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H Duan

Publications and source records attributed to H Duan.

At least 73 records · Page 4Linked to original sources

[Influence of smear layer and adhesive resin on the retentive force of amalgam restoration in vitro study].

UNLABELLED: The purposes of this in vitro study were to determine whether removing of smear layer and using of self-cured adhesive can increase retentive strength of amalgam restoration and to understand the adhesive mechanism between amalgam and adhesive. Class I cavities without mechanical retention were prepared in the occlusal surfaces of 45 extracted molars which were randomly divided into 3 groups. Group 1: 10%EDTA(pH 7.4) was applied to cavity walls for 1 minute prior to amalgam condensation. Group 2: 10%EDTA was applied in the same manner as in group 1, then the walls were water-sprayed and dried. Miradapt adhesive was applied, and amalgam must be packed into cavity before the adhesive cures. CONTROL GROUP: no special treatment before amalgam condensation. The tensile strength of the restorations were measured. The adhesive interface of two samples from group 2 were evaluated by SEM and EDS. As a result, removing smear layer had little effect on retentive force of amalgam (P > 0.05), while removing smear layer and applying adhesive improved the retentive strength of amalgam fillings significantly (P < 0.05), and there were micromechanical interlock between amalgam and adhesive according to SEM and EDS observation.

Adhesives↗

Degradation of macrophage ApoE in a nonlysosomal compartment. Regulation by sterols.

Macrophage-derived apoE has been shown to play an important role in the susceptibility of the vessel wall to atherosclerosis. Previous studies have shown that macrophage sterol content modulates apoE synthesis and secretion, associated with a large transcriptional response of the apoE gene. The current studies were undertaken to evaluate the existence of additional post-transcriptional regulatory loci for the effect of sterols on apoE synthesis and secretion. Using a macrophage cell line transfected to constitutively express an apoE cDNA to facilitate detection of a post-transcriptional regulatory locus, we demonstrated that preincubations in 25-hydroxycholesterol and cholesterol lead to increased apoE secretion in pulse/chase experiments. Examination of cell lysates in these experiments showed that apoE not secreted by control cells was degraded and not detectable, suggesting that the preincubation in sterols increased secretion by decreasing degradation of newly synthesized apoE. The measurement of total protein and apoE degradation in cell fractions revealed an intermediate density fraction that degraded significant amounts of newly synthesized total protein and newly synthesized apoE. In this fraction, degradation of total protein and apoE was unaffected by chloroquine but was substantially reduced by N-acetyl-Leu-Leu-norleucinal plus N-acetyl-Leu-Leu-methioninal or by lactacystin, suggesting the involvement of proteasomes. Preincubation in sterol/oxysterol or acetylated low density lipoprotein did not modify total protein degradation by this fraction but inhibited apoE degradation. Similar results were obtained using intermediate density fractions isolated from human monocyte-derived macrophages. The results of our studies indicate that newly synthesized apoE in the macrophage can be degraded in an intermediate density nonlysosomal cellular compartment, which is sensitive to proteasomal inhibitors. Alteration of cellular lipid homeostasis by preincubation in sterol/oxysterol or acetylated low density lipoprotein inhibits apoE, but not total protein, degradation in this fraction. Inhibition of the degradation of apoE in this fraction likely contributes to the increased apoE secretion observed in sterol-enriched cells.

Apolipoproteins E↗

RAIDD is a new 'death' adaptor molecule.

The effector arm of the cell-death pathway is composed of cysteine proteases belonging to the ICE/CED-3 family. In metazoan cells these exist as inactive polypeptide precursors (zymogens), each composed of a prodomain, which is cleaved to activate the protease, and a large and small catalytic subunit. The coupling of these 'death' proteases to signalling pathways is probably mediated by adaptor molecules that contain protein-protein interaction motifs such as the death domain. Here we describe such an adaptor molecule, RAIDD, which has an unusual bipartite architecture comprising a carboxy-terminal death domain that binds to the homologous domain in RIP, a serine/threonine kinase component of the death pathway. The amino-terminal domain is surprisingly homologous with the sequence of the prodomain of two ICE/CED-3 family members, human ICH-1 (ref. 5) and Caenorhabditis elegans CED-3 (ref. 6). This similar region mediates the binding of RAIDD to ICH-1 and CED-3, serving as a direct link to the death proteases, indicating that the prodomain may, through homophilic interactions, determine the specificity of binding of ICE/CED-3 zymogens to regulatory adaptor molecules. Finally, alternations in the sequence of the N-terminal domain that are equivalent to inactivating mutations in the C. elegans ced-3 gene prevent homophilic binding, highlighting the potentially primordial nature of this interaction.

