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Biomedical subjects

L Cui

Publications and source records attributed to L Cui.

At least 145 records · Page 8Linked to original sources

Histopathological analysis of invasive bladder carcinomas induced by 3,2'-dimethyl-4-aminobiphenyl in hamsters.

Histopathological characteristics of urinary bladder tumors induced in Syrian golden hamsters by 3,2'-dimethyl-4-aminobiphenyl (DMAB) were analyzed. DMAB was subcutaneously injected in corn oil at a concentration of 100 mg/kg once a week for 20 weeks and ethinyl estradiol (EE) was administered in the diet at a dose of 0.75 ppm throughout the experiment. A small group of animals was killed at week 20 and all survivors were killed at week 50. Urinary bladder carcinomas were induced in 14 of 18 hamsters (78%; 0.89/animal) in the DMAB+EE group and 11 of 17 (65%; 0.88/animal) in the DMAB alone group in males, and in 11 of 14 (79%; 0.79/animal) in the DMAB+EE group and 4 of 5 (80%; 0.80/animal) in the DMAB alone group in females examined between weeks 20 and 50. All were non-papillary invasive transitional cell carcinomas partly demonstrating glandular and/or squamous differentiation, and most carcinomas developed in the bladder neck. Degree of invasion was clearly correlated with degree of morphological atypism in the transitional cell carcinomas, but not with squamous or glandular differentiation. No sex difference or modifying effect of EE on DMAB urinary bladder carcinogenesis was evident. No bladder carcinomas were observed in non-DMAB-treated animals.

Aminobiphenyl Compounds↗

Direct effects of testosterone, dihydrotestosterone and estrogen on 3,2'-dimethyl-4-aminobiphenyl-induced prostate carcinogenesis in castrated F344 rats.

The present experiment was carried out to explore the effect of endogenous androgen on rat prostate carcinogenesis induced by 3,2'-dimethyl-4-aminobiphenyl (DMAB) and testosterone propionate (TP) or 5alpha-dihydrotestosterone (DHT) with or without ethinyl estradiol (EE). In order to eliminate the influence of endogenous androgen, F344 rats were orchiectomized just after initiation with the prostate carcinogen, DMAB, and then given TP, DHT, TP plus EE or DHT plus EE for 40 weeks. The results demonstrated that while administration of TP following DMAB treatment causes invasive carcinomas in the lateral and anterior prostate and seminal vesicles, DHT does not exhibit equivalent effects. Synergistic enhancement was also evident with TP plus EE, but not with DHT plus EE. The incidences of prostatic and seminal vesicle lesions in all groups of the present experiment, except for the group given castration without hormonal supplement, were equivalent to those previously found in non-castrated animals. Therefore, the present findings indicate that endogenous testosterone may not be required for promotion by TP/EE of DMAB-initiated prostate carcinogenesis and that it may not contribute to the actions of DHT.

Aminobiphenyl Compounds↗

Dose-dependent induction of 8-hydroxyguanine and preneoplastic foci in rat liver by a food-derived carcinogen, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline, at low dose levels.

Male F344 rats were administered 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) in the diet at doses of 200, 50, 12.5, 3.2, 0.8, 0.2 and 0.05 ppm for six weeks, and partially hepatectomized 1 week after the beginning of MeIQx administration. Quantitative values for glutathione S-transferase placental form (GST-P)-positive foci in the liver were dose-dependently increased by the MeIQx treatment. 8-Hydroxyguanine (8-OHG) levels assessed after 1 week of dietary MeIQx administration were also dose-dependently increased, although the effect was no longer observed at the end of the treatment period. The correlation between numbers of GST-P-positive foci at week 6 and 8-OHG levels at week 1 was linear, values for both parameters being higher than the control levels even in the 0.8 ppm dose group. These findings indicate that, in addition to the previously reported MeIQx-DNA adduct formation, DNA modifications due to oxidative damage may play an important role in MeIQx liver carcinogenesis in rats.

Animals↗

[Quantitative study on the effect of osthole on proximal tibiae in ovariectomized (OVX) rats].

