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Biomedical subjects

Li Song

Publications and source records attributed to Li Song.

At least 37 records · Page 2Linked to original sources
PubMed2006

[Gene mutation of high affinity immunoglobulin E receptor beta-chain in children with asthma].

OBJECTIVE: To investigate the association of the polymorphism of I181L, V183L and E237G in the high affinity immunoglobulin E receptor beta-chain (FcepsilonR1beta) with the susceptibility of childhood asthma and the serum total immunoglobulin E (IgE) level. METHODS: The coding variants of I181L, V183L and E237G and the serum total IgE level were detected using amplification refractory mutation systemdouble ended arrowpolymerase chain reaction (ARMS-PCR) and double antibody sandwich ELISA respectively in 50 asthmatic children and 40 normal controls from Sichuan Province. The association of gene mutation with the susceptibility of asthma and the serum total IgE level was analyzed. RESULTS: There were 5 cases of I181L mutation, 2 of V183L mutation, and 7 of E237G mutation in the Asthmatic group. There was no mutation in the Normal control group. The frequency of I181L and E237G mutation in the Asthmatic group were statistically higher than in the Normal control group (P < 0.01). The serum total IgE level in the Asthmatic subgroup with I181L mutation (2.837 +/- 0.407) or E237G mutation (3.044 +/- 0.419) was significantly higher than in the Asthmatic subgroup without gene mutation (2.156 +/- 0.638) and the Normal control group (1.348 +/- 1.291) (P < 0.05 or 0.01). CONCLUSIONS: The polymorphism of Fc epsilonR1betaI181L and E237G is a susceptible gene of childhood asthma and closely associates with the increased serum total IgE level.

Adolescent↗
PubMed2006

[Effect of valsatan on hepatocyte growth factor in the airways of asthmatic rats].

OBJECTIVE: To study the effect of valsatan (angiotensin II receptor antagonist, AT1) on hepatocyte growth factor (HGF) in the airways and airway remodeling in asthmatic rats. METHODS: Thirty two rats were randomly assigned into A-D four groups. Group A was normal control without treatment. Groups B-D were challenged by ovalbumin (OVA) for 2 weeks, 4 weeks and 4 weeks respectively to induce asthma. Group D received intragastric administration of valsatan (30 microg/kg daily for 4 weeks) after OVA challenge. The expressions of HGF, angiotonin II (AngII) and transforming growth factor (TGF-beta1) in the airways were detected by immunihistochemical staining. The pathological changes of airways were observed by Haematoxylin and Eosin staining. RESULTS: The HGF expression of Group B was significantly higher than that of Group A (10.69 +/- 0.96% vs 5.49 +/- 1.34%; P < 0.05). Group C also showed an increased HGF level (11.85 +/- 0.87%) compared with Group A (P < 0.05). The HGF level in Group D (15.58 +/- 1.06%) was significantly higer than that of both Group B and Group C (P < 0.05). The expressions of TGF-beta1 and AngII increased with the challenged time, while valsatan treatment decreased significantly the levels of both. Valsatan treatment attenuated airway injuries of asthmatic rats induced by OVA sensitization/challenge. CONCLUSIONS: HGF has protective effects on airways and anti-fibrotic effects. Valsatan can improve airway remodeling possibly by increasing HGF levels in asthmatic rats.

Angiotensin II↗
PubMed2005

Low-temperature growth and photoluminescence property of ZnS nanoribbons.

At a low temperature of 450 degrees C, ZnS nanoribbons have been synthesized on Si and KCl substrates by a simple chemical vapor deposition (CVD) method with a two-temperature-zone furnace. Zinc and sulfur powders are used as sources in the different temperature zones. X-ray diffraction (XRD), selected area electron diffraction (SEAD), and transmission electron microscopy (TEM) analysis show that the ZnS nanoribbons are the wurtzite structure, and there are two types-single-crystal and bicrystal nanoribbons. Photoluminescence (PL) spectrum shows that the spectrum mainly includes two parts: a purple emission band centering at about 390 nm and a blue emission band centering at about 445 nm with a weak green shoulder around 510 nm.

