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Biomedical subjects

Y Yu

Publications and source records attributed to Y Yu.

At least 469 records · Page 26Linked to original sources
PubMed1996

[The effects of intensive DMPA regimen in the treatment of Graves' ophthalmopathy].

35 patients with Graves' ophthalmopathy were treated with DMPA regimen which included dexamethasone (D) 20-30 mg and Methotrexate (M) 15-20 mg i.v. once a week and prednisone (P) 20 mg/d p. o. 4 times a week for 4 weeks followed by addition of azathioprine (A) or 6-MP 75-100 mg/d and the increment of prednisone (20 mg/d) to 5 times a week in the fifth and sixth weeks. The full intensive course of therapy lasted for 6 weeks. If necessary, the similar course of therapy might be repeated. Later on, each patient was mintainted on a therapy with P and A or P and 6-MP for another 1-2 months then the P and A or P and 6-MP for another 1-2 months, and then the P and A or 6-MP were tapered and finally discontinued at the end of sixth month. The symptoms and signs of the opthalmopathy were evaluated blindedly at the beginning and the end of the first and second courses of the therapy by two ophthalmologists. The results showed that the symptoms and signs were significantly improved in 33 (94.3%) cases. A decrease of eyeball protrusion of 1.22 +/- 1.15 and 1.28 +/- 1.15 mm in the left and right eyes respectively was shown by eophthalmometry reading (both P < 0.0005, compared with before and after the therapy). The decrease of exophthalmos was more remarkable in the cases with ophthalmopathy for < or = 1 year than that > 1 year. 11/22 patients recovered their ability to close eyes adequately. The diplopia was corrected in 8/15 cases. The mobility of eye ball returned to normal in 5/15 cases. Exposed lesion and/or ulceration of the cornea found in 7 patients were cured. Serious side and/or toxic effects of the drugs were not present during the course of therapy. It is suggested that DMPA regimen is an effective, safe and cheap approach to the treatment of Graves' ophthalmopathy.

Adult↗
PubMed1996

[Early result comparison following mitral valve replacement with partial or entire subvalvular structure preservation].

21 patients after mitral valve replacement with partial subvalvular structure preservation and 20 patients with entire subvalvular structure preservation were compared with 26 patients after mitral valve replacement with entire subvalvular structure excision. We found that patients after mitral valve replacement with partial or entire subvalvular structure preservation had a more uneventful postoperative course with less inotropic therapy and more decreased left atrial dimension when compared to those with conventional mitral valve replacement. But the patients after mitral valve replacement with entire mitral structure preservation had more decreased left ventricular dimension and short hospital stay when compared to those of the other two groups. The authors suggest that mitral subvalvular structure should be preserved, and we especially recommend the procedure of intravalvular implantation of mitral prosthesis with entire mitral subvalvular structure preservation.

Adult↗
PubMed1996

[Clinical treatment of post-thrombotic deep veins of lower limbs].

From 1989 to 1995, 213 patients with chronic post-thrombotic syndrome of the deep veins of lower limbs were treated. The surgical approaches consisted of establishment of temporary distal arteriovenous fistula for iliac and iliofemoral occlusion, and bypass of suitable length of autogenous vein with temporary distal arteriovenous fistula. Those who were not candidates for surgery were treated continuously by conservative methods with periodical short-term thrombolysis. A mean follow-up of 37.3 months the cure rate and the effective rate were 50.9% and 83.5% respectively. The authors suggest that different methods may be used in different patients, and the temporary distal arteriovenous fistula is a new approach of the posthrombotic legs.

Adult↗
PubMed1996

[Prognostic factors of primary liver cancer].

To investigate the prognostic factors of primary liver cancer (PLC) and improve the long-term results, 1,248 cases of PLC were analysed. Univariate analysis demonstrated that discovery approach, staging of PLC, original gamma-GPT, resection, radical resection, original AFP, tumor size, tumor number, and tumor capsule have very significant effects on prognosis of PLC (all P < 0.001); cirrhosis, HBsAg, local resection, and tumor embolus in portal vein were also significant difference (all P < 0.05); age, sex, original AFP, hepatitis, and differentiation of PLC cells were no significant difference (all P > 0.05). Multivariate analysis demonstrated that original gamma-GPT, radical resection, tumor size, and tumor number were the most significant prognostic factors (all P < 0.001). Some aspects improving long-term survival were discussed.

Adolescent↗
PubMed1996

[Long-term results of multimodality treatment in patients with primary liver cancer].

