Search PubMed⌕ Search

Biomedical subjects

Tao Song

Publications and source records attributed to Tao Song.

At least 19 recordsLinked to original sources

p90 RSK-1 associates with and inhibits neuronal nitric oxide synthase.

Evidence is presented that RSK1 (ribosomal S6 kinase 1), a downstream target of MAPK (mitogen-activated protein kinase), directly phosphorylates nNOS (neuronal nitric oxide synthase) on Ser847 in response to mitogens. The phosphorylation thus increases greatly following EGF (epidermal growth factor) treatment of rat pituitary tumour GH3 cells and is reduced by exposure to the MEK (MAPK/extracellular-signal-regulated kinase kinase) inhibitor PD98059. Furthermore, it is significantly enhanced by expression of wild-type RSK1 and antagonized by kinase-inactive RSK1 or specific reduction of endogenous RSK1. EGF treatment of HEK-293 (human embryonic kidney) cells, expressing RSK1 and nNOS, led to inhibition of NOS enzyme activity, associated with an increase in phosphorylation of nNOS at Ser847, as is also the case in an in vitro assay. In addition, these phenomena were significantly blocked by treatment with the RSK inhibitor Ro31-8220. Cells expressing mutant nNOS (S847A) proved resistant to phosphorylation and decrease of NOS activity. Within minutes of adding EGF to transfected cells, RSK1 associated with nNOS and subsequently dissociated following more prolonged agonist stimulation. EGF-induced formation of the nNOS-RSK1 complex was significantly decreased by PD98059 treatment. Treatment with EGF further revealed phosphorylation of nNOS on Ser847 in rat hippocampal neurons and cerebellar granule cells. This EGF-induced phosphorylation was partially blocked by PD98059 and Ro31-8220. Together, these data provide substantial evidence that RSK1 associates with and phosphorylates nNOS on Ser847 following mitogen stimulation and suggest a novel role for RSK1 in the regulation of nitric oxide function in brain.

Amino Acid Sequence↗

Insight into the solvent effect: a density functional theory study of cisplatin hydrolysis.

The solvent effect on reactions in solutions is crucial for many systems. In this study, the reaction barrier with respect to the number of solvent molecules included in the system is systematically studied using density function theory calculations. Our results show that the barriers rapidly converge with respect to the number of solvent molecules. The solvent effect is investigated by calculating cisplatin hydrolysis in several types of solvents. The results are analyzed and a linear relationship between the reaction barrier and the interaction strength of solvent-reactants is found. Insight into the general solvent effect is obtained.

Journal Article↗

A simple and accurate method for quantification of magnetosomes in magnetotactic bacteria by common spectrophotometer.

A simple apparatus for measuring the magnetism of magnetotactic bacteria was developed with a common laboratory spectrophotometer, which was based on measuring the change in light scattering resulting from cell alignment in a magnetic field. A multiple coils were built around the cuvette holder of the spectrophotometer to compensate geomagnetic field and to generate two mutually perpendicular magnetic fields. In addition, we defined a novel magnetism parameter, R(mag), by modifying the definition of C(mag) to a normalized parameter with the culture absorbance obtained without application of magnetic field. The number of magnetosomes in each cell was determined by transmission electron microscopy to assess the relationship between the two magnetism parameters and the distribution of magnetosomes in the cells. We found that both R(mag) and C(mag) were linearly correlated rather with the percentage of magnetosome-containing bacteria than with the average magnetosome numbers, and R(mag) exhibited a better linearity than C(mag) with respect to the percentage of magnetosome-containing bacteria.

Electromagnetic Phenomena↗

Recombined DNA vaccines encoding calreticulin linked to HPV6bE7 enhance immune response and inhibit angiogenic activity in B16 melanoma mouse model expressing HPV 6bE7 antigen.

