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Biomedical subjects

L Cui

Publications and source records attributed to L Cui.

At least 73 records · Page 4Linked to original sources
PubMed2000

Suppressive effects of dietary genistin and daidzin on rat prostate carcinogenesis.

High intake of phytoestrogens through soybeans and their products is thought to be associated with low incidences of prostate and / or breast cancer in Asian countries. Possible chemopreventive effects of genistin or daidzin on rat prostate carcinogenesis were therefore investigated. Male F344 rats were given 10 biweekly subcutaneous injections of 3,2'-dimethyl-4-aminobiphenyl (DMAB) and then either genistin or daidzin in the diet at a concentration of 0.1% for 40 weeks. Other groups of rats given DMAB were treated with genistin or daidzin together with a high dose of testosterone propionate (TP). Both genistin and daidzin reduced the numbers of ventral prostate carcinomas (P < 0.05), with a tendency for decrease in incidence. Invasive carcinomas which developed in the anterior prostate and seminal vesicles with TP were, however, not influenced by the two isoflavones. Thus, the present data suggest that genistin and daidzin possess anti-cancer effects at relatively early stages of prostate cancer development, providing experimental support for epidemiological findings.

Aminobiphenyl Compounds↗
PubMed2000

Differential effects of antiretroviral nucleoside analogs on mitochondrial function in HepG2 cells.

Numerous studies have reported effects of antiviral nucleoside analogs on mitochondrial function, but they have not correlated well with the observed toxic side effects. By comparing the effects of the five Food and Drug Administration-approved anti-human immunodeficiency virus nucleoside analogs, zidovudine (3'-azido-3'-deoxythymidine) (AZT), 2',3'-dideoxycytidine (ddC), 2', 3'-dideoxyinosine (ddI), 2',3'-didehydro-2',3'-deoxythymidine (d4T), and beta-L-2',3'-dideoxy-3'-thiacytidine (3TC), as well as the metabolite of AZT, 3'-amino-3'-deoxythymidine (AMT), on mitochondrial function in a human hepatoma cell line, this issue has been reexamined. Evidence for a number of mitochondrial defects with AZT, ddC, and ddI was found, but only AZT induced a marked rise in lactic acid levels. Only in mitochondria isolated from AZT (50 microM)-treated cells was significant inhibition of cytochrome c oxidase and citrate synthase found. Our investigations also demonstrated that AZT, d4T, and 3TC did not affect the synthesis of the 11 polypeptides encoded by mitochondrial DNA, while ddC caused 70% reduction of total polypeptide content and ddI reduced by 43% the total content of 8 polypeptides (including NADH dehydrogenase subunits 1, 2, 4, and 5, cytochrome c oxidase subunits I to III, and cytochrome b). We hypothesize that in hepatocytes the reserve capacity for mitochondrial respiration is such that inhibition of respiratory enzymes is unlikely to become critical. In contrast, the combined inhibition of the citric acid cycle and electron transport greatly enhances the dependence of the cell on glycolysis and may explain why apparent mitochondrial dysfunction is more prevalent with AZT treatment.

Anti-HIV Agents↗
PubMed2000

Contribution of a thickened cell wall and its glutamine nonamidated component to the vancomycin resistance expressed by Staphylococcus aureus Mu50.

Staphylococcus aureus Mu50, which has reduced susceptibility to vancomycin, has a remarkably thickened cell wall with an increased proportion of glutamine nonamidated muropeptides. In addition, Mu50 had enhanced glutamine synthetase and L-glutamine D-fructose-6-phosphate aminotransferase activities, which are involved in the cell-wall peptidoglycan synthesis pathway. Furthermore, significantly increased levels of incorporation of (14)C-labeled D-glucose into the cell wall was observed in Mu50. Unlike a femC mutant S. aureus strain, increased levels of production of nonamidated muropeptides in Mu50 was not caused by lower levels of glutamine synthetase activity but was considered to be due to the glutamine depletion caused by increased glucose utilization by the cell to biosynthesize increased amounts of peptidoglycan. After the cells were allowed to synthesize cell wall in the absence or presence of glucose and glutamine, cells with different cell-wall thicknesses and with cell walls with different levels of cross-linking were prepared, and susceptibility testing of these cells demonstrated a strong correlation between the cell-wall thickness and the degree of vancomycin resistance. Affinity trapping of vancomycin molecules by the cell wall and clogging of the outer layers of peptidoglycan by bound vancomycin molecules were considered to be the mechanism of vancomycin resistance of Mu50. The reduced cross-linking and the increased affinity of binding to vancomycin of the Mu50 cell wall presumably caused by the increased proportion of nonamidated muropeptides may also contribute to the resistance to some extent.

