Electrochemical enzyme immunoassay for serum prostate-specific antigen at low concentrations.
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Alkaline Phosphatase↗
Biomedical subjects
S F Chen
Publications and source records attributed to S F Chen.
[Analysis of divergent angle and length of CEJ to furcation entrance in extracted molars].
The purposes of this study were to investigate the furcation entrance angle (FEA) and the distance between cemento-enamel junction (CEJ) and furcation entrance (FE) of the extracted maxillary and mandibular molars. Assay teeth comprised 89 maxillary molars and 93 mandibular molars. All the FEAs and CEJ-FEs of the molars were measured by a stereomicroscope at 2.5 x equipped with a Bioscan OPTIMAS Image Analyzer (BOIA). The results were summarized as follows: (1) The mean FEAs in the buccal, mesial and distal furcations were 96.3 +/- 10.0, 103.8 +/- 9.7, and 107.2 +/- 12.2 degrees in the maxillary molars, and 91.6 +/- 11.7, 101.7 +/- 11.5, and 97.1 +/- 10.7 degrees in the maxillary second molars, respectively. At the buccal and lingual furcations of mandibular first and second molars, they measured 100.5 +/- 9.7/102.7 +/- 8.5, and 93.3 +/- 11.5/91.7 +/- 10.8 degrees, respectively. (2) The mean distance of CEJ-FEs at the buccal, mesial and distal furcations of maxillary molars were 3.42 +/- 1.5mm, 3.55 +/- 0.97 mm, and 3.69 +/- 0.98mm for the first molars, and 3.01 +/- 1.04mm, 4.04 +/- 1.58mm and 3.00 +/- 1.14mm for the second molars. At the buccal and lingual furcations of the mandibular first and second molars, they were recorded as 1.90 +/- 0.08mm and 2.90 +/- 0.07mm, and 2.82 +/- 1.34mm and 3.46 +/- 1.03mm, respectively. It was concluded that buccal FEA of maxillary 2nd molar was the smallest (91.56 +/- 9.68 degrees) as compared to the mesial and distal FEAs; whereas the mean distance of CEJ-FEs at the buccal surface was the smallest (1.90mm +/- 0.08mm) when compared to the others.
Humans↗
Human telomerase inhibition by 7-deaza-2'-deoxypurine nucleoside triphosphates.
Telomeres play an important role in chromosome organization and stability. Human telomerase is a terminal transferase that adds TTAGGG units onto the telomere end. In general, telomerase activity is not detected in normal somatic cells but is present in immortalized cells. Consequently, telomerase might be a selective target for cancer chemotherapy. Using cell-free biochemical telomerase assay, we have found that 7-deaza-2'-deoxyguanosine-5'-triphosphate (7-deaza-dGTP) and 7-deaza-2'-deoxyadenosine-5'-triphosphate (7-deaza-dATP) were potent telomerase inhibitors. The concentrations of inhibitors in which 50% of the telomerase activity was inhibited (IC50 values) were 11 and 8 microM for 7-deaza-dGTP and 7-deaza-dATP, respectively. Additional studies show that both 7-deaza-dGTP and 7-deaza-dATP were also incorporated into telomeric DNA by telomerase. However, incorporation of 7-deaza-dATP or 7-deaza-dGTP results in a telomeric ladder that is prematurely shortened. No difference in the number or position of pause sites were observed when 7-deaza-dATP was compared to dATP as substrates. On the other hand, both a shift and an increase in pause sites was observed when dGTP was replaced by 7-deaza-dGTP. Incorporation of 7-deaza nucleotides by telomerase may be used as a tool for the study of telomerase mechanism and function. In addition, this may be a novel approach in the design of new telomerase inhibitors.
Cells, Cultured↗
Involvement of cytokine gene expression in the age-dependent decline of NK cell response.
