138 research outputs found

    The Application of Near Infrared (Nir) Spectroscopy to Inorganic Preservative-Treated Wood

    Get PDF
    There is a growing need to find a rapid, inexpensive, and reliable method to distinguish between treated and untreated waste wood. This paper evaluates the ability of near infrared (NIR) spectroscopy with multivariate analysis (MVA) to distinguish preservative types and retentions. It is demonstrated that principal component analysis (PCA) can differentiate lumber treated with CCA, ACZA, or ACQ preservatives. Furthermore, separation according to wood species and assay zone was also observed. Within the range of preservative concentrations available, partial least squares (PLS) regression was also performed on the NIR data, from which retention levels were predicted. The results highlight the potential for this technique to predict the concentration, as well as identify the type, of inorganic preservatives present

    Human COL2A1-directed SV40 T antigen expression in transgenic and chimeric mice results in abnormal skeletal development

    Get PDF
    The ability of SV40 T antigen to cause abnormalities in cartilage development in transgenic mice and chimeras has been tested. The cis- regulatory elements of the COL2A1 gene were used to target expression of SV40 T antigen to differentiating chondrocytes in transgenic mice and chimeras derived from embryonal stem (ES) cells bearing the same transgene. The major phenotypic consequences of transgenic (pAL21) expression are malformed skeleton, disproportionate dwarfism, and perinatal/neonatal death. Expression of T antigen was tissue specific and in the main characteristic of the mouse α1(II) collagen gene. Chondrocyte densities and levels of α1(II) collagen mRNAs were reduced in the transgenic mice. Islands of cells which express cartilage characteristic genes such as type IIB procollagen, long form α1(IX) collagen, α2(XI) collagen, and aggrecan were found in the articular and growth cartilages of pAL21 chimeric fetuses and neonates. But these cells, which were expressing T antigen, were not properly organized into columns of proliferating chondrocytes. Levels of α1(II) collagen mRNA were reduced in these chondrocytes. In addition, these cells did not express type X collagen, a marker for hypertrophic chondrocytes. The skeletal abnormality in pAL21 mice may therefore be due to a retardation of chondrocyte maturation or an impaired ability of chondrocytes to complete terminal differentiation and an associated paucity of some cartilage matrix components.published_or_final_versio

    Ability of Near Infrared Spectroscopy to Monitor Air-Dry Density Distribution and Variation of Wood

    Get PDF
    Process control of wood density with near infrared spectroscopy (NIR) would be useful for pulp mills that need to maximize pulp yield without compromising paper strength properties. If models developed from the absorbance at wavelengths in the NIR region could provide density histograms, fiber supply personnel could monitor chip density variation as the chips enter the mill. The objectives of this research were to a) develop density histograms from actual density versus density histograms developed through NIR modeling, and b) determine the precision of density models developed from absorbance in the NIR region with a recommendation for the sample size needed to estimate the standard deviation of density at a given precision.Models for density were developed from calibration samples (n = 170) and then validated with 93 randomly held aside samples. The samples were systematically removed from 10 longleaf pine trees of equal age, but different growth rates. The histogram patterns for actual density almost paralleled the histogram patterns developed from predictive models. Subsequently, the validation data set was randomly categorized into groups of three, and the standard deviations of density were measured. For three measurements per data point, the predicted standard deviation covaried with the actual standard deviation of density with an R2 = 0.61 and 0.55 for the calibration and validation data set, respectively. A sample size of 30 was recommended to estimate the standard deviation of density with a precision of 0.01 g/cm3

    The Response of Visible/Near Infrared Absorbance to Wood-Staining Fungi

    Get PDF
    The influence of blue-stain fungi [Ophiostoma minus (Hedgcock) H. and P. Sydow and Leptographium serpens (Goid.) Siemaszko] on absorbance at the visible and near infrared wavelengths was investigated. Forty trees were sampled at breast height from longleaf pine (Pinus palustris Mill.). One half of each increment core was inoculated with one of two fungi treatments while the other half served as a control. Visible and near infrared spectra were acquired between rings 3-40 for the stained and control-clear wood samples (n = 304). Absorbance was greater for the stained than the control wood at wavelengths between 464 to 1334 nm. Statistical techniques were applied to the NIR data to determine which wavelengths, and their corresponding chemical assignments, were most affected by the fungi. First and 2nd derivative pretreatments to the original spectra resulted in some blue-stain sensitive wavelengths throughout the 350 to 2500 nm range, some of which are associated with nitrogen in the melanin present in blue stain. However, for the 2nd derivative pretreatment, the stained wood exhibited a different signal to noise ratio than the control wood, and thus the pretreatment method should be used with vigilance. For the raw, 1st, and 2nd derivatives, the absorbance of L. serpens (n = 164) significantly differed from O. minus (n = 140) between 424-554 nm. The results of this study are important because the absorbance at visible and NIR wavelengths may be used to classify stained wood

