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Biomedical subjects

W Y Hu

Publications and source records attributed to W Y Hu.

At least 19 recordsLinked to original sources
PubMed2001

Determination of 2-amino-1-methyl-6-phenylimidazo[4,5- b]pyridine (PhIP) and its metabolite 2-hydroxyamino-PhIP by liquid chromatography/electrospray ionization-ion trap mass spectrometry.

2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is the most abundant heterocyclic aromatic amine found in cooked meat. It is metabolically activated by the human cytochrome P450 enzymes to form the carcinogenic metabolite N2-OH-PhIP. PhIP has been found to induce tumors in rats and is a suspected human carcinogen. In the present work, we have developed and validated a liquid chromatography-electrospray ionization/ion trap mass spectrometry (LC-ESI/ITMS) method for the determination of PhIP and N2-OH-PhIP. PhIP was incubated with microsomes prepared from the human liver; the PhIP and N2-OH-PhIP formed were isolated from the biomatrices by solid-phase extraction using C18 cartridges, with recoveries greater than 86%. Subsequently, the products were separated on a microbore reversed-phase C18 liquid chromatograph coupled to an ESI-ITMS. The ESI interface and the ITMS were tuned for various parameters, and data acquisition was performed in selective ion monitoring mode. The detection limit of PhIP and N2-OH-PhIP was 1 and 10 pg, respectively. The method is highly sensitive and selective, has simple sample preparation protocols, and should be applicable to the study of the metabolic activation of PhIP in various human tissues.

Chromatography, Liquid↗
PubMed2001

Anatomy of a preferred target site for the bacterial insertion sequence IS903.

Like many transposons the bacterial insertion sequence IS903 was thought to insert randomly. However, using both genetic and statistical approaches, we have derived a target site for IS903 that is used 84% of the time. Computational and genetic analyses of multiple IS903 insertion sites predicted a preferred target consisting of a 21 bp palindromic pattern centered on the 9 bp target duplication generated during transposition. Here we show that targeting can be dissected into four components: the 5 bp flanking sequences, the most important sequences required for site-specific insertion; the 7 bp palindromic core within the target duplication; the dinucleotide pair at the transposon-target junction; and the local DNA context. Finally, using a substrate with multiple target sites we show that a target site is more likely found by a local bind-and-slide model and not by extended DNA tracking.

Adenine↗
PubMed2001

Hammerhead ribozyme targeting human platelet-derived growth factor A-chain mRNA inhibited the proliferation of human vascular smooth muscle cells.

Platelet-derived growth factor (PDGF) A-chain contributes to the pathogenesis of cardiovascular proliferative diseases, such as hypertensive vascular disease, atherosclerosis, and re-stenosis of an artery after angioplasty. To develop a ribozyme against human PDGF A-chain mRNA as a gene therapy for human arterial proliferative diseases, we designed and synthesized a 38-base hammerhead ribozyme to cleave human PDGF A-chain mRNA at the GUC sequence at nucleotide 591. In the presence of MgCl(2), synthetic hammerhead ribozyme to human PDGF A-chain mRNA cleaved the synthetic target RNA to two RNA fragments at a predicted size. Doses of 0.01-1.0 microM hammerhead ribozyme to human PDGF A-chain mRNA significantly inhibited angiotensin II (Ang II) and transforming growth factor (TGF)-beta(1)-induced DNA synthesis in vascular smooth muscle cells (VSMC) from human in a dose-dependent manner. One micromolor of hammerhead ribozyme to human PDGF A-chain mRNA significantly inhibited Ang II-induced PDGF A-chain mRNA and PDGF-AA protein expressions in VSMC from humans. These results indicate that the designed hammerhead ribozyme to human PDGF A-chain mRNA effectively inhibited growth of human VSMC by cleaving the PDGF A-chain mRNA and inhibiting the PDGF-AA protein expression in human VSMC. This suggests that the designed hammerhead ribozyme to PDGF A-chain mRNA is a feasible gene therapy for treating arterial proliferative diseases.

Arterial Occlusive Diseases↗
PubMed2001

Sedation for refractory symptoms of terminal cancer patients in Taiwan.

