Search PubMed⌕ Search

Biomedical subjects

W C Chen

Publications and source records attributed to W C Chen.

At least 19 recordsLinked to original sources
PubMed2006

Identification and mapping of Rf-I an inhibitor of the Rf5 restorer gene for Cms-C in maize (Zea mays L.).

The restoration of the C-type cytoplasmic male sterility (Cms) has been a common agriculture practice in the production of hybrid seed for many years. In this study, a series of crosses between select sterile and restorer lines, as well as a backcross population of (Cms-C77 x 6233) x 6233, were used to investigate the restoration of C-type Cms. Our results demonstrated that there was an inhibitor of the Rf5 restorer gene. This inhibitor gene, Rf-I, maps to chromosome 7 and is tightly linked with SSR markers, umc2326 and umc2327, at a genetic distance 4.7 and 3.4 cM, respectively. After analyzing our data combined with previous studies, we propose that the restoration of C-type Cms has two dominant genes, Rf4 and Rf5. Rf4 has the ability to restore all genotypes of Cms-C lines; however, there exists an inhibitor for the other restorer gene, Rf5; thus, it can restore only those genotypes of Cms-C lines lacking the Rf-I inhibitor.

Genes, Plant↗
PubMed2006

Limits to the polarization for spin-exchange optical pumping of 3He.

Based on measurements of the temperature dependence of 3He relaxation in a wide range of spin-exchange optical pumping cells, we report evidence for a previously unrecognized surface relaxation process. The relaxation rate was found to be linearly proportional to the alkali-metal density with a slope that exceeds the spin-exchange rate, which limits the polarization for current applications, including neutron spin filters, polarized targets, and polarized gas magnetic resonance imaging. We find that the magnitude of this excess relaxation can vary widely between cells, and that the variation is larger for cells of higher surface to volume ratio. We have observed 3He polarization as high as 81%, but further improvements require understanding the origin of this relaxation.

Journal Article↗
PubMed2006

Safrole-induced Ca2+ mobilization and cytotoxicity in human PC3 prostate cancer cells.

The effect of the carcinogen safrole on intracellular Ca2+ mobilization and on viability of human PC3 prostate cancer cells was examined. Cytosolic free Ca2+ levels ([Ca2+]i) were measured by using fura-2 as a probe. Safrole at concentrations above 10 microM increased [Ca2+]i in a concentration-dependent manner with an EC50 value of 350 microM. The Ca2+ signal was reduced by more than half after removing extracellular Ca2+ but was unaffected by nifedipine, nicardipine, nimodipine, diltiazem, or verapamil. In Ca2+-free medium, after treatment with 650 microM safrole, 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor) failed to release Ca2+. Neither inhibition of phospholipase C with U73122 nor modulation of protein kinase C activity affected safrole-induced Ca2+ release. Overnight incubation with 0.65-65 microM safrole did not affect cell viability, but incubation with 325-625 microM safrole decreased viability. Collectively, the data suggest that in PC3 cells, safrole induced a [Ca2+]i increase by causing Ca2+ release from the endoplasmic reticulum in a phospholipase C- and protein kinase C-independent fashion, and by inducing Ca2+ influx. Safrole can decrease cell viability in a concentration-dependent manner.

Calcium Channel Blockers↗
PubMed2006

Effect of riluzole on Ca2+ movement and cytotoxicity in Madin-Darby canine kidney cells.

Riluzole is a drug used in the treatment of amyotrophic lateral sclerosis; however, its in vitro action is unclear. In this study, the effect of riluzole on intracellular Ca2+ concentration ([Ca2+]i) in Madin-Darby canine kidney (MDCK) cells was investigated using the Ca2+ -sensitive fluorescent dye, fura-2. Riluzole (100-500 microM) caused a rapid and sustained increase of [Ca2+]i in a concentration-dependent manner (EC50 = 150 microM). Some 40 and 50% of this [Ca2+]i increase was prevented by the removal of extracellular Ca2+ and the addition of La3+, respectively, but was unchanged by dihydropyridines, verapamil and diltiazem. In Ca2+ -free medium, thapsigargin - an inhibitor of the endoplasmic reticulum (ER) Caz+ -ATPase--caused a monophasic [Ca2+]i increase, after which the increasing effect of riluzole on [Ca2+]i was attenuated by 70%; in addition, pre-treatment with riluzole abolished thapsigargin-induced [Ca2+]i increases. U73122, an inhibitor of phospholipase C (PLC), abolished ATP (but not riluzole)-induced [Ca2+]i increases. At concentrations of 250 and 500 microM, riluzole killed 40 and 95% cells, respectively. The cytotoxic effect of riluzole (250 microM) was unaltered by pre-chelating cytosolic Ca2+ with BAPTA. Collectively, in MDCK cells, riluzole rapidly increased [Ca2+]i by stimulating extracellular Ca2+ influx via an La3+ -sensitive pathway and intracellular Ca2+ release from the ER via, as yet, unidentified mechanisms. Furthermore, riluzole caused Ca2+ -unrelated cytotoxicity in a concentration-dependent manner.

