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Biomedical subjects

S Zhan

Publications and source records attributed to S Zhan.

35 records · Page 2Linked to original sources
PubMed1999

[The apoptosis and proliferation after photorefractive keratectomy].

OBJECTIVE: To search the correlation between the apoptosis and proliferation of keratocytes and investigate the influence of phototherapeutic keratectomy (PTK) and mechanical epithelial scrape (MES) on keratocyte apoptosis and proliferation. METHODS: Rabbit corneas received photorefractive keratectomy (PRK, -9.9 diopters, 6 mm diameter). Animals were evaluated subsequently up to 6 months after surgery by in vivo confocal microscopy. Corneas were prepared for H.E. staining, corneal cell apoptosis was evaluated by terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) to detect DNA fragmentation. RESULTS: Loss of keratocytes and keratocyte death were found anteriorly in the remaining stroma at 4h after PRK. Activated keratocytes observed by confocal microscopy repopulated within 1 month. A significant elevation of apoptosis was detected in keratocytes and epithelium at 4h, 3d, 1m after PRK. The level of keratocyte apoptosis was parallel to the loss of keratocytes at the early stage and was correlated with keratocyte proliferation in the later stage, PTK-PRK was associated with lower levels of central corneal apoptosis and activated keratocytes than MES-PRK. CONCLUSION: It is suggested that the loss of keratocytes and keratocyte apoptosis be correlated with keratocyte activation and proliferation, which may result in haze and regression after PRK, and PTK-PRK induce lower level of early keratocyte apoptosis and late keratocyte activation than MES-PRK.

Animals↗
PubMed1999

[Excimer laser photorefractive keratectomy for lower to moderate myopia: 5 year follow-up].

OBJECTIVE: To evaluate the long-term effectiveness and safety of photorefractive keratectomy (PRK) for patient with lower to moderate myopia. METHODS: 148 myopic eyes (-1.5 to -6.00 D) after PRK follow-up of more than 5 years were analyzed. RESULTS: Uncorrected visual acuity was >or= 1.0 in 136 eyes (91.9%), >or= 0.8 in 4 eyes (2.7%) and >or= 0.6 in 8 eyes (5.4%). The mean spherical equivalent change was from (-4.43 +/- 0.97) D to (-0.12 +/- 0.22) D, and the keratometric power (K value) was reduced from (43.81 +/- 1.10) D to (41.36 +/- 1.30) D in the 5 years of follow-up (P < 0.01). CONCLUSION: The long-term effectiveness of PRK for myopia (-1.5 to -6.00 D) is satisfactory.

Female↗
PubMed1998

AP-2 may contribute to IGF-II overexpression in rhabdomyosarcoma.

The human insulin-like growth factor II gene is regulated in a development-dependent manner and is not expressed in most adult tissues. However, high levels of insulin-like growth factor II mRNA are detected in many human tumors including rhabdomyosarcoma, an embryonal tumor of skeletal muscle origin. In this study, we demonstrate that the developmentally regulated transcription factor AP-2 is expressed at higher levels in human fetal skeletal muscle and rhabdomyosarcoma cells compared to human adult skeletal muscle. Endogenous insulin-like growth factor II mRNA derived from the P3 as well as transfected P3 promoter activity were modestly and consistently increased to the same extent following treatment of the rhabdomyosarcoma cell line RD with forskolin, a compound implicated in AP-2 transactivation. This effect of AP-2 on increased transcriptional activity was confirmed by nuclear run-on assays. Expression of AP-2B, a dominant-negative inhibitor of AP-2, suppressed the P3 promoter activity in AP-2 expressing RD cells. Furthermore, five AP-2 protected regions corresponding to six AP-2 specific binding sites were detected in the insulin-like growth factor II P3 promoter. These data together suggest that AP-2 may contribute to the high expression of IGF-II in rhabdomyosarcoma cells.

Binding Sites↗
PubMed1998

Biallelic expression of all four IGF-II promoters and its association with increased methylation of H19 gene in human brain.