Journal Article↗
PubMed2005

Plasma homocysteine thiolactone adducts associated with risk of coronary heart disease.

BACKGROUND: Homocysteine thiolactone adducts have been proposed as the culprit of homocysteine related cardiovascular diseases. We studied the association of these adducts in plasma, and the gene polymorphism of paraoxonase-2 with coronary heart disease. METHODS: 254 patients and 308 controls were recruited for the study. Homocysteine thiolactone adducts were determined with ELISA. The codon 311 polymorphism of paraoxonase-2 gene was genotyped by using polymerase chain reaction and restrictive digestion. RESULTS: The plasma level of homocysteine thiolactone adducts were significantly higher in patients than in controls (40.65 +/- 10.87 u/ml vs. 30.58 +/- 10.20 u/ml, P <0.01), with odds ratio of 7.34 (95% confidence interval 4.020-13.406, P <0.01), and increased according to the number of atherosclerotic coronary arteries: 35.59 +/- 10.34 units/ml (n = 76); 41.88 +/- 8.83 (n = 70) and 43.13 +/- 11.47 (n = 108) in subjects with 1, 2 and 3 affected arteries, respectively (r =0.174, P < 0.01). The frequency of CC genotype was significantly higher in patients with coronary heart disease (7.48%) than in controls (1.62%, P < 0.01), with adjusted odds ratio of 4.367 (95% confidence interval: 1.178 to 16.191, P < 0.01), so was the C allele (23.2% vs. 14.9%, P < 0.05). CONCLUSIONS: High plasma homocysteine thiolactone adducts and the CC 311 genotype of paraoxonase-2 gene may be the emerging risk factor for coronary heart disease.

Adult↗
PubMed2005

CD8+ T cell depletion amplifies hepatitis C virus replication in peripheral blood mononuclear cells.

We investigated the ability of CD8+ T cells to inhibit hepatitis C virus (HCV) replication in peripheral blood mononuclear cells (PBMCs). PBMCs isolated from 11 of 20 HCV-infected subjects had no detectable HCV RNA. Removal of CD8+ T cells from these PBMCs resulted in detection of HCV RNA, and depletion of CD8+ T cells from PBMCs that had detectable HCV RNA amplified HCV replication. Reconstitution of CD8- PBMCs with autologous CD8+ T cells led to inhibition of HCV replication. Interferon-gamma produced by CD8+ T cells was partially responsible for CD8+ T cell-mediated noncytotoxic anti-HCV activity in PBMCs. This noncytotoxic anti-HCV activity was confirmed in HCV replicon cells. Supernatants from CD8+ T cell cultures inhibited HCV RNA expression in the replicon cells. These findings may have important implications for the immunopathogenesis of HCV in both immune and hepatic cells and are relevant to the development of host innate immunity-based anti-HCV interventions.

Antiviral Agents↗
PubMed2005

CCR2 expression by brain microvascular endothelial cells is critical for macrophage transendothelial migration in response to CCL2.

While the expression of chemokine receptors by endothelial cells is now well established, little is known of the function of these receptors at this cellular locale. However, given that chemokines are instrumental in directing leukocytes to specific parenchymal sites, one possibility is that endothelial chemokine receptors play a role in the process of leukocyte extravasation. To test this hypothesis, we investigated the contribution of CCR2, the major cognate receptor for the chemokine CCL2 (formerly known as MCP-1), to CCL2-stimulated transendothelial migration of macrophages (mØ) across cultured brain microvascular endothelial cells (BMEC). Specifically, we prepared both BMEC and mØ from wild-type (WT) mice and mice deficient in CCR2; i.e., CCR2 (-/-), and compared the ability of WT and CCR2 (-/-) BMEC to support CCL2-stimulated transendothelial migration of WT and CCR2 (-/-) mØ. In response to CCL2, WT mØ, but not CCR2 (-/-) mØ, were stimulated to migrate across WT BMEC, consistent with the recognized obligatory role for CCR2 in mediating CCL2-stimulated responses. Remarkably, however, neither WT nor CCR2 (-/-) mØ were stimulated by CCL2 to migrate across CCR2 (-/-) BMEC. In contrast, both types of mØ were able to migrate similarly across both types of BMEC in response to another chemokine--CCL3 (formerly known as MIP-1alpha)--which utilizes receptors other than CCR2. Lastly, CCL2-induced mØ transendothelial migration was blocked by treatment of WT BMEC with pertussis toxin, suggesting that CCR2 is functionally coupled to the inhibitory G protein Galphai, much as it is in other cell types. These results highlight a heretofore-unrecognized role for endothelial CCR2 in mediating transendothelial migration.

