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R Tao

Publications and source records attributed to R Tao.

At least 19 recordsLinked to original sources

Differential effect of orexins (hypocretins) on serotonin release in the dorsal and median raphe nuclei of freely behaving rats.

Orexin (hypocretin)-containing neurons in the perifornical hypothalamus project to widespread regions of the brain, including the dorsal and median raphe nuclei [Peyron C, Tighe DK, van den Pol AN, de Lecea L, Heller HC, Sutcliffe JG, Kilduff TS (1998) Neurons containing hypocretin (orexin) project to multiple neuronal systems. J Neurosci 18:9996-10015; Wang QP, Koyama Y, Guan JL, Takahashi K, Kayama Y, Shioda S (2005) The orexinergic synaptic innervation of serotonin- and orexin 1-receptor-containing neurons in the dorsal raphe nucleus. Regul Pept 126:35-42]. Orexin-A or orexin-B was infused by reverse microdialysis into the dorsal raphe nucleus or median raphe nucleus of freely behaving rats, and extracellular serotonin was simultaneously collected by microdialysis and analyzed by high-performance liquid chromatography. We have found that orexin-A produced a dose-dependent increase of serotonin in the dorsal raphe nucleus, but not in the median raphe nucleus. However, orexin-B elicited a small but significant effect in both the dorsal raphe nucleus and median raphe nucleus. Orexins may have regionally selective effects on serotonin release in the CNS, implying a unique interaction between orexins and serotonin in the regulation of activities including sleep-wakefulness.

Analysis of Variance↗

Interactions between a rotating polarized sphere and a stationary one in an electric field.

Precise measurement of the attracting force between two polarized spheres inside an electric field indicates that the rotation of one sphere along the axis perpendicular to the electric field reduces the attracting force between them. The important difference between the experimental results and the existing theory indicated that this reduction is due to several factors. In addition to the reduction of polarization due to the free surface charges, the rotation may also weaken the local field near the rotating sphere, making the main contribution to the reduction of the attracting force. Moreover, the experiment also suggests that the polarization due to the molecular polarizability cannot be ignored.

Journal Article↗

Effects on serotonin of (-)nicotine and dimethylphenylpiperazinium in the dorsal raphe and nucleus accumbens of freely behaving rats.

The aim of this study was to investigate the neurochemical mechanism underlying the effect of nicotine and dimethylphenylpiperazinium (DMPP) on 5-hydroxytryptamine (5-HT) release in the dorsal raphe nucleus and nucleus accumbens of freely behaving rats. For comparison, lobeline, cytisine and RJR-2403 were also investigated. It was found that all drugs, when infused locally, evoked an increase of 5-HT in the dorsal raphe nucleus. However, the magnitudes of the 5-HT increase were comparatively different between the drugs in the ranking of their potency: DMPP>RJR 2403>>nicotine>lobeline>cytisine. Both methyllycaconitine, a nicotinic acetylcholine receptor (nAChR) antagonist and methyllycaconitine, a selective alpha7-containing nAChR antagonist blocked the effects of nicotine and DMPP, suggesting that alpha7 subunit mediated the increases in 5-HT. However, DMPP was reported to increase 5-HT using non-nAChR mechanism [Lendvai B, Sershen H, Lajtha A, Santha E, Baranyi M, Vizi ES (1996) Differential mechanisms involved in the effect of nicotinic agonists DMPP and lobeline to release [3H]5-HT from rat hippocampal slices. Neuropharmacology 35:1769-1777]. To test if 5-HT carriers were involved, a selective 5-HT reuptake inhibitor citalopram (1 microM) was infused into the dorsal raphe nucleus before administration of nicotine or DMPP. As a result, citalopram significantly blocked the effect of DMPP, whereas it had no influence on nicotine. Finally, the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) was used to test whether the increases in 5-HT were depolarization-dependent. Administration of 8-OH-DPAT (0.1 mg/kg, s.c.) produced significant decreases in 5-HT in the animals treated with nicotine. In contrast, the effect of DMPP was not altered by 8-OH-DPAT, suggesting that the increases in 5-HT were independent of cell membrane depolarization. In conclusion, there are different mechanisms involved in nicotine- and DMPP-evoked increases in 5-HT. This is consistent with prior work suggesting DMPP may primarily act on 5-HT carriers.

