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Biomedical subjects

T Li

Publications and source records attributed to T Li.

At least 361 records · Page 20Linked to original sources
PubMed1997

[Outward character and inner quality of Bombyx Batryticatus, Carapax Trionycis, Squama Manitis and endothelium corneum Gigeriae Galli after frying].

According to the requirement for outward character in processing traditional Chinese medicines, Bombyx Batryticatus, Carapax Trionycis, Squama Manitis and Endothelium Corneum Gigeriae Galli, which are four kinds of often used traditional Chinese animal medicines, were fried, the contents of amino acids in each kind were determined, and investigate the inner quality of each kind of the processed product was investigated with reference to other standards.

Amino Acids↗
PubMed1997

[Chemical studies on peptidepolysaccharides of Ganoderma lucidum (W. Curt. Fr.) Karst].

Seven homogeneous peptidepolysaccharides have been obtained from the fruit-body of Ganoderma lucidum. The main constituents are TGLP-2, TGLP-3, TGLP-6 and TGLP-7, whose molecular weights are 20.9 x 10(4), 4.5 x 10(4), 3.2 x 10(4) and 10 x 10(4) respectively. TGLP-2 is a heteroglycan peptide, TGLP-3 and TGLP-6 are glycan peptides and TGLP-7 is a galactan peptide.

Drugs, Chinese Herbal↗
PubMed1997

[Experimental study on antitumor effect in vitro of modified DNL of oral squamous cell carcinoma with TNF-alpha gene].

The gene coding for TNF-alpha was introduced into DNL of human oral squamous carcinoma by retroviral-mediated gene transduction, and experiments proved that the gene had been introduced into the DNL and the DNL could secrete TNF-alpha of high activity with PCR analysis, bioactivity analysis of TNF-alpha, selection test in G418. Cytotoxicity of gene-transduced and nontransduced DNL to Tca8113 cell was compared with MTT method. The result showed that cytotoxicity of the former was higher than that of the latter.

Carcinoma, Squamous Cell↗
PubMed1997

[Dual wavelength multiplication subtractive spectrophotometric determination of sulfadiazinum and trimethoprimum in compound sulfadiazine tablets].

This paper described the simultaneous determination of sulfadiazine (SD) and trimethoprim (TMP) in tablets co-Trimediazini by dual wavelength spectrophotometry multriplication subtractive method. This method was based on the measurement of both absorbance of standard solution of SD (8-14) x 10(-6)g/mL, TMP (1-2) x 10(-6)g/mL and sample solution at wavelength 242.5 nm and 228.0nm. The average recovery and RSD of SD and TMP were 100.60%, 0.33% and 98.27%, 1.58%, respectively (n=20). The method was simple, quick and results satisfactory.

Drug Combinations↗
PubMed1997

[Surface photovoltaic spectroscopic investigation of Bacteriorhodopsin (BR)].

The surface photovoltaic spectra (SPS) of Bacteriorhodopsin-based films were systematically measured. The results show that the BR films are characterized by the specific photovoltaic effect. The SPS response of the BR films depends on the fabrication and humidity of the film. The intermediate M412 and O640 of BR are observed in the SPS of HEPES-containing BR film, indicating that HEPES has very important function to stabilize intermediate M412. The observations are explained in terms of the photocycle of BR and the mechanism of photovoltage generation.

Bacteriorhodopsins↗
PubMed1997

Alcohol dehydrogenase-2*3 allele protects against alcohol-related birth defects among African Americans.

