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Lin Li

Publications and source records attributed to Lin Li.

At least 199 records · Page 11Linked to original sources
PubMed2003

Antigens in tea-beverage prime human Vgamma 2Vdelta 2 T cells in vitro and in vivo for memory and nonmemory antibacterial cytokine responses.

Human gammadelta T cells mediate innate immunity to microbes via T cell receptor-dependent recognition of unprocessed antigens with conserved molecular patterns. These nonpeptide alkylamine antigens are shared by tumor cells, bacteria, parasites, and fungi but also by edible plant products such as tea, apples, mushrooms, and wine. Here we show that priming of gammadelta T cells with alkylamine antigens in vitro results in a memory response to these antigens. Such priming results also in a nonmemory response to whole bacteria and to lipopolysaccharide, characterized by IL-12-dependent secretion of IFN-gamma by gammadelta T cells and by gammadelta T cell proliferation. Drinking tea, which contains l-theanine, a precursor of the nonpeptide antigen ethylamine, primed peripheral blood gammadelta T cells to mediate a memory response on reexposure to ethylamine and to secrete IFN-gamma in response to bacteria. This unique combination of innate immune response and immunologic memory shows that gammadelta T cells can function as a bridge between innate and acquired immunity. In addition, these data provide an explanation for the health benefits of tea.

Anti-Bacterial Agents↗
PubMed2003

Role of actin microfilament in hyposmotic membrane stretch-induced increase in muscarinic current of guinea-pig gastric myocytes.

To investigate the relationship between cytoskeleton and hyposmotic membrane stretch-induced increase in muscarinic current, the role of actin microfilament in hyposmotic membrane stretch-induced increase in muscarinic current was studied with the whole-cell patch clamp technique in guinea-pig gastric myocytes. In this study, the muscarinic current was induced by carbachol (50 micromol/L) or GTPgammaS (0.5 mmol/L). The results showed that hyposmotic superfusate (202 mOsmol/L) increased carbachol-induced current (I(CCh)) by 145+/-27% and increased GTPgammaS-induced current by 183+/-30%; but in the presence of cytochalasin-B (Cyt-B, 20 micromol/L), an actin cytoskeleton disruptor, hyposmotic membrane stretch increased I(CCh) by 70+/-6%. However, hyposmotic membrane stretch induced increase in I(CCh) was potentiated to 545+/-81% by phalloidin (20 micromol/L), an actin microfilament stabilizer. The results demonstrated that hyposmotic membrane stretch increased the muscarinic currents induced by carbachol or GTPgammaS and that the actin microfilament is involved in the process in guinea-pig gastric myocytes.

Actin Cytoskeleton↗
PubMed2003

Role of unsaturated fatty acids in the enhancement of muscarinic current by hyposmotic membrane stretch in guinea pig smooth muscle cells.

To investigate the function of exogenous unsaturated fatty acids in hyposmotic membrane stretch enhancement of muscarinic current (ICCh) in antral circular smooth muscle cells of guinea pig, we recorded the membrane current with the conventional whole cell patch-clamp technique. I(CCh) elicited by 50 micromol/L carbachol (CCh) at the holding potential of 20 mV under isosmotic condition was taken as control. Hyposmotic membrane stretch increased I(CCh) to 226.0+/-21.0%. When the cells were pretreated with 5 micromol/L arachidonic acid (AA), linoleic acid (LA) or oleic acid (OA), I(CCh)was inhibited to 3.8+/-0.6%, 35.2+/-0.8% and 66.6+/-0.6% respectively. Hyposmotic membrane stretch increased I(CCh) to 106.0+/-2.5%, 173.2+/-6.8% and 222.1+/-11.0% of the control respectively. Five micromol/L AA inhibited hyposmotic membrane stretch-enhanced I(CCh) by 51.2+/-3.8%, while the control I(CCh) under isosmotic condition was inhibited by 96.2+/-1.6%. The results suggest that unsaturated fatty acids inhibited I(CCh) and the inhibitory effect is more significant when the unsaturation degree is increased. However, the unsaturated fatty acids are not involved in the increase of I(CCh) induced by hyposmotic membrane stretch.

Animals↗
PubMed2003

gp49B1 suppresses stem cell factor-induced mast cell activation-secretion and attendant inflammation in vivo.