Amino Acid Sequence↗

[Influence of smear layer and adhesive resin on the adaptation of amalgam restoration to cavity walls].

This in vitro study evaluated the effect of removing smear layer and applying adhesive on the marginal adaptation of amalgam fillings to cavity walls. Three groups were established, cavities in group 1 were exposed to 10% EDTA (pH7.4) for 1 minute to remove smear layer before amalgam condensation; cavities in group 2 were also subjected to EDTA, then Miradapt adhesive was applied on the walls, finally amalgam condensed into cavities before the adhesive set; cavities in group 3 received no special treatment before amalgam condensation. After thermocycling, all teeth were subjected to SEM and image analyser. Results showed: Space between restorations and tooth structure in group 1 was 6.31 microns, space in group 2 with adhesive was 3.49 microns and micromechanical interlocking was observed while space in control group was 14.22 microns. Difference among the three groups was statistical significant. It was indicated that removing smear layer and using adhesive resin significantly improved the adaptation of amalgam to cavity walls.

Composite Resins↗

[Effect of age and ginsenoside Rg1 on nitric oxide content and nitric oxide synthase activity of cerebral cortex in rats].

Nitric oxide(NO) content and nitric oxide synthase(NOS) activity were measured in cerebral cortex isolated from Wistar rats of three age groups(young: 3 months; adult: 9 months; and old: 27 months). No significant differences in NO content and NOS activity between young and adult rats were found(P > 0.05). The NO content and NOS activity in old rats were shown to be significantly higher than those of young and adult rats(P < 0.01). When treated with Rg1(10, 20, 40 mg.kg-1), the NO content and NOS activity in old rats decreased. The inhibitory effect of Rg1 on NOS was found to be dose-dependent in the range of 10-40 mg.kg-1. The optimal reduction in NO content and NOS activity induced by Rg1 occurred at 40 mg.kg-1 for old rats(P < 0.01). In view of the close relationship of NO content and NOS activity with aging, the inhibitory effect of Rg1 on NOS activity, as shown by our results, might provide an explanation for its antiaging function.

Aging↗

[Effects of tyrosine alone and tyrosine in combination with RU486 on early pregnancy in mice and the mechanism of action].

Treatment with tyrosine at the dosage of 85 mg.kg-1 on day 6-8 of gestation did not have significant effect to terminate early pregnancy in mice. Tyrosine combined with RU486 was shown to have a synergistic effect to terminate early pregnancy. Tyrosine 170 mg.kg-1 on day 6-10 of gestation significantly decreased the concentration of serum progesterone in early pregnant mice. Further study with luteal cells in rats showed that tyrosine 50 micrograms.ml-1 inhibited hCG-induced progesterone production when used alone, and inhibited basal production when used together with (+) PG05. These results suggest that the inhibiting effect of tyrosine on steroidogenesis may contribute to the termination of early pregnancy.

Abortifacient Agents, Steroidal↗

[Analysis of 158 cases of hysteroscopic surgery for hysteromyoma].

OBJECTIVE: To treat hysteromyoma by hysteroscopic surgery and to examine the treatment results in relation to the extent of surgery. METHODS: 177 patients admitted from May, 1990 to Dec. 1994 for abnormal uterine bleeding caused by hysteromyoma were subjected to transcervical resection of myoma (TCRM) and/or transcervical resection of endometrium (TCRE). Except for 19 patients lost to follow-up, 158 patients were closely observed postoperatively. The mean follow-up was 29.3 months (range 5-60). These patients were divided into four groups according to the extent of the resected myoma. Analysis was based on 3 categories: the degree of bleeding control, the rate of growth of myoma and the need of subsequent surgery, and the treatment results were grouped into: perfection, satisfaction and dissatisfaction. RESULTS: The growth of myoma and bleeding were controlled in 150 patients (94.9%) after resection. The result was much better than that of abdominal myomectomy. The treatment success of total resection of pediculate submucosal myoma was as high as 100%. If only > or = 50% of sessile submucosal myoma and intramural myoma were resected, the results of hysteroscopic surgery were satisfactory although there might be small residual intramural myoma or subserous myoma. Long term follow-up showed the residual myomata seemed to have stopped growing. CONCLUSION: Transcervical resection is one of the effective treatments for abnormal uterine bleeding in hysteromyoma. Preoperative accuracy in appraisal of the extent of the myoma to be resected may help to correctly predict the prognosis and to improve the surgical cure rate.

