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Biomedical subjects

C L Yu

Publications and source records attributed to C L Yu.

At least 91 records · Page 5Linked to original sources
PubMed1995

Reducing effect of 3,4',5-trihydroxystibene-3-beta-mono-D-glucoside on arterial thrombosis induced by vascular endothelial injury.

AIM: To study the effect of 3,4',5-trihydroxystibene-3-beta-mono-D-glucoside (Polydatin, Pol) on rabbit arterial thrombosis. METHODS: Rabbit arterial thrombosis was induced by vascular endothelial damage with trypsin. RESULTS: It was showed that the moist weights of the thrombus were 6.6 +/- 1.8 and 4.8 +/- 1.6 mg in Pol 5 and 10 mg.kg-1 groups, respectively, which was lighter than that in control (10.9 +/- 1.9 mg, P < 0.05, P < 0.01); the platelet aggregation was inhibited simultaneously. In vitro, Pol 0.30-1.15 mmol.L-1 reduced TXA2 produced in platelets. It did not affect the production of PGI2 in cultured human umbilical vein endothelial cells. CONCLUSION: Thrombosis was abated by Pol. The selective inhibition of production of TXA2 rather than PGI2, is one of the mechanisms involved.

Animals↗
PubMed1995

Anti-dsDNA antibodies cross-react with ribosomal P proteins expressed on the surface of glomerular mesangial cells to exert a cytostatic effect.

Affinity-purified human polyclonal anti-double-stranded DNA antibodies (anti-dsDNA) exerted a cytostatic effect towards human and rat glomerular mesangial cells (MC). In order to identify the cognate antigens for anti-dsDNA on the surface of MC, we used these autoantibodies to probe a human renal lambda gt11 cDNA expression library. Two cDNA clones encoding the cognate proteins for the autoantibodies were isolated. Sequencing analysis of the two cDNA showed that they had 98.6% homology with the gene of the P0 and 99.2% homology with the gene of the P1 human acidic ribosomal phosphoproteins (P protein). Two galactosidase fusion proteins (125,000 and 150,000 MW) derived from the two cDNA inserts expressed in lysogenic Escherichia coli Y1089 could react with the original screening antibodies in an immunoblotting analysis. After transformation and expression of the full-length P1 clone in prokaryotic cells, the purified P1 protein was able to react with anti-dsDNA. In a cross-inhibition experiment, the dsDNA binding activity of anti-dsDNA was inhibited by a synthetic polypeptide corresponding to the carboxyl-terminal 20 amino acids of P protein and purified P1 protein in a dose-dependent manner, but this was less potent than the inhibition caused by calf thymus dsDNA. By use of well-defined systemic lupus erythematosus (SLE) sera, we found only sera containing a high titre of anti-dsDNA activity (> 300 IU/ml) reacted with P1 of rat MC lysate. Furthermore, the 38,000 and 19,000 MW macromolecules were proved to be the cognate antigens for anti-dsDNA expression on the surface of the MC, by Western blot of the MC plasma membrane lysates. These results suggest that anti-dsDNA may cross-react with ribosomal P proteins expressed on the surface of the MC and exert cytostasis towards these cells.

Animals↗
PubMed1995

Influence of 3,4',5-trihydroxystibene-3-beta-mono-D-glucoside on vascular endothelial epoprostenol and platelet aggregation.

AIM: To study the relationship between the inhibiting effect on platelet aggregation and the enhancing effect on epoprostenol (PGI2) released from vascular endothelium with 3,4',5-trihydroxystibene-3-beta-mono-D-glucoside (polydatin, Pol). METHODS: After having been incubated with Pol, the incubating medium was withdrawn from the bottles with newborn umbilical vein endothelial cells (VEC group, trypsin digesting method) and added to the platelets (washing method). The medium withdrawn from the bottles without VEC was designated as control group. Reduction of platelet aggregation rates (PAR, turbidity method) and changes of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) (radioimmunoassay method) in the supernatant of the aggregated platelets induced by thrombin were scrutinized. RESULTS: PAR in the control group showed no reduction, whereas PAR reduction (-10 +/- 10) and 6-keto-PGF1 alpha increase (108 +/- 30 ng.L(-1)) in the VEC group treated 10 min with Pol 0.41 mmol.L(-1) (vs that of distilled water, ie, 2 +/- 12 and 54 +/- 20 ng.L(-1)) occurred. CONCLUSION: Increase of PGI2 from VEC by Pol was involved in its (Pol's) inhibition effect of platelet aggregation.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Intraoperative somatosensory evoked potentials for localization in excision of recurrent parasagittal meningioma--a case report.