Thirty-one 3-month-old Female Sprague-Dawley rats were randomly divided into 5 groups, basal control (group 1, killed at the begining), aging control (group 2), ovariectomized (OVX, group 3), OVX with nilestriol treatment group (group 4) and OVX with osthole treatment group (group 5). Group 2 and group 3 ig with water 5 ml.kg-1 and group 5 ig with osthole 6.7 mg.kg-1, all once a day for 6 d; group 4 ig with nilestriol 1 mg.kg-1, once a week. After 12 weeks, all rats were killed. The proximal tibiae of rats were processed to undecalcified sections at 20 microns thickness for histomorphometric analysis. OVX was shown to reduce markedly the trabecular bone mass (%Tb. Ar-59%) due to increase of bone turnover with the result that bone resorption exceeded bone formation, as compared with aging controls. In contrast, treatment of OVX rats with Osthole and nilestriol increased significantly the trabecular area (increased 68% and 27.1% compared with that of OVX respectively). Our results indicate that osthole and nilestriol treatment provides protection against osteoporosis in OVX rats. The protective mechanism of osthole and nilestriol involves supression of bone turnover, but the effects of osthole is lower than that of nilestriol (trabecular area decreased 55% more in osthole group than that with nilestriol treatment). Our finding may provide theoretical evidence for the clinical use of osthole or nilestriol for treatment and prevention of osteoporosis.

Animals↗

A comparative study of intravenous accelerated streptokinase dose regimen with conventional dose regimen for coronary thrombolysis.

The aim of this study is to test the patency rate and safety of the accelerated streptokinase dose regimen for coronary thrombolysis compared with the conventional one. One hundred and four patients entering three hospitals up to 12 hours after the onset of definite acute myocardial infarction were randomizely treated with intravenous accelerated streptokinase dose regimen (1.5 million units/30 min) (group A, 47 cases) and conventional dose regimen (1.5 million units/60 min) (group B, 57 casese). The reperfusion rate of infarct-related arteries determined by clinical evidence of reperfusion was 76.6% (36/47) in group A VS 61.4% (35/57) in group B. There was significant difference in reperfusion rates among patients within 6 hours after the onset of chest pain: 87.9% (29/33) in group A VS 67.4 (29/43) in group B (P < 0.05). The incidence of mild bleeding, allergic reaction, hypotension was 12.8% (6/47), 4.3% (2/47), 12.8 (6/47) respectively in group A vs 21.1 (12/57), 3.5 (2/57), 17.5% (10/57) respectively in group B. Compared to conventional dose regimen, intravenous accelerated streptokinase dose regimen for coronary thrombolysis seems to improve reperfusion rate markedly without increasing adverse events such as bleeding, allergic reaction and hypotension. It suggests that accelerated streptokinase therapy deserves more extensive investigation.

Aged↗

Site-directed mutagenesis of conserved histidines in the helix VIII domain of PsaB impairs assembly of the photosystem I reaction center without altering spectroscopic characteristics of P700.

The chloroplast psaB gene encodes one of the polypeptides of the photosystem I reaction center heterodimer that coordinates the electron transfer components P700, A0, and A1. Histidine residues in the most highly conserved region of the PsaB protein are predicted to coordinate the P700 reaction center chlorophyll(s) and the initial electron acceptor, A0. Oligonucleotide-mediated site-directed mutagenesis and chloroplast transformation of Chlamydomonas reinhardtii have been used to determine the importance of these conserved histidines in photosystem I reaction center biogenesis and function. It is demonstrated that these histidine residues are essential for stable accumulation of the photosystem I reaction center. Protein pulse-labeling shows that changing the histidine residues impairs a post-translational step in reaction center assembly. Photosystem I complexes from the mutants have been characterized by Electron Nuclear Double Resonance and Electron Spin Echo Envelope Modulation spectroscopy to determine the impact of any mutations on P700+. In all cases we determine that spectroscopic characteristics of P700+ remain unchanged. The implications of these results to current models of the photosystem I reaction center and related bacterial reaction centers are discussed.

Amino Acid Sequence↗

Olfactory event-related potentials in normal human subjects: effects of age and gender.

