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Biomedical subjects

K D Yang

Publications and source records attributed to K D Yang.

At least 37 records · Page 2Linked to original sources
PubMed2000

Profiles of inflammatory cytokines in bronchoalveolar lavage fluid from premature infants with respiratory distress disease.

In view of cytokine's effects in promoting or inhibiting inflammation, the objective of this study was to explore the characteristics of the proinflammatory cytokine, interleukin-8 (IL-8), and the inhibitory cytokine, interleukin-10 (IL-10), in the bronchoalveolar lavage (BAL) fluid of premature infants suffering from respiratory distress disease. Eighteen premature neonates with respiratory distress disease with gestational age (GA) ranging from 24 to 37 weeks were recruited for study. BAL fluids were collected following endotracheal intubation during an episode of hypoxemia or dyspnea. A series of BAL samples were obtained on day 1, 2, 4 and 7 after intubation for measuring IL-8 and IL-10 levels. The results indicate that premature infants with GA ranging from 24 to 32 weeks had a higher level of IL-8 (p = 0.029), but not level of IL-10 (p = 0.109), in the BAL obtained during the first intubation compared to premature infants with GA ranging from 33 to 37 weeks. The administration of exogenous surfactant did not influence the profiles of IL-8 and IL-10, as compared to those in-patients without treatment. Levels of IL-8 were correlated with IL-10 levels (r = 0.613, p = 0.007) in BAL fluid samples obtained on the day of intubation. The level of IL-8, but not IL-10, was significantly correlated with the duration of intubation. IL-8 and IL-10 levels in BAL fluid samples collected on the day of intubation were correlated with the development of chronic lung disease (CLD). The results suggest that extreme prematurity tends to have increased IL-8 and IL-10 levels in BAL fluid compared to premature infants with older GA, and that these increased levels are associated with the development of CLD.

Bronchoalveolar Lavage Fluid↗
PubMed2000

Childhood asthma: aspects of global environment, genetics and management.

The prevalence of asthma in children dramatically increased over the past two decades. In Taiwan, the prevalence of childhood asthma has risen to around 10% in the 1990s, in contrast to a prevalence of about 1% in the 1970s. Currently, Australia and New Zealand have the highest prevalence in the world (> 15%). African and Asian countries have a low prevalence of about 5 to 10%. In general, countries in coastal, temperate and subtropical zones have the highest mite-sensitive asthma prevalence. Countries in the subarctic or in semiarid areas have a lower prevalence. Indoor allergens such as house dust mites, cockroaches and fungi usually cause perennial asthma; outdoor allergens such as grass and tree pollens as well as outdoor fungi induce seasonal asthma. A gene on chromosome 11q13 is significantly linked to maternal inheritance of asthma, and possibly involves polymorphisms in the beta subunit of the high affinity IgE receptor. Cytokine genes in chromosome 5q31-33 are known to regulate IgE production resulting in various severities of allergic diseases. Recent studies suggest that pollutants such as diesel exhaust, O3, NO2, and SO2, together with allergens and susceptible genes are likely to promote IgE production and allergic reactions. As a result, asthma is apparently not a single gene disorder, but a disease determined by the interaction between gene and environment. In practice, immunopharmacological interventions to block IgE-mediated early bronchospasm and late inflammatory reactions are the major regimens for asthma treatments. This makes possible a step-wise self-management based on portable monitoring of airway resistance using the peak expiratory flow rate (PEFR). Early avoidance of allergen exposure in utero as well as early anti-inflammatory therapy in infancy have decreased the prevalence of allergic diseases. A combination of both strategies may bring much more benefit in the prevention of childhood asthma. As progress in therapeutic gene vaccines as well as genetic immunoregulation continues, we expect early environmental avoidance and genetic vaccines may prevent childhood asthma in the near future.

Allergens↗
PubMed2000

Atopic cataracts in a child with atopic dermatitis: a case report and review of the literature.