Removal of tumors that are located in the motor area is a challenge to neurosurgeons because of the possibility of injuring the motor cortex. We present our experience in excision of a recurrent parasagittal meningioma located in the central area. With the help of somatosensory evoked potentials (SSEP) monitoring, the tumor was removed totally without any neurologic sequela.

Aged↗
PubMed1995

Production of the third component of complement (C3) by peripheral polymorphonuclear neutrophils of the patients with rheumatoid arthritis.

Normal human polymorphonuclear neutrophils (PMN) can spontaneously produce the third component of complement (C3) in in vitro culture as detected by ELISA. This C3-producing capacity of PMN can be augmented by TNF-alpha (20 ng/ml) and bacterial lipopolysaccharide (100 ng/ml), but not by IL-1 beta or IL-8. The C3 production by PMN was found to be temperature dependent and was suppressed by the addition of protein inhibitor. The C3 mRNA in PMN could be detected by reverse transcription assisted polymerase chain reaction (RT-PCR) after TNF-alpha or LPS stimulation for 6 hours. To further understand C3 production by peripheral blood PMN in rheumatoid arthritis (RA), spontaneous and TNF-alpha stimulated production of C3 by peripheral PMN were compared in 15 cases of active RA, 15 inactive RA and 15 normal individuals. We failed to find any significant difference among the three groups. We conclude that PMN plays a negligible role in C3 hypercomplementemia in patients with active RA.

Arthritis, Rheumatoid↗
PubMed1995

Prostaglandin E2 suppresses the expression and release of beta 2-microglobulin from mitogen-activated normal human mononuclear cells.

BACKGROUND: Prostaglandin E2 (PGE2) is a feedback suppressor of immune response. Beta 2-Microglobulin (beta 2M) is part of HLA class I molecule that mediates viral antigen presentation to cytotoxic T lymphocytes as well as graft rejection. It has been known that beta 2M can be synthesized by both stimulated and unstimulated lymphocytes, but it is unknown whether beta 2M can be modulated by PGE2. This investigation aimed to clarify this point. METHODS: Normal human mononuclear cells (MNC) were isolated, stimulated by phytohemagglutinin (PHA), and cultured for 3 days in the presence or absence of PGE2. The culture supernatants were collected and detected for beta 2M concentration by enzyme linked immunosorbent assays (ELISA). The cell pellets were stained indirectly with immunofluorescence for HLA-class I antigen and beta 2M expression on the surface membranes. In addition, the membrane potential of stimulated or unstimulated cells was measured by flow cytometry to evaluate the effect exerted by PGE2. RESULTS: PGE2 at a concentration of more than 1 x 10(-8)M markedly suppressed the expression and release of beta 2M from PHA-stimulated MNC in a dose-dependent manner. Expression of HLA-class I molecule on PHA-stimulated MNC was also suppressed by PGE2. Kinetic study demonstrated that PGE2 began to suppress beta 2M synthesis of PHA-stimulated MNC from the 3rd day of culture. It also inhibited beta 2M release from lymphocytes in mixed lymphocyte reaction. This inhibitory effect was not due to cell death as confirmed by trypan blue exclusion. PGE2 per se exerts negligible effect on membrane potential of MNC but can normalize the depolarized state of the membrane induced by PHA as demonstrated by 3,3'-dihexyloxacarbocyanine iodide stain. CONCLUSIONS: PGE2 down-regulates the production of HLA-class I antigens and beta 2M molecules. This effect is associated with the suppression of cytotoxic T cell function by PGE2 and may be relevant to the underlying mechanism of PGE2 on this population of cells.

