Offshore CO2 storage: Sleipner natural gas field beneath the North Sea

Sleipner is the world's longest-running industrial-scale storage project and the first example of underground CO2 storage arising as a direct response to environmental legislation. It began in 1996, injecting around one million tonnes (1 Mt) of CO2 per year into the Utsira Sand, a relatively shallow saline aquifer. By late 2011 over 13 Mt of CO2 had been securely stored. A comprehensive research-focused monitoring programme was carried out with multiple time-lapse surveys; predominantly 3D seismic but also 2D seismic, gravimetry and controlled-source electromagnetics (CSEM). The time-lapse seismic data image the CO2 plume clearly in the reservoir with very high detection capability and show no evidence of CO2 migration from the storage reservoir. Although not specifically designed for this purpose, the monitoring programme fulfils most of the requirements of the recently developed European regulatory framework for CO2 underground storage

Saline aquifer CO2 storage : a demonstration project at the Sleipner Field : Work Area 5 (Geophysics) : gravity modelling of the CO2 bubble

A principal aim of the SACS project is to monitor the injected CO2 by geophysical methods and to develop a robust and repeatable monitoring and verification methodology for future CO2 sequestration operations. This report evaluates the applicability of microgravity surveys as a means of monitoring the future subsurface distribution and migration of the Sleipner CO2 bubble. Time-lapse seismic data acquired in 1999, after 2.3 MT of CO2 injection, show an exceptionally clear image of the CO2 bubble, characterised by very high reflection amplitudes. The outer envelope of the amplitude anomaly roughly defines an elliptical cylindrical ‘bubble envelope’, ~ 225 m high, with a major axis of ~ 1500 m oriented NNE and a minor axis of ~ 600 m. Gravity modelling was based on a number of scenarios. Two ‘in situ’ scenarios assume that the CO2 is entirely contained within the bubble envelope. The 1999 and 2001 in situ models assume respectively that 2.3 MT and 4MT of CO2 are contained within the envelope. Two migration scenarios are also modelled. The first assumes that 2.3MT of CO2 migrate vertically upwards into the overlying caprock succession to between depths of 375 and 600 m. The second migration model looks further ahead to the situation where 3 x 107 m3 (~ 10.5 – 21.0 MT depending on the density) of CO2 have been injected, and migrate laterally beneath the caprock at the top of the reservoir. Results depend strongly on the assumed density of the injected CO2 at reservoir conditions, which is subject to significant uncertainty. Only one, poorly-constrained, reservoir temperature measurement of 37 ° C is available. A density-depth profile based on this suggests that the density of CO2 in the reservoir is ~ 700 kgm-3. However the possibility of significantly lower densities cannot be discounted and modelling also includes a lower density case of 350 kgm-3. The 1999 and 2001 in situ cases produce anomalies which would be barely detectable if the higher density of CO2 is assumed. With the lower density however anomalies should be readily detectable with a modern seabed gravimeter. The vertical migration scenario indicates that large-scale vertical migration into the caprock, to depths where densities would be unequivocally lower, would be readily detected. The lateral migration scenario, whereby a single thin layer of CO2 migrates beneath the top reservoir seal, produces small anomalies which may be locally detectable but with insufficient resolution to enable effective migration mapping. However if lateral migration is via several layers, beneath intra-reservoir shales, then anomalies should be more usefully measurable. Obtaining time-lapse gravimeter readings directly above the bubble would appear to offer the best chance of obtaining useful information. Coupled with geometric information provided by the time-lapse seismic data, the gravity should be able to discriminate between the low and high CO2 density scenarios. This would provide important constraints on future reservoir modelling and also the volume estimates based on the seismic velocity pushdown effect. Related to this, gravity data would offer the potential to provide independent verification of the amount of CO2 sequestered. In addition gravimetric surveys above the bubble could provide an effective ‘early warning’ of major caprock breaching

Cutaneous exposure to hypoxia does not affect skin perfusion in humans.

