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Biomedical subjects

C H Yeh

Publications and source records attributed to C H Yeh.

At least 37 records · Page 2Linked to original sources
PubMed1999

Determinants of parental decisions on 'drop out' from cancer treatment for childhood cancer patients.

Little is known about the psychosocial process of parental decisions on 'drop out' from cancer treatment for paediatric patients in Taiwan. This study, based on structured in-depth interviews, attempted to document the determinants of parental decisions on drop out. A total of 19 parents of paediatric cancer patients who dropped out from a cancer treatment for at least a month within 3 years since first treatment were interviewed. Content analysis of qualitative data revealed six categories of determinants associated with parental decisions: suffering severe pain from medical treatments and adverse side-effects; desire for better and less painful treatments; adverse effect of other patients' experiences; searching for possible explanations for disease after prolonged denial of diagnosis; lack of empathy from health care professionals; and misinterpretation of improved prognostics. These findings reflected the deficiency of psychological and emotional support for parents from health care professionals prior to and during cancer treatment.

Adult↗
PubMed1999

Role of the outward delayed rectifier K+ current in ceramide-induced caspase activation and apoptosis in cultured cortical neurons.

We studied the novel hypothesis that an up-modulation of channels for outward delayed rectifier K+ current (I(K)) plays a key role in ceramide-induced neuronal apoptosis. Exposure for 6-10 h to the membrane-permeable C2-ceramide (25 microM) or to sphingomyelinase (0.2 unit/ml), but not to the inactive ceramide analogue C2-dihydroceramide (25 microM), enhanced the whole-cell I(K) current without affecting the transient A-type K+ current and increased caspase activity, followed by neuronal apoptosis 24 h after exposure onset. Tetraethylammonium (TEA) or 4-chloro-N,N-diethyl-N-heptylbenzenebutanaminium tosylate (clofilium), at concentrations inhibiting I(K), attenuated the C2-ceramide-induced caspase-3-like activation as well as neuronal apoptosis. Raising extracellular K+ to 25 mM similarly blocked the C2-ceramide-induced cell death; the neuroprotection by 25 mM K+ or TEA was not eliminated by blocking voltage-gated Ca2+ channels. An inhibitor of tyrosine kinases, herbimycin A (10 nM) or lavendustin A (0.1-1 microM), suppressed I(K) enhancement and/or apoptosis induced by C2-ceramide. It is suggested that ceramide-induced I(K) current enhancement is mediated by tyrosine phosphorylation and plays a critical role in neuronal apoptosis.

Animals↗
PubMed1999

Surgical treatment of bronchiectasis: 10 years' experience.

BACKGROUND: Since antibiotic therapy and vaccination have been widely used in medical practice, the incidence of bronchiectasis has decreased steadily. The principal role of surgery associated with this disease is for the treatment of complications. We present an analysis of surgical results during a 10-year period. METHODS: The medical records of bronchiectasis patients who were surgically treated were retrospectively reviewed from July, 1987, to March, 1998. The surgical indications, complications and recurrences of bronchiectasis were evaluated. RESULTS: A total of 41 bronchiectasis patients underwent surgical treatment from 1987 to 1998 at our hospital. There were 18 males (mean age, 37.8 +/- 15.3 years; range, 16-73 years), and 23 females (mean age, 33 +/- 7.1 years; range, 21-46 years). The indications for surgery were hemoptysis in 30, failed medical treatment in eight, suspected neoplasm in two and retention of a foreign body in one patient. Anatomic resections of the diseased sites were carried out more frequently on the left lower lobes of the lungs. In total, there were 20 left lower lobes, five right lower lobes, 10 left lingular lobes, five right middle lobes, four left upper lobes and one right upper lobe that required surgery. Surgical complications included hemorrhage in one patient, bronchopleural fistula in one and galactorrhea in one patient. The follow-up intervals were from two to 131 months (mean, 72.5 +/- 37.6 months; median, 74 months). There were two cases of recurrent symptoms and six cases of recurrent hemoptysis; all were easily controlled by medication. There were no mortalities. CONCLUSIONS: Surgical treatment of bronchiectasis yields immediate resolution of symptoms, better quality of life and no mortalities. Cessation of smoking, avoiding air pollution and careful medical follow-up are mandatory.