Cells, Cultured↗
PubMed1995

Proximal promoter region of the junB gene mediates attenuation of serum inducibility in Src-transformed cells.

Transcription of the junB gene is rapidly and transiently induced following stimulation of susceptible cells by growth factors in serum. Our previous studies demonstrated that serum inducibility of junB and other immediate-early genes is markedly attenuated in fibroblasts chronically transformed by the viral Src oncoprotein. Moreover, attenuation of junB induction occurs at the transcriptional level. To characterize further the molecular mechanisms of this attenuation, various full-length and recombinant junB constructs were transfected into normal and viral Src-transformed rat fibroblasts. A stable transfection system was used to faithfully reproduce regulation of the junB gene. Analyses of pooled populations of stably transfected cells demonstrate that sequences between -89 and +32 (relative to the transcriptional start site) are sufficient to confer both serum inducibility of the junB gene in normal cells and its attenuation in viral Src-transformed cells. By contrast, attenuation of c-fos serum inducibility by Src transformation involves element(s) distinct from regulatory elements identified previously in the c-fos promoter. These results identify a proximal promoter region of the junB gene that is involved in a novel negative regulation of its transcription.

Animals↗
PubMed1994

Cerebrospinal fluid interleukin-6, prostaglandin E2 and autoantibodies in patients with neuropsychiatric systemic lupus erythematosus and central nervous system infections.

Cerebrospinal fluid (CSF) from patients with a variety of central nervous system (CNS) disorders was assayed for cytokines, prostaglandins, and autoantibodies. CSF interleukin-6 (IL-6) in patients with CNS infection (374.24 +/- 92.61 pg/mL) and neuropsychiatric systemic lupus erythematosus (NP-SLE) (71.40 +/- 5.89 pg/mL) were significantly higher than in patients with CNS inflammation (33.92 +/- 29.36 pg/mL) or controls (non-inflammatory CNS diseases) (4.35 +/- 3.00 pg/mL). Interleukin-1 beta, interferon alpha, and tumor necrosis factor alpha were undetectable in these samples: CSF prostaglandin E2 (PGE2) also exhibited similar patterns as IL-6. CSF immunoglobulin G (IgG) in patients with NP-SLE (8.84 +/- 1.80 mg/dL) was much higher than in patients with CNS infection (4.65 +/- 3.09 mg/dL), CNS inflammation (2.54 +/- 1.24 mg/dL), or controls (2.11 +/- 1.03 mg/dL). CSF autoantibodies against calf thymus antigens were present in patients with NP-SLE but not in patients with CNS infection as demonstrated by immunoblot. These results suggest that high IL-6 and PGE2 in CSF favors the diagnosis of CNS infection, while modestly elevated IL-6, high IgG, and autoantibodies against calf thymus antigens in CSF are the features of NP-SLE.

Autoantibodies↗
PubMed1994

The elevation of plasma DNA in patients with systemic lupus erythematosus is attributable to increased DNA release and defective DNA binding of mononuclear cells.

BACKGROUND: Although immunoprecipitable DNA has been found in a subgroup of patients with systemic lupus erythematosus (SLE) exhibiting systemic vasculitis and/or central nervous system involvement, the mechanism for elevated plasma DNA in these patients is poorly understood. METHODS: The plasma DNA concentrations and reactivity of serum and lymphocytes to six species of double-stranded DNA from calf thymus, human placenta, Escherichia coli, Micrococcus lysodeikticus, Clostridium perfringens and poly (dG.dC). poly (dG.dC) were measured in twenty-seven patients with active SLE. To understand the mechanism of increased plasma DNA in SLE, the DNA binding and release of the mononuclear cells were examined. RESULTS: Compared with the controls, the incidence of the presence of plasma DNA was markedly increased in SLE (59.3% in SLE vs. 7.4% in controls) as detected by counterimmunoelectrophoresis. Except for DNA from Clostridium perfringens, the reactivity of lupus sera to various DNA samples was significantly higher than that of the controls. The reactivity of lymphocytes to 6 species of DNA (as defined by 3H-thymidine incorporation of the cells) was also higher in SLE patients. In DNA binding and releasing experiments, patients with SLE were found to have decreased 3H-DNA binding activity (0.169 +/- 0.018 micrograms/2 x 10(6) cells in SLE vs. 0.283 +/- 0.02 micrograms/2 x 10(6) cells in controls, p = 0.001) but to have increased spontaneous release of DNA (1,465 +/- 412 cpm in SLE vs. 630 +/- 179 cpm in controls, p = 0.0173) in mononuclear cells. CONCLUSIONS: The results suggest that some subsets of lymphocytes can be sensitized by different DNA samples in vivo to increase endogenous DNA release from mononuclear cells, which in addition to decreased DNA clearance as has been previously reported, may be responsible for the elevation of plasma DNA in patients with SLE.