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

No association between the PTGS2/PLA2G4A locus and schizophrenia in a Chinese population.

The present study was undertaken to replicate an association between the PTGS2/PLA2G4A locus and schizophrenia among a Chinese population. We recruited 168 Chinese parent-offspring trios of Han descent, consisting of fathers, mothers and affected offspring with schizophrenia. Of 3 informative SNPs genotyped, no one showed allelic association with schizophrenia; the haplotype analysis also failed to capture a haplotypic association with the illness. Because the frequencies of alleles and genotypes of SNPs analyzed differ in the Chinese population as compared with a British population that initially showed the genetic association between the PTGS2/PLA2G4A locus and schizophrenia, the ethnic background may be a major reason for poor replication of the initial finding.

Asian People↗

Application of recipient-derived dendritic cells to induce donor-specific T-cell hyporesponsiveness.

Administration of donor-derived immature dendritic cells (DC) treated with NF-kappaB oligodeoxyribonucleotides (ODN) prevents allograft rejection. We attempted to explore the use of recipient-derived DC pulsed with donor antigens, in which the donor antigens were presented to host T cells via an indirect pathway (cross-priming). Expression of CD40, CD80, and CD86 on DC was significantly inhibited by treatment with NF-kappaB ODN, whereas MHC class I and II were minimally affected. Normal C3H DC pulsed with B10 antigens stimulated proliferative responses and donor-specific CTL activity in C3H T cells, both of which were, however, markedly inhibited when DC were treated with NF-kappaB ODN. This manipulation was associated with reduced IFN-gamma and increased IL-10 production in the supernate, suggesting a Th2 bias. More frequent apoptotic T cells were observed in cultures with NF-kappaB ODN DC. In contrast to administration of normal DC pulsed with donor antigens that accelerated rejection of B10 cardiac allografts (median survival time [MST] 7 days versus 10 days in no-DC treatment control, P < .05), a single injection of 2 x 10(6) NF-kappaB ODN DC significantly prolonged allograft survival (MST 50 days, P < .05 compared with no-DC treatment control). The anti-donor CTL activity in infiltrating T cells isolated from cardiac grafts in recipients that received NF-kappaB ODN DC was significantly suppressed. These data indicate that vaccination with immature DC, propagated from recipient BM is an attractive approach to induce T-cell hyporesponsiveness.

Animals↗

Identification of a non-S RNase, a possible ancestral form of S-RNases, in Prunus.

This study identifies and characterizes a basic non-S RNase in the styles with stigmas of sweet cherry (Prunus avium L.), a member of the Rosaceae subfamily Amygdaloideae, which has an RNase-based gametophytic self-incompatibility system. Internal sequences of putative non-S RNases (RNase PA1 and PA2) were determined, and a cDNA for PA1 was obtained. The deduced amino acid sequence of PA1 contained two conserved sequence motifs essential for T2/ S-type RNase activity. PA1 shows 20-30% sequence identity to S-RNases of Rosaceae, Solanaceae and Scrophulariaceae, and non-S RNases of higher plants. Transcription of the PA1 gene was specific to the styles with stigmas, and the gene was not expressed in other tissues. Although PA1 resembles RNase X2, a non-S RNase from Petunia inflata, the placement of PA1 and RNase X2 in the phylogenetic tree was quite different. Placement of PA1 was also distinct from that of rosaceous S-RNases, while RNase X2 was incorporated in the clade of S-RNases from the Solanaceae. The sole intron in the PA1 gene is located at a position equivalent to that of the second intron of amygdaloid S-RNase genes, and that of the only intron in most other S-RNase genes. Genomic Southern analysis revealed the presence of sequences homologous to PA1 in all of the other four Prunus species tested, suggesting that PA1 has an important physiological function. The significance of the discovery of PA1 is discussed in terms of the origin and evolution of S-RNases and self-incompatibility in Rosaceae.

