Classification and regression trees are machine-learning methods for constructing prediction models from data. The models are obtained by recursively partitioning the data space and fitting a simple prediction model within each partition. As a result, the partitioning can be represented graphically as a decision tree. Classification trees are designed for dependent variables that take a finite number of unordered values, with prediction error measured in terms of misclassification cost. Regression trees are for dependent variables that take continuous or ordered discrete values, with prediction error typically measured by the squared difference between the observed and predicted values. This article gives an introduction to the subject by reviewing some widely available algorithms and comparing their capabilities, strengths, and weakness in two examples. © 2011 John Wiley & Sons, Inc. WIREs Data Mining Knowl Discov 2011 1 14-23 DOI: 10.1002/widm.8

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Technologies > Classification
Technologies > Machine Learning
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Technologies > Statistical Fundamentals

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Classification and regression trees

RNA interference (RNAi) is the process of sequence-specific, post-transcriptional gene silencing in animals and plants, initiated by double-stranded RNA (dsRNA) that is homologous in sequence to the silenced gene. The mediators of sequence-specific messenger RNA degradation are 21- and 22-nucleotide small interfering RNAs (siRNAs) generated by ribonuclease III cleavage from longer dsRNAs. Here we show that 21-nucleotide siRNA duplexes specifically suppress expression of endogenous and heterologous genes in different mammalian cell lines, including human embryonic kidney (293) and HeLa cells. Therefore, 21-nucleotide siRNA duplexes provide a new tool for studying gene function in mammalian cells and may eventually be used as gene-specific therapeutics.

Duplexes of 21-nucleotide RNAs mediate RNA interference in cultured mammalian cells

One of the mechanisms by which the innate immune system senses the invasion of pathogenic microorganisms is through the Toll-like receptors (TLRs), which recognize specific molecular patterns that are present in microbial components. Stimulation of different TLRs induces distinct patterns of gene expression, which not only leads to the activation of innate immunity but also instructs the development of antigen-specific acquired immunity. Here, we review the rapid progress that has recently improved our understanding of the molecular mechanisms that mediate TLR signalling.

Toll-like receptor signalling

The innate immune system in drosophila and mammals senses the invasion of microorganisms using the family of Toll receptors, stimulation of which initiates a range of host defense mechanisms. In drosophila antimicrobial responses rely on two signaling pathways: the Toll pathway and the IMD pathway. In mammals there are at least 10 members of the Toll-like receptor (TLR) family that recognize specific components conserved among microorganisms. Activation of the TLRs leads not only to the induction of inflammatory responses but also to the development of antigen-specific adaptive immunity. The TLR-induced inflammatory response is dependent on a common signaling pathway that is mediated by the adaptor molecule MyD88. However, there is evidence for additional pathways that mediate TLR ligand-specific biological responses.

Toll-like receptors.

Since the first application of the surface plasmon resonance (SPR) phenomenon for sensing almost two decades ago, this method has made great strides both in terms of instrumentation development and applications. SPR sensor technology has been commercialized and SPR biosensors have become a central tool for characterizing and quantifying biomolecular interactions. This paper attempts to review the major developments in SPR technology. Main application areas are outlined and examples of applications of SPR sensor technology are presented. Future prospects of SPR sensor technology are discussed.

