22 research outputs found

    Effects of regional and local stresses on fault slip tendency in the southern Taranaki Basin, New Zealand

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    © 2019 Elsevier Ltd Determining the potential for faults to slip is widely employed for evaluating fault slip potential and associated earthquake hazards, and characterising hydrocarbon seal integrity and reservoir properties. Here we use borehole and 3D seismic reflection data to estimate stress orientations and magnitudes, fault geometries and slip tendency in the southern Taranaki Basin, New Zealand. Late Cenozoic normal faults in the basin range in strike from E-W to NE-SW and are associated with stress changes from basin to borehole scales. The Maui and Maari-Manaia regions, part of the eastern mobile belt, show a strike-slip/normal stress regime (SHmax ≄ Sv > Shmin). The Tui region, part of the western stable platform, shows a normal stress regime (Sv > SHmax > Shmin). Both regions have a mean SHmax azimuth of ENE-WSW. Although the southern Taranaki basin is undergoing active deformation at plate tectonic scales, the stress magnitudes appear insufficiently high to reactivate the faults assuming a classic coefficient of friction. SHmax azimuths and SHmax:Sv magnitude ratios vary locally between boreholes and with depth. A borehole that intersects an inactive seismic-scale fault and borehole-scale faults over a 150-m interval shows SHmax to rotate by up to 30° proximal to the faults, which are favourably orientated for slip in both strike-slip and normal regimes. The small borehole-scale faults may, however, be active within the inactive seismic scale fault's damage zone. We highlight changes of slip tendency along faults resulting from local variations in the stress field and non-planar fault geometries that could not be resolved using only seismic reflection data and regional stress tensor. In the Taranaki Basin additional sub-seismic fault mapping, stress information and mechanical rock property testing are required to realise the potential of stress-based prediction of along-fault permeability and fluid migration

    Dense gas formation and destruction in a simulated Perseus-like galaxy cluster with spin-driven black hole feedback

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    Extended filamentary Hα\alpha emission nebulae are a striking feature of nearby galaxy clusters but the formation mechanism of the filaments, and the processes which shape their morphology remain unclear. We conduct an investigation into the formation, evolution and destruction of dense gas in the center of a simulated, Perseus-like, cluster under the influence of a spin-driven jet. We particularly study the role played by condensation of dense gas from the diffuse intracluster medium, and the impact of direct uplifting of existing dense gas by the jets, in determining the spatial distribution and kinematics of the dense gas. We present a hydrodynamical simulation of an idealised Perseus-like cluster using the adaptive mesh refinement code {\sc ramses}. Our simulation includes a supermassive black hole (SMBH) that self-consistently tracks its spin evolution via its local accretion, and in turn drives a large-scale jet whose direction is based on the black hole's spin evolution. We show that the formation and destruction of dense gas is closely linked to the SMBH's feedback cycle, and that its morphology is highly variable throughout the simulation. While extended filamentary structures readily condense from the hot intra-cluster medium, they are easily shattered into an overly clumpy distribution of gas during their interaction with the jet driven outflows. Condensation occurs predominantly onto infalling gas located 5 - 15 kpc from the center during quiescent phases of the central AGN, when the local ratio of the cooling time to free fall time falls below 20, i.e. when tcool/tff<20t_{\rm cool}/t_{\rm ff} < 20. We find evidence for both condensation and uplifting of dense gas, but caution that purely hydrodynamical simulations struggle to effectively regulate the cluster cooling cycle and produce overly clumpy distributions of dense gas morphologies, compared to observation

    Pathologic tearfulness after limbic encephalitis: A novel disorder and its neural basis

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    Objective We investigated the nature and neural foundations of pathologic tearfulness in a uniquely large cohort of patients who had presented with autoimmune limbic encephalitis (aLE). Methods We recruited 38 patients (26 men, 12 women; median age 63.06 years; interquartile range [IQR] 16.06 years) in the postacute phase of aLE who completed questionnaires probing emotion regulation. All patients underwent structural/functional MRI postacutely, along with 67 age- and sex-matched healthy controls (40 men, 27 women; median age 64.70 years; IQR 19.87 years). We investigated correlations of questionnaire scores with demographic, clinical, neuropsychological, and brain imaging data across patients. We also compared patients diagnosed with pathologic tearfulness and those without, along with healthy controls, on gray matter volume, resting-state functional connectivity, and activity. Results Pathologic tearfulness was reported by 50% of the patients, while no patient reported pathologic laughing. It was not associated with depression, impulsiveness, memory impairment, executive dysfunction in the postacute phase, or amygdalar abnormalities in the acute phase. It correlated with changes in specific emotional brain networks: volume reduction in the right anterior hippocampus, left fusiform gyrus, and cerebellum, abnormal hippocampal resting-state functional connectivity with the posteromedial cortex and right middle frontal gyrus, and abnormal hemodynamic activity in the left fusiform gyrus, right inferior parietal lobule, and ventral pons. Conclusions Pathologic tearfulness is common following aLE, is not a manifestation of other neuropsychiatric features, and reflects abnormalities in networks of emotion regulation beyond the acute hippocampal focus. The condition, which may also be present in other neurologic disorders, provides novel insights into the neural basis of affective control and its dysfunction in disease