Bacterial Proteins↗
PubMed2000

Making rats rise to erect bipedal stance for feeding partially prevented orchidectomy-induced bone loss and added bone to intact rats.

The objectives of this study were to investigate the different effects on muscle mass and cancellous (proximal tibial metaphysis [PTM]) and cortical (tibial shaft [TX]) bone mass of sham-operated and orchidectomized (ORX) male rats by making rats rise to erect bipedal stance for feeding. Specially designed raised cages (RC) were used so that the rats had to rise to erect bipedal stance to eat and drink for 12 weeks. Dual-energy X-ray absorptiometry (DEXA) and peripheral quantitative computerized tomography (pQCT) were used to estimate the lean leg mass and bone mineral. Static and dynamic histomorphometry were performed on the triple-labeled undecalcified sections. We found that making the intact rats rise to erect bipedal stance for feeding increased muscle mass, cortical bone volume, and periosteal bone formation. Orchidectomy increased net losses of bone next to the marrow by increasing bone turnover. Making the ORX rats rise to erect bipedal stance increased muscle mass, partially prevented cancellous bone loss in the PTM, and prevented net cortical bone loss in TX induced by ORX by depressing cancellous and endocortical high bone turnover and stimulating periosteal bone formation. The bone-anabolic effects were achieved mainly in the first 4 weeks in the PTM and by 8 weeks in the TX. These findings suggested that making the rats rise to erect bipedal stance for feeding helped to increase muscle mass and cortical bone mass in the tibias of intact rats, increase muscle mass, and partially prevented cancellous and net cortical bone loss in ORX rats.

Animals↗
PubMed2000

Comparison of two PCR techniques used in amplification of microdissected plant chromosomes from rice and wheat.

Linker adaptor-mediated PCR (LAM-PCR) and degenerate oligonucleotide primed PCR (DOP-PCR) are major ways to generate chromosome-specific libraries. In this study, these two PCR techniques were used to amplify the microdissected mitotic and meiotic chromosomes from rice and wheat. The results of amplifications were compared, and the advantages and limitations between the two techniques are presented.

Blotting, Southern↗
PubMed2000

[Experiment research on the mechanism of skin contracture after expansion].

OBJECTIVE: The aim of this study is to observe the repairing process of skin chronic injury due to expansion and explore the mechanism of skin contracture after expansion. METHODS: 20 dogs used in this study were divided randomly into four groups. Skin samples were collected from the back of dogs when expansion finished and 3 months, 6 months, 1 year after expansion. Normal skim from the other side on the back of dogs was used as control group. The dermal ultrastructure was observed by electriscope. The expression of alpha-SMA in dermis at different stage has been analyzed by immunohistochemistry, and the concentration of intracellular free Ca2+ in the fibroblast has been measured by Fura-2 fluorescen indicator. Meanwhile we constructed a 3-dimension system in vitro to analyze the afgfect of different cell density and collagen concentration to fibroblast contracture. RESULTS: (1) The microfilment in fibroblast was fragile, and the features of myofibroblast was absent, the collagen fibers were returned to reticular arrangement along with time. One after expansion few of the collagen remained irregular in arrangement and aparse. (2) After expansion the concentration of Ca2+ increased significantly. (3) In 3-D culture system the density of fibroblasts positively corresponded to fibroblast contracture and the collagen concentration negatively corresponded to it. CONCLUSION: After expansion the dog skin has a structure between scar tissue and thoroughly regeneration skin. Dermal fibroblast is the dynamic source of the skin contracture, meanwhile the density of fibroblast and collagen concentration are two essential factors during skin contracture.

Actins↗
PubMed2000

[Effects of excessive iodine on apoptosis and expression of bcl-2, bax genes in the cells of brain and thyroid gland in guinea pigs].

OBJECTIVE: To investigate the effects of excessive iodine intake on apoptosis and the expression of bcl-2, bax genes in the cells of brain and thyroid gland. METHODS: Guinea pigs, divided into two groups at random, were fed with distilled water containing iodine 50 microg/L (a control group with appropriate iodine) and 10,000 microg/L (a trial group with excessive iodine), respectively for six months. Apoptosis rate and expression of bcl-2, bax gene in the cells of cerebral cortex, hippocampus and thyroid gland in guinea pigs were quantitatively determined by flow cytometry and immunofluorescent techniques. RESULTS: The proportion of apoptosis in the cells of cerebral cortex, hippocampus and thyroid gland was significantly higher in the group with excessive iodine intake than that in the control one (P < 0.01). The level of expression of bcl-2 gene was notably decreased (P < 0.05), but that of bax was notably increased (P < 0.01), in the cerebral cortex, hippocampus and thyroid gland in the group with excessive iodine than in the control one. The ratio of bcl-2 to bax in the cerebral cortex, hippocampus and thyroid gland of the group with excessive iodine was decreased significantly (P < 0.01) than that of the control one. CONCLUSION: Excessive iodine intake may induce apoptosis in the cells of cerebral cortex, hippocampus and thyroid gland. The over-expression of bax gene and the down-regulation of bcl-2, which can then cause the decrease in a ratio of bcl-2 to bax, appear to play an important role in the course of apoptosis induced by excessive iodine intake.