Animals↗
PubMed2005

Effect of celecoxib on Ca2+ fluxes and proliferation in MDCK renal tubular cells.

The effect of celecoxib on renal tubular cells is largely unexplored. In Madin Darby canine kidney (MDCK) cells, the effect of celecoxib on intracellular CaCa2+ concentration ([Ca2+]i) and proliferation was examined by using the Ca(2 +)-sensitive fluorescent dye fura-2 and the viability detecting fluorescent dye tetrazolium, respectively. Celecoxib (> or =1 micro M) caused an increase of [CaCa2+]i in a concentration-dependent manner. Celecoxib-induced [CaCa2+]i increase was partly reduced by removal of extracellular CaCa2+. Celecoxib-induced CaCa2+ influx was independently suggested by MnCa2+ influx-induced fura-2 fluorescence quench. In Ca(2 +)-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca(2 +)-ATPase, caused a monophasic [CaCa2+]i increase, after which celecoxib only induced a tiny [CaCa2+]i increase; conversely, pretreatment with celecoxib completely inhibited thapsigargin-induced [CaCa2+]i increases. U73122, an inhibitor of phospholipase C, abolished ATP (but not celecoxib)-induced [CaCa2+]i increases. Overnight incubation with 1 or 10 micro M celecoxib decreased cell viability by 80% and 100%, respectively. These data indicate that celecoxib evokes a [CaCa2+]i increase in renal tubular cells by stimulating both extracellular CaCa2+ influx and intracellular CaCa2+ release and is highly toxic to renal tubular cells in vitro.

Animals↗
PubMed2005

Econazole induces increases in free intracellular Ca2+ concentrations in human osteosarcoma cells.

Econazole is an antifungal drug with different in vitro effects. However, econazole's effect on osteoblast-like cells is unknown. In human MG63 osteosarcoma cells, the effect of econazole on intracellular Ca2+ concentrations ([Ca2+]i) was explored by using fura-2. At a concentration of 0.1 microM, econazole started to cause a rise in [Ca2+]i in a concentration-dependent manner. Econazole-induced [Ca2+]i rise was reduced by 74% by removal of extracellular Ca2+. The econazole-induced Ca2+ influx was mediated via a nimodipine-sensitive pathway. In Ca2+ -free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca+ -ATPase, caused a [Ca2+]i rise, after which the increasing effect of econazole on [Ca2+]i was abolished. Pretreatment of cells with econazole to deplete Ca2+ stores totally prevented thapsigargin from releasing Ca2+. U73122, an inhibitor of phospholipase C, abolished histamine (an inositol 1,4,5-trisphosphate-dependent Ca2+ mobilizer)-induced, but not econazole-induced, [Ca2+]i rise. Econazole inhibited 76% of thapsigargin-induced store-operated Ca2+ entry. These findings suggest that in MG63 osteosarcoma cells, econazole increases [Ca2+]i by stimulating Ca2+ influx and Ca2+ release from the endoplasmic reticulum via a phospholipase C-independent manner. In contrast, econazole acts as a potent blocker of store-operated Ca2+ entry.

Antifungal Agents↗
PubMed2004

Randomization of heavily damaged regions in annealed low energy Ge(+)-implanted (001)Si.

Apparent growth of amorphous layers during low temperature annealing was observed in low energy Ge(+)-implanted (001)Si by high-resolution transmission electron microscopy. The occurrence of abnormal growth is due to the randomization of heavily damaged regions beneath the original amorphous/crystalline interfaces. The randomization process is attributed to the strain, incurred by the presence of a high density of large Ge atoms in the heavily damaged Si substrate, relaxation to lower the free energy of the systems. The randomization upon annealing may be fruitfully applied to minimize the transient enhanced diffusion in shallow junction formation.

Journal Article↗
PubMed2004

Signals in the activation of opioid mu-receptors by loperamide to enhance glucose uptake into cultured C2C12 cells.