Adult↗

[Analysis of the outcomes of transcervical resection of endometrium in 400 cases with menorrhagia].

OBJECTIVE: To report the efficacy and outcomes of transcervical resection of the endometrium (TCRE) in treatment of menorrhagia. METHODS: 400 patients with menorrhagia due to fatigue causes who had failed in medical therapy and did not desire pregnancy and surgery underwent TCRE under hysteroresectoscope. Among them, 72 patients with submucous uterine myoma less than 5cm in diameter had their myoma resected simultaneously, 366 cases were followed up postoperatively for 3 months to 4 years. RESULTS: TCRE was performed successfully except 16 cases, giving a success rate of 95.6%. Three cases sustained uterine perforation. During follow-up, 146 cases (41.7%) became amenorrhea, 119 (34.0%) had only spotting. The remaining 85 (24.3%) had normal periods. 78.3% of the cases who previously had dysmenorrhea had relieved their pain. Long-term complications were recurrent abnormal uterine bleeding (22 cases 13 of them had a second operation), hematometra (5) and adenomyosis (4 cases). CONCLUSION: TCRE is an effective procedure in treating menorrhagia and small submucous uterine myoma.

Adult↗

ICE-LAP6, a novel member of the ICE/Ced-3 gene family, is activated by the cytotoxic T cell protease granzyme B.

Members of the ICE/Ced-3 gene family are likely effector components of the cell death machinery. Here, we characterize a novel member of this family designated ICE-LAP6. By phylogenetic analysis, ICE-LAP6 is classified into the Ced-3 subfamily which includes Ced-3, Yama/CPP32/apopain, Mch2, and ICE-LAP3/Mch3/CMH-1. Interestingly, ICE-LAP6 contains an active site QACGG pentapeptide, rather than the QACRG pentapeptide shared by other family members. Overexpression of ICE-LAP6 induces apoptosis in MCF7 breast carcinoma cells. More importantly, ICE-LAP6 is proteolytically processed into an active cysteine protease by granzyme B, an important component of cytotoxic T cell-mediated apoptosis. Once activated, ICE-LAP6 is able to cleave the death substrate poly(ADP-ribose) polymerase into signature apoptotic fragments.

Amino Acid Sequence↗

Cytotoxic T-cell-derived granzyme B activates the apoptotic protease ICE-LAP3.

Cytotoxic T lymphocytes (CTLs) and natural killers (NK) cells provide immune surveillance against viruses and neoplasms, and play a central role in the pathogenesis of autoimmune disease, AIDS and graft rejection. Thus, it is important to understand the precise molecular mechanism(s) whereby cytotoxic lymphocytes destroy susceptible target cells. Granule-mediated cytotoxicity requires a combination of both perforin and granzyme B. Perforin polymerizes to form transmembrane channels and presumably allows granzyme B access to target cell substrates, which until recently, were unknown. One clue to the identity of the physiological substrate(s) activated by granzyme B comes from its unusual specificity for cleaving synthetic substrates after aspartate residues. Members of the ICE/CED-3 family of cysteine proteases are prime candidates as they are important apoptotic effectors and are expressed as zymogens, which can be processed to form active heterodimeric enzymes after cleavage at specific aspartate residues. Previous studies have shown that granzyme B proteolytically activates the cell death effector Yama/CPP32/apopain (referred to here as Yama). Here we report that granzyme B also activates ICE-LAP3/Mch3/CMH-1 (referred to here as ICE-LAP3), which, along with Yama and Mch2, forms a subset of the ICE/CED-3 family of cysteine proteases most closely related to the Caenorhabditis elegans cell death gene, CED-3. Importantly, Jurkat T cells incubated with granzyme B and a sublytic concentration of perforin undergo apoptosis, which is preceded by the activation of endogenous ICE-LAP3. Thus, we propose that granzyme B mediates apoptosis by directly engaging the target cell's death effector machinery, which is probably composed of an arsenal of intracellular, CED-3-like cysteine proteases.

Apoptosis↗

Molecular ordering of the cell death pathway. Bcl-2 and Bcl-xL function upstream of the CED-3-like apoptotic proteases.