Adolescent↗
PubMed1998

A new short chain RGD-containing disintegrin, accutin, inhibits the common pathway of human platelet aggregation.

A new short-chain disintegrin, accutin, was purified from the Formosan Agkistrodon acutus venom by using of gel filtration, ion exchanger and reverse phase HPLC. The homogeneous protein is a 47-residue polypeptide with a molecular mass of 5241 Da containing an Arg-Gly-Asp sequence and seven cysteinyl residues at positions highly homologous to other disintegrins. Accutin dose-dependently inhibited human platelet aggregation stimulated by ADP, collagen, thrombin or the thromboxane analogue U46619 in platelet suspension with IC50 values of 66-267 nM. It was also active in inhibiting platelet aggregation of platelet-rich plasma. However, accutin apparently did not affect the shape change caused by these agonists. Accutin also inhibited fibrinogen-induced aggregation of human elastase-treated platelets in a dose-dependent manner. Furthermore, accutin dose-dependently inhibited the binding reaction of fluorescein isothiocyanate (FITC)-conjugated arietin, a member of the disintegrin family, to human platelets. In addition, the binding of FITC-conjugated accutin to platelets was almost completely blocked by a monoclonal antibody, 7E3, raised against the platelet glycoprotein IIb/IIIa complex. On the other hand, accutin as well as other disintegrins, rhodostomin and arietin, exhibited an inhibitory effect on 7E3 binding toward platelets and endothelial cells in a dose-dependent manner. It is concluded that accutin, a new platelet aggregation inhibitor belonging to the short-chain disintegrin family, acts specifically on a binding epitope of GPIIb/IIIa overlapping with that of 7E3, leading to the blockade of fibrinogen binding to its receptor.

Amino Acid Sequence↗
PubMed1998

Accutin, a new disintegrin, inhibits angiogenesis in vitro and in vivo by acting as integrin alphavbeta3 antagonist and inducing apoptosis.

Endothelial integrins play an essential role in angiogenesis and cell survival. Accutin, a new member of disintegrin family derived from venom of Agkistrodon acutus, potently inhibited human platelet aggregation caused by various agonists (eg, thrombin, collagen, and, adenosine diphosphate [ADP]) through the blockade of fibrinogen binding to platelet glycoprotein IIb/IIIa (ie, integrin alphaIIbbeta3). In this report, we describe that accutin specifically inhibited the binding of monoclonal antibody (MoAb) 7E3, which recognizes integrin alphavbeta3, to human umbilical vein endothelial cells (HUVECs), but not those of other anti-integrin MoAbs such as alpha2beta1, alpha3beta1, and alpha5beta1. Moreover, accutin, but not the control peptide GRGES, dose-dependently inhibited the 7E3 interaction with HUVECs. Both 7E3 and GRGDS, but not GRGES or Integrelin, significantly blocked fluorescein isothiocyanate-conjugated accutin binding to HUVEC. In functional studies, accutin exhibited inhibitory effects on HUVEC adhesion to immobilized fibrinogen, fibronectin and vitronectin, and the capillary-like tube formation on Matrigel in a dose- and RGD-dependent manner. In addition, it exhibited an effective antiangiogenic effect in vivo when assayed by using the 10-day-old embryo chick CAM model. Furthermore, it potently induced HUVEC apoptotic DNA fragmentation as examined by electrophoretic and flow cytometric assays. In conclusion, accutin inhibits angiogenesis in vivo and in vitro by blocking integrin alphavbeta3 of endothelial cells and by inducing apoptosis. The antiangiogenic activity of disintegrins might be explored as the target of developing the potential antimetastatic agents.