The molecular mechanism responsible for the age-dependent decline of natural killer (NK) cell response was examined. The responses of NK cells to poly(I:C), Con A, and LPS were compared between the young and the aged animals. We observed that both basal and induced NK cell activity declined with age. To further determine the basis for this change, an effort was made to identify the cytokine genes that might be involved. In addition, the capacity of acetyl-L-carnitine (ALC) to restore NK cell activity was evaluated. In this study, 51Cr release assay and reverse transcriptase-polymerase chain reaction assay were used to measure the NK cell activity and the changes in cytokine gene expression, respectively. Our results show that the decline in NK cell response to poly(I:C) and LPS in aged animals was correlated with decreased expression of the IFN-gamma gene. The decline in the NK cell response to Con A in aged animals was, however, independent of the expression of IL-2 or IFN-gamma genes. Although ALC was reported to restore functions of T cells and macrophages in aged animals, we found that long-term treatment (4 months) with ALC had no effect on either the basal or the induced age-dependent loss of NK cell activity. Our observations suggest that cytokine gene therapy could be a potential approach to improving or even preventing the decline of certain immune functions in the elderly.
Acetylcarnitine↗
Activation of mu-opioid receptors are required for the conditioned enhancement of NK cell activity.
The type of opioid receptors involved in the conditioned enhancement of natural killer (NK) cell activity is identified in the present study. In our previous observations, we have demonstrated that the conditioned enhancement of NK cell activity was dependent on beta-endorphin and methionine-enkephalin, but not dynorphin. Based on the interaction of opioids with their homologous receptors, we concluded that mu- and delta-opioid receptors might be involved. To further classify the type(s) of opioid receptors involved in eliciting the conditioned NK cell activity, three opioid receptor antagonists, cyprodime hydrobromide, ICI-174864, and nor-binaltorphimine dihydrochloride, were used to block the conditioned NK cell activity in BALB/c mice. Blocking was conducted by intracisternal injection of the drugs. The results showed that the activation of mu-opioid receptors was required in the conditioned enhancement of NK cell activity, but not the delta- or kappa-type of receptors.
Animals↗
Immunological abnormality in C3H/HeJ mice with heritable inflammatory bowel disease.
To explore the immunological abnormality of a heritable inflammatory bowel disease developed in a new substrain of C3H/HeJ mice, we examined the expression of integrins beta7 and other cell adhesion molecules on normal and disease mice lymphocytes by flow cytometry. We also examined the cytotoxicity of small intestinal intraepithelial lymphocytes to epithelial cells and the proliferation and aggregation of intestinal lymphocytes. There are several significant changes in the expression levels of alpha4 and alphaM290beta7 integrins, CD11a, ICAM-1, CD45RB, CD4, CD44, and CD45 in different lymphocyte populations. The cytotoxicity of small intestinal intraepithelial lymphocytes from disease mice was higher than that from normal mice and could be stimulated by PHA and inhibited by mAb to alphaM290beta7. The proliferation of both normal and disease small intestinal intraepithelial lymphocytes was enhanced by costimulation by mAb to CD2 or CD3 and ProNectin. In comparison to disease mice, normal small intestinal intraepithelial lymphocytes proliferated at a significantly higher rate in response to sheep RBC and mAb to CD2 or CD3 and ProNectin costimulation. Homotypic aggregation of small intestinal intraepithelial lymphocytes isolated from disease mice was greater than in those from normal mice. The abnormality of expression of integrin beta7 and other cell adhesion molecules and cytotoxic, proliferative, and aggregative responses of lymphocytes from disease mice may play important roles in the pathogenesis of this heritable inflammatory bowel disease.
Animals↗
Agents that target telomerase and telomeres.
Telomeres are guanine-rich regions that are located at the ends of chromosomes and are essential for preventing aberrant recombination and protecting against exonucleolytic DNA degradation. Telomeres are maintained by telomerase, an RNA-dependent DNA polymerase. Because telomerase is known to be expressed in tumor cells, which concurrently have short telomeres, and not in most somatic cells, which usually have long telomeres, telomerase and telomere structures have been recently proposed as attractive targets for the discovery of new anticancer agents. The most exciting current strategies are aimed at specifically designing new drugs that target telomerase or telomeres and new models have been formulated to study the biological effects of inhibitors of telomerase and telomeres both in vitro and in vivo.