Genetic analyses of Caenorhabditis elegans has identified three genes that function in the regulation of nematode cell death. Mammalian homologs of two of these genes, ced-9 and ced-3, have been identified and comprise proteins belonging to the Bcl-2 and ICE families, respectively. To date, it is unclear where the negative regulators, ced-9 and bcl-2, function relative to the death effectors, ced-3 and the mammalian ced-3 homologs, respectively. Here, the molecular order of the cell death pathway is defined. Our results establish that Bcl-2 and Bcl-xL function upstream of two members of the ICE/CED-3 family of cysteine proteases, Yama (CPP32/apopain) and ICE-LAP3 (Mch3).

Amino Acid Sequence↗

ICE-LAP3, a novel mammalian homologue of the Caenorhabditis elegans cell death protein Ced-3 is activated during Fas- and tumor necrosis factor-induced apoptosis.

Members of the ICE/ced-3 gene family have been implicated as components of the cell death pathway. Based on similarities with the structural prototype interleukin-1 beta-converting enzyme (ICE), family members are synthesized as proenzymes that are proteolytically processed to form active heterodimeric enzymes. In this report, we describe a novel member of this growing gene family, ICE-LAP3, which is closely related to the death effector Yama/CPP32/Apopain. Pro-ICE-LAP3 is a 35-kDa protein localized to the cytoplasm and expressed in a variety of tissues and cell lines. Overexpression of a truncated version of ICE-LAP3 (missing the pro-domain) induces apoptosis in MCF7 breast carcinoma cells. Importantly, upon receipt of a death stimulus, endogenous ICE-LAP3 is processed to its subunit forms, suggesting a physiological role in cell death. This is the first report to demonstrate processing of a native ICE/ced-3 family member during execution of the death program and the first description of the subcellular localization of an ICE/ced-3 family member.

Adult↗

Cholesterol homeostasis is modulated by amphiphiles at transcriptional and post-transcriptional loci.

A variety of amphiphiles inhibit plasma membrane cholesterol esterification and induce 3-hydroxy-3-methylglutaryl-coenzyme A reductase accumulation in cultured cells; among these are steroids, hydrophobic amines, phenothiazines, ionophores, colchicine, and lysophosphatides. It has been proposed that these amphiphiles signal a sterol deficiency to regulatory sites by blocking the movement of plasma membrane cholesterol into the cell (Lange, Y., and Steck, T. L. 1994. J. Biol. Chem. 269: 29371-29374). If this were the case, these agents also should enhance transcription of sterol responsive genes and stabilize 3-hydroxy-3-methylglutaryl-coenzyme A reductase. As a test of this hypothesis, the effect of the amphiphiles on such transcriptional and post-transcriptional events was assessed. A mouse embryo cell line was transfected with a construct containing the promoter for the human low density lipoprotein receptor upstream of the DNA sequence coding for chloramphenicol acyltransferase (CAT). Incubation of these cells for 7-18 h with the aforementioned agents caused the level of expression of the promoter/CAT construct to increase 2- to 9-fold. We showed further that the amphiphiles stimulated 3-hydroxy-3 methylglutaryl-coenzyme A reductase activity by increasing gene transcription as well as by decreasing degradation of the enzyme. These are the predicted homeostatic responses to cell cholesterol deficiency. These findings support the hypothesis that certain amphiphiles falsely signal a cholesterol deficiency to the intracellular sites regulating cholesterol homeostasis.

3T3 Cells↗

[Diagnosis of uterine diseases by combined hysteroscopy and ultrasonography].

OBJECTIVE: To investigate the diagnostic value of combined hysteroscopy with ultrasonography. METHODS: 477 patients were diagnosed by hysteroscopy, ultrasonography, or hysteroscopy combined with ultrasound. The results of the 3 groups were compared with the findings after operations. RESULTS: This study indicated to diagnose intrauterine lesions, intramural diseases or pelvic disorders, hysteroscopy with ultrasonography was significantly better than either methods alone. The accuracy rate, false positive rate as well as false negative rate were 98.32%, 1.26% and 0.04% respectively. CONCLUSION: Hysteroscopy is used for diagnosis and treatment of intrauterine lesions, and ultrasonography is difficult to show actual location of lesions within uterine cavity. The present study has shown that hysteroscopy combined with ultrasound could increase the effectiveness and accuracy of uterine diseases' diagnosis.

Adult↗

[The role of urokinase type plasminogen activator in invasion of bile duct carcinoma].

