Biomedical subjects

Y L Lee

Publications and source records attributed to Y L Lee.

At least 19 recordsLinked to original sources

PubMed2005

Demonstration of different modes of cell death upon herpes simplex virus 1 infection in different types of oral cells.

The effects of Herpes simplex virus 1 (HSV-1) infection on five different types of oral cancerous cells (neck metastasis of gingival carcinoma (GNM) cells and tongue squamous cells of carcinoma (TSCCa) and non-cancerous cells (buccal mucosal fibroblasts (BF), gingival fibroblasts (GF), oral submucosal fibrosis cells (OSF)) and one type of non-oral cancerous cells (KB cells) were investigated. In HSV-1-infected cells the cell viability, CPE, viral antigens accumulation, caspase-3 activity, annexin V binding and DNA fragmentation were estimated. Three different forms or pathways of cell death were considered: apoptosis (the presence or rise of caspase-3 activity, DNA fragmentation and annexin V binding), slow cell death (the presence or rise of DNA fragmentation, the absence or decline of caspase-3 activity and annexin V binding), and necrosis (the absence of decline of caspase-3 activity, DNA fragmentation and annexin V binding). The viability of all cell types, except for KB cells, was reduced by the infection. CPE and viral antigens data demonstrated that all six types of cells could be infected with HSV-1. Upon HSV-1 infection there occurred (i) a classical apoptosis in GF cells, (ii) apoptosis in the early phase of infection and necrosis in the late phase of infection in GNM and TSCCa cells, (iii) slow cell death followed by necrosis in BF and OSF cells (however, these cells showed a different type of CPE), (iv) a classical slow cell death in KB cells. It is hypothesized that HSV-1 infection has a potential to induce several distinct pathways leading to cell death or several forms of cell death. Moreover, more than one pathway may be involved in the death of particular cell type. As HSV-1 was demonstrated to infect different oral and non-oral cells and cause different pathways or forms of cell death, the safety of using HSV-1 as a vector for gene therapy should be re-considered.

Annexin A5↗

PubMed2005

Effect of cordycepin on Hantaan virus 76-118 infection of primary human embryonic pulmonary fibroblasts--characterization of apoptotic effects.

The cDNA microarray technique was used to study gene epression in human embryonic pulmonary fibroblasts (HEPF) infected with Hantaan virus (HTNV) under the influence of cordycepin (Cor), an inhibitor of post-transcriptional pre-mRNA polyadenylation. Four apoptotic genes, the insulin-like growth factor binding protein 1, NFkB inhibitor alpha, caspase-3 and NFkB1 were up-regulated in both infected and uninfected Cor-treated cells and two cell cycle-associated genes, CDC-like kinase and beta-induced transforming growth factor were up-regulated in Cor-untreated cells but down-regulated in Cor-treated cells. Cell morphology examination, quantitative RT-PCR, and immunofluorescence (IF) test suggested that following the Cor treatment the HTNV infection took place, but late viral gene expression was slightly reduced. Three parameters, namely caspase-3 activity, annexin V binding, and cell cycle were used to detect apoptosis. The results suggested that the induction of apoptosis in HEPF by HTNV started at 6 hrs post infection (p.i.). Following the Cor treatment, however, the caspase-3 activity began to increase at 24 hrs p.i. Thus it is suggested that inhibition of de novo late viral protein synthesis by Cor changes the apoptosis pathway and cell cycle by delaying caspase-3 gene expression and by up/down-regulating of expression of other apoptotic and cell cycle-associated genes. This implicates that HTNV can induce apoptosis in HEPF even without de novo viral protein synthesis and with a reduced and slowed viral maturation.

Animals↗

PubMed2004

Embryotrophic factor-3 from human oviductal cells enhances proliferation, suppresses apoptosis and stimulates the expression of the beta1 subunit of sodium-potassium ATPase in mouse embryos.

