Novel Characterization Techniques for Agricultural and Environmental Applications

ABSTRACT

Using the recently proposed open-photoacoustic-cell (OPC) detection technique the thermal diffusivity of potato skin has been found. Skin samples were taken from potatoes that were grown on different soils. The measurements were carried out with samples that, after being removed from the potatoes, were left in the air for different periods of time. Apparently, the process of the dehydration/oxidation resulted not only in the expected shrinkage of skin layers but also entailed chemical and/or structural changes that have produced a noticeable decrease of the thermal diffusivity coefficient.     

Near-lossless and lossy compression of imaging spectrometer data: comparison of information extraction performance

We investigate the ability to derive meaningful information from decompressed imaging spectrometer data. Hyperspectral images are compressed with near-lossless and lossy coding methods. Linear prediction between the bands is used in both cases. Each band is predicted by a previously transmitted band. The residual is formed by subtracting the prediction from the original data and then is compressed either with a near-lossless bit-plane coder or with the lossy JPEG2000 algorithm. We study the effects of these two types of compression on hyperspectral image processing such as mineral and vegetation content classification using whole- and mixed pixel analysis techniques. The results presented in this paper indicate that an efficient lossy coder outperforms near-lossless method in terms of its impact on final hyperspectral data applications.     

Altered glycosylation of the env-sea oncoprotein inhibits intracellular transport and transformation

The transforming gene product of the S13 avian erythroblastosis virus, env-sea, is a member of the growth factor receptor class of tyrosine kinases. The env-sea precursor protein gp155env-sea is proteolytically processed into the mature cleavage products gp85env and gp70env-sea, which are subsequently terminally glycosylated and transported to the cell surface. Previous studies have shown that the abnormal glycosylation of gp155env-sea induced by the carbohydrate processing inhibitor castanospermine blocks the proteolytic cleavage of gp155env-sea and impairs its transforming ability. We have shown recently that an uncleaved but fully glycosylated sea-encoded protein retains the ability to transform chicken embryo fibroblasts, indicating that proteolytic processing is not essential for transformation by the env-sea tyrosine kinase. To address the question of how castanospermine blocks transformation by env-sea, differential sucrose gradient centrifugation was performed on env-sea-transformed cells treated with the inhibitor. This report shows that no surface forms of env-sea could be detected in inhibitor-treated cells, suggesting that castanospermine acts by blocking the transport of sea-encoded proteins to the cell surface.     

Imaging evaluation of artificial nipples during bottle feeding

OBJECTIVE: To report a case of probable famotidine-induced mixed hepatocellular jaundice. CASE SUMMARY: A 55-year-old man presented with a one-month history of mid-epigastric pain. Initial physical examination and laboratory studies, including liver enzyme concentration tests, were unrevealing. A diagnosis of gastritis was made and ranitidine was prescribed. Following one week of therapy, the patient's symptoms had not improved and therapy was changed to famotidine and sucralfate. Approximately one week later the patient presented with jaundice. Liver enzyme concentrations were elevated and the patient was hospitalized for further evaluation. Five days following discontinuation of famotidine, liver enzyme concentrations were normal and jaundice had resolved. Further tests did not reveal any pathologic etiology. DISCUSSION: Hepatic changes have occurred in patients receiving histamine2-antagonists; ranitidine and cimetidine have been cited most frequently. In general, the elevations are mild, transient, and return to baseline with continued therapy. This is one of the first case reports of probable famotidine-induced mixed hepatocellular jaundice. CONCLUSIONS: There was a temporal relationship between the patient's signs and symptoms and initiation of famotidine. No identifiable factors contributed to the elevated liver enzyme concentrations and jaundice.     