Surface plasmon resonance sensors: review

. The contents of prealbumin, retinol binding protein, and retinol in normal human serum have been estimated. The amounts of prealbumin were, on average, 6 times larger than those of RBP, that is a two-fold molar excess of prealbumin over RBP. Retinol and RBP were present in about the same molar amounts. Prealbumin occurred in two molecular forms in serum. About half of the prealbumin was bound to RBP (prealbumin-RBP complex) and half was in free form. In spite of the molar excess of prealbumin, small amounts of free RBP were encountered. The free RBP was isolated from normal serum and displayed about the same characteristics as RBP isolated from the prealbumin-RBP complex. Some significant differences were noted however. The free RBP had a lower content of retinol and one amino acid residue less of arginine. The contents of prealbumin, RBP, and retinol were also estimated in the sera of patients subjected to chronic haemodialysis. The amounts of prealbumin and retinol were normal or somewhat low whereas the values for RBP were considerably elevated. The size distribution of RBP and retinol in the serum of one of these patients showed that the amount of free RBP was considerably elevated whereas the amount of the prealbumin-RBP complex was normal. Retinol was apparently associated only with the prealbumin-RBP complex. Various analyses revealed that RBP, isolated in free form from serum, did not bind to prealbumin in contrast to RBP from the prealbumin-RBP complex. It is suggested that the free species of RBP, present in serum, represents a transitory form which has fulfilled its physiological role and will rapidly be degraded by the kidney.

Demonstration in Serum of two Physiological Forms of the Human Retinol Binding Protein

The assembly of MHC Ia molecules in the endoplasmic reticulum requires the presence of peptide ligands and β 2 m and is facilitated by chaperones in an ordered sequence of molecular interactions. A crucial step in this process is the interaction of the class I α-chain/β 2 m dimer with TAP, which is believed to ensure effective peptide loading of the empty class I molecule. We have previously demonstrated impaired intracellular transport of the class Ib molecule HLA-E in mouse myeloma cells cotransfected with the genes for HLA-E and human β 2 m, which is most likely attributable to inefficient intracellular peptide loading of the HLA-E molecule. We therefore analyzed the ability of HLA-E in the transfectant cell line to bind synthetic peptides by means of their ability to enhance cell surface expression of HLA-E. Peptide binding was confirmed by testing the effect on the thermostability of soluble empty HLA-E/human β 2 m dimers. Two viral peptides binding to HLA-E were thus identified, for which the exact positioning of the N terminus appeared critical for binding, whereas the contribution of the length of the C terminus seemed to be minor, allowing peptides as short as seven amino acids and up to 16 amino acids to exhibit considerable binding activity. Furthermore, we demonstrate that HLA-E interacts with TAP and that this interaction can be prolonged by the proteasome inhibitor N -acetyl-l-leucyl-l-leucyl-l-norleucinal, which reduces the intracellular peptide pool. The presented data indicate that HLA-E is capable of presenting peptide ligands similar to the repertoire of HLA class Ia molecules.

Interaction of HLA-E with Peptides and the Peptide Transporter In Vitro: Implications for its Function in Antigen Presentation

Publisher Summary This chapter presents different aspects of the metabolism of retinol-binding protein (RBP) and retinol. RBP is not significantly decreased until the liver reserves of the vitamin are virtually abolished. The diminished concentration of RBP in plasma in manifest vitamin A deficiency reflects the impaired transport of retinol to the various tissues. The catabolism of RBP is probably greatly dependent on renal function, since a small fraction of free RBP exists in plasma although most is bound to prealbumin. The biological half-life of RBP was increased by about 50% in protein deficiency while the rate of synthesis was diminished to one-third of the normal value. The cellular accumulation of retinol is a temperature-dependent process. Incubations of the cells in the absence of oxygen or in the presence of metabolic inhibitors like sodium azide and EDTA did not change their ability to extract retinol from RBP. It is seen that the labeled RBP component exhibited a slower electrophoretic mobility than genuine RBP, which could complex with prealbumin. The low pH was chosen to minimize charge differences due to variable content of amide groups in the two forms of RBP.

Aspects of the metabolism of retinol-binding protein and retinol.

https://febs.onlinelibrary.wiley.com/doi/pdf/10.1016/0014-5793%2879%2981084-4

Per A. Peterson

Papers

Demonstration in Serum of two Physiological Forms of the Human Retinol Binding Protein

Interaction of HLA-E with Peptides and the Peptide Transporter In Vitro: Implications for its Function in Antigen Presentation

Aspects of the metabolism of retinol-binding protein and retinol.

The primary structure of the human retinol-binding protein

In Vivo Characterization of the Proteasome Regulator PA28