We report that gp49B1, a mast cell membrane receptor with two immunoreceptor tyrosine-based inhibitory motifs (ITIM), constitutively inhibits mast cell activation-secretion induced by stem cell factor (SCF), a tissue-derived cytokine that also regulates mast cell development. The intradermal injection of SCF into the ears of gp49B1 null (gp49B(-/-)) mice elicited approximately 4- and 2.5-fold more degranulating mast cells and tissue swelling caused by edema, respectively, than in gp49B(+/+) mice. SCF did not induce tissue swelling in mast cell-deficient mice, and the responsiveness of gp49B(-/-) mice to mast cell-associated amine and lipid mediators was unaltered. When gp49B(+/+) and gp49B(-/-) mice were pretreated with antagonists of the amines, SCF-induced tissue swelling was reduced by >90% and 60%, respectively, and it was reduced by >90% in both genotypes when a cysteinyl leukotriene receptor antagonist was also provided. Hence, the dominant contribution of secretory granule amines to SCF-induced tissue swelling is the result of gp49B1-mediated inhibition of the production of cysteinyl leukotrienes by mast cells. Our findings also provide the first example of an ITIM-bearing receptor that constitutively suppresses inflammation generated in vivo independently of the adaptive immune response by a receptor that signals through intrinsic tyrosine kinase activity rather than immunoreceptor tyrosine-based activation motifs.

Animals↗
PubMed2003

Arterial spin labeling perfusion fMRI with very low task frequency.

Functional magnetic resonance imaging (fMRI) has become the most widely used modality for visualizing regional brain activation in response to sensorimotor or cognitive tasks. While the majority of fMRI studies have used blood oxygenation level-dependent (BOLD) contrast as a marker for neural activation, baseline drift effects result in poor sensitivity for detecting slow variations in neural activity. By contrast, drift effects are minimized in arterial spin labeling (ASL) perfusion contrast, primarily as a result of successive pairwise subtraction between images acquired with and without labeling. Recent data suggest that ASL contrast shows stable noise characteristics over the entire frequency spectrum, which makes it suitable for studying low-frequency events in brain function. The present study investigates the relative sensitivities of ASL and BOLD contrast in detecting changes in motor cortex activation over a spectrum of frequencies of experimental design, where the alternating period between the resting state and activation is varied from 30 s up to 24 hr. The results demonstrate that 1) ASL contrast can detect differences in motor cortex activation over periods of minutes, hours, and even days; 2) the functional sensitivity of ASL contrast becomes superior to that of BOLD contrast when the alternating period between the resting state and activation is greater than a few minutes; and 3) task activation measured by ASL tends to have less intersubject variability than BOLD contrast. The improved sensitivity of the ASL contrast for low task frequency and longitudinal studies, along with its superior power in group analysis, is expected to extend the range of experimental designs that can be studied using fMRI.

Adult↗
PubMed2003

Up-regulation of phosphorylated/activated p70 S6 kinase and its relationship to neurofibrillary pathology in Alzheimer's disease.

The ribosomal S6 protein kinase p70 S6 kinase is known for its role in modulating cell-cycle progression, cell size, and cell survival. In response to mitogen stimulation, p70 S6 kinase activation up-regulates ribosomal biosynthesis and enhances the translational capacity of the cell. In Alzheimer's disease (AD), there is a marked increase in total tau protein in the form of abnormally hyperphosphorylated tau (PHF-tau) in neurons with neurofibrillary tangles (NFTs). In the present study, we investigated whether p70 S6 kinase activation is associated with PHF-tau accumulation in AD. By immunohistochemistry, we found that the levels of phosphorylated p70 S6 kinase (at Thr389 or at Thr421/Ser424) were increased in accordance with the progressive sequence of neurofibrillary changes according to Braak's criteria. Confocal microscopy showed that in AD brain, phosphorylated p70 S6 kinase appeared especially in neurons that are known to later develop NFTs. This pattern of neurons showed dot-like structures of phosphorylated p70 S6 kinase and hyperphosphorylated tau, which partially correlated with rab5 (endosome marker), lamp-1 (lysosome marker), and ubiquitin (ubiquitin-proteasomal system marker). By indirect enzyme-linked immunosorbent assay, phosphorylated p70 S6 kinase (Thr389 or Thr421/Ser424), total tau, and PHF-tau were found to be significantly increased in AD brain as compared to control cases. The levels of total p70 S6 kinase and p70 S6 kinase phosphorylated at Thr421/Ser424 showed significant correlations with the levels of both total tau and PHF-tau. Regression analyses revealed a significant dependence of total tau or PHF-tau on p70 S6 kinase phosphorylated at Thr421/Ser424 rather than at Thr389. The levels of ribosomal protein S6 as well as the levels of markers for the proteolytic system were also significantly increased in AD as compared to control brain. Using a SH-SY5Y neuroblastoma cell model, we found that 100 micro mol/L zinc sulfate could induce p70 S6 kinase phosphorylation and activation, in particular at Thr421/Ser424. This up-regulation of the activated kinase resulted in an increased expression and phosphorylation of tau. Pretreatment of cells with rapamycin (an inhibitor of FRAP/mTOR which is the immediate upstream kinase of the p70 S6 kinase) attenuated the effects induced by zinc. In primary cultured neurons of rat cortical cortex, zinc sulfate treatment could repeat p70 S6 kinase phosphorylation and activation at Thr421/Ser424, followed by increased expression and phosphorylation of tau. Taken together, these data suggest that activated p70 S6 kinase could mediate an up-regulation of tau translation. The partial co-localization of phosphorylated p70 S6 kinase with rab5, lamp-1 and ubiquitin, or PHF-tau with ubiquitin suggests that the activated proteolytic system might not be sufficient to degrade the over-produced and over-phosphorylated tau protein. A p70 S6 kinase modulated up-regulation of tau translation might contribute to PHF-tau accumulation in neurons with neurofibrillary changes.

