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Jing-Yu Yang

Publications and source records attributed to Jing-Yu Yang.

8 recordsLinked to original sources

Topology description for data distributions using a topology graph with divide-and-combine learning strategy.

The topologies of data distributions are very important for data description. Usually, it is not easy to find a description that can give us an intuitional understanding of the topologies for general distributions. In this paper, a novel concept, a topology graph, is proposed as a description for the principal topology of data distribution. The topology graph builds a one-to-one correspondence between the principal topology of the distribution and the topology itself: annularity features of the principal topology correspond to the loops of the graph, and the divarication features correspond to the branches of the graph. In general, the topology graph can be considered as the skeleton of the data distribution. A divide-and-combine learning strategy is developed to find the topology graphs for general data distributions. The learning strategy is focused on the constrained local description learning and automatic topology generation. Following the learning strategy, a cluster growing algorithm is developed. Experimental results on both artificial datasets and real-world applications show good performance of the proposed algorithm.

Journal Article↗

Morphine modulates glutamate release in the hippocampal CA1 area in mice.

Opiate abuse is associated with long-lasting neural adaptative changes in the brain. Increasing evidence demonstrates that opiates significantly alter the function of the glutamatergic system, while how the system is regulated still remains elusive. In the present study, we studied the effect of morphine on extracellular glutamate concentration in the hippocampus, a nucleus rich of the glutamatergic neurons. The results showed that glutamate concentration in the extracellular fluid of the hippocampus was decreased following either acute or chronic treatment of morphine. However, naloxone-induced withdrawal increased glutamate concentration significantly. These results suggest an adaptation of the glutamatergic neuronal transmission in the hippocampus after morphine treatment.

Adaptation, Physiological↗

KPCA plus LDA: a complete kernel Fisher discriminant framework for feature extraction and recognition.

This paper examines the theory of kernel Fisher discriminant analysis (KFD) in a Hilbert space and develops a two-phase KFD framework, i.e., kernel principal component analysis (KPCA) plus Fisher linear discriminant analysis (LDA). This framework provides novel insights into the nature of KFD. Based on this framework, the authors propose a complete kernel Fisher discriminant analysis (CKFD) algorithm. CKFD can be used to carry out discriminant analysis in "double discriminant subspaces." The fact that, it can make full use of two kinds of discriminant information, regular and irregular, makes CKFD a more powerful discriminator. The proposed algorithm was tested and evaluated using the FERET face database and the CENPARMI handwritten numeral database. The experimental results show that CKFD outperforms other KFD algorithms.

Algorithms↗

Roles of ginsenosides on morphine-induced hyperactivity and rewarding effect in mice.

Ginsenosides, the main effective components of the root of Panax ginseng, have been reported to modulate morphine action. In the present study, ginsenosides Rd, Rb2, Rgl and Re were divided into two groups according to their effects in mice on morphine-induced hyperactivity and conditioned place preference (CPP). Ginsenosides Rd, Rb2, Rgl had no effect on morphine-induced hyperactivity, but antagonized morphine-induced CPP. On the contrary, ginsenoside Re increased morphine-induced hyperactivity whereas it showed no effect on morphine-induced CPP.Furthermore, Re antagonized the inhibitory effect of the mixture involving Rd, Rb2 and Rgl on the morphine action. These results suggest that ginsenosides with different structures have antagonizing properties in the regulation of morphine-induced reinforcement.

Animals↗

The serotonergic system may be involved in the sleep-inducing action of oleamide in rats.

The mechanism underlying the sleep-inducing effect of oleamide, an endogenous fatty acid amide, was studied in rats. Animals implanted with cerebrocortical and dorsal neck muscle electrodes were monitored continuously by electroencephalograph (EEG) and electromyograph (EMG) for 4 h after i.p. or s.c. injection of drugs. Oleamide induced a dose-dependent increase in slow-wave sleep (SWS), a decrease in wakefulness (W) and sleep latency, but had no effect on rapid-eye-movement sleep (REMS). The oleamide-induced increase in SWS was prevented by 5-HT reuptake inhibitors such as fluoxetine or fenfluramine and by agonists at 5-HT(1A) receptors such as buspirone or 8-hydroxy-2-(di- N-propylamino) tetralin (8-OH-DPAT). Moreover, the selective 5-HT(1A) receptor antagonist WAY100635 markedly antagonized the suppression of the oleamide-induced increase in SWS by 8-OH-DPAT. These data provide the first behavioural evidence that the serotonergic system may be involved in the sleep-inducing action of oleamide in rats.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Selective effect of oleamide, an endogenous sleep-inducing lipid amide, on pentylenetetrazole-induced seizures in mice.

The anti-seizure effect of oleamide, an endogenous sleep-inducing fatty acid amide, was studied in mice. Oleamide, in the dose range 43.7-700.0 mg kg(-1), significantly and dose-dependently inhibited the seizures induced by pentylenetetrazole. However, oleamide showed no inhibitory action on the seizures induced by picrotoxin, strychnine, caffeine or semicarbazide. These results provide the first evidence for the anti-seizure effect of oleamide, and suggest that this effect may be selective to the seizure model induced by pentylenetetrazole.

Animals↗

Oleamide attenuates apoptotic death in cultured rat cerebellar granule neurons.

The effect of oleamide on apoptosis was investigated by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction assay, DNA staining assay with propidium iodide and caspase-3 activity analyses. The present results showed that oleamide significantly attenuated the cell death and nuclear condensation of cultured rat cerebellar granule neurons induced by K(+) deprivation in a dose-dependent manner. The oleamide actions were well parallel with the attenuation of caspase-3 activity in the process of apoptotic death. Moreover, neither elaidic acid nor stearic acid, two fatty acids structurally related to oleamide without the Delta(9)-cis double bond, had similar effects on the cell death, suggesting the selectively structural features of oleamide required for this action. These data provided the first evidence of a protective effect of oleamide against apoptosis in a structurally specific manner.

Animals↗

Hypnotic activity of melatonin: involvement of semicarbazide hydrochloride, blocker of synthetic enzyme for GABA.

AIM: To assess the effect of semicarbazide hydrochloride (SCZ), the blocker of synthetic enzyme for GABA, on the hypnotic activity of melatonin. METHODS: Righting reflex method in mice and electroencephalography (EEG) in rats were used to determine effects of SCZ on sleep and hypnotic activity of melatonin. RESULTS: Melatonin displayed a marked hypnotic activity both in righting reflex experiment and EEG recording. SCZ had no influence on sleep parameters in mice and rats when it was used alone. However, it blocked the sleep-potentiation effect of melatonin in mice. SCZ also inhibited melatonin-induced increase in total sleep time, slow wave sleep time, and paradoxical sleep time, and prevented melatonin-induced decrease in awake time in rats. CONCLUSION: SCZ antagonized the hypnotic activity of melatonin. It is thought that the hypnotic activity of melatonin is mediated by GABAergic system.

Animals↗