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Biomedical subjects

W C Chen

Publications and source records attributed to W C Chen.

At least 73 records · Page 4Linked to original sources

Ticlopidine-induced hepatitis.

Ticlopidine is a commonly prescribed drug in cerebrovascular or cardiovascular diseases. Since the first introduction in 1970's, ticlopidine was shown to be a relatively safe drug. The adverse effects of ticlopidine were mainly bone marrow toxicity and elevation of liver function tests. Ticlopidine-induced hepatitis is rare and only 33 cases were reported in previous English literature. The 33 cases were mostly categorized in cholestatic liver injury; only 2 cases were hepatocellular. In Taiwan, a case of ticlopidine-induced cholestatic hepatitis was ever reported. Herein, we present another rare case of ticlopidine-induced hepatitis in Taiwan with the nature of hepatocellular injury.

Aged↗

Proton magnetic resonance spectroscopy of cerebral glioma after irradiation.

BACKGROUND: Conventional magnetic resonance imaging (MRI) is commonly employed to assess cerebral gliomas after radiotherapy, but it cannot always differentiate tumor regrowth from post-irradiation changes. In this study, we utilized magnetic resonance spectroscopy (MRS) to evaluate changes in cerebral metabolites in patients with a cerebral glioma after irradiation. METHODS: Over a period of 3 years, we performed MRS after MRI whenever soft tissue masses were found on magnetic resonance (MR) images. A total of 122 MR spectra of 58 patients was used for analysis. Spectral interpretations were based on integral values of the N-acetylaspartate (NAA) and choline (Cho) compounds relative to phosphocreatine/creatine (Cr). RESULTS: Our MRS study showed that higher Cho/Cr ratios occurred in regrowing gliomas than for stable diseases (range, 0.9 to 9.5 vs. 0.4 to 2.1; mean, 3.0 vs. 1.2). A greater increment in the Cho/Cr ratio between successive studies was also noted in regrowing gliomas than for stable disease (range, 41% to 87% vs. < 32%). No significant differences in NAA/Cr ratios or lactate were found between these 2 groups. None of our patients exhibited abnormal MR spectra in the mirror area of the contralateral brain. CONCLUSION: MRS provides valuable information about the metabolism of irradiated gliomas and can be used to exclude radiation encephalopathy of the contralateral brain. Cho is the most reliable indicator of a regrowing glioma. A high Cho/Cr ratio or substantial elevation in the Cho/Cr ratio between serial studies increases the likelihood of tumor regrowth. However, lower Cho/Cr ratios were inconclusive for determining if tumor regrowth or a stable process was occurring.

Brain↗

The effects on vesicourethral function following laparoscopic hysterectomy.

The aim of our study is to determine whether laparoscopic hysterectomy is associated with increased postoperative urinary symptoms and to assess the change in urodynamic parameters after operation. Forty-five women were arranged for laparoscopic hysterectomy (LH). Each patient received urinalysis, interview, and urodynamic study including uroflowmetry, filling and voiding cystometry and urethral pressure profilometry before and after hysterectomy. A total of 27 patients (60%) had urinary symptoms preoperatively. After operation, only 22 patients (48.9%) remained symptomatic. There was no significant change in the number of women with one or more voiding symptoms before and after surgery, but the incidence of urinary frequency and stress incontinence decreased significantly after laparoscopic hysterectomy (P < 0.05). In addition, maximal urethral closure pressure and maximal cystometric capacity showed significant increases after operation. They were 73.1 cm H2O (range: 49-114) vs 104.4 cm H2O (range: 60-147) (P < 0.001), and 363.3 ml (range: 287-423) vs 396.1 ml (range: 265-515) (P < 0.001), respectively. The result indicated that laparoscopic hysterectomy did not significantly increase the subjective or objective incidence of vesicourethral dysfunction. On the contrary, some patients might be cured of urinary frequency or stress incontinence postoperatively.