Considerable variation in offspring outcome is observed after intrauterine alcohol exposure. The underlying mechanism may include genetic diversity in the enzymes responsible for alcohol metabolism. Of the known genetic polymorphisms, differences at the alcohol dehydrogenase-2 locus (ADH2) are likely most critical because the resulting enzymes are >30-fold different in their kinetic constants. To test whether differences in maternal or offspring ADH2 genotype are determinants of risk for alcohol-related birth defects, maternal-infant pairs (n = 243) were enrolled on the basis of maternal alcohol intake during pregnancy and maternal ADH2 genotype. Infant outcome was measured using the Bayley Scales of Infant Development Mental Index (MDI) at 12 months of age. Drinking during pregnancy was associated with lower MDI scores but only in the offspring of mothers without an ADH2*3 allele (P < .01, analysis of variance, post hoc). The offspring of drinking women with at least one ADH2*3 allele had MDI scores similar to those of nondrinking women of either ADH2 genotype. Lower MDI scores were associated with the three-way interaction among increasing alcohol intake and maternal and offspring absence of the ADH2*3 allele (P < .01, multiple linear regression). We suggest that the protection afforded by this allele is secondary to its encoding of the high-Km/high-Vmax ADH beta3 isoenzyme, which would provide more efficient alcohol metabolism at high blood alcohol concentrations. These observations are supportive of alcohol, rather than acetaldehyde, being the more important proximate teratogen and are the first observations of a specific genetic explanation for susceptibility differences to alcohol-related birth defects.

Abnormalities, Drug-Induced↗
PubMed1997

Adriamycin depresses in vivo and in vitro phosphatidylethanolamine N-methylation in rat heart sarcolemma.

Adriamycin, an effective anticancer chemotherapeutic agent, causes an insidious and delayed cardiotoxicity. Different subcellular abnormalities including calcium transport changes in the sarcolemma (SL) as well as downregulation of the adrenergic system have been shown to be associated with the development of this cardiomyopathy. Since both of these activities are influenced by phospholipid methylation, effects of adriamycin on the three catalytic sites of SL phosphatidylethanolamine N-methyltransferase were examined. Rats were administered with a cumulative dose of adriamycin (15 mg/kg) over 2 weeks and examined after 3 weeks. Vehicle injected animals served as controls. Dyspnea, high mortality rate, ascites and decrease in aortic and left ventricular systolic pressure, as well as increase in left ventricular end diastolic pressure were seen in the adriamycin group. Myocardial cell damage typical of adriamycin cardiomyopathy, i.e. sarcotubular swelling, vacuolization and myofibrillar drop-out, was also apparent. Total methyl group incorporation into SL phosphatidylethanolamine using radiolabeled S-adenosyl-L-methionine as the donor was significantly depressed in the 3 week group at catalytic sites II and III. Decreased production of methylated intermediates, phosphatidyl-N-monomethylethanolamine and phosphatidyl-N,N-dimethylethanolamine as well as phosphatidylcholine (PC) was seen. Depression of phosphatidylethanolamine N-methylation was also noticed when SL, isolated from untreated hearts, was exposed in vitro to different concentrations (10, 100 and 1000 microM) of adriamycin. Inhibition of phosphatidylethanolamine N-methylation appears to be mediated by adriamycin-induced increase in the oxidative stress and may contribute in the pathogenesis of subcellular changes associated with this cardiomyopathy.

Analysis of Variance↗
PubMed1997

Highly efficient induction of sugar beet plant regeneration.

A method for high-frequency in vitro regeneration of adventitious shoots from petiole explants of a tetraploid breeding line 405 of Beta vulgaris L. was established. Plant regeneration was obtained by direct bud formation from petioles. Explants were precultured in a medium containing MS inorganic salts supplemented with Gamborg's vitamins, named MSB. Adventitious shoots were developed when petiole explants excised from 20-30-day-old seedlings grown on MSB containing 0.3 mg/L naphthalene acetic acid (NAA), 1.0 mg/L 6-benzylaminopurine (BA), and were then cultured on MS with 0.3 mg/L NAA and 1.0 mg/L BA. Shoots rooted on half-strength MS medium containing 0.5-1.0 mg/L NAA. This procedure of the culture method may be very useful both for multiplication of sugar beet and for the introduction of foreign genes into Beta vulgaris. The proliferation rate of induced plantlets is as high as 51.3%.

Chenopodiaceae↗
PubMed1997

[Digital subtraction angiography and selective arterial embolization in the treatment of vascular tumors in nasopharynx and nasal sinuses].

The paper presents the treatment of vascular tumors in nasopharynx and nasal sinuses with digital subtraction angiography (DSA) and selective arterial embolization. By using preoperative embolization of blood supply arteries, the intraoperative bleeding was reduced significantly, the tumors were shrank and the tumor limits were clear. We recommend that DSA and selective arterial embolization should be used as a routine preoperative method adjunct to surgery for the treatment of vascular tumors of nasopharynx and nasal sinuses.