Calreticulin (CRT) has been reported to have an effect of upregulating MHC class I presentation as well as inhibiting angiogenesis in vitro and in vivo. Combination of dual mechanisms of enhanced immunogenicity of human papillomavirus (HPV) 6bE7 antigen and antiangiogenesis may be introduced in the strategy of vaccines against condyloma acuminatum (CA) resulting from HPV infection. Therefore, we constructed DNA vaccines by employing different lengths of CRT chimerically linked to a model antigen HPV6bE7 and investigated the immunological and antiangiogenic effects of these vaccines in a B16 melanoma model that express HPV6bE7 antigen. Our results showed that vaccination with CRT180/HPV6bE7 or CRT120/HPV6bE7 enhanced the presence of CD8(+) T cells and TCRgammadelta T cells in vivo, increased the specific lysis activity against E7-expressing cells and secretion levels of IL-2 and IFN-gamma by activating T cells in vitro significantly. Moreover, recombined CRT180 or CRT120 with HPV6bE7 vaccines could elicit a more efficient E7-specific immune response than HPV6bE7 alone. The similarity of immunological enhancement of CRT180/HPV6bE7 and CRT120/HPV6bE7 implies that the immunologically active region mainly exist in fragment 1-120 aa. Furthermore, CRT180/HPV6bE7 and CRT180 displayed remarkable superiority over CRT120/HPV6bE7 in vivo angiogenesis assay, suggesting that the antiangiogenic activity of CRT resides in a domain between aa 120 and 180. Vaccination with CRT180/HPV6bE7 generated the best protective effect of delaying tumor formation and reduction of tumor size in tumor growth inhibition experiment among all DNA constructs. Therefore, CRT180/HPV6bE7 vaccine may enhance the immunological response to HPV6bE7 and inhibit angiogenesis. This construct may be useful in preventing HPV-associated dermatosis and may be developed as a promising strategy to control CA.

Animals↗

Vector-based spatial-temporal minimum L1-norm solution for MEG.

Minimum L1-norm solutions have been used by many investigators to analyze MEG responses because they provide high spatial resolution images. However, conventional minimum L1-norm approaches suffer from instability in spatial construction, and poor smoothness of the reconstructed source time-courses. Activity commonly "jumps" from one grid point to (usually) the neighboring grid points. Equivalently, the time-course of one specific grid point can show substantial "spiky-looking" discontinuity. In the present study, we present a new vector-based spatial-temporal analysis using a L1-minimum-norm (VESTAL). This approach is based on a principle of MEG physics: the magnetic waveforms in sensor-space are linear functions of the source time-courses in the imaging-space. Our computer simulations showed that VESTAL provides good reconstruction of the source amplitude and orientation, with high stability and resolution in both the spatial and temporal domains. "Spiky-looking" discontinuity was not observed in the source time-courses. Importantly, the simulations also showed that VESTAL can resolve sources that are 100% correlated. We then examined the performance of VESTAL in the analysis of human median-nerve MEG responses. The results demonstrated that this method easily distinguishes sources very spatially close to each other, including individual primary somatosensory areas (BA 1, 2, 3b), primary motor area (BA 4), and other regions in the somatosensory system (e.g., BA 5, 7, SII, SMA, and temporal-parietal junction) with high temporal stability and resolution. VESTAL's potential for obtaining information on source extent was also examined.

Adult↗

A hybrid tissue segmentation approach for brain MR images.

A novel hybrid algorithm for the tissue segmentation of brain magnetic resonance images is proposed. The core of the algorithm is a probabilistic neural network (PNN) in which weighting factors are added to the summation layer, such that partial volume effects can be taken into account in the modeling process. The mean vectors for the probability density function estimation and the corresponding weighting factors are generated by a hierarchical scheme involving a self-organizing map neural network and an expectation maximization algorithm. Unlike conventional PNN, this approach circumvents the need for training sets. Tissue segmentation results from various algorithms are compared and the effectiveness and robustness of the proposed approach are demonstrated.

Algorithms↗

A possible involvement of beta-endorphin, substance P, and serotonin in rat analgesia induced by extremely low frequency magnetic field.

Most of the research concerning magnetic antinociception was focused on brief exposure less than 1 h. The main purpose of the present study was to determine the effect of extremely low frequency (ELF) magnetic field (MF) repeated exposures on rats in inducing antinociception and to find the effective analgesic "time window." Meanwhile this investigation was to examine the role of central beta-endorphin, substance P, and 5-HT in magnetic analgesia. We found tail flick latencies (TFLs) increased significantly after the rats were exposed to 55.6 Hz, 8.1 mT magnetic field for 4 days, 6 h each day. The analgesic effects seemed to decrease gradually when the rats were exposed daily for another 10 days. Their levels of TFLs decreased within 1 day when the rats were removed after a 4-day exposure. The concentrations of hypothalamus beta-endorphin, substance P, and brainstem serotonin (5-HT) were increased significantly on Day 4. However, no differences were found when rats were exposed for another 10 days, and there were no significant increases when rats were removed after the fourth day of exposure and tested for nociception on Days 5 and 7 with no changes in the biochemical markers at 7 days. These results suggest that the ELF magnetic field has analgesic effect, but only on Days 3 and 4. The effect may be associated with increases in endogenous beta-endorphin, substance P, and 5-HT stimulated by the 55.6 Hz, 8.1 mT magnetic field.