Adult↗

The effect of nodal status on determinants of initial treatment response and patterns of relapse-free survival in nasopharyngeal carcinoma.

PURPOSE: To study the effect of regional nodal status on predictors of treatment response, failure patterns, and the time-dependent nature of the various pattern of relapse via a hazard function analysis. METHODS AND MATERIALS: We reviews tumor control data of 496 patients with nasopharyngeal carcinoma (NPC) to whom a radical course of radiotherapy (RT) with or without induction chemotherapy (CT) was given. All alive patients had a median follow-up period of 131 months. Primary tumor (T) and nodal (N) status were staged according to the TNM system of the American Joint Committee. Remote after-loading brachytherapy may be added to teletherapy in T1-2 lesions while induction CT could be given for N3 and/or T4 lesions. Hazard function analysis over 1-year interval was carried out for locoregional or distant relapse. RESULTS: T stage and brachytherapy were two independent predictors for complete response (CR) at the primary site irrespective of nodal status, whereas N stage and brachytherapy are major determinants for regional CR in node (+) patients. Multivariate analysis revealed that contributors to a relatively long disease-free interval in (1) node (-) patients were for locoregional relapse, induction CT(-) (p = 0.0062) or brachytherapy (+) (p = 0.0268) and for distant relapse, none; (2) node (+) patients were for locoregional relapse, early T stage (p = 0.0377) or regional CR (p = 0.0075) and for distant relapse, induction CT(-) (p = 0.0001) or regional CR (p = 0.0001). In node (-) or (+) patients, primary CR rate yield no independent prognostic value on various types of disease-free survival. Hazard function analysis for relapse revealed that hazard rates are in general negatively correlated with time, being highest at the first year post-treatment, decreasing from time to time, and approaching zero after a longer follow-up period in patients with locoregional CR than in patients without. CONCLUSION: Nodal status had no significant impact on predictors of primary CR, whereas in node (+) patients regional CR rate had an independent value in predicting disease-free survival to locoregional and distant relapse. Hazard function analysis revealed a decreasing hazard rate over a protracted post-treatment time in primary and regional CR patients. This indicates the continued risk of late recurrence in this subset of patients for whom long-term observation is recommended.

Adult↗

Dual action of palmitoyl trifluoromethyl ketone (PACOCF3) on Ca2+ signaling: activation of extracellular Ca2+ influx and alteration of ATP- and bradykinin-induced Ca2+ responses in Madin Darby canine kidney cells.

The effect of the phospholipase A2 inhibitor palmitoyl trifluoromethyl ketone (PACOCF3) on Ca2+ signaling in Madin Darby canine kidney (MDCK) cells was examined using fura-2 as the fluorescent Ca2+ indicator. At a concentration of 20 microM, PACOCF3 did not change basal cytosolic free calcium concentrations ([Ca2+]i), but at concentrations of 50-250 microM PACOCF3 induced an increase in [Ca2+]i by activating extracellular Ca2+ entry which was partly suppressed by 50 microM La3+. The effect of PACOCF3 was abolished by removal of extracellular Ca2+. PACOCF3 (10 microM) enhanced both the peak value and the area under the curve of the [Ca2+]i increase induced by 10 microM ATP and 1 microM bradykinin by potentiating extracellular Ca2+ influx without affecting internal Ca2+ release. Several other phospholipase A2 inhibitors had no effect on basal [Ca2+]i or agonist-induced [Ca2+]i increases. Collectively, the results suggest that PACOCF3 alters Ca2+ signaling in renal tubular cells in a manner independent of phospholipase A2 inhibition.

Adenosine Triphosphate↗

Distributions of p53 codon 72 polymorphism in bladder cancer--proline form is prominent in invasive tumor.

