Biomedical subjects

L Li

Publications and source records attributed to L Li.

At least 1,171 records · Page 65Linked to original sources

PubMed1998

[Determination of trace selenium and tellurium in steel by hydride-generation nondispersive atomic fluorescence spectrometry].

A method was developed for the determination of trace Se and Te in steel by ion-exchange-separation hydride-generation nondispersive atomic fluorescence spectrometry. 40% (V/V) chlorhydric acid was selected as the best medium for hydride reaction. The detection limits of Se and Te are 0.27 and 0.33 ng/mL, relative standard deviations are 6.99 and 6.11%, respectively. The recovery was in the range of 96.7-102.0%. The results are satisfactory.

English Abstract↗

PubMed1998

[Cyclodextrin induced-room temperature phosphorescence for the determination of quinoline without deoxidization].

A cyclodextrininduced-room temperature phosphorescence (CD-RTP) system for the determination of quinoline without deoxidization procedure was developed based on the external heavy atom effect of dibromopropane (DBP), the RTP maximum wavelengths lambda(ex)/lambda(em) = 273/496nm. The difference of heavy atom effect between dibromopropane DBP and dibromoethane (DBE) was examined and the apparent formation constants of the ternary inclusion complexes for quinoline/beta-CD/DBP and quinoline/beta-CD/DBE systems were determined. As compared with DBE, the heavy atom effect of DBP was higher and the RTP intensity was stronger. The RTP intensity was linear for quinoline/beta-CD/DBP systems with quinoline concentration in the ranges of 5.0 x 10(-7)-5.0 x 10(-5)mol/L and 5.0 x 10(-5)-5.0 x 10(-4)mol/L, respectively. The detection limit was 7.8 x 10(-8)mol/L. The determination precision was satisfactory.

Calibration↗

PubMed1998

[Synthesis and molecular recognition study of 6-Cs-beta-CD].

The reagents 6-Cs-beta-CD with molecular recognition function were synthesized and confirmed. Both basic condition and enough illumination were necessary for obtaining stable and strong fluorescence. With 6-Cs-beta-CD as the host, cyclohexanol, cyclohexene, cyclohexane and bromocyclohexane as the guest, the recognition properties were studied. The affinity of 6-Cs-beta-CD and the guest is distinct with different hydrophobicity of the guest.

Hydrophobic and Hydrophilic Interactions↗

PubMed1998

[Phenomena of supramolecular assembly fluid room temperature phosphorescence (II)--effects of alcohols on room temperature phosphorescence of cyclodextrin/4-iodo-4'-ethyl-biphenyl/bromocyclohexane system].

Beta-cyclodextrin( beta/-CD)can induce 4-iodo-4'-ethyl-biphenyl(IEBP)to emit room temperature phosphorescence(RTP) in the presence of bromocyclohexane (BCH). If butyl alcohol (BuOH) is presented as a fourth component at the same time, RTP intensity of the system is enhanced obviously. Effects of different alcohols, CDs and derivatives of beta-CD on RTP emission of the system are studied. The results show that a ternary host-guest inclusion complex is formed among beta-CD, IEBP and BCH, but the alcohol hydroxyl bonds to the rim of the CD cavities by hydrogen-bonding and the alkyl end of alcohol flips over the two tops of the CD due to hydrophobic interaction force. Accordingly, the alcohol acts as a lid for CD cup, thereby shielding IEBP from oxygen and decreasing the collision quenching of oxygen, and decreasing the micro polarity of the CD cavity and the formation constant of ternary inclusion complex increases. As a result, the RTP of the system is enhanced. As far as we can see that the system studied is a typical supramolecular assembly one and the BuOH acts as a molecular regulation for RTP emitting.

Alcohols↗

PubMed1998

Distinct roles of synapsin I and synapsin II during neuronal development.

The synapsins are a family of neuron-specific proteins, associated with the cytoplasmic surface of synaptic vesicles, which have been shown to regulate neurotransmitter release in mature synapses and to accelerate development of the nervous system. Using neuronal cultures from mice lacking synapsin I, synapsin II, or both synapsins I and II, we have now found that synapsin I and synapsin II play distinct roles in neuronal development. Deletion of synapsin II, but not synapsin I, greatly retarded axon formation. Conversely, deletion of synapsin I, but not synapsin II, greatly retarded synapse formation. Remarkably, the deletion of both synapsins led to partial restoration of the wild phenotype. The results suggest that the synapsins play separate but coordinated developmental roles.