Animals↗
Effects of dextran sulphate sodium on intestinal epithelial cells and intestinal lymphocytes.
BACKGROUND AND AIMS: The effects of dextran sulphate sodium (DSS) on mouse intestinal epithelial cells and intraepithelial lymphocytes were analysed to investigate the mechanism by which DSS induces colitis and tumours in mice. Cytotoxicity of DSS towards intestinal epithelial cells and intestinal intraepithelial lymphocyte hybridomas or fresh intestinal intraepithelial lymphocytes seems to have concentration, time, and cell type dependency with increasing concentrations and time causing increased cytotoxicity. RESULTS: Integrin alpha 4 expression was marginally down regulated by 0.5% of DSS, while alpha M290 expression was up regulated. DSS inhibits the binding of 9.1 gamma delta cells to both extracellular matrix (ECM) and epithelial cells. Conversely at high concentrations it increases binding to all ECM except poly-L-lysine. Various cytokines including TGF beta, interleukin 2, and tumour necrosis factor alpha as well as prostaglandin alter the expression of the integrin alpha 4 and M290 subunits at the cell surface, and also alter the adhesion of 9.1 gamma delta cells to epithelial monolayers. The expression of a large number of cell adhesion molecules expressed on intraepithelial lymphocytes is affected by a combination of the abundant gut cytokine TGF beta and DSS, suggesting that DSS induced colitis may ultimately arise from a combination of gut cytokine and DSS. DSS also triggers intraepithelial lymphocyte aggregation on all ECM coated plate tested. CONCLUSIONS: These data suggest that the potential roles of DSS induced colitis may be: (a) direct cytotoxicity; (b) interference with the normal interaction between intestinal lymphocytes, epithelial cells, and ECMs; (c) aberrant modulation of the expression of the integrin beta 7 receptors, other cell receptors, and their functions.
Animals↗
Attenuation of acute and chronic damage following traumatic brain injury in copper, zinc-superoxide dismutase transgenic mice.
To elucidate the role of oxygen-derived free radicals and superoxide dismutase in traumatic brain injury (TBI), blood-brain barrier (BBB) permeability, brain edema, behavioral function, and necrotic cavity volume (CV) were evaluated after TBI using nontransgenic (nTg) mice and heterozygous and homozygous transgenic (Tg) mice with a 1.5- (Tg 1.5x), 3.1-(Tg3.1x) and five- (Tg5x) fold increase in human copper, zinc-superoxide dismutase (CuZn-SOD) activity. Traumatic brain injury was produced by the weight-drop method. Evans blue dye leakage 4 hours after injury was attenuated in a CuZn-SOD dose-dependent manner with decreases of 18.6%, 40.9%, and 48.8%, in the Tg1.5x, Tg3.1x, and Tg5x groups, respectively. The water content 6 hours after injury in the Tg3.1x (79.64%) and Tg5x (79.45%) groups was significantly lower than in nTg mice (81.37%). There was an initial decrease in body weight and in motor performance, as measured by beam walk and beam balance tasks undertaken 1 day after TBI. However, the average reduction in beam balance and beam walk performance deficits and changes in body weight postinjury were significantly ameliorated in Tg mice. The CV was significantly smaller in Tg mice than in nTg mice (p < 0.01). These results indicate that superoxide radicals play a deleterious role following TBI. Furthermore, Tg mice provide a useful model for demonstrating the beneficial role of an antioxidant enzyme in TBI without the confounding effect of pharmacokinetics, toxicity, and BBB permeability associated with exogenous agents.
Animals↗
Neuroprotective role of CuZn-superoxide dismutase in ischemic brain damage.
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Animals↗
Mechanism of extracellular ATP-induced proliferation of vascular smooth muscle cells.