Adolescent↗
PubMed1997

[The relations between mutations of p53 anti-oncogene in atherosclerosis and levels of lipids in serum].

OBJECTIVE: To further understanding the pathogenesis of human atherosclerosis, we studied the mutations of p53 anti-oncogene in Chinese atherosclerosis lesions and the relations between p53 gene mutations with the levels of serum lipoprotein and the contents of lipids in AS tissues. METHODS: p53 gene mutations were detected by a-32P-dCTP labelled radiative PCR-SSCP and the biochemical analyses of lipids in serum and AS tissues. RESULTS: In 89 cases studied, 9 were found the p53 gene multi-hotsports exons mutations. The TC, TG and CE contents in vascular AS tissues in p53 gene mutation group were higher than those in non-mutations group (ANOV: F = 4.56-9.97, P < 0.05-0.01, no differences in PL contents). But there were no statistic differences in serum levels of TC, TG, CE and apoAI between the two groups (P > 0.05-0.25). All the levels of the serum lipoproteins studied were almost in normal ranges. CONCLUSION: The DNA structural mutations of p53 anti-oncogene in Chinese adults' AS tissues have remarkable relations with the severity of AS lesions. The mutations of p53 gene may play some important roles in the formation of human atherosclerosis. In addition to serum lipid disorders, this may be a new mechanism in the pathogenesis of human atherosclerosis.

Adult↗
PubMed1996

Transgenic mice carrying the dominant rhodopsin mutation P347S: evidence for defective vectorial transport of rhodopsin to the outer segments.

To explore the pathogenic mechanism of dominant mutations affecting the carboxyl terminus of rhodopsin that cause retinitis pigmentosa, we generated five lines of transgenic mice carrying the proline-347 to serine (P347S) mutation. The severity of photoreceptor degeneration correlated with the levels of transgene expression in these lines. Visual function as measured by the electroretinogram was approximately normal at an early age when there was little histologic evidence of photoreceptor degeneration, but it deteriorated as photoreceptors degenerated. Immunocytochemical staining showed the mutant rhodopsin predominantly in the outer segments prior to histologically evident degeneration, a finding supported by quantitation of signal intensities in different regions of the photoreceptor cells by confocal microscopy. A distinct histopathologic abnormality was the accumulation of submicrometer-sized vesicles extracellularly near the junction between inner and outer segments. The extracellular vesicles were bound by a single membrane that apparently contained rhodopsin as revealed by ultrastructural immunocytochemical staining with anti-rhodopsin antibodies. The outer segments, although shortened, contained well-packed discs. Proliferation of the endoplasmic reticulum as reported in Drosophila expressing dominant rhodopsin mutations was not observed. The accumulation of rhodopsinladen vesicles likely represents aberrant transport of rhodopsin from the inner segments to the nascent disc membranes of the outer segments. It is possible that photoreceptor degeneration occurs because of a failure to renew outer segments at a normal rate, thereby leading to a progressive shortening of outer segments, or because of the loss of cellular contents to the extracellular space, or because of both.

Animals↗
PubMed1996

Measurement of genetic structure within populations using Moran's spatial autocorrelation statistics.

Spatial structure of genetic variation within populations, an important interacting influence on evolutionary and ecological processes, can be analyzed in detail by using spatial autocorrelation statistics. This paper characterizes the statistical properties of spatial autocorrelation statistics in this context and develops estimators of gene dispersal based on data on standing patterns of genetic variation. Large numbers of Monte Carlo simulations and a wide variety of sampling strategies are utilized. The results show that spatial autocorrelation statistics are highly predictable and informative. Thus, strong hypothesis tests for neutral theory can be formulated. Most strikingly, robust estimators of gene dispersal can be obtained with practical sample sizes. Details about optimal sampling strategies are also described.

Biological Evolution↗
PubMed1996

Induction of alpha-helix in the beta-sheet protein tumor necrosis factor-alpha: thermal- and trifluoroethanol-induced denaturation at neutral pH.