Animals↗
PubMed2005

Where is the blood-brain barrier ... really?

Few terms in the biomedical lexicon are as widely recognized as the phrase blood-brain barrier (BBB). Indeed, it immediately conjures up a "barricade" between the blood and the brain, a feature often considered more obstacle than safeguard. In truth, the BBB performs in both capacities, and it is precisely this duality that imparts such a vital role to the BBB in influencing physiological and pathophysiological processes in the CNS. Although the concept is more than a century old, the BBB continues to remain enigmatic in both substance and idea, with seemingly resolved issues once again beckoning for clarification. In this regard, recent technological advancements, such as sequencing of the human genome and development of microarray analysis, have illuminated novel aspects of vascular gene expression and provoked reconsideration of the cellular and biochemical makeup of the BBB. In light of the critical impact of the BBB in the realms of science and medicine, this Mini-Review will revisit the topic of the composition of the BBB, specifically highlighting how recent developments in endothelial biology have prompted a reevaluation of its precise vascular location. We have intentionally avoided discussing generalized features of the BBB, as these have been skillfully described elsewhere as noted.

Animals↗
PubMed2005

Synthesis of long indium nitride nanowires with uniform diameters in large quantities.

Large quantities of indium nitride (InN) nanowires are synthesized by the in situ nitriding of indium oxide (In(2)O(3)) powders in an ammonia (NH(3)) flux. Tens of milligrams of nanowires are obtained in one batch. Every 100 mg of In(2)O(3) starting powder can produce up to 65 mg of InN nanowires under the optimized conditions. The synthesized nanowires grow along the [001] direction with excellent crystallinity. They are of high purity and are 30-50 microm in length with an almost uniform diameter of about 100 nm. Photoluminescence measurements of the nanowires exhibit a strong peak at 707 nm. An optical bandgap of about 1.7 eV is estimated based on the absorption spectrum. The experimental results also demonstrate that the approach of nitriding In(2)O(3) powders in situ is feasible for the synthesis of high-purity InN nanowires in large quantities, with good reproducibility and without catalyst materials. The synthesis of InN nanowires in large quantities would be of benefit to the further study and understanding of their intrinsic properties, as well as being advantageous for their potential application in nanodevices.

Indium↗
PubMed2005

Characterization of the F198S prion protein mutation: enhanced glycosylation and defective refolding.

Prion diseases are associated with the accumulation of a misfolded, protease resistant form of the prion protein, PrPres. In humans there are a variety of different prion related diseases that are sporadic, inherited, or acquired by infection. Gerstmann-Straussler-Sheinker syndrome (GSS) is an inherited prion disease in which PrPres accumulates as amorphous aggregates as well as in amyloid plaques. GSS has been associated with a variety of point mutations in the prion protein: 102, 105, 117, 131, 145, 187, 198, 202, 212, 217, and 232. The F198S mutation was discovered in a large Indiana kindred. Previous studies in vitro have shown that the 198 mutation results in structural instability of the prion protein. In the current study, we demonstrate in a cell model that the F198S mutant protein can be folded properly in a cellular context, but is unable to refold to a native state after denaturation. Further, the F198S mutation significantly affects glycosylation of the mutant protein.