This paper report the long-term results of multimodality treatment in 2388 patients with pathologically proven primary liver cancer (PLC) over the last three decades. The 5-and 10-year survival after resection of PLC was 39.3% and 29.2% respectively for the whole series (n = 1650), and 61.9% and 45.4% respectively for patients with small PLC (< or = 5 cm, n = 569). The 5-year survival after cryosurgery was 37.9% for the whole series (n = 191), and 53.1% for patients with small PLC (n = 56). The 5-year survival of 71 patients receiving sequential resection after cytoreduction therapy was 66.0%. The 5-year survival after re-resection for recurrence tumor (n = 147) was 34.5%. 214 patients survived more than 5 years; of these 113 patients (52.8%) were small PLC, and 57 patients survived more than 10 rears. It is concluded that early detection and resection of small PLC is the leading approach to get long-term survivors, cytoreduction and sequential resection might be an important approach to improving the prognosis of patients with unresectable PLC, re-resection for subclinical recurrance and metastasis after an initial curative resection was also important to prolong survival further.

Adolescent↗
PubMed1995

Determining the requirements for cooperative DNA binding by Swi5p and Pho2p (Grf10p/Bas2p) at the HO promoter.

SW15 encodes a zinc finger DNA binding protein required for the transcription of the Saccharomyces cerevisiae HO gene, and PHO2 encodes a homeodomain DNA binding protein. In vitro biochemical studies using purified Swi5p and Pho2p proteins have demonstrated that Swi5p and Pho2p bind cooperatively to the HO promoter. In this report we investigate the regions of the Swi5p and Pho2p proteins required for cooperative DNA binding. The analysis of each protein gives a similar result: the zinc finger or homeodomain DNA binding domains are each sufficient for in vitro DNA binding, but additional regions of each protein are required for cooperative DNA binding. In vitro and in vivo experiments were conducted with promoters with altered spacing between the Pho2p and Swi5p binding sites. Mutations that increased the distance between the two binding sites had minimal effects on either in vitro cooperative DNA binding or in vivo upstream activating sequence activity. These observations suggest that the interaction domains of Swi5p and Pho2p are flexible and can tolerate an increase in distance between the two binding sites. The mechanism of the cooperative DNA binding by Swi5p and Pho2p is discussed.

Base Sequence↗
PubMed1995

Functional analysis of the transforming growth factor beta responsive elements in the WAF1/Cip1/p21 promoter.

The transforming growth factor beta s (TGF-beta s) are a group of multifunctional growth factors that inhibit cell cycle progression in many cell types. The TGF-beta-induced cell cycle arrest has been partially attributed to the regulatory effects of TGF-beta on both the levels and activities of the G1 cyclins and their cyclin-dependent kinase partners. The ability of TGF-beta to inhibit the activity of these kinase complexes derives in part from its regulatory effects on the cyclin-dependent kinase inhibitors, p21/WAF1/Cip1, p27Kip1, and p15. Upon treatment of cells with TGF-beta, these three inhibitors bind to and block the activities of specific cyclin-cyclin-dependent kinase complexes to cause cell cycle arrest. Little is known, however, on the mechanism through which TGF-beta activates these cyclin-dependent kinase inhibitors. In the case of p21, TGF-beta treatment leads to an increase in p21 mRNA. This increase in p21 mRNA is partly due to transcriptional activation of the p21 promoter by TGF-beta. To further define the signaling pathways through which TGF-beta induces p21, we have performed a detailed functional analysis on the p21 promoter. Through both deletion and mutation analysis of the p21 promoter, we have defined a 10-base pair sequence that is required for the activation of the p21 promoter by TGF-beta. In addition, this sequence is sufficient to drive TGF-beta-mediated transcription from a previously nonresponsive promoter. Preliminary gel shift assays demonstrate that this TGF-beta responsive element binds specifically to several proteins in vitro. Two of these proteins are the transcription factors Sp-1 and Sp-3. These studies represent the initial steps toward defining the signaling pathways involved in TGF-beta-mediated transcriptional activation of p21.

Base Sequence↗
PubMed1995

Iron regulates the intracellular degradation of iron regulatory protein 2 by the proteasome.

Iron regulatory proteins (IRP1 and IRP2) are RNA-binding proteins that bind to specific structures, termed iron-responsive elements (IREs), that are located in the 5'- or 3'-untranslated regions of mRNAs that encode proteins involved in iron homeostasis. IRP1 and IRP2 RNA binding activities are regulated by iron; IRP1 and IRP2 bind IREs with high affinity in iron-depleted cells and with low affinity in iron-repleted cells. The decrease in IRP1 RNA binding activity occurs by a switch between apoprotein and 4Fe-4S forms, without changes in IRP1 levels, whereas the decrease in IRP2 RNA binding activity reflects a reduction in IRP2 levels. To determine the mechanism by which iron decreases IRP2 levels, we studied IRP2 regulation by iron in rat hepatoma and human HeLa cells. The iron-dependent decrease in IRP2 levels was not due to a decrease in the amount of IRP2 mRNA or to a decrease in the rate of IRP2 synthesis. Pulse-chase experiments demonstrated that iron resulted in a 3-fold increase in the degradation rate of IRP2. IRP2 degradation depends on protein synthesis, but not transcription, suggesting a requirement for a labile protein. IRP2 degradation is not prevented by lysosomal inhibitors or calpain II inhibitors, but is prevented by inhibitors that block proteasome function. These data suggest the involvement of the proteasome in iron-mediated IRP2 proteolysis.

