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Biomedical subjects

L Li

Publications and source records attributed to L Li.

At least 1,477 records · Page 82Linked to original sources
PubMed1996

[Effect of organic fertilizer and mineral fertilizer on the tuber yield of Curcuma longa L].

Regression method of orthogonal conic substitution with factors was employed to build up the tuber models for yield, quality and benefit. Three main measures affecting the tuber yield, quality and benefit were analyzed by these mathematical models. The effect of agronomic measures on the tuber yield is human and livestock excreta, rape cake > Ca3(PO4)2 > KCl. The optimal combination of farming practices has been obtained according to the analysis of these models.

Fertilizers↗
PubMed1995

Inactivation and conformation changes of the glycated and non-glycated D-glyceraldehyde-3-phosphate dehydrogenase during guanidine-HCl denaturation.

The glycated D-glyceraldehyde-3-phosphate dehydrogenases have been isolated from rabbit muscle and erythrocytes (He et al. (1995) Biochem. J. 309, 133-139). The circular dichroism spectrum in the near-ultraviolet of gGAPDH was different from that of GAPDH. Changes in intrinsic protein fluorescence and in the 410 nm fluorescence of the NAD derivatives introduced at the active sites of both the glycated and non-glycated GAPDH from rabbit were compared on inactivation during denaturation in GuHCl. Complete inactivation for the non-glycated enzyme occurred in 0.5 M GuHCl solution, however, that for the glycated enzyme occurred in the 0.35 M solution. The kinetic inactivation of gGAPDH was a biphasic process (the fast and slow phases). The fast phase for gGAPDH was faster than that of GAPDH. The kinetic exposure of the fluorescent NAD derivatives at the active sites of both enzymes was also biphasic with fast phase rates which approach those of the inactivation. It appears that glycation of the enzyme may disturb the spatial geometry of the functional groups responsible for the catalytic mechanism and affect the activity.

Animals↗
PubMed1995

Positive regulation of human alpha 1 (I) collagen promoter activity by transcription factor Sp1.

Analysis of the regulatory promoter region of the human alpha 1 (I) collagen-encoding gene (COL1A1) gene indicated the presence of G+C-rich sequence elements that are potential binding sites for the transcription factor Sp1. As a step toward understanding transcriptional regulation of the human COL1A1, we examined Sp1 binding in the promoter region using DNase I footprinting, and analyzed the effect of Sp1 expression on COL1A1 promoter activity in transiently transfected Drosophila melanogaster cells in vivo. The results indicated that recombinant human Sp1 interacted specifically with two G+C-rich sequences within the COL1A1 promoter. Binding of factors in nuclear extracts prepared from human dermal fibroblasts to a 22-nucleotide deoxyribonucleotide (oligo) spanning the 5' G+C-rich sequence required Zn2+, and was abolished by excess Sp1 consensus binding site oligos, or by anti-Sp1 antibodies. Studies in which a series of progressively 5'-deleted COL1A1 promoter::cat constructs were co-expressed with an Sp1 expression plasmid in a cellular background devoid of Sp1 homology demonstrated that Sp1 markedly enhanced the COL1A1 promoter activity. These results suggest that the transcriptional activity of the human COL1A1 can be positively regulated by Sp1.

Adult↗
PubMed1995

Different effects of two aldose reductase inhibitors on nociception and prostaglandin E.

This study examined the effect of two structurally dissimilar aldose reductase inhibitors, N-[[5-(trifluoromethyl)-6-methoxy-1- napthalenyl]thioxomethyl]-N-methlyglycine (tolrestat) and 4-amino-2,6-dimethylphenyl-sulphonyl nitromethane (ICI 222155), on formalin-evoked behavioural responses in control and diabetic rats and on capsaicin-evoked release of prostaglandin E from spinal cord slices in vitro. Both compounds, given orally for 4 weeks, prevented hyperalgesia in diabetic rats 5-20 min after hindpaw formalin injection. ICI 222155 also prevented hyperalgesia in diabetic rats 21-60 min after formalin, whereas tolrestat suppressed activity in diabetic rats below controls and also suppressed activity in controls when given orally or intrathecally. Capsaicin-evoked release of prostaglandin E from spinal cord slices of control rats was significantly reduced by tolrestat, but not ICI 222155. These data suggest that hyperalgesia in diabetic rats is related to glucose metabolism by aldose reductase, whereas tolrestat has specific effects on formalin-evoked nociception associated with an ability to reduce spinal prostaglandin release.

Aldehyde Reductase↗
PubMed1995

Dual-analyte fiber-optic sensor for the simultaneous and continuous measurement of glucose and oxygen.