BACKGROUND: Embrytrophic factor-3 (ETF-3) from human oviductal cells enhanced the development of mouse preimplantation embryos. This report studied the embryotrophic mechanisms of the molecule. METHODS AND RESULTS: Mouse embryos were incubated with ETF-3 for 24 h at different stages of development. ETF-3 treatment between 96 and 120 h post-HCG increased the cell count of blastocysts, whilst treatment between 72 and 96 h post-HCG enhanced the expansion and hatching of the blastocysts. ETF-3 increased the cell number of the embryos by suppressing apoptosis and increasing proliferation as determined by TUNEL and bromodeoxyuridine uptake assays, respectively. Real-time quantitative PCR showed that the in vivo developed and ETF-3-treated blastocysts had a significantly higher mRNA copy number of Na/K-ATPase-beta1, but not of hepsin, than that of blastocysts cultured in medium alone. The former gene was associated with cavitation of blastocysts while the latter was related to hatching of blastocyst. The beneficial effect of ETF-3 on blastocyst hatching was also seen when ETF-3-supplemented commercially available sequential culture medium for human embryo culture was used to culture mouse embryos. CONCLUSIONS: ETF-3 improves embryo development by enhancing proliferation, suppressing apoptosis and stimulating expression of genes related to blastocyst cavitation. Supplementating human embryo culture medium with ETF-3 may improve the success rate in clinical assisted reproduction.

Animals↗

PubMed2004

Peritonsillar infections: local experience.

INTRODUCTION: The disease pattern and management of peritonsillar infections in Singapore General Hospital are studied. Other objectives are to determine if a seasonal variation exists and to examine the role of routine bacterial cultures and interval tonsillectomy. METHODS: This is a retrospective review of the management and outcome of patients with peritonsillar infections who were admitted acutely to Singapore General Hospital over a three-year period. RESULTS: Of 185 patients studied, 151 (81.6 percent) had peritonsillar abscess or quinsy and 34 (18.4 percent) had peritonsillar cellulitis. There were 139 males and 46 females, with a racial predisposition among Malays (p value is less than 0.0005). There may be a seasonal variation with a bi-annual trend, though no correlation with upper respiration tract infections was noted. Treatment consisted mainly of incision and drainage (66 percent) or needle aspiration (34 percent). No significant difference in the length of stay was noted in patients receiving penicillin alone, penicillin with metronidazole, or broad-spectrum antibiotics (p value is equal to 0.062). Fourteen (7.6 percent) patients had recurrences, all of which occurred after the first month. Two patients (1 percent) had bilateral quinsy. CONCLUSION: Peritonsillar infections remain a common admitting diagnosis to the Otolaryngology department. A single episode of infection should no longer be an indication for tonsillectomy as the incidence of recurrence is low.

Acute Disease↗

PubMed2003

Embryotrophic factor-3 from human oviductal cells affects the messenger RNA expression of mouse blastocyst.

Our previous results showed that embryotrophic factor-3 (ETF-3) from human oviductal cells increased the size and hatching rate of mouse blastocysts in vitro. The present study investigated the production of ETF-3 by an immortalized human oviductal cell line (OE-E6/E7) and the effects of ETF-3 on the mRNA expression of mouse embryos. The ETF-3 was purified from primary oviductal cell conditioned media using sequential liquid chromatographic systems, and antiserum against ETF-3 was raised. The ETF-3-supplemented Chatot-Ziomek-Bavister medium was used to culture Day 1 MF1 x BALB/c mouse embryos for 4 days. The ETF-3 treatment significantly enhanced the mouse embryo blastulation and hatching rate. The antiserum, at concentrations of 0.03-3%, abolished the embryotrophic effect of ETF-3. Positive ETF-3 immunoreactivity was detected in the primary oviductal cells, OE-E6/E7, and blastocysts derived from ETF-3 treatment. Vero cells (African Green Monkey kidney cell line), fibroblasts, and embryos cultured in control medium did not possess ETF-3 immunoreactivity. The mRNA expression patterns of the treated embryos were studied at the blastocyst stage by mRNA differential display reverse transcription-polymerase chain reaction (DDRT-PCR). The DDRT-PCR showed that some of the mRNAs were differentially expressed after ETF-3 treatment. Twelve of the differentially expressed mRNAs that had high homology with cDNA sequences in the GenBank were selected for further characterization. The differential expression of seven of these mRNAs (ezrin, heat shock 70-kDa protein, cytochrome c oxidase subunit VIIa-L precursor, proteinase-activated receptor 2, eukaryotic translation initiation factor 2beta, cullin 1, and proliferating cell nuclear antigen) was confirmed by semiquantitative RT-PCR. In conclusion, immortalized oviductal cells produce ETF-3, which influences mRNA expression of mouse blastocyst.

