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Biomedical subjects

Song Han

Publications and source records attributed to Song Han.

At least 19 recordsLinked to original sources

Activations of nPKCepsilon and ERK1/2 were involved in oxygen-glucose deprivation-induced neuroprotection via NMDA receptors in hippocampal slices of mice.

Accumulated reports have suggested that activation of protein kinase C (PKC) isoforms may involve the activation of extracellular signal-regulated kinases (ERKs) in the neuronal response to ischemic/hypoxic stimuli. We have previously demonstrated that the membrane translocation of novel PKC (nPKC) epsilon increased in the early phase of cerebral ischemic/hypoxic preconditioning of mice. In this study, we used Western blot analysis and propidium iodide stain to determine whether the activations of nPKCepsilon and ERKs were involved in oxygen-glucose deprivation (OGD)-induced neuroprotection via N-methyl-D-aspartate (NMDA) receptors. The hippocampal slices of mice were exposed to OGD for 10 (OGD10) or 45 minutes (OGD45) to mimic mild (causing ischemic/hypoxic preconditioning) and severe (causing severe OGD) ischemia/hypoxia, respectively. We found that OGD10-induced nPKCepslilon membrane translocation was mediated by NMDA receptors, and both OGD10 and NMDA (1 microM, 30 min) pretreatment could protect Cornu Ammonis region 1 neurons against the subsequent severe OGD45. In addition, nPKCepsilon translocation inhibitor, epsilonV1-2 (1 microM, 30 min), and ERKs upstream mitogen-activated protein/extracellular signal regulated kinase kinase inhibitor, PD-98059 (20 microM, 30 min), could significantly inhibit OGD10 and NMDA-induced neuroprotection. These results suggest that OGD10-induced neuroprotection against severe OGD45 in the Cornu Ammonis region 1 region of the hippocampal slices was mediated by the activations of NMDA receptors, nPKCepsilon, and the downstream ERKs.

Animals↗

Increased isoform-specific membrane translocation of conventional and novel protein kinase C in human neuroblastoma SH-SY5Y cells following prolonged hypoxia.

Several studies have suggested that protein kinase C (PKC) plays a key role in the mechanism of cerebral ischemic/hypoxic preconditioning (I/HPC). However, detailed information regarding PKC isoforms in response to brain ischemia/hypoxia and their potential role in neuroprotection is unclear. Previous studies in our laboratory have demonstrated that the levels in membrane translocation of conventional PKC (cPKC) betaII, gamma, and novel PKCepsilon (nPKC), but not cPKCalpha, betaI, nPKCdelta, eta, mu, theta, and atypical PKC (aPKC) zeta and iota/lambda, were increased significantly in the hippocampus and cortex of intact mice with hypoxic preconditioning. To further detect cPKC and nPKC isoforms activation following prolonged hypoxia in vitro, we tested the membrane translocation (an indicator of PKC activation) of cPKCalpha, betaI, betaII, and gamma, and nPKCdelta, epsilon, eta, mu, and theta in a human neuroblastoma SH-SY5Y cell line following sustained hypoxic exposure (1% O(2)/5% CO(2)/94% N(2)). Using Western blot and immunocytochemistry methods, we found that the levels of cPKCalpha, betaI, betaII, and nPKCepsilon, but not nPKCdelta, eta, mu, and theta, membrane translocation were increased significantly (P < 0.05, n = 8) in a time-dependent manner (from 0.5 to 24 h) following sustained hypoxic exposure. Similarly, the immunostaining experiment also showed a noticeable translocation of cPKCalpha, betaI, betaII, and nPKCepsilon from the cytosol to the perinuclear or membrane-related areas after 6 h posthypoxic exposure. In addition, no cPKCgamma was detected in this cell line under either a normoxic or hypoxic condition. These results suggested that prolonged hypoxia may induce the activation of cPKCalpha, betaI, betaII, and nPKCepsilon by triggering their membrane translocation in SH-SY5Y cells.

Blotting, Western↗

Decreased phosphorylation and protein expression of ERK1/2 in the brain of hypoxic preconditioned mice.