Behavioral and electrophysiological testing of olfactory function was performed in 33 normal human male and female subjects, 18-83 years of age. Acuity for odor identification and odor detection was verified by standard psychophysical tests. For evoked potential testing, a constant flow olfactometer provided odorant stimuli (amyl acetate) or air control stimuli that were presented to the right nostril by a nasal cannula at a flow rate of 5 l/min, duration of 40 msec and random interstimulus intervals of 6-30 sec. The behavioral tests revealed no significant difference between males and females, whereas increasing age was associated with a decline in performance on the odor identification test. No reproducible evoked potentials were recorded in response to the air control stimulus. Potentials to the odorant stimulus consisted of 4 components named P1, N1, P2 and N2. A significant correlation was found between P2 latency and odor identification test scores, suggesting a relationship between the generation of the P2 component and olfactory processing. P2 peak latency increased significantly with age at 2.5 msec/year. An age-related decline in N1-P2 interpeak amplitude was seen in male subjects. Topographic differences were seen in the P2 peak amplitude and the N1-P2 and P2-N2 interpeak amplitudes such that their amplitudes were greatest at Cz and Pz. On average, N1-P2 interpeak amplitudes were larger in the female subjects than in the male subjects, possibly revealing a hormonal influence on the olfactory event-related potential.

Adolescent↗

Cellular and molecular events leading to mitochondrial toxicity of 1-(2-deoxy-2-fluoro-1-beta-D-arabinofuranosyl)-5-iodouracil in human liver cells.

We have explored the mechanism(s) related to FIAU-induced liver toxicity, particularly focusing on its effect on mitochondrial function in a human hepatoma cell line-HepG2. The potential role of FMAU and FAU, metabolites detected in FIAU-treated patients were also ascertained. FIAU and FMAU inhibited cell growth and were effectively phosphorylated. A substantial increase in lactic acid production in medium of cells incubated with 1-10 microM FIAU or FMAU was consistent with mitochondrial dysfunction. Slot blot analysis demonstrated that a two week exposure to 10 microM FIAU or FMAU was not associated with a decrease in total mitochondrial (mt) DNA content. However, FIAU and FMAU were incorporated into nuclear and mtDNA and relative values suggest that both compounds incorporate at a much higher rate into mtDNA. Electron micrographs of cells incubated with 10 microM FIAU or FMAU revealed the presence of enlarged mitochondria with higher cristae density and lipid vesicles. In conclusion, these data suggest that despite the lack of inhibition of mtDNA content, incorporation of FIAU and FMAU into mtDNA of HepG2 cells leads to marked mitochondrial dysfunction as evidenced by disturbance in cellular energy metabolism and detection of micro- and macrovesicular steatosis.

Adenosine Triphosphate↗

[Impact of placental hormone withdrawal on postpartum depression].

Prenatal and postpartum measurements of serum beta-hCG, estradiol (E2) and progesterone (P) concentration were done by radioimmunoassay in 20 cases of postpartum depression (PD) and 20 cases without postpartum depression (NPD). The results showed significantly higher serum levels of P and beta-hCG (at 36-37 gestational week) in PD, but no difference in the serum P and beta-hCG concentration between the PD and NPD after childbirth. The falling of the two hormones was faster in PD than in NPD. In neither prenatal nor postpartum test was any difference seen in serum E2 concentration between PD and NPD. These results suggest that supposely, the endogenous risk factor, the rapid withdrawal of the placental hormones (P and beta-hCG) after delivery, leads to PD.

Chorionic Gonadotropin↗

[A study on duration of using VCu200 intrauterine device].

OBJECTIVE: To make certain of the duration of using V-copper 200mm2 intrauterine device (VCu200 IUD). METHODS: Six hundreds and sixty six pieces of VCu200 IUD used for different time period and removed for various reasons were analyzed. The life span of VCu200 IUD depended on corrosion, fragmentation and damage of copper wire and these parameters were measured on VCu200 IUD removed. RESULTS: There were significant difference in copper wire fragmentation rate between tenth year-group and fifteenth year group which were 12.36%, 25.53% respectively (P < 0.001), and so were the expulsion rate of copper wire 2.54%, 9.57% respectively (P < 0.05). The copper loss and copper releasing rate in tenth year-group were 39.73%, 22.95%micrograms/day respectively. Copper corrosion resulted in fragmentation of copper wire which occurred the earliest in three years of use and expulsion of copper wire segment occurred after five years of use. CONCLUSION: Comparing the above results with other copper intrauterine devices, it was suggested that the suitable duration of VCu200 IUD use was ten years.

