C- or 19°C-grown algae. Both respiration and photosynthesis acclimated to long-term changes in temperature, irrespective of the N availability under which the algae were grown; respiration displayed strong acclimation, whereas photosynthesis only exhibited a partial acclimation response to changing growth temperatures. The ratio of respiration to gross photosynthesis was higher in 12°C-grown algae, but displayed little difference between the algae grown at 19°C and 26°C. We propose that it is unlikely that respiration in G. lemaneiformis would increase significantly with global warming, although photosynthesis would increase at moderately elevated temperatures. “
“In November 2004, Chaetoceros spp. (diatom) cells were collected from 5 m at Station ALOHA (22º45′ N, 158º0′ W) in the subtropical North Pacific Ocean. Attached to the spines of several Chaetoceros spp. were symbiotic heterocystous cyanobacterial cells, identified as Calothrix rhizosoleniae Lemmerm. The symbiotic diatom cells were handpicked and placed in N-deplete media.

huxleyi virus 1 (EhV1). Resistant E. huxleyi strains were consistently characterized by low caspase specific activity and a relatively simple metacaspase expression profile. In contrast, sensitive E. huxleyi strains had markedly elevated caspase specific activity and consistently expressed more diverse metacaspase proteins. Using pooled data sets from triplicate experiments, we observed statistically significant linear correlations between infectivity, caspase activity, and metacaspase expression, with each strain forming distinct clusters, within a gradient in viral susceptibility. At the same time, we observed positive

correlations between the expression of a subset of metacaspase proteins and lower susceptibility, suggestive of potential protective roles. Our findings implicate the importance of Ibrutinib subtle differences in the basal physiological regulation of the PCD machinery to viral resistance or sensitivity and cell fate. “
“The responses of respiration and photosynthesis to temperature fluctuations in marine macroalgae have the potential to significantly affect coastal carbon fluxes learn more and sequestration. In this study, the marine red macroalga Gracilaria lemaneiformis was cultured at three different temperatures (12, 19, and 26°C) and at high- and low-nitrogen (N) availability, to investigate the

acclimation potential of respiration and photosynthesis to temperature change. Measurements of respiratory and photosynthetic rates

were made at five temperatures (7°C–33°C). An instantaneous change in temperature resulted in a change in the rates of respiration and medchemexpress photosynthesis, and the temperature sensitivities (i.e., the Q10 value) for both the metabolic processes were lower in 26°C-grown algae than 12°C- or 19°C-grown algae. Both respiration and photosynthesis acclimated to long-term changes in temperature, irrespective of the N availability under which the algae were grown; respiration displayed strong acclimation, whereas photosynthesis only exhibited a partial acclimation response to changing growth temperatures. The ratio of respiration to gross photosynthesis was higher in 12°C-grown algae, but displayed little difference between the algae grown at 19°C and 26°C. We propose that it is unlikely that respiration in G. lemaneiformis would increase significantly with global warming, although photosynthesis would increase at moderately elevated temperatures. “
“In November 2004, Chaetoceros spp. (diatom) cells were collected from 5 m at Station ALOHA (22º45′ N, 158º0′ W) in the subtropical North Pacific Ocean. Attached to the spines of several Chaetoceros spp. were symbiotic heterocystous cyanobacterial cells, identified as Calothrix rhizosoleniae Lemmerm. The symbiotic diatom cells were handpicked and placed in N-deplete media.