Abciximab↗
PubMed1998

Involvement of de novo ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced cerebral endothelial cell death.

Cytokines, including tumor necrosis factor-alpha (TNF-alpha), may elicit cytotoxic response through the sphingomyelin-ceramide signal transduction pathway by activation of sphingomyelinases and the subsequent release of ceramide: the universal lipid second messenger. Treatment of bovine cerebral endothelial cells (BCECs) with TNF-alpha for 16 h followed by cycloheximide (CHX) for 6 h resulted in an increase in ceramide accumulation, DNA fragmentation, and cell death. Application of a cell permeable ceramide analogue C2 ceramide, but not the biologically inactive C2 dihydroceramide, also induced DNA laddering and BCEC death in a concentration- and time-dependent manner. TNF-alpha/CHX-mediated ceramide production apparently is not a result of sphingomyelin hydrolysis because sphingomyelin content does not decrease in this death paradigm. In addition, an acidic sphingomyelinase inhibitor, desipramine, had no effect on TNF-alpha/CHX-induced cell death. However, addition of fumonisin B1, a selective ceramide synthase inhibitor, attenuated TNF-alpha/CHX-induced intracellular ceramide elevation and BCEC death. Together, these findings suggest that ceramide plays at least a partial role in this paradigm of BCEC death. Our results show, for the first time, that ceramide derived from de novo synthesis is an alternative mechanism to sphingomyelin hydrolysis in the BCEC death process initiated by TNF-alpha/CHX.

Animals↗
PubMed1998

Enhancement of outward potassium current may participate in beta-amyloid peptide-induced cortical neuronal death.

In light of recent evidence implicating the upregulation of outward K+ current in mediating several forms of neuronal apoptosis, we tested the hypothesis that such an upregulation might specifically contribute to the pathogenesis of beta-amyloid peptide (A beta)-induced neuronal death. Exposure to A beta fragment 25-35 (20 microM) or 1-42 (20 microM) enhanced the delayed rectifier K+ current IK, shifting its activation voltage relationship toward hyperpolarized levels and increasing maximal conductance, but did not affect the transient K+ current IA or charybdotoxin-sensitive BK current. Reducing IK by adding the channel blocker tetraethylammonium (TEA, 5 mM) or raising extracellular K+ to 25 mM attenuated A beta-induced neuronal death, even in the presence of nifedipine or gadolinium to block associated increases in Ca2+ influx. The IA blocker 4-aminopyridine (4-AP, 5 mM) and the CI- channel blocker anthracene-9-carboxylic acid (ACA, 500 microM) were not neuroprotective. These data raise the intriguing possibility that manipulations aimed at reducing outward K+ current may provide an approach to reducing neuronal degeneration in patients with Alzheimer's disease.

Amyloid beta-Peptides↗
PubMed1998

Computed tomography in the diagnosis of adult midgut rotational anomalies: a report of two cases.

Adult midgut rotational anomalies are difficult to diagnose. Any symptoms present in adults may be the result of intermittent volvulus of the midgut. Successful outcome of this clinical condition depends on prompt diagnosis and timely surgical intervention. Computed tomography (CT) is useful in early identification of these lesions in the abdomen. However, the specific CT signs, the "superior mesenteric vein rotation" sign and the "whirl" sign, are easy to overlook if not kept in mind, as occurred in one of our two patients. In the other patient, CT played the major role in preoperative diagnosis.

Adenocarcinoma↗
PubMed1998

Totally minimally invasive cardiac surgery for coronary artery disease.