Amyloid↗
PubMed2004

[Correlation of thrombospondin-1 G1678A polymorphism to stroke: a study in Chinese population].

OBJECTIVE: To assess whether thrombospondin-1 (THBS-1) gene G1678A polymorphism is associated with stroke. METHODS: Samples of venous blood were collected from 1634 patients with stroke, including cerebral thrombosis, lacunar cerebral infarction, and cerebral hemorrhage confirmed by CT or MRI, and sex-, and age-matched 1171 controls without cerebrovascular diseases. Genotypes were determined with polymerase chain reaction and allele-specific restriction enzyme analysis. RESULTS: The frequency of the THBS-1 gene 1678 AA genotype (0.503 vs. 0.441) was significantly higher in the cerebral thrombosis group than in the controls (P = 0.008). The frequency of the G allele (0.299 vs. 0.339) was significantly lower in the cerebral thrombosis group than in the controls (P = 0.009). No significant difference was seen in THBS-1 gene 1678 AA polymorphism either between the lacunar cerebral infarction group and the control group or between the cerebral hemorrhage group and the control group (all P > 0.05). Multiple logistic regression analysis showed that the AA genotype of THBS-1 gene G1678A carriers had a higher risk of cerebral thrombosis (OR: 1.4; 95% CI 1.083 - 1.693; P = 0.008) after adjustment for age, sex, SBP, DBP, BMI, smoking, TC, TG, HDL-C, LDL-C and Glu. CONCLUSION: AA genotypes in THBS-1 gene G1678A polymorphism may be a genetic risk factor of cerebral thrombosis in Chinese population.

Aged↗
PubMed2004

Machinable long PVP-stabilized silver nanowires.

PVP-capped silver nanowires with a diameter range from 150 to 200 nm and a length range from 50 to 100 microm have been synthesized in large quantity by using a soft-template liquid-phase method. The so-obtained longer and thicker metallic nanowires exhibit fivefold-twinned structures bound by five [1 0 0] wall-planes and two spearlike ends around five [1 1 1] facets. X-ray photoelectron spectroscopy (XPS) investigations show that a strong interaction exists between the carboxyl oxygen atom (C=O) of PVP and the Ag core interface. The PVP-capped Ag nanowires can either self-assemble into ordered raft structures or form a complicated network, depending on the dispersive solvent employed. In addition, the Ag nanowires can also be specifically bent into various angles, demonstrating their excellent mechanical stability.

Journal Article↗
PubMed2004

IL-6 and the acute phase response in murine atherosclerosis.

Numerous studies have implicated C-reactive protein (CRP) and the acute phase response (APR) in the development of atherosclerotic heart disease. Interleukin (IL)-6, which regulates both CRP expression and the APR, has also been identified as a risk factor for heart disease. To more directly evaluate the role of IL-6 in the development of atherosclerosis, IL-6 knockout mice were crossed with atherosclerosis prone LDL receptor (LDL-R) knockout mice. Lesion development was evaluated on Chow, Western type and Paigen diets. As anticipated, the Paigen diet stimulated the expression of APR genes in LDL-R[-/-] mice, but not IL-6[-/-]/LDL-R[-/-] mice. Despite this difference in acute phase response, only modest and statistically not significant differences were noted in the development of atherosclerotic lesions in LDL-R[-/-] and IL-6[-/-]/LDL-R[-/-] mice. These observations suggest that IL-6 and the acute phase response may not play as significant role in atherogenesis as other studies have indicated.

Acute-Phase Reaction↗
PubMed2004

Monocyte chemoattractant protein-1 alters expression of tight junction-associated proteins in brain microvascular endothelial cells.