The mitogenic effect of extracellular ATP was examined in cultured rat aortic smooth muscle cells (VSMCs). ATP, 2-methylthio-ATP, and ADP stimulated [3H]thymidine and [3H]leucine incorporation and cell growth. AMP, adenosine, UTP, and P2x agonists showed little of these effects. Reactive blue 2, a P2Y purinoceptor antagonist, was effective in suppressing the mitogenic effect of ATP and 2-methylthio-ATP, indicating that extracellular ATP-induced VSMC proliferation is mediated by P2Y purinoceptors. The P2Y purinoceptor activation was coupled to a pertussis toxin (PTX)-insensitive G protein (Gq) and triggered phosphoinositide hydrolysis with subsequent activation of protein kinase C (PKC), Raf-1, and mitogen-activated protein kinase (MAPK) in VSMCs. In response to ATP, both 42-and 44-kDa MAPKs were activated, and tyrosine was phosphorylated. Western blot analysis using PKC isozyme-specific antibodies indicated that VSMCs express PKC-alpha, PKC-delta, and PKC-zeta. A complete down-regulation of PKC-alpha and PKC-delta was seen after 24-hr treatment with 12-O-tetradecanoylphorbol-13-acetate. When cells were pretreated with 12-O-tetradecanoyl-phorbol-13-acetate for 24 hr and subsequently challenged with ATP, Raf-1 activation and 42-kDa as well as 44-kDa MAPK tyrosine phosphorylation failed to be induced. These results demonstrate that ATP-induced Raf-1 and MAPK activations involve the activation of PKC-alpha and PKC-delta. P2Y purinoceptor stimulation with ATP also caused accumulation of c-fos and c-myc mRNAs. Both Reactive blue 2 and staurosporine significantly blocked this increase by ATP. In conclusion, the mitogenic effect of ATP seemed to be triggered by activation of the Gq protein-coupled P2Y purinoceptor that led to the formation of inositol trisphosphate and activation of PKC. PKC and, in turn, Raf-1 and MAPK were then activated, leading eventually to DNA synthesis and cell proliferation.
Adenosine Triphosphate↗
[Furcation entrance dimension, divergent angle and length of CEJ to furcation entrance relate to periodontal therapy].
In previous studies we have investigated the furcation entrance dimension (FED), furcation entrance angle (FEA) and the distance between cementoenamel junction and furcation entrance (CEJ-FE) of the first and second molars and compared the Chinese with the Caucasians. The aim of the present study was to relate the FED, FEA, and distance of CEJ-FE to the clinical significance of periodontal therapy of molar furcations. All the FEDs, FEAs, and distance of CEJ-FEs of the molars were measured by a stereomicroscope equipped with a Bioscan OPTIMAS Image Analyzer and statistically analyzed by Student's paired t-test, multiple regression of ANOVA and correlation analysis. The results are summarized below. (1) There is a significant relationship between FEA and location of buccal, mesial, and distal furcations of maxillary first and second molars (16& 26, p < 0.001; 17&27, p < 0.01). (2) There exists a significant relationship between FEA and FED in the mandibular first and second molars. (3) There exists a significant relationship between FED and FEA in the mandibular second molar (r = 0.370, p < 0.05). (4) The prevalence of mean FED and FEA (type D, FED < or = 0.75 mm and FEA < or = 90 degree) of the maxillary first molar (45%) is twice as high as the maxillary first molar (24%). (5) The prevalence of type D of the buccal (32%) and lingual (37%) furcations on the mandibular second molar is markedly higher than the first molar (buccal = 12%; lingual = 4%, respectively). These results reveal that those topographics of the FED, FEA, and distance of CEJ-FE in second molars have poor prognosis in periodontal therapy when compared with first molars.
Humans↗
Expression of the conditioned NK cell activity is beta-endorphin dependent.
We are interested in identifying the pathways which are responsible for triggering the conditioned enhancement of natural killer (NK) cell activity. Earlier studies have suggested that central opioid(s) are involved in eliciting the expression of the conditioned NK cell activity. The purpose of this study was to identify the central opioid peptides that allow the central nervous system (CNS) to communicate with the immune system. Mediators that activate the efferent pathway of communication between the CNS and immune system was examined by injection of the mediator via the cisterna magna (CM). Conditioning was used as a tool to show that the bi-directional communication between the CNS and the immune system does take place. We found that beta-endorphin but not dynorphin could stimulate NK cell activity, when beta-endorphin or dynorphin was injected into the CM. In addition, when anti-beta-endorphin or anti-dynorphin antibody was injected into the conditioned animals via CM the conditioned response was blocked by anti-beta-endorphin but not by anti-dynorphin antibody. These observations suggest that beta-endorphin appears to be one of the signals that is induced in the brain at the CS recall step of the conditioned response to trigger the elevation of NK cell activity.