Animals↗

PubMed2003

Climate, traffic-related air pollutants and allergic rhinitis prevalence in middle-school children in Taiwan.

The prevalence of allergic rhinitis, a common respiratory disorder, may be rapidly increasing. Epidemiological studies, however, indicate little about its association with climatic factors and air pollution. The relationship between traffic-related air pollutants and allergic rhinitis in middle-school students was therefore investigated. In a nationwide survey of middle-school students in Taiwan conducted in 1995/1996, the lifetime prevalence of physician-diagnosed allergic rhinitis and typical symptoms of allergic rhinitis were compared with air-monitoring station data on temperature, relative humidity, sulphur dioxide (SO2), nitrogen oxides (NOx), ozone (O3), carbon monoxide (CO) and particulate matter with a 50% cut-off aerodynamic diameter of 10 microm (PM10). A total of 331,686 nonsmoking children attended schools located within 2 km of 55 stations. Mean (range) annual exposures were: CO 853 (381-1,610) parts per billion (ppb), NOx 35.1 (10.2-72.4) ppb, SO2 7.57 (0.88-21.2) ppb, PM10 69.2 (40.1-116.2) microg x m(-3), O3 21.3 (12.4-34.1) ppb, temperature 22.9 (19.6-25.1) degrees C, and relative humidity 76.2 (64.8-86.2)%. The prevalence of physician-diagnosed allergic rhinitis was 28.6 and 19.5% in males and females, respectively, with prevalence of questionnaire-determined allergic rhinitis 42.4 and 34.0%. After adjustment for age, parental education and history of atopic eczema, physician-diagnosed allergic rhinitis was found to be associated with higher nonsummer (September-May) warmth and traffic-related air pollutants, including CO, NOx and O3. Questionnaire-determined allergic rhinitis correlated only with traffic-related air pollutants. Nonsummer warmth and traffic-related air pollution, probably mediated through exposure to common allergens such as dust mites, are possible risk factors for allergic rhinitis in middle-school-aged children.

Adolescent↗

PubMed2001

The proteins of synaptic vesicle membranes are affected during ageing of rat brain.

Low molecular weight GTP-binding proteins are molecular switches that are believed to play pivotal roles in cell growth, differentiation, cytoskeletal organization, and vesicular trafficking. Rab proteins are key players in the regulation of vesicular transport, while Rho family members control actin-dependent cell functions, i.e. the regulation of cytoskeletal organization in response to extracelluar growth factors and in dendritic neuron development. In this study, we have examined the regulation of small GTP-binding proteins that are implicated in neurosecretion and differentiation of neuron during ageing processes. Comparison of small GTP-binding proteins from the synaptosome and crude synaptic vesicles (LP2 membranes) of 2 months and 20 months old rat brain respectively showed no difference in the level of Rab family proteins (Rab3A and Rab5A). However, Rho family proteins such as RhoA and Cdc42 were elevated in LP2 membranes of the aged brain. The dissociation of Rab3A by Ca2+/calmodulin (CaM) from SV membranes was not changed during aging. Ca2+/CaM stimulated phosphorylation of the 22 and 55-kDa proteins in SV membranes from the aged rat brain, and inhibited phosporylation of 30-kDa proteins. GTPgammaS inhibited phosphorylation of the 100-kDa proteins and stimulated phosphorylation of the 70 kDa in LP2 membranes from both the young and aged rat brains, whereas GDPbetaS caused just the opposite reaction. These results suggest that protein phosphorylation and regulation of Rho family GTPases in rat brain appears to be altered during ageing processes.

