Why human color vision cannot reliably detect cerebrospinal fluid xanthochromia

Background - Visual assessment of cerebrospinal fluid (CSF) for xanthochromia ( yellow color) is practiced by the majority of laboratories worldwide as a means of diagnosing intracranical bleeds.Methods - Colorimetric and spectrophotometric analysis of CSF samples for recognizing the presence of bilirubin either in low concentrations or in the presence of hemolysed blood.Results - The experiments provide the physiological and colorimetric basis for abandoning visual assessment of CSF for xanthochromia.Conclusion - We strongly recommend relying on spectrophotometry as the analytical method of choice

Mainstream parallel array programming on cell

We present the E] compiler and runtime library for the ‘F’ subset of the Fortran 95 programming language. ‘F’ provides first-class support for arrays, allowing E] to implicitly evaluate array expressions in parallel using the SPU coprocessors of the Cell Broadband Engine. We present performance results from four benchmarks that all demonstrate absolute speedups over equivalent ‘C’ or Fortran versions running on the PPU host processor. A significant benefit of this straightforward approach is that a serial implementation of any code is always available, providing code longevity, and a familiar development paradigm

Spectrophotometry for cerebrospinal fluid pigment analysis

The use of spectrophotometry for the analysis of the cerebrospinal fluid (CSF) is reviewed. The clinically relevant CSF pigments--oxyhemoglobin and bilirubin--are introduced and discussed with regard to clinical differential diagnosis and potentially confounding variables (the four T's: traumatic tap, timing, total protein, and total bilirubin). The practical laboratory aspects of spectrophotometry and automated techniques are presented in the context of analytical and clinical specificity and sensitivity. The perceptual limitations of human color vision are highlighted and the use of visual assessment of the CSF is discouraged in light of recent evidence from a national audit in the United Kingdom. Finally, future perspectives including the need for longitudinal CSF profiling and routine spectrophotometric calibration are outlined

The role of phonology in error recovery.

Thesis (M.S.

Examination of the Non-linear V̇O2p Response to Exercise: Non-invasive Evidence of Linear Systems Control Using V̇O2p Kinetic Analyses

The pulmonary O2 uptake (V̇O2p) response to exercise has been characterized by exponential kinetics that remain constant regardless of the exercise protocol used to force the change in V̇O2p (kinetics are invariant). A system that responds in this way is classified as “dynamically linear”, implying that a first-order rate reaction controls V̇O2 at the muscle level (V̇O2m). However, slowed V̇O2p kinetics when initiating exercise from raised baseline intensities challenges this notion. The purpose of this thesis was to characterize the rate (τV̇O2p) and magnitude (gain) of adjustment of V̇O2p in response to step-transitions initiated from a wide range of exercise intensities to examine whether V̇O2 kinetics at the muscle level function as a dynamically linear system. In silico experiments were included to corroborate responses measured in vivo. Using breath-by-breath V̇O2p during step- and ramp-incremental exercise it was demonstrated that: 1) V̇O2p kinetics were invariant and fast (τV̇O2p ~20s) when transitions of varying ∆WR were initiated from a common WR (Chapter III); and 2) the V̇O2p response to ramp exercise was linearly related to WR and well described by a mono-exponential (Chapter IV) – consistent with dynamically linear control. However, it was also demonstrated in the same groups of participants that τV̇O2p and gain increased as a function of baseline intensity (Chapters III and IV) – refuting this notion. Modelling the summed influence of muscle compartments based on in vivo measurements in Chapter III revealed that τV̇O2p could appear fast (20s) despite being derived from τV̇O2m values ranging 15-40s and τQ̇m ranging 20-45s. Additionally, it was demonstrated that the V̇O2p response to ramp exercise in Chapter IV could also be characterized by an exponential function with τV̇O2p and gain parameters that vary as a function of WR. Collectively, these data suggest that V̇O2p kinetics are slowed dependent on WR and may be strongly influenced by muscle metabolic and circulatory heterogeneity. Therefore, it is proposed that at the muscle level V̇O2 kinetics operate as a linear system and that non-linear V̇O2p responses to exercise may reflect a “heterogeneity of linear responses” within the range of muscle fibres recruited to address the exercise challenge

Quantification of neurodegeneration by measurement of brain-specific proteins

Quantification of neurodegeneration in animal models is typically assessed by time-consuming and observer-dependent immunocytochemistry. This study aimed to investigate if newly developed ELISA techniques could provide an observer-independent, cost-effective and time-saving tool for this purpose. Neurofilament heavy chain (NfH(SM135)), astrocytic glial fibrillary acidic protein (GFAP), S100B and ferritin, markers of axonal loss, gliosis, astrocyte activation and microglial activation, respectively, were quantified in the spinal cord homogenates of mice with chronic relapsing experimental allergic encephalomyelitis (CREAE, n=8) and controls (n=7). Levels of GFAP were found to be threefold elevated in CREAE (13 ng/mg protein) when compared to control animals (4.5 ng/mg protein, p<0.001). The inverse was observed for NfH(SM135) (21 ng/mg protein vs. 63 ng/mg protein, p<0.001), ferritin (542 ng/mg protein vs. 858 ng/mg protein, p<0.001) and S100B (786 ng/mg protein vs. 2080 ng/mg protein, N.S.). These findings were confirmed by immunocytochemistry, which demonstrated intense staining for GFAP and decreased staining for NfH(SM135) in CREAE compared to control animals. These findings indicate that axonal loss and gliosis can be estimated biochemically using the newly developed ELISA assays for NfH(SM135) and GFAP. These assays may facilitate the quantification of pathological features involved in neurodegeneration