Adult↗
PubMed1994

Increased production of tumor necrosis factor-alpha and release of soluble CD4 and CD8 molecules, but decreased responsiveness to phytohemagglutinin in patients with nasopharyngeal carcinoma.

Twelve patients with nasopharyngeal carcinoma (NPC) were studied for spontaneous and phytohemagglutin (PHA)-stimulated production of cytokines, soluble markers and [3H] thymidine incorporation by mononuclear cells. The same number of patients with skin cancer and healthy subjects were used as control groups. Our results showed that the NPC group produced much more tumor necrosis factor-alpha (TNF alpha), soluble CD4 (sCD4) and CD8 (sCD8) in PHA-stimulated mononuclear cell supernatants than those in the other two groups. The levels of soluble interleukin-2 receptor (sIL-2R) and gamma-interferon (IFN gamma) in PHA-stimulated supernatants were at the same high level in the NPC and healthy subjects groups while the concentrations were much lower in the skin cancer group. We also noticed that the early stage group in NPC patients had higher levels of interleukin-1 alpha (IL-1 alpha), TNF alpha, IFN gamma and sIL-2R in both spontaneous and PHA-stimulated mononuclear cell supernatants. The stimulation index of PHA-responsiveness was 155, 5.2 and 37, respectively, in the healthy subjects, skin cancer and NPC groups. The PHA-responsiveness was depressed in both the NPC and skin cancer groups. It seems that cancer patients have an impaired T cell mitogenic response after mitogen stimulation. NPC patients had better immune response than skin cancer patients in immune factor release or PHA-responsiveness.

Adolescent↗
PubMed1994

Small cell carcinoma of the lung in a patient with rheumatoid arthritis: a case report.

We describe an occurrence of small cell carcinoma of the lung in a 37-year-old woman with rheumatoid arthritis who did not receive any kind of cytotoxic agents for the rheumatic condition. There seemed to have no predisposing factor for the development of malignancy. The diagnosis of small cell carcinoma was based on repeated hemoptysis and cytologic finding of a rapidly growing mass over the forehead. The patient responded dramatically to chemotherapy with rapid resolution of forehead mass, relief of arthritis in the hands, and decrease of serum rheumatoid factor from 4800U/ml to 1200U/ml. This appeared to be the first report of small cell carcinoma of the lung developing in a patient with rheumatoid arthritis.

Adult↗
PubMed1993

Prostaglandin E2 suppresses phytohemagglutinin-induced immune responses of normal human mononuclear cells by decreasing intracellular glutathione generation, but not due to increased DNA strand breaks or apoptosis.