The unfolding and refolding of alpha-helical proteins has been extensively studied, demonstrating formation of intermediate structures which retain the native-like alpha-helix but lack the tertiary structure. Studies on the folding of proteins consisting primarily of beta-sheet are interesting since, unlike the alpha-helix, the beta-sheet requires the formation of peptide hydrogen bonds between two or more polypeptide segments which may be far apart in the linear sequence. Here we have studied the unfolding of the beta-sheet-containing protein tumor necrosis factor-alpha (TNF-alpha). This protein exists as a symmetric trimer in solution. Murine TNF-alpha begins to melt at 60 degrees C and unfolds to a soluble structure with a transition midpoint of 66 degrees C. This reaction is irreversible. This unfolded form contains a considerable amount of (approximately 30%) alpha-helix, as determined by circular dichroism. Human TNF-alpha begins to melt at 60 degrees C and precipitates concurrently with unfolding, such that there is no soluble protein present by 70 degrees C. The secondary and tertiary structures of murine TNF-alpha unfold simultaneously, suggesting that unfolding from the native to the unfolded state occurs cooperatively. The thermal-induced denaturation is very insensitive to protein concentration, indicating that trimer to monomer conversion, if it occurs, is not rate-limiting. Trifluoroethanol induces alpha-helix in both human and murine TNF-alpha, further demonstrating the propensity of TNF-alpha to form alpha-helix. The different behavior of human versus murine TNF-alpha upon thermal unfolding is due to differences in the solubility of the unfolded protein, the murine form being more soluble. These results indicate that TNF-alpha can form alpha-helix when the long range interactions conferred by the native structure are removed during unfolding.

Animals↗
PubMed1996

Induction of alpha-helix in the beta-sheet protein tumor necrosis factor-alpha: acid-induced denaturation.

Acid-induced unfolding of proteins often results in an intermediate structure, called the molten globule structure or "A" state, which retains at least partial secondary structure but lacks a rigid tertiary structure. Acid-induced unfolding has been studied extensively for alpha-helical proteins, while few studies have been done on proteins containing only beta-strands. Tumor necrosis factor-alpha (TNF-alpha) is a trimer in which the individual subunits consist of antiparallel beta-sheet, organized into a jellyroll beta-sandwich. We have found previously [Narhi et al. (1996) Biochemistry 35, 11447-11453] that thermal denaturation of TNF-alpha results in an aggregate which contains a substantial amount of alpha-helix and that the addition of trifluoroethanol induces alpha-helix in both murine and human TNF-alpha. Here we show that acid also can induce alpha-helix in these proteins. At acidic pH (below 4), both human and murine TNF-alpha convert to a monomeric form, as determined by sedimentation and diffusion constants obtained from sedimentation velocity experiments. The sedimentation coefficient indicated that this monomer was only slightly expanded relative to the native state. Near-UV circular dichroic (CD) analysis showed a loss of tertiary structure. These structural features coincide with the notion that the acid-induced structure of TNF-alpha is a molten globule. What is unique in this protein is that TNF-alpha acquires alpha-helical structure, which is not present in the native structure as determined by both CD and Fourier transform infrared spectroscopy. Even more surprising is that TNF-alpha at pH 3.3 undergoes a very gradual noncooperative change in secondary structure upon heating, which results in an increase in alpha-helical content. At pH 2.2 in the absence of salt, TNF-alpha shows considerable alpha-helix, although heating does not change the spectrum. At pH 2.2, physiological salt decreases the amount of alpha-helix at ambient temperature, and upon heating, we see the noncooperative increase in alpha-helix as observed at pH 3.3 with low salt. The addition of salt at low pH induces reassociation but to a range of oligomers rather than a unique trimer structure. This acid-induced formation of an alpha-helical monomer of TNF-alpha may be related to its known interaction with lipid bilayers.

Animals↗
PubMed1996

The serotonin transporter is a potential susceptibility factor for bipolar affective disorder.