Aging↗

PubMed2001

Construction of single-chain interleukin-12 DNA plasmid to treat airway hyperresponsiveness in an animal model of asthma.

Allergic asthma is strongly associated with the airway inflammation caused by the dysregulated production of cytokines secreted by the allergen-specific type-2 T helper (Th2) cells. Interleukin (IL)-12 is a heterodimeric cytokine, which strongly promotes the differentiation of naive CD4(+) T cells to the type-1 T helper (Th1) phenotype and suppresses the expression of Th2 cytokines. Therefore, immunotherapy with IL-12 has been suggested as a possible therapy for asthma. In previous studies, we developed a murine model of airway inflammation based on the purified, house dust-mite allergen Der p 1 (Dermatophagodies pteronyssinus) as a clinically relevant allergen. We hypothesized that the expression of IL-12 in the airway may represent an effective therapy for allergic airway diseases. In this study, we investigate whether the local transfer of the IL-12 gene to respiratory tissues modifies allergic inflammation and airway hyper-responsiveness (AHR) in our disease model. To enhance the in vivo delivery of the IL-12 gene, we expressed the murine single-chain IL-12 protein from a nonviral vector to which the two IL-12 subunits (p35 and p40) were linked by a 14- to 18-amino-acid linker. One of these single-chain IL-12s, containing an 18 amino-acid polypeptide linker, was stably expressed and had a high level of biological activity comparable to that of native IL-12 in vitro. In mice with Der p 1-induced asthma, the local administration of this IL-12 fusion gene into the lungs significantly prevented the development of AHR, abrogated airway eosinophilia, and inhibited type-2 cytokine production. These findings indicate that the local transfer of the single-chain IL-12 gene is effective in modulating pulmonary allergic responses and may be a convenient method for future applications of DNA vaccination.

Allergens↗

PubMed2001

Observation of a (6)(LambdaLambda)He double hypernucleus.

A double-hyperfragment event has been found in a hybrid-emulsion experiment. It is identified uniquely as the sequential decay of ( 6)(LambdaLambda)He emitted from a Xi(-) hyperon nuclear capture at rest. The mass of ( 6)(LambdaLambda)He and the Lambda-Lambda interaction energy DeltaB(LambdaLambda) have been measured for the first time devoid of the ambiguities due to the possibilities of excited states. The value of DeltaB(LambdaLambda) is 1.01+/-0.20(+0.18)(-0.11) MeV. This demonstrates that the Lambda-Lambda interaction is weakly attractive.

Journal Article↗

PubMed2001

Ammonium ions induce inactivation of Kir2.1 potassium channels expressed in Xenopus oocytes.

1. The decay of inward currents was studied using the giant patch-clamp technique and a cloned inward rectifier K(+) channel, Kir2.1, expressed in Xenopus oocytes. 2. In inside-out patches, inward currents carried by NH4(+) or Tl(+) decayed over time. When the voltage was more negative, the degree and rate of decay were greater. The rate of NH4(+)-induced decay saturated at a symmetrical [NH4(+)] of approximately 100 mM. The decay rate was slow (2.6 x 10(3) M(-1) s(-1)) at -140 mV with 10 mM [NH4(+)]. 3. Upon a 10 degrees C increase in temperature, the single-channel NH4(+) current amplitude increased by a factor of 1.57, whereas the NH4(+)-induced decay rate increased by a factor of 2.76. In the R148Y Kir2.1 mutant (tyrosine 148 is at the external pore mouth), NH4(+)-induced inactivation was no longer observed. 4. NH4(+) single-channel currents revealed one open and one closed state. The entry rate into the closed state was voltage dependent whereas the exit rate from the closed state was not. An increase of internal [NH4(+)] not only decreased the entry rate into but also elevated the exit rate from the closed state, consistent with the occupancy model modified from the foot-in-the-door model of gating. 5. These results suggest that the decay of NH4(+) current is unlikely to be due to a simple bimolecular reaction leading to channel block. We propose that NH4(+) binding to Kir2.1 channels induces a conformational change followed by channel closure. 6. The decay induced by permeant ions other than K(+) may serve as a secondary selectivity filter, such that K(+) is the preferred permeant ion for Kir2.1 channels.