Accumulated reports have suggested that activation of protein kinase C (PKC) isoforms may involve the activation of extracellular signal-regulated kinases 1/2 (ERK1/2) in the neuronal response to hypoxic stimuli. We have previously demonstrated that the membrane translocation or activation of conventional PKC (cPKC) betaII, gamma and novel PKC (nPKC) epsilon are increased in the early phase of cerebral hypoxic preconditioning in mice. However, the role of ERK1/2 in the development of cerebral hypoxic preconditioning is unclear. In the current study, we used Western blot analysis to investigate the effects of repetitive hypoxic exposure (H0-H6, n=6 for each group) on the levels of phosphorylation and protein expression of ERK1/2 in the frontal cortex and the whole hippocampus of mice. We found that the levels of phosphorylated ERK1/2, not protein expression of ERK1/2, decreased significantly in both cortex and hippocampus of the early hypoxic preconditioned mice (H1-H4), when compared to that of the normoxic group (p<0.05). In addition, a significant decrease (p<0.05) in the ERK1/2 protein expression, not the phosphorylated form of ERK1/2, was found both in the frontal cortex and hippocampus of mice followed hypoxia with previous hypoxia (H5 and H6). These results suggest that the decreased phosphorylation and downregulation of protein expression of ERK1/2 might be involved in the development of hypoxic preconditioning.

Animals↗

[Expression of AIV subtype H5HA, H7HA and H9HA hemagglutinin gene in Pichia pastoris].

The expression of the hemagglutinins of Avian influenza virus H5 H7and H9 subtypes was studied in this article by Pichia pastoris, one of the eukaryotis expression systems. Three reconstructed expression plasmids and engineering strains, named pPIC9K-H5HA, pPIC9K-H7HA, pPIC9K-H9HA and GS115/pPIC9K-H5HA, GS115/pPIC9K-H7HA, GS115/pPIC9K-H9HA repectively, were obtained. The reconstructed yeast engineering strains were identified by MD and MM plate selecting and PCR. The induced interests proteins were examined by SDS-PAGE and Western-bloting,the results showed that the interest genes were expressed exactly. And this will be helpful in the future study of antigen detection and antibody detection kit, as well in the subunit vaccines developing.

Animals↗

Novel nanotube-on-insulator (NOI) approach toward single-walled carbon nanotube devices.

We present a novel nanotube-on-insulator (NOI) approach for producing high-yield nanotube devices based on aligned single-walled carbon nanotubes. First, we managed to grow aligned nanotube arrays with controlled density on crystalline, insulating sapphire substrates, which bear analogy to industry-adopted silicon-on-insulator substrates. On the basis of the nanotube arrays, we demonstrated registration-free fabrication of both top-gated and polymer-electrolyte-gated field-effect transistors with minimized parasitic capacitance. In addition, we have developed a way to transfer these aligned nanotube arrays to flexible substrates successfully. Our approach has great potential for high-density, large-scale integrated systems based on carbon nanotubes for both micro- and flexible electronics.

Journal Article↗

Resistance imparted by vitamin C, vitamin E and vitamin B12 to the acute hepatic glycogen change in rats caused by noise.

The effects of vitamin C, vitamin E and vitamin B12 on the noise-induced acute change in hepatic glycogen content in rats were investigated. The exposure of rats to 95 dB and 110 dB of noise acutely reduced their hepatic glycogens. Vitamin C (ascorbic acid) and vitamin E (alpha-tocopherol) attenuated the noise-induced acute reduction in the hepatic glycogen contents. This result suggests that antioxidants could reduce the change via reactive oxygen species. Vitamin B12 (cobalamin) delayed the noise-induced change, a finding that suggests that vitamin B12 could postpone the acute change via compensating for vitamin B12 deficiency.

Animals↗

Enhanced phosphorylation of cyclic AMP response element binding protein in the brain of mice following repetitive hypoxic exposure.

Cerebral ischemic/hypoxic preconditioning (I/HPC) is a phenomenon of endogenous protection that renders the brain tolerant to sustained ischemia/hypoxia. This profound protection induced by I/HPC makes it an attractive target for developing potential clinical therapeutic approaches. However, the molecular mechanism of I/HPC is unclear. Cyclic AMP (cAMP) response element binding protein (CREB), a selective nuclear transcriptional factor, plays a key role in the neuronal functions. Phosphorylation of CREB on Ser-133 may facilitate its transcriptional activity in response to various stresses. In the current study, we observed the changes in CREB phosphorylation (Ser-133) and protein expression in the brain of auto-hypoxia-induced HPC mice by using Western blot analysis. We found that the levels of phosphorylated CREB (Ser-133), but not protein expression of CREB, increased significantly (p<0.05) in the hippocampus and the frontal cortex of mice after repetitive hypoxic exposure (H2-H4, n=6 for each group), when compared to that of the normoxic (H0, n=6) or hypoxic exposure once group (H1, n=6). In addition, a significant enhancement (p<0.05) of CREB phosphorylation (Ser-133) could also be found in the nuclear extracts from the whole hippocampus of hypoxic preconditioned mice (H2-H4, n=6 for each group). These results suggest that the phosphorylation of CREB might be involved in the development of cerebral hypoxic preconditioning.

