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Biomedical subjects

Y Shi

Publications and source records attributed to Y Shi.

At least 487 records · Page 27Linked to original sources
PubMed1996

A scanning electron microscopy and computer image processing morphometric study of the pharmacological regulation of patency of the peritoneal stomata.

The experiment on mice was carried out by injecting intraperitoneally Chinese materia medica for treating hepatocirrhosis with ascites. Observations and a quantitative analysis were carried out on the pharmacological regulation of the peritoneal stomata by using a scanning electron microscope (SEM) and a computer image processing system attached to the SEM. There was a significant increase in both the diameter (P < 0.05) and distribution density (P < 0.01) of the peritoneal stomata in the red sage root and alismatis rhizome groups, whereas the effect of poria and poria peel was not significant compared with the control group (P > 0.05). Our findings confirm the effect of red sage root and alismatis rhizome on the regulation of the peritoneal stomata, which can enhance the absorption of ascitic fluid, taking into consideration the absorbent function of these stomata. They indicate that the patency of peritoneal stomata can vary in response to the effect of some Chinese materia. They also suggest that the ascites is drained mainly by means of enhancing the patency of the stomata and lymphatic absorption of the stomata during the process of treatment by traditional Chinese medicine.

Animals↗
PubMed1996

Evidence of gene deletion of p21 (WAF1/CIP1), a cyclin-dependent protein kinase inhibitor, in thyroid carcinomas.

Eukaryotic cell cycle progression is controlled by a host of cyclin/cyclin-dependent kinases (Cdks), that are themselves regulated by multiple factors, including a group of small cyclin-Cdk inhibitor proteins (p15, p16, p21 and p27). The involvement of Cdk inhibitors in carcinogenesis has been demonstrated by the studies of p16. p53 is frequently mutated in thyroid carcinomas and p21/Waf1 is a downstream effector of p53. It is conceivable that genetic defects of genes downstream in the p53 pathway could also be oncogenic. We, therefore, examined a series of 57 thyroid tumour specimens (eight follicular adenomas and 49 carcinomas) for deletion and point mutation of the p21/Waf1 gene. Three different kinds of deletions ranging from 349 to 450 bp were detected in five papillary carcinoma specimens by reverse transcription-polymerase chain reaction (RT-PCR). All the deletions were involved in the second exon of the p21/Waf1 gene. RT-PCR single strand conformational polymorphism (SSCP) analysis of remaining samples failed to reveal any point mutations in the coding region of the gene, except for a polymorphism at codon 31 (Ser to Arg). Genomic Southern blot analysis did not demonstrate any gene deletion or rearrangement in these samples, indicating abnormal RNA splicing may be involved. Analysis of intron-exon boundary and the coding region of the second exon did not reveal any mutation except for a point mutation (C to G) located 16 bp downstream from the splice donor site of the second intron in three out of five samples with p21/Waf1 deletions. Whether the mutation plays any role in aberrant RNA splicing remains to be determined. Among the five samples with p21/Waf1 gene deletions, none of them simultaneously carried a p53 or retinoblastoma (Rb) gene mutation. No p21/Waf1 abnormality was found in the benign adenomas. Thus, 12.5% (5/40) of thyroid papillary carcinoma specimens harboured p21/Waf1 gene deletions. Our data suggest that p21/Waf1 gene deletion is involved in thyroid carcinogenesis and may play an important role in thyroid cell transformation.

Adenocarcinoma, Follicular↗
PubMed1996

Studies on the hypomethylation of c-myc, c-Ha-ras oncogenes and histopathological changes in human gastric carcinoma.

In order to study the status of DNA methylation of specific oncogenes and the relationship between them and the pathological changes in gastric carcinoma, we analysed the methylated status of c-myc, c-Ha-ras oncogenes by Southern blot hybridization. Genomic DNA from cancerous, paracancerous and non-cancerous areas of surgically resected specimens were examined in 22 cases of advanced human gastric carcinoma. Specimens were digested by the restriction endonucleases MspI/HpaII, which are able to cleave between methylated and non-methylated cytosine at their nucleotide recognition site the DNA 5'-CCGG sequence, and were hybridized with c-myc, c-Ha-ras oncogene probes. Moreover, the corresponding pathological changes in gastric carcinoma were observed. The results showed that c-myc, c-Ha-ras oncogenes from cancerous (10/22, 5/10) and paracancerous areas (13/22, 4/10) were hypomethylated and that there was no significant relationship between them and the histopathological changes.

