PubMed Health⌕ Search

Biomedical subjects

S F Luo

Publications and source records attributed to S F Luo.

At least 19 recordsLinked to original sources
PubMed1995

Pharmacological characterization of bradykinin receptors in canine cultured tracheal smooth muscle cells.

1. [3H]-bradykinin was used to characterize the bradykinin receptors associated with canine cultured tracheal smooth muscle cells (TSMCs). Receptor binding assay showed that TSMCs had specific, saturable, high-affinity binding sites for [3H]-bradykinin. 2. The specific [3H]-bradykinin binding increased linearly with increasing cell concentrations. The equilibrium for association of [3H]-bradykinin with the bradykinin receptors was attained within 2 h at 4 degrees C and 1 h at room temperature, respectively. 3. Analysis of binding isotherms yielded an apparent equilibrium dissociation constant (KD) of 2.5 +/- 0.3 nM and a maximum receptor density (Bmax) of 25.1 +/- 0.3 fmol mg-1 protein. The Hill coefficient for [3H]-bradykinin binding was 1.00 +/- 0.02. The association (K1) and dissociation (K-1) rate constants were (8.67 +/- 2.60) x 10(6) M-1 min-1 and 0.024 +/- 0.005 min-1, respectively. KD, calculated from the ratio of K-1 and K1 was 2.8 +/- 0.5 nM, a value close to that of KD calculated from Scatchard plots of binding isotherms. 4. The B1 receptor selective agonist, (des-Arg9-bradykinin, 0.1 nM-10 microM) and antagonist ([Leu8, des-Arg9]-bradykinin, 0.1 nM-10 microM) did not did not inhibit the [3H]-bradykinin binding to TSMCs, which excludes the presence of B1 receptors in canine TSMCs. 5. The specific binding of [3H]-bradykinin to canine TSMCs was inhibited by B2 receptor selective antagonists ([D-Arg0, Hyp3, Thi5, D-Tic7, Oicl-bradykinin, Hoe 140, 0.1 nM-10 micro M and [D-Arg0, Hyp3,Thi5,8, D-Phe7-bradykinin, 0.1 nM-10 micro M) and agonists (bradykinin and kallidin, 0.1 nM-10 micro M) with a best fit by a one-binding site model. The order of potency for the inhibition of [3H]-bradykinin binding was kallidin = bradykinin = Hoe 140> [D-Arg0, Hyp3, Thi5,8, D-Phel-bradykinin.6. Preincubation of TSMCs with forskolin for 24 h led to an up-regulation of B2 receptors, increasing in Bmax from 25.1 +/- 0.3 to 218 +/- 24 fmol mg-1 protein without changing the KD values. [3H]-bradykinin binding to TSMCs was inhibited by the B2 receptor selective antagonists and agonists, but not by the B1 receptor selective reagents. The up-regulation of the B2 receptor by forskolin was mediated through protein synthesis, since cycloheximide blocked this response.7 It is concluded that the pharmacological characteristics of the bradykinin receptors in canine cultured TSMCs are primarily of the B2 receptor subtype.

Animals↗
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

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↗
PubMed1994

Effect of phorbol ester on phosphoinositide hydrolysis and calcium mobilization in cultured canine tracheal smooth muscle cells.

In cultured canine tracheal smooth muscle cells (TSMCs), muscarinic receptor stimulation led to phosphoinositide (PI) hydrolysis, formation of inositol phosphates (IPs), and mobilization of intracellular Ca2+. Desensitization of IPs accumulation and Ca2+ mobilization evoked by carbachol was investigated using [3H]inositol labelling and Ca(2+)-sensitive dye fura-2. Treatment of TSMCs with phorbol 12-myristate 13-acetate (PMA) for 30 min blocked the carbachol-stimulated formation of IPs and mobilization of Ca2+. The concentrations of PMA that gave half-maximal and maximal inhibition of carbachol-induced IPs accumulation were 70 nM and 1 microM, respectively. The inhibitory effect of PMA on carbachol-induced responses was reversed by staurosporine, a protein kinase C (PKC) inhibitor, suggesting that the inhibitory effect of PMA was mediated through the activation of PKC. Treatment of TSMCs with PMA for 24 h, the cells remained the ability to response to carbachol-induced IPs accumulation and Ca2+ mobilization with the same extent as that observed in the control group. Inactive phorbol ester, 4 alpha-phorbol 12, 13-didecanoate at 1 microM, did not inhibit the responses. The KD and Bmax of the muscarinic receptor for [3H]N-methyl scopolamine binding were not significantly changed by PMA treatment for either 30 min or 24 h. The locus of this inhibition was further investigated by examining the effect of PMA on AlF4(-)-stimulated IPs accumulation in canine TSMCs. AlF4(-)-induced response was inhibited by PMA treatment, supporting that G protein(s) can be directly activated by AlF4- which was uncoupled to phospholipase C (PLC) by PMA treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Bradykinin-stimulated calcium mobilization in cultured canine tracheal smooth muscle cells.