In an attempt to understand the signal pathways of opioid mu-receptors for glucose metabolism, we used loperamide to investigate the glucose uptake into the myoblast C2C12 cells. Loperamide enhanced the uptake of radioactive deoxyglucose into C2C12 cells in a concentration-dependent manner that was abolished in cells pre-incubated with naloxone or naloxonazine at concentrations sufficient to block opioid mu-receptors. Pharmacological inhibition of phospholipase C (PLC) by U73122 resulted in a concentration-dependent decrease in loperamide-stimulated uptake of radioactive deoxyglucose into C2C12 cells. This inhibition of glucose uptake by U73122 was specific since the inactive congener, U73343, failed to modify loperamide-stimulated glucose uptake. Moreover, both chelerythrine and GF 109203X diminished the action of loperamide at concentrations sufficient to inhibit protein kinase C (PKC). The obtained data suggest that an activation of opioid mu-receptors in C2C12 cells by loperamide may increase glucose uptake via the PLC-PKC pathway.

Animals↗
PubMed2003

Rough set-based hybrid fuzzy-neural controller design for industrial wastewater treatment.

Recent advances in control engineering suggest that hybrid control strategies, integrating some ideas and paradigms existing in different soft computing techniques, such as fuzzy logic, genetic algorithms, rough set theory, and neural networks, may provide improved control performance in wastewater treatment processes. This paper presents an innovative hybrid control algorithm leading to integrate the distinct aspects of indiscernibility capability of rough set theory and search capability of genetic algorithms with conventional neural-fuzzy controller design. The methodology proposed in this study employs a three-stage analysis that is designed in series for generating a representative state function, searching for a set of multi-objective control strategies, and performing a rough set-based autotuning for the neural-fuzzy logic controller to make it applicable for controlling an industrial wastewater treatment process. Research findings in the case study clearly indicate that the use of rough set theory to aid in the neural-fuzzy logic controller design can produce relatively better plant performance in terms of operating cost, control stability, and response time simultaneously, which is effective at least in the selected industrial wastewater treatment plant. Such a methodology is anticipated to be capable of dealing with many other types of process control problems in waste treatment processes by making only minor modifications.

Artificial Intelligence↗
PubMed2003

Isolation of non-tuberculous mycobacteria from hospital cockroaches (Periplaneta americana).

This study attempted to isolate mycobacteria from hospital and household cockroaches from 90 hospitals and 40 households in Kaohsiung City and Kaohsiung County, South Taiwan. Among 203 cockroaches (139 Periplaneta americana and 64 Blattella germanica) collected from the hospitals, six Mycobacterium spp. were isolated and identified by polymerase chain reaction-restriction fragment length polymorphism analysis. In 12 cockroaches (P. americana): four Mycobacterium kansaii, three Mycobacterium xenopi, two Mycobacterium gordonae, one Mycobacterium hemophilium, one Mycobacterium fortuitum, and one Mycobacterium avium. However, no mycobacteria were obtained form the hospital B. germanica or 226 household cockroaches (123 P. americana and 103 B. germanica). As cockroach infestation occurs commonly in the hospital environment, they may potentially be implicated as a cause of hospital-acquired infections due to non-tuberculous mycobacteria.

Animals↗
PubMed2003

Release of beta-endorphin by caffeic acid to lower plasma glucose in streptozotocin-induced diabetic rats.

The role of alpha 1A -adrenoceptors in the regulation of opioid secretion from the adrenal glands of streptozotocin-induced diabetic rats (STZ-diabetic rats) was examined in an attempt to determine the mechanism of plasma glucose-lowering action of caffeic acid. In agreement with a previous report, we showed that caffeic acid produced a dose-dependent lowering of the plasma glucose concentration in STZ-diabetic rats along with an increase of plasma beta-endorphin-like immunoreactivity (BER). These actions of caffeic acid were abolished by pretreatment with WB 4101 or RS 17 056 at doses sufficient to block alpha 1A -adrenoceptors. In addition, naloxone and naloxonazine at doses effective for blocking opioid micro -receptors abolished the plasma glucose-lowering action of caffeic acid. Also, unlike that in wild-type diabetic mice, caffeic acid failed to produce a plasma glucose lowering effect in opioid micro -receptor knockout diabetic mice. We observed that caffeic acid could enhance BER release from isolated rat adrenal medulla in a concentration-dependent manner; inhibitors of alpha 1A -adrenoceptors such as WB 4101 and RS 1705 abolished this action. Investigations of the signal pathways further supported that activation of alpha 1A -adrenoceptor is responsible for the stimulatory effect of caffeic acid on BER secretion from the adrenal medulla. In the presence of U73312, a specific inhibitor of phospholipase C, the caffeic acid-induced increase of BER was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control of U73312. Chelerythrine and GF 109203X also diminished the action of caffeic acid at concentrations sufficient for inhibiting protein kinase C. Moreover, bilateral adrenalectomy in STZ-diabetic rats resulted in the loss of this plasma glucose-lowering effect of caffeic acid, and there was no increase in plasma BER with caffeic acid. Therefore, beta-endorphin release from the adrenal gland appears to be responsible for the lowering of plasma glucose in STZ-diabetic rats induced by caffeic acid, through the activation of alpha 1A -adrenoceptors.