This study assessed sedation in terminal cancer patients in terms of three characteristics: frequency; relationship to intractable symptoms; and the extent to which medical staff, family, and patients found sedation to be ethically acceptable and efficacious. Two hundred seventy-six consecutive patients, who were admitted to the palliative care unit of National Taiwan University Hospital in Taiwan between August 1998 and the end of May 1999, were enrolled. A recording form was completed every day. This included demographic data, pain and common symptom scores, and the use of sedation in the terminal phase. Seventy (27.9%) of 251 patients who died received sedation. Sedation was administered to relieve agitated delirium in 40 (57.1%), dyspnea in 16 (22.8%), severe pain in 7 (10%) and insomnia in 5 (7.2%). The drugs used for sedation were haloperidol in 35 (50%), midazolam in 17 (24.3%), and rapidly increasing dosage of morphine in 9 (12.9%). In fewer than half (42.9%) of the patients, sedation was with the consent of both patient and family, and half (50%) had the consent of family alone. The overwhelming majority of medical staff and family felt the decision to use terminal sedation was ethically acceptable. There was no significant difference in survival time between sedated and non-sedated patients (28.49 vs. 24.71 days, t = -0.791, P = 0.430). Positive ethical acceptability and higher satisfaction with symptom control with terminal sedation were found in both medical staff and family in this study. Further work is needed to find the most appropriate time of intervention and to improve management of refractory symptoms in dying patients.

Adolescent↗
PubMed2001

Inhibition of vascular smooth muscle cell proliferation by DNA-RNA chimeric hammerhead ribozyme targeting to rat platelet-derived growth factor A-chain mRNA.

BACKGROUND: Spontaneously hypertensive rats (SHR)-derived vascular smooth muscle cells (VSMC) show exaggerated growth and increasingly express platelet-derived growth factor (PDGF) A-chain mRNA compared to VSMC from normotensive Wistar-Kyoto (WKY) rats. OBJECTIVE: To investigate the effects of designed DNA-RNA chimeric hammerhead ribozyme to rat PDGF A-chain on exaggerated growth of VSMC from SHR. DESIGN AND METHODS: We designed and synthesized a 38-base DNA-RNA chimeric hammerhead ribozyme with two phosphorothioate linkages at the 3' terminal to cleave rat PDGF A-chain mRNA at the GUC sequence at nucleotide 921. We confirmed the cleavage activity of designed ribozyme by in vitro cleavage reaction and by lipofectin-mediated transfection of ribozyme into VSMC. RESULTS: Doses of 0.1 and 1 micromol/l DNA-RNA chimeric ribozyme dose-dependently inhibited basal DNA synthesis in VSMC from SHR. A dose of 1 micromol/l DNA-RNA chimeric ribozyme time-dependently inhibited basal DNA synthesis in VSMC from SHR. However, the same doses of all-RNA ribozyme had no effects on DNA synthesis in VSMC from SHR. Fluorescein isothiocyanate-labeled DNA-RNA chimeric ribozyme was recognized in cytosol at 30 min, and in nucleus at 60 min after lipofectin transfection. A dose of 1 micromol/l DNA-RNA chimeric ribozyme significantly inhibited expressions of both PDGF A-chain mRNA and PDGF-AA protein in VSMC from SHR, but not from WKY rats. CONCLUSION: These results indicated that the designed DNA-RNA chimeric ribozyme to PDGF A-chain mRNA effectively and specifically inhibited the exaggerated growth of VSMC from SHR at low concentrations, which were mediated by the reduction of PDGF A-chain mRNA and PDGF-AA protein expressions.

Animals↗
PubMed2001

Endogenous angiotensin II suppresses insulin signaling in vascular smooth muscle cells from spontaneously hypertensive rats.

BACKGROUND: Angiotensin II (Ang II) has been reported to inhibit insulin signaling at multiple levels in vascular smooth muscle cells (VSMC) in vitro. We have demonstrated that VSMC from spontaneously hypertensive rats (SHR) produce Ang II in a homogeneous culture. OBJECTIVE: In the current study, we investigated influences of endogenous Ang II on insulin signaling in VSMC from SHR. DESIGN AND METHODS: Phosphatidylinositol 3-kinase (PI3-kinase) activity, insulin receptor substrate-1 (IRS-1) associated tyrosine phosphorylation, and p85 subunit of PI3-kinase were measured in VSMC from SHR and normotensive Wistar-Kyoto (WKY) rats in the absence and presence of Ang II type 1 receptor antagonist RNH6270 and mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) inhibitor U0126. RESULTS: Insulin treatment increased PI3-kinase activity in VSMC from WKY rats in a dose-dependent manner. In contrast, insulin treatment of VSMC from SHR did not affect PI3-kinase activity. However, co-treatment of VSMC from SHR with RNH6270 and insulin, increased PI3-kinase activity. PI3-kinase activity, IRS-1-associated tyrosine phosphorylation and p85 subunit of PI3-kinase in VSMC from WKY rats decreased in response to treatment with Ang II and returned to control levels upon co-treatment with U0126. Basal levels of PI3-kinase activity, IRS-1-associated tyrosine phosphorylation, and p85 subunit of PI3-kinase were significantly lower in VSMC from SHR than in cells from WKY rats. U0126 treatment of VSMC from SHR significantly increased levels of PI3-kinase activity, IRS-1-associated tyrosine phosphorylation, and p85 subunit of PI3-kinase. CONCLUSION: These results indicate that endogenous Ang II suppresses insulin signaling in VSMC from SHR by activating extracellular signal-regulated kinase. These findings suggest that tissue Ang II may play a role in insulin resistance in hypertension.

