ALUM SHALE BITUMEN MATURATION AND MIGRATION: IMPLICATIONS FOR GOTLAND'S OIL

Thermal maturation of Swedish Alum Shale kerogen and bitumen has been determined from core samples from Eastern and Central Sweden. In samples from Eastern Sweden (Öland and Gotland), the kerogen and bitumen are thermally immature with respect to petroleum generation. In some areas of Central Sweden (Närke, ÖstergÖtland, and Kinnekulle in VästergÖtland), the kerogen is immature, whereas the bitumen is marginally mature to mature. In other areas of Central Sweden (Halleberg-Hunneberg in VästergÖtland), the kerogen is supermature and the bitumen mature. This suggests that bitumen from a mature source-rock has migrated into the Alum Shales of Central Sweden. Migration in Central Sweden is further evidenced by the occurrence of obviously-migrated bituments in vugs and voids in the organicpoor Ordovician limestone overlying the Alum Shale in Central Sweden, and in concretions within the Alum Shale itself. Based on biomarker distributions of extracted bitumen, Alum Shale kerogen pyrolysate and obviously-migrated oils, and the fact that the Alum Shale in most of the areas studied is the only petroleum source-rock extant, it is suggested that the migrated bitumen in Central Sweden is from the Alum Shale itself. Bitumen has migrated from areas where the Alum Shale is in close proxmity to Permo-Carboniferous intrusions, such as Halleberg-Hunneberg, into nearby areas such as Närke and ÖstergÖtland, where there is no evidence of intrusion and the indigenous organic matter is thermally immature. Other areas, where Alum Shales were associated with intrusions and consequently sourced oil, may have been eroded away. There are producing wells on the island of Gotland, where the Alum Shale is also thermally immature. It is therefore assumed that heating which was responsible for generating Gotland's oil was very localized (such as by an intrusion) or that the oil has migrated from a thermally moremature, distant area. On the basis of reservoir rock porosity, and the fact that the Alum Shale of Gotland contains no migrated component, localized heating is favored.     

The boundary contour method for two-dimensional Stokes flow and incompressible elastic materials

 A variant of the boundary element method, called the boundary contour method (BCM), offers a further reduction in dimensionality. Consequently, boundary contour analysis of two-dimensional (2-D) problems does not require any numerical integration at all. While the method has enjoyed many successful applications in linear elasticity, the above advantage has not been exploited for Stokes flow problems and incompressible media. In order to extend the BCM to these materials, this paper presents a development of the method based on the equations of Stokes flow and its 2-D kernel tensors. Potential functions are derived for quadratic boundary elements. Numerical solutions for some well-known examples are compared with the analytical ones to validate the development. Received 28 August 2001 / Accepted 15 January 2002     

Spatial learning deficits in mice with a targeted glucocorticoid receptor gene disruption

Previous studies in rats using the Morris water maze suggested that the processing of spatial information is modulated by corticosteroid hormones through mineralocorticoid and glucocorticoid receptors in the hippocampus. Mineralocorticoid receptors appear to be involved in the modulation of explorative behaviour, while additional activation of glucocorticoid receptors facilitates the storage of information. In the present study we used the water maze task to examine spatial learning and memory in mice homozygous and heterozygous for a targeted disruption of the glucocorticoid receptor gene. Compared with wild-type controls, homozygous and heterozygous mice were impaired in the processing of spatial but not visual information. Homozygous mutants performed variably during training, without specific platform-directed search strategies. The spatial learning disability was partly compensated for by increased motor activity. The deficits were indicative of a dysfunction of glucocorticoid receptors as well as of mineralocorticoid receptors. Although the heterozygous mice performed similarly to wild-type mice with respect to latency to find the platform, their strategy was more similar to that of the homozygous mice. Glucocorticoid receptor-related long-term spatial memory was impaired. The increased behavioural reactivity of the heterozygous mice in the open field points to a more prominent mineralocorticoid receptor-mediated function. The findings indicate that (i) the glucocorticoid receptor is of critical importance for the control of spatial behavioural functions, and (ii) mineralocorticoid receptor-mediated effects on this behaviour require interaction with functional glucocorticoid receptors. Until the development of site-specific, inducible glucocorticoid receptor mutants, glucocorticoid receptor-knockout mice present the only animal model for the study of corticosteroid-mediated effects in the complete absence of a functional receptor.     

Myoblast-mediated gene transfer to the joint

Several genetic and acquired pathologic conditions of the musculoskeletal system, such as arthritis and damage to ligament, cartilage, and meniscus, may be amenable to gene therapy. Even though ex vivo gene transfer with synovial cells has been shown to deliver genes encoding for anti-arthritic proteins into the rabbit knee joint, its success has been limited by a transient transgene expression. In this study, data were investigated regarding the use of muscle cells as an alternative gene-delivery vehicle to the joint in newborn rabbit and adult severe combined immunodeficiency mice. We demonstrated that myoblasts were transduced more efficiently than synovial cells with use of the same adenoviral preparation in vitro. After intra-articular injection, the engineered muscle cells adhered to several structures in the joint, including the ligament, capsule, and synovium. In addition, myoblasts fused to form many post-mitotic myotubes and myofibers at different locations of the joint of the newborn rabbit 5 days after the injection. In the knee of the adult mouse, myoblasts fused and expressed the reporter gene for at least 35 days after the injection. The presence of post-mitotic myofibers in the knee joint raises the possibility of long-term expression of the secreted protein. Currently, numerous tissues in the joint (ligament, meniscus, and cartilage) have poor intrinsic healing capacity and frequently need surgical corrections. A stable gene-delivery vehicle to the joint producing proteins that ameliorate these different musculoskeletal conditions may change the clinical implications of these pathologies.     

GABA and glutamate levels in the substantia nigra reticulata following repetitive cerebral ischemia in gerbils

Repetitive cerebral ischemia produces more severe damage than a similar single duration insult. We have previously shown that, in gerbils, damage in the substantia nigra reticulata (SNr) is seen with repetitive insults rather than a single insult. We have also shown that there is a progressive decrease in the extracellular GABA in the striatum in the days preceding such damage, speculating that a loss of GABA may be in part responsible for this damage. This study evaluates the GABA levels in the SNr in animals exposed to repetitive ischemic insults. Each animal received a total of three ischemic insults of 3-min duration at hourly intervals. In vivo microdialysis was carried out to analyze the GABA and glutamate dialysate levels on Days 1, 3, 5, 7, and 14 following the ischemic insult. In the control and treated (ischemic) animals, there was a significant increase in the GABA levels with the introduction of nipecotic acid on Days 1, 3, 5, and 14. However, on Day 7 there was a significant attenuation in the GABA response to nipecotic acid in the treated animals in comparison to the controls. The glutamate levels in the treated animals were similar to the control animals on Days 1, 3, 5, and 7. However, on Day 14 the glutamate levels were significantly lower than on previous days. Our experiments for the first time measure extracellular glutamate and GABA responses in the SNr in animals exposed to repetitive ischemic insults. Our experiments show that there is a significant decrease in the GABA concentrations at a time when ischemic damage is developing in this region. This confirms our hypothesis that a decrease in GABA may be one factor contributing to neuronal damage during the period following repetitive ischemic insults. Further, the rebound increase in GABA levels on Day 14 with a concomitant fall in glutamate levels would indicate that reparative processes are still active in the 2 weeks following the insult.