Adrenalectomy↗
PubMed2002

Gamma spectra resulting from the annihilation of positrons with electrons in a single core level.

The first gamma spectra associated with the annihilation of positrons with individual core levels (Cu 3p and Ag 4p) are presented. The spectra were obtained by measuring the energy of gamma rays time coincident with Auger electrons emitted as a result of positrons annihilating with a selected core level. Relativistic calculations show good agreement with experiment over a limited range of momenta. However, statistically significant differences indicate that the measurements can provide an impetus to new calculations of many body effects in positron-core electrons annihilation.

Journal Article↗
PubMed2002

Effect of triethyltin on Ca2+ movement in Madin-Darby canine kidney cells.

The effects of the environmental toxicant, triethyltin, on Ca2+ mobilization in Madin-Darby canine kidney (MDCK) cells have been examined. Triethyltin induced an increase in cytosolic free Ca2+ levels ([Ca2+]i) at concentrations larger than 2 microM in a concentration-dependent manner. Within 5 min, the [Ca2+]i signal was composed of a gradual rise and a sustained phase. The [Ca2+]i signal was partly reduced by removing extracellular Ca2+. In Ca(2+)-free medium, pretreatment with thapsigargin (1 microM), an endoplasmic reticulum Ca2+ pump inhibitor, reduced 50 microM triethyltin-induced [Ca2+]i increase by 80%. Conversely, pretreatment with triethyltin abolished thapsigargin-induced Ca2+ release. Pretreatment with U73122 (2 microM) to inhibit phospholipase C-coupled inositol 1,4,5-trisphosphate formations failed to alter 50 microM triethyltin-induced Ca2+ release. Incubation with triethyltin at a concentration (1 microM) that did not increase basal [Ca2+]i for 3 min did not alter ATP (10 microM)- and bradykinin (1 microM)-induced [Ca2+]i increases. Collectively, this study shows that triethyltin altered Ca2+ movement in renal tubular cells by releasing Ca2+ from multiple stores in an inositol 1,4,5-trisphosphate-independent manner, and by inducing Ca2+ influx.

Animals↗
PubMed2001

Molecular approach to echinoderm regeneration.

Until very recently echinoderm regeneration research and indeed echinoderm research in general has suffered because of the lack of critical mass. In terms of molecular studies of regeneration, echinoderms in particular have lagged behind other groups in this respect. This is in sharp contrast to the major advances achieved with molecular and genetic techniques in the study of embryonic development in echinoderms. The aim of our studies has been to identify genes involved in the process of regeneration and in particular neural regeneration in different echinoderm species. Our survey included the asteroid Asterias rubens and provided evidence for the expression of Hox gene homologues in regenerating radial nerve cords. Present evidence suggests: 1) ArHox1 expression is maintained in intact radial nerve cord and may be upregulated during regeneration. 2) ArHox1 expression may contribute to the dedifferentiation and/or cell proliferation process during epimorphic regeneration. From the crinoid Antedon bifida, we have been successful in cloning a fragment of a BMP2/4 homologue (AnBMP2/4) and analysing its expression during arm regeneration. Here, we discuss the importance of this family of growth factors in several regulatory spheres, including maintaining the identity of pluripotent blastemal cells or as a classic skeletal morphogenic regulator. There is clearly substantial scope for future echinoderm research in the area of molecular biology and certain aspects are discussed in this review.

Amino Acid Sequence↗
PubMed2001

Relation of the estrogen receptor alpha gene microsatellite polymorphism to bone mineral density and the susceptibility to osteoporosis in postmenopausal Chinese women in Taiwan.