A fiber-optic sensor for the continuous and simultaneous determination of glucose and oxygen is described. The sensor is comprised of dual-analyte sensing sites in defined positions on the distal end of an imaging fiber (350 microns o.d.). Each sensing site is an individual polymer cone covalently attached to the activated fiber surface using localized photopolymerization. The oxygen sensor consists of a double-layer polymer cone. The inner polymer cone is a hydrophobic gas-permeable copolymer containing an oxygen-sensitive ruthenium dye, and the outer layer is a poly(hydroxyethyl methacrylate) (HEMA) polymer. The glucose sensor is an oxygen sensor with a poly-HEMA outer layer containing immobilized glucose oxidase. The fluorescence images of both sensing sites are captured with a CCD camera, and the measured fluorescence intensities are related to analyte concentrations. Oxygen quenching data for both sensing sites fit a two-site Stern-Volmer quenching model. The sensor has been used to simultaneously monitor independent changes in glucose and oxygen concentrations. Glucose calibration curves were obtained under varying oxygen tensions, and the detection limit is 0.6 mM glucose. The effect of fluctuations in oxygen partial pressure on the glucose response can be used to calibrate the sensor. The sensor response time varies from 9 to 28 s, depending on the different thicknesses of the enzyme layer. The sensor maintains the same sensitivity for 2 days. Multiple glucose sensing sites with different enzymatic activities can be immobilized on the distal end of the fiber, affording control of the linear range.

Fiber Optic Technology↗
PubMed1995

Rescue of adult mouse motoneurons from injury-induced cell death by glial cell line-derived neurotrophic factor.

Glial cell line-derived neurotrophic factor (GDNF) has been shown to rescue developing motoneurons in vivo and in vitro from both naturally occurring and axotomy-induced cell death. To test whether GDNF has trophic effects on adult motoneurons, we used a mouse model of injury-induced adult motoneuron degeneration. Injuring adult motoneuron axons at the exit point of the nerve from the spinal cord (avulsion) resulted in a 70% loss of motoneurons by 3 weeks following surgery and a complete loss by 6 weeks. Half of the loss was prevented by GDNF treatment. GDNF also induced an increase (hypertrophy) in the size of surviving motoneurons. These data provide strong evidence that the survival of injured adult mammalian motoneurons can be promoted by a known neurotrophic factor, suggesting the potential use of GDNF in therapeutic approaches to adult-onset motoneuron diseases such as amyotrophic lateral sclerosis.

Animals↗
PubMed1995

Direct analysis of enzymatic reactions of oligosaccharides in human serum using matrix-assisted laser desorption ionization mass spectrometry.

Matrix-assisted laser desorption ionization mass spectrometry has been developed for direct mass analysis of enzymatic reaction products of oligosaccharides in human blood serum without the use of extraction or chromatographic separation. Molecular labeling of the substrate is used to achieve both the detection sensitivity and selectivity required in rapid analysis of reaction products in serum. It is found that tetramethylrhodamine (TMR)-labeled oligosaccharides provide 100-fold sensitivity enhancement over the corresponding underivatized oligosaccharides. In order to selectively retain the TMR-labeled molecules on the sample probe while washing away contaminants in a serum sample, a sample/matrix preparation method is developed. This technique provides detection sensitivity of labeled oligosaccharides in the range of hundreds of femtomoles per microliter. The mass measurement accuracy is better than 0.01% when a linear time-of-flight mass spectrometer is used. The application of the technique is illustrated for the subpicomole detection and quantitation of the conversion of the disaccharide alpha Fuc(1-->2)beta Gal-TMR to the blood group B active trisaccharide alpha Fuc(1-->2)[alpha Gal(1-->3)]beta Gal-TMR, catalyzed by the blood group B galactosyltransferase present in human serum.

Enzymes↗
PubMed1995

Impairment of axonal development and of synaptogenesis in hippocampal neurons of synapsin I-deficient mice.

Synapsin I, the most abundant of all neuronal phosphoproteins, is enriched in synaptic vesicles. It has been hypothesized to regulate synaptogenesis and neurotransmitter release from adult nerve terminals. The evidence for such roles has been highly suggestive but not compelling. To evaluate the possible involvement of synapsin I in synaptogenesis and in the function of adult synapses, we have generated synapsin I-deficient mice by homologous recombination. We report herein that outgrowth of predendritic neurites and of axons was severely retarded in the hippocampal neurons of embryonic synapsin I mutant mice. Furthermore, synapse formation was significantly delayed in these mutant neurons. These results indicate that synapsin I plays a role in regulation of axonogenesis and synaptogenesis.

Animals↗
PubMed1995

Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice.