Adult↗
PubMed1996

Utilization of individual cellodextrins by three predominant ruminal cellulolytic bacteria.

Growth of the ruminal bacteria Fibrobacter succinogenes S85, Ruminococcus flavefaciens FD-1, and R. albus 7 followed Monod kinetics with respect to concentrations of individual pure cellodextrins (cellobiose, cellotriose, cellotetraose, cellopentaose, and cellohexaose). Under the conditions tested, R. flavefaciens FD-1 possesses the greatest capacity to compete for low concentrations of these cellodextrins.

Animals↗
PubMed1996

A novel C/EBP beta-YY1 complex controls the cell-type-specific activity of the human papillomavirus type 18 upstream regulatory region.

The human papillomavirus type 18 (HPV-18) upstream regulatory region (URR) controls viral gene transcription in a cell-type-specific manner. The HPV-18 URR is active in HeLa cells but inactive in HepG2 cells. The activating activity of YY1 in HeLa cells is dependent on its functional interactions with the switch region which is critical for the HPV-18 URR activity in HeLa cells. Here, we show that a protein complex composed of C/EBP beta and YY1 binds the switch region which is detected only in HeLa cells, not in HepG2 cells. Transfection of C/EBP beta into HepG2 cells restored the formation of the C/EBP beta-YY1-switch region complex, accompanied by increased transcription directed by the HPV-18 URR. Mutations in the switch region that abolished the complex formation also abrogated C/EBP beta-induced transcriptional activation. This provides a strong correlation between the binding of the C/EBP beta-YY1 complex to the switch region and cell-type-specific URR activity. Taken together, we have identified a novel C/EBP beta-YY1 complex that binds the switch region and contributes to cell-type-specific HPV-18 URR activity.

CCAAT-Enhancer-Binding Proteins↗
PubMed1996

A novel repressor, par-4, modulates transcription and growth suppression functions of the Wilms' tumor suppressor WT1.

The tumor suppressor WT1 represses and activates transcription. The loss and/or imbalance of the dual transcriptional activity of WT1 may contribute to Wilms' tumor. In this study, we identified par-4 (for prostate apoptosis response) as a WT1-interacting protein that itself functions as a transcriptional repressor. par-4 contains a putative leucine zipper domain and is specifically upregulated during apoptosis of prostate cells (S. F. Sells, D. P. Wood, Jr., S. S. Joshi-Barve, S. Muthukkumar, R. J. Jacob, S. A. Crist, S. Humphreys, and V. M. Rangnekar, Cell Growth Differ. 5:457-466, 1994). The leucine repeat domain of par-4 was shown to interact with the zinc finger DNA binding domain of WT1. Immunoprecipitation-Western blot (immunoblot) analyses demonstrated in vivo WT1-par-4 interactions. par-4 was ubiquitously expressed, and the protein was found in both the nucleus and the cytoplasm. Functionally, par-4 inhibited transcription activated by WT1, but not by the related protein EGR1. Inhibition of WT1-mediated transcription was dependent on the domain of par-4 that mediates its physical association with WT1. In addition, par-4 augmented WT1-mediated repression, possibly by contributing an additional repression domain. Consistent with these results, par-4 functioned as a transcriptional repressor when brought to a promoter via a heterologous DNA binding domain. Significantly, par-4, but not a mutant unable to interact with WT1, rescued growth suppression caused by WT1. Thus, we identified a novel repressor that modulates transcription as well as growth suppression functions of WT1.

Amino Acid Sequence↗
PubMed1996

Adenovirus E1A downregulates cJun- and JunB-mediated transcription by targeting their coactivator p300.

Transcription factors and cofactors play critical roles in cell growth and differentiation. Alterations of their activities either through genetic mutations or by viral oncoproteins often result in aberrant cell growth and tumorigenesis. The transcriptional cofactor p300 has recently been shown to be complexed with transcription factors YY1 and CREB. Adenovirus E1A oncoproteins target these transcription complexes via physical interactions with p300, resulting in alterations of transcription mediated by these transcription factors. Here we show that p300 is also critical for repression by E1A of the activities of cJun and JunB, two members of the AP-1 transcriptional complexes. This repressive effect of E1A is dependent on the p300-binding domain of E1A and can be relieved by overexpression of p300. These results suggest that p300 serves as a mediator protein for downregulation of AP-1 activity by E1A. This hypothesis was further supported by the following observations: (i) in the absence of E1A, overexpression of p300 stimulated transcription both through an AP-1 site present in the collagenase promoter and through Jun proteins in GAL4 fusion protein-based assays; and (ii) overexpression of a mutant p300 lacking the E1A-interacting domain reduced the responsiveness of Jun-dependent transcription to E1A repression. As predicted from the functional results, p300 physically interacted with the Jun proteins. These findings thus established that p300 is a cofactor for cJun and JunB. We propose that p300 is a common mediator protein through which E1A gains control over multiple transcriptional regulatory pathways in the host cells.