Bradykinin (BDK)-induced increases in intracellular Ca2+ concentration ([Ca2+]i) were monitored in cultured canine tracheal smooth muscle cells (TSMCs) using a fluorescent Ca2+ indicator, Fura-2. BDK and kallidin caused an initial transient peak followed by a sustained elevation of [Ca2+]i in a concentration-dependent manner, with half-maximal stimulation (log EC50) obtained at -8.10 M and -8.04 M, respectively. The BDK-induced rise in [Ca2+]i was not affected by the BDK B1 receptor antagonist, des-Arg9[Leu8]-BDK (10 microM). However, the BDK B2 receptor antagonists des-Arg[Hyp3, Thi5,8, D-Phe7]-BDK and Hoe 140 had high affinity in antagonizing BDK with pKB values of 7.5 +/- 0.3 and 8.7 +/- 0.3, respectively. The sustained phase of the rise in [Ca2+]i was dependent on the presence of external Ca2+, as evidenced by a decline to the resting level on addition of EGTA. In the absence of external Ca2+, only an initial transient peak was seen which then declined to the resting level; a sustained elevation of [Ca2+]i could then be evoked by addition of 1.8 mM Ca2+ in the continued presence of BDK. Ca2+ influx was required for the changes in [Ca2+]i, since Ca(2+)-channel blockers, diltiazem, verapamil, and Ni2+, decreased both the initial and sustained elevation of [Ca2+]i in response to BDK. In conclusion, these findings indicate that the initial increase in [Ca2+]i stimulated by BDK acting on BDK B2 receptors is due to the release of Ca2+ from internal stores, followed by the influx of external Ca2+ into the cells. The influx of extracellular Ca2+ partially involves a diltiazem- and verapamil-sensitive Ca2+ channel.

Animals↗
PubMed1994

The effect of cyclic AMP elevating agents on bradykinin- and carbachol-induced signal transduction in canine cultured tracheal smooth muscle cells.

1. The effects of cholera toxin (CTX), forskolin and dibutyryl cyclic AMP on bradykinin (BK)- and carbachol-induced accumulation of inositol phosphates (IPs) and Ca2+ mobilization were investigated in canine cultured tracheal smooth muscle cells (TSMCs). The BK-induced responses were mediated via a G protein which was not inhibited by CTX or pertussis toxin treatment. 2. BK-stimulated IPs accumulation and Ca2+ mobilization were potentiated by CTX (10 micrograms ml-1) pretreatment which was time-dependent. Maximal increase of these responses occurred after 24 h treatment with CTX. The concentration-effect relationship of BK-induced responses were shifted to the left and BK was substantially more effective in CTX-treated cells than in the control cells. This enhancing effect of CTX did not occur with carbachol. 3. Short-term (< 4 h) treatment with forskolin (10 microM) or dibutyryl cyclic AMP (1 mM) failed to accentuate BK-induced responses, but long-term (> 4 h) treatment of TSMCs with these agents mimicked the enhancing effect of CTX, suggesting that CTX-induced enhancement of BK responsiveness might be due to a rise in cyclic AMP. 4. Prolonged treatment of TSMCs with these agents was accompanied by an increase in cell surface [3H]-BK binding sites, which was inhibited by concurrent incubation with cycloheximide, an inhibitor of protein biosynthesis. Cycloheximide also abolished the potentiating actions of CTX, forskolin, and dibutyryl cyclic AMP on BK-induced IPs formation and Ca2+ mobilization. 5. The locus of this enhancement was further investigated by examining the effects of CTX, forskolin and dibutyryl cyclic AMP on A1F4(-)-induced IPs accumulation in canine TSMCs. AIF4-induced IPs accumulation was not affected by CTX, forskolin, or dibutyryl cyclic AMP treatment, supporting the contention that this stimulatory effect is located at the BK receptor level.6. These results demonstrate that the augmentation of BK-induced IPs accumulation and Ca2+mobilization produced by CTX, forskolin and dibutyryl cyclic AMP involves a cyclic AMP-dependent mechanism which is induced by a sustained increase in the level of intracellular cyclic AMP. CTX and forskolin may promote an increase of the synthesis of BK receptors, and thereby enhance BK-induced responses.