Aged↗
PubMed2003

Bioeffects of selenite on the growth of Spirulina platensis and its biotransformation.

The bioeffects of selenium on the growth of Spirulina platensis and the selenium distribution were investigated. S. platensis was batch cultured in Zarrouk medium containing increasing concentrations of sodium selenite. The biotransformation characteristic of selenium was analysed by the determination of the detailed selenium distribution forms. At 35 degrees C, 315.2 microEm(-2) x s(-1), sodium selenite concentrations below 400 mg x l(-1) were found to stimulate algal growth, especially in the range of 0.5-40 mg x l(-1). However, above 500 mg x l(-1) sodium selenite was toxic to this alga with the toxicity being related to the sulfite level in the medium. S. platensis was found to resist higher selenite by reducing toxic Se(IV) to nonsoluble Se(0). Selenium was accumulated efficiently in S. platensis during cultivation with accumulated selenium increasing with selenite concentration in the medium. It was demonstrated that inorganic selenite could be transformed into organic forms through binding with protein, lipids and polysaccharides and other cell components. The organic selenium accounted for 85.1% of the total accumulated selenium and was comprised of 25.2% water-soluble protein-bound, 10.6% lipids-bound and 2.1% polysaccharides-bound selenium. Among the organic fractions lipid possessed the strongest ability to accumulate Se (6.47 mg x kg(-1)). The 14.9% inorganic selenium in S. platensis was composed of Se(IV) (13.7%) and Se(VI) (1.2%).

Biotransformation↗
PubMed2003

Measurement of histone acetyltransferase and histone deacetylase activities and kinetics of histone acetylation.

Dynamic histone acetylation has a role in chromatin remodeling and in the regulation of transcription. Histone deacetylases (HDACs) and histone acetyltransferases (HATs) catalyze reversible histone acetylation. HATs and HDACs exist as multiprotein complexes that have coactivator and corepressor activities, respectively. The steady-state level of acetylation at a chromatin site is determined by the local net activities of these enzymes. Here we describe methods to isolate different subcellular fractions (cytosol, nuclei, tightly bound nuclear, loosely bound nuclear, immunoprecipitated multiprotein complexes, and nuclear matrix) to determine the subcellular distribution of HAT and HDAC activities. Procedures to assay the activities of these enzymes and to measure the kinetics of histone acetylation and deacetylation are presented.

Acetylation↗
PubMed2003

Chromatin immunoprecipitation: a tool for studying histone acetylation and transcription factor binding.

The function of a protein in gene expression can often be explained, in part, by the location of that protein along a specific gene sequence. In recent years, the chromatin immunoprecipitation (ChIP) assay has been developed to study the association of proteins located within 2 A of DNA such as transcription factors and modified histones. Numerous important findings have been published using the ChIP assay and many questions about transcription have been answered. In this article, we present the ChIP assay currently used in our lab and discuss the various ways to optimize this assay for one's own use.

Acetylation↗
PubMed2003

Study on Escherichia coli alkaline phosphatase conformation by phosphorimetry in the presence of denaturant.