Analgesia↗

Use of tissue water as a concentration reference for proton spectroscopic imaging.

A strategy for using tissue water as a concentration standard in (1)H magnetic resonance spectroscopic imaging studies on the brain is presented, and the potential errors that may arise when the method is used are examined. The sensitivity of the method to errors in estimates of the different water compartment relaxation times is shown to be small at short echo times (TEs). Using data from healthy human subjects, it is shown that different image segmentation approaches that are commonly used to account for partial volume effects (SPM2, FSL's FAST, and K-means) lead to different estimates of metabolite levels, particularly in gray matter (GM), owing primarily to variability in the estimates of the cerebrospinal fluid (CSF) fraction. While consistency does not necessarily validate a method, a multispectral segmentation approach using FAST yielded the lowest intersubject variability in the estimates of GM metabolites. The mean GM and white matter (WM) levels of N-acetyl groups (NAc, primarily N-acetylaspartate), choline (Ch), and creatine (Cr) obtained in these subjects using the described method with FAST multispectral segmentation are reported: GM [NAc] = 17.16 +/- 1.19 mM; WM [NAc] = 14.26 +/- 1.38 mM; GM [Ch] = 3.27 +/- 0.47 mM; WM [Ch] = 2.65 +/- 0.25 mM; GM [Cr] = 13.98 +/- 1.20 mM; and WM [Cr] = 7.10 +/- 0.67 mM.

Adult↗

Inhibitory effects of cariporide on LPC-induced expression of ICAM-1 and adhesion of monocytes to smooth muscle cells in vitro.

AIM: To explore the effects of cariporide on the expression of intercellular adhesion molecule-1 (ICAM-1) and the adhesion of monocytes to vascular smooth muscle cells (SMC) in vitro. METHODS: Monocytes were isolated from human peripheral blood by the Ficoll-Hypaque method. The expression of ICAM-1 in SMC was detected by ELISA. The adhesion of monocytes to SMC was stimulated by lysophosphatidylcholine (LPC). The adhesion ratio of monocytes was assayed by measuring protein contents. The intracellular pH ([pH]i) of SMC was measured with 2' ,7' -bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF). RESULTS: Preincubation of SMC with LPC alone (5 microg/mL) for 4 h markedly enhanced the expression of ICAM-1 in SMC and the rate of the adhesion of monocytes to SMC in a concentration-dependent and time-related manner. LPC simultaneously also induced an increase of [pH]i value in SMC. Cariporide concentration-dependently reduced the adhesion ratio of monocytes to SMC and the expression of ICAM-1 in SMC induced by LPC. The inhibitory effects of cariporide on the expression of ICAM-1 in SMC and the adhesion of monocytes to SMC also were associated with blocking LPC-induced elevation of the [pH]i value in SMC. CONCLUSION: LPC-induced monocyte-SMC adhesion may be mediated via activation of the Na+/H+ (NHE) exchanger. The action mechanism of cariporide may be related with inhibition of activation of the Na+/H+ exchanger of plasma membranes and ICAM-1 expression on the surface of SMC induced by LPC.

Animals↗

[Effects of xuezhikang and simvastatin on cerebral ischemia-reperfusion injury in rat].

OBJECTIVE: To observe the effects of Xuezhikang and simvastatin on cerebral ischemia/reperfusion injury in rat, as well as the influences after intervention with L-NAME. METHOD: Rats were given orally with Xuezhikang and simvastatin or vehicle for 2 weeks, and then subjected to middle cerebral artery occlusion for 120 min using intraluminal filament model. L-NAME were injected into the lateral ventricles in half of the rats treated with Xuezhikang and simvastatin 45 min before the ischemia. The neurological deficits examinations were performed at 2, 24, 48 h after reperfusion. After the last examination the animals were sacrificed, the infarct volumes were determined by TTC staining, and MDA levels were also measured. RESULT: Xuezhikang and simvastatin both significantly reduced the infarct volume and improved the functional recovery when compared to vehicle. Xuezhikang and simvastatin both significantly decreased the MDA accumulation after reperfusion. L-NAME partially inhibited the protective effect of Xuezhikang but nearly completely abolished the protective effect of simvastatin. CONCLUSION: Xuezhikang has protective effects on ischemic brain damage in rats, which the beneficial effects are partly due to the statins components. The other components in Xuezhikang may also account for the neuroprotective effects, which is worth further investigations.