Angiotensin II↗
PubMed2001

Role of endogenous angiotensin II in the increased expression of growth factors in vascular smooth muscle cells from spontaneously hypertensive rats.

In culture, vascular smooth muscle cells (VSMC) derived from spontaneously hypertensive rats (SHR) show exaggerated growth compared with cells from normotensive Wistar-Kyoto (WKY) rats. SHR-derived VSMC express higher levels of transforming growth factor (TGF)-beta1, platelet-derived growth factor (PDGF) A-chain, and basic fibroblast growth factor (bFGF) mRNAs than cells from WKY rats. We have recently observed production of angiotensin II (Ang II) in homogeneous cultures of VSMC from SHR. In the current study we investigated the contribution of endogenous Ang II to increased expression of the above-mentioned growth factors in VSMC from SHR. The levels of mRNAs encoding TGF-beta1, PDGF A-chain, and bFGF were determined by reverse transcription-polymerase chain reaction and were much higher in VSMC from SHR than in cells from WKY rats. The basal level of Ang II-like immunoreactivity (LI) in conditioned medium as determined by radioimmunoassay was significantly higher in VSMC from SHR than in cells from WKY rats. Isoproterenol is known to induce angiotensinogen gene significantly increased Ang II-LI in VSMC from both WKY rats and SHR. Isoproterenol also increased angiotensinogen, TGF-beta1, PDGF A-chain, and bFGF mRNAs in VSMC from SHR. An angiotensin-converting enzyme inhibitor delapril significantly decreased Ang II-LI in VSMC from WKY rats and SHR. Delapril considerably decreased the levels of TGF-beta1, PDGF A-chain, and bFGF mRNAs in VSMC from SHR. An Ang II type 1 receptor antagonist CV 11974 decreased the levels of TGF-beta1, PDGF A-chain, and bFGF mRNAs, and the levels of TGF-beta1, PDGF-AA, and bFGF proteins in VSMC from SHR. These findings suggest that increased generation of Ang II is associated with enhanced expression of TGF-beta1, PDGF A-chain, and bFGF, and the increases in the levels of these growth factors by endogenous Ang II may contribute to the exaggerated growth of VSMC from SHR.

Adrenergic beta-Agonists↗
PubMed2001

Effects of the L- and N-type calcium channel blocker cilnidipine on growth of vascular smooth muscle cells from spontaneously hypertensive rats.

Cultured vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) show exaggerated growth compared with cells from Wistar-Kyoto (WKY) rats. Calcium antagonists have recently been reported to have an in vivo antiproliferative effect on hypertensive cardiovascular organs. We investigated the effects of the calcium antagonist cilnidipine that blocks both L- and N-type calcium channels on the growth of VSMC from SHR. Cilnidipine (1 and 10 microM) significantly inhibited basal DNA synthesis in VSMC from both rat strains; the inhibition was significantly larger in VSMC from SHR than in cells from WKY rats, and was significantly greater than effects of nifedipine. Cilnidipine (1 microM) significantly inhibited serum-stimulated DNA synthesis in VSMC from both rat strains. The inhibition was more marked in VSMC from SHR than in cells from WKY rats. Angiotensin II, platelet-derived growth factor (PDGF)-AA, and phorbol-12-myristate-13-acetate dose-dependently increased DNA synthesis in VSMC from SHR but not in cells from WKY rats. Cilnidipine (1 microM) significantly suppressed this increase in DNA synthesis in VSMC from SHR. Expression of basic fibroblast growth factor (bFGF), transforming growth factor-beta1, and PDGF A-chain mRNAs was markedly greater in VSMC from SHR than in cells from WKY rats. Cilnidipine (1 microM) significantly inhibited the expression of TGF-beta1 mRNA in VSMC from SHR but not in cells from WKY rats. These findings suggest that cilnidipine exerts its antiproliferative effects through the inhibition of DNA synthesis induced by growth-promoting factors and by inhibiting the expression of TGF-beta1 mRNA in VSMC from SHR.