    Pegylated derivatives of recombinant human arginase (rhArg1) for sustained in vivo activity in cancer therapy: preparation, characterization and analysis of their pharmacodynamics in vivo and in vitro and action upon hepatocellular carcinoma cell (HCC)

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Protein used in medicine, e.g. interferon, are immunogenic and quickly broken down by the body. Pegylation is a recognized way of preserving their integrity and reducing immune reactions, and works well with enzymes used to degrade amino acids, a recent focus of attention in controlling cancer growth. Of the two arginine-degrading enzymes being explored clinically, arginine deiminase is a decidedly foreign mycoplasm-derived enzyme, whereas human arginase 1 is a native liver enzyme. Both have been pegylated, the former with adjuncts of 20 kD, the latter with 5 kD PEG. Pegylation is done by several different methods, not all of which are satisfactory or desirable.</p> <p>Methods</p> <p>The preparation of novel polyethylene glycol (PEG) derivatives for modifying proteins is described, but directed specifically at pegylation of recombinant human arginase 1 (rhArg1). rhArg1 expressed in <it>Escherichia coli </it>was purified and coupled in various ways with 5 different PEG molecules to compare their protective properties and the residual enzyme activity, using hepatocellular cell lines both in vitro and in vivo.</p> <p>Results</p> <p>Methoxypolyethylene glycol-succinimidyl propionate (mPEG-SPA 5,000) coupled with very high affinity under mild conditions. The resulting pegylated enzyme (rhArg1-peg<sub>5,000 mw</sub>) had up to 6 PEG chains of 5K length which not only protected it from degradation and any residual immunogenicity, but most importantly let it retain >90% of its native catalytic activity. It remained efficacious in depleting arginine in rats after a single ip injection of 1,500 U of the conjugate as the native enzyme, plasma arginine falling to >0.05 μM from ~170 μM within 20 min and lasting 6 days. The conjugate had almost the same efficacy as unpegylated rhArg1 on 2 cultured human liver cancer (HCC) cell lines. It was considerably more effective than 4 other pegylated conjugates prepared.</p> <p>Conclusion</p> <p>Valuable data on the optimization of the pegylation procedure and choice of ligand that best stabilizes the enzyme arginase 1 are presented, a protocol that should equally fit many other enzymes and proteins. It is a long lasting arginine-depleting enzyme in vivo which will greatly improve its use in anti-cancer therapy.</p

    Mutations of PIK3CA in gastric adenocarcinoma

    Get PDF
    BACKGROUND: Activation of the phosphatidylinositol 3-kinase (PI3K) through mutational inactivation of PTEN tumour suppressor gene is common in diverse cancer types, but rarely reported in gastric cancer. Recently, mutations in PIK3CA, which encodes the p110α catalytic subunit of PI3K, have been identified in various human cancers, including 3 of 12 gastric cancers. Eighty percent of these reported mutations clustered within 2 regions involving the helical and kinase domains. In vitro study on one of the "hot-spot" mutants has demonstrated it as an activating mutation. METHODS: Based on these data, we initiated PIK3CA mutation screening in 94 human gastric cancers by direct sequencing of the gene regions in which 80% of all the known PIK3CA mutations were found. We also examined PIK3CA expression level by extracting data from the previous large-scale gene expression profiling study. Using Significance Analysis of Microarrays (SAM), we further searched for genes that show correlating expression with PIK3CA. RESULTS: We have identified PIK3CA mutations in 4 cases (4.3%), all involving the previously reported hotspots. Among these 4 cases, 3 tumours demonstrated microsatellite instability and 2 tumours harboured concurrent KRAS mutation. Data extracted from microarray studies showed an increased expression of PIK3CA in gastric cancers when compared with the non-neoplastic gastric mucosae (p < 0.001). SAM further identified 2910 genes whose expression levels were positively associated with that of PIK3CA. CONCLUSION: Our data suggested that activation of the PI3K signalling pathway in gastric cancer may be achieved through up-regulation or mutation of PIK3CA, in which the latter may be a consequence of mismatch repair deficiency
    corecore