Equipment Failure↗

Phenotypic alteration of hepatocellular foci in rats treated with clofibrate and phenobarbital.

In male F344 rats pretreated with diethylnitrosamine (DEN), subsequent administration of clofibrate increased the proportion of eosinophilic foci, to become the most abundant type, and reduced numbers of basophilic, clear and vacuolated foci, the total not being changed. A similar shift towards eosinophilia was also observed in phenobarbital-treated animals, but in this case clear increases in total number and area were apparent. Expression of the glutathione S-transferase placental form (GST-P) in foci was much lowered by clofibrate treatment, while the proportion of positive foci was very high in both phenobarbital and control groups. A marked contrast was found with eosinophilic foci, with 74% positive after phenobarbital as compared to only 15% for clofibrate. Thus, the decrease in GST-P positive foci by clofibrate was mainly due to increased negativity in the most abundant eosinophilic type foci. In a long-term feeding study without DEN initiation, similar negativity of foci was observed and, furthermore, only minimal effects of clofibrate on foci development was revealed in both young and old animals.

Animals↗

In vitro mutational spectrum of aflatoxin B1 in the human hypoxanthine guanine phosphoribosyltransferase gene.

The in vitro mutational spectrum of aflatoxin B1 (AFB1) in exon 3 of the human hypoxanthine guanine phosphoribosyltransferase gene in B-lymphoblasts was examined by a combination of polymerase chain reaction and denaturing gradient gel electrophoresis. The cell line used in this study contained an expression vector that produced high levels of human cytochrome P450 CYP1A1. CYP1A1 metabolizes AFB1 to form an epoxide intermediate which can react with DNA. About 1200 independent mutants were induced at the hypoxanthine guanine phosphoribosyltransferase locus by AFB1 and were selected en masse by addition of 6-thioguanine to the bulk culture. Two independent cultures were treated with AFB1. Polymerase chain reaction was used to amplify exon 3 from the complex mutant population, and denaturing gradient gel electrophoresis was used to separate wild-type DNA sequences from mutant sequences. Mutational hotspots were visible as discrete bands on the denaturing gradient gel. Scanning densitometry was used to determine the fraction of the complex population that was represented in each non-wild-type band. The bands containing the mutations were excised from the denaturing gradient gel and sequenced. In this way, the nature and frequency of mutational hotspots in a population of > 1000 mutants were determined. AFB1 produced one strong mutational hotspot in exon 3. Between 10 and 17% of the AFB1-induced mutants contained a single GC-->TA base substitution at base pair 209. This hotspot occurred in a GGGGGG sequence (the mutated base is underlined). This mutation was observed reproducibly in two independently treated cultures. Several other mutations were observed in only one culture but at a lower frequency. Our results are the first report of the mutational spectrum of AFB1 in a native human gene.

Aflatoxin B1↗

Database and software for the analysis of mutations in the human p53 gene.

Mutations of the human p53 gene are of importance in the development of cancer. Perhaps 50% of all human cancers contain a mutation in the p53 oncogene and many laboratories are investigating mutations at this locus. In an effort to centralize and standardize the information regarding human p53 mutations, we have created a computerized database that contains information about DNA sequence alterations for > 3000 p53 mutants. Information on the cancer type, the origin of the cells, the specific mutation, the amino acid change, the literature citation, and other data are provided for each mutant. We have also produced a software package for the analysis of the p53 database. Routines have been developed for the analysis of single-base substitutions, including programs to (a) determine whether two mutational spectra are different, (b) display the number of mutations and mutable sites in each exon, (c) determine whether mutations show a DNA strand bias, (d) determine the frequency of transitions and transversions, (e) display the number and kind of mutations observed at each base in the coding region, (f) perform nearest neighbor analysis, and (g) display mutable amino acids in the p53 protein. The software runs only on IBM-compatible machines with MS-DOS. The software and p53 database are freely available via the Internet, using the remote file transfer protocol. These programs simplify the analysis of the rapidly increasing body of information about p53 mutations. The programs permit facile comparison between different p53 data sets, as well as the identification of mutational patterns that may be of importance to experimenters studying the mechanisms of mutation and the etiology of cancers.

Base Sequence↗