Animals↗

Efficient synthesis and electronic studies of core-shell nanowires based on colossal magnetoresistive manganites.

We report our recent study on the pulsed laser deposition process in the synthesis of colossal magnetoresistive MgO/LaCaMnO3 and MgO/LaSrMnO3 core-shell nanowires. A highly efficient process has been developed by depositing an epitaxial layer of manganite onto randomly oriented MgO nanowires grown on SiO2/Si substrates. In addition, in-depth studies revealed that the sample-target distance played a critical role in determining the core-shell nanowire quality. The MgO/LaCaMnO3 and MgO/LaSrMnO3 nanowires opened up the unique opportunity to explore a number of intriguing physical properties at the nanoscale. Remarkable metal-insulator phase transitions and pronounced colossal magnetoresistance have been observed in both LaCaMnO3 and LaSrMnO3 nanostructures.

Journal Article↗

Kinetics and dynamics of N2 formation in a steady-state N2O + CO reaction on Pd(110).

The N(2)O decomposition kinetics and the product (N(2) and CO(2)) desorption dynamics were studied in the course of a catalyzed N(2)O+CO reaction on Pd(110) by angle-resolved mass spectroscopy combined with cross-correlation time-of-flight techniques. The reaction proceeded steadily above 400 K, and the kinetics was switched at a critical CO/N(2)O pressure ratio. The ratio was about 0.03 at 450 K and reached approximately 0.08 at higher temperatures. Below it, the reaction was first order in CO, and negative orders above it. Throughout the surveyed conditions, the N(2) desorption sharply collimated along about 45 degrees off the normal toward the [001] direction. Desorbing N(2) showed translational temperatures in the range of 2000-5000 K. It is proposed that the decomposition proceeds in N(2)O(a) oriented along the [001] direction. On the other hand, the CO(2) desorption sharply collimated along the surface normal, showing a translational temperature of about 1600 K.

Journal Article↗

Identification of protein kinase C isoforms involved in cerebral hypoxic preconditioning of mice.

Recently, accumulated studies have suggested that protein kinases C (PKC) play a central role in the development of ischemic-hypoxic preconditioning (I/HPC) in the brain. However, which types of PKC isoforms might be responsible for neuroprotection is still not clear, especially when the systematic investigation of PKC isoform-specific changes in brain regions was rare in animals with ischemic-hypoxic preconditioning. By using Western blot, we have demonstrated that the levels of cPKC betaII and gamma membrane translocation were increased in the early phase of cerebral hypoxic preconditioning. In this study, we combined the Western blot and immunostaining methods to investigate the effects of repetitive hypoxic exposure (H1-H4, n = 6 for each group) on membrane translocation and protein expression of several types of PKC isoforms, both in the cortex and hippocampus of mice. We found that the increased membrane translocation of nPKCepsilon (P < 0.05, versus normoxic H0) but not its protein expression levels in both the cortex and hippocampus during development of cerebral HPC in mice. However, there were no significant changes in both membrane translocation and protein expression levels of nPKCdelta, theta, eta, mu, and aPKC iota/lambda, zeta in these brain areas after hypoxic preconditioning. Similarly, an extensive subcellular redistribution of cPKCbetaII, gamma, and nPKCepsilon was observed by immunostaining in the cortex after three series of hypoxic exposures (H3). These results indicate that activation of cPKCbetaII, gamma, and nPKCepsilon might be involved in the development of cerebral hypoxic preconditioning of mice.

Animals↗

Increased phosphorylation of neurogranin in the brain of hypoxic preconditioned mice.