Adenovirus E1A Proteins↗
PubMed1996

Transforming growth factor-beta 1 expression and myofibroblast formation during arterial repair.

Transforming growth factor-beta 1 (TGF-beta 1) plays a central role in tissue repair owing to its modulating effects on cell growth and the synthesis of extracellular matrix. We have previously shown that adventitial fibroblasts differentiate to myofibroblasts after endoluminal injury, thereby contributing to arterial remodeling. Since TGF-beta 1 exerts several biologic actions attributed to myofibroblasts, we examined its role in myofibroblast formation in a porcine model of balloon overstretch coronary artery injury. TGF-beta 1 transcripts were induced in numerous adventitial cells 2 days after injury (47 +/- 10%, P < .001 versus control). These cells displayed no smooth muscle (SM) markers, i.e., alpha-SM actin or desmin, which suggested their fibroblastic origin. This was further corroborated by the rare presence of macrophages in the injured adventitia (3 +/- 1%). At 7 to 8 days, most TGF-beta 1-expressing cells demonstrated alpha-SM actin immunoreactivity. Their myofibroblast phenotype was confirmed by electron microscopy, which revealed microfilaments (stress fibers) and a well-developed rough endoplasmic reticulum. The distribution of TGF-beta 1 transcripts by in situ hybridization was paralleled by the immunolocalization of intracellular and extracellular TGF-beta 1 epitopes. At later times (> 14 days after injury), the decrease in TGF-beta 1 coincided with the disappearance of adventitial myofibroblasts, whereas the neointima exhibited longer TGF-beta 1 expression. In conclusion temporal and spatial relationships between TGF-beta 1 and myofibroblast formation suggest an important role for autocrine TGF-beta 1 in the phenotypic modulation of vascular fibroblasts. Induction of TGF-beta 1 expression may provide a differentiation signal for adventitial fibroblasts to become myofibroblasts, which affect arterial remodeling via their mechanical and synthetic properties.

Animals↗
PubMed1996

[Effects of ACM sequential chemotherapy on ovarian function in trophoblastic tumors].

OBJECTIVE: To study the changes of ovarian function during and after ACM sequential chemotherapy on trophoblastic tumors. METHODS: 17 patients with trophoblastic tumors, received totally 48 cycles of ACM chemotherapy. Of these, 7 underwent hysterotomy and focal ectomy and ovarian biopsy. Changes of menstruation and BBT were observed. beta-hCG, E2, FSH and LH were assayed and histological and immunohistochemical studies in ovaries biopsied were made. RESULTS: Amenorrhea and anovulatory BBT were predominant at the onset of chemotherapy and high level of beta-hCG. Following chemotherapy and decrease of beta-hCG, menstruation recovered with less amount and BBT transformed into ovulatory types with shorter luteal phase. The E2 level appeared to be lower and the FSH and LH level higher. The different kinds of follicles were decreased, but estrogen receptors unchanged. Follow-up showed that ovarian function of 12 of the 17 patients returned to normal in one year. CONCLUSION: ACM chemotherapy suppresses ovarian function mildly and temporarily. Trophoblastic tumor also affects ovarian function. ACM chemotherapy seems to be suitable for young patients with trophoblastic tumors who desire child-bearing.

Adult↗
PubMed1996

[Study on cellular proliferation activity of placental site trophoblastic tumor].

OBJECTIVE: To study the relationship among the cellular proliferation activity, benign clinical process and pathologic characteristics of placental site trophoblastic tumor (PSTT). METHODS: Paraffin-embedded blocks from ten patients with PSTT were reexamined by mitotic count, argyrophilic nucleolar organizer regions (AgNOR) staining and flow cytometric DNA analysis. Five cases of hydatidiform mole (HM) and 5 choriocarcinoma (CC) were chosen as controls. RESULTS: Mean mitotic figures of PSTT were 1.3 (0-3) per 10 high power field, while those of HM and CC were 0.8 (0-2) and 2.2 (1-4) respectively. AgNOR number of PSTT was 2.70 +/- 0.55 per cell, while those of HM and CC were 1.96 +/- 0.38 and 4.50 +/- 0.73 respectively. Flow cytometric DNA content revealed that PSTT had DNA index (DI) of 1.10, S phase of 16.7% and proliferating index (PI) of 26.6%. Eight of 10 Cases were followed up, 7 are alive and 1 died of primary lung cancer. CONCLUSION: PSTT has relative low cellular proliferation activity. The good clinical procedure and benign pathological feature of PSTT may be associated with its diploidy DNA and low cellular proliferation activity.

