A comparison of the floras of the Colchester (No. 2) Coal and Francis Creek Shale

Abundant data from spore studies of the Colchester (no. 2) Coal Member and from investigations of plant compressions in the Francis Creek Shale provide an opportunity to compare the flora of the coal with that of the overlying shale in the northeastern part of the Illinois Basin. As both floras were investigated by different methods and since different systems of form genera were used, it is first necessary to review the plant taxa found in the 2 facies and to arrange them according to major plant groups. Paleoenvironmental interpretations of Pennsylvanian floras are rare and widely scattered in the literature; therefore some of the research on fossil spores and plant assemblages from other strata is discussed in this report. Finally, the report presents an interpretation of paleoecological conditions that existed during deposition of peat and mud, which eventually formed the No. 2 Coal and Francis Creek Shale

Inhibition of Growth of Toxoplasma Gondii in Cultured Fibroblasts by Human Recombinant Gamma Interferon.

The growth of Toxoplasma gondii in cultured human fibroblasts was inhibited by recombinant human gamma interferon at concentrations of 8 to 16 U/ml. The interferon was titrated by observing a total inhibition of parasite plaque formation 7 days after infection. Inhibition of the growth of T. gondii in the early days after infection was measured by marked reductions in the incorporation of radioactive uracil, a precursor that can only be used by the parasites. This assay showed that when cells were pretreated with gamma interferon for 1 day and then infected, inhibition of T. gondii growth could be readily detected 1 or 2 days after infection. When the pretreatment was omitted and parasites and gamma interferon were added at the same time, no inhibition of parasite growth could be detected 1 day later, although it was apparent after 2 days. Cultures from which the gamma interferon had been removed by washing after a 1-day treatment showed inhibition of T. gondii growth. Gamma interferon had no effect on the viability of extracellular parasites, but it did inhibit the synthesis of host cell RNA and protein by ca. 50% 3 days after treatment. This degree of inhibition is unlikely, of itself, to compromise the growth of T. gondii. Recombinant alpha and beta interferons had no effect on the growth of T. gondii

User-Centric Monitoring and Steering of the Execution of Large Job Sets

Processing of large data sets with high through put is one of the major focus of Grid computing today. If possible, data are split up into small chunks that are processed independently. Thus, job sets of hundreds > or even thousands of individual jobs are possible. For the job submitter or the resource providers such a scenario is a nightmare currently, as it is hard to keep track of such an amount of jobs or to identify failure reasons. We present a system that will support gLite users to track and monitor their jobs and their resource usage, to nd and identify failure reasons and even to steer running applications

Antiparasitic and Antiproliferative Effects of Indoleamine 2,3-dioxygenase Enzyme Expression in Human Fibroblasts.

Studies were carried out to evaluate the proposed role of indoleamine 2,3-dioxygenase (INDO) induction in the antimicrobial and antiproliferative effects of gamma interferon (IFN-gamma) in human fibroblasts. The INDO cDNA coding region was cloned in the pMEP4 expression vector, containing the metallothionein (MTII) promoter in the sense (+ve) or the antisense (-ve) orientation. Human fibroblasts (GM637) stably transfected with the sense construct expressed INDO activity after treatment with CdCl2 or ZnSO4, but cells transfected with the antisense construct did not. The growth of Chlamydia psittaci was strongly inhibited in INDO +ve cells but not in INDO -ve cells after treatment with Cd2+ or Zn2+. The inhibition correlated with the level of INDO activity induced and could be reversed by the addition of excess tryptophan to the medium. The growth of Toxoplasma gondii was also strongly inhibited in INDO +ve cells but not in INDO -ve cells after treatment with Cd2+. Expression of Cd(2+)-induced INDO activity also inhibited thymidine incorporation and led to cytotoxicity in INDO +ve cells but not in INDO -ve cells. Thus, the induction of INDO activity by IFN-gamma may be an important factor in the antimicrobial and antiproliferative effects of IFN-gamma in human fibroblasts

Regional astrocyte IFN signaling restricts pathogenesis during neurotropic viral infection

Type I IFNs promote cellular responses to viruses, and IFN receptor (IFNAR) signaling regulates the responses of endothelial cells of the blood-brain barrier (BBB) during neurotropic viral infection. However, the role of astrocytes in innate immune responses of the BBB during viral infection of the CNS remains to be fully elucidated. Here, we have demonstrated that type I IFNAR signaling in astrocytes regulates BBB permeability and protects the cerebellum from infection and immunopathology. Mice with astrocyte-specific loss of IFNAR signaling showed decreased survival after West Nile virus infection. Accelerated mortality was not due to expanded viral tropism or increased replication. Rather, viral entry increased specifically in the hindbrain of IFNAR-deficient mice, suggesting that IFNAR signaling critically regulates BBB permeability in this brain region. Pattern recognition receptors and IFN-stimulated genes had higher basal and IFN-induced expression in human and mouse cerebellar astrocytes than did cerebral cortical astrocytes, suggesting that IFNAR signaling has brain region–specific roles in CNS immune responses. Taken together, our data identify cerebellar astrocytes as key responders to viral infection and highlight the existence of distinct innate immune programs in astrocytes from evolutionarily disparate regions of the CNS