Animals↗

Transmission of digital images consisting of white-light dark solitons.

A distortion-free digital image is transmitted through parallel propagation of white-light photovoltaic dark solitons. The waveguide channels induced by white-light dark solitons can guide both the laser beam and the white-light beam well. We determine experimentally the critical separations of the dark solitons in the directions parallel and perpendicular to the crystalline c axis for the given crystal thickness.

Journal Article↗

Inhibition of neuronal nitric-oxide synthase by phosphorylation at Threonine1296 in NG108-15 neuronal cells.

We demonstrate that neuronal nitric-oxide synthase (nNOS) is directly inhibited through the phosphorylation of Thr(1296) in NG108-15 neuronal cells. Treatment of NG108-15 cells expressing nNOS with calyculin A, an inhibitor of protein phosphatase 1 and 2A, revealed a dose-dependent inhibition of nNOS enzyme activity with concomitant phosphorylation of Thr(1296) residue. Cells expressing a phosphorylation-deficient mutant in which Thr(1296) was changed to Ala proved resistant to phosphorylation and suppression of NOS activity. Mimicking phosphorylation mutant of nNOS in which Thr(1296) is changed to Asp showed a significant decrease in nNOS enzyme activity, being competitive with NADPH, relative to the wild-type enzyme. These data suggest that phosphorylation of nNOS at Thr(1296) may involve the attenuation of nitric oxide production in neuronal cells through the decrease of NADPH-binding to the enzyme.

Animals↗

50-Hz magnetic field (0.1-mT) alters c-fos mRNA expression of early post implantation mouse embryos and serum estradiol levels of gravid mice.

BACKGROUND: We exposed pregnant mice to magnetic or sham fields for 24 hr/day during Gestation Day (GD) 5.5-8.5 to study the effects of 50-Hz 0.1-mT sinusoidal magnetic fields on early pregnancy in mouse embryos and mice. METHODS: Mice were sacrificed on GD 8.5. Embryos and blood samples were collected. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of embryo c-fos mRNA. The blood samples were tested through radioimmunoassay for serum estradiol levels and general examinations. RESULTS: We found that the expression of c-fos mRNA of embryos under exposure was enhanced. We reported that 50-Hz 0.1-mT magnetic exposure induced the decline of serum estradiol levels of pregnancy mice on GD 8.5. General examinations of blood including white blood cell (WBC) count, red blood cell (RBC) count, and hemoglobin (HGB) did not show significant differences between the exposure group and the control group (sham exposure). CONCLUSIONS: Under the experimental conditions, 50-Hz 0.1-mT sinusoidal magnetic fields affected the development of early pregnancy mouse embryos and the dams to some extent.

Animals↗

Captopril restores endothelium-dependent relaxation induced by advanced oxidation protein products in rat aorta.

To explore whether advanced oxidation protein products (AOPP) can cause endothelial dysfunction in vitro, and whether captopril exerts beneficial effect on impaired endothelium-dependent relaxation induced by exogenous advanced oxidation protein products and to investigate the potential mechanisms. Both the Acetylcholine (ACh)-induced endothelium-dependent relaxation (EDR), sodium nitroprusside-induced endothelium-independent relaxation of aortic rings were measured by recording isometric tension after the rings were exposed to AOPP-BSA in the absence or presence of captopril to assess the injury effect of AOPP-BSA and the protective effect of captopril on the aortic endothelium, respectively. Co-incubation of aortic rings with AOPP-BSA (3 mmol/L) for 90 minutes resulted in a significant inhibition of EDR to ACh, but had no effects on endothelium-independent relaxation to SNP. After incubation of the rings in the co-presence of captopril (3 to 30 micromol/L) or enalaprilat (30 micromol/L) with AOPP-BSA (3 mmol/L) for 90 minutes, captopril significantly and enalaprilat only partly attenuated the inhibition of EDR induced by AOPP-BSA. This protective effect of captopril (30 micromol/L) was abolished by N-nitro-L-arginine methyl ester (10 micromol/L), an inhibitor of nitric oxide synthase. Furthermore, the superoxide anion scavenger superoxide dismutase (SOD, 200 U/mL), and the nitric oxide precursor L-arginine (3 mmol/L) also ameliorated the impaired EDR caused by AOPP-BSA. But D-arginine had no effect on the impaired EDR caused by AOPP-BSA. AOPP-BSA can trigger endothelial dysfunction and captopril can protect the endothelium against functional damage induced by AOPP-BSA in rat aorta, increase nitric oxide bioavailability. The mechanisms of endothelial dysfunction induced by AOPP-BSA may include the decrease of NO and the generation of oxygen-free radicals.