Cataracts induced by atopic dermatitis rarely occur in adolescent and young adult patients suffering from this problem. Lenticular opacity is an important ocular complication in atopic dermatitis. Although the cause of atopic dermatitis and its ocular complications are unknown, cataracts have been observed to develop and progress during periods of exacerbation of the dermatitis. We report the case of a 16-year-old boy with atopic dermatitis who abruptly developed cataracts in both eyes while suffering from severe skin itching which began 2 months before the initial examination. His peroxidation test result was very high, and we postulate the retinal peroxidation might play a key role in cataractogenesis. Lens aspiration and intraocular artificial lens implantation were performed smoothly with restoration of visual acuity in both eyes.

Adolescent↗
PubMed1999

Hypokalemia and salbutamol therapy in asthma.

Hypokalemia is a common side effect in adult asthmatic patients on beta 2 adrenergic therapy. There is limited information in regard to hypokalemia and its relation to the clinical responses following administration of beta 2 agonist therapy in children with asthma. We observed that salbutamol inhalation significantly improved asthmatic symptoms as demonstrated by increases in peak expiratory flow (PEF: 122.37+/-75.38 vs. 152.59+/-80.29; P < 0.001) and venous oxygen tension (Pv,O2: 33.24+/-4.95 vs. 58.16+/-2.31; P < 0.001), and decreases in respiratory rate (RR: 36.39+/-3.78 vs. 28.62+/-3.12; P< 0.01), clinical scores (CS: 3.59+/-1.28 vs. 1.59+/-0.71), and venous PCO2 tensions (Pv,CO2: 40.84+/-2.67 vs. 34.75+/-2.31; P < 0.001). Salbutamol-induced hypokalemia was correlated with a decrease in RR, and an increase of Pv,O2 and PEF. These findings suggest that the same mechanism is involved in eliciting hypokalemia and bronchodilatation.

Administration, Inhalation↗
PubMed1999

Effect of glutamine on Th1 and Th2 cytokine responses of human peripheral blood mononuclear cells.

Decreased glutamine concentrations are found in patients with catabolic stress and are related to susceptibility to infections. In this study, we evaluated the role of glutamine in Th1/Th2 cytokine responses. Peripheral blood mononuclear cells were stimulated with phytohemagglutinin (PHA), live attenuated bacillus Calmette-Guérin (BCG), or measles virus in the presence of different glutamine concentrations. We found that glutamine at an optimal concentration (0.6 mM) significantly enhanced PHA-stimulated lymphocyte proliferation as well as Th1 [interferon-gamma (IFN-gamma) and interleukin-2 (IL-2)] and Th2 cytokine (IL-4 and IL-10) production. In the absence of glutamine, BCG and measles virus elicited minimal lymphocyte proliferation, whereas BCG enhanced Th1 cytokine response and measles virus promoted Th2 cytokine response. Interestingly, addition of glutamine promoted the BCG-elicited Th1 cytokine response (IFN-gamma), but suppressed the measles-induced Th2 cytokine response (IL-10). These results suggest that appropriate glutamine levels may influence host responses to different antigens and microorganisms. Furthermore, predominately Th1, but not Th2, cytokine responses required the presence of optimal concentrations of glutamine.

BCG Vaccine↗
PubMed1999

Lymphocyte proliferation modulated by glutamine: involved in the endogenous redox reaction.