Neurogranin/RC3 (Ng/rodent cortex-enriched mRNA clone #3), a postsynaptic neuronal protein kinase C (PKC) substrate, binds calmodulin (CaM) at low Ca(2+) levels. Neurotransmitters triggering influx calcium induce neurogranin phosphorylation by PKC in physiological or pathophysiological conditions. Phosphorylated Ng reduces the affinity of Ng to bind CaM, which may affect the activities of calmodulin-dependent downstream enzymes, such as nitric oxide synthase (NOS), CaM-dependent protein kinase II (CaMKII) and adenylate cyclase (AC). These protein enzymes have been reported to play key roles in the development of ischemic/hypoxic preconditioning (I/HPC). We previously demonstrated that activation of cPKCbetaII and gamma isoforms may be involved in the early phase of cerebral hypoxic preconditioning. However, as a substrate of PKC, the role of Ng in the onset of cerebral hypoxic preconditioning is unknown. In this study, we examined the effects of repetitive hypoxic exposure on the status of Ng phosphorylation in the cortex and hippocampus of mice. Using Western blot analysis, we found that the levels of Ng phosphorylation in the cortex and hippocampus of the hypoxic group of mice increased significantly from that of the normoxic group (p<0.05). These results suggest that neurogranin protein may be involved in the development of cerebral hypoxic preconditioning.

Animals↗

Collision-induced desorption in 193-nm photoinduced reactions in (O2+CO) adlayers on Pt(112).

The spatial distribution of desorbing O(2) and CO(2) was examined in 193-nm photoinduced reactions in O(2)+CO adlayers on stepped Pt (112)=[(s)3(111)x(001)]. The O(2) desorption collimated in inclined ways in the plane along the surface trough, confirming the hot-atom collision mechanism. In the presence of CO(a), the product CO(2) desorption also collimated in an inclined way, whereas the inclined O(2) desorption was suppressed. The inclined O(2) and CO(2) desorption is explained by a common collision-induced desorption model. At high O(2) coverage, the CO(2) desorption collimated closely along the (111) terrace normal.

Journal Article↗

Template-free directional growth of single-walled carbon nanotubes on a- and r-plane sapphire.

We report high-throughput growth of highly aligned single-walled carbon nanotube arrays on a-plane and r-plane sapphire substrates. This is achieved using chemical vapor deposition with ferritin as the catalyst. The nanotubes are aligned normal to the [0001] direction for growth on the a-plane sapphire. They are typically tens of micrometers long, with a narrow diameter distribution of 1.34 +/- 0.30 nm. In contrast, no orientation was achieved for growth on the c-plane and m-plane sapphire, or when Fe films, instead of ferritin, were used as the catalyst. Such orientation control is likely related to the interaction between carbon nanotubes and the sapphire substrate, which is supported by the observation that when a second layer of nanotubes was grown, they followed the gas flow direction. These aligned nanotube arrays may enable the construction of integrable and scalable nanotube devices and systems.

Journal Article↗

Single crystalline magnetite nanotubes.

We descried a method to synthesize single crystalline Fe3O4 nanotubes by wet-etching the MgO inner cores of MgO/Fe3O4 core-shell nanowires. Homogeneous Fe3O4 nanotubes with controllable length, diameter, and wall thickness have been obtained. Resistivity of the Fe3O4 nanotubes was estimated to be approximately 4 x 10-2 Omega cm at room temperature. Magnetoresistance of approximately 1% was observed at T = 77 K when a magnetic field of B = 0.7 T was applied. The synthetic strategy presented here may be extended to a variety of materials such as YBCO, PZT, and LCMO which should provide ideal candidates for fundamental studies of superconductivity, piezoelectricity, and ferromagnetism in nanoscale structures.

Ferrosoferric Oxide↗

[Hypoxic preconditioning increases cPKCgamma membrane translocation in murine brain].