Animals↗

Protective effects of cariporide on endothelial dysfunction induced by high glucose.

AIM: To explore the effects of cariporide, a selective sodium-hydrogen antiporter inhibitor, on endothelial dysfunction induced by high glucose. METHODS: Acetylcholine (ACh)-induced endothelium-dependent relaxation (EDR), sodium nitroprusside (SNP)-induced endothelium-independent relaxation and biochemical parameters including malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) were measured in rat isolated aorta. RESULTS: A 6-h incubation of aortic rings with high glucose (44 mmol/L) resulted in a significant inhibition of EDR, but had no effects on endothelium-independent relaxation. After the 6-h incubation of aortic rings in the co-presence of cariporide (0.01, 0.1, and 1 micromol/L) with high glucose, cariporide prevented the inhibition of EDR caused by high glucose in concentration-dependent manners. Similarly, high glucose decreased SOD activity and contents of NO, and increased MDA concentration in aortic tissue. Cariporide (1 micromol/L) significantly resisted the decrease of NO content and SOD activity, and elevation of MDA concentration caused by high glucose in aortic tissues. Mannitol (44 mmol/L) or cariporide (1 micromol/L) alone had no effect on EDR, endothelium-independent relaxation and biochemical parameters. CONCLUSION: Cariporide significantly prevented endothelial dysfunction induced by high glucose. The mechanisms of endothelial dysfunction induced by high glucose may involve the activation of sodium-hydrogen antiporter and the generation of oxygen-free radicals, but it is not related to the change of osmolarity.

Animals↗

Calcium/calmodulin-dependent protein kinase I inhibits neuronal nitric-oxide synthase activity through serine 741 phosphorylation.

We demonstrate here that neuronal nitric-oxide synthase (nNOS) is phosphorylated and inhibited by a constitutively active form of Ca2+/calmodulin (CaM)-dependent protein kinase I (CaM-K I1-293). Substitution of Ser741 to Ala in nNOS blocked the phosphorylation and the inhibitory effect. Mimicking phosphorylation at Ser741 by Ser to Asp mutation resulted in decreased binding of and activation by CaM, since the mutation was within the CaM-binding domain. CaM-K I1-293 gave phosphorylation of nNOS at Ser741 in transfected cells, resulting in 60-70% inhibition of nNOS activity. Wild-type CaM-K I also did phosphorylate nNOS at Ser741 in transfected cells, but either CaM-K II or CaM-K IV did not. These results raise the possibility of a novel cross-talk between nNOS and CaM-K I through the phosphorylation of Ser741 on nNOS.

Alanine↗

Phosphohippolin expression in the rat central nervous system.

The FXYD family is a small single-span membrane protein family; recently, we have identified a novel member of this family from the cDNA library of the rat hippocampus and named phosphohippolin (Php) (Mol. Br. Res. vol. 86, 2001). The deduced amino acid sequence of this novel Php comprises 93 residues with a core motif of FXYD and a single transmembrane domain. This indicates that Php belongs to FXYD6 subfamily of the seven FXYD subfamilies (FXYD1-7). Php shows a 48.1% homology with rat phospholemman (FXYD1), a transmembrane family protein. In this study, polyclonal antibodies against the carboxyl-terminal sequence of rat Php were raised and purified. The spatial expression of the Php protein was in the neuronal fibers of the medial part of lateral habenula nucleus, thalamus, hypothalamus, stria terminalis, zona incerta, amygdaloid body and cingulum, olfactory bulb, hippocampus, cerebral cortex and cerebellum. A unique Php distribution was identified in the cerebellum, with a predominant expression pattern in the granule layer of lobules VI-IX of the posterior lobe. Developmental studies demonstrated that the highest level of Php expression was seen in the postnatal (PN) 3-week-old rat brain, and a significant amount of Php still existed in the adult brain. These findings suggest that Php may play an important role in the excitability of neurons in the central nervous system during postnatal development, as well as those in the adult brain.

Aging↗