Raman spectroscopy has attracted interest as a non‐invasive optical technique to study the composition and structure of a wide range of materials at the microscopic level. The intrinsic fluorescence background can be orders of magnitude stronger than the Raman scattering, and so, background removal is one of the foremost challenges for quantitative analysis of Raman spectra in many samples. A range of methods anchored in instrumental and computational programming approaches have been proposed for removing fluorescence background signals. An enhanced adaptive weighting scheme for automated fluorescence removal is reported, applicable to both polynomial fitting and penalized least squares approaches. Analysis of the background fitting results for ensembles of simulated spectra suggests that the method is robust and reliable and can significantly improve the background fit over the range of signal, shot noise and background parameters tested, while reducing the subjective nature of the process. The method was also illustrated by application to experimental data generated from aqueous solutions of bulk protein fibrinogen mixed with dextran. Copyright © 2013 John Wiley & Sons, Ltd.

Background: Mercury is a prominent environmental contaminant that causes detrimental effects to human health. Although the liver has been known to be a main target organ, there is limited information onin vivomolecular mechanism of mercury-induced toxicity in the liver. By using transcriptome analysis, phenotypic anchoring and validation of targeted gene expression in zebrafish, mercury-induced hepatotoxicity was investigated and a number of perturbed cellular processes were identified and compared with those captured in thein vitrohuman cell line studies.Results: Hepato-transcriptome analysis of mercury-exposed zebrafish revealed that the earliest deregulated genes were associated with electron transport chain, mitochondrial fatty acid beta-oxidation, nuclear receptor signaling and apoptotic pathway, followed by complement system and proteasome pathway, and thereafter DNA damage, hypoxia, Wnt signaling, fatty acid synthesis, gluconeogenesis, cell cycle and motility. Comparative meta-analysis of microarray data between zebrafish liver and human HepG2 cells exposed to mercury identified some common toxicological effects of mercury-induced hepatotoxicity in both models. Histological analyses of liver from mercury-exposed fish revealed morphological changes of liver parenchyma, decreased nucleated cell count, increased lipid vesicles, glycogen and apoptotic bodies, thus providing phenotypic evidence for anchoring of the transcriptome analysis. Validation of targeted gene expression confirmed deregulated gene-pathways from enrichment analysis. Some of these genes responding to low concentrations of mercury may serve as toxicogenomic-based markers for detection and health risk assessment of environmental mercury contaminations.Conclusion: Mercury-induced hepatotoxicity was triggered by oxidative stresses, intrinsic apoptotic pathway, deregulation of nuclear receptor and kinase activities including Gsk3 that deregulates Wnt signaling pathway, gluconeogenesis, and adipogenesis, leading to mitochondrial dysfunction, endocrine disruption and metabolic disorders. This study provides important mechanistic insights into mercury-induced liver toxicity in a whole-animal physiology context, which will help in understanding the syndromes caused by mercury poisoning. The molecular conservation of mercury-induced hepatotoxicity between zebrafish and human cell line reveals the feasibility of using zebrafish to model molecular toxicity in human for toxicant risk assessments.

Bisphenol-A is an important environmental contaminant due to the increased early-life exposure that may pose significant health-risks to various organisms including humans. This study aimed to use zebrafish as a toxicogenomic model to capture transcriptomic and phenotypic changes for inference of signaling pathways, biological processes, physiological systems and identify potential biomarker genes that are affected by early-life exposure to bisphenol-A. Phenotypic analysis using wild-type zebrafish larvae revealed BPA early-life exposure toxicity caused cardiac edema, cranio-facial abnormality, failure of swimbladder inflation and poor tactile response. Fluorescent imaging analysis using three transgenic lines revealed suppressed neuron branching from the spinal cord, abnormal development of neuromast cells, and suppressed vascularization in the abdominal region. Using knowledge-based data mining algorithms, transcriptome analysis suggests that several signaling pathways involving ephrin receptor, clathrin-mediated endocytosis, synaptic long-term potentiation, axonal guidance, vascular endothelial growth factor, integrin and tight junction were deregulated. Physiological systems with related disorders associated with the nervous, cardiovascular, skeletal-muscular, blood and reproductive systems were implicated, hence corroborated with the phenotypic analysis. Further analysis identified a common set of BPA-targeted genes and revealed a plausible mechanism involving disruption of endocrine-regulated genes and processes in known susceptible tissue-organs. The expression of 28 genes were validated in a separate experiment using quantitative real-time PCR and 6 genes, ncl1, apoeb, mdm1, mycl1b, sp4, U1SNRNPBP homolog, were found to be sensitive and robust biomarkers for BPA early-life exposure toxicity. The susceptibility of sp4 to BPA perturbation suggests its role in altering brain development, function and subsequently behavior observed in laboratory animals exposed to BPA during early life, which is a health-risk concern of early life exposure in humans. The present study further established zebrafish as a model for toxicogenomic inference of early-life chemical exposure toxicity.

Carrot juice (straight, 8.5 Brix and concentrated, 15.2 Brix) was fermented by lactic acid bacteria (Lactobacillus gasseri strain DSM 20604 or DSM 20077). Fermentation enhanced the nutritional profile of carrot juice. There was a greater sugar reduction (27%) in fermented straight carrot juices than in the fermented concentrated juices (15%). The sugar reduction was independent of the strain used for fermentation. The two L. gasseri strains synthesised fructosyltransferase enzymes during fermentation of carrot juice samples that enabled conversion of simple sugars primarily into polysaccharides. The level of conversion to polysaccharides was dependent on the L. gasseri strain and juice concentration. Fermentation of carrot juice by L. gasseri enables the production of a nutritionally-enhanced beverage with reduced calorie and prebiotic potential. An additional benefit is the increased carotenoid content observed in straight and concentrated juices fermented by Lactobacillus gasseri DSM 20077 and the concentrated juice fermented by Lactobacillus gasseri DSM 20604.