The influence of different denaturants on the phosphorescence spectrum and lifetime decay of Escherichia coli alkaline phosphatase (AP) was investigated. Phosphorescence intensity and lifetime of tryptophan residue (Trp-109) decrease upon addition of guanidine hydrochloride, ethylene diamine tetraacetic acid, and urea or decreasing acidity. The experiments show that AP undergoes different pathways with different denaturants and that the activation energy data, DeltaS degrees (not equal) and deltaH degrees (not equal) further confirm that there is a stable intermediate state between the folded and unfolded AP states in solution.

Alkaline Phosphatase↗
PubMed2003

Effect of protein kinase C activation and inhibition on rat hepatic stellate cell activation.

Protein kinase C (PKC) may play a role in the intracellular signaling pathways responsible for transforming hepatic stellate cells into myofibroblasts. This study examined the effects of inhibitors and activators of PKC on hepatic stellate cell activation. Stellate cells isolated from normal rats were incubated with either 10(-5) M chelerythrine, 10(-7) M bisindolylmaleimide I hydrochloride (BIM), or 10(-6) M staurosporine (PKC inhibitors), or 10(-7) M phorbol myristate acetate (PMA) or 10(-6) M thymeleatoxin (PKC activators). Chelerythrine suppressed alpha-smooth muscle actin expression and proliferation by 49% and 33%, respectively. BIM inhibited alpha-smooth muscle actin expression by 60%, but had no significant effect on proliferation. Staurosporine decreased proliferation by 86% and completely prevented alpha-smooth muscle actin expression. PKC activators had divergent effects on proliferation and alpha-smooth muscle actin expression. PMA and thymeleatoxin caused a 2.8- to 3.2-fold increase in proliferation, while suppressing alpha-smooth muscle actin expression by 50-70%. The demonstration that hepatic stellate cell activation can be suppressed by PKC inhibitors suggests a role for PKC in the regulation of hepatic stellate cell activation.

Actins↗
PubMed2003

Genistein protects primary cortical neurons from iron-induced lipid peroxidation.

Neuroprotective role of isoflavones in particular genistein might be resulted from their antioxidant activities in addition to their estrogenic actions. In the present study, we investigated effect of genistein on iron-induced free radical reaction in cultured cortical neurons. Thiobarbituric-acid-reactive species (TBARS) and superoxide dismutase (SOD) were measured after incubation of the cells with different concentrations of genistein in the absence or presence of iron (12.5 microM) for 24 h. Genistein at 100 microM significantly reduced the iron-induced TBARS, implying that genistein has an inhibitory role on iron-induced lipid peroxidation. Also, genistein (100 microM) led to a relatively higher SOD level than that in iron treatment although no significant difference was found. The findings imply that the antioxidative effect of genistein is partly associated with its neuroprotective function.

Animals↗
PubMed2003

Magnetic susceptibility quantitation with MRI by solving boundary value problems.

Magnetic susceptibility measurement is of considerable research interest in MRI and MRS. A rigorous method was previously developed to quantify the susceptibility of an arbitrarily shaped uniform object in an inhomogeneous external field. However, it requires using the field distribution information on a spherical surface or shell in the surrounding homogeneous medium enclosing the object. In this work, a new approach was developed through solving the boundary value problems of the Laplace equation, which has an advantage that the boundary providing the necessary field distribution information can have an arbitrary shape. This method has been validated on rectangular boundaries with both numerical simulation as well as experimental data. It has also been realized that MRI provides an experimental means of solving some boundary value problems of partial differential equations, if proper boundary condition can be set up.

Computer Simulation↗
PubMed2003

[Cloning and sequence analysis of tomato fruit-specific E8 promoter from Lycopersicon esculentum (Zhongshu No.5)].

OBJECTIVE: To obtain the gene encoding tomato fruit-specific E8 promoter therefore to prepare for exogenous gene transcription and expression in transgenic tomato fruit. METHODS: The cotyledons of tomato Lycopersicon esculentum (Zhongshu No.5) were collected for extracting the genomic DNA of this plant. The fruit-specific E81.1 and E82.2 promoter DNA were then amplified by PCR, the product of which was subcloned into pGEM-T vector. After identification by restriction enzymes, the recombinant T-vectors were subjected to sequence analysis. RESULTS: The fragments of the promoter as amplified by PCR were of predicted length. Digestion with Xba I and Hind III /BamH I proved correct insertion of the target fragments with expected length into the recombinant T vectors. As indicated by homology analysis, the resultant tomato fruit-specific E8 promoter was highly conservative, and E82.2 promoter of Zhongshu No.5, with GenBank submission number of AF515784, proved to share 99% homology with E82.2 promoter of Zhongshu No.5 Cherry as reported by Deikman J. CONCLUSION: Tomato fruit-specific E8 promoter of Zhongshu No.5 has been successfully cloned, thus making possible the subsequent research in oral vaccine of transgenic tomato.