Synapsin I has been proposed to be involved in the modulation of neurotransmitter release by controlling the availability of synaptic vesicles for exocytosis. To further understand the role of synapsin I in the function of adult nerve terminals, we studied synapsin I-deficient mice generated by homologous recombination. The organization of synaptic vesicles at presynaptic terminals of synapsin I-deficient mice was markedly altered: densely packed vesicles were only present in a narrow rim at active zones, whereas the majority of vesicles were dispersed throughout the terminal area. This was in contrast to the organized vesicle clusters present in terminals of wild-type animals. Release of glutamate from nerve endings, induced by K+,4-aminopyridine, or a Ca2+ ionophore, was markedly decreased in synapsin I mutant mice. The recovery of synaptic transmission after depletion of neurotransmitter by high-frequency stimulation was greatly delayed. Finally, synapsin I-deficient mice exhibited a strikingly increased response to electrical stimulation, as measured by electrographic and behavioral seizures. These results provide strong support for the hypothesis that synapsin I plays a key role in the regulation of nerve terminal function in mature synapses.

Animals↗
PubMed1995

Inhibition of nucleotide excision repair by the cyclin-dependent kinase inhibitor p21.

p21, a p53-induced gene product that blocks cell cycle progression at the G1 phase, interacts with both cyclin-dependent kinases and proliferating cell nuclear antigen (PCNA). PCNA functions as a processivity factor for DNA polymerases delta and epsilon and is required for both DNA replication and nucleotide excision repair. Previous studies have shown that p21 inhibits simian virus 40 (SV40) DNA replication in HeLa cell extracts by interacting with PCNA. In this report we show that p21 blocks nucleotide excision repair of DNA that has been damaged by either ultraviolet radiation or alkylating agents, and that this inhibition can be reversed following addition of PCNA. We have determined that p21 is more effective in blocking DNA resynthesis than in inhibiting the excision step. We further show that a peptide derived from the carboxyl terminus of p21, which specifically interacts with PCNA, inhibits polymerase delta-catalyzed elongation of DNA chains almost stoichiometrically relative to the concentration of PCNA. When added at higher levels, this peptide also blocks both SV40 DNA replication and nucleotide excision repair in HeLa cell extracts. These results indicate that p21 interferes with the function of PCNA in both in vitro DNA replication and nucleotide excision repair.

Amino Acid Sequence↗
PubMed1995

17-beta-Estradiol stimulation of endothelial K+ channels.

Whole-cell membrane current recordings under voltage clamp were made from freshly isolated rabbit aortic endothelial cells. Intracellular Ca2+ signals of fura-2 loaded both native single aortic endothelial cells and intact endothelium from rabbit cardiac valves were measured using imaging fluorescence microscopy. Application of 17-beta-estradiol stimulated rapid discharge of transient outward currents and induced an increase in the intracellular free Ca2+ concentration ([Ca2+]i. The stimulated discharge of outward currents and [Ca2+]i were reduced by extracellulary applied tetraethylammonium (TEA).

Animals↗
PubMed1995

Unexpected presence of polyreactive catalytic antibodies in IgG from unimmunized donors and decreased levels in rheumatoid arthritis.

Polyclonal IgG from healthy humans and unimmunized mice was screened for peptide-methylcoumarinamide (peptide-MCA) hydrolyzing activity. The activity was detected in every IgG sample examined. Contaminant enzymes were precluded as an explanation, as the activity tracked exactly with the 150-kDa IgG peak separated by gel filtration in denaturing solvent (6 M guanidine hydrochloride) and with the 50-kDa Fab fragment peak produced by papain-digestion of the IgG. Patients with rheumatoid arthritis displayed a 3.2-fold reduced peptide-MCA hydrolyzing activity (mean) compared to healthy subjects. Control osteoarthritis patients showed no diminution in activity. A progressive decrease in the activity by 7.4-fold of the pre-immune levels was observed in mice over the course of hyperimmunization with SRBC, indicating that exogenous Ag challenge, like rheumatoid arthritis, is associated with decreased catalytic activity. Apparent Km values of the IgG for Pro-Phe-Arg-MCA were 0.39 to 0.53 mM, values approximately 3-orders of magnitude greater than observed previously for Ag-specific catalysis by Abs. The only common structural feature in peptide-MCA conjugates utilized by the Abs as substrates was the presence of Arg-MCA and Lys-MCA bonds. The IgG hydrolyzed Pro-Phe-Arg-Phe at the Arg-Phe peptide bond, showing that the activity is relevant to cleavage of peptide bonds in natural Ags. The universal occurrence of this polyreactive catalytic activity in unimmunized donors and its diminution in an autoimmune disease and nonspecific Ag challenge suggest that it may possess an important, but as yet unidentified, biologic role.

Adult↗
PubMed1995

The Cockayne syndrome group A gene encodes a WD repeat protein that interacts with CSB protein and a subunit of RNA polymerase II TFIIH.

