61) for water depths of 2 m to <5 m (Fig. 2A). The probability declined as water depth increased, reaching its minimum (0.29) in water 10 m to <15 m deep and remained Pirfenidone datasheet relatively low in water up to 25 m deep. In water depths ≥25 m, the dugongs spent almost as much time in the detection zone (0.57) as they did in water depths 2 to <5 m. Between water depths of 5 and 25 m, these probabilities were lower than the average probability of availability (0.47) across water of all depths. when the detection zone was deeper, the probability of a dugong being available for detection was higher in most depth

categories (Fig. 2B). Although habitat affected detection probabilities, the difference between seagrass and offshore habitats was only substantial in the two shallowest depth categories (that

is, water depths up to 10 m). In deeper water, the confidence intervals for the seagrass habitat included the mean of the offshore habitat. The depth-specific probabilities were lower than the constant probability (0.67) in water depths 3 m to <5 m for offshore waters and between 5 m and 15 m for both habitats. Most dugongs were sighted in water depths of 2 m to <15 m in the 2001 (80%), 2005 (90%), and 2011 (70%) aerial surveys of Hervey Bay (details in Sobtzick et al. 2011). For the detection zone 0–2.5 m, similarly large numbers of dugongs were sighted from water 3 m to <15 m: 58% in 2001, 70% in 2005, and 57% in 2011. In most water depth ranges except 2 m to <5 m (or 3 m to <5 m) and ≥25 m, depth-specific corrections resulted in higher dugong numbers Palbociclib manufacturer estimated than the constant corrections (Fig. 3). The differences in the estimated numbers based on the depth-specific and constant corrections were larger when the detection zone was 0–1.5 m than 0–2.5 m. The total numbers of dugongs estimated across the water depth MCE range were also

higher when finer corrections at each water depth bin were applied than those using constant corrections. The availability of dugongs for detection by aerial observers varied with water depth. Where the detection zone was narrow (0–1.5 m), the probability of a dugong being available for detection reached 50% only in very shallow water (2 m to <5 m) and very deep water (≥25 m). When the detection zone was wider (0–2.5 m), the availability for detection was larger but showed some evidence of variation between habitats. The habitat effect was largely confined to shallow water depths. Our expectation was that the dugongs would be less available for detection over seagrass beds than in offshore waters because they would be spending more time on the sea floor feeding on seagrass. This pattern was observed in water 5–10 m deep, but for water depths below 5 m the pattern was reversed, with very low estimated availability in the offshore habitat and high availability over seagrass meadows.

61) for water depths of 2 m to <5 m (Fig. 2A). The probability declined as water depth increased, reaching its minimum (0.29) in water 10 m to <15 m deep and remained find more relatively low in water up to 25 m deep. In water depths ≥25 m, the dugongs spent almost as much time in the detection zone (0.57) as they did in water depths 2 to <5 m. Between water depths of 5 and 25 m, these probabilities were lower than the average probability of availability (0.47) across water of all depths. when the detection zone was deeper, the probability of a dugong being available for detection was higher in most depth

categories (Fig. 2B). Although habitat affected detection probabilities, the difference between seagrass and offshore habitats was only substantial in the two shallowest depth categories (that

is, water depths up to 10 m). In deeper water, the confidence intervals for the seagrass habitat included the mean of the offshore habitat. The depth-specific probabilities were lower than the constant probability (0.67) in water depths 3 m to <5 m for offshore waters and between 5 m and 15 m for both habitats. Most dugongs were sighted in water depths of 2 m to <15 m in the 2001 (80%), 2005 (90%), and 2011 (70%) aerial surveys of Hervey Bay (details in Sobtzick et al. 2011). For the detection zone 0–2.5 m, similarly large numbers of dugongs were sighted from water 3 m to <15 m: 58% in 2001, 70% in 2005, and 57% in 2011. In most water depth ranges except 2 m to <5 m (or 3 m to <5 m) and ≥25 m, depth-specific corrections resulted in higher dugong numbers 5-Fluoracil in vivo estimated than the constant corrections (Fig. 3). The differences in the estimated numbers based on the depth-specific and constant corrections were larger when the detection zone was 0–1.5 m than 0–2.5 m. The total numbers of dugongs estimated across the water depth 上海皓元医药股份有限公司 range were also

higher when finer corrections at each water depth bin were applied than those using constant corrections. The availability of dugongs for detection by aerial observers varied with water depth. Where the detection zone was narrow (0–1.5 m), the probability of a dugong being available for detection reached 50% only in very shallow water (2 m to <5 m) and very deep water (≥25 m). When the detection zone was wider (0–2.5 m), the availability for detection was larger but showed some evidence of variation between habitats. The habitat effect was largely confined to shallow water depths. Our expectation was that the dugongs would be less available for detection over seagrass beds than in offshore waters because they would be spending more time on the sea floor feeding on seagrass. This pattern was observed in water 5–10 m deep, but for water depths below 5 m the pattern was reversed, with very low estimated availability in the offshore habitat and high availability over seagrass meadows.