Adult↗
PubMed1996

[Effects of assisted ovarian stimulation with leuprolide acetate on alterations of plasma estradiol levels and newly synthesized endometrial proteins].

OBJECTIVE: To evaluate the effects of leuprolide acetate (LA)-assisted ovarian stimulation on endometrial protein synthesis in hamsters. METHODS: Hamsters were treated separately with three different regimens: (1) 40 IU of pregnant mare's serum gonadotropin (PMSG) followed by 100 IU of hCG after 52 hours (PMSG alone group). (2) Same volumes of normal saline on the same schedule (control group). (3) 40 micrograms of LA daily prior to the same regimen of PMSG-hCG treatment in order to down-regulate the pituitary-ovarian functions (LA-PMSG group). The newly synthesized endometrial proteins were characterized and quantitated in vitro by 3H-leucine incorporation test and 10% SDS-PAGE technique. RESULTS: The levels of newly synthesized 3H-labelled endometrial proteins were not different between LA-PMSG and control groups. However, those of low and middle molecular weight (< 31,000 and 45,000) proteins in the PMSG alone group were significantly lower than the levels in both LA-PMSG and control groups (P < 0.05, P < 0.01). CONCLUSIONS: The addition of LA in ovarian stimulation protocol resulted in more physiological endometrial protein synthesis. This phenomenon may causally related to higher pregnancy rate when applied in vitro fertilization-embryo transfer programs.

Animals↗
PubMed1996

Study on bovine serum albumin recovery from reversed micellar solutions.

From near-infrared spectra, it was confirmed that CTAB/hexanol-octane reversed micellar solution is a suitable medium for BSA solubilization. The effects of various factors, e.g., PH, and the type and concentration of salt in stripping solution, on Bovine Serum Albumin (BSA) back extraction were studied. The suitable conditions for stripping have been ascertained, i.e., 1.0-2.0 mol/L KBr, pH = 4.3-4.9. Spectroscopic studies showed that no significant change is observed in the structure of the main chain of BSA after extraction and back extraction. In addition, the problem of how long the reversed micellar solution can be recycled has been examined. Finally, the recovery and concentration of protein were successfully obtained with suitable phase ratio.

Cetrimonium↗
PubMed1996

The role of GRH mediated AC-cAMP system in the pathogenesis of human pituitary GH-secreting adenomas.

OBJECTIVE: To investigate the role of AC-cAMP system in the transmission of the action of the growth hormone releasing hormone (GRH) on growth hormone (GH) release in pituitary GH-secreting adenomas. METHODS: The effects of GRH (10(-7) mol/L) on intracellular cAMP levels and GH release and the effects of AC-cAMP stimulators, cholera toxin (Ct, 50 micrograms/L), forskolin (10(-5) ml/L) and db-cAMP (10(-3) mol/L) on GH secretion were studied in cultured cells of 21 GH-secreting adenomas obtained from operation for acromegalic patients. RESULTS: GRH and Ct failed to stimulate GH secretion in 61.9% (13/21 cases) and 57.1% (12/21 cases) pituitary GH adenoma cell cultures respectively. Forskolin stimulated GH release in 88.9% (8/9 cases), while db-cAMP induced GH secretion in all cases tested (5/5 cases). The intracellular cAMP levels were elevated by GRH in the 4 out of 9 cases of tumor cell cultures, but not in the other 5 cases. According to the GH secretory responses to GRH and Ct, the 21 GH tumors were divided into 4 groups. In group A and B, GRH can stimulate GH release, but Ct has stimulative role only in group A. In group C and D, GRH fails to stimulate GH secretion. However group A can respond to Ct, but group D has no response. CONCLUSIONS: The GH hypersecretion in most acromegalic patients is mainly due to the defects of pituitary adenoma cells, especially the abnormalities of GRH receptor and/or stimulative guanosine protein.

Adenoma, Acidophil↗