Animals↗
PubMed1994

Bradykinin-stimulated phosphoinositide metabolism in cultured canine tracheal smooth muscle cells.

1. Stimulation of bradykinin (BK) receptors coupled to phosphoinositide (PI) hydrolysis was investigated in canine cultured tracheal smooth muscle cells (TSMCs). BK, kallidin, and des-Arg9-BK, stimulated [3H]-inositol phosphates (IPs) accumulation in a dose-dependent manner with half-maximal responses (EC50) at 20 +/- 5, 13 +/- 4, and 2.3 +/- 0.7 nM, (n = 5), respectively. 2. D-Arg[Hyp3, D-Phe7]-BK and D-Arg[Hyp3, Thi5,8, D-Phe7]-BK, B2 receptor antagonists, were equipotent in blocking the BK-induced IPs accumulation with pKB = 7.1 and 7.3, respectively. 3. Short-term exposure of TSMCs to phorbol 12-myristate 13-acetate (PMA, 1 microM) attenuated BK-stimulated IPs accumulation. The concentrations of PMA that gave half-maximal and maximal inhibition of BK-induced IPs accumulation were 15 +/- 4 nM and 1 microM, n = 3, respectively. The inhibitory effect of PMA on BK-induced response was reversed by staurosporine, a protein kinase C (PKC) inhibitor, suggesting that the inhibitory effect of PMA was mediated through the activation of PKC. 4. Prolonged incubation of TSMCs with PMA for 24 h, resulted in a recovery of receptor responsiveness which may be due to down-regulation of PKC. The inactive phorbol ester, 4 alpha-phorbol 12, 13-didecanoate at 1 microM, did not inhibit this response. 5. The site of this inhibition was further investigated by examining the effect of PMA on AlF(4-)-induced IPs accumulation in canine TSMCs. AlF(4-)-stimulated IPs accumulation was inhibited by PMA treatment, suggesting that the G protein(s) can be directly activated by AlF4-, which is uncoupled from phospholipase C by PMA treatment. 6. Incubation of TSMCs in the absence of external Ca2+ or upon removal of Ca2+ by addition of EGTA, caused a decrease in IPs accumulation without changing the basal levels. Addition of Ca2+ (3-620 nM) to digitonin-permeabilized TSMCs stimulated IPs accumulation was obtained by inclusion of either guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) or BK. The combination of GTP gamma S and BK caused an additive effect on IPs accumulation.7. Pretreatment of TSMCs with cholera toxin enhanced BK-stimulated IPs accumulation, whereas there was no effect with pertussis toxin.8. These data suggest that BK-stimulated PI metabolism is mediated by the activation of BK B2 receptors coupling to a G protein which is not blocked by cholera toxin or pertussis toxin treatment and dependent on external Ca2+. The transduction mechanism of BK coupled to PI hydrolysis is sensitive to feedback regulation by PKC.

Animals↗
PubMed1994

[Experimental pathological study of brain damage in rats with copper deficiency].

Pathological observations on brain damage in baby rats with experimental copper deficiency were carried out and the following observations were made: 1. The cerebrum were decreased in size and weight, the cortex became thinner and the corpus striatum atrophic. 2. Vacuolar degeneration and swelling of the mitochondria in the extrapyramidal system within the corpus striatum resulted in axon damage and disintegration of the myelin sheath. 3. Proliferation of endoplasmic reticulum in the dark neurons, swelling and rupture of mitochondria in the light neurons, which can result in necrosis of both types of neurons. The damage due to copper deficiency could not be reversed by copper supplements in diet.

Animals↗
PubMed1994

The morbidity and mortality associated with childhood onset systemic lupus erythematosus.