    Immune enhancement by novel vaccine adjuvants in autoimmune-prone NZB/W F1 mice: relative efficacy and safety

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    <p>Abstract</p> <p>Background</p> <p>Vaccines have profoundly impacted global health although concerns persist about their potential role in autoimmune or other adverse reactions. To address these concerns, vaccine components like immunogens and adjuvants require critical evaluation not only in healthy subjects but also in those genetically averse to vaccine constituents. Evaluation in autoimmune-prone animal models of adjuvants is therefore important in vaccine development. The objective here was to assess the effectiveness of experimental adjuvants: two phytol-derived immunostimulants PHIS-01 (phytanol) and PHIS-03 (phytanyl mannose), and a new commercial adjuvant from porcine small intestinal submucosa (SIS-H), relative to a standard adjuvant alum. Phytol derivatives are hydrophobic, oil-in water diterpenoids, while alum is hydrophilic, and SIS is essentially a biodegradable and collagenous protein cocktail derived from extracellular matrices.</p> <p>Results</p> <p>We studied phthalate -specific and cross-reactive anti-DNA antibody responses, and parameters associated with the onset of autoimmune disorders. We determined antibody isotype and cytokine/chemokine milieu induced by the above experimental adjuvants relative to alum. Our results indicated that the phytol-derived adjuvant PHIS-01 exceeded alum in enhancing anti-phthalate antibody without much cross reactivity with ds-DNA. Relatively, SIS and PHIS-03 proved less robust, but they were also less inflammatory. Interestingly, these adjuvants facilitated isotype switching of anti-hapten, but not of anti-DNA response. The current study reaffirms our earlier reports on adjuvanticity of phytol compounds and SIS-H in non autoimmune-prone BALB/c and C57BL/6 mice. These adjuvants are as effective as alum also in autoimmune-prone NZB/WF1 mice, and they have little deleterious effects.</p> <p>Conclusion</p> <p>Although all adjuvants tested impacted cytokine/chemokine milieu in favor of Th1/Th2 balance, the phytol compounds fared better in reducing the onset of autoimmune syndromes. However, SIS is least inflammatory among the adjuvants evaluated.</p

    Human pancreatic islet transplantation: an update and description of the establishment of a pancreatic islet isolation laboratory

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    Type 1 diabetes mellitus (T1DM) is associated with chronic complications that lead to high morbidity and mortality rates in young adults of productive age. Intensive insulin therapy has been able to reduce the likelihood of the development of chronic diabetes complications. However, this treatment is still associated with an increased incidence of hypoglycemia. In patients with "brittle T1DM", who have severe hypoglycemia without adrenergic symptoms (hypoglycemia unawareness), islet transplantation may be a therapeutic option to restore both insulin secretion and hypoglycemic perception. The Edmonton group demonstrated that most patients who received islet infusions from more than one donor and were treated with steroid-free immunosuppressive drugs displayed a considerable decline in the initial insulin independence rates at eight years following the transplantation, but showed permanent C-peptide secretion, which facilitated glycemic control and protected patients against hypoglycemic episodes. Recently, data published by the Collaborative Islet Transplant Registry (CITR) has revealed that approximately 50% of the patients who undergo islet transplantation are insulin independent after a 3-year follow-up. Therefore, islet transplantation is able to successfully decrease plasma glucose and HbA1c levels, the occurrence of severe hypoglycemia, and improve patient quality of life. The goal of this paper was to review the human islet isolation and transplantation processes, and to describe the establishment of a human islet isolation laboratory at the Endocrine Division of the Hospital de ClĂ­nicas de Porto Alegre - Rio Grande do Sul, Brazil

    Feeding behaviour of broiler chickens: a review on the biomechanical characteristics

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    Network-wide abnormalities explain memory variability in hippocampal amnesia

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    Patients with hippocampal amnesia play a central role in memory neuroscience but the neural underpinnings of amnesia are hotly debated. We hypothesized that focal hippocampal damage is associated with changes across the extended hippocampal system and that these, rather than hippocampal atrophy per se, would explain variability in memory between patients. We assessed this hypothesis in a uniquely large cohort of patients (n = 38) after autoimmune limbic encephalitis, a syndrome associated with focal structural hippocampal pathology. These patients showed impaired recall, recognition and maintenance of new information, and remote autobiographical amnesia. Besides hippocampal atrophy, we observed correlatively reduced thalamic and entorhinal cortical volume, resting-state inter-hippocampal connectivity and activity in posteromedial cortex. Associations of hippocampal volume with recall, recognition, and remote memory were fully mediated by wider network abnormalities, and were only direct in forgetting. Network abnormalities may explain the variability across studies of amnesia and speak to debates in memory neuroscience. </p
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