The human IGF-II gene is maternally imprinted in all tissues except adult liver and the choroid plexus/leptomeninges of the central nervous system where IGF-II is biallelically expressed. In human liver, it has recently been reported that this biallelic expression only involves the promoter P1 while the promoters P2-P4 direct IGF-II transcription monoallelically. To explore whether or not biallelic expression of the IGF-II promoters in human CNS displays the same pattern as in liver, we examined the allelic expression status of the four IGF-II promoters in human brain. We found that all four IGF-II promoters in human fetal and adult brain were expressed from both parental alleles. Furthermore, the levels of methylation of the 3' region of H19 gene in fetal brain were higher than those in other tissues with monoallelic expression of IGF-II. Since similar findings have been reported in Wilms' tumor, these data suggest a similar mechanism may be responsible for loss of imprinting of IGF-II in normal brain and Wilms' tumor.

Adult↗
PubMed1998

p53 regulates human insulin-like growth factor II gene expression through active P4 promoter in rhabdomyosarcoma cells.

The developmentally regulated human insulin-like growth factor II (IGFII) gene is expressed at high levels in many types of tumors and promotes the proliferation of tumor cells with a high incidence of p53 gene defects. We have previously shown that p53 inhibits IGFII P3 promoter activity and decreases endogenous IGFII gene expression derived from the P3 promoter in rhabdomyosarcomas by interfering with TBP binding to the TATA element of the IGFII P3 promoter. In this report, we demonstrate that wild-type p53 expression in rhabdomyosarcoma cell lines containing mutant p53 leads to a decrease in the activity of another active IGFII promoter, P4, and a 5-fold reduction of IGFII mRNA derived from the P4 promoter. This inhibition of P4 activity is associated with direct binding of p53 to the P4 proximal promoter element despite the lack of a p53 consensus binding site. Our results suggest that p53 inhibits IGFII P4 promoter activity by a mechanism different than its effect on the P3 promoter. These data also supply further evidence of cross-talk between the IGF and p53 signaling pathways.

DNA, Neoplasm↗
PubMed1998

[Myopic regression after photorefractive keratectomy].

OBJECTIVE: To investigate myopic regression after excimer laser photorefractive keratectomy (PRK) in patients with myopia. METHODS: 103 eyes with regression (>or= -1.00 D) found in the follow-up for more than 1 year were included in this study. The preoperative spherical equivalent was -4.00 - -14.50 D (-8.72 +/- 2.65 D). Patients were divided into two groups: (1) moderate myopia (-4.00 - -7.90 D) and (2) high myopia (>or= -8.00 D). RESULTS: A significant positive correlation was found between regression and the extent of attempted correction, the rate of regression in high myopia group was 6.93% and that in moderate group, 1.17%. The rate of regression in older age group was higher than that in younger cases. (P < 0.01). Relatively severe haze under the corneal epithelium often accompanies the regression, and decrease of the dosage of topical corticosteroid application or its withdrawal because of the development of corticosteroid ocular hypertention could lead to the regression. The stability of the refraction is not related to the difference in sex. The regression is often accompanied by the increase in K value. CONCLUSION: The regression is significantly related to the extent of attempted correction, patients' age, corneal haze and topical application of corticosteroid.

Adrenal Cortex Hormones↗
PubMed1997

[A correlation study on homocysteine metabolism in pregnant women and neural tube defects in urban and rural areas].

Serum levels of homocysteine, folic acid and vitamin B12 in pregnant women in urban and rural areas were compared to study the relationship between homocysteine metabolism and neural tube defects. Four hundred and eleven serum specimens were sampled randomly from a serum bank for women with early pregnancy in Beijing area, 195 from urban and 216 from rural. Their levels of homocysteine were determined by high performance liquid chromatography combined with electrochemical methods, and those of folic acid and vitamin B12 by radioimmunoassay. Results showed that level of homocysteine was significantly higher in rural pregnant women than that in urban, with 9.31 mumol/L and 5.73 mumol/L, respectively, level of vitamin B12 was lower in rural than that in urban women, with 210.09 pmol/L and 233.35 pmol/L, respectively, and level of folic acid was higher in rural than that in urban women, but no significant difference in deficiency of folic acid between rural and urban was found. The average ratio of folic acid to homocysteine and that of vitamin B12 to homocysteine were higher in rural than those in urban women. It suggests that abnormal metabolism of homocysteine usually correlates with high incidence of neural tube defects in rural area.