Amino Acid Motifs↗

A gain-control model relating nulling results to the duration of dynamic motion aftereffects.

Strength of the motion aftereffect (MAE) is most often quantified by its duration, a high-variance and rather 'subjective' measure. With the help of an automatic gain-control model we quantitatively relate nulling-thresholds, adaptation strength, direction discrimination threshold, and duration of the dynamic MAE (dMAE). This shows how the nulling threshold, a more objective two-alternative forced-choice measure, relates to the same system property as MAE-durations. Two psychophysical experiments to test the model use moving random-pixel-arrays with an adjustable luminance signal-to-noise ratio. We measure MAE-duration as a function of adaptation strength and compare the results to the model prediction. We then do the same for nulling-thresholds. Model predictions are strongly supported by the psychophysical findings. In a third experiment we test formulae coupling nulling threshold, MAE-duration, and direction-discrimination thresholds, by measuring these quantities as a function of speed. For the medium-to-high speed range of these experiments we found that nulling thresholds increase and dMAE-durations decrease about linearly, whereas direction discrimination thresholds increase exponentially with speed. The model description then suggests that the motion-gain decreases, while the noise-gain and model's threshold increase with speed.

Adaptation, Physiological↗

Transformation of Japanese persimmon (Diospyros kaki Thunb.) with apple cDNA encoding NADP-dependent sorbitol-6-phosphate dehydrogenase.

Japanese persimmon (Diospyros kaki Thunb. cv Jiro) was transformed with apple (Malus x domestica Borkh.) cDNA encoding NADP-dependent sorbitol-6-phosphate dehydrogenase (S6PDH) by an Agrobacterium-mediated leaf-disc transformation system. Integration and expression of the transgene were confirmed by genomic DNA blot and immunoblot analyses. Sorbitol accumulation in five of six transgenic plants obtained was confirmed by GC-MS. The amount of sorbitol in the leaves of transgenic plants varied from 14.5 to 61.5 µmol g(-1) fr wt(-1). Sorbitol was not found in leaves of non-transformed 'Jiro' or the line PS7 that produced S6PDH protein with no S6PDH activity. Eventually, two transformed lines producing high (PS1) and medium (PS6) amounts of sorbitol, one control transformed line (PS7), and non-transformed 'Jiro' were selected and evaluated for salt-stress tolerance. Under NaCl stress, the activity of photosystem II in leaves was determined in terms of the ratio of the variable (Fv) to the maximum (Fm) fluorescence of chlorophyll. The rate of decline in Fv/Fm under NaCl stress was lower in PS1 than the other three lines, suggesting that PS1 is more tolerant to NaCl stress than the other three lines. The factors that caused enhanced salt stress tolerance in PS1 are discussed in relation to sorbitol biosynthesis and its growth.

Journal Article↗

Characterization of the S-locus region of almond (Prunus dulcis): analysis of a somaclonal mutant and a cosmid contig for an S haplotype.

Almond has a self-incompatibility system that is controlled by an S locus consisting of the S-RNase gene and an unidentified "pollen S gene." An almond cultivar "Jeffries," a somaclonal mutant of "Nonpareil" (S(c)S(d)), has a dysfunctional S(c) haplotype both in pistil and pollen. Immunoblot and genomic Southern blot analyses detected no S(c) haplotype-specific signal in Jeffries. Southern blot showed that Jeffries has an extra copy of the S(d) haplotype. These results indicate that at least two mutations had occurred to generate Jeffries: (1) deletion of the S(c) haplotype and (2) duplication of the S(d) haplotype. To analyze the extent of the deletion in Jeffries and gain insight into the physical limit of the S locus region, approximately 200 kbp of a cosmid contig for the S(c) haplotype was constructed. Genomic Southern blot analyses showed that the deletion in Jeffries extends beyond the region covered by the contig. Most cosmid end probes, except those near the S(c)-RNase gene, cross-hybridized with DNA fragments from different S haplotypes. This suggests that regions away from the S(c)-RNase gene can recombine between different S haplotypes, implying that the cosmid contig extends to the borders of the S locus.