Base Sequence↗
PubMed2003

Effect of unsaturated fatty acid on muscarinic current in guinea pig gastric antral circular myocytes.

AIM: To investigate the effect of ectogenesis unsaturated fatty acid on carbachol-induced muscarinic current (ICCh) and its mechanism. METHODS: Using the whole-cell patch-clamp technique, ICCh was recorded in single smooth muscle cell isolated from the antral circular smooth muscles of guinea-pig stomach. RESULTS: Arachidonic acid (AA) was added in external perfusing solution and AA inhibited ICCh to 46 %+/-8 %, 23 %+/-5 %, and 3.8 %+/-0.9 % at 1, 3, and 5 micromol/L. Another unsaturated fatty acid, linoleic acid (LA) also inhibited ICCh in a dose-dependant manner. LA inhibited ICCh to 69 %+/-10 %, 35 %+/-5 %, and 7.4 %+/-1.2 % at 1, 5, and 10 micromol/L, respectively. The same concentration (5 micromol/L) of AA, LA, and oleic acid (OA) suppressed ICCh to 3.8 %+/-0.9 %, 35 %+/-5 %, and 67 %+/-9 %, respectively. The inhibitory potency sequence of these unsaturated fatty acids was AA>LA>OA. After 10-15 min of pretreatment with H-7 (a protein phosphorylation C inhibitor) 100 micromol/L or indomethacin (a cyclooxygenase inhibitor) 10 micromol/L, ICCh was inhibited by 5 micromol/L of AA to 5.5 %+/-0.7 % and 3.0 %+/-1.0 %, respectively. CONCLUSION: The unsaturated fatty acids directly inhibited ICCh, and the inhibitory potency was related to the number of double bonds in fatty acid chain.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2003

[Effect of congsheng capsule on intracellular calcium concentration in mice after ischemic cerebral injury].

OBJECTIVE: To investigate the effect of Congsheng Capsule (CSC) in intracellular Ca2+ concentration in cerebral intra-synaptosomes of ischemia/reperfusion mice and analogous ischemic injured neurons to estimate the mechanism of CSC in antagonizing ischemic cerebral injury. METHODS: The concentration of Ca2+ in cerebral intra-synaptosomes of mice and in neurocyte suspension of fetal mice were determined using Fura-2/AM double wavelength fluorescence spectrophotometer. RESULTS: CSC 3 g/kg and 9 g/kg through gastrogavage could relieve the degree of calcium overloading of intra-synaptosomes in mice after cerebral ischemia/reperfusion. The CSC containing serum could inhibit the elevation of Ca2+ content in neurocytes induced by 1 hour hypoxia and glutamate of high concentration (200 mumol/L). CONCLUSION: CSC plays a role in antagonizing ischemic injury through relieving the calcium overloading after cerebral ischemia.

Animals↗
PubMed2003

[Relation between activation of NF-kappa B and chemotherapy induced apoptosis of leukemic cells].

OBJECTIVE: To analyze the relation between activation of NF-kappa B and chemotherapy induced apoptosis of leukemic cells and the effect of vincristine (VCR) on them. METHODS: Electrophoretic mobility shift assay (EMSA) was used to detect the activation of NF-kappa B and tunel DNA electrophoresis was adopted to observe the apoptosis induced by cytosine arabinoside (Ara-C) and etopside (Vp-16) in P388 leukemic cells. RESULTS: The activation of NF-kappa B induced by Ara-C and Vp-16 was obviously correlated to apoptosis in P388 cells. VCR (0.1 micromol/L) could suppress activation of NF-kappa B by 52% and 63% and significantly increase the apoptosis by 89% and 123% as induced by Ara-C (100 micromol/L) and Vp-16 (100 micromol/L). The activity of NF-kappa B could be found in P388 cells before being exposed to chemotherapeutic agent. CONCLUSION: Chemotherapeutic agents can induce apoptosis and activation of NF-kappa B of P388 cells. The mechanism of VCR potentiating chemotherapeutics induction of leukemia cell apoptosis may be related to its suppression of the NF-kappa B activity in the P388 cells.

Animals↗