Animals↗

PubMed1998

Prevalence and risk factors of illicit drug use by people with disabilities.

The authors examined patterns and risk factors of illicit drug use among people with disabilities by use of a random sample of 1,876 persons actively involved in vocational rehabilitation services in three Midwestern states. Compared with regional drug use data from the general population, respondents with disabilities reported higher rates of illicit drug use for nearly every drug category. Factors significantly associated with illicit drug use included level of disability acceptance, best friends' drug use, attitude of disability entitlement, self-esteem, and risk-taking. These findings provide additional insight into illicit drug use among people with disabilities. The authors discuss implications from these findings for rehabilitation and disability policy.

Adaptation, Psychological↗

PubMed1998

Relaxing effects of NO donors on guinea pig trachea in vitro are mediated by calcium-sensitive potassium channels.

The relaxing effects of the nitric oxide (NO) donors 1,2,3,4-oxatriazolium,3-(3-chloro-2-methylphenyl-5-[[(4-methoxyphe nyl) sulfonyl]amino]-,hydroxide inner salt (GEA 3268) 1,2,3,4-oxatriazolium,3-(3-chloro-2-methyphenyl-5-[methys ulfonyl)amino]- hydroxide inner salt (GEA 5145), 3-morpholinosydnonimine (SIN-1) and S-nitroso-N-acetylpenicillamine (SNAP) were inhibited in vitro by iberiotoxin (IbTX) and charybdotoxin (ChTX), the two selective inhibitors of Ca(++)-activated K+ channels (KCa) in guinea pig trachea. When studied in cumulative concentrations in metacholine constriction, the relaxing effects of the NO donors were inhibited by at least 70% in the presence of the toxins, with the exception of SIN-1 in the presence of ChTX. The inhibitory effect of ChTX was less marked than that of IbTX. This suggests that the relaxing effects of the structurally different NO donors are mediated through KCa channels and that IbTX is more potent than ChTX. A selective inhibitor of soluble guanylate cyclase, 1H-[1,2,4]oxadiazolo[4,3-a]quinozalin-1-one (ODQ), significantly inhibited the relaxing effects of GEA 3268 and GEA 5145 on metacholine and KCl constriction and almost totally inhibited the relaxing effects of SIN-1 and SNAP. The inhibitor of the delayed rectifier K+ channel current 4-aminopyridine did not influence the relaxations of the NO donors, and under the experimental conditions of this study, the ATP-sensitive K+ channel inhibitor glibenclamide had no effect. In conclusion, the relaxing effects of the structurally different NO-releasing compounds are mediated via KCa channels. However, the significance of some other possible mechanisms unrelated to K+ channels cannot be excluded.

4-Aminopyridine↗

PubMed1998

Resistance of chylomicron and VLDL remnants to post-heparin lipolysis in ApoE-deficient mice: the role of apoE in lipoprotein lipase-mediated lipolysis in vivo and in vitro.

The interaction of lipoprotein lipase (LPL) with triglyceride-rich lipoproteins is governed by a number of factors, such as apolipoprotein (apo) C-II. The role of apoE in lipolysis is controversial. We made the unexpected observation that apoE-deficient mice were resistant to heparin-induced lipolysis; this study aims at examining the underlying mechanism for this observation. Compared to wild-type mice, apoE-deficient mice had significantly higher very low density lipoprotein (VLDL) and chylomicron remnant (VLDL/CMR) concentrations and moderately lower lipase activity (15.5 +/- 1.3 mU/ml vs. 22.9 +/- 2.5 mU/ml). Unlike in wild-type mice where the injection of heparin reduced total plasma triglycerides by 50% and VLDL/CMR triglycerides by over 95%, the injection of heparin into apoE-deficient mice did not significantly affect plasma lipids. Similarly, in vitro, purified human LPL (hLPL) almost completely hydrolyzed VLDL/CMR isolated from wild-type mice, but had no effect on VLDL/CMR from apoE-deficient mice. However, when the amount of apoE-deficient VLDL/CMR was reduced to an equivalent level as in wild-type mice, LPL hydrolyzed 94% of VLDL/CMR triglycerides. In order to increase the ratio of LPL to VLDL/CMR in vivo, we injected an adenovirus containing the human LPL cDNA into apoE-deficient mice, which produced marked liver-specific overexpression of LPL and significant reduction of VLDL/CMR (93%) and total plasma triglyceride concentrations (87%). Thus, apoE is not required for LPL activity in vivo or in vitro. Under certain pathological conditions, such as severe hyperlipidemia, the LPL pathway may be saturated and efficient lipolysis can proceed only if the ratio of substrate particles to LPL is adjusted to a more normal range.