Ammonium Chloride↗
PubMed1995

Characterization and expression of iron regulatory protein 2 (IRP2). Presence of multiple IRP2 transcripts regulated by intracellular iron levels.

Iron regulatory proteins (IRP1 and IRP2) are RNA-binding proteins that bind to stem-loop structures, termed iron-responsive elements (IREs), present in either the 5'- or 3'-untranslated regions of specific mRNAs. The binding of IRPs to 5'-IREs inhibits translation of mRNA, whereas the binding of IRPs to 3'-IREs stabilizes mRNA. To study the structure and regulation of IRP2, we isolated cDNAs for rat and human IRP2. The derived amino acid sequence of rat IPR2 is 93% identical with that of human IRP2 and is present in lower eukaryotes, indicating that IRP2 is highly conserved. IRP1 and IRP2 share 61% overall amino acid identity. IRP2 is ubiquitously expressed in rat tissues, the highest amounts present in skeletal muscle and heart. IRP2 is encoded by multiple mRNAs of 6.4, 4.0, and 3.7 kilobases. The 3'-untranslated region of rat IRP2 contains multiple polyadenylation signals, two of which could account for the 4.0-kb and 3.7-kb mRNAs. The 3.7-kb mRNA is increased in iron-depleted cells and occurs with a reciprocal decrease in the 6.4-kb transcript. These data suggest that the 3.7-kb mRNA is produced by alternative poly(A) site utilization in iron-depleted cells.

Amino Acid Sequence↗
PubMed1995

Absence of radiation-induced G1 arrest in two closely related human lymphoblast cell lines that differ in p53 status.

In order to examine more precisely the role of p53 in the activation of the G1/S checkpoint by ionizing radiation, we examined two human lymphoblast cell lines derived from the same donor. The TK6 line had a doubling time of 12.2 h and expressed wild type p53, while the WTK1 line had a doubling time of 12.7 h and expressed mutant p53. The two lines differ significantly in their susceptibility to radiation-induced cell killing and apoptosis. Cells were examined by flow cytometry at regular intervals from 0 to 12 h after irradiation with two different doses designed to yield equivalent survival levels in both cell lines. In some experiments, cells were incubated with colcemid to block them in the first postirradiation mitosis and prevent contamination of the flow cytometric profiles with second cycle cells. There was no significant difference between the two cell lines in the progression of irradiated cells out of G1 and into the S and G2 phases of the cell cycle. In particular, there was no evidence for a prolonged arrest in G1 in the TK6 cell line expressing wild type p53. Furthermore, expression of the p53 downstream genes WAF1/CIP1 and RB appeared normal in TK6 cells. These results suggest that factors other than those in the p53 signal transduction pathway alone may be required to activate the G1/S checkpoint in irradiated human cells and that apoptosis and G1 arrest may utilize different pathways.

Apoptosis↗
PubMed1995

Stage-specific isoforms of complex II (succinate-ubiquinone oxidoreductase) in mitochondria from the parasitic nematode, Ascaris suum.

Complex II from mitochondria of the adult parasitic nematode, Ascaris suum, exhibits high fumarate reductase activity and plays a key role in the anaerobic electron transport observed in these organelles. In contrast, mitochondria isolated from free living second stage larvae (L2) of A. suum show much lower fumarate reductase activity than those from adults, whereas succinate dehydrogenase activities of mitochondria in both stages are comparable. In the present study, biochemical and antigenic properties of the partially purified enzymes from both larval and adult mitochondria were compared. Larval complex II eluted from the DEAE-Cellulofine column chromatography at a lower salt concentration than adult enzyme, whereas the apparent molecular size of both enzyme complexes estimated by gel permeation column chromatography was the same. The fumarate reductase activity of larval complex II was less than 3% of that of adult enzyme, and the Km values for substrates were significantly different between the two complexes. The flavoprotein subunit of larval complex II could be distinguished from that of adult complex II by two-dimensional gel electrophoresis and peptide mapping. The antibody against the smallest subunit (small subunit of cytochrome b558) of the adult enzyme did not cross-react with that of the larval enzyme. These results suggest that larval complex II differs from adult enzyme and is more similar to aerobic mammalian enzymes with low fumarate reductase activity. This is the first direct indication of the two different stage-specific forms of mitochondrial complex II.

Animals↗
PubMed1995

Molecular nature of spontaneous mutations at the hypoxanthine-guanine phosphoribosyltransferase (hprt) locus in Chinese hamster ovary cells.