2 or pHBC1.2. There was no difference in the number of HBc-positive cells and serum HBV-DNA levels between NOG mice transfected by pHBA1.2 and pHBC1.2 1 day after injection. Serum levels of HBV-DNA, HBs Ag and HBe Ag were detected for 3 months in NOG mice transfected pHBA1.2 and pHBC1.2, but not detectable in immune-competent Roxadustat mouse NOD mice 28 days after injection. NOD-scid mice showed intermediated pheno-type between NOG mice and NOD mice. These results suggested that immune response for HBV-transfected hepatocytes were

required for clearance of HBV. In contrast, all strain mice transfected with pHBA1.2 showed higher HBV-DNA levels than those transfected with pHBC1.2. Together with the finding that no difference were observed in the expression of type 1 IFN between pHBA1.2 and pHBC1.2 in any strain mice, it is suggested that mechanisms which are independent of immune response would exist for the difference in clearance between HBV genotypes. Conclusion: Although Immune system is critical for HBV clearance, the different levels of HBV viremia in genotype

A and C remains even in immune deficient mice. It is indicated that immune system is not enough for explaining the difference in HBV genotype A and C clearance. Disclosures: Tetsuo selleck inhibitor Takehara – Grant/Research Support: Chugai Pharmaceutical Co., MSD K.K. The following people have nothing to disclose: Yoshinobu Yokoyama, Hayato Hikita, Teppei Yoshioka, Kaori Mukai, Satoshi Aono, Takatoshi Nawa, Ryotaro Sakamori, Takuya Miyagi, Kazuyoshi Ohkawa, Naoki Hiramatsu, Tomohide Tatsumi Background: It has been reported that interferon treatment could reduce HBs

antigen (HBsAg) production in patients with chronic hepatitis B virus (HBV) infection. However, only limited 上海皓元 HBsAg reduction is observed in patients treated with interferon therapy. One cause of this limitation may be that interferon responsiveness in human hepatocytes is suppressed by HBV infection, and, therefore, interferon stimulated genes (ISGs) are not induced sufficiently to promote anti-viral effects. In the present study, we analyzed whether the suppression of HBV replication using nucleotide analogues (NAs) could improve interferon responsiveness in HBV infected human hepatocytes. Methods: Thirty-seven chronic hepatitis B patients were enrolled. Twenty patients underwent sequential interferon therapy, which included 6 months of conventional interferon therapy, running from one month prior to discontinuation until 5 months after discontinuation of NA therapy. The remaining 17 patients underwent interferon mono-therapy. Serum HBsAg titers were measured every year for 5 years after interferon therapy. To confirm the clinical results, we performed an in vitro study using T23 cells, which were generated from HepG2 cells stably transfected with an HBV expression plasmid.

460) Conclusions:  Children with chronic liver disease, whether in a compensated or decompensated state, had lower serum zinc levels compared with the healthy controls. As the severity of liver disease worsened, the zinc levels decreased. The study suggests that zinc supplementation should constitute part of the micronutrient intake of children with chronic liver disease. “
“Genetic factors are believed to play a role on the development of NAFLD, as even in individuals closely matched for all clinical variables, some do not develop

hepatic steatosis, many develop only simple steatosis, while others steatohep-atitis and eventually, cirrhosis. In order to assess the role of genetic factors that may be associated with NAFLD and NASH, PNPLA3 selleckchem (patatin-like phospholipase domain-containing protein 3), APOC3 (apolipoprotein C3), and PPARG (peroxisome Ixazomib concentration pro-liferator-activated receptor-gamma) single nucleotide polymorphisms (SNPs) were analyzed. A total of 176 patients were included