Animals↗
PubMed2001

Use of the Alberta Stroke Program Early CT Score (ASPECTS) for assessing CT scans in patients with acute stroke.

BACKGROUND AND PURPOSE: Clinicians are insecure reading CT scans by using the one-third rule for acute middle cerebral artery stroke (1/3 MCA rule) before treating patients with recombinant tissue plasminogen activator. The 1/3 MCA rule is a poorly defined volumetric estimate of the size of cerebral infarction of the MCA. A 10-point quantitative topographic CT scan score, the Alberta Stroke Program Early CT Score (ASPECTS), is described and illustrated. A sharp increase in dependence and death occurs with an ASPECTS of 7 or less. We describe how to use ASPECTS and why it works with CT scans obtained on all commonly used axial baselines. We also describe interobserver reliability among clinicians from different specialties and with different experience in reading CT scans in the context of acute stroke. METHODS: The six physicians who developed ASPECTS answered a questionnaire on precisely how they interpret and use ASPECTS. The ASPECTS areas as interpreted by these physicians were compared with one another and with standards in the literature. kappa statistics were used to assess the interobserver reliability of ASPECTS versus the 1/3 MCA rule. RESULTS: The exact methods of interpretation varied among the six individual observers, with either a 3:3 or 4:2 split on the specific questions. The overall interobserver agreement was good compared with that of the 1/3 MCA rule. Normal anatomic vascular and interobserver variations explain why ASPECTS can be applied with different CT axial baselines. CONCLUSION: ASPECTS is a systematic, robust, and practical method that can be applied to different axial baselines. Clinician agreement is superior to that of the 1/3 MCA rule.

Aged↗
PubMed2000

Ribozyme to human TGF-beta1 mRNA inhibits the proliferation of human vascular smooth muscle cells.

Transforming growth factor-beta (TGF-beta) has been reported to be involved in the pathogenesis of cardiovascular proliferative diseases such as hypertensive vascular disease, atherosclerosis, and arterial restenosis after angioplasty. We designed a 38-base DNA-RNA chimeric hammerhead ribozyme to cleave human TGF-beta1 mRNA as a gene therapy for human arterial proliferative diseases. In the presence of MgCl(2), synthetic ribozyme to human TGF-beta1 mRNA cleaved the synthetic target RNA into two RNA fragments of predicted size. A control mismatch ribozyme, with one different base in the catalytic loop region, was inactive. DNA-RNA chimeric ribozyme (0. 01-1.0 microM) significantly inhibited angiotensin II (Ang II)-stimulated DNA synthesis in a dose-dependent manner in human vascular smooth muscle cells (VSMC). The mismatch ribozyme did not affect Ang II-stimulated DNA synthesis in the cells. DNA-RNA chimeric ribozyme (1.0 microM) inhibited the proliferation of human VSMC in the presence of Ang II. DNA-RNA chimeric ribozyme (1.0 microM) significantly inhibited Ang II-stimulated TGF-beta1 mRNA and protein expression in human VSMC. These results indicate that the designed DNA-RNA chimeric hammerhead ribozyme targeted to human TGF-beta1 mRNA can effectively and potentially inhibit growth of human VSMC by cleaving the TGF-beta1 mRNA. This finding suggests that this ribozyme will be useful in the gene therapy of arterial proliferative diseases.

Base Sequence↗
PubMed2000

Effect of methylene methylimino linkage of antisense oligonucleotide to the platelet-derived growth factor A-chain on growth of vascular smooth muscle cells from spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR)-derived vascular smooth muscle cells show exaggerated growth and increased expression of platelet-derived growth factor (PDGF) A-chain mRNA. We examined the effect of methylene methylimino linkage of antisense oligodeoxynucleotide, a novel modification of antisense oligodeoxynucleotide designed to increase nuclease resistance, to PDGF A-chain on the exaggerated growth of vascular smooth muscle cells from SHR. Methylene methylimino-linked oligodeoxynucleotide provided complete resistance against S1 nuclease. Methylene methylimino linkage of antisense oligodeoxynucleotide to PDGF A-chain resulted in a rapid inhibition of basal DNA synthesis of vascular smooth muscle cells from SHR. This inhibition was much greater than that produced by phosphorothioate linkage of antisense oligodeoxynucleotide to PDGF A-chain. The methylene methylimino linkage of antisense oligodeoxynucleotide to PDGF A-chain may prove useful in the treatment of arterial proliferative diseases including hypertension.