Decreased glutamine concentrations are found during catabolic stress and are related to susceptibility to infections. However, little is known about the mechanism of glutamine modulation of lymphocyte functions. Glutamine is not only an important energy source in mitochondria, but is also a precursor of glutamate, which is used for cellular glutathione (GSH) biosynthesis in lymphocytes. In this study, we investigated the effects of glutamine on the redox reaction during lymphocyte proliferation. Peripheral blood mononuclear cells, obtained from healthy adult volunteers, were cultured and stimulated by phytohaemagglutinin (PHA) in the presence of different glutamine concentrations. Cells were harvested and prepared for analysis of lymphocyte proliferation, cell cycle propagation, intracellular glutathione levels and reactive oxygen species (ROS) production. We found that glutamine supplementation significantly enhanced PHA-stimulated lymphocyte proliferation and propagation of the cell cycle from the G1 to S and G2/M phases. Glutamine also enhanced production of both intracellular ROS and GSH levels in PHA-stimulated lymphocytes. Flow cytometric analysis by the mercury orange staining method showed that glutamine significantly enhanced intracellular non-protein thiols in PHA-stimulated CD4+, but not CD8+ lymphocyte subsets. Furthermore, intracellular GSH detected by monochlorobimane dye probe showed that glutamine enhanced GSH both in PHA-stimulated CD4+ and CD8+ lymphocyte subsets. Inadequate glutamine supplementation resulted in decreased lymphocyte proliferation in association with decreased levels of intracellular GSH. Addition of exogenous GSH significantly enhanced lymphocyte proliferation, whereas blockade of GSH synthesis enhanced ROS production and suppressed lymphocyte proliferation. These results suggest that the modulation of PHA-stimulated lymphocyte proliferation by glutamine is closely related to the maintenance of appropriate intracellular redox status.

Adult↗
PubMed1998

Pentoxifylline synergizes with all-trans retinoic acid to induce differentiation of HL-60 myelocytic cells, but suppresses tRA-augmented clonal growth of normal CFU-GM.

All-trans retinoic acid (tRA) has been shown to promote terminal differentiation of promyelocytic leukemia cells, but frequently induce hyperleukocytosis and pulmonary leakage syndrome. Employing pentoxifylline (PTX), a phosphodiesterase inhibitor which could raise intracellular cAMP and modulate leukocyte activation, we sought to investigate if PTX could enhance tRA-induced promyelocytic leukemic cell differentiation but suppress tRA-augmented growth and activation of human granulocytes. tRA could significantly suppress clonal growth of U937 and HL-60 leukemic cells but enhanced the CFU-GM formation of normal bone marrow cells (22 +/- 6 vs. 90 +/- 16 CFU/well). PTX significantly augmented tRA suppression of clonal growth of U937 and HL-60 leukemic cells but suppressed tRA-augmented CFU-GM formation of normal bone marrow cells (90 +/- 16 vs. 25 +/- 9 CFU/well). In addition, PTX enhanced tRA-induced growth inhibition and differentiation of promyelocytic HL-60 leukemic cells, but suppressed respiratory burst activation by the immature granulocytic HL-60 cells and suppressed CD11b adhesion molecule expression by mature granulocytes. PTX similar to dibutyric cAMP promoted HL-60 myelocytic leukemic cell differentiation and growth inhibition, whereas PTX, in contrast to dibutyric cAMP which could augment phorbol myristate acetate (PMA)-elicited respiratory burst activity by immature granulocytes, suppressed the PMA-elicited respiratory burst activity by immature and mature granulocytes. PTX did not raise the intracellular cAMP level of HL-60 cells, but partly suppressed the dibutyric cAMP-elicited elevation of intracellular cAMP level. Results from these studies suggest that PTX might act through different signaling pathways to enhance tRA-induced myelocytic leukemic cell differentiation but prevent from hyperreactive normal granulopoiesis and granulocyte activation.

Bone Marrow Cells↗
PubMed1997

Application of chromosome 4q35-qter marker (pFR-1) for DNA rearrangement of facioscapulohumeral muscular dystrophy patients in Taiwan.