Animals↗

PubMed1998

Isolation of synaptotagmin as a receptor for types A and E botulinum neurotoxin and analysis of their comparative binding using a new microtiter plate assay.

Clostridium botulinum neurotoxin acts on nerve endings to block acetylcholine release. Binding of the neurotoxin to a membrane receptor through its heavy chain is the first essential step in its mode of toxin action. Type E botulinum neurotoxin (BoNT/E) or type A botulinum neurotoxin (BoNT/A) receptor was purified from rat brain synaptosomes employing a neurotoxin affinity column chromatography. The protein fraction eluted from the affinity column with 0.5 M NaCl contained a 57 kDa protein as a major eluant. Immunoblotting the eluant with anti-synaptotagmin antibodies revealed that the 57 kDa protein was synaptotagmin I. Rat synaptotagmin I has been suggested as the receptor for BoNT/B (Nishiki et al., J. Biol. Chem. 269, 10498-10503, 1994) in rat brain. In this study, binding of BoNT/A and BoNT/E to synaptotagmin I was studied by a microtiter plate-based method. Binding of synaptotagmin I to BoNT/A coated on the plate was competitively reduced upon preincubation of the proteins with BoNT/E, suggesting a competitive binding of BoNT/A and BoNT/E to the receptor. Taken together, these results suggest that the same receptor protein binds to all three BoNT serotypes tested.

Animals↗

PubMed1998

Do changes in the hydration of the diabetic human lens precede cataract formation?

Cataract formation in diabetic lenses has been attributed to polyol-osmotic pressure-generated influx of water. The ensuing swelling in the form of pocket and lake accumulations cause light scattering. The authors tested whether clear lenses of diabetic patients show different hydration properties than age matched normal lenses. Normal and diabetic human lenses were investigated for their nonfreezable water content by differential scanning calorimetry. The total water content of the lens sections were studied by thermogravimetric analysis. Non-cataractous diabetic lenses in all three regions showed a higher total water content than normal lenses. The nonfreezable water content, seems to increase with age in diabetic lenses and decrease with age in normal human lenses. Thus, hydration changes in human diabetic lenses precede cataract formation. While syneresis, the release of bound water into the bulk, is part of the normal aging process, it appears to occur in the younger diabetics only. In older diabetics syneresis is halted or even reversed. This may be due to the glycation of lens proteins in diabetic patients which tends to immobilize water and therefore, reverse the syneresis due to aging.

Adult↗

PubMed1997

Role of gamma-carboxyglutamic acid in the calcium-induced structural transition of conantokin G, a conotoxin from the marine snail Conus geographus.

Conantokin G is a gamma-carboxyglutamic acid- (Gla-) containing conotoxin isolated from the venom of the marine cone snail Conus geographus. This 17-residue polypeptide, which contains five gamma-carboxyglutamic acid residues, is a N-methyl-d-aspartate- (NMDA-) type glutamate receptor antagonist. To investigate the role of gamma-carboxyglutamic acid in the calcium-induced structural transition of conantokin G, we determined the three-dimensional structure of the conantokin G/Ca2+ complex by two-dimensional 1H NMR spectroscopy and compared it to the high-resolution structure of conantokin G in the absence of metal ions [Rigby et al. (1997) Biochemistry 36, 6906]. Complete resonance assignments were made by two dimensional 1H NMR spectroscopy at pH 5.6 in the presence of saturating amounts of Ca2+. Distance geometry and simulated annealing methods were used to derive 23 convergent structures from a set of 302 interproton distance restraints and two torsion angle measurements. A high-resolution structure, with the backbone root mean square deviation to the geometric average of the 23 structures of 0.6 +/- 0.1 A, contains a linear alpha-helix from Gla 3 to Lys 15. Gla residues 3, 7, 10, and 14 are aligned in a linear array on one face of the helix. A genetic algorithm was applied to determine the calcium positions in conantokin G, and the conantokin G/Ca2+ complex refined by molecular simulation. Upon binding of Ca2+ to gamma-carboxyglutamic acid, conantokin G undergoes a conformational transition from a distorted curvilinear 310 helix to a linear alpha-helix. Occupancy of the metal binding sites, defined by gamma-carboxyglutamic acids, results in formation of a calcium-carboxylate network that linearizes the helix and exposes the hydrophobic amino acids on the opposite face of the helix.