Alkenes↗
PubMed2000

Instrumental and bioanalytical measures of persistent organochlorines in blue mussel (Mytilus edulis) from Korean coastal waters.

Blue mussels (Mytilus edulis) collected from 34 locations along the south and east coast of Korea were analyzed for polychlorinated biphenyls (PCBs) and organochlorine (OC) pesticides. Maximum concentrations of PCBs and total OC pesticides were 98.5 and 20.5 ng/g, wet weight, respectively. Extracts were fractionated by Florisil chromatography and each fraction was screened for dioxin-like activity in vitro, using recombinant rat hepatoma cells (H4IIE-luc). Fraction 2 (F-2), which contained hexachlorocyclohexanes, chlordanes, p,p'-DDD, and p,p'-DDT, generally elicited significant dioxin-like activity compared to control, whereas Fraction 1 (F-1), which contained PCBs, p,p'-DDE, and hexachlorobenzene, did not. The greatest magnitude of dioxin-like response observed was 44% of the maximum response elicited by a 2,000 pM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) standard. The relatively low magnitudes of dioxin-like response observed for F-1 samples were consistent with the relatively low PCB concentrations. At concentrations equal to the maximum observed in the mussel samples, neither individual OC pesticides nor a mixture of OC pesticides yielded a significant dioxin-like response in the H4IIE-luc assay. Thus, the concentrations of OC pesticides in F-2 did not appear to have accounted for the dioxin-like activity observed. This suggests the presence of unidentified and/or unknown, acid-stable, dioxin-like compounds in F-2. This study suggests that in vitro bioassays are useful in assessing the contamination of mussels collected from coastal marine locations.

Animals↗
PubMed2000

Prevalence and severity of symptoms in terminal cancer patients: a study in Taiwan.

This paper reports a prospective study conducted between September 1997 and July 1998 in 232 consecutive patients with terminal cancer. A structured data collection form was used daily to evaluate symptoms, which were analyzed at the time of admission, 1 week after admission and 48 h before death. Terminal cancer patients in this study were polysymptomatic. There were no statistically significant differences in the prevalence of most symptoms with the primary site of cancer. The majority of symptoms improved at the end of the 1st week after admission, but many symptoms worsened just before death. The high prevalence of symptoms and lack of significant difference among primary tumor sites may be related to shorter survival times caused by late referral, which is common in Taiwan.

Aged↗
PubMed2000

DNA-RNA chimeric hammerhead ribozyme to transforming growth factor-beta(1) mRNA inhibits the exaggerated growth of vascular smooth muscle cells from spontaneously hypertensive rats.

OBJECTIVE: The purpose of this study was to develop DNA-RNA chimeric hammerhead ribozyme against transforming growth factor-beta(1) (TGF-beta(1)) mRNA as a gene therapy agent for arterial proliferative diseases. METHODS: A 38-base hammerhead ribozyme against rat TGF-beta(1) mRNA, to produce cleavage at the GUC sequence at nucleotide 825 according to the secondary structure of rat TGF-beta(1) mRNA was designed. To enhance its stability, we synthesized a DNA-RNA chimeric ribozyme with two phosphorothioate linkages at the 3'-terminal. We also synthesized a mismatch ribozyme with single base change in the catalytic loop region as a control. These ribozymes were delivered into rat vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats by lipofectin-mediated transfection, and their biological effects were investigated. RESULTS: According to in vitro cleavage studies, the synthetic ribozyme can cleave the synthetic substrate RNA into two RNA fragments. Chimeric ribozyme significantly inhibited DNA synthesis in VSMC from SHR but not in cells from WKY rats. Mismatch ribozyme showed only a little effect on growth of VSMC from SHR. Chimeric ribozyme significantly inhibited proliferation of VSMC from SHR; in contrast, the proliferation of VSMC from WKY rats was significantly increased by this chimeric ribozyme. Mismatch ribozyme did not affect proliferation of VSMC from either rat strain. Chimeric hammerhead ribozyme to rat TGF-beta(1) dose-dependently inhibited TGF-beta(1) mRNA expression detected by reverse transcription and polymerase chain reaction analysis in VSMC from both rat strains. Chimeric hammerhead ribozyme to rat TGF-beta(1) also dose-dependently inhibited TGF-beta(1) protein production detected by Western blot analysis. CONCLUSIONS: The present results demonstrated that our designed DNA-RNA chimeric hammerhead ribozyme to TGF-beta(1) mRNA might be a useful gene therapy agent for hypertensive vascular diseases.