From 1977 till 1991, the diagnosis of systemic lupus erythematosus was made on 137 children aged 18 years or under in Chang Gung Memorial Hospital. The medical records were reviewed and the clinical data were analysed with emphasis on the morbidity and mortality of this disease. The clinical and laboratory characteristics were similar to the findings from most other reports. Renal failure accounted for 8% of the initial presentation. The non-infectious complications were, in the order of frequencies, hypertension, avascular necrosis of femoral head, cataract, encephalopathy, and venous thrombosis. Sepsis, cutaneous infection and urinary tract infection were the frequently encountered infectious complications. The major causes of death in childhood onset systemic lupus erythematosus were sepsis (42%) and renal failure (30.7%). Forty patients were lost to follow-up. The 5-year survival rate, calculated by life-table, was 76.3%.

Adolescent↗
PubMed1992

Systemic lupus erythematosus and pheochromocytoma.

A 40-year-old Chinese woman with systemic lupus erythematosus (SLE) developed labile blood pressure 3 years after her onset of high blood pressure. Pheochromocytoma was subsequently found and removed. Postoperatively her hypertension improved without change in her SLE activity. Our case demonstrates pheochromocytoma can be a cause of hypertension in SLE.

Adrenal Gland Neoplasms↗
PubMed1992

Expression of cytolytic mediators by synovial fluid lymphocytes in rheumatoid arthritis.

To understand the role of cytolytic lymphocytes in the pathogenesis of rheumatoid arthritis, we investigated the expression of lymphocyte cytotoxicity mediators, perforin, and serine esterases, in lymphocytes derived from the synovial fluid of 15 patients with rheumatoid arthritis. Previous work has shown that CD8+ lymphocytes that possess markers of activation appear to be present in rheumatoid arthritis (RA). By means of in situ hybridization techniques and immunohistochemical analysis, the authors show that perforin and two serine esterases (serine esterase 1/Hanukah factor/granzyme A, and serine esterase 2/granzyme B) are expressed by subpopulations of CD8+ and CD56+ lymphocytes obtained from synovial fluid. The presence of these cytotoxic mediators suggests a possible mechanism for tissue damage, and provides evidence implicating cytolytic lymphocytes in the pathogenesis of RA.

Arthritis, Rheumatoid↗
PubMed1990

[Influences of 3,4,5-trihydroxystibene-3-beta-mono-D-glucoside on beat rate and injury of cultured newborn rat myocardial cells].

3,4,5-Trihydroxystibene-3-beta-mono-D-glucoside (PD) from Polygonum cuspidatum 0.05-0.45 mmol/L increased beat rate of myocardial cells from 100% to 112-220%. This action of PD 0.15 mmol/L was agonized by nisoldipine 0.1, propranolol 10 and phentolamine 1 mumol/L. PD (0.05, 0.15 mmol/L) decreased the lactate dehydrogenase (LDH) amount liberated by myocardial cells, from 98 +/- 11 IU/ml of deprivation of oxygen and glucose (DOG) to 55 +/- 16, 68 +/- 14 IU/ml (P less than 0.01) 6 h after injury of DOG; 77 +/- 9, 80 +/- 6 IU/ml (P less than 0.01) 9 h after injury of DOG. PD 0.15 mmol/L decreased the LDH amount liberated by myocardial cells, from 311 +/- 34 to 231 +/- 42 IU/ml (P less than 0.05) 9 h after injury of chlorpromazine (CPZ). It is suggested that PD can protect myocardial cells injured by DOG and CPZ.

Animals↗
PubMed1989

[Mosquito bite allergies terminating as hemophagocytic histiocytosis: report of a case].

A 21-year-old woman had suffered from repeated vasculitis and panniculitis with fever and chills after following mosquito bites since age 7. These manifestations were confirmed with a direct mosquito bite test during her admission to another hospital at age 17. The patient presented to our hospital with progressive dyspnea, productive cough and intermittent fever for one week. In addition to the bilateral infiltrative lesions on chest roentgenography, hepatosplenomegaly with an abnormal liver function test, pancytopenia, and elevated IgE were also detected. Blood and sputum cultures grew no microorganisms. Epstein-Barr virus-IgM, Cytomegalovirus-IgM and Mycoplasma pneumonia antibodies were all negative. Bone marrow aspiration and biopsy revealed histiocytosis with hemophagocytosis. No atypical histiocyte was found. The patient was put on dexamethasone treatment with improvement. Unfortunately, symptoms relapsed two weeks later. A repeated bone marrow aspiration and biopsy revealed a picture similar to the previous one. Despite antibiotic administration and ventilator support, a rapidly deteriorated course terminated in the patient's death by respiratory failure. Mosquito bite allergies were reported to be associated with malignant histiocytosis in Japan. However, atypical histiocytes were not found in our case upon repeated bone marrow aspirations, biopsies and skin biopsies. Mature histiocytes with hemophagocytosis were prominent instead. Reactive histiocytosis was thus favored rather than malignant histiocytosis. Although opportunistic infection cannot be excluded, we propose that a mosquito bite allergy with consequent histiocytic activation by antigen, immune complex or IgE is the possible pathogenetic mechanism for hemophagocytic histiocytosis in this patient.