OBJECTIVE: To study the role of urokinase type plasminogen activator (u-PA) in the invasive process of bile duct carcinoma. METHODS: The secretion of u-PA and the invasive potential of tumor cell in vitro in a newly established cell line of bile duct carcinoma, QBC939, were observed by using an amnion invasion culture system. RESULTS: QBC939 cells secreted u-PA with high invasive potential. The inhibitors of u-PA and plasmin, tranexamic acid and 6-aminocaproic acid, obviously inhibited the u-PA activity and the invasive potential of QBC939 cells. CONCLUSION: u-PA is one of the important enzymes in tumor invasion. Inhibiting u-PA or plasmin may be a prospective therapy for tumor treatment.

Bile Duct Neoplasms↗

[Changes of Kupffer cell DNA and RNA synthetic functions after partial hepatectomy in cirrhotic rats].

We studied the changes of DNA and RNA synthetic functions of regenerating liver cells after partial hepatectomy in cirrhotic rats and discussed the relationship between liver regeneration and liver functional failure. Seventy healthy male Wistar rats weighing 200 approximately 250 g, were randomized into sham-operated (SO), partial hepatectomy in cirrhotic rats (C-PH) and partial hepatectomy in normal rats (N-PH). The left and middle lobes were dissected. The synthetic DNA peak of Kupffer cells (KC) in the G2 and M phase in C-PH was found after 24 hr of operation. The regenerating index peak of KC was at 48 hr after operation, which was higher than the other groups, but the liver weights in C-PH was lower than that in the N-PH at 1 week after operation. The RNA content of KC markedly decreased and returned to normal levels at 1 week after operation. We think that KC functions are suppressed after partial hepatectomy in cirrhotic rats. It is an important cause of hepatocyte regeneration function decrease and liver functional failure for delay of liver cell regeneration "start" and the regeneration cell cycle.

Animals↗

The Ret receptor protein tyrosine kinase associates with the SH2-containing adapter protein Grb10.

Ret is a receptor protein tyrosine kinase that has been implicated in the development of the enteric nervous, endocrine, and renal systems. Mutations associated with multiple endocrine neoplasia types 2A and 2B (MEN 2A and 2B) have been shown to activate the intrinsic kinase and transforming ability of ret (Santoro, M., Carlomagno, F., Romano, A., Bottaro, D. P., Dathan, N. A., Grieco, M., Fusco, A., Vecchio, G., Matoskova, B., Kraus, M. H., and Paolo DiFiore, P. (1995) Science 267, 381-383). Using the cytoplasmic domain of Ret as bait in a yeast two-hybrid screen of a mouse embryonic library, it was discovered that the src homology 2 (SH2) domain containing protein Grb10 bound Ret. Grb10 belongs to an emerging family of SH2 containing adapter proteins, the prototypical member being Grb7. Using glutathione S-transferase fusion proteins, it was demonstrated that the SH2 domain of Grb10 specifically interacted with Ret. Additionally, using an EGFR/Ret chimera, it was shown that Grb10 bound Ret in an activation dependent manner in vivo. This is the first description of a receptor protein tyrosine kinase that utilizes Grb10 as a signaling intermediate.

Animals↗

Characterization of a novel Src-like adapter protein that associates with the Eck receptor tyrosine kinase.

The Eph family of receptor protein tyrosine kinases (RPTKs) is the largest family of RPTKs. The signal transduction pathways initiated by this family have only recently begun to be explored. Using a yeast two-hybrid screen to identify molecules that interact with the cytoplasmic domain of Eck, it was previously shown that activated Eck RPTK bound to and stimulated phosphatidylinositol 3-kinase (Pandey, A., Lazar, D.F., Saltiel, A. R., and Dixit, V.M. (1994) J. Biol. Chem. 269, 30154-30157). Also isolated from this same screen was a novel protein containing SH3 and SH2 adapter modules that had striking homology to those found in the Src family of non-receptor tyrosine kinases. However, unlike other Src family members, it lacked a catalytic tyrosine kinase domain. Hence, this protein was designated SLAP for Src-like adapter protein. Using glutathione S-transferase fusion Proteins, it was demonstrated that SLAP bound to activated Eck receptor tyrosine kinase. Therefore, SLAP is a novel candidate downstream signaling intermediate and the first member of the Src family that resembles an adapter molecule.

Adaptor Proteins, Signal Transducing↗