in the study. Liver magnetic resonance imaging and spectroscopy (1H-MRS) and a liver biopsy (n=131) were performed to characterize liver disease. An oral glucose tolerance test was performed to determine diabetes status and insulin resistance was calculated during the fasting state (HOMA-IR and AdipoIR [fasting plasma free fatty acids × insulin]). Polymorphisms associated with increased liver fat by 1H-MRS after adjusting for age, gender, and ethnicity 上海皓元医药股份有限公司 included: rs738409 (PNPLA3: +3.4% liver fat per G allele, p=0.03) and rs2281135 (PNPLA3: +3.1% liver fat per T allele, p=0.05). Moreover,

both of these SNPs were also associated with higher plasma alanine aminotransferase levels (an increase of 7±3 IU/L per risk allele for both SNPs after adjustments for age, gender and ethnicity, p=0.04). Neither PPARG nor APOC3 had any association with liver fat content by 1H-MRS. To further characterize the mechanisms by which these SNPs may affect liver fat, their relationship with different measurements of insulin resistance was assessed. None of the examined SNPs were associated with liver (HOMA-IR), or adipose tissue (AdipoIR) insulin resistance. Regarding severity of liver disease, PNPLA3 and APOC3 SNPs were not associated with the presence of NASH, worse necroinflammation, or fibrosis. However, PPARG rs17817276 was associated with the presence of NASH: patients with the GG genotype had a lower prevalence of NASH versus other variants: 50% vs. 86%, p=0.004 (OR=0.39, p=0.03) after adjusting for age, and ethnicity. Conclusions: genetic variants may hold the answer to individual variations in the severity of NAFLD and NASH. Although PNPLA3 SNPs were associated with liver fat content, no significant association was observed with insulin resistance or with severity of NASH. PPARG rs17817276 was associated with a higher prevalence of NASH, which emphasizes the important role that thiazolidinediones (i.e.

460) Conclusions:  Children with chronic liver disease, whether in a compensated or decompensated state, had lower serum zinc levels compared with the healthy controls. As the severity of liver disease worsened, the zinc levels decreased. The study suggests that zinc supplementation should constitute part of the micronutrient intake of children with chronic liver disease. “
“Genetic factors are believed to play a role on the development of NAFLD, as even in individuals closely matched for all clinical variables, some do not develop

hepatic steatosis, many develop only simple steatosis, while others steatohep-atitis and eventually, cirrhosis. In order to assess the role of genetic factors that may be associated with NAFLD and NASH, PNPLA3 Selleckchem GDC-0068 (patatin-like phospholipase domain-containing protein 3), APOC3 (apolipoprotein C3), and PPARG (peroxisome Decitabine mw pro-liferator-activated receptor-gamma) single nucleotide polymorphisms (SNPs) were analyzed. A total of 176 patients were included

in the study. Liver magnetic resonance imaging and spectroscopy (1H-MRS) and a liver biopsy (n=131) were performed to characterize liver disease. An oral glucose tolerance test was performed to determine diabetes status and insulin resistance was calculated during the fasting state (HOMA-IR and AdipoIR [fasting plasma free fatty acids × insulin]). Polymorphisms associated with increased liver fat by 1H-MRS after adjusting for age, gender, and ethnicity medchemexpress included: rs738409 (PNPLA3: +3.4% liver fat per G allele, p=0.03) and rs2281135 (PNPLA3: +3.1% liver fat per T allele, p=0.05). Moreover,

both of these SNPs were also associated with higher plasma alanine aminotransferase levels (an increase of 7±3 IU/L per risk allele for both SNPs after adjustments for age, gender and ethnicity, p=0.04). Neither PPARG nor APOC3 had any association with liver fat content by 1H-MRS. To further characterize the mechanisms by which these SNPs may affect liver fat, their relationship with different measurements of insulin resistance was assessed. None of the examined SNPs were associated with liver (HOMA-IR), or adipose tissue (AdipoIR) insulin resistance. Regarding severity of liver disease, PNPLA3 and APOC3 SNPs were not associated with the presence of NASH, worse necroinflammation, or fibrosis. However, PPARG rs17817276 was associated with the presence of NASH: patients with the GG genotype had a lower prevalence of NASH versus other variants: 50% vs. 86%, p=0.004 (OR=0.39, p=0.03) after adjusting for age, and ethnicity. Conclusions: genetic variants may hold the answer to individual variations in the severity of NAFLD and NASH. Although PNPLA3 SNPs were associated with liver fat content, no significant association was observed with insulin resistance or with severity of NASH. PPARG rs17817276 was associated with a higher prevalence of NASH, which emphasizes the important role that thiazolidinediones (i.e.