Prostaglandin E2 (PGE2) at concentrations more than 1 x 10(-8) M markedly suppressed the cell proliferation and release of soluble molecules of interleukin-2 receptor (sIL-2R), CD4 (sCD4) and CD8 (sCD8) from phytohemagglutinin (PHA)-stimulated normal human mononuclear cells (MNC) in a dose-related manner. To further elucidate the subcellular mechanism of the inhibitory effect of PGE2 on PHA-stimulated MNC, intracellular concentration of glutathione (GSH) in PHA-stimulated MNC was sequentially measured from day 1 to day 3 by enzymic method. Furthermore, the effect of PGE2 on nuclear DNA including DNA strand breaks in alkali treatment and DNA fragmentation (apoptosis) of PHA-stimulated MNC were also measured. We found intracellular GSH levels were significantly decreased in the early stage of lymphocyte activation (day 1), but no evidence of increased DNA strand breaks or apoptotic process appeared in 3-day culture. In addition, butathione sulfoximine (a specific GSH inhibitor) and dibutyryl cyclic AMP also exhibited both proliferation inhibition and GSH-decreasing effects on PHA-stimulated MNC as well as PGE2. These results suggest that the immunosuppressive effect of PGE2 is mediated by the decreased generation of intracellular GSH, but not by the increased DNA strand breaks or apoptotic mechanism in the cells.

Antimetabolites↗
PubMed1993

Coexistence and relationship of antikeratinocyte and antimelanocyte antibodies in patients with non-segmental-type vitiligo.

To test for autoantibodies in patients with vitiligo, skin biopsies from 16 patients with active vitiligo and 12 patients with stable vitiligo were examined by direct immunofluorescence. In periodate-lysine-paraformaldehyde-fixed biopsy specimens, the presence of IgG deposits in keratinocytes and the number of keratinocytes with focal IgG in active vitiligo were significantly greater than in stable vitiligo. To test whether the antibodies to normal human keratinocytes or melanocytes are present in vitiligo, we used an indirect immunofluorescent test and enzyme-linked immunosorbent assay to test the serum of 43 patients. With unfixed viable melanocytes, we found a granular pattern of IgG staining on the plasma membrane of melanocytes incubated with patients' sera but not in cells incubated with the control sera. With methanol-fixed melanocytes, however, we found a homogeneous pattern of IgG staining in the cytoplasm of melanocytes. With unfixed viable keratinocytes as targets, there was no deposit of IgG on the cells. A homogeneous pattern of IgG binding in the cytoplasm of methanol-fixed keratinocytes suggested the presence of antikeratinocyte autoantibodies to cytoplasmic keratinocyte components. The fluorescence staining for IgG binding was more prominent in active or extensive vitiligo. Vitiligo sera were cytotoxic for melanocytes but not for keratinocytes in vitro. Antimelanocytic antibodies may play a role in melanocytotoxicity, whereas antikeratinocyte antibodies may occur secondary to cellular damage.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1993

Attenuation of serum inducibility of immediate early genes by oncoproteins in tyrosine kinase signaling pathways.

Immediate early genes involved in controlling cell proliferation are rapidly and transiently induced following stimulation of susceptible cells with serum. To study how oncoproteins regulate immediate early genes, we examined serum inducibility of these genes in cells transformed by various oncoproteins. We found that induction of the immediate early gene, c-fos, by serum stimulation was markedly attenuated in four independent cell lines stably transformed by the v-Src tyrosine kinase. Cells chronically transformed by other oncoproteins implicated in tyrosine kinase signaling pathways, including v-Sis, v-Ras, and v-Raf, showed the same pattern of attenuation. In contrast, serum inducibility of c-fos was not attenuated in cells transformed by simian virus 40, which is thought to transform cells through a different pathway. Cell cycle analyses showed that proliferation of these transformed cell lines could be arrested effectively in 0.1% serum, demonstrating that the attenuation was not simply due to continuous cycling of transformed cells after serum deprivation. Moreover, serum inducibility of other immediate early genes, including c-jun, junB, egr-1, and NGFI-B, also was strikingly attenuated by these same oncoproteins. Nuclear run-on transcription assays established that this attenuation of serum inducibility occurred at the transcriptional level. Finally, flow cytometric analysis demonstrated that serum-starved v-Src-transformed cells were viable and able to progress into S phase of the cell cycle after serum stimulation, even though the induction of immediate early genes was greatly attenuated in these cells. Our results suggest that activation of immediate early genes is repressed by chronic stimulation of tyrosine kinase signaling pathways in transformed cells.

