Open bibliography for science, technology, and medicine.

The concept of Open Bibliography in science, technology and medicine (STM) is introduced as a combination of Open Source tools, Open specifications and Open bibliographic data. An Openly searchable and navigable network of bibliographic information and associated knowledge representations, a Bibliographic Knowledge Network, across all branches of Science, Technology and Medicine, has been designed and initiated. For this large scale endeavour, the engagement and cooperation of the multiple stakeholders in STM publishing - authors, librarians, publishers and administrators - is sought.

Ami - The chemist's amanuensis.

The Ami project was a six month Rapid Innovation project sponsored by JISC to explore the Virtual Research Environment space. The project brainstormed with chemists and decided to investigate ways to facilitate monitoring and collection of experimental data.A frequently encountered use-case was identified of how the chemist reaches the end of an experiment, but finds an unexpected result.

Respiratory function following bilateral mid-cervical contusion injury in the adult rat.

The consequences of spinal cord injury (SCI) are often viewed as the result of white matter damage. However, injuries occurring at any spinal level, especially in cervical and lumbar enlargement regions, also entail segmental neuronal loss. Yet, the contributions of gray matter injury and plasticity to functional outcomes are poorly understood.

Neuronal progenitor transplantation and respiratory outcomes following upper cervical spinal cord injury in adult rats.

Despite extensive gray matter loss following spinal cord injury (SCI), little attention has been given to neuronal replacement strategies and their effects on specific functional circuits in the injured spinal cord. In the present study, we assessed breathing behavior and phrenic nerve electrophysiological activity following transplantation of microdissected dorsal or ventral pieces of rat fetal spinal cord tissue (FSC(D) or FSC(V), respectively) into acute, cervical (C2) spinal hemisections. Transneuronal tracing demonstrated connectivity between donor neurons from both sources and the host phrenic circuitry.

Apolipoprotein E genotype and oxidative stress response to traumatic brain injury.

Traumatic Brain Injury (TBI) is known to result in oxidative stress, and as variation at the Apolipoprotein E (APOE) gene has been shown to influence outcome following TBI, but through as yet unclear mechanisms, we used transgenic APOE mouse models to examine the relationship between APOE genotype and oxidative stress following TBI. We administered a controlled cortical impact (CCI) injury or sham injury to transgenic mice expressing either human APOE3 or APOE4 on a murine APOE-deficient background. RNA was prepared from the ipsilateral hippocampi and cortices retrieved at 24 h and 1 month post-TBI.

Apolipoprotein E-genotype dependent hippocampal and cortical responses to traumatic brain injury.

The different alleles of the apolipoprotein E gene (APOE-gene, ApoE-protein) have been reported to influence recovery after traumatic brain injury (TBI) in both human patients and animal models, with the e4 allele typically conferring poorer prognosis for recovery. How the E4 allele, and consequently the ApoE4 isoform, affects recovery is unknown, but proposed mechanisms include neurogenesis, inflammatory response and amyloid processing or metabolism. Using the controlled cortical impact (CCI) model of brain injury and microarray technology we have characterized the genomic response to injury in the brains of APOE2, APOE3 and APOE4 transgenic mice and identified quantitatively and qualitatively significantly different profiles of gene expression in both the hippocampus and the cortex of the APOE3 mice compared to APOE4.

Genomic analysis of response to traumatic brain injury in a mouse model of Alzheimer's disease (APPsw).

Numerous studies have shown that the beta-amyloid peptide (Abeta) or beta-amyloid deposits impact many processes that can contribute to neurodegeneration, ranging from immune and inflammatory processes to cell death and apoptosis, processes characteristic of both Alzheimer's disease and head injury. Human and animal studies of traumatic brain injury (TBI) have shown that Abeta production is increased acutely following injury, and there is evidence for increased amyloid deposition and risk for Alzheimer's disease following TBI. Given the poorer outcome after injury observed both in transgenic mice overproducing Abeta, as well as in humans subjected to repetitive head injury, one may conclude that the presence of elevated brain levels of Abeta, whether endogenous or as a consequence of previous injury, exacerbates many of the deleterious processes triggered by TBI.

Alpha-II-spectrin after controlled cortical impact in the immature rat brain.

Proteolytic processing plays an important role in regulating a wide range of important cellular functions, including processing of cytoskeletal proteins. Loss of cytoskeletal proteins such as spectrin is an important characteristic in a variety of acute central nervous system injuries including ischemia, spinal cord injury and traumatic brain injury (TBI). The literature contains extensive information on the proteolytic degradation of alpha-II-spectrin after TBI in the adult brain.

Extensive degradation of myelin basic protein isoforms by calpain following traumatic brain injury.

Axonal injury is one of the key features of traumatic brain injury (TBI), yet little is known about the integrity of the myelin sheath. We report that the 21.5 and 18.

Rapid discovery of putative protein biomarkers of traumatic brain injury by SDS-PAGE-capillary liquid chromatography-tandem mass spectrometry.

We report the rapid discovery of putative protein biomarkers of traumatic brain injury (TBI) by SDS-PAGE-capillary liquid chromatography-tandem mass spectrometry (SDS-PAGE-Capillary LC-MS(2)). Ipsilateral hippocampus (IH) samples were collected from naive rats and rats subjected to controlled cortical impact (a rodent model of TBI). Protein database searching with 15,558 uninterpreted MS(2) spectra, collected in 3 days via data-dependent capillary LC-MS(2) of pooled cyanine dye-labeled samples separated by SDS-PAGE, identified more than 306 unique proteins.

A novel marker for traumatic brain injury: CSF alphaII-spectrin breakdown product levels.

Currently, there is no definitive diagnostic test for traumatic brain injury (TBI) to help physicians determine the seriousness of injury or the extent of cellular pathology. Calpain cleaves alphaII-spectrin into breakdown products (SBDP) after TBI and ischemia. Mean levels of both ipsilateral cortex (IC) and cerebral spinal fluid (CSF) SBDP at 2, 6, and 24 h after two levels of controlled cortical impact (1.