Analysis of Variance↗
PubMed2000

Angiotensin II upregulates transforming growth factor-beta type I receptor on rat vascular smooth muscle cells.

Angiotensin II (Ang II) and transforming growth factor-beta (TGF-beta) modulate cell growth and metabolism. Our objective was to evaluate the effect of Ang II on the characteristics and expression of TGF-beta receptors on vascular smooth muscle cells (VSMC) from Wistar-Kyoto rats. The addition of TGF-beta1 elicited a biphasic response on DNA synthesis in cultured VSMC in the absence of Ang II, but TGF-beta1 did not stimulate DNA synthesis in the presence of Ang II. TGF-beta binding data showed that Ang II increased the specific binding of 125I-TGF-beta1 by enhancing the expression of lower affinity receptors and increasing the number of binding sites. Ang II alone did not stimulate DNA synthesis in these cultures. However, Ang II significantly stimulated DNA synthesis after the inhibition of endogenous TGF-beta with a neutralizing antibody. The DNA synthesis stimulated by phorbol ester milisterol (PMA) was not affected by the TGF-beta neutralizing antibody. Affinity labeling data revealed receptor-ligand complexes of 280, 85, and 70 kDa, corresponding to TGF-beta type III, II, and I receptors, respectively. Incubation of VSMC with Ang II but not with PMA markedly increased the expression of the TGF-beta type I receptor. Reverse transcription and polymerase chain reaction data also indicated that Ang II, but not PMA, significantly increased the expression of TGF-beta type I receptor mRNA. Results suggest that Ang II increases the binding of TGF-beta with upregulation of TGF-beta type I receptor via a C-kinase-independent pathway. The enhanced expression of the TGF-beta type I receptor may counteract Ang II-promoted growth of VSMC.

Activin Receptors, Type I↗
PubMed2000

Polyoxygenated bipyridine, pyrrolylpyridine, and bipyrrole alkaloids from Speranskia tuberculata.

Five novel polyoxygenated alkaloids, speranculatines A-C (3-5), speranskilatine A (6), and speranberculatine A (7), have been isolated from Speranskia tuberculata. Compounds 3-5, 6, and 7, have bipyridine, pyrrolylpyridine, and bipyrrole skeletons, respectively. This is the first time that these three alkaloid structural types have been reported. The structures of 3-7 were elucidated by spectroscopic methods, including 2D NMR techniques and X-ray crystallographic analysis.

Alkaloids↗
PubMed2000

Ethical dilemmas in palliative care: a study in Taiwan.

OBJECTIVES: To investigate the incidence and solution of ethical dilemmas in a palliative care unit. DESIGN: Health care workers recorded daily all dilemmas in caring for each patient. SETTING: Palliative care unit of National Taiwan University Hospital in Taiwan. PATIENTS: Two hundred and forty-six consecutive patients with terminal cancer during 1997-8. MAIN MEASUREMENT: Ethical dilemmas in the questionnaire were categorised as follows: telling the truth; place of care; therapeutic strategy; hydration and nutrition; blood transfusion; alternative treatment; terminal sedation; use of medication, and others. RESULTS: The type and frequency of ethical dilemmas encountered were: place of care (33.3%); truth-telling (32.1%); hydration and nutrition (25.2%); therapeutic strategy (24.8%), and use of medication (19.1%). Ethical problems relating to the place of care and to therapeutic strategy were unlikely to be solved with increased hospital stay and some ethical dilemmas remained unsolved even in the final week in hospital, including place of care (23.2%), truth-telling (17.1%) and therapeutic strategy (11.4%). Problems of truth-telling occurred in nearly half (42.6%) of patients over sixty-five-years-old. Conflicts about blood transfusion were experienced in all patients below 18-years-old, and the dilemmas concerning the place of care occurred most frequently with head and neck cancer patients (43.8%). CONCLUSIONS: The solution of ethical dilemmas required refocusing by medical professionals on the importance of continuing communication. Improved ethical training for professionals would contribute to solving the moral dilemmas of palliative care.

Aged↗