Intelligent Extraction of Salient Feature From Electroencephalogram Using Redundant Discrete Wavelet Transform.

At present, electroencephalogram (EEG) signals play an irreplaceable role in the diagnosis and treatment of human diseases and medical research. EEG signals need to be processed in order to reduce the adverse effects of irrelevant physiological process interference and measurement noise. Wavelet transform (WT) can provide a time-frequency representation of a dynamic process, and it has been widely utilized in salient feature analysis of EEG. In this paper, we investigate the problem of translation variability (TV) in discrete wavelet transform (DWT), which causes degradation of time-frequency localization. It will be verified through numerical simulations that TV is caused by downsampling operations in decomposition process of DWT. The presence of TV may cause severe distortions of features in wavelet subspaces. However, this phenomenon has not attracted much attention in the scientific community. Redundant discrete wavelet transform (RDWT) is derived by eliminating the downsampling operation. RDWT enjoys the attractive merit of translation invariance. RDWT shares the same time-frequency pattern with that of DWT. The discrete delta impulse function is used to test the time-frequency response of DWT and RDWT in wavelet subspaces. The results show that DWT is very sensitive to the translation of delta impulse function, while RDWT keeps the decomposition results unchanged. This conclusion has also been verified again in decomposition of actual EEG signals. In conclusion, to avoid possible distortions of features caused by translation sensitivity in DWT, we recommend the use of RDWT with more stable performance in BCI research and clinical applications.

Exogenous GM1 Ganglioside Attenuates Ketamine-Induced Neurocognitive Impairment in the Developing Rat Brain.

BACKGROUND: A prolonged exposure to ketamine triggers significant neurodegeneration and long-term neurocognitive deficits in the developing brain. Monosialotetrahexosylganglioside (GM1) can limit the neuronal damage from necrosis and apoptosis in neurodegenerative conditions. We aimed to assess whether GM1 can prevent ketamine-induced developmental neurotoxicity. METHODS: Postnatal day 7 (P7) rat pups received 5 doses of intraperitoneal ketamine (20 mg/kg per dose) at 90-minute intervals for 6 hours. Cognitive functions, determined by using Morris water maze (MWM) including escape latency (at P32-36) and platform crossing (at P37), were compared among the ketamine-exposed pups treated with or without exogenous GM1 (30 mg/kg; n = 12/group). The effect of GM1 on apoptosis in hippocampus was determined by terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick end labeling (TUNEL) staining and activated caspase 3 measurement. The hippocampal expression of brain-derived neurotrophic factor (BDNF), along with the phosphorylation of protein kinase B (AKT) and extracellular signal-related kinases 1 and 2 (ERK1/2), was detected by western blotting (n = 6/group). Anti-BDNF antibody (2 µg per rat) administered before GM1 treatment was applied to determine the neuroprotective mechanisms of GM1. RESULTS: The rats receiving ketamine exposure experinced cognitive impairment in MWM test compared to the control rats, indicated by prolonged escape latency at P34 (P = .006), P35 (P = .002), and P36 (P = .005). However, in GM1-pretreated rats, ketamine exposure did not induce prolonged escape latency. The exogenous GM1 increased the platform-crossing times at P37 (3.00 ± 2.22 times vs 5.40 ± 1.53 times, mean ± standard deviation; P = .041) and reduced the hippocampal TUNEL-positive cells and cleaved-caspase 3 expression in ketamine-exposed young rats. Ketamine decreased BDNF expression and phosphorylation of AKT and ERK in the hippocampus, whereas exogenous GM1 blocked these ketamine-caused effects. However, for the ketamine-exposed rat pups receiving exogenous GM1, compared to immunoglobulin Y (IgY) isotype control, the BDNF-neutralizing antibody treatment counteracted the exogenous GM1-induced improvement of the escape latency at P36 (41.32 ± 12.37 seconds vs 25.14 ± 8.97 seconds, mean ± standard deviation; P = .036), platform-crossing times at P37 (2.16 ± 1.12 times vs 3.92 ± 1.97 times, mean ± standard deviation; P < .036), apoptotic activity, as well as AKT and ERK1/2 phosphorylation in the hippocampus of ketamine-challenged young rats. CONCLUSIONS: Our data suggest that the exogenous GM1 acts on BDNF signaling pathway to ameliorate the cognitive impairment and hippocampal apoptosis induced by ketamine in young rats. Our study may indicate a potential use of GM1 in preventing the cognitive deficits induced by ketamine in the young per se.

Monosialoganglioside 1 may alleviate neurotoxicity induced by propofol combined with remifentanil in neural stem cells.

Monosialoganglioside 1 (GM1) is the main ganglioside subtype and has neuroprotective properties in the central nervous system. In this study, we aimed to determine whether GM1 alleviates neurotoxicity induced by moderate and high concentrations of propofol combined with remifentanil in the immature central nervous system. Hippocampal neural stem cells were isolated from newborn Sprague-Dawley rats and treated with remifentanil (5, 10, 20 ng/mL) and propofol (1.0, 2.5, 5.0 µg/mL), and/or GM1 (12.5, 25, 50 µg/mL). GM1 reversed combined propofol and remifentanil-induced decreases in the percentage of 5-bromodeoxyuridine(+) cells and also reversed the increase in apoptotic cell percentage during neural stem cell proliferation and differentiation. However, GM1 with combined propofol and remifentanil did not affect ß-tubulin(+) or glial fibrillary acidic protein(+) cell percentage during neural stem cell differentiation. In conclusion, we show that GM1 alleviates the damaging effects of propofol combined with remifentanil at moderate and high exposure concentrations in neural stem cells in vitro, and exerts protective effects on the immature central nervous system.