460) Conclusions:  Children with chronic liver disease, whether in a compensated or decompensated state, had lower serum zinc levels compared with the healthy controls. As the severity of liver disease worsened, the zinc levels decreased. The study suggests that zinc supplementation should constitute part of the micronutrient intake of children with chronic liver disease. “
“Genetic factors are believed to play a role on the development of NAFLD, as even in individuals closely matched for all clinical variables, some do not develop

hepatic steatosis, many develop only simple steatosis, while others steatohep-atitis and eventually, cirrhosis. In order to assess the role of genetic factors that may be associated with NAFLD and NASH, PNPLA3 Stem Cells antagonist (patatin-like phospholipase domain-containing protein 3), APOC3 (apolipoprotein C3), and PPARG (peroxisome Dabrafenib clinical trial pro-liferator-activated receptor-gamma) single nucleotide polymorphisms (SNPs) were analyzed. A total of 176 patients were included

in the study. Liver magnetic resonance imaging and spectroscopy (1H-MRS) and a liver biopsy (n=131) were performed to characterize liver disease. An oral glucose tolerance test was performed to determine diabetes status and insulin resistance was calculated during the fasting state (HOMA-IR and AdipoIR [fasting plasma free fatty acids × insulin]). Polymorphisms associated with increased liver fat by 1H-MRS after adjusting for age, gender, and ethnicity MCE included: rs738409 (PNPLA3: +3.4% liver fat per G allele, p=0.03) and rs2281135 (PNPLA3: +3.1% liver fat per T allele, p=0.05). Moreover,

both of these SNPs were also associated with higher plasma alanine aminotransferase levels (an increase of 7±3 IU/L per risk allele for both SNPs after adjustments for age, gender and ethnicity, p=0.04). Neither PPARG nor APOC3 had any association with liver fat content by 1H-MRS. To further characterize the mechanisms by which these SNPs may affect liver fat, their relationship with different measurements of insulin resistance was assessed. None of the examined SNPs were associated with liver (HOMA-IR), or adipose tissue (AdipoIR) insulin resistance. Regarding severity of liver disease, PNPLA3 and APOC3 SNPs were not associated with the presence of NASH, worse necroinflammation, or fibrosis. However, PPARG rs17817276 was associated with the presence of NASH: patients with the GG genotype had a lower prevalence of NASH versus other variants: 50% vs. 86%, p=0.004 (OR=0.39, p=0.03) after adjusting for age, and ethnicity. Conclusions: genetic variants may hold the answer to individual variations in the severity of NAFLD and NASH. Although PNPLA3 SNPs were associated with liver fat content, no significant association was observed with insulin resistance or with severity of NASH. PPARG rs17817276 was associated with a higher prevalence of NASH, which emphasizes the important role that thiazolidinediones (i.e.

The primary team was alerted to these

findings, and immediately revised her shunt with normalization of ICP and selleck chemical TCD. Serial TCD monitoring allowed identification of an imminently fatal complication in time to allow a life saving intervention. TCD is a portable, inexpensive, real-time tool providing important physiologic data regarding blood flow velocities and intracranial pressure that is crucial to the care of critically ill patients. “
“Three-dimensional (3D) ultrasound imaging is a new technique that maximizes the information and image quality of traditional 2-dimensional (2D) B-mode scanning. The aim of this study was to evaluate the ability of the 3D ultrasound technique to characterize ulcerated atherosclerotic carotid plaque. Using conventional

2D ultrasound, we examined 284 carotid arteries from 142 consecutive patients (101 men and 41 women; average age, 64 years). Eighty-two carotid arteries were symptomatic with atherosclerotic plaque causing 50-99% stenosis. In 62 arteries, the atherosclerotic plaques were visualized completely AZD6244 price and were further processed to construct 3D images. Two independent observers rated plaque morphology according to a standardized protocol. The 3D ultrasound showed carotid plaque ulceration more frequently than the 2D method (16.1% and 14.5% of plaques, for observers 1 and 2, respectively, versus 6.5% and 9.7% of plaques, for observers 1 and 2, respectively, P= .125 and P= .063, for observers 1 and 2, respectively). The interobserver reproducibility was very good for both methods (κ= .973, SE = .027, P < .001 for 3D, and κ= .885, SE = .055, P < .001 for 2D), although the 3D method was slightly superior to 2D. 3D ultrasound reliably characterized the surface morphology of atherosclerotic