Facioscapulohumeral muscular dystrophy (FSHD) has been found to be linked to chromosome 4qter. A chromosome 4q35-ter marker, pFR-1 (subclone of the cosmid c51), has been recently isolated and used as a probe for mapping near, or within, the FSHD gene. To examine FSHD-associated DNA rearrangements in the Taiwan population, we used the pFR-1 probe to perform Southern blot analysis on 142 individuals, including 32 FSHD patients within 9 autosomal dominant families, five sporadic FSHD patients from 4 families (include one pair of twins), three sporadic scapuloperoneal syndrome (SPS) patients and two sporadic polymyositis patients with their unaffected parents, and 29 healthy controls. In 29 healthy individuals, 3 SPS and 2 polymyositis patients with their families, probe pFR-1 analysis revealed that all had polymorphic restriction fragments that were larger than 28 kb in length. All but 1 FSHD-affected individual had specific smaller EcoRI fragments (ranging in size from 10.5 to 27 kb). Two point linkage analysis between pFR-1 and the FSHD locus provided significant evidence for FSHD linkage (Z(max)=6.84). A similar smaller fragment was also present in 5 sporadic patients, while this smaller fragment could not be found in one of their parents. Identical EcoRI restriction fragment length polymorphism (RFLP) patterns linked to FSHD were shown in the monozygotic twins, even though they showed extreme variability in the expression of FSHD. We conclude that the pFR-1 probe is a tightly linked marker of FSHD and can be used to detect most DNA rearrangements associated with this disease in the Taiwan population. However, the same RFLP patterns may represent extreme variability in the expression of the FSHD gene.

Adolescent↗
PubMed1996

When do human macrophages release nitric oxide? Variable effects of certain in vitro cultural and in vivo resident conditions.

Nitric oxide (NO) release from mouse and rat macrophages is implicated in tumor cell cytotoxicity and the killing of intracellular organisms. Evidence, however, suggests that human monocyte-derived macrophages or myeloid leukemic cells differentiated along the monocytic lineage do not consistently release NO. Results presented herein that human monocyte-derived macrophages in response to lipopolysaccharide can release NO, but markedly less than mouse macrophages (1.26 +/- 0.20 vs 42.5 +/- 6.3 microM). Different in vitro and in vivo conditions have variable effects on NO production by human macrophages. Monocytes cultured in plastic wells, but not teflon beakers, for 7 days can release NO (1.22 +/- 0.13 vs 0.14 +/- 0.07 microM). In addition, human resident macrophages derived from patients with certain diseases possess a calcium- and protein kinase C-dependent pathway to produce NO, in contrast to the calcium-independent and phosphatase-dependent NO release in murine macrophages. Above results suggest that the mechanism of producing NO by macrophages in humans is not only different from that in mice, but also depends on certain in vitro and in vivo conditions.

Adult↗
PubMed1995

Pentoxifylline augments but does not antagonize TNF alpha-mediated neuroblastoma cell differentiation: modulation of calcium mobilization but not cAMP.

We described here that pentoxifylline (PTX), which is well known to counteract tumor necrosis factor alpha (TNF alpha)-mediated inflammatory responses, augmented TNF alpha-induced neuroblastoma cell differentiation in conjunction with growth inhibition and cell-cycle arrest in G1 phase. PTX also enhanced TNF alpha-induced down-regulation of acetylcholine-mediated [Ca2+]i mobilization in neuroblastoma cells. Furthermore, we found that addition of cAMP failed to induce neuroblastoma cell differentiation, whereas blockade of [Ca2+]i mobilization by 8-(N,N-diethyl-amino)octyl-3,4,5-trimethoxybenzoate HCl (TMB-8, 10 microM) did induce neuroblastoma cell differentiation. Taken together, these results indicated that PTX possessed a novel signal transduction, down-regulation of [Ca2+]i mobilization, to augment but not counteract TNF alpha-mediated functions.

Acetylcholine↗
PubMed1995

Cytotoxic factors released by dengue virus-infected human blood monocytes.