Animals↗
PubMed2000

[The experimental study of intracellular actin in the scar fibroblasts].

OBJECTIVE: To study the relationship between intracellular actin and scar contracture. METHODS: Fibroblasts from 10 cases of hypertrophic scar and 5 cases of keloid were cultured in vitro. Total actin, filamentous actin(F actin), globular actin (G actin) and the ratio of F to G actin(F/G) were measured by densitometry after differential extraction and separation by polyacrylamide gel electrophoresis in the presence of sodium sulfate. RESULTS: Total actin, F actin, G actin and F/G in hypertrophic scar fibroblasts were 2.38 ng/10(4) cells, 0.98 ng/10(4) cells, 1.42 ng/10(4) cells and 0.68 respectively, while in keloid fibroblasts were 1.68 ng/10(4) cells. 0.46 ng/10(4) cells, 1.26 ng/10(4) cells, and 0.36 respectively. There was significant differences between two tissues fibroblasts in the items of total actin, F actin, G actin, and F/G (P < 0.01), while no significant difference in G actin (P > 0.05). CONCLUSION: Total intracellular actin, F actin, and F/G may play an important role in the scar contracture. The hypertrophic scar and keloid can be distinguished by the contents of total intracellular actin, F actin and F/G.

Actins↗
PubMed2000

[Interaction between biofilm formed by Pseudomonas aeruginosa and antibacterial agents].

UNLABELLED: We hypothesized that bacterial biofilm formation could be an important factor that make some infection intractable. Interaction of P. aeruginosa biofilm with antibactial agents was examined in vitro. METHODS: P. aeruginosa incubated for 6 days in a saline-teflon system formed biofilm on the surfaces of the teflon piece. The biofilm were characteried by dense colonization of bacteria and thick membranous structure that covered the colonies, it was observed with a scanning electron microscopy. CPFX, CAM, ROX and Herba Andrographitis were added to the biofilm bacteria. RESULTS: The rate of survial of the floating bacteria decreased to 0.02% after 4 hours of contact with 2MIC of Ciprofloxacin (CPFX), but that of biofilms was 41% When 10 micrograms/mL of Clarithromycin (CAM per mL was combined with CPFX, the survial rate for the biofilm bacteria decreased to 0.2%. When 12 micrograms/mL of Roxithromycin (ROX) was combined with CPFX, the survial rate for the biofilm bacteria decreased to 0.5%. When 0.05 g of Burm. f. per mL was combined with CPFX the survial rate for the biofilm bacteria decreased to 2.7%. CONCLUSION: We conclude that biofilm bacteria are much more resistant to CPFX than the floating bacteria. The combination of CPFX and CAM, ROX HA were more effective in decreasing the biofilm bacteria survial rate than CPFX alone. The results suggest that the combination of CPFX and CAM, ROX, HA can be one of the therapeutic manauvers against biofilm bacteria.

Anti-Bacterial Agents↗
PubMed1999

Carcinogenicity of 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP) in the rat prostate and induction of invasive carcinomas by subsequent treatment with testosterone propionate.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) at 400 ppm in the diet for 52 weeks was found to induce non-invasive microscopic carcinomas in the ventral prostate of the treated rats, in addition to colon and mammary carcinomas. The current experimental data demonstrate that only a 20-week period of PhIP treatment is sufficient for induction of ventral carcinomas and that long-term pharmacological dosing with testosterone propionate which applied through a Silastic tube embedded in the subcutis after PhIP treatment can induce invasive carcinomas in the anterior prostate and seminal vesicles. Thus, PhIP may provide the basis for a good two stage carcinogenesis model for investigation of prostate carcinogenesis.

Animals↗
PubMed1999

Effect of 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl)-5-ethyluracil on mitochondrial functions in HepG2 cells.