Animals↗
PubMed1993

Polyclonal IgG anti-dsDNA antibodies exert cytotoxic effect on cultured rat mesangial cells by binding to cell membrane and augmenting apoptosis.

IgG anti-double stranded DNA antibodies (anti-dsDNA) purified from serum of patients with active systemic lupus erythematosus (SLE), have been found to be cytotoxic to the cultured rat mesangial cells (MC). In the present study, by use of immunofluorescent staining, immunoblotting, radioimmunoprecipitation, and cell cycle analysis, we showed that IgG anti-dsDNA could bind to the membrane of MC. The bound epitope was a 28 kDa protein, which would disappear if the cells were treated in advance with proteinase K (100 micrograms/ml). In addition, binding of MC by 20 micrograms/ml of anti-dsDNA IgG F(ab')2 activated plasma membrane (equivalent to 80 IU/ml of calf thymus double-stranded DNA binding activity) resulted in release of much more 3H-arachidonic acid than binding by 20 micrograms/ml of human IgG F(ab')2 (26.71 +/- 3.75% in the case of anti-dsDNA vs. 4.73 +/- 2.86% in the case of IgG). To understand further the cytotoxic mechanism of anti-dsDNA, we incubated MC with anti-dsDNA, for a variety of periods (from 10 minutes to 24 hours). After incubation, the cells were fixed and stained with hematoxylin-eosin for morphologic observation. Simultaneously, the genomic DNA was extracted and analyzed in 1.8% agarose gel electrophoresis. We found that cell death caused anti-dsDNA followed a process of apoptosis rather than necrosis. These results suggest that binding of anti-dsDNA with MC membrane may activate endonuclease which will fracture the DNA and lead to programmed cell death.

Animals↗
PubMed1992

Platelet-derived growth factor (PDGF) alpha receptor activation modulates the calcium mobilizing activity of the PDGF beta receptor in Balb/c3T3 fibroblasts.

In order to determine whether distinct platelet-derived growth factor (PDGF) receptors (alpha and beta) can modulate the activity of one another, PDGF isoform (AA, BB, and AB)-stimulated changes in Ca2+i were monitored by digitized video microscopy in single cells upon sequential addition of PDGF isoforms. In Balb/c 3T3 fibroblasts, all PDGF isoforms were capable of stimulating increases in Ca2+i of 200-600% above basal levels, although with different potencies: BB greater than or equal to AB greater than AA. All cells were BB-PDGF-responsive, but only 74% of cells examined responded to AA-PDGF. The Ca2+i response elicited by BB-PDGF was inhibited by 60-75% in cells stimulated 10 min earlier with the AA isoform. The half-life of this inhibition was 22 min. In cells in which the alpha receptor was down-regulated by prolonged incubation with AA-PDGF, BB-induced Ca2+i responses were not inhibited. Pretreatment of cells with phorbol ester did not inhibit BB-PDGF-induced increases in Ca2+i, yet down-regulation of PKC activity prevented the AA-PDGF inhibition of BB-PDGF-induced Ca2+i responses. An increase in Ca2+i induced by AlF(4-)-stimulated IP3 generation did not inhibit a subsequent BB-PDGF Ca2+i response; however, attenuation of AA-PDGF-induced extracellular Ca2+ influx with EGTA prevented the inhibition of BB-PDGF-induced Ca2+i increases. Readdition of Ca2+ to the medium after removal of EGTA restored the inhibition of the BB-PDGF Ca2+i response. The inhibition of the BB-PDGF Ca2+i response by AA-PDGF was not caused by inhibition of PDGF receptor tyrosine autophosphorylation, which was unchanged after pretreatment with AA-PDGF. These results demonstrate: (a) that only a subpopulation of cells possess a functional alpha receptor-mediated response as assessed by AA-PDGF-induced increases in Ca2+i, whereas all cells possess the beta receptor-mediated responses; and (b) AA-PDGF and its associated alpha receptor can modulate the activity of the beta receptor through a mechanism that is dependent upon Ca(2+)-influx which may be controlled in part by PKC activation.

3T3 Cells↗