Adult↗
PubMed1996

Genomic structure, chromosomal localization, start of transcription, and tissue expression of the human p40-phox, a new component of the nicotinamide adenine dinucleotide phosphate-oxidase complex.

p40-phox is a newly isolated cytosolic component of the nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase that copurifies with p67-phox. Although its function is not well defined, preliminary evidence indicates that it is a component of the cytosolic complex. We report the characterization of the human p40-phox gene, which is single copy and spans approximately 18 kb with 10 exons. Based on fluorescent in situ hybridization (FISH) studies and analysis of somatic hybrid cell lines, the chromosomal location of p40-phox is human chromosome 22q13.1. The start of transcription has been mapped to bp -156. The expression of p40-phox message is restricted to hematopoietic cells. In addition to identifying the mRNA transcript on Northern blot analysis in cells known to express components of the NADPH-oxidase, polymorphonuclear leukocytes, monocytes, B lymphoblastoid cell lines, and eosinophils, p40-phox is also expressed in two other cell types of white cell lineage, mast cells, and basophils. In addition, the mRNA for p40-phox is expressed in megakaryocytic cells, but not in erythroid cells.

Base Sequence↗
PubMed1996

Regulation of insulin-like growth factor II P3 promotor by p53: a potential mechanism for tumorigenesis.

Human insulin-like growth factor (IGF)-II mRNA has been shown to be expressed at high levels in a variety of tumors, including rhabdomyosarcomas. In addition, many tumors have alterations in p53 expression. To investigate whether p53 regulates IGF-II gene expression, we transfected wild-type p53 expression vectors and luciferase constructs driven by IGF-II P3 promotors into multiple cell lines. We found that p53 reduced, in a dose-dependent manner, both endogenous IGF-II P3 transcripts and transfected P3 luciferase expression. The inhibition of P3 luciferase expression by p53 was more pronounced in the two cell lines that expressed mutant p53 protein, RD, and HTB114. The element responsible for this inhibition was mapped to the minimal promoter region. We also transfected an HPV-16 E6 expression plasmid into CCL13 cells containing functional p53 and found that E6 up-regulated IGF-II P3 activity. Wild-type, but not mutant, p53 interfered with the binding of TATA-binding protein to the TATA motif of P3, although both could directly associate with human TATA-binding protein. Our results suggest that p53 may play a role in regulation of IGF-II gene expression.

Gene Expression Regulation, Neoplastic↗
PubMed1996

Calcium channel blockade and anti-free-radical actions of panaxatriol saponins in cultured myocardiocytes.

AIM: To identify the calcium channel blockade and anti-free-radical actions of panaxatriol saponins Re, Rf, Rg1, Rg2, Rh1, and oleanolic acid saponin Ro. METHODS: On ventricular myocytes of Wistar rats, single channel activities of B, L, and T type calcium channels were recorded with the cell-attached configuration of patch-clamp technic, and free radical contents were measured with electron spin resenance method. RESULTS: Re, Rg1, Rg2, and Rh1 shortened the open times, prolonged the close times, and reduced the open-state probabilities of B, L, and T type calcium channels; Rf shortened the open time, prolonged the close time and reduced the open-state probability of L type calcium channel; Ro did not influence the activity of calcium channels (60 mumol.L-1). Re, Rg1, Rg2, and Rh1 antagonized the increase of free radical content induced by xanthine 0.42 mmol.L-1-xanthine oxidase 5.3 nmol.L-1; Ro and Rf had no effect (30 mumol.L-1). CONCLUSION: Re, Rg1, Rg2, and Rh1 had both the calcium channel blockade and antifree-radical actions. Rf had blockade action on L type calcium channel.

Animals↗
PubMed1995

Loss of imprinting of IGF2 in Ewing's sarcoma.