Animals↗

PubMed2001

Highly sulfated forms of heparin sulfate are involved in japanese encephalitis virus infection.

Japanese encephalitis virus (JEV) infects a broad range of cell types in vitro, though little is known about the initial events of JEV infection. In the present study, we found that highly sulfated glycosaminoglycans (GAGs) are involved in infection of both neurovirulent (RP-9) and attenuated (RP-2ms) JEV strains. Competition experiments using highly sulfated GAGs, heparin and dextran sulfate, demonstrated an inhibition of JEV's attachment and subsequent infection of BHK-21 cells. Treatment of target cells by a potent sulfation inhibitor, sodium chlorate, greatly reduced viral binding ability as well as infection, suggesting a critical role of GAGs' sulfation status on the cellular surface in JEV infection. This phenomenon was confirmed by the manifestation of a distinct binding efficiency of JEV to the wild-type CHO cell line and its mutants with defects in GAG biosynthesis. We also demonstrated the binding of JEV particles and virus envelope glycoprotein to immobilized heparin beads. Furthermore, the addition of heparin suppressed the cytopathic effects induced by JEV infection in cultured cells. Our results establish that the highly sulfated form of GAGs on cell surfaces plays a determining role in the early stage of in vitro JEV infection.

Animals↗

PubMed2001

Chemokine antagonist infusion promotes axonal sparing after spinal cord contusion injury in rat.

Spinal cord injury produced by mechanical contusion causes the onset of acute and chronic degradative events. These include blood brain barrier disruption, edema, demyelination, axonal damage and neuronal cell death. Posttraumatic inflammation after spinal cord injury has been implicated in the secondary injury that ultimately leads to neurologic dysfunction. Studies after spinal cord contusion have shown expression of several chemokines early after injury and suggested a role for them in the ordered recruitment of inflammatory cells at the lesion site (McTigue et al. [1998] J. Neurosci. Res. 53:368-376; Lee et al., [2000] Neurochem Int). We have demonstrated previously that infusion of the broad-spectrum chemokine receptor antagonist (vMIPII) in the contused spinal cord initially attenuates leukocyte infiltration, suppresses' gliotic reaction and reduces neuronal damage after injury. These changes are accompanied by increased expression of bcl-2, the endogenous apoptosis inhibitor, and reduced neuronal apoptosis (Ghirnikar et al. [2000] J. Neurosci. Res. 59:63-73). We demonstrate that 2 and 4 weeks of vMIPII infusion in the contusion-injured spinal cord also results in decreased hematogenous infiltration and is accompanied by reduced axonal degeneration in the gray matter. Luxol fast blue and MBP immunoreactivity indicated reduced myelin breakdown in the dorsal and ventral funiculi. Increased neuronal survival in the ventral horns of vMIPII infused cords was seen along with increased bcl-2 staining in them. Immunohistochemical identification of fiber phenotypes showed increased presence of calcitonin gene related peptide, choline acetyl transferase and tyrosine hydroxylase positive fibers as well as increased GAP43 staining in treated cords. These results suggest that sustained reduction in posttraumatic cellular infiltration is beneficial for tissue survival. A preliminary report of this study has been published (Eng et al. [2000] J. Neurochem. 74(Suppl):S67B). In contrast to vMIPII, infusion of MCP-1 (9-76), a N-terminal analog of the MCP-1 chemokine showed only a modest reduction in cellular infiltration at 14 and 21 dpi without significant tissue survival after spinal cord contusion injury. Comparing data on tissue survival obtained with vMIPII and MCP-1 (9-76) further validate the importance of the use of broad-spectrum antagonists in the treatment of spinal cord injury. Controlling the inflammatory reaction and providing a growth permissive environment would enhance regeneration and ultimately lead to neurological recovery after spinal cord injury. J. Neurosci. Res. 64:582-589, 2001. Published 2001 Wiley-Liss, Inc.

