Oriented colorings of 2-outerplanar graphs

A graph G is 2-outerplanar if it has a planar embedding such that the subgraph obtained by removing the vertices of the outer face is outerplanar. The oriented chromatic number of an oriented graph H is defined as the minimum order of an oriented graph H^′ such that H has a homomorphism to H^′. In this paper, we prove that 2-outerplanar graphs are 4-degenerate. We also show that oriented 2-outerplanar graphs have a homomorphism to the Paley tournament QR₆₇, which implies that their (strong) oriented chromatic number is at most 67.     

Closed form solution for the sensor registration problem using only position information

Sensors, mounted on the dexterous end of a robot, can be used for feedback control or calibration. When you mount a sensor on a robot it becomes necessary to find the pose (orientation and position) of the sensor relative to the robot. This is the sensor registration problem. Many researchers have provided closed-form solutions to the sensor registration problem; however, the published solutions apply only to sensors that can measure a complete pose (three positions and three orientations). Many sensors, however, can provide only position information; they cannot measure the orientation of an object. This article provides a closed-form solution to the sensor registration problem applicable when: (1) the sensor can provide only position information and (2) the robot can move along and rotate about straight lines. © 1994 John Wiley & Sons, Inc.     

A Novel Band-Reject Element for Pseudoelliptic Bandstop Filters

A novel band-reject element for the design of inline waveguide pseudoelliptic band-reject filters is introduced. The element consists of an offset partial-height post in a rectangular waveguide in which the dominant TE₁₀ mode is propagating. The location of the attenuation pole is primarily determined by the height of the post that generates it. The element allows the implementation of weak, as well as strong coupling coefficients that are encountered in asymmetric band-reject responses with broad stopbands. The coupling strength is controlled by the offset of the post with respect to the center of the main waveguide. The posts are separated by uniform sections of the main waveguide. An equivalent low-pass circuit based on the extracted pole technique is first used in a preliminary design. An improved equivalent low-pass circuit that includes a more accurate equivalent circuit of the band-reject element is then introduced. A synthesis method of the enhanced network is also presented. Filters based on the introduced element are designed, fabricated, and tested. Good agreement between measured and simulated results is achieved     

Display modulation by Fourier transform: A preferred method

Abstract— A preferred method for determining the grating modulation of a rear‐projection display using a grating image and Fourier analysis is prescribed. This method is insensitive to spatial image noise and is in better correspondence with the response of the human visual system than is the standard technique. This method is not limited to rear‐projection displays and can be applied to any display technology.     

Random sampling, randomization, and equivalence of contrasted groups in psychotherapy outcome research.

Random sampling and random assignment (randomization) are some of the most popular methods of equating contrasted groups on pre-existing nuisance variables. However, the small samples typically used in psychotherapy outcome studies raise some questions about the extent to which these methods eliminate the pretreatment nonequivalence of groups in this area of research. This article identifies conditions under which equivalence is likely (and unlikely) to be attained with simple random sampling and randomization in psychotherapy efficacy studies of the kind examined in recent meta-analyses. Some consequences of nonequivalence are viewed as manifestations of Simpson's paradox. Misinterpretations of estimates of the relative efficacy of treatments are expected in view of belief in the law of small numbers. The minimum sample sizes needed to protect against nonequivalence are compared with those needed to satisfy several other criteria. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Pharmacology and subcellular distribution of [3H]rilmenidine binding sites in rat brain