Base Sequence↗

Study on DNA strand breaks induced by sodium nitroprusside, a nitric oxide donor, in vivo and in vitro.

Nitric oxide (NO) as well as its donors has been shown to generate mutation and DNA damage in in vitro assays. The objective of this study was to identify that DNA single-strand breaks (SSBs) could be elicited by NO, not only in vitro but also in vivo. The alkaline single-cell gel electrophoresis (SCGE) was performed to examine the DNA damage in g12 cells and the cells isolated from the organs of mice exposed to sodium nitroprusside (SNP). A modified method, in which neither collagenase nor trypsin was necessary, was used to prepare the single-cell suspension isolated from organs of mice. Results showed that the exposure of g12 cells to 0.13-0.5 micromol/ml SNP with S9 for 1 h induced a concentration-dependent increase in DNA SSBs in g12 cells. The significant increase in DNA migration and comet frequency has appeared in the cells isolated from the spleen, thymus, and peritoneal macrophages of mice after injecting i.p. SNP in the dosage range of 0.67-6.0 mg/kg b.wt for 1 h. However, no obvious increase in DNA strand breaks was observed in the cells isolated from the liver, kidney, lung, brain and heart obtained from the same treated mice. These results suggested that DNA SSBs could be induced by NO in some cells both in vivo and in vitro. There were organ differences in sensitivity in the mice exposed to NO. Spleen, thymus, and macrophages might be the important targets of NO.

Akathisia, Drug-Induced↗

Association of the R485K polymorphism of the factor V gene with poor response to activated protein C and increased risk of coronary artery disease in the Chinese population.

Inherited predisposition to thrombosis contributes to the initiation and progression of coronary artery disease (CAD). The present study was designed to explore the relationship between genetic variation of coagulation factor V and occurrence of CAD. A total of 141 unrelated patients with CAD and 175 healthy controls were analyzed by polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) for variation detection in all 25 exons of the factor V gene. Among the study subjects, 55 CAD patients and 73 controls were evaluated at random for response to activated protein C (APC) by Coatest APC resistance test. Polymorphisms in exon 4, 10, 13 and 16 of factor V gene were documented [642G-->T(S156), 1628--> A(R485K), 4070A-->G(H1299R) and 5380G A(V1736M), respectively]. The study also identified a novel polymorphism 327A G in exon 2 which did not alter the amino acid residue. Leiden mutation (R506Q) was not detected in any of our 316 subjects. Among the five polymorphisms, the allele frequency of 1628G--> A was significantly different between the CAD patients and the controls (0.36 vs. 0.21, p < 0.05). Subjects homozygous or heterozygous for the A allele of 1628G-->A polymorphism had lower normalized APC ratios than those with the GG genotype in the CAD group (1.16+/-0.13 and 1.18+/-0.23 vs. 1.36+/-0.33, p <0.05) and in the controls, indicating that A(1628) allele was associated with a poor response to APC. We conclude that the 1628G-->A (R485K) polymorphism of factor V is associated with a poor response to APC and increased risk for CAD.

Activated Protein C Resistance↗

Regulation of serotonin release by GABA and excitatory amino acids.