Ethyl 2-isopropyl-amino-6-methyl-8-oxo-3-phenyl-3H,8H-furo[2,3-d][1,2,4]triazolo[1,5-a]pyrimidine-7-carboxyl-ate.

In the title compound, C(20)H(21)N(5)O(4), the ring system containing the three fused rings is essentially planar (r.m.s. deviation for all 12 non-H atoms = 0.041 Å). The phenyl ring makes a dihedral angle of 54.41 (6)° with this ring system. The isopropyl group is disordered over two positions, with site-occupancy factors of 0.753 (9) and 0.247 (9). The structure is mainly stabilized by weak inter-molecular N-H⋯O and intra-molecular C-H⋯O hydrogen-bonding inter-actions and π-π inter-actions, with inter-planar distances of 3.415 (1) Šbetween adjacent furan ring centroids and 3.420 (1) Šbetween the benzene and pyrimidinone rings.

Characteristics and sources of atmospheric polycyclic aromatic hydrocarbons (PAHs) in Shanghai, China.

A field campaign was conducted to measure and analyze 13 polycyclic aromatic hydrocarbons (PAHs) in six major zones in the city of Shanghai, P.R. China from August 2006 to April 2007. Ambient air samples were collected seasonally using passive air samplers, and gas chromatography-mass spectroscopy was used in this field campaign. The results showed that there was a sequence of 13 PAHs at Phen > FA > Pyr > Chr > Fl > An > BaA > BbFA > BghiP > IcdP > BkFA > BaP > DahA and the sum of these PAHs is 36.01 +/- 10.85 ng/m(3) in gas phase. FL, Phen, FA, Pyr, and Chr were the dominant PAHs in gas phase in the city. They contributed 90% of total PAHs in the gas phase. Proportion of measured PAHs with three, four, five, and six rings to total PAHs was 53%, 42%, 3%, and 2%, respectively. The highest concentration of SigmaPAHs (the sum of 13 PAHs) occurred in the wintertime and the lowest was in the summer. This investigation suggested that traffic, wood combustion, and metal scrap burn emissions were dominant sources of the concentrations of PAHs in six city zones compared with coal burning and industry emissions. Further, the traffic emission sources of PAHs in the city were attributed mostly to gasoline-powered vehicles compared with diesel-powered vehicles. It was revealed that the seasonal changes in PAHs in the city depended on different source types. Metal scrap burn was found to be the major source of PAHs during the autumn, while the PAH levels in the atmosphere for winter and spring seasons were mainly influenced by wood and biomass combustion. Comparisons of PAHs among different city zones and with several other cities worldwide were also made and discussed.

[Analgesic effect of intrathecal transplant of immortalized rat astrocyte strain genetically modified by human preproenkephalin gene on rat chronic neuropathic pain].

OBJECTIVE: To observe the analgesic effect of intrathecal transplant of immortalized rat astrocyte genetically modified by human preproenkephalin gene (IAST/hPPE) on chronic neuropathic pain. METHODS: 40 adult male Sprague-Dawley rats were randomly divided into four groups, 10 rats for each group. Naive group, SNI group, SNI + IAST group and SNI + IAST/hPPE group. The immortalized rat astrocyte (IAST) or IAST/hPPE co-incubated with bromodeoxyuridine (BrdU) in vitro were transplanted in the lumbar 4 to 6 subarachnoid space near the spinal cord 1 week after right side spared nerve injury (SNI). All animals were tested for bilateral 50% hindpaw withdrawal threshold (PWT) to a graded series of Von Frey hairs stimulation once a week from one week before SNI to six weeks after transplant, the difference value for right 50% PWT minus left 50% PWT was calculated and the effect of intraperitoneal naloxone on the analgesic efficacies was also observed. The content of L-EK in the spinal cord of L4 - 6 and was determined using immunohistochemistry and radioimmunoassay, and the expression of BrdU in grafts was determined using immunohistochemistry. RESULTS: Allodynia-like behaviour after 1 week following SNI was observed. As compared with Naive group, the difference value for the right 50% PWT minus left 50% PWT in the other three groups was higher significantly (P < 0.01). The tactile allodynia induced by SNI was significantly alleviated during the 1 to 6 week period after transplantation of IAST/hPPE cells, but transplants of IAST cells had no effect on the allodynia-like behaviour. The difference value for the right 50% PWT minus left 50% PWT in SNI + IAST/hPPE group was lower significantly than that in the SNI and SNI +I AST group (P < 0.01), but there was no significant difference between SNI and SNI + IAST group (P > 0.05). The efficacies were reversed by intraperitoneal naloxone in SNI + IAST/hPPE group. The content of L-EK in the lumbar spinal cord in IAST/hPPE group (108.1 pg/mg +/- 12.5 pg/mg) was significantly higher than that in other three groups (P < 0.01), but there was no significant difference between SNI and SNI + IAST group (25.4 pg/mg +/- 1.9 pg/mg vs 28.0 pg/mg +/- 2.1 pg/mg, P > 0.05). Furthermore, The grafts in the surface of dorsal horn were still stained positively for BrdU, they survived greater than 6 weeks on the pia mater around the spinal cord. CONCLUSION: Intrathecal transplant of IAST/hPPE cells could alleviate the allodynia-like behaviour after chronic neuropathic pain, which is associated with enkephalin secreted continuously from the grafts and conducted via opiate receptors.