The serotonin transporter is a strong candidate for aetiological involvement in affective disorders and psychosis. We analysed a VNTR in intron 2 of the human serotonin transporter gene (hSERT) for allelic association with bipolar affective disorder, unipolar depression and schizophrenia. An increased frequency of allele 12 of the VNTR was observed in subjects with bipolar affective disorder (n = 191; chi 2 p = 0.00048 by allele) but not unipolar depression (n = 86; chi 2 p = 0.18, ns) or schizophrenia (n = 129; chi 2 p = 0.08, ns), although a trend towards an excess of allele 12 was observed for the latter. There was also a significant difference in the frequency of allele 12 between bipolar affective disorder and unipolar depression (p = 0.0087). The relative risk for bipolar affective disorder with respect to allele 12 was 1.84 (95% CI 0.97-3.56) for heterozygotes, and 3.10 (95% CI 1.60-6.07) for homozygotes, with evidence for a gene-dosage effect. Because allele 12 is common in the population, the attributable risk is 50.8% (95% CI 14.5%-73.3%). We hypothesize that either the VNTR affects regulation of expression of hSERT at the transcriptional level or it is in linkage disequilibrium with another functional polymorphism in the gene, and this results in an increased risk for the development of bipolar affective disorder.

Alleles↗
PubMed1996

Mechanism of NO-induced oxidation of myoglobin and hemoglobin.

Nitric oxide (NO) has been implicated as mediator in a variety of physiological functions, including neurotransmission, platelet aggregation, macrophage function, and vasodilation. The consumption of NO by extracellular hemoglobin and subsequent vasoconstriction have been suggested to be the cause of the mild hypertensive events reported during in vivo trials of hemoglobin-based O2 carriers. The depletion of NO from endothelial cells is most likely due to the oxidative reaction of NO with oxyhemoglobin in arterioles and surrounding tissue. In order to determine the mechanism of this key reaction, we have measured the kinetics of NO-induced oxidation of a variety of different recombinant sperm whale myoglobins (Mb) and human hemoglobins (Hb). The observed rates depend linearly on [NO] but show no dependence on [O2]. The bimolecular rate constants for NO-induced oxidation of MbO2 and HbO2 are large (k.ox,NO = 30-50 microM-1 s-1 for the wild-type proteins) and similar to those for simple nitric oxide binding to deoxygenated Mb and Hb. Both reversible NO binding and NO-induced oxidation occur in two steps: (1) bimolecular entry of nitric oxide into the distal portion of the heme pocket and (2) rapid reaction of noncovalently bound nitric oxide with the iron atom to produce Fe(2+)-N=O or with Fe(2+)-O-O delta- to produce Fe(3+)-OH2 and nitrate. Both the oxidation and binding rate constants for sperm whale Mb were increased when His(E7) was replaced by aliphatic residues. These mutants lack polar interactions in the distal pocket which normally hinder NO entry into the protein. Decreasing the volume of the distal pocket by replacing Leu(B10) and Val(E11) with aromatic amino acids markedly inhibits NO-induced oxidation of MbO2. The latter results provide a protein engineering strategy for reducing hypertensive events caused by extracellular hemoglobin-based O2 carriers. This approach has been explored by examining the effects of Phe(B10) and Phe(E11) substitutions on the rates of NO-induced oxidation of the alpha and beta subunits in recombinant human hemoglobin.

Animals↗
PubMed1996

PDGF-A is required for normal murine cardiovascular development.

Several lines of evidence suggest that platelet-derived growth factor A chain (PDGF-A) is required for normal embryonic cardiovascular development. To test this directly, we introduced anti-PDGF-A neutralizing antibodies into mouse deciduas in utero at Embryonic Days (E) 8.5, 9.5, and 10.5. This resulted in the selective disruption of PDGF-A ligand-receptor interactions in vivo for a period of 18-24 hr and allowed us to assess both if PDGF-A is required for cardiovascular development and when it is required. Embryos collected 48 hr after antibody treatment displayed severe cardiovascular abnormalities. These included both atrial and ventricular myocardial hypertrophy, epicardial and endocardial abnormalities, and aortic dilation, among others. Although heart abnormalities were observed in embryos treated at all three ages, they were more common in embryos treated at E8.5. In contrast, only embryos treated at E10.5 exhibited significant aortic dilation. This work (1) demonstrates directly for the first time that PDGF-A is required for normal cardiovascular development, (2) identifies several processes that require PDGF-A, and (3) defines discreet developmental periods during which these PDGF-A-dependent processes require the factor.

Animals↗