Adult↗
PubMed1989

Neonatal lupus erythematosus: report of a case.

We present the first report of neonatal lupus erythematosus from Taiwan. A female baby, born to a mother with documented systemic lupus erythematosus (SLE), developed cutaneous lupus lesions after phototherapy for hyperbilirubinemia. She had additional clinical features of hemolytic anemia and thrombocytopenia. Detailed serological and immunogenetic studies were performed. Transplacental passage of both anti-SSA/Ro and anti-SSB/La antibodies were demonstrated and their disappearance at the age of 6 months correlated with regression of clinical symptoms. This patient inherited human leukocyte antigen (HLA) A11, Bw60 Cw3, DR2 and Aw33, Bw57, Cw7, DRw6 from her father and mother, respectively. A long-term follow-up is required for observing whether she will develop SLE in the future.

Adult↗
PubMed1989

Effect of ethanol on natural killer cell activity in vitro.

The effect of ethanol on kinetic stages of natural killer (NK) cell activity was studied in vitro. Peripheral blood mononuclear cells (MNC) were either co-cultured or pre-incubated with various ethanol concentrations and assayed for NK cell activity with a "4-hour chromium release assay" and a "single cell cytotoxicity assay in agarose" simultaneously. Direct addition of ethanol to the assay system resulted in a dose-dependent inhibition of NK cell activity. The percentage of lysed conjugated target cells was suppressed from a control value of 21.2% to 17.0%, 15.1%, 11.8% and 10.0% with an ethanol concentration of 0.125%, 0.25%, 0.5% and 1.0%, respectively. NK cell recycling was also inhibited. A 24-hour pre-incubation with ethanol, however, resulted in NK cell activity enhancement. The enhancement was around 20% with a 0.25% ethanol concentration and around 45% with a 0.5% and a 1.0% ethanol concentrations. The enhancing effect was noted mainly at the cytolysis stage after binding of effector cell with target cells.

Cells, Cultured↗
PubMed1989

Reiter's syndrome in uremia: report of a case.

A 35-year-old male uremic patient developed the classical presentation of Reiter's syndrome after 3 years of regular hemodialysis. He had painful swelling of the left knee, sacroilitis, urethritis, balanitis, painless oral ulcers, acute uveitis and positive HLA-B27. Disease activity persisted and was aggravated although immune function studies showed depressed cellular immunity. The clinical course of this patient seemed to contradict our belief that activity of immunologically mediated disease will abate after uremia, but it concurred with the report that Reiter's activity was unchanged in AIDS despite the significant immunodeficiency of AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Association of ankylosing spondylitis with IgA-multiple myeloma: report of a case and pathogenetic considerations.

Multiple myeloma has rarely been reported in patients with ankylosing spondylitis. We observed a patient with a 20-year history of ankylosing spondylitis, who subsequently developed IgA myeloma. This association may not be simply coincidental. It has been proposed that the protracted stimulation of immunocytes by inflammatory lesions on the mucosal surfaces of the gastrointestinal, respiratory, and biliary tracts, where lymphocytes are already committed to IgA production, may be implicated in the pathogenesis of IgA myeloma in some patients. Ankylosing spondylitis is a chronic inflammatory disease, probably resulting from the interaction of a genetic predisposition involving HLA-B27 with an environmental event such as enteric bacterial infection. We propose that ankylosing spondylitis and IgA myeloma occurring concomitantly in our patient implies a possible pathogenetic relationship. In ankylosing spondylitis, persistent reticuloendothelial stimulation, due to chronic subclinical gastrointestinal infection, may lead to IgA-producing plasma cell activation and proliferation, and subsequent IgA myeloma development.

Humans↗