Potential Matrix Effects in Iodometry Determination of Peroxides Induced by Olefins.

Peroxides (H2O2, ROOR, and ROOH) are an important reaction intermediate involved in a number of natural processes, including atmospheric autoxidation and lipid peroxidation in oils and animal tissues. Iodometry is an established spectroscopic technique that has been widely used to quantify total peroxide concentration in food, indoor, and outdoor samples. Iodometry provides selectivity toward peroxides through a quantitative reaction between I- and peroxides to form I3- via a molecular iodine (I2) intermediate. However, equilibrium changes caused by a potential interaction between olefinic species and I2 can suppress I3- formation, thereby underestimating peroxide concentration. For the first time in the current study, this unrecognized interference posed by olefins (OEs) is systematically investigated to gauge its effects on the accuracy of iodometry. A number of model molecules were investigated. The interference was observed to be unique to OEs, but universally affecting different peroxide species such as H2O2, tert-butyl hydroperoxide, and aerosol-bound peroxides. A simple kinetic box model was built to explain this chemistry. The measured rate constant for 3-octenoic acid was found to be 0.84 ± 0.02 M-1 s-1. Overall, our results show matrix effects induced by OEs can underestimate peroxide concentration determined by iodometry for edible oils, indoor environments, and animal fat, but absent in most of the atmospheric samples. Nonetheless, our results point out the importance of this interfering chemistry in matrices enriched with OEs.

iTools: a framework for classification, categorization and integration of computational biology resources.

The advancement of the computational biology field hinges on progress in three fundamental directions--the development of new computational algorithms, the availability of informatics resource management infrastructures and the capability of tools to interoperate and synergize. There is an explosion in algorithms and tools for computational biology, which makes it difficult for biologists to find, compare and integrate such resources. We describe a new infrastructure, iTools, for managing the query, traversal and comparison of diverse computational biology resources. Specifically, iTools stores information about three types of resources--data, software tools and web-services. The iTools design, implementation and resource meta-data content reflect the broad research, computational, applied and scientific expertise available at the seven National Centers for Biomedical Computing. iTools provides a system for classification, categorization and integration of different computational biology resources across space-and-time scales, biomedical problems, computational infrastructures and mathematical foundations. A large number of resources are already iTools-accessible to the community and this infrastructure is rapidly growing. iTools includes human and machine interfaces to its resource meta-data repository. Investigators or computer programs may utilize these interfaces to search, compare, expand, revise and mine meta-data descriptions of existent computational biology resources. We propose two ways to browse and display the iTools dynamic collection of resources. The first one is based on an ontology of computational biology resources, and the second one is derived from hyperbolic projections of manifolds or complex structures onto planar discs. iTools is an open source project both in terms of the source code development as well as its meta-data content. iTools employs a decentralized, portable, scalable and lightweight framework for long-term resource management. We demonstrate several applications of iTools as a framework for integrated bioinformatics. iTools and the complete details about its specifications, usage and interfaces are available at the iTools web page http://iTools.ccb.ucla.edu.

Computational fluid flow and mass transfer of a functionally integrated pediatric pump-oxygenator configuration.

Ension, Inc., under a contract with the National Heart, Lung, and Blood Institute (HHSN268200448189C), is currently developing a pediatric cardiopulmonary assist system (pCAS). This work reports on the utilization of computational fluid dynamics to predict the performance of the first of two device iterations before physical fabrication and in vitro testing. Fluent, Inc. was consulted to assist with key technical aspects of model development. Activities included porous model development and verification, generation of predictive fluid velocity fields, and incorporation of postprocessing subroutines for calculating oxygenation, decarbonation, and hemolytic blood damage. Experimental validation was conducted using bovine blood and good quantitative agreement with computational predictions was demonstrated. The success of this work suggests that the generated models and subroutines can be used as a practical tool for design and analysis of subsequent candidate pCAS design configurations.

LONI visualization environment.

Over the past decade, the use of informatics to solve complex neuroscientific problems has increased dramatically. Many of these research endeavors involve examining large amounts of imaging, behavioral, genetic, neurobiological, and neuropsychiatric data. Superimposing, processing, visualizing, or interpreting such a complex cohort of datasets frequently becomes a challenge. We developed a new software environment that allows investigators to integrate multimodal imaging data, hierarchical brain ontology systems, on-line genetic and phylogenic databases, and 3D virtual data reconstruction models. The Laboratory of Neuro Imaging visualization environment (LONI Viz) consists of the following components: a sectional viewer for imaging data, an interactive 3D display for surface and volume rendering of imaging data, a brain ontology viewer, and an external database query system. The synchronization of all components according to stereotaxic coordinates, region name, hierarchical ontology, and genetic labels is achieved via a comprehensive BrainMapper functionality, which directly maps between position, structure name, database, and functional connectivity information. This environment is freely available, portable, and extensible, and may prove very useful for neurobiologists, neurogenetisists, brain mappers, and for other clinical, pedagogical, and research endeavors.

Heme oxygenase-1 overexpression protects rat hearts from cold ischemia/reperfusion injury via an antiapoptotic pathway.

BACKGROUND: Ischemia/reperfusion (I/R) injury is one of the most important causes of the early graft loss. We have shown that overexpression of heme oxygenase-1 (HO-1), an inducible heat shock protein 32, protects rat livers against I/R injury. We report on the cytoprotective effects of HO-1 in a rat cardiac I/R injury model, using cobalt protoporphyrin (CoPP) as HO-1 inducer and zinc protoporphyrin (ZnPP) as HO-1 inhibitor. METHODS: Three groups of Lewis rats were studied: group 1 control donors received phosphate-buffered saline 48 hr before the harvest; group 2 donors were pretreated with CoPP at -48 hr; and in group 3, donors received CoPP at -48 hr and ZnPP was given to recipients at reperfusion. Hearts were harvested, stored in University of Wisconsin solution (4 degrees C) for 24 hr, and then transplanted to syngeneic (Lewis) rats. RESULTS: Sixty percent of control grafts ceased their function in <15 min. In contrast, 80% of CoPP-pretreated grafts survived 14 days. All grafts stopped functioning within 24 hr after CoPP + ZnPP therapy. Cardiac HO-1 enzymatic activity and protein expression correlated with beneficial effects of CoPP and deleterious effects of adjunctive ZnPP treatment. Markedly less apoptotic (TUNEL+) myocyte/endothelial cells could be detected in CoPP cardiac grafts, as compared with controls. The expression of antiapoptotic (Bcl-2/Bag-1) proteins was up-regulated in the CoPP group. CONCLUSION: HO-1 overexpression provides potent protection against cold I/R injury in a stringent rat cardiac model. This effect depends, at least in part, on HO-1-mediated up-regulation of a host antiapoptotic mechanism, especially in the early postreperfusion period.