The effects of 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl)-5-ethyluracil (D-FEAU) on mitochondrial functions were examined in HepG2 cells. D-FEAU between 0.1 and 10 microM had no apparent inhibitory effect on cell proliferation for 2-week period; however, D-FEAU caused a decrease in mitochondrial DNA (mtDNA) content in a dose-dependent manner with an IC50 value of 2.7 microM. A 20.9% of increase in lactic acid production was observed after the cells were incubated with 10 microM of D-FEAU for 4 days without substantial effect being detected at 0.1 and 1 microM. In addition, no significant changes on mitochondrial morphology were observed in the cells treated with 10 microM of D-FEAU for 14 days under the electron microscope.

Arabinofuranosyluracil↗
PubMed1999

Effects of acute and chronic ethanol exposure on the hepatic gamma-aminobutyric acid transport system in rats.

Ethanol-induced increases in gamma-aminobutyric (GABA)ergic activity contribute to the impairment in hepatic regeneration associated with alcohol-induced liver disease. To determine the mechanism(s) whereby ethanol increases GABAergic activity in the liver, we documented the effects of acute (5 g/kg x 1) and chronic (36% of total calories over 6 weeks) ethanol exposure as well as exogenous GABA (500 microg/g body weight) administration on GABA transport protein (GABA-TP) mRNA expression in the livers of adult male Sprague-Dawley rats at various times (0-72 h) post 70% partial hepatectomy (PHx). We also documented the in vitro effects of ethanol (30-90 microM) on [3H]-GABA uptake in isolated rat hepatocytes. The results of the study revealed that compared to saline-exposed controls, acute but not chronic ethanol exposure resulted in significant decreases in GABA-TP mRNA expression at 12, 24, and 48 h post PHx (saline exposed, 1.04 +/- 0.06, 1.19 +/- 0.21, and 1.15 +/- 0.05. vs. acute ethanol exposed, 0.80 +/- 0.16, 0.88 +/- 0.09, and 0.86 +/- 0.16 optical density units, p < 0.01, 0.05, and 0.05, respectively). An inhibitory effect was also observed following exogenous GABA administration (GABA-TP mRNA expression at 3 h was approximately 40% that of baseline, p < 0.05). [3H]-GABA uptake in isolated rat hepatocytes in vitro was unaffected by the presence of ethanol. In conclusion, the results of this study indicate that acute but not chronic ethanol exposure and exogenously administrated GABA inhibit hepatic GABA-TP mRNA expression following partial hepatectomy in the rat. These findings suggest that the increased GABAergic activity that occurs in the liver following acute ethanol exposure results from alterations in the hepatic GABA transport system at a transcriptional level.

Animals↗
PubMed1999

Removal of multiple arginine-framed trafficking signals overcomes misprocessing of delta F508 CFTR present in most patients with cystic fibrosis.

Many cystic fibrosis transmembrane conductance regulator (CFTR) mutants are recognized as aberrant by the quality control apparatus at the endoplasmic reticulum (ER) and are targeted for degradation. The mechanism whereby nascent chains are distinguished as either competent or incompetent for ER export has not been elucidated. Here we show that export-incompetent chains display multiple arginine-framed tripeptide sequences like the one recently identified in ATP-sensitive K+ channels. Replacement of arginine residues at positions R29, R516, R555, and R766 with lysine residues to inactivate four of these motifs simultaneously causes delta F508 CFTR, present in approximately 90% of CF patients, to escape ER quality control and function at the cell surface. Interference with recognition of these signals may be helpful in the management of CF.

Arginine↗
PubMed1999

Anabolic effect of prostaglandin E2 on cortical bone of aged male rats comes mainly from modeling-dependent bone gain.

In this study, prostaglandin E2 (3 mg/kg per day) was administered to 20-month-old male Wistar rats for 10 and 30 days. Histomorphometric analyses were performed on double-fluorescent-labeled undecalcified tibial shaft sections. Thirty days of prostaglandin E2 (PGE2) administration increased bone formation rate/total bone surface from undetectable levels to 0.6 microm/day at the periosteal surface and from 0.5 to 2.1 microm/day at the endocortical surface. Endocortical osteoid surface area increased from 2% to 67% at day 10 and decreased to 6% at day 30; woven and lamellar bone formation started at day 0, but was most obvious at day 30, resulting in a 12% increase of total bone mass. The red to yellow marrow ratio was 0.2 in pretreatment controls, and increased to 1.6 by day 10 and 2.4 by day 30 with PGE2 administration. Intracortical cavity number and area increased after 10 days of PGE2 treatment, but with forming osteon number and area far exceeding those of resorption cavities at day 30. Endocortical modeling surface/endocortical surface was only 1.5%, and remodeling was 11.1% in pretreatment controls. PGE2 treatment increased modeling to 24.5% in the 10 day group and 93.7% in the 30 day group, whereas remodeling remained unchanged at 10 days, and decreased to 6.2% at 30 days. Osteoprogenitor cells and osteoblasts could not be detected in pretreatment controls, but increased by day 10, and returned almost to control levels by 30 days. Our data indicate that PGE2 induced periosteal and endocortical bone formation mainly by modeling-dependent bone gain, accompanied by increases in intracortical remodeling and red bone marrow, and a transient increase in the osteoprogenitor cells adjacent to the endocortical surface. These findings suggest that 20-month-old male Wistar rats were very responsive to the anabolic action of PGE2 in the tibial shaft, a site consisting mainly of cortical bone and yellow marrow.

