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Eduardo Gonzalez Toledo

Publications and source records attributed to Eduardo Gonzalez Toledo.

2 recordsLinked to original sources

Creating an IHE ATNA-based audit repository.

Compliance with the Health Insurance Portability and Accountability Act (HIPAA) requires gathering audit information from picture archiving and communications systems (PACS) regarding evidence trails of human interactions. Until recently, most PACS users have had limited access to auditing information. Access required resources to handle manual inspection of audit logs, and access to proprietary databases was not always available. Some vendors now produce eXtensible Markup Language (XML) audit logs based on certain events occurring in PACS. However, it is up to the user to convert this information into an easily mined data repository supporting compliance and quality control. This process can be handled in multiple ways, which could mean different audit mechanisms depending on the PACS (or other hospital system) used. It is apparent that an organized method of dealing with audit information is needed. This help may be provided within the Integrating the Healthcare Environment (IHE) framework. The IHE initiative defines a set of profiles, actors, and transactions that create common scenarios for particular workflow processes. The Integration Profiles depict security as a fundamental requirement of the framework. Specifically, the Audit Trail and Node Authentication (ATNA) profile defines standards based mechanisms for securely transmitting and storing audit records in a central repository. The data structure defined by the profile provides a number of record types that capture different audit events. A general feasibility study for storing currently available PACS audit information following the profile is defined, and steps to an automated solution are discussed.

Feasibility Studies↗

Pathogenesis of brain and spinal cord atrophy in multiple sclerosis.

For more than a century, multiple sclerosis was viewed as a disease process characterized by oligodendrocyte and myelin loss, and research into the pathogenesis of multiple sclerosis was mainly focused on the mechanisms of inflammation. However, with development of more sophisticated neuroimaging and molecular biology techniques, attention has shifted to new aspects of pathogenesis of multiple sclerosis: axonal loss and neurodegeneration. Evidence is increasing that tissue destruction, primarily axonal loss and neurodegeneration, is a key element in the pathogenesis of multiple sclerosis. In addition, it is now known that brain and spinal cord atrophy begins early in the disease process of multiple sclerosis and advances relentlessly throughout the course of the disease. Cumulative data suggest that axonal loss is the major determinant of progressive neurologic disability in patients with multiple sclerosis. Magnetic resonance imaging and magnetic resonance spectroscopy in patients with multiple sclerosis for < 5 years indicate brain atrophy and loss of axonal integrity. Neurodegeneration and axonal loss in patients with multiple sclerosis are initially accompanied by a local response from oligodendrocyte progenitor cells and some remyelination. However, these repair mechanisms eventually fail, and patients typically develop generalized brain atrophy, cognitive decline, and permanent disability. Although the exact mechanisms underlying central nervous system atrophy in patients with multiple sclerosis are largely unknown, evidence exists that atrophy may represent an epiphenomenon related to the effects of dynamic inflammation within the central nervous system, including demyelination, axonal injury, neuronal loss, Wallerian degeneration, and possibly iron deposition. This article summarizes the potential mechanisms involved in central nervous system atrophy in patients with multiple sclerosis.

Apoptosis↗