OBJECTIVE: Osteoporosis is a common disorder with a strong genetic component. Our aim was to investigate the correlation of the estrogen receptor alpha gene microsatellite polymorphism (TA dinucleotide repeat polymorphism 5' upstream of exon 1) with bone mineral density and their relationship to osteoporosis. METHODS: We determined the estrogen receptor alpha gene microsatellite polymorphism using polymerase chain reaction-based microsatellite analysis in postmenopausal Chinese women in Taiwan. Bone mineral density of the lumbar spine and proximal femur were measured using dual-energy X-ray absorptiometry. RESULTS: The ERalpha genotype was classified into '12' through '27' according to the number of TA dinucleotide repeats they contained, as a 'signpost'. After adjustment for potential confounding factors including age, height, and weight, subjects with genotype 18+ (n=4) had lower bone mineral density values and a 54.5 times greater risk for osteoporosis when compared with subjects with genotype 18- (n=170) at the lumbar spine. This should be interpreted with caution because of the small number of subjects with the unfavorable genotype 18+. According to mean number of TA dinucleotide repeats, women with a high number of repeats (TA > or =20) (n=38) had the lowest bone mineral density and a 6.1 times greater risk for osteoporosis than women with a low number of repeats (TA < or =15) (n=61) at the femoral neck, after adjustment for potential confounding factors such as age, height, and weight. CONCLUSION: The present study suggests that the estrogen receptor alpha gene microsatellite polymorphism may be a candidate genetic marker for risk of osteoporosis in postmenopausal Chinese women in Taiwan.

Absorptiometry, Photon↗
PubMed2001

Effect of oleamide on Ca(2+) signaling in human bladder cancer cells.

The effect of oleamide, a sleep-inducing endogenous lipid in animal models, on intracellular free levels of Ca(2+) ([Ca(2+)](i)) in non-excitable and excitable cells was examined by using fura-2 as a fluorescent dye. [Ca(2+)](i) in pheochromocytoma cells, renal tubular cells, osteoblast-like cells, and bladder cancer cells were increased on stimulation of 50 microM oleamide. The response in human bladder cancer cells (T24) was the greatest and was further explored. Oleamide (10-100 microM) increased [Ca(2+)](i) in a concentration-dependent fashion with an EC(50) of 50 microM. The [Ca(2+)](i) signal comprised an initial rise and a sustained plateau and was reduced by removing extracellular Ca(2+) by 85 +/- 5%. After pre-treatment with 10-100 microM oleamide in Ca(2+)-free medium, addition of 3 mM Ca(2+) increased [Ca(2+)](i) in a manner dependent on the concentration of oleamide. The [Ca(2+)](i) increase induced by 50 microM oleamide was reduced by 100 microM La(3+) by 40%, but was not altered by 10 microM nifedipine, 10 microM verapamil, and 50 microM Ni(2+). In Ca(2+)-free medium, pre-treatment with thapsigargin (1 microM), an endoplasmic reticulum Ca(2+) pump inhibitor, abolished 50 microM oleamide-induced [Ca(2+)](i) increases; conversely, pretreatment with 50 microM oleamide reduced 1 microM thapsigargin-induced [Ca(2+)](i) increases by 50 +/- 3%. Suppression of the activity of phospholipase C with 2 microM U73122 failed to alter 50 microM oleamide-induced Ca(2+) release. Linoleamide (10-100 microM), another sleep-inducing lipid with a structure similar to that of oleamide, also induced an increase in [Ca(2+)](i). Together, it was shown that oleamide induced significant [Ca(2+)](i) increases in cells by a phospholipase C-independent release of Ca(2+) from thapsigargin-sensitive stores and by inducing Ca(2+) entry.

Animals↗
PubMed2001

Mechanism of bifonazole-induced [Ca2+]i increases in MDCK renal tubular cells.

The effect of the antifungal drug bifonazole on Ca2+ homeostasis in Madin Darby canine kidney (MDCK) cells was investigated. Cell suspensions were loaded with the Ca2+-sensitive dye fura-2, and the fluorescence changes were measured with a spectrofluorophotometer. At concentrations between 10-80 microM bifonazole increased cytosolic free Ca2+ levels ([Ca2+]i) in a concentration-dependent manner. The Ca2+ signals were partly inhibited by removing extracellular Ca2+. Bifonazole (40 microM) released Ca2+ from the store sensitive to 1 microM thapsigargin, an endopolasmic reticulum Ca2+ pump inhibitor. Bifonazole (40 microM) per se induced capacitative Ca2+ entry while reduced 1 microM thapsigargin-induced capacitative Ca2+ entry. Inositol 1,4,5-trisphosphate may be involved in bifonazole-induced Ca2+ release because inhibiting phospholipase C with 2 microM U73122 partly reduced the bifonazole response. Together, bifonazole increased [Ca2+]i in renal tubular cells by inducing intracellular Ca2+ release and extracellular Ca2+ influx.

Adenosine Triphosphate↗