$\textbf{Aim:}$ Experiments have indicated that skin perfusion in mice is sensitive to reductions in environmental O$_2$ availability. Specifically, a reduction in skin-surface PO$_2$ attenuates transcutaneous O$_2$ diffusion, and hence epidermal O$_2$ supply. In response, epidermal HIF-1$\alpha$ expression increases and facilitates initial cutaneous vasoconstriction and subsequent nitric oxide-dependent vasodilation. Here, we investigated whether the same mechanism exists in humans. $\textbf{Methods:}$ In a first experiment, eight males rested twice for 8 h in a hypobaric chamber. Once, barometric pressure was reduced by 50%, while systemic oxygenation was preserved by O$_2$-enriched (42%) breathing gas (Hypoxia$_\text{Skin}$), and once barometric pressure and inspired O$_2$ fraction were normal (Control$_1$). In a second experiment, nine males rested for 8 h with both forearms wrapped in plastic bags. O$_2$ was expelled from one bag by nitrogen flushing (Anoxia$_\text{Skin}$), whereas the other bag was flushed with air (Control$_2$). In both experiments, skin blood flux was assessed by laser Doppler on the dorsal forearm, and HIF-1$\alpha$ expression was determined by immunohistochemical staining in forearm skin biopsies. $\textbf{Results:}$ Skin blood flux during Hypoxia$_\text{Skin}$ and Anoxia$_\text{Skin}$ remained similar to the corresponding Control trial ($P$ = 0.67 and $P$ = 0.81). Immunohistochemically stained epidermal HIF-1$\alpha$ was detected on 8.2 ± 6.1 and 5.3 ± 5.7% of the analysed area during Hypoxia$_\text{Skin}$ and Control$_1$ ($P$ = 0.30) and on 2.3 ± 1.8 and 2.4 ± 1.8% during Anoxia$_\text{Skin}$ and Control$_2$ ($P$ = 0.90) respectively. $\textbf{Conclusion:}$ Reductions in skin-surface PO$_2$ do not affect skin perfusion in humans. The unchanged epidermal HIF-1$\alpha$ expression suggests that epidermal O$_2$ homoeostasis was not disturbed by Hypoxia$_\text{Skin}$/Anoxia$_\text{Skin}$, potentially due to compensatory increases in arterial O$_2$ extraction.Gösta Fraenckel Foundatio

Inverse correlation between PDGFC expression and lymphocyte infiltration in human papillary thyroid carcinomas