1-Carboxyglutamic Acid↗

PubMed1997

A long-lived, highly luminescent Re(I) metal-ligand complex as a biomolecular probe.

A highly luminescent rhenium (I) metal-ligand complex [Re(bcp)(CO)3(4-COOHPy)](ClO4), where bcp is 2,9-dimethyl-4,7-diphenyl-1,10-phenanthroline and 4-COOHPy is isonicotinic acid, has been synthesized and characterized. High quantum yields (> 0.5) and long excited-state lifetimes (0.3-10 micronseconds) in fluid solutions at room temperature were found for this complex, with remarkable emission sensitivity to microenvironment. This compound also displays highly polarized emission with a maximum anisotropy near 0.3 in the absence of rotational diffusion. This Re complex was conjugated to several biomolecules, including the proteins human serum albumin and bovine immunoglobulin G, as well as an amine-containing lipid. When bound to a protein or lipid, the decay time is near 3 microseconds and the quantum yield is approximately 0.12 in aqueous oxygenated solution at room temperature. This compound's unique spectral properties along with its conjugatability allowed us to utilize it as biomolecular probe in a variety of environments.

Anisotropy↗

PubMed1997

Separate bisphosphatase domain of chicken liver 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase: the role of the C-terminal tail in modulating enzyme activity.

The separate bisphosphatase domain (amino acid residues 243-468) of the chicken liver bifunctional enzyme 6-phosphofructo-2-kinase-fructose-2,6-bisphosphatase was expressed in Escherichia coli and purified to homogeneity. The fructose-2, 6-bisphosphatase activity of the separate domain was 7-fold higher than that of the native bifunctional enzyme, and exhibited substrate inhibition characteristic of the native enzyme. The inhibition of the enzymes by fructose 2,6-bisphosphate could be overcome by Pi, glycerol 3-phosphate and GTP. Deletion of 30 amino acid residues from the C-terminus of the separate domain resulted in around a 5-fold increase in the Vmax of the bisphosphatase. Also, the truncated form was more accessible to chemical modification by diethyl pyrocarbonate and N-ethylmaleimide, suggesting a more open structure than the wild-type form. In addition, the mutation of cysteine-389 to alanine increased bisphosphatase activity by 20% and the Km value for fructose 2,6-bisphosphate by 3-fold, and both the point mutation at cysteine-389 and the deletional mutation led to the predominantly insoluble expression of the enzyme. The results indicated that the C-terminal tail plays a role in modulating the enzyme activity and suggested that the difference in the C-terminal tail sequence is responsible for the difference in activity of the chicken and rat liver fructose-2,6-bisphosphatases. It is postulated that an interaction between the C-terminal tail and the active site might be present.

Animals↗

PubMed1997

Alx-4: cDNA cloning and characterization of a novel paired-type homeodomain protein.

Homeodomain containing transcription factors serve important functions in patterning the embryo during vertebrate development. We have isolated cDNA clones encoding a novel protein, named Alx-4, that contains a paired-type homeodomain. Analysis of the homeodomain sequence shows that Alx-4 belongs to a family of genes that are related to the Drosophila gene aristaless, and includes the mammalian genes Alx3, Cart-1, MHox, and S8. We have analyzed the expression of Alx-4 during development by Northern blot and whole mount in situ hybridization. In addition, we have generated antibodies to recombinant Alx-4 protein and identified Alx-4 protein in nuclear extracts prepared from mouse embryos. The expression pattern of Alx-4 suggests that it may play a role in the patterning of structures derived from craniofacial mesenchyme, the first branchial arch, and the limb bud. Our results provide a starting point for the analysis of a new member of the family of paired type homeodomain proteins.

Amino Acid Sequence↗

PubMed1997

Brain-derived neurotrophic factor fails to arrest neuromuscular disorders in the paralysé mouse mutant, a model of motoneuron disease.

Several new neurotrophic factors have been recently identified and shown to prevent motoneuron death in vitro and in vivo. One such agent is brain-derived neurotrophic factor (BDNF). In this study, we tested BDNF on an animal model of early-onset motoneuron disease: the paralysé mouse mutant, characterized by a progressive skeletal muscle atrophy and the loss of 30-35% of spinal lumbar motoneurons between the first and second week post-natal. The results show that subcutaneous injections of 1 or 10 mg/kg BDNF did not have any significant effect in increasing the mean survival time of mutant mice or in preventing the loss of motor function and total body weight in paralysé mice. The weight and choline acetyltransferase activity of specific muscles and the number of motoneurons in the spinal cords were identical in BDNF-treated and placebo-injected paralysé mice. These results suggest that BDNF does not act on the disease process in paralysé mice in the conditions we used. By contrast, BDNF has previously been shown to partially prevent the loss of motor function in the wobbler mouse, a suggested model of later-onset motoneuron disease. Taken together these findings suggest that BDNF acts differently on early and late-onset motoneuron diseases. It is however possible that treatment of paralysé mice with BDNF or combinations of different neurotrophic factors prior to the phenotypical expression of the paralysé mutation may prevent the loss of motor function and motoneurons in mutant mice.

