38 research outputs found

    Adding run history to CLIPS

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    To debug a C Language Integrated Production System (CLIPS) program, certain 'historical' information about a run is needed. It would be convenient for system builders to have the capability to request such information. We will discuss how historical Rete networks can be used for answering questions that help a system builder detect the cause of an error in a CLIPS program. Moreover, the cost of maintaining a historical Rete network is compared with that for a classical Rete network. We will demonstrate that the cost for assertions is only slightly higher for a historical Rete network. The cost for handling retraction could be significantly higher; however, we will show that by using special data structures that rely on hashing, it is also possible to implement retractions efficiently

    MIRO: A debugging tool for CLIPS incorporating historical Rete networks

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    At the last CLIPS conference, we discussed our ideas for adding a temporal dimension to the Rete network used to implement CLIPS. The resulting historical Rete network could then be used to store 'historical' information about a run of a CLIPS program, to aid in debugging. MIRO, a debugging tool for CLIPS built on top of CLIPS, incorporates such a historical Rete network and uses it to support its prototype question-answering capability. By enabling CLIPS users to directly ask debugging-related questions about the history of a program run, we hope to reduce the amount of single-stepping and program tracing required to debug a CLIPS program. In this paper, we briefly describe MIRO's architecture and implementation, and the current question-types that MIRO supports. These question-types are further illustrated using an example, and the benefits of the debugging tool are discussed. We also present empirical results that measure the run-time and partial storage overhead of MIRO, and discuss how MIRO may also be used to study various efficiency aspects of CLIPS programs

    Ultrasound evidence of altered lumbar connective tissue structure in human subjects with chronic low back pain

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    <p>Abstract</p> <p>Background</p> <p>Although the connective tissues forming the fascial planes of the back have been hypothesized to play a role in the pathogenesis of chronic low back pain (LBP), there have been no previous studies quantitatively evaluating connective tissue structure in this condition. The goal of this study was to perform an ultrasound-based comparison of perimuscular connective tissue structure in the lumbar region in a group of human subjects with chronic or recurrent LBP for more than 12 months, compared with a group of subjects without LBP.</p> <p>Methods</p> <p>In each of 107 human subjects (60 with LBP and 47 without LBP), parasagittal ultrasound images were acquired bilaterally centered on a point 2 cm lateral to the midpoint of the L2-3 interspinous ligament. The outcome measures based on these images were subcutaneous and perimuscular connective tissue thickness and echogenicity measured by ultrasound.</p> <p>Results</p> <p>There were no significant differences in age, sex, body mass index (BMI) or activity levels between LBP and No-LBP groups. Perimuscular thickness and echogenicity were not correlated with age but were positively correlated with BMI. The LBP group had ~25% greater perimuscular thickness and echogenicity compared with the No-LBP group (ANCOVA adjusted for BMI, p < 0.01 and p < 0.001 respectively).</p> <p>Conclusion</p> <p>This is the first report of abnormal connective tissue structure in the lumbar region in a group of subjects with chronic or recurrent LBP. This finding was not attributable to differences in age, sex, BMI or activity level between groups. Possible causes include genetic factors, abnormal movement patterns and chronic inflammation.</p

    Neutron-Unbound Excited States of 23N

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    Neutron unbound states in 23N were populated via proton knockout from an 83.4 MeV/nucleon 24O beam on a liquid deuterium target. The two-body decay energy displays two peaks at E1∼100keV and E2∼1MeV with respect to the neutron separation energy. The data are consistent with shell model calculations predicting resonances at excitation energies of ∼3.6MeV and ∼4.5MeV. The selectivity of the reaction implies that these states correspond to the first and second 3/2− states. The energy of the first state is about 1.3 MeV lower than the first excited 2+ in 24O. This decrease is largely due to coupling with the πp−13/2 hole along with a small reduction of the N=16 shell gap in 23N

    Design of the Nephrotic Syndrome Study Network (NEPTUNE) to evaluate primary glomerular nephropathy by a multidisciplinary approach

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    The Nephrotic Syndrome Study Network (NEPTUNE) is a North American multi-center collaborative consortium established to develop a translational research infrastructure for Nephrotic Syndrome. This includes a longitudinal observational cohort study, a pilot and ancillary studies program, a training program, and a patient contact registry. NEPTUNE will enroll 450 adults and children with minimal change disease, focal segmental glomerulosclerosis and membranous nephropathy for detailed clinical, histopathologic, and molecular phenotyping at the time of clinically-indicated renal biopsy. Initial visits will include an extensive clinical history, physical examination, collection of urine, blood and renal tissue samples, and assessments of quality of life and patient-reported outcomes. Follow-up history, physical measures, urine and blood samples, and questionnaires will be obtained every 4 months in the first year and bi-annually, thereafter. Molecular profiles and gene expression data will be linked to phenotypic, genetic, and digitalized histologic data for comprehensive analyses using systems biology approaches. Analytical strategies were designed to transform descriptive information to mechanistic disease classification for Nephrotic Syndrome and to identify clinical, histological, and genomic disease predictors. Thus, understanding the complexity of the disease pathogenesis will guide further investigation for targeted therapeutic strategies

    Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

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    In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

    A capstone course for a computer information systems major

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