Amino Acid Sequence↗

PubMed2001

Overexpression of macrophage colony-stimulating factor receptor on microglial cells induces an inflammatory response.

Microglia are important in the inflammatory response in Alzheimer's disease (AD). We showed previously that macrophage colony-stimulating factor receptor (M-CSFR), encoded by the c-fms protooncogene, is overexpressed on microglia surrounding amyloid beta (Abeta) deposits in the APP(V717F) mouse model for AD. The M-CSFR is also increased on microglia after experimental brain injury and in AD. To determine the relevance of these findings, we transiently expressed M-CSFR on murine BV-2 and human SV-A3 microglial cell lines using an SV40-promoted c-fms construct. M-CSFR overexpression resulted in microglial proliferation and increased expression of inducible nitric-oxide synthase, the proinflammatory cytokines interleukin-1alpha, macrophage inflammatory protein 1-alpha, and interleukin-6 and of macrophage colony-stimulating factor (M-CSF) itself. Antibody neutralization of M-CSF showed that the M-CSFR-induced proinflammatory response was dependent on M-CSF in the culture media. By using a co-culture of c-fms-transfected murine microglia and rat organotypic hippocampal slices and a species-specific real time reverse transcriptase-polymerase chain reaction assay and enzyme-linked immunosorbent assay, we showed that M-CSFR overexpression on exogenous microglia induced expression of interleukin-1alpha by the organotypic culture. These results show that increased M-CSFR expression induces microglial proliferation, cytokine expression, and a paracrine inflammatory response, suggesting that in APP(V717F) mice increased M-CSFR on microglia could be an important factor in Abeta-induced inflammatory response.

Amidohydrolases↗

PubMed2001

Cancer cells surviving hypoxia obtain hypoxia resistance and maintain anti-apoptotic potential under reoxygenation.

In solid tumors hypoxia and reoxygenation may be important factors in secondary expansion after anti-cancer therapy. Our study examined the effect of hypoxia and reoxygenation on the apoptotic potential of cancer cells. Four experimental groups were studied using a human colorectal cancer cell line (HCT116) that is apoptosis-competent in conventional culture: (1) sham, cells grown under conventional conditions; (2) hypoxic, cells cultured in 95% N2 and 5% CO2 for 24 hr; (3) continued hypoxic, cells cultured for 48 hr; and (4) reoxygenation, cells grown in hypoxic conditions for 24 hr followed by another 24 hr under conventional conditions. Protein expression of p53, bcl-2 and PCNA were determined by immunohistochemistry and immunoblotting (p53), and viable cell growth rate was determined. Hypoxia for 24 hr induced significant up-regulation of p53 and bcl-2 expression, accompanied by significant decreases of cell growth rate and PCNA expression. Up-regulation of p53 and bcl-2 expression persisted with both continued hypoxia and reoxygenation, despite increased cell growth rate and PCNA expression. Cells escaping hypoxia acquired sustained resistance to apoptosis and proliferate despite an elevated p53 level, suggesting that p53 transfer to hypoxic solid tumor should be reevaluated as a cancer gene therapy approach.

Apoptosis↗

PubMed2001

Regulation of an endogenous locus using a panel of designed zinc finger proteins targeted to accessible chromatin regions. Activation of vascular endothelial growth factor A.

We have mapped conserved regions of enhanced DNase I accessibility within the endogenous chromosomal locus of vascular endothelial growth factor A (VEGF-A). Synthetic zinc finger protein (ZFP) transcription factors were designed to target DNA sequences contained within the DNase I-hypersensitive regions. These ZFPs, when fused to either VP16 or p65 transcriptional activation domains, were able to activate expression of the VEGF-A gene as assayed by mRNA accumulation and VEGF-A protein secretion through a range exceeding that induced by hypoxic stress. Importantly, multiple splice variants of VEGF-A mRNA with defined physiological functions were induced by a single engineered ZFP transcription factor. We present evidence for an enhanced activation of VEGF-A gene transcription by ZFP transcription factors fused to VP16 and p65 targeted to two distinct chromosomal sites >500 base pairs upstream or downstream of the transcription start site. Our strategy provides a novel approach for dissecting the requirements for gene regulation at a distance without altering the DNA sequence of the endogenous target locus.

