The Nature of Novelty Detection

Sentence level novelty detection aims at reducing redundant sentences from a sentence list. In the task, sentences appearing later in the list with no new meanings are eliminated. Aiming at a better accuracy for detecting redundancy, this paper reveals the nature of the novelty detection task currently overlooked by the Novelty community $-$ Novelty as a combination of the partial overlap (PO, two sentences sharing common facts) and complete overlap (CO, the first sentence covers all the facts of the second sentence) relations. By formalizing novelty detection as a combination of the two relations between sentences, new viewpoints toward techniques dealing with Novelty are proposed. Among the methods discussed, the similarity, overlap, pool and language modeling approaches are commonly used. Furthermore, a novel approach, selected pool method is provided, which is immediate following the nature of the task. Experimental results obtained on all the three currently available novelty datasets showed that selected pool is significantly better or no worse than the current methods. Knowledge about the nature of the task also affects the evaluation methodologies. We propose new evaluation measures for Novelty according to the nature of the task, as well as possible directions for future study.Comment: This paper pointed out the future direction for novelty detection research. 37 pages, double spaced versio

MAP7 regulates axon morphogenesis by recruiting kinesin-1 to microtubules and modulating organelle transport.

Neuronal cell morphogenesis depends on proper regulation of microtubule-based transport, but the underlying mechanisms are not well understood. Here, we report our study of MAP7, a unique microtubule-associated protein that interacts with both microtubules and the motor protein kinesin-1. Structure-function analysis in rat embryonic sensory neurons shows that the kinesin-1 interacting domain in MAP7 is required for axon and branch growth but not for branch formation. Also, two unique microtubule binding sites are found in MAP7 that have distinct dissociation kinetics and are both required for branch formation. Furthermore, MAP7 recruits kinesin-1 dynamically to microtubules, leading to alterations in organelle transport behaviors, particularly pause/speed switching. As MAP7 is localized to branch sites, our results suggest a novel mechanism mediated by the dual interactions of MAP7 with microtubules and kinesin-1 in the precise control of microtubule-based transport during axon morphogenesis

Volumetric error compensation for industrial robots and machine tools

“A more efficient and increasingly popular volumetric error compensation method for machine tools is to compute compensation tables in axis space with tool tip volumetric measurements. However, machine tools have high-order geometric errors and some workspace is not reachable by measurement devices, the compensation method suffers a curve-fitting challenge, overfitting measurements in measured space and losing accuracy around and out of the measured space. Paper I presents a novel method that aims to uniformly interpolate and extrapolate the compensation tables throughout the entire workspace. By using a uniform constraint to bound the tool tip error slopes, an optimal model with consistent compensation capability is constructed. In addition to machine tools, industrial robots, are also becoming popularly used in manufacturing field. However, typical robot volumetric error compensation methods only consider constant errors such as link length and assembly errors while neglecting complicated kinematic errors such as strain wave gearing and out of rotating plane errors. Paper II presents a high-order joint-dependent model which describes both simple and complicated robot kinematic errors. A laser tracker with advantages of rapid data collection and a self-oriented position retroreflector are used for data collection. The experimental results show that nearly 20% of the robot kinematic errors are joint-dependent which are successfully captured by the proposed method. Paper III continues using the high-order joint-dependent robot error model while utilizing a new retroreflector with the ability of measuring robot position and orientation information simultaneously. More than 60% of measurement time is saved. Both position and orientation accuracy are also further improved”--Abstract, page iv

Inhibition of food intake in obese subjects by peptide YY3-36

Background: The gut hormone fragment peptide YY3-36 (PYY) reduces appetite and food intake when infused into subjects of normal weight. In common with the adipocyte hormone leptin, PYY reduces food intake by modulating appetite circuits in the hypothalamus. However, in obesity there is a marked resistance to the action of leptin, which greatly limits its therapeutic effectiveness. We investigated whether obese subjects were also resistant to the anorectic effects of PYY.Methods: We compared the effects of PYY infusion on appetite and food intake in 12 obese and 12 lean subjects in a double-blind, placebo-controlled, crossover study. The plasma levels of PYY, ghrelin, leptin, and insulin were also determined.Results: Caloric intake during a buffet lunch offered two hours after the infusion of PYY was decreased by 30 percent in the obese subjects (P<0.001) and 31 percent in the lean subjects (P<0.001). PYY infusion also caused a significant decrease in the cumulative 24-hour caloric intake in both obese and lean subjects. PYY infusion reduced plasma levels of the appetite-stimulatory hormone ghrelin. Endogenous fasting and postprandial levels of PYY were significantly lower in obese subjects (the mean [+/-SE] fasting PYY levels were 10.2+/-0.7 pmol per liter in the obese group and 16.9+/-0.8 pmol per liter in the lean group, P<0.001). Furthermore, the fasting PYY levels correlated negatively with the body-mass index (r=-0.84, P<0.001).Conclusions: We found that obese subjects were not resistant to the anorectic effects of PYY. Endogenous PYY levels were low in the obese subjects, suggesting that PYY deficiency may contribute to the pathogenesis of obesity

The η(2225)\eta(2225) observed by the BES Collaboration

In the framework of the $^3P_0$ meson decay model, the strong decays of the $3 ^1S_0$ and $4 ^1S_0$ $s\bar{s}$ states are investigated. It is found that in the presence of the initial state mass being 2.24 GeV, the total widths of the $3 ^1S_0$ and $4 ^1S_0$ $s\bar{s}$ states are about 438 MeV and 125 MeV, respectively. Also, when the initial state mass varies from 2220 to 2400 MeV, the total width of the $4 ^1S_0$ $s\bar{s}$ state varies from about 100 to 132 MeV, while the total width of the $3 ^1S_0$ $s\bar{s}$ state varies from about 400 to 594 MeV. A comparison of the predicted widths and the experimental result of $(0.19\pm 0.03^{+0.04}_{-0.06})$ GeV, the width of the $\eta(2225)$ with a mass of $(2.24^{+0.03+0.03}_{-0.02-0.02})$ GeV recently observed by the BES Collaboration in the radiative decay $J/\psi\to\gamma\phi\phi\to\gamma K^+K^-K^0_SK^0_L$, suggests that it would be very difficult to identify the $\eta(2225)$ as the $3 ^1S_0$ $s\bar{s}$ state, and the $\eta(2225)$ seams a good candidate for the $4 ^1S_0$ $s\bar{s}$ state.Comment: 14 pages, 3 figures, typos corrected, Accepted by Physical Review