OBJECTIVE: We report our experience using minimally invasive techniques both to perform coronary artery bypass and harvesting of saphenous vein grafts in 25 patients with left main or triple vessels disease. METHODS: From March 1997 to June 1997, 25 patients received elective coronary artery bypass grafting using minimally invasive surgical techniques for left main or triple vessels disease. Saphenous vein grafts were harvested using minimally invasive techniques under direct vision. The coronary artery bypass grafting was performed through a limited left anterior parasternal minithoracotomy under femoro-femoral or aorto-atrial cardiopulmonary bypass. The myocardium was protected by antegrade infusion of cold blood cardioplegic solution while the aorta was cross-clamped. RESULTS: Three to four distal anastomoses were performed with the saphenous vein graft and the left internal thoracic arterial graft. The aortic cross-clamp time was 60-135 min. The duration of cardiopulmonary bypass was 89-172 min. The postoperative course was uneventful for all patients. All patients were found to be in New York Heart Association functional class I or II on follow-up from 3-7 months after surgery. CONCLUSIONS: Minimally invasive coronary artery surgery is technically feasible and can be performed in left main or triple vessel disease safely and effectively for complete revascularization.

Cardiopulmonary Bypass↗
PubMed1998

Association between interleukin-8 concentration in nasal secretions and severity of symptoms of experimental rhinovirus colds.

The purpose of this study was to examine the association between experimental rhinovirus infection and the elaboration of interleukin-8 (IL-8) into nasal secretions of volunteers and to determine the effect of pentoxifylline on IL-8 elaboration and rhinovirus-associated common cold symptoms. Fifty-four subjects with experimental rhinovirus infections and 20 sham-inoculated subjects were studied. Pentoxifylline had no effect on rhinovirus-induced symptoms or nasal-secretion IL-8 concentrations. IL-8 concentrations were significantly greater in nasal secretions from infected symptomatic subjects than in those from infected asymptomatic or sham-challenged subjects on days 2-4 after virus challenge. In infected subjects, there was significant rank correlation between nasal obstruction severity, rhinorrhea severity, and nasal-wash albumin concentrations and the change in IL-8 concentration from baseline on days 2-4 after virus challenge.

Adolescent↗
PubMed1998

Effects of treatment of secondary hyperparathyroidism on the lipid profile in patients on hemodialysis.

Abnormalities in circulating lipoprotein concentrations are a characteristic finding in patients undergoing dialytic therapy. A substantial number of these patients display type IV hyperlipoproteinemia. Certain data suggest that secondary hyperparathyroidism may induce disturbances in lipid metabolism. To evaluate the effects of pulse calcitriol therapy on the lipid profile in these patients, we undertook a prospective study in 12 patients on stable bicarbonate hemodialysis. Lipid parameters comprising cholesterol and the low- as well as the high-density lipoprotein subfractions, triglycerides, apolipoproteins A and B, serum parathyroid hormones (iPTH), alkaline phosphatase, calcium, phosphorus, hematocrit, and blood urea were obtained prior to commencement of pulse calcitriol therapy and again 8-10 weeks later. Calcitriol therapy was associated with a decrease in serum iPTH levels (701 +/- 103.9 vs. 220.3 +/- 50.5 pmol/l; p < 0.001). Significant increases in high-density lipoprotein cholesterol (32.8 +/- 2.7 vs. 38.8 +/- 2.3 mmol/l; p < 0.05) and apolipoprotein A-I (107.8 +/- 6.1 vs. 121.8 +/- 5.8 g/l; p < 0.05) were noted during the course of the study. Moreover, serum iPTH correlated inversely with high-density lipoprotein cholesterol and apolipoprotein A-I. There were no changes in other lipid parameters except for low-density lipoprotein cholesterol which showed a tendency to increase. We conclude that in short-term study, pulse oral calcitriol therapy is associated with an improvement in the lipid profile in patients with secondary hyperparathyroidism. However, it remains to be established whether ameliorating the uremic dyslipidemia results in any long-term clinical benefits.

Administration, Oral↗
PubMed1997

Mediation of neuronal apoptosis by enhancement of outward potassium current.

Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (IK) current and loss of total intracellular K+. This IK augmentation was not seen in neurons undergoing excitotoxic necrosis or in older neurons resistant to staurosporine-induced apoptosis. Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented. Furthermore, exposure to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced apoptosis. Enhanced K+ efflux may mediate certain forms of neuronal apoptosis.