Cell Line, Transformed↗

PubMed2001

Establishment and characterization of an immortalized human oviductal cell line.

Human oviductal cells stimulate embryo development in vitro partly by the production of embryotrophic glycoproteins. The identity of these glycoproteins is not yet known mainly because oviductal samples are limited and that the cultured parental oviductal cells cannot produce sufficient amount of embryotrophic factors for characterization. In this study, human oviductal epithelial cells (OE) were immortalized by HPV 16 E6/E7 open reading frame (ORF) by retroviral expression. The characteristics of this immortalized cell line (OE-E6/E7) were compared to the parental OE. HPV 16 E6/E7 DNA was found only in OE-E6/E7 but not in OE. Human oviduct-specific glycoprotein, estrogen receptors, and cytokeratin were found in both cell types. Both OE and OE-E6/E7 possessed telomerase activities but the former had much lower activity. OE-E6/E7 also produced glycoproteins with chromatographic behavior similar to the embryotrophic glycoproteins derived from OE. These results showed that OE-E6/E7 retained a number of characteristics of OE. The development of preimplantation mouse embryo was significantly better after coculture with OE-E6/E7 when compared to medium alone culture in term of blastulation rates (52% vs. 32%) and blastocyst diameter (113.0 +/- 2.07 microm vs. 83.9 +/- 5.23 microm). This immortalized cell line can be used as a continuous and stable in vitro system for the study of the oviductal embryotrophic activity. Mol. Reprod. Dev. 59: 400-409, 2001.

Animals↗

PubMed2001

Image display for collision avoidance of radiation therapy: treatment planning.

Patient treatment in a medical linear accelerator is characterized by many angular and translational movements of the gantry and couch. The direction and orientation of each treatment beam is specified by a set of gantry, turntable, and collimator angles. It is possible that some selected treatment field configurations will result in gantry/couch or gantry/patient collisions that remain undetected during the treatment planning process. In this work, a digital camera has been used to record all the workable gantry/ patient set-up images, and a Windows programming language is used to edit and display these images on a personal computer for the treatment planner to screen the treatment plans. These graphical displays enable the planner to be aware of any potential collision hazards by an actual visualization of each selected gantry/turntable or gantry/patient angle configuration.

Accident Prevention↗

PubMed2001

Development and deployment of a web-based physician order entry system.

The computer-based Physician Order Entry System (POES) has been employed in many clinical institutes in Taiwan. Most of the POES systems are developed in the two-tier client-server architecture, and a large portion of the systems are constructed on a mainframe or even a single PC. The exponential growth of the Internet has had a tremendous impact on our society in recent years. In consideration of the future user interface and system architecture, we have developed a three-tier web-based Physician Order Entry System and successfully deployed it in the Wang-Fang Hospital in Taipei. The system is the first POES based on three-tier and World Wide Web (WWW) in Taiwan. The system provides the Subjective, Objective, Assessment, and Plan (SOAP) structure for the physician to enter subject, object, diagnoses, medicine dosage, treatment and laboratory test request, and prints out the prescription and necessary document. The doctor can also retrieve the patient's medical record on the system. One of the special characteristics of the system is its personalized design. The doctor can define their own diagnosis, medicine and treatment database and any combination of these to facilitate their clinical work. The system has been reviewed since February 1999. The result shows that the clinical procedure has become more efficient, and the chances of omission have been reduced. The system is very stable and the Open Database Connectivity (ODBC) database access did not show any delay in the network. Since we have incorporated many new web-programming techniques, the progress of the techniques will improve the system performance in the future.

Computer Systems↗