The phosphorylation of eukaryotic initiation factor eIF4E in response to phorbol esters, cell stresses, and cytokines is mediated by distinct MAP kinase pathways

Initiation factor eIF4E binds to the 5'-cap of eukaryotic mRNAs and plays a key role in the mechanism and regulation of translation. It may be regulated through its own phosphorylation and through inhibitory binding proteins (4E-BPs), which modulate its availability for initiation complex assembly. eIF4E phosphorylation is enhanced by phorbol esters. We show, using specific inhibitors, that this involves both the p38 mitogen-activated protein (MAP) kinase and Erk signaling pathways. Cell stresses such as arsenite and anisomycin and the cytokines tumor necrosis factor-alpha and interleukin-1beta also cause increased phosphorylation of eIF4E, which is abolished by the specific p38 MAP kinase inhibitor, SB203580. These changes in eIF4E phosphorylation parallel the activity of the eIF4E kinase, Mnk1. However other stresses such as heat shock, sorbitol, and H2O2, which also stimulate p38 MAP kinase and increase Mnk1 activity, do not increase phosphorylation of eIF4E. The latter stresses increase the binding of eIF4E to 4E-BP1, and we show that this blocks the phosphorylation of eIF4E by Mnk1 in vitro, which may explain the absence of an increase in eIF4E phosphorylation under these conditions.     

Bayes estimates for immunological progression rates in HIV disease

We develop Bayesian methods for calculating shrinkage estimates of immunological progression rates (for example, CD4 count decline rates) in populations of HIV-infected patients. These methods make the assumption that decline of immunological markers may be modelled as approximately linear on some suitable chosen scale. They are applicable in situations where seroconversion times are unknown and follow-up of patients is variable, with some patients having only sparse measurements of immunological markers. Fitting of models is achieved by Gibbs sampling and CD4 count data from 603 members of the Edinburgh City Hospital Cohort with at least two CD4 determinations are analysed to provide an illustration. It is found that Bayesian shrinkage estimates for CD4 slopes on the square root scale are much more effective predictors of future CD4 counts than the least squares estimates, with respect to squared error loss. Of various shrinkage estimators considered, the most effective corresponds to the simplest model, which can also be fitted using SAS. A characterization of the pattern of CD4 loss in the Edinburgh cohort is obtained (mean rate of decline on root scale-1.61 per annum, standard deviation 1.03) and the effect of various covariates (sex, age, risk category and HLA antigen type) on immunological progression is considered. It is found that homosexual men in Edinburgh and patients with HLA haplotype A1B8DR3 experience significantly faster loss of CD4.     

Enhanced cyclooxygenase-2 gene expression in alcoholic liver disease in the rat

BACKGROUND & AIMS: Inflammatory stimuli and lipid peroxidation up-regulate cyclooxygenase (COX)-2. This study evaluated the relationship between inflammatory mediators, COX expression, and pathological changes in experimental alcoholic liver disease. METHODS: Rats (5 per group) were fed ethanol and a diet containing saturated fat, corn oil, or fish oil by intragastric infusion. Dextrose isocalorically replaced ethanol in controls. In the first set of experiments, whole livers were analyzed. In the second set of experiments, Kupffer cells, endothelial cells, and hepatocytes were isolated from rats in each group. Pathological analyses and measurements of lipid peroxidation, tumor necrosis factor (TNF)-alpha, COX-1 and COX-2 messenger RNA (mRNA), endotoxin, and liver and plasma thromboxane were performed. RESULTS: Increased expression of COX-2 mRNA was detected in the livers of rats showing necroinflammatory changes. The Kupffer cell was the cell primarily responsible for the increase in COX-2 mRNA level. Increased expression of COX-2 was associated with increased levels of endotoxin, TNF-alpha mRNA, lipid peroxidation, and synthesis of thromboxane. COX-1 mRNA was decreased in Kupffer cells in rats with the most severe liver injury. CONCLUSIONS: Up-regulation of COX-2 in alcoholic liver injury occurred in the presence of proinflammatory stimuli and resulted in increased synthesis of inflammatory and vasoactive eicosanoids. Down-regulation of COX-1 may result in decreased synthesis of cytoprotective eicosanoids and additionally exacerbate liver injury.