Human monocyte-derived cytotoxic factors (CF) induced by dengue virus were studied. Using several human leukemia cell lines as precursors, the biological activities of CF in conditioned medium from dengue virus-infected monocytes were demonstrated through the measurement of tumor cell growth inhibition. The conditioned medium from dengue virus infected monocytes suppressed significantly growth of CEM, HL60, K562, and U937 cells. In the presence of 10% conditioned medium (v/v) from dengue virus infected monocytes, DNA synthesis of U937 cells, as measured by [3H]thymidine incorporation, decreased by 99% in contrast to their synthesis in conditioned medium from noninfected control monocytes, which did not have any suppressive effect. Partial characterization of CF showed that it is a proteinase-K-sensitive and heat-labile protein with a molecular mass over 100 kDa. Employing a flow cytometric analysis of the cell cycle, it was found that U937 cells, treated either with conditioned medium from dengue virus infected monocytes or with CF, but not treated with conditioned medium from noninfected monocytes, showed cell-cycle arrest in G1 phase by 48 hr. This suppressive effect of CF on U937 growth was dose- and time-dependent. These results suggest that dengue virus-infected monocytes may produce CF to target myeloid cells, resulting in the hematological changes observed in patients with dengue fever.

Adult↗
PubMed1995

Generation of interleukin-8 from human monocytes in response to Trichomonas vaginalis stimulation.

Neutrophils are the predominant inflammatory cells found in the vaginal discharges of patients with Trichomonas vaginalis infection. We have investigated the possible role of interleukin-8 (IL-8) in the inflammatory response elicited by T. vaginalis infection. This study has shown that T. vaginalis induces blood monocytes to produce large amounts of bioactive IL-8, mainly by membrane components of T. vaginalis (MTV). Monocyte-derived IL-8 induced by MTV was dose and time dependent. The peak level of IL-8 was 102 +/- 11 ng/ml of conditioned media (mean +/- standard error; n = 5) obtained from MTV-stimulated monocytes (MTVCM) at 36 h of cultivation. With a multichamber chemotactic assay, we found an optimal neutrophil chemotaxis (177 +/- 14 migrated cells) induced by MTVCM collected at 16 h of cultivation when the level of IL-8 was 42 +/- 8 ng/ml. A neutralizing monoclonal antibody directed against IL-8, but not the irrelevant antibodies, significantly blocked the neutrophil chemotactic activity (decreased from 153 +/- 6 to 23 +/- 3 migrated cells; n = 3 [P < 0.001]) induced by MTVCM. Moreover, the maximum increase of the IL-8 mRNA level from MTV-treated monocytes was observed after a 5-h cultivation and decreased thereafter. Monocytes cocultured with MTV in the presence of a neutralizing monoclonal antibody directed against tumor necrosis factor alpha, but not against IL-1 beta, decreased IL-8 production by 25% (P < 0.05), indicating that the release of IL-8 in MTV-stimulated monocytes is partially dependent on tumor necrosis factor alpha. The capacity of MTV-induced monocytes to synthesize IL-8 suggests that these cells can contribute to the induction of the acute inflammatory response seen in T. vaginalis infection.

Animals↗
PubMed1995

A model to study cytokine profiles in primary and heterologously secondary Dengue-2 virus infections.

Roles of cytokines in primary and secondary Dengue virus (DV) infections are not completely understood. In this study, we challenged mononuclear leukocytes (MNLs) obtained from non-immune and DV-1-infected donors with DV-2 in vitro to mimic primary and heterologously secondary DV-2 infections, respectively. We found that MNLs in response to DV-2 could release a large amount of interleukin-1 (IL-1 beta) and tumor necrosis factor alpha (TNF alpha). However, IL-1 beta and TNF alpha released by MNLs with primary or heterologously secondary exposure to DV-2 were not significantly different. In contrast, MNLs with heterologously secondary DV-2 infections produced significantly higher amount of interferon gamma (IFN gamma) than those with primary DV-2 infections. These results suggest that IFN gamma, but not TNF alpha or IL-1 beta, may in part participate in the pathogenesis of Dengue shock syndrome (DSS) frequently found in heterologously secondary DV-2 infections.