Insulin-like Growth Factor 2 (IGF2) has recently been demonstrated to be maternally imprinted in both mice and humans. We previously reported loss of imprinting (LOI) of IGF2 in rhabdomyosarcoma (RMS) where IGF2 has been shown to act as an autocrine growth factor and play an important role in pathogenesis. Since IGF2 does not appear to play a role in the pathogenesis of Ewing's sarcoma, we sought to determine whether normal IGF2 imprinting was maintained in these tumors. Of 32 Ewing's tumors examined for imprinting of IGF2, 10 were informative heterozygotes and three of these expressed IGF2 biallelically. Furthermore, all three tumors with LOI and five of seven tumors with normal imprinting transcribed IGF2 mRNA at lower levels while relatively higher levels of IGF2 expression was observed in the remaining two tumors with normal imprinting. These data demonstrate altered imprinting of IGF2 occurs in some Ewing's sarcomas. However, LOI of IGF2 in Ewing's sarcoma was not associated with increased expression of IGF2 mRNA, suggesting that LOI may not be involved in the regulation of IGF2 expression and may be related to genetic or epigenetic abnormalities in tumors independent of IGF2 expression.

Base Sequence↗
PubMed1995

Concordant loss of imprinting of the human insulin-like growth factor II gene promoters in cancer.

The human insulin-like growth factor II (IGFII) gene has been shown to be imprinted for the promoters P2, P3, and P4 but not for the promoter P1 in liver and chondrocytes. Loss of imprinting of the IGFII gene has been found in a variety of human tumors including rhabdomyosarcoma and lung cancer. In this report, we determined whether loss of imprinting in tumors displays a promoter-specific pattern. We examined allelic expression of all four IGFII promoters in rhabdomyosarcoma, lung cancer, and normal skeletal muscle. We demonstrate that the imprinting of all IGFII promoters is relaxed in rhabdomyosarcoma and lung cancer. These data suggest that loss of imprinting of IGFII gene promoters may be regulated coordinately by a common mechanism in these tumors. Unexpectedly, we also found that P1, in addition to P2, P3, and P4 is monoallelically expressed in three informative adult skeletal muscle tissues. This indicates that imprinting of the IGFII promoter P1 occurs in a tissue-specific manner.

Adult↗
PubMed1995

A dominant negative bone morphogenetic protein 4 receptor causes neuralization in Xenopus ectoderm.

Injection of DN-BR mRNA encoding a dominant negative type I receptor for bone morphogenetic protein 4 (BMP4) converted prospective ectoderm into neural tissue in Xenopus animal cap explants, in the absence of expression of mesodermal marker genes. The injected caps expressed a general neural marker NCAM and the forebrain marker opsin. Coinjection of wild-type BMP4 receptor mRNA completely reversed the neuralization by DN-BR. No expression of known neuralizing factors, i.e., noggin and follistatin, was detected in the DN-BR-injected animal caps. Furthermore, neuralization elicited by noggin or 3m, a LIM domain mutant of Xlim-1, was substantially inhibited by co-injection of BMP4 mRNA. Since BMP4 is expressed in the prospective ectoderm during gastrulation, our results suggest that the ventralizing factor BMP4 acts also as a physiological inhibitor of neuralization in the development of Xenopus ectoderm.

Animals↗
PubMed1994

Activation of an imprinted allele of the insulin-like growth factor II gene implicated in rhabdomyosarcoma.

The insulin-like growth factor II (IGF2) gene is exclusively silent at the maternal allele in the mouse as well as in normal human tissues and is expressed at a high level in rhabdomyosarcoma (RMS). We report here that the normally imprinted allele of the IGF2 gene is activated in RMS tumors as well as in one RMS cell line. Since overexpression of IGF2 has been shown to be important in the pathogenesis of RMS, our data suggest that loss of imprinting (LOI) may lead to overexpression of IGF2 and play an important role in the onset of RMS. Furthermore, embryonal RMS usually has loss of heterozygosity (LOH) with paternal disomy of the IGF2 locus. One informative embryonal RMS tumor evaluated in this study was heterozygous at the IGF2 allele and had LOI, raising the possibility that LOI may be the functional equivalent of LOH in this tumor with both events leading to overexpression of IGF2.

Alleles↗
PubMed1992

[Studies and preparations of fufang danshen granules].

With the preparation of borneol-beta-cyclodextrin inclusion compound, the stability of the product was improved. In the studies on quality standards, TLC method was used in the identification of three medicinal ingredients and TLC-ultraviolet spectrophotometry was used in the content determination of the chemical constituent tanshinone II A in Salvia miltiorrhiza.

Abietanes↗