We have previously reported that in rat brain membranes, [3H]rilmenidine, in addition to labelling alpha2-adrenoceptors and the I2B-subtype of imidazoline receptor binding site (I2B-RBS), may label an additional I-RBS population, distinct from previously classified I1-RBS and I2-RBS. In this study, using crude or fractionated rat brain membranes we examined the possible association of [3H]rilmenidine-labelled I-RBS with the A- and B-isoforms of monoamine oxidase (MAO) by studying the inhibition of [3H]rilmenidine binding by a number of MAO inhibitors; and comparing the maximal binding density (Bmax) and subcellular distribution of [3H]rilmenidine binding sites with that of MAO-A and MAO-B catalytic sites labelled by [3H]RO41-1049 and [3H]RO19-6327 and 12-RBS labelled by [3H]2-BFI. Inhibition of [3H]rilmenidine binding by all MAO inhibitors tested produced very shallow curves (slope 0.29-0.56). Clorgyline and moclobemide (selective MAO-A inhibitors) displayed moderate affinities (60-140 nM), while pargyline (non-selective MAO-inhibitor), RO41-1049 (selective MAO-A inhibitor) and RO19-6327 (selective MAO-B inhibitor) exhibited very low affinities (> 2 microM) for 50-75% of [3H]rilmenidine-labelled I-RBS in crude brain membranes and even lower affinity for the remaining binding. Under identical buffer conditions, the Bmax of [3H]rilmenidine-labelled I-RBS (1.45+/-0.14 pmol/mg protein) was considerably lower than those of MAO-A (13.10+/-0.15 pmol/mg) and MAO-B (10.35+/-0.50 pmol/mg) sites. These results suggest that [3H]rilmenidine does not interact directly with the active catalytic site of either MAO enzyme and could at best only associate with a subpopulation of MAO molecules. Binding studies on five fractions of rat cortex homogenates-nuclear (N), heavy (M) and light (L) mitochondrial, microsomal non-mitochondrial (P), and soluble cytosolic (S) fractions-revealed that 45% of total [3H]rilmenidine binding was present in the P fraction cf. 20 and 23% in the M and L fractions, in contrast to [3H]RO19-6327 and [3H]2-BFI which bound 11-13% in the P fraction and 36-38% and 35-44% in the M and L fractions, respectively. Binding of all ligands in the N fraction was 6-15% of total. These studies reveal that [3H]rilmenidine-labelled I-RBS, unlike the I2-RBS, are not predominantly associated with mitochondrial fractions containing the MAO enzymes (and cytochrome oxidase activity), but appear to be distributed in both the mitochondrial and plasma membrane fractions in rat cerebral cortex.     

Hydrophilic peptides derived from the transframe region of Gag-Pol inhibit the HIV-1 protease

The HIV-1 transframe region (TFR) is between the structural and functional domains of the Gag-Pol polyprotein, flanked by the nucleocapsid and the protease domains at its N and C termini, respectively. Transframe octapeptide (TFP) Phe-Leu-Arg-Glu-Asp-Leu-Ala-Phe, the N terminus of TFR, and its analogues are competitive inhibitors of the action of the mature HIV-1 protease. The smallest, most potent analogues are tripeptides: Glu-Asp-Leu and Glu-Asp-Phe with Ki values of approximately 50 and approximately 20 microM, respectively. Substitution of the acidic amino acids in the TFP by neutral amino acids and d or retro-d configurations of Glu-Asp-Leu results in an >40-fold increase in Ki. Protease inhibition by Glu-Asp-Leu is dependent on a protonated form of a group with a pKa of 3.8; unlike other inhibitors of HIV-1 protease which are highly hydrophobic, Glu-Asp-Leu is extremely soluble in water, and its binding affinity decreases with increasing NaCl concentration. However, Glu-Asp-Leu is a poor inhibitor (Ki approximately 7.5 mM) of the mammalian aspartic acid protease pepsin. X-ray crystallographic studies at pH 4.2 show that the interactions of Glu at P2 and Leu at P1 of Glu-Asp-Leu with residues of the active site of HIV-1 protease are similar to those of other product-enzyme complexes. It was not feasible to understand the interaction of intact TFP with HIV-1 protease under conditions of crystal growth due to its hydrolysis giving rise to two products. The sequence-specific, selective inhibition of the HIV-1 protease by the viral TFP suggests a role for TFP in regulating protease function during HIV-1 replication.