The hypoxanthine-guanine phosphoribosyltransferase (hprt) locus has been widely used as a selectable genetic marker for studies of mammalian cell mutagenesis. We report here the spontaneous mutation spectrum at the hprt locus in 64 independently isolated mutants of Chinese hamster ovary (CHO) cells. All nine hprt exons were simultaneously analyzed via multiplex polymerase chain reaction (PCR) for rapid detection of gene deletions or insertions. Structural point mutations were identified by direct sequence analysis of the PCR amplified cDNA. The molecular nature of RNA splicing errors and insertions was analyzed by solid-phase direct exon sequencing. Single base substitutions were found in 24 mutants (38%), of which 21 were missense and 3 were nonsense mutations. Transversions were about twice as frequent as transitions. Fifteen mutants (23%) had deletions involving either intragenic small fragments (2), single exons (9), or multiple exons (4). The majority of deletion breakpoints (71%) were located in regions surrounding exons 4, 5, and 6. RNA splicing mutations were observed in 15 mutants (23%) and affected exons 3-8; most (6/15) resulted in the loss of exon 7. Two insertion mutants, one with a 209 bp insert in exon 4 and the other with a 88 bp insert accompanied by a 24 bp deletion in exon 6, represent novel mutations reported for the first time in spontaneous mutants of the mammalian hprt gene.

Animals↗
PubMed1995

Transforming growth factor-beta 1 modulates adenylyl cyclase signaling elements and epidermal growth factor signaling in cardiomyocytes.

Studies presented in this report were designed to investigate the effects of transforming growth factor-beta 1 (TGF-beta 1) on epidermal growth factor (EGF)-mediated stimulation of cAMP accumulation in cardiac myocytes and elucidate the mechanism(s) involved in this modulation. TGF-beta 1 (20 pM) treatment of cardiac myocytes, in a time-dependent manner, decreased the ability of EGF (100 nM) to increase cAMP accumulation. Significant attenuation of EGF-elicited cAMP accumulation was observed 2 h after exposure to TGF-beta 1 and 18 h after addition of TGF-beta 1, the ability of EGF to increase cAMP accumulation was completely obliterated. TGF-beta 1 neither decreased immunoprecipitable EGF receptors in membranes from cardiomyocytes nor altered the specific binding of [125I]EGF to cardiomyocyte membranes. However, TGF-beta 1 decreased the ability of EGF to phosphorylate membrane proteins on tyrosine residues. TGF-beta 1 treatment of cardiomyocytes also decreased the ability of forskolin to augment cAMP accumulation in intact cells and stimulate adenylyl cyclase activity. Similarly, in membranes of TGF-beta 1-treated cells, neither isoproterenol nor EGF stimulated adenylyl cyclase activity. Interestingly, as assessed by the ability of A1F4- to stimulate adenylyl cyclase, TGF-beta 1 did not alter the coupling between Gs and catalytic subunits. Likewise, TGF-beta 1 did not alter the functional activity of the inhibitory regulatory element of the system, Gi. Western analysis of cellular proteins revealed that TGF-beta 1 did not alter the amounts of Ga alpha, Gi alpha 2, and Gi alpha 3. We conclude that TGF-beta 1 attenuates EGF-elicited cAMP accumulation in cardiomyocytes, in part, by decreasing the EGF receptor kinase function and that TGF-beta 1-mediated alterations in the activity of adenylyl cyclase catalytic subunit also contribute toward the regulation of adenylyl cyclase by various agonists.

Adenylyl Cyclases↗
PubMed1995

Combinations of multiple serum markers are superior to individual assays for discriminating malignant from benign pelvic masses.

To determine whether measurement of the levels of multiple tumor markers in the preoperative serum of women presenting with a pelvic mass distinguished benign from malignant disease better than the assay of CA 125 alone, sera from 429 patients, 192 of whom had malignant histology, were assayed for 8 different markers: CA 125, macrophage colony-stimulating factor, OVX1, lipid-associated sialic acid (LASA), CA15-3, CA72-4, CA19-9, and CA54/61. The sensitivity and specificity of CA 125 alone (> 35 U/ml) was 78.1 and 76.8%, respectively. A panel consisting of CA 125, OVX1, LASA, CA15-3, and CA72-4 had a sensitivity of 83.3% and specificity of 84.0% when two or more markers were elevated. Using the concentrations of these five markers, logistic regression analysis had a sensitivity of 85.4% and a specificity of 83.1%. Considering the values of markers in different sequences, classification and regression tree analysis substantially improved the sensitivity to 90.6% and the specificity to 93.2%. When applied in clinical practice this approach could improve the management of women presenting with a pelvic mass and may also have application in screening for ovarian cancer.

Biomarkers, Tumor↗