Measurement of Tool-Workpiece Interface Temperature Distribution in Friction Stir Welding

The objective of this work is to develop an improved temperature measurement system for friction stir welding (FSW). FSW is a solid-state joining process enabling welds with excellent metallurgical and mechanical properties, as well as significant energy consumption and cost savings compared to traditional fusion welding processes. The measurement of temperatures during FSW is needed for process monitoring, heat transfer model verification and process control, but current methods have limitations due to their restricted spatial and temporal resolution. Previous work showed that temperatures at the tool shoulder-workpiece interface can be measured and utilized for closed-loop control of temperature. Adding an additional thermocouple at the tool pin-workpiece interface and performing a calibration of the measurement to gain better insight into the temperature distribution in the weld zone improved the method. Both thermocouples were placed in through holes right at the interface of tool so that the sheaths are in direct contact with the workpiece material. This measurement strategy reveals dynamic temperature variations at the shoulder and the pin within a single rotation of the tool in realtime. It was found that the highest temperatures are at the shoulder interface between the advancing side and the trailing edge of the tool, closer to the advancing side. The temperature distribution was mostly affected by travel speed and the temperature difference within one tool rotation was found to be between 10 C and 50 C, depending on the process parameters. The dynamic temperature measurements obtained with the current system are of unmatched resolution, fast, and reliable and are likely to be of interest for both fundamental studies and process control of FSW

Cysteinyl Leukotriene Levels in Esophageal Mucosal Biopsies of Children with Eosinophilic Inflammation: Are They All the Same?

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75498/1/j.1572-0241.2006.00557.x.pd

Kynurenine pathway inhibition reduces central nervous system inflammation in a model of human African trypanosomiasis

Human African trypanosomiasis, or sleeping sickness, is caused by the protozoan parasites <i>Trypanosoma brucei rhodesiense</i> or <i>Trypanosoma brucei gambiense</i>, and is a major cause of systemic and neurological disability throughout sub-Saharan Africa. Following early-stage disease, the trypanosomes cross the blood-brain barrier to invade the central nervous system leading to the encephalitic, or late stage, infection. Treatment of human African trypanosomiasis currently relies on a limited number of highly toxic drugs, but untreated, is invariably fatal. Melarsoprol, a trivalent arsenical, is the only drug that can be used to cure both forms of the infection once the central nervous system has become involved, but unfortunately, this drug induces an extremely severe post-treatment reactive encephalopathy (PTRE) in up to 10% of treated patients, half of whom die from this complication. Since it is unlikely that any new and less toxic drug will be developed for treatment of human African trypanosomiasis in the near future, increasing attention is now being focussed on the potential use of existing compounds, either alone or in combination chemotherapy, for improved efficacy and safety. The kynurenine pathway is the major pathway in the metabolism of tryptophan. A number of the catabolites produced along this pathway show neurotoxic or neuroprotective activities, and their role in the generation of central nervous system inflammation is well documented. In the current study, Ro-61-8048, a high affinity kynurenine-3-monooxygenase inhibitor, was used to determine the effect of manipulating the kynurenine pathway in a highly reproducible mouse model of human African trypanosomiasis. It was found that Ro-61-8048 treatment had no significant effect (P = 0.4445) on the severity of the neuroinflammatory pathology in mice during the early central nervous system stage of the disease when only a low level of inflammation was present. However, a significant (P = 0.0284) reduction in the severity of the neuroinflammatory response was detected when the inhibitor was administered in animals exhibiting the more severe, late central nervous system stage, of the infection. <i>In vitro</i> assays showed that Ro-61-8048 had no direct effect on trypanosome proliferation suggesting that the anti-inflammatory action is due to a direct effect of the inhibitor on the host cells and not a secondary response to parasite destruction. These findings demonstrate that kynurenine pathway catabolites are involved in the generation of the more severe inflammatory reaction associated with the late central nervous system stages of the disease and suggest that Ro-61-8048 or a similar drug may prove to be beneficial in preventing or ameliorating the PTRE when administered as an adjunct to conventional trypanocidal chemotherap