Cerebral hypoxic preconditioning (CHP), which was induced by repetitive sub-lethal hypoxic insult, is an endogenous protection of neuron against subsequent severe hypoxic injury. Although a number of possible induction pathways have been investigated, such as neuroactive cytokines, activation of glutamate receptors, the ATP-sensitive potassium channel, nitric oxide and oxidative stress, the exact mechanism underlying CHP-induced protection remains unclear. It is interesting that all the above-mentioned mechanisms are involved in the activation of protein kinases C (PKC). Recently we reported that the level of PKCs membrane translocation was significantly increased in the brain of hypoxic preconditioned mice. In order to explore the role of conventional protein kinases C (cPKC) in the development of cerebral hypoxic preconditioning, biochemical techniques of SDS-PAGE and Western bolt were applied to observe the effects of repetitive hypoxic exposure (H1-H4) on the level of cPKCalpha and gamma membrane translocation in the cortex and hippocampus of mice. Experiments were carried out in accordance with the National Institutes of Health guide for the care and use of laboratory animals. The hypoxic preconditioned mice model was adapted with minor modification from our previous report. In brief, healthy adult BALB/C mice weighing 18-20 g of either sex were randomly divided into 5 groups: control group (H0), hypoxic control group (H1, hypoxic exposure once ), hypoxic preconditioned group (H2-H4, repetitive hypoxic exposure for 2-4 times respectively). The first sign of gasping breath was taken as the end of each hypoxic exposure, and then the mice were kept in normal control condition for a 30-min interval to recover before the following hypoxic insult. We found that the level of cPKCgamma membrane translocation was increased significantly (*P<0.05, n=6) with the increase of the hypoxic exposure times in both hippocampus (H0: 100% vs H1 approximately H4: 119.2%+/-7.0% *, 139.3% +/-7.4%*, 134.2% +/-8.95%*, 184.0% +/-10.8%*) and cortex (H0: 100% vs H1-H4: 129.7% +/-13.8%, 143.3% +/-13.9%*, 204.0% +/-12.1%*, 229.5% +/-14.6%*) of mice. But there were no significant changes in cPKCalpha membrane translocation in cortex and hippocampi of hypoxic preconditioned mice. These results suggest that cPKCgamma plays an important role in the development of cerebral hypoxic preconditioning. The changes in some other forms of novel and atypical PKCs are still under investigation.

Animals↗

Characterization of the somatic mutational spectrum of the neurofibromatosis type 1 (NF1) gene in neurofibromatosis patients with benign and malignant tumors.

One of the main features of neurofibromatosis type 1 (NF1) is benign neurofibromas, 10-20% of which become transformed into malignant peripheral nerve sheath tumors (MPNSTs). The molecular basis of NF1 tumorigenesis is, however, still unclear. Ninety-one tumors from 31 NF1 patients were screened for gross changes in the NF1 gene using microsatellite/restriction fragment length polymorphism (RFLP) markers; loss of heterozygosity (LOH) was found in 17 out of 91 (19%) tumors (including two out of seven MPNSTs). Denaturing high performance liquid chromatography (DHPLC) was then used to screen 43 LOH-negative and 10 LOH-positive tumors for NF1 microlesions at both RNA and DNA levels. Thirteen germline and 12 somatic mutations were identified, of which three germline (IVS7-2A>G, 3731delT, 6117delG) and eight somatic (1888delG, 4374-4375delCC, R2129S, 2088delG, 2341del18, IVS27b-5C>T, 4083insT, Q519P) were novel. A mosaic mutation (R2429X) was also identified in a neurofibroma by DHPLC analysis and cloning/sequencing. The observed somatic and germline mutational spectra were similar in terms of mutation type, relative frequency of occurrence, and putative underlying mechanisms of mutagenesis. Tumors lacking mutations were screened for NF1 gene promoter hypermethylation but none were found. Microsatellite instability (MSI) analysis revealed MSI in five out of 11 MPNSTs as compared to none out of 70 neurofibromas (p=1.8 x 10(-5)). The screening of seven MPNSTs for subtle mutations in the CDKN2A and TP53 genes proved negative, although the screening of 11 MPNSTs detected LOH involving either the TP53 or the CDKN2A gene in a total of four tumors. These findings are consistent with the view that NF1 tumorigenesis is a complex multistep process involving a variety of different types of genetic defect at multiple loci.

Alleles↗

Resistance imparted by traditional Chinese medicines to the acute change of glutamic pyruvic transaminase, alkaline phosphatase and creatine kinase activities in rat blood caused by noise.

The activities of serum glutamic pyruvic transaminase (GPT), alkaline phosphatase (ALP) and creatine kinase (CK) in rats injected or not with the Chinese medicines, Astragali, Rhodiolae and Ligusticum, were determined after noise exposure. Noise at 95 and 105 dB significantly increased the activities of GPT, ALP and CK, and showed a dependence on the exposure time. The injection of each medicine significantly suppressed the increased enzyme activities by 95 and 105 dB noise.

Alanine Transaminase↗