Animals↗
A new simple method for isolation of microvascular endothelial cells avoiding both chemical and mechanical injuries.
Our study indicates that when small pieces of lung or muscles of chest wall are cultured, erythrocytes and leukocytes (PMNs) leave the tissues first, followed by vascular endothelial cells (ECs). Fibroblasts and other mixed cells grow after 72 hr culture. The ECs can then be isolated avoiding mechanical and chemical injuries. The lung tissue is obtained from the peripheral surface and muscles from the chest. It is then cut into pieces and cultured with DMEM containing 20% fetal bovine serum. After 60 hr culture, the tissues are discarded. The flask contains only ECs and blood cells. Blood cells can be cleared out after the cells are subcultured once or twice. The primary cells and the subcultured cells cultured on gelatinized culture dish give the capillary-like structure. Cells cultured on untreated dishes have regular cobblestone morphology and junctional contacts. The isolated cells were not mesothelial cells because the cells did not react to antibody against cytokeratin 18, while mesothelial cells reacted strongly to the antibody. The cells can be isolated from the lung tissue without pleura. The primary microvascular ECs are also cultured on microcarriers (cytodex 3). Because both mechanical and proteolytic injuries are avoided, the cells may be more similar to cells in the in vivo state. There are no significant differences in PMN-endothelium adherence and monolayer responses to second messengers, platelet activating factor, and phospholipase A2 when pulmonary and muscular microvascular endothelial cells are compared.
Animals↗
A multicentred phase III comparative clinical trial of Mesigyna, Cyclofem and Injectable No. 1 given monthly by intramuscular injection to Chinese women. I. Contraceptive efficacy and sid effects.
A phase III clinical study was carried out among 5680 fertile Chinese women to evaluate efficacy and side effects of three monthly injectable contraceptives: Mesigyna, Cyclofem and Chinese Injectable No. 1. When used in a once-a-month treatment schedule (part 1 of study), the effectiveness of Chinese Injectable No. 1 was unacceptably low; 36 pregnancies occurred during the first 1743 women-months of use, 16 before the second injection. The study was restarted with a revised injection schedule for Injectable No. 1: two injections separated by 9 +/- 1 days during the first month and subsequent injections given 10-12 days after the onset of bleeding, or if no bleeding occurred, 28 days after previous injection. In part 2 of the study, 988, 990 and 992 subjects were provided Mesigyna, Cyclofem and Injectable No. 1, respectively. Life-table pregnancy rates at one year were 0.41%, 0% and 0.77% (p < 0.05), respectively; the overall discontinuation rates at one year were 13.9%, 19.1% and 20.4% (p < 0.001). Discontinuation rates for bleeding problems were significantly different between the groups: discontinuation rates for amenorrhea were 0.58%, 3.71% and 0.68% (p < 0.001) for Mesigyna, Cyclofem and Injectable No. 1; for other bleeding problems, the rates were 4.88%, 8.38% and 12.64% (p < 0.001). There were no significant differences between the groups regarding discontinuation for other medical or non-medical reasons. Mean weight changes after one year of use were small: 0.73, 0.86 and 0.17 kg for the three groups, respectively. Both Mesigyna and Cyclofem were very effective for contraception, but Mesigyna appeared to be tolerated slightly better with regard to cycle control; the modified dose regimen for Injectable No. 1 also gave a low pregnancy rate but was associated with higher rates of discontinuation.
Adolescent↗
A multicentred phase III comparative clinical trial of Mesigyna, Cyclofem and Injectable No. 1 given by intramuscular injection to Chinese women. II. The comparison of bleeding patterns.