Regulation of serotonin release by gamma-aminobutyric acid (GABA) and glutamate was examined by microdialysis in unanaesthetized rats. The GABA(A) receptor agonist muscimol, or the glutamate receptor agonists kainate, alpha-amino-3-hydroxy-5-methyl-4-isoxazolaproprionate or N-methyl-D-aspartate were infused into the dorsal raphe nucleus (DRN) while extracellular serotonin was measured in the DRN and nucleus accumbens. Muscimol produced decreases, and the glutamate receptor agonists produced increases in serotonin. To determine if these receptors have a tonic influence on serotonergic neurons, glutamate or GABA(A) receptor antagonists were infused into the DRN. Kynurenate, a nonselective glutamate receptor blocker, produced a small, 30% decrease in serotonin. A similar decrease was obtained with combined infusion of AP-5 and DNQX into the DRN. The GABAA receptor blocker bicuculline produced an approximately three-fold increase in DRN serotonin. In conclusion, glutamate neurotransmitters have a weak tonic excitatory influence on serotonergic neurons in the rat DRN. However, the predominate influence is mediated by GABA(A) receptors.

Animals↗

Differential effect of local infusion of serotonin reuptake inhibitors in the raphe versus forebrain and the role of depolarization-induced release in increased extracellular serotonin.

Systemic administration of selective serotonin reuptake inhibitors (SSRIs) elicits larger increases in serotonin (5-HT) in raphe than in forebrain sites. Because serotonergic neuronal activity is suppressed, the mechanism underlying SSRI-induced increases in extracellular 5-HT is unclear. This study determined whether local infusion of SSRIs also elicited regionally selective increases in extracellular 5-HT, and whether changes depended on serotonergic neuronal depolarization. Conventional microdialysis methods were used to measure 5-HT in dorsal raphe (DRN), median raphe, nucleus accumbens (NAcc), and frontal cortex of unanesthetized rats. During infusion of SSRIs into each site, the maximum response was an approximately 6- to 7-fold increase in 5-HT in NAcc and frontal cortex, and an approximately 20-fold increase in DRN and median raphe. The larger increase in 5-HT in raphe was confirmed using zero-net-flux microdialysis. In NAcc, baseline 5-HT was 0.7 nM, and levels increased to a maximum of 3.1 nM during infusion of the SSRI citalopram. Baseline 5-HT in DRN was greater, 1.3 nM, and increased to 12.4 nM in response to citalopram. Consistent with evidence that autoreceptor activation inhibits serotonergic neuronal discharge, SSRI infusion into DRN produced a moderate decrease in 5-HT in NAcc. However, increases in 5-HT in DRN elicited by SSRI infusion were attenuated by 8-hydroxydipropylaminotetralin and tetrodotoxin. These data indicate that depolarization-dependent 5-HT release was not fully inhibited during SSRI infusion into DRN. In summary, SSRIs produce larger increases in extracellular 5-HT in raphe than in forebrain sites. Increases depend in part on depolarization-induced release, which may be greater in raphe than in forebrain.

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

[Recent trends in the standardization of laboratory automation].

Laboratory automation systems have been introduced to many clinical laboratories since early 1990s. Meanwhile, it was found that the difference in the specimen tube dimensions, specimen identification formats, specimen carrier transportation equipment architecture, electromechanical interfaces between the analyzers and the automation systems was preventing the systems from being introduced to a wider extent. To standardize the different interfaces and reduce the cost necessary for the laboratory automation, NCCLS and JCCLS started establishing standards for the laboratory automation in 1996 and 1997 respectively. NCCLS has published five proposed standards which that are expected to be approved by the end of 2000.

Automation↗

[Standardization of operation monitoring and control of the clinical laboratory automation system].

Laboratory automation systems showed up in the 1980s and have been introduced to many clinical laboratories since early 1990s. Meanwhile, it was found that the difference in the specimen tube dimensions, specimen identification formats, specimen carrier transportation equipment architecture, electromechanical interfaces between the analyzers and the automation systems was preventing the systems from being introduced to a wider extent. To standardize the different interfaces and reduce the cost of laboratory automation, NCCLS and JCCLS started establishing standards for laboratory automation in 1996 and 1997 respectively. Operation monitoring and control of the laboratory automation system have been included in their activities, resulting in the publication of an NCCLS proposed standard in 1999.

Automation↗

Arg485Lys polymorphism of factor V increases the risk of coronary artery disease in a Chinese population.