Amino Acid Chloromethyl Ketones↗
PubMed1997

Expression of a gene encoding a 16.9-kDa heat-shock protein, Oshsp16.9, in Escherichia coli enhances thermotolerance.

A gene encoding the rice 16.9-kDa class I low-molecular-mass (LMM) heat-shock protein (HSP), Oshsp16.9, was introduced into Escherichia coli using the pGEX-2T expression vector to analyze the possible function of this LMM HSP under heat stress. It is known that E. coli does not normally produce class I LMM HSPs. We compared the survivability of E. coli XL1-Blue cells transformed with a recombinant plasmid containing a glutathione S-transferase (GST)-Oshsp16.9 fusion protein (pGST-FL cells) with the control E. coli cells transformed with the pGEX-2T vector (pGST cells) under heat-shock (HS) after isopropyl beta-D-thiogalactopyranoside induction. The pGST-FL cells demonstrated thermotolerance at 47.5 degrees C, a treatment that was lethal to the pGST cells. When the cell lysates from these two E. coli transformants were heated at 55 degrees C, the amount of protein denatured in the pGST-FL cells was 50% less than that of the pGST cells. Similar results as pGST-FL cells were obtained in pGST-N78 cells (cells produced a fusion protein with only the N-terminal 78 aa in the Oshsp16.9 portion) but not in pGST-C108 cells (cells produced a fusion protein with C-terminal 108 aa in the Oshsp16.9 portion). The acquired thermotolerant pGST-FL cells synthesized three types of HSPs, including the 76-, 73-, and 64-kDa proteins according to their abundance at a lethal temperature of 47.5 degrees C. This finding indicates that a plant class I LMM HSP, when effectively expressed in transformed prokaryotic cells that do not normally synthesize this class of LMM HSPs, may directly or indirectly increase thermotolerance.

Cloning, Molecular↗
PubMed1997

Midodrine for the treatment of intradialytic hypotension.

Recurrent intradialytic hypotension is probably the most severely disabling feature in dialysis patients and the etiology is multifactorial. We assessed the efficacy and safety of midodrine, a selective alpha1-adrenergic pressor agent in 12 patients with recurrent intradialytic hypotension. Symptomatic intradialytic hypotension was defined as hypotensive symptoms occurring with a systolic blood pressure < 100 mm Hg or with 25% decrease in systolic blood pressure in those patients with a basal systolic blood pressure of 100 mm Hg. The patients who suffered from symptomatic intradialytic hypotension and failed to improve after cautious body weight adjustment were included into the study. The lowest intradialytic and postdialysis blood pressures were monitored for 18 consecutive dialysis sessions before and after midodrine treatment. Clinical signs and symptoms were also recorded during both periods. With midodrine, the mean (+/- SE) lowest systolic and diastolic blood pressure increased significantly from 68.7 +/- 3.1 and 42.8 +/- 2.0 mm Hg to 84.7 +/- 3.9 and 52.7 +/- 2.7 mm Hg respectively during the study (p < 0.01). Midodrine treatment also significantly increased postdialysis systolic and diastolic blood pressures from baseline values of 90.8 +/- 3.8 and 58.3 +/- 3.0 mm Hg to 113.3 +/- 7.1 and 70.6 +/- 3.1 mm Hg (p < 0.01 and p < 0.01 respectively). In addition, oral administration of midodrine also significantly decreased the total volume of intravenous fluid administered during symptomatic hypotension. The clinical signs and symptoms during dialysis were improved in all patients. There were no differences in hemoglobin, serum albumin, urea, creatinine, fasting blood sugar or volume removed per dialysis between both periods of the study. In conclusion, our study has demonstrated that midodrine is a safe and effective treatment for the prevention of recurrent intradialytic hypotension if routinely premedicated before each dialysis session.