Between 1988 and 1992, a randomized phase III clinical trial was conducted in China to compare three monthly injectable contraceptives: Mesigyna, Cyclofem and Injectable No. 1. This paper presents a detailed analysis of the menstrual diaries provided by 5098 (89%) of the subjects. In total, 902, 903 and 913 diaries were analyzed to compare bleeding patterns induced by Mesigyna, Cyclofem and Injectable No. 1. The first withdrawal bleeding usually occurs 14-20 days after the first injection for all three of these preparations. Thereafter, 50% of Mesigyna users had precisely 3 bleeding/spotting episodes every 90 days, 50% of Cyclofem users had 2-3 and 50% of Injectable No. 1 users had 3-4 episodes every 90 days. Relative to users of Mesigyna or Cyclofem, Injectable No. 1 users had 2-3 more bleeding/spotting days, and a shorter length of bleeding/spotting-free intervals in each period. 63.7%, 41.4% and 60.6% of subjects using Mesigyna, Cyclofem and Injectable No. 1, respectively, had bleeding patterns similar to their untreated patterns in the first 90-day period. The percentages increased to 82.2% 67.8% and 75.0% in the fourth 90-day period. A total of 1815 diaries for Mesigyna and 1802 for Cyclofem were analyzed for more in depth comparison of these two methods. The number of bleeding/spotting days over four periods showed little difference between the two group, but there were more spotting days and there was greater individual variability among Cyclofem users.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
1 alpha, 25-Dihydroxyvitamin D3 decreased ICAM-1 and ELAM-1 expressions on pulmonary microvascular endothelial cells and neutrophil motivation.
Preincubation of pulmonary microvascular endothelial cells (PMVECs) with platelet activating factor (PAF) for 3.5 h increased the adhesion rate of polymorphonuclear leukocytes (PMNs) to PMVECs from 57.3 to 72.8% (P < 0.01). Coincubations of 1 alpha, 25-dihydroxyvitamin D3 (VD) or MC903 (VD analog) decreased the ability of PAF to increase PMN-PMVEC adhesion rate significantly. Preincubation of PMNs with PAF also increased PMN-PMVEC adhesion rate. Coincubation of VD but not MC903 blocked PAF-induced adherence of PMNs to PMVECs. Both VD and MC903 decreased PAF-increased expression of ICAM-1 on PMVECs, PMN chemotaxis to zymosan activated serum and histamine, and PMN aggregation induced by PAF significantly. VD but not MC903 decreased the expression of ELAM-1 on PMVECs. VD and MC903 did not affect PAF-induced release of acid phosphatase from PMNs. The results suggest that VD may be a good drug to inhibit PMN motivation by acting on both ECs and PMNs.
Animals↗
1 alpha,25-Dihydroxyvitamin D3 decreases scalding- and platelet-activating factor-induced high vascular permeability and tissue oedema.
We have previously demonstrated that 1,25-dihydroxyvitamin D3 decreases endotoxin-induced mortalities of rat and mouse from 80% and 70% to 14% and 10% (unpublished results). In the present study, pretreatment of 1,25-dihydroxyvitamin D3 decreased pad oedema and pulmonary vascular permeability induced by scalding and platelet-activating factor. 1,25-Dihydroxyvitamin D3 in a dose of 4 x 10(-9) mol/kg decreased pulmonary extravascular Evans blue concentration increased by platelet-activating factor from 6.32 +/- 0.63 ng/g to 2.57 +/- 0.28 ng/g (P < 0.01), and lung water/dry lung weight from 3.79 +/- 0.57 to 1.51 +/- 0.13 (P < 0.01). 1,25-Dihydroxyvitamin D3 of 4 x 10(-11) moles/kg and calcipotriol (a vitamin D analogue which has limited hypercalcaemic effect) of 4 x 10(-9) moles/kg had similar effects. Karyocyte counting of bronchoalveolar lavage fluid and the reduction of mean arterial pressure were also reduced to some extent. These results suggest that 1,25-dihydroxyvitamin D3 may be a new and effective drug to reduce vascular permeability and ameliorate oedema.
Animals↗