OBJECTIVE: To explore the relationship between genetic variation in coagulation factor V and the occurrence of coronary arterial disease (CAD). METHODS: Unrelated 86 patients with CAD and 102 healthy controls were analyzed by polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) to detect variations in the entire twenty-five exons of the factor V gene. RESULTS: Polymorphisms in exon 4 [642 G-->T (Ser156)], exon 10 [1628 G-->A (Arg485Lys)], exon 13 [4070 A-->G (His1299Arg)] and exon 16 [5380 G-->A (Val1736Met)] were documented. The study also identified a novel polymorphism in exon 2 (327 A-->G) which did not result in amino acid residue substitution. The Leiden mutation (Arg506Gln) was not detected in any of our 188 subjects. Among the 5 polymorphisms, the allele frequency of 1628 G-->A was significantly different between CAD patients and controls (0.69 vs 0.81, chi 2 = 6.908, P < 0.01). This is the first report of this finding in a Chinese population. CONCLUSION: 1628 G-->A polymorphism is associated with CAD and it may be a risk factor for CAD morbidity in the Chinese population.

Aged↗

[Study on the chemical form and extraction rate of Cr, Cu, Fe, Mn, Ni and Zn in tea].

The content of Cr, Cu, Fe, Mn, Ni and Zn in the tea commonly available in China market were measured by inductivity coupled plasma-optical emission spectrometry (ICP-OES). The extraction rates of the six elements in tea leachate were measured. The solubilitied were 39.8% for Cr, 42.5% for Cu, 8.6% for Fe, 45.5% for Mn, 87.1% for Ni and 71.0% for Zn. The process of making tea leachate affects the elements extraction rates. The content of the microelements in tea leave extracts decreases gradually with the processing. About 80% of Cr, Cu, Mn, Ni and Zn and 60% of Fe were in the first infusion of tea. Moreover, the chemical forms of six elements were determined. The ratios of organic to inorganic forms were 0.33 for Cr, 0.022 for Cu, 0.18 for Fe, 0.002 for Mn, 0.01 for Ni and 0.18 for Zn. It is concluded that the six elements from the tea infusion extracted from 5 g tea are too little to meet the recommend dietary allowance (RDA). Therefore, tea is not a rich food source of Cr, Cu, Fe, Mn, Ni and Zn.

Plant Extracts↗

Glial cell responses, complement and apolipoprotein J expression following axon injury in the neonatal rat.

Immature motoneurons are highly susceptible to degeneration following axon injury. The response of perineuronal glia to axon injury may significantly influence neuronal survival and axon regeneration. We have examined the central reactions to neonatal facial nerve transection with emphasis on the expression of complement component C3 (C3) and the multifunctional apolipoprotein J (ApoJ). Axotomy was performed on one-day-old rats. Animals were perfused from eight hours to two weeks after the lesion. The astroglial marker, glial fibrillary acidic protein (GFAP) was increased from one day and the microglial marker OX-42 from two days after injury. ApoJ immunoreactivity was increased in axotomized neuronal perikarya and astroglial cells from one day postaxotomy, but no C3 immunoreactive profiles were found at any postoperative survival time. Cell proliferation as judged by bromodeoxyuridine labeling and immunoreactivity for the cyclin Ki-67 antigen (antibody MIB5) occurred only at two days after injury. Double immunostaining revealed that the vast majority of proliferating cells were microglia, although occasional cells double labeled astrocytes were found as well. Our results indicate that the non-neuronal response in neonatal animals differ from that of adult ones as follows: 1) microglia transform rapidly into phagocytes in parallel with the degeneration of axotomized neurons, 2) despite the presence of neuronal degeneration, no expression of C3 was found, and the upregulation of the expression of the complement C3 receptor (CR3) is delayed, 3) ApoJ is strongly upregulated in perineuronal astrocytes as well as in the axotomized motoneurons. The marked upregulation of ApoJ in both instances suggests a general role of this protein in the neuronal response to axotomy.

Aging↗