Administration, Oral↗
PubMed1995

The Ser36-Ser37 pair in HeLa nuclear protein p21/SIIR mediates Ser/Thr phosphorylation and is essential for Rous sarcoma virus long terminal repeat repression.

Phosphorylation of HeLa SII (or TFIIS)-related nuclear protein p21/SIIR was demonstrated in transfected COS-1 cells. To test for a possible functional link between phosphorylation and the previously described Rous sarcoma virus (RSV) long terminal repeat (LTR) repression (Yeh, C.H., and Shatkin, A.J. (1994) Proc. Natl. Acad. Sci. U.S.A. 91, 11002-11006), p21/SIIR mutants were constructed and assayed for phosphorylation level and effect on RSV LTR-driven chloramphenicol acetyltransferase (CAT) reporter expression. A major phosphorylation target in p21/SIIR was localized to the Arg/Ser-rich region between amino acids 12 and 49. Deletion of this region impaired the ability of p21/SIIR to down-regulate RSV LTR promoter function. Four serine pairs, all displaying the Arg/Lys-Ser-Ser motif typical of phosphorylation sites, are present in p21/SIIR between positions 31 and 48. Conversion of these individual serine pairs to alanine resulted in decreased phosphorylation in each case. Mutation of the Ser36-Ser37 pair also diminished by severalfold the repression activity of p21/SIIR. The single tyrosine (Tyr155) in p21/SIIR was not detectably phosphorylated in transfected COS-1 cells, suggesting that the Ser36-Ser37 pair mediates Ser/Thr phosphorylation of p21/SIIR and is critical for LTR repression function.

Amino Acid Sequence↗
PubMed1995

A cis-acting element in Rous sarcoma virus long terminal repeat required for promoter repression by HeLa nuclear protein p21.

HeLa cell basic nuclear protein (p21), which represses Rous sarcoma virus long terminal repeat (RSV LTR) promoter activity, diminished v-src expression and the appearance at permissive temperature of the transformed phenotype in tsRSVLA23 Rat-1, a cell line transformed with a temperature-sensitive mutant of RSV. Nuclear run-on analyses using COS-1 cells cotransfected with p21 cDNA and chloramphenicol acetyltransferase reporter indicated that p21 inhibits transcription initiation by targeting a region in the RSV LTR promoter between positions -108 and -85 upstream of the cap site. Insertion of this 24-base pair sequence in place of one of the 72-base pair enhancers in the SV40 early promoter rendered it sensitive to p21 repression. Electrophoretic mobility shift assays using a synthetic oligomer corresponding to the 24-base pair LTR promoter element revealed that p21 altered the pattern of protein.DNA complex formation apparently without binding DNA directly. Complex formation assayed by UV cross-linking and DNA affinity chromatography indicated further that a cellular factor which can interact with this element was decreased in cells transfected with p21 expression plasmid. The results indicate that p21 repression of RSV LTR is mediated by a cis-acting element and may occur by alteration of protein complexes formed on this promoter element.

Animals↗
PubMed1995

A recombinant rice 16.9-kDa heat shock protein can provide thermoprotection in vitro.

It is difficult to obtain large amounts of purified low-molecular-mass heat shock proteins (LMM HSPs), which are unique to plants, for biochemical and physiological studies. Therefore, an attempt was made to produce such a HSP by applying recombinant DNA technology. We fused the cDNA for a rice class I 16.9-kDa HSP, pTS1, to the gene for glutathione S-transferase (GST) of Schistosoma japonicum and we obtained large amounts of the fusion protein from transformed Escherichia coli cells. In addition, we found that the 16.9-kDa HSP obtained by cleavage of the recombinant protein could also form a protein complex of approximately 310 kDa under nondenaturing conditions as can the small, native, class I HSPs from heat-shocked rice seedlings. An assay in vitro to examine the thermoprotection of rice soluble proteins from heat denaturation revealed the strong stabilizing effect of the recombinant HSP.

Amino Acid Sequence↗