Animals↗

PubMed1997

Hypersensitivity of Ku80-deficient cell lines and mice to DNA damage: the effects of ionizing radiation on growth, survival, and development.

We recently have shown that mice deficient for the 86-kDa component (Ku80) of the DNA-dependent protein kinase exhibit growth retardation and a profound deficiency in V(D)J (variable, diversity, and joining) recombination. These defects may be related to abnormalities in DNA metabolism that arise from the inability of Ku80 mutant cells to process DNA double-strand breaks. To further characterize the role of Ku80 in DNA double-strand break repair, we have generated embryonic stem cells and pre-B cells and examined their response to ionizing radiation. Ku80(-/-) embryonic stem cells are more sensitive than controls to gamma-irradiation, and pre-B cells derived from Ku80 mutant mice display enhanced spontaneous and gamma-ray-induced apoptosis. We then determined the effects of ionizing radiation on the survival, growth, and lymphocyte development in Ku80-deficient mice. Ku80(-/-) mice display a hypersensitivity to gamma-irradiation, characterized by loss of hair pigmentation, severe injury to the gastrointestinal tract, and enhanced mortality. Exposure of newborn Ku80(-/-) mice to sublethal doses of ionizing radiation enhances their growth retardation and results in the induction of T cell-specific differentiation. However, unlike severe combined immunodeficient mice, radiation-induced T cell development in Ku80(-/-) mice is not accompanied by extensive thymocyte proliferation. The response of Ku80-deficient cell lines and mice to DNA-damaging agents provides important insights into the role of Ku80 in growth regulation, lymphocyte development, and DNA repair.

Animals↗

PubMed1997

Cell-cycle regulation of DNA damage-induced expression of the suppressor gene PML.

The promyelocytic leukemia (PML) gene, which encodes a growth- and transformation-suppressor, has been identified at the non-random chromosomal translocation break point t(15; 17)(q22; q12) of acute promyelocytic leukemia. To elucidate if PML may play a role in cellular response to DNA damage, PML expression was analyzed by immunofluorescence staining in HeLa cells treated with ionizing radiation (IR) and cisplatin. Our studies demonstrated IR at 20Gy, and cisplatin at 6 micrograms/ml caused more than 5-10 fold increases in PML protein expression in the PML Oncogenic Domain (POD) by immunofluorescent staining. Northern blotting showed that there was no gross increase in mRNA levels indicating that the induction is a post-transcriptional event. Flow cytometry showed that HeLa cells treated with IR were progressively arrested in G1, which correlates with the optimal expression of PML in the cell cycle. To determine if PML expression was under the control of the tumor suppressor p53, which is known to arrest cells in G1, HeLa cells were transfected with the wild-type p53 gene. PML expression in p53 transduced cells were 5-10 fold higher than the control, indicating that the enhanced expression of PML is apparently dependent on the p53 pathway. These data also indicate that PML may play an important role in cellular response to DNA damage such as DNA repair or apoptosis during G1 arrest.

Blotting, Northern↗

PubMed1997

Myc represses transcription of the growth arrest gene gas1.

Cell proliferation is regulated by the induction of growth promoting genes and the suppression of growth inhibitory genes. Malignant growth can result from the altered balance of expression of these genes in favor of cell proliferation. Induction of the transcription factor, c-Myc, promotes cell proliferation and transformation by activating growth promoting genes, including the ODC and cdc25A genes. We show that c-Myc transcriptionally represses the expression of a growth arrest gene, gas1. A conserved Myc structure, Myc box 2, is required for repression of gas1, and for Myc induction of proliferation and transformation, but not for activation of ODC. Activation of a Myc-estrogen receptor fusion protein by 4-hydroxytamoxifen was sufficient to repress gas1 gene transcription. These findings suggest that transcriptional repression of growth arrest genes, including gas1, is one step in promotion of cell growth by Myc.

3T3 Cells↗