Animals↗
PubMed1995

A higher production of platelet activating factor in ex vivo heterologously secondary dengue-2 virus infections.

Patients with a dengue-1 virus (DV-1) infection followed by another DV-2 infection were reported to have a higher incidence of dengue haemorrhagic fever (DHF). Mononuclear leukocytes (MNLs) are principal cells for DV replication so that we challenge MNLs obtained from non-immune and previously DV-1-infected donors with DV-2 to mimic primary and heterologously secondary DV-2 infections. Production of platelet activating factor (PAF), thromboxane B2 (TxB2), and prostaglandin D2 (PGD2) by MNLs in the DV-2 infections was measured by radioimmunoassay. We found that MNLs, no matter primary or heterologously secondary exposure to DV-2, could release significant amount of PAF, TxB2, and PGD2. PAF but not TxB2 or PGD2 levels released by MNLs were significantly higher in those obtained from previously DV-1-infected donors (75.8 +/- 28.5 vs 21.2 +/- 13.4 pg/ml; p < 0.05). These results suggest that PAF, which is known to enhance inflammatory reactions and to augment platelet aggregation, may in part participate in the pathogenesis of DHF.

Dengue↗
PubMed1994

Hydroxyl radicals as an early signal involved in phorbol ester-induced monocytic differentiation of HL60 cells.

A useful model for the study of monocytic differentiation has been the induction of myeloid leukemic cell differentiation. Employing human HL60 leukemic cells, we sought to clarify whether reactive oxygen intermediates (ROI) are involved in phorbol myristate acetate (PMA)-induced monocytic differentiation. We found that hydroxyl radical (OH.) scavenger pyrrolinodimethylthiocarbamate (PDTC), but not O2-, H2O2 or 1O2 scavenger, suppressed PMA-mediated HL60 cell differentiation in a dose dependent fashion (0.1 to 1.0 microM). PDTC suppressed OH. but not O2- or H2O2 production by HL60 cells stimulated with PMA (32 nM). Addition of PDTC before and right after, but not 16 hours after, PMA stimulation inhibited PMA-induced HL60 cell differentiation. Taken together, these findings indicate that OH., but not O2-, H2O2, or 1O2, is a critical early signal involved in the PMA-induced monocytic differentiation of HL60 cells.

Cell Differentiation↗
PubMed1994

All-trans retinoic acid reverses phorbol ester resistance in a human myeloid leukemia cell line.

Treatment of human HL-60 leukemic cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with activation of protein kinase C (PKC) and induction of monocytic differentiation. An HL-60 variant cell line, termed HL-525, derived from long-term exposure to TPA (Homma et al, Proc Natl Acad Sci USA 83: 7316, 1986) is resistant to TPA-induced differentiation and displays decreased PKC beta expression compared with the HL-60 parent line. However, this variant exhibits features of granulocytic differentiation, including nitroblue tetrazolium reduction, when exposed to all-trans retinoic acid (ATRA). Whereas treatment of HL-525 cells with ATRA or TPA alone had no effect on features of monocytic differentiation, these agents in combination resulted in cellular adhesion, nonspecific esterase staining, and induction of the c-fms (monocyte growth factor receptor) gene. In order to measure PKC expression associated with the reversal of TPA resistance by ATRA, we exposed HL-525 cells to ATRA and analyzed PKC-mRNA and protein levels. Exposure of HL-525 cells to ATRA for 3 days resulted in induction of PKC beta transcripts, whereas there was little change in PKC alpha mRNA levels. ATRA treatment was also associated with an increase in PKC activity and an induction of cytosolic PKC beta protein levels. These findings are consistent with the hypothesis that ATRA reverses TPA resistance in HL-525 cells by enhancing the expression of PKC.

Cell Differentiation↗