<p>Abstract</p> <p>Background</p> <p>Members of the PDGF family have been suggested as potential biomarkers for papillary thyroid carcinomas (PTC). However, it is known that both expression and stimulatory effect of PDGF ligands can be affected by inflammatory cytokines. We have performed a microarray study in a collection of PTCs, of which about half the biopsies contained tumour-infiltrating lymphocytes or thyroiditis. To investigate the expression level of PDGF ligands and receptors in PTC we measured the relative mRNA expression of all members of the PDGF family by qRT-PCR in 10 classical PTC, eight clinically aggressive PTC, and five non-neoplastic thyroid specimens, and integrated qRT-PCR data with microarray data to enable us to link PDGF-associated gene expression profiles into networks based on recognized interactions. Finally, we investigated potential influence on PDGF mRNA levels by the presence of tumour-infiltrating lymphocytes.</p> <p>Methods</p> <p>qRT-PCR was performed on <it>PDGFA</it>, <it>PDGFB</it>, <it>PDGFC</it>, <it>PDGFD</it>, <it>PDGFRA PDGFRB </it>and a selection of lymphocyte specific mRNA transcripts. Semiquantitative assessment of tumour-infiltrating lymphocytes was performed on the adjacent part of the biopsy used for RNA extraction for all biopsies, while direct quantitation by qRT-PCR of lymphocyte-specific mRNA transcripts were performed on RNA also subjected to expression analysis. Relative expression values of PDGF family members were combined with a cDNA microarray dataset and analyzed based on clinical findings and PDGF expression patterns. Ingenuity Pathway Analysis (IPA) was used to elucidate potential molecular interactions and networks.</p> <p>Results</p> <p>PDGF family members were differentially regulated at the mRNA level in PTC as compared to normal thyroid specimens. Expression of <it>PDGFA </it>(p = 0.003), <it>PDGFB </it>(p = 0.01) and <it>PDGFC </it>(p = 0.006) were significantly up-regulated in PTCs compared to non-neoplastic thyroid tissue. In addition, expression of <it>PDGFC </it>was significantly up-regulated in classical PTCs as compared to clinically aggressive PTCs (p = 0.006), and <it>PDGFRB </it>were significantly up-regulated in clinically aggressive PTCs (p = 0.01) as compared to non-neoplastic tissue. Semiquantitative assessment of lymphocytes correlated well with quantitation of lymphocyte-specific gene expression. Further more, by combining TaqMan and microarray data we found a strong inverse correlation between <it>PDGFC </it>expression and the expression of lymphocyte specific mRNAs.</p> <p>Conclusion</p> <p>At the mRNA level, several members of the PDGF family are differentially expressed in PTCs as compared to normal thyroid tissue. Of these, only the <it>PDGFC </it>mRNA expression level initially seemed to distinguish classical PTCs from the more aggressive PTCs. However, further investigation showed that <it>PDGFC </it>expression level correlated inversely to the expression of several lymphocyte specific genes, and to the presence of lymphocytes in the biopsies. Thus, we find that <it>PDGFC </it>mRNA expression were down-regulated in biopsies containing infiltrated lymphocytes or thyroiditis. No other PDGF family member could be linked to lymphocyte specific gene expression in our collection of PTCs biopsies.</p

Wolcott-Rallison syndrome

Wolcott-Rallison syndrome (WRS) is a rare autosomal recessive disease, characterized by neonatal/early-onset non-autoimmune insulin-requiring diabetes associated with skeletal dysplasia and growth retardation. Fewer than 60 cases have been described in the literature, although WRS is now recognised as the most frequent cause of neonatal/early-onset diabetes in patients with consanguineous parents. Typically, diabetes occurs before six months of age, and skeletal dysplasia is diagnosed within the first year or two of life. Other manifestations vary between patients in their nature and severity and include frequent episodes of acute liver failure, renal dysfunction, exocrine pancreas insufficiency, intellectual deficit, hypothyroidism, neutropenia and recurrent infections. Bone fractures may be frequent. WRS is caused by mutations in the gene encoding eukaryotic translation initiation factor 2α kinase 3 (EIF2AK3), also known as PKR-like endoplasmic reticulum kinase (PERK). PERK is an endoplasmic reticulum (ER) transmembrane protein, which plays a key role in translation control during the unfolded protein response. ER dysfunction is central to the disease processes. The disease variability appears to be independent of the nature of the EIF2AK3 mutations, with the possible exception of an older age at onset; other factors may include other genes, exposure to environmental factors and disease management. WRS should be suspected in any infant who presents with permanent neonatal diabetes associated with skeletal dysplasia and/or episodes of acute liver failure. Molecular genetic testing confirms the diagnosis. Early diagnosis is recommended, in order to ensure rapid intervention for episodes of hepatic failure, which is the most life threatening complication. WRS should be differentiated from other forms of neonatal/early-onset insulin-dependent diabetes based on clinical presentation and genetic testing. Genetic counselling and antenatal diagnosis is recommended for parents of a WRS patient with confirmed EIF2AK3 mutation. Close therapeutic monitoring of diabetes and treatment with an insulin pump are recommended because of the risk of acute episodes of hypoglycaemia and ketoacidosis. Interventions under general anaesthesia increase the risk of acute aggravation, because of the toxicity of anaesthetics, and should be avoided. Prognosis is poor and most patients die at a young age. Intervention strategies targeting ER dysfunction provide hope for future therapy and prevention