Aging↗
PubMed1999

Effective and safe gene therapy for colorectal carcinoma using the cytosine deaminase gene directed by the carcinoembryonic antigen promoter.

We have recently isolated carcinoembryonic antigen (CEA) promoter regions consisting of 419 bp and 204 bp from CEA-producing human colorectal carcinoma (CRC). We constructed CEA419/CD and CEA204/CD retroviruses carrying the bacterial cytosine deaminase (CD) gene directed by the CEA promoter regions. pCD2 retroviruses carrying the CD gene directed by the retrovirus long terminal repeat promoter were also used. CEA419/CD or CEA204/CD retrovirus-infected CRC cells were found to be susceptible to 5-fluorocytosine (5-FC), while non-CRC cells infected with the same retroviruses were not. CD-transduced CRC xenografts in nude mice were sensitive to 5-FC treatment, resulting in arrest of tumor growth. When mice with intraperitoneally disseminated CRCs were given intraperitoneal injections of CEA419/CD retrovirus-producing cells followed by 5-FC treatment, significantly prolonged survival rates were observed compared with animals injected with pCD2 retrovirus-producing cells followed by 5-FC treatment. Importantly, bone marrow suppression was not observed in animals injected with CEA419/CD retrovirus-producing cells and 5-FC, while profound bone marrow suppression was observed in those injected with pCD2 retrovirus-producing cells and 5-FC. These results indicate that effective and safe in vivo gene therapy for advanced CRC may be feasible by transferring the CD gene controlled by the CEA promoter followed by 5-FC treatment.

Animals↗
PubMed1999

Postoperative toxic shock syndrome caused by a highly virulent methicillin-resistant Staphylococcus aureus strain.

We report on a rare fatal case of postoperative toxic shock syndrome caused by infection with a highly virulent methicillin-resistant Staphylococcus aureus strain, designated Sak-1, which was found to be characteristic in its increased production of toxic shock syndrome toxin 1 in human whole blood (about 30-fold more than produced in Tod Hewitt broth). The strain also produced a high level of toxic shock syndrome toxin 1 in the circulating blood of mice experimentally infected with the strain.

Adult↗
PubMed1999

Nitric oxide synthase inhibitor attenuates intestinal damage induced by zinc deficiency in rats.

A nitric oxide synthase (NOS) inhibitor, NG-nitro-L -arginine methyl ester (L-NAME), was given to zinc-deficient (ZD) rats to determine whether it prevents the intestinal damage usually observed under these conditions. Weanling male rats were given free access to a ZD diet (2 mg zinc/kg), whereas control rats including pair-fed (PF) and ad libitum consumption (AL) groups were given a zinc-supplemented (50.8 mg zinc/kg) diet for 4 wk. Half of the ZD rats received L-NAME (0.3 g/L in drinking water) for 3 wk starting at the wk 2 of the deficient period. Plasma zinc concentration in ZD rats was significantly lower (P < 0.05) than that of AL and PF rats. Administration of L-NAME did not alter this concentration. Intestinal zinc concentration did not differ among groups. However, metallothionein-1 (MT-1) mRNA level was significantly lower in the intestine of ZD rats than in AL or PF rats. Treatment of ZD rats with L-NAME did not affect this level. Intestinal microvascular permeability evaluated by Evans blue showed significantly higher extravasation in ZD rats than in AL rats, whereas L-NAME administration inhibited the extravasation. Expression of inducible NOS mRNA was observed in intestine of ZD but not of AL or PF rats, and there was no significant difference between ZD rats, regardless of L-NAME treatment. The activity ratio of inducible NOS to total NOS in ZD rats not receiving L-NAME was significantly higher than that in AL rats or ZD rats treated with L-NAME (P < 0.05). The number of apoptotic-positive and goblet cells in intestinal villi was significantly higher in ZD rats compared with AL or PF rats. L-NAME administration in ZD rats reversed this effect. These results indicate that inhibition of NOS ameliorates zinc deficiency-induced intestinal damage in rats.

Animals↗