carotid plaques. A trend of superiority of 3D ultrasound over 2D was found in detecting ulcers of carotid artery plaque. “
“Basilar artery occlusion (BAO) is generally considered an emergency and is associated with high mortality and poor functional outcome. Although cases with more benign course without thrombolysis treatment have occasionally been reported, to our knowledge 上海皓元医药股份有限公司 there is only one previous report in which angiography, almost accidentally revealed a clinically unsuspected BAO. A 45-year-old man with treated hypertension and lipidemia had three distinct isolated episodes of dizziness, 2-3 months before he was referred by an internist for an ultrasound neurovascular evaluation. Neurological examination and extensive laboratory work-up was normal; however, transcranial Doppler (TCD) unexpectedly provided findings that first raised the suspicion of BAO, alerting for further work-up. Cerebral angiography demonstrated BAO, just beyond the anterior inferior cerebellar artery origin, as well as extensive intracerebellar collateral circulation.

M OOI, S CHAMBERS, A THOMSON The Canberra Hospital, ACT, Australia Background: EDNAPS, in which propofol is given after the administration of other more traditional sedative agents, has been used for most endoscopic procedures at our hospital since the year 2000. Respiratory compromise related to EDNAPs, including unplanned

endotracheal intubation is much more common with gastroscopies than colonoscopies. It is not clear whether experience with this sort of sedation leads to a fall in unplanned respiratory events. Aims: To assess the safety of EDNAPS for gastroscopies over a 9 year period (2004–2012) and to determine if there is any change in unplanned respiratory events, in particular endotracheal intubation, during this period. Method: A retrospective analysis

Selleckchem HKI 272 was performed of a prospectively entered Medical Emergency Team Calls(METCALLs) database of all the activated METCALLs due to respiratory compromise defined as threatened airway, respiratory arrest, oxygen desaturation <90%, respiratory rate >36 breaths or <5 breaths per minute and decreased level of consciousness. Need for endotracheal intubation post gastroscopy was recorded. The database also included patients’ demographics, indication, complications, total sedation administered and clinical outcomes after the METCALLs. Results: Of the 16393 gastroscopies performed using EDNAPS between 1st January 2004 and 1st Nov 2012, there were 18 METCALLs with an age range of 28- 84 years (mean age 61.5: 76.4% males, 23.6% females; 12 were inpatients and 6 outpatients. The ASA AZD6244 score for these patients were II (n = 3), III (n = 13), IV (n = 1) and one patient with no ASA score recorded. Indications for the gastroscopies were gastrointestinal haemorrhage (n = 6: 4 variceal, 2 non-variceal), dysphagia (n = 5), PEG removal (n = 1) and dyspepsia (n = 1). All activated METCALLs were associated with significant oxygen desaturation 上海皓元医药股份有限公司 – range 51–86%. Outcomes: 11 patients made a full recovery and were discharged from the unit. 7 required

endotracheal intubation and went to the Intensive Care Unit (ICU) of whom 6 were emergency cases for upper gastrointestinal bleeding. The other patient, who had previously undergone major facialmaxillary surgery, had undergone PEG removal. One intubation occurred in 2004, 3 in 2005, 2 in 2006 and 1 in 2008 There were 2 deaths in the intubated group – one in 2004 and one in 2005. They were in a 57 yo male, ASA score III, with Child Pugh C liver disease who presented with variceal haemorrhage and was subsequently found to have a large hepatocellular carcinoma. The other occurred in an 86 year old male with ASA score IV who presented with melena due to a malignant gastric ulcer. He was subsequently found to have Stage IV metastatic lung cancer and was palliated and died 8 days post extubation.

The human hepatic cell lines Huh7 and HepG2 and 293T cells were obtained from the Cell Bank of the Chinese Academy of Sciences. The HepG2-derived HBV-producing stable cell lines HepG2.215 and HepAD38 were kindly provided by Yumei Wen. The cells

were routinely cultured as described.8 Additionally, HepAD38 cells were treated with or without 1 μg/mL doxycycline (Dox) to regulate HBV pregenomic RNA transcription.9 Plasmids used for transfection are listed in Supporting Table 1. All plasmids were prepared using Endo-Free Plasmid Kits (Omega). Human recombinant IFN-α (Calbiochem) was used at 500 U/mL unless specified otherwise. check details Rottlerin was obtained from Sigma. The small interfering RNAs (siRNAs) targeting Pol (Supporting Table 2) and an unrelated control siRNA were purchased from Ribobio (China). Liver biopsies were collected from CHB patients in Shanghai Public Health Clinical Center with informed consent and the approval of the institutional ethics committee. The liver biopsies were obtained percutaneously with a Menghini needle. A part of the biopsy was used for routine histopathological diagnosis, and the remaining fresh tissue was incubated with