The chemokine monocyte chemoattractant protein (MCP-1) is recognized to mediate extravasation of mononuclear leukocytes into the brain during a variety of neuroinflammatory conditions. In large part produced by parenchymal neural cells during these disease states, it is unclear how this chemokine can stimulate the migration of circulating leukocytes that lie behind the highly impermeant blood-brain barrier (BBB). Based on the premise that disruption of tight junctions (TJs) could foster leukocyte extravasation, experiments were conducted to test the hypothesis that MCP-1 alters the expression and/or distribution of the TJ-associated proteins zonulae occludens-1 (ZO-1) and occludin in brain microvascular endothelial cells (BMEC) comprising the BBB. Exposure to MCP-1 caused a loss in immunostaining of ZO-1 at inter-endothelial junctional regions in both cultured BMEC and isolated brain microvessels, as well as a similar effect on occludin in cultured BMEC, but did not alter occludin staining in microvessels. In cellular fractionation experiments, ZO-1 associated predominantly with the detergent-resistant cytoskeletal framework (CSK) in both cultured BMEC and brain microvessels, while a slimmer majority of occludin partitioned with the CSK. Following MCP-1 exposure, ZO-1 was reduced in the CSK fraction of cultured BMEC and microvessels, with a shift of ZO-1 to the detergent-soluble fraction in both cases. Occludin exhibited a similar pattern of MCP-1-induced loss and shift from the CSK in cultured BMEC, but remained nearly constant in microvessels. Lastly, expression of caveolin-1, a major structural component of membrane microdomains thought to be functionally complexed with TJs, was additionally altered by MCP-1 treatment of both cultured BMEC and microvessels. These results indicate that, in addition to its chemotactic activity, MCP-1 might alter BBB integrity during CNS inflammation.

Animals↗
PubMed2004

Effects of lipopolysaccharide on actin reorganization and actin pools in endothelial cells.

OBJECTIVE: To investigate the dose and time-dependent effects of lipopolysaccharide (LPS) on cytoskeletal F-acitn and G-actin reorganizations by visualizing their distribution and measuring their contents in human umbilical vein endothelial cell line ECV-304. METHODS: F-actin was labeled with rhodamine-phalloidin and G-actin with deoxyribonuclease I (DNase I)conjugated with fluorescein isothiocyanate (FITC). Contents of cytoskeletal proteins were obtained by flow cytometry. RESULTS: F-actin was mainly distributed peripherally in endothelial cells under normal conditions. LPS stimulation caused the formation of stress fibers and filopodia. G-actin was normally seen in perinuclear and nuclear areas in control ECV-304 cells. Under LPS stimulation, G-actin dots appeared in the cytoplasmic region. The actin disorganization was accompanied by the time- and dose- dependent decrease in F-actin pool and increase in G-actin pool. CONCLUSIONS: LPS can induce characteristic morphological alterations of actin cytoskeleton and formation of intercellular gap in endothelial cells, accompanied by changes in F-actin and G-actin pools.

Actins↗
PubMed2004

Interaction of two classes of release factors from Euplotes octocarinatus.

Translation termination on the ribosome is an essential process for cell viability. This process is maintained by two classes of peptide release factors (RF1/RF2, RF3 and eRF1, eRF3 in prokaryotes and eukaryotes, respectively). In protozoa ciliates Euplotes octocarinatus, an unicellular eukaryotes, universal stop codon UGA is reassigned for cysteine suggesting the specificity of evolution of translation termination system. We cloned two classes of release factors from Euplotes octocarinatus previously. In this paper, three in-frame stop codons UGA in Eo-eRF3 gene were mutated mediated by PCR site directed mutagenesis method. The interaction between eRF1 and eRF3 from E. octocarinatus was assayed in vivo using Yeast Two-hybrid System, which has an advantage of highly sensitivity. The results showed that the eRF1 x eRF3 complex was formed in living cells to function in the process of translation termination, differing from that in prokaryotes in which RF1/RF2 and RF3 function separately. The evolution of translation termination of life-form was analyzed using phylogenetic tree of amino acids sequences of RFs (32 (e) RF1s and 24 (e) RF3s) obtained from GenBank. Two classes of RFs are useful information in analysis of evolution of life-form and further elucidation of mechanism of translation termination of protein synthesis on ribosome.

Animals↗