The impact of potential leakage from the sub-seabed CO2 storage site on the phosphorus transformation in marine sediments - An experimental study.

Carbon Capture and Storage (CCS) in the sub-seabed geological formations is a method of mitigation of carbon dioxide (CO2) emissions to avoid anthropogenic climate change. While CCS can be one of the most promising technologies to reduce atmospheric CO2 in the short and medium term, it raises serious concerns about the potential leakage of gas from storage sites. In the present study, the impact of acidification induced by CO2 leakage from a sub-seabed storage site on geochemical pools, and thus the mobility, of phosphorus (P) in sediment was investigated during laboratory experiments. The experiments were conducted in a hyperbaric chamber at a hydrostatic pressure of 900 kPa, which simulates pressure conditions at a potential sub-seabed CO2 storage site in the southern Baltic Sea. We performed three separate experiments in which the partial pressure of CO2 was: 352 µatm (corresponding pH = 7.7); 1815 µatm (corresponding pH = 7.0), and 9150 µatm (corresponding pH = 6.3). Under pH 7.0 and 6.3, apatite P is transformed into organic and non-apatite inorganic forms, which are less stable than CaP bonds and can be more easily released into the water column. At pH 7.7, P released during mineralization of organic matter and microbial reduction of FeP phases is bound with Ca, and the concentration of this form increases. The obtained results indicate that acidification of bottom water can reduce the efficiency of P burial in marine sediments, which contributes to an increase in P concentration in the water column and promote eutrophication especially in shallow areas.

Stable COX17 Downregulation Leads to Alterations in Mitochondrial Ultrastructure, Decreased Copper Content and Impaired Cytochrome c Oxidase Biogenesis in HEK293 Cells.

Cox17 is an assembly factor that participates in early cytochrome c oxidase (COX, CcO) assembly stages. Cox17 shuttles copper ions from the cytosol to the mitochondria and, together with Sco1 and Sco2, provides copper ions to the Cox1 and Cox2 mitochondrially encoded subunits. In Saccharomyces cerevisiae, Cox17 also modulates mitochondrial membrane architecture due to the interaction of Cox17 with proteins of the MICOS complex (mitochondrial contact site and cristae organizing system). There is currently no data regarding the impact of long-term Cox17 deficiency in human cells. Here, we present construction and characterization of three stable COX17 shRNA-downregulated HEK293 cell lines that have less than 10 % of the residual Cox17 protein level. Cox17-depleted cell lines exhibited decreased intramitochondrial copper content, decreased CcO subunit levels (Cox1, Cox4 and Cox5a) and accumulation of CcO subcomplexes. Similarly to yeast cells, mitochondria in Cox17-downregulated HEK293 cell lines exhibited ultrastructural changes including cristae reduction and mitochondrial swelling. Characterization of the molecular pathogenesis of long-term Cox17 deficiency complements our knowledge of the mitochondrial copper metabolism and assembly of cytochrome c oxidase in human cells.

The relationship between the concentrations and distribution of organic pollutants and black carbon content in benthic sediments in the Gulf of Gdansk, Baltic Sea.

The influence of the sediment's physico-chemical properties and black carbon content, on the distribution of polycyclic aromatic hydrocarbons and polychlorinated biphenyls in benthic sediments of the Gulf of Gdansk (Baltic Sea) was determined. Sediments from port, marine dump site of dredged spoils, the Vistula river mouth, Gdansk Deep were selected. The concentrations of ∑PAHs (fluoranthene, pyrene, benzo(a)anthracene, benzo(k)fluoranthene, benzo(a)pyrene, dibenzo(ah)anthracene, benzo(ghi)perylene) were 294-2200 ng/g d.w. and for ∑PCBs (28, 52, 101, 118, 138, 153, 180) were 2.4-11.3 ng/g d.w. The sediments content of loss on ignition was 1.13-16.15%, total organic carbon was 0.89-7.15%, black carbon was 0.20-1.15%. The highest correlation coefficient values (r=0.76-0.92, p<0.05) for a relationship between the concentrations of organic pollutants, and organic matter, organic and black carbon contents were obtained in harbor sediments with low content of organic matter (<5%) and high share of black carbon in total carbon (up to 40%).

[Left ventricular electromechanical latency period is an additional indicator to upgrade from right to biventricular DDD pacing]. / Die linksventrikuläre elektromechanische Latenzzeit ist ein zusätzlicher Indikator für ein Upgrading zur biventrikulären Stimulation.

In DDD pacing, the left-ventricular electromechanical latency period defines the duration between premature ventricular stimulation and the prematurely ending left-atrial contribution to left-ventricular filling. It has to be considered in diastolic AV delay optimization. Individual duration of this parameter seemed to reflect the ventricular function. Therefore, we compared the left-ventricular electromechanical latency period due to right ventricular stimulus with the documented ejection fraction of two groups, 33 congestive heart failure patients carrying biventricular systems and 13 right ventricular paced bradycardia patients. A mean latency period of 168+/-26 ms was found in the heart failure patients (ejection fraction: 25+/-5%) which was significantly longer (p=0.0039) compared to the bradycardia patients (ejection fraction: 51+/-12%) with a mean latency of 119+/-13 ms. Thus, an increasing latency period during right ventricular DDD pacing therapy indicates decreasing ejection fraction. A cut-off interval of 135 ms allowed the discrimination of 93% of our patients as having an individual ejection fraction of either up to 35% or above. Thus, the left ventricular electromechanical latency period can be used as an additional parameter indicating the necessity to upgrade from right to biventricular DDD pacing.

Effect of nitric oxide in ischemia/reperfusion of the pancreas.

BACKGROUND: Ischemia/reperfusion injury, and thus graft pancreatitis, remains a major problem in pancreas transplantation. Contradictory results about the role of nitric oxide (NO) in pancreatic ischemia/reperfusion have been reported; however, in none of the reports has a detailed comparison between inhibition of NO synthase and NO supplementation been carried out. METHODS: Vascular isolation of the pancreatic tail was performed in landrace pigs. After splenectomy catheters placed in the distal part of the splenic vessels allowed collection of the venous effluent and perfusion of the pancreatic tail. Three hours of complete warm ischemia was followed by 6 h of reperfusion. The effect of the NO donor sodium nitroprusside (SNP) and L-arginine was compared to a control group and NO synthase inhibition with L-NAME. RESULTS: Lipase in the venous effluent of the pancreas was significantly decreased in the SNP and the L-arginine groups. Vascular resistance was markedly elevated in the L-NAME group and reduced in the NO donor groups. Tissue pO2 after reperfusion was only significantly elevated in the SNP group. Granulocyte infiltration and also overall histological tissue injury were most severe in the control group followed by the L-NAME group, the SNP group, and the L-ARG group. CONCLUSION: The data show that supplementation of nitric oxide is clearly protective in pancreatic ischemia/reperfusion. However, inhibition of NO synthesis does not lead to an equally clear aggravation of tissue injury.