The hereditary disease Cockayne syndrome (CS) is characterized by a complex clinical phenotype. CS cells are abnormally sensitive to ultraviolet radiation and are defective in the repair of transcriptionally active genes. The cloned CSB gene encodes a member of a protein family that includes the yeast Snf2 protein, a component of the transcriptional regulator Swi/Snf. We report the cloning of the CSA cDNA, which can encode a WD repeat protein. Mutations in the cDNA have been identified in CS-A cell lines. CSA protein interacts with CSB protein and with p44 protein, a subunit of the human RNA polymerase II transcription factor IIH. These observations suggest that the products of the CSA and CSB genes are involved in transcription.

Amino Acid Sequence↗
PubMed1995

Incremental doses of dobutamine induce a biphasic response in dysfunctional left ventricular regions subtending coronary stenoses.

BACKGROUND: Dobutamine stress echocardiography has been proposed as a diagnostic tool to identify viable myocardium. How regional wall thickening responds to dobutamine in the ischemic or short-term hibernating myocardium has not been adequately defined. We hypothesized that regional wall thickening would improve initially and subsequently deteriorate with incremental doses of dobutamine in viable myocardial regions supplied by a stenotic coronary artery. This study was undertaken to determine whether this biphasic pattern of regional function characterizes the response of ischemic or hibernating myocardium to dobutamine and to explore the factors and mechanisms that determine this response. METHODS AND RESULTS: Twenty-six pigs in four groups were studied: a control group (n = 5) to assess the response of myocardium perfused by nonstenotic coronary artery to incremental doses of dobutamine, and three experimental groups with a left anterior descending coronary artery stenosis producing acute myocardial ischemia (n = 7), short-term myocardial hibernation for 90 minutes (n = 7), and short-term hibernation for 24 hours (n = 7) to determine the functional and metabolic response to dobutamine under these conditions. Regional coronary flow was reduced to 40% to 60% of baseline, with significant reductions of regional wall thickening as measured by two-dimensional echocardiography and sonomicrometers. An incremental dobutamine infusion from 2.5 to 25 micrograms.kg-1.min-1 increased wall thickening and coronary flow without lactate production in the control group. In the other three groups, during the incremental dobutamine infusion, regional wall thickening improved initially, from 11.4 +/- 7.5% to 19.8 +/- 11.4%, P < .01, at dobutamine doses of 2.5 to 10 (4.5 +/- 2.2) micrograms.min-1.kg-1 but deteriorated subsequently to 5.0 +/- 5.8% at the maximal dose of dobutamine of 12.6 +/- 4.1 micrograms.min-1.kg-1. The initial improvement of regional wall thickening was associated with a small increase in regional coronary flow (from 0.53 +/- 0.18 to 0.68 +/- 0.25 mL.min-1.g-1 myocardium, P < .05) and with regional lactate production. High doses of dobutamine did not further increase regional coronary flow but markedly increased lactate production and induced regional myocardial acidosis (pH 7.26 +/- 0.07). The biphasic pattern of response to dobutamine was observed in each of the three experimental groups. Both peak improvement and peak deterioration occurred earlier and at lower dobutamine dose levels in the group with acute ischemia compared with the group with short-term hibernation for 24 hours (P < .05). CONCLUSIONS: A biphasic response of wall thickening to incremental dobutamine with initial improvement and subsequent deterioration is characteristic of ischemic or short-term hibernating myocardium. The initial low-dose dobutamine infusion improved wall thickening in the ischemic or hibernating myocardial region to a modest level. This initial modest improvement was transient and at the expense of metabolic deterioration of myocardial ischemia, so that at higher doses during prolonged dobutamine infusion, wall thickening deteriorated, lactate accumulated, and myocardial acidosis developed.

Animals↗
PubMed1995

Insulin-like growth factor-I is an autocrine regulator for the brain metastatic variant of a human non-small cell lung cell line.

Insulin-like growth factor (IGF-I) is associated with autocrine and paracrine stimulation for cell growth and development of brain tumor cells. The function of IGF-I in the brain metastatic variant of human lung cancer cells is investigated. The cells used here were derived in vivo with intracarotid injection of human non-small cell lung carcinoma NCI-H226. The tumor was developed as a cultured cell line, H226Br. Unlike the parental cells, H226Br was tumorigenic in nu/nu nude mice. Reverse transcriptase-polymerase chain reaction showed that IGF-I transcript of H226Br is increased compared to that of parental cells. The amount of IGF-I secreted in cultured medium of H226Br is higher than that of cultured parental cells. The IGF-I receptor-specific antibody, alpha IR3, inhibits H226Br growth in serum-free culture. The results established that IGF-I is an autocrine growth regulator for human non-small cell lung cancer cells that progressed to brain.

Animals↗