500 U/mL IFN-α for 0.5 hours at 37°C and then fixed in formaldehyde, embedded in paraffin, and sectioned for immunostaining. The clinical characteristics of the patients are shown in Supporting Table 3. Co-IP and glutathione S-transferase (GST) pull-down were performed as described10 with minor modifications. MCE公司 Anti-Flag M2 agarose affinity beads (Sigma) were used to precipitate Flag-tagged proteins. Native polyacrylamide gel electrophoresis was performed8 to detect the STAT1/2 heterodimer. Immunoblotting see more was performed with the appropriate antibodies (Supporting Table 4) according to standard protocols. Results are representative of at least three experiments. Total

RNA was extracted using the RNAsimple Total RNA Kit (TianGen) and reverse-transcribed using ReverTra Ace qPCR RT Kit (Toyobo). The complementary DNA samples were subjected to real-time polymerase chain reaction (PCR) using primers specific for the genes listed in Supporting Table 5. For comparisons, the expression of each gene was normalized to that of glyceraldehyde 3-phosphate dehydrogenase. Each PCR was performed in duplicate using Thunderbird SYBR qPCR Mix (Toyobo) in a StepOne Real-Time PCR System (ABI). The results are representative of three independent experiments. Immunofluorescence was performed as described.8 Paraffin sections of liver biopsies were dewaxed, rehydrated, and microwaved before incubation with the primary antibodies. Cytoplasm and nuclear fractions were obtained as described.6 Extracts were analyzed by immunoblotting. Antibodies against β-tubulin and lamin A/C were used as cytoplasmic and nuclear markers, respectively. The hydrodynamic-based HBV mouse model was as described by Huang et al.11 The methods are described in detail in the Supporting Information.

For this purpose, we carried out continuous culture experiments with the diatom Thalassiosira weissflogii (Grunow) G. Fryxell & Hasle exposed to various conditions of light and N supply. The results revealed that a decrease in N acquisition occurred when a significant proportion of the

population was in mitosis. This observation suggests that N acquisition is incompatible with mitosis and therefore that its acquisition rate is not constant during the cell cycle. In addition, environmental conditions, such as light and nutrient supply disrupt the cell cycle at the level of the individual cell, which impacts synchrony of the population. “
“Coralline algae are considered among the most sensitive species to near future ocean RG7422 mw acidification. We tested the effects of elevated pCO2 on the metabolism of the free-living coralline alga Lithothamnion corallioides (“maerl”) and the interactions with changes Enzalutamide in temperature. Specimens were collected in North Brittany (France) and grown for 3 months at pCO2 of 380 (ambient pCO2), 550, 750, and 1000 μatm (elevated pCO2) and at successive temperatures

of 10°C (ambient temperature in winter), 16°C (ambient temperature in summer), and 19°C (ambient temperature in summer +3°C). At each temperature, gross primary production, respiration (oxygen flux), and calcification (alkalinity flux) rates were assessed in the light and dark. Pigments were determined by HPLC. Chl a, carotene, and zeaxanthin were the three major pigments found in L. corallioides thalli. Elevated pCO2 did

not affect pigment content while temperature slightly decreased zeaxanthin and carotene content at 10°C. Gross production was not affected by temperature but was significantly affected by pCO2 with an increase between 380 and 550 μatm. Light, dark, and diel (24 h) calcification rates strongly decreased with increasing pCO2 regardless of the temperature. Although elevated pCO2 only slightly affected gross production in L. corallioides, diel net calcification was reduced by up to 80% under MCE the 1,000 μatm treatment. Our findings suggested that near future levels of CO2 will have profound consequences for carbon and carbonate budgets in rhodolith beds and for the sustainability of these habitats. “
“As part of their strategy to infect the globally important coccolithophore, Emiliania huxleyi (Lohmann) W.W. Hay & H.P. Mohler, Coccolithoviruses trigger and regulate the host’s programmed cell death (PCD) machinery during lytic infection. The induction and recruitment of host metacaspases, specialized, ancestral death proteases that facilitate viral lysis, suggests they may be important subcellular determinants to infection. We examined the “basal” levels and patterns of caspase activity and metacaspase expression in exponentially growing resistant and sensitive E.