Abnormal function of p53 is commonly associated with various cancer formations. High-grade and late-stage bladder cancers have been reported to have mutated or become inactive p53 when using immunohistochemical stains. Recently, p53 codon 72 polymorphism was extensively studied to determine the risk factors responsible for cancer formation. There was a general population of codon 72 sequence polymorphism of the wild type p53. A single base change from G to C caused the alteration of amino acid residue 72 from arginine to proline. The arginine form is considered to be a significant risk factor in the development of cancer. However, various reports had indicated discrepancies with regard to this polymorphism; some showed no significant difference between the control and cancer groups, while other series were associated with high risks in the proline form homozygotes. To resolve the undefined distribution of this polymorphism in bladder cancers, 58 patients with bladder cancer were enrolled onto this study. When checked using the Chi-squared test (P = 0.952) there were no differences between the control subjects and bladder cancer patients in the distribution of polymorphism. However, proline form homozygotes were more frequently found in the invasive group than the non-invasive group by Fisher's exact test (25% and 2.9%, respectively, P < 0.001). More than 70% of the non-invasive bladder cancers were the arginine form homozygotes. This result is consistent with those reported for hepatocellular carcinoma that showed a history of chronic liver disease and proline form homozygotes in a report by Yu et al. Our data suggest that proline form homozygotes are associated with invasive bladder cancer.

Adult↗

Biological effects and metabolism of 9-cis-retinoic acid and its metabolite 9,13-di-cis-retinoic acid in HaCaT keratinocytes in vitro: comparison with all-trans-retinoic acid.

9-cis-Retinoic acid (9cRA), a geometric isomer of all-trans-retinoic acid (atRA), is an endogenous high-affinity ligand for retinoid X receptors and retinoic acid receptors activating them with high potency. 9,13-di-cis-Retinoic acid (9,13dcRA) has been described as a major plasma metabolite of 9cRA. In this study, the biological activity and the metabolism of 9cRA and 9,13dcRA were investigated and compared with those of atRA in a retinol-free culture system of HaCaT keratinocytes. 9cRA exhibited a slightly weaker activity overall than atRA in inhibiting cell proliferation, inducing cellular retinoic acid binding protein II (CRABP II) mRNA levels and upregulating cytokeratin 19 expression. 9,13dcRA regulated HaCaT keratinocyte activity only at the highest concentration tested (10(-6) M). In cultures of HaCaT keratinocytes with atRA and 9cRA, rapid intracellular accumulation of atRA was observed within 2 h, and atRA levels were higher with atRA treatment than with 9cRA treatment. 9,13dcRA remained relatively stable in the medium with intracellular 9,13dcRA levels below the level of detection. Taken together, 9cRA seems to be slightly less potent than atRA in regulating the biological activity of HaCaT keratinocytes, while its metabolite 9,13dcRA is effectively inactive at biologically relevant concentrations. Our data suggest a prodrug/drug relationship between 9cRA and atRA in human keratinocytes. 9,13dcRA seems to be a weaker prodrug of atRA or an inactive metabolic derivative.

Alitretinoin↗

Fendiline increases [Ca2+]i in Madin Darby canine kidney (MDCK) cells by releasing internal Ca2+ followed by capacitative Ca2+ entry.

The effect of fendiline, a documented inhibitor of L-type Ca2+ channels and calmodulin, on Ca2+ signaling in Madin Darby canine kidney (MDCK) cells was investigated using fura-2 as a Ca2+ probe. Fendiline at 5-100 microM significantly increased [Ca2+]i concentration-dependently. The [Ca2+]i rise consisted of an initial rise and a slow decay. External Ca2+ removal partly inhibited the Ca2+ signals induced by 25-100 microM fendiline by reducing both the initial rise and the decay phase. This suggests that fendiline triggered external Ca2+ influx and internal Ca2+ release. In Ca(2+)-free medium, pretreatment with 50 microM fendiline nearly abolished the [Ca2+]i rise induced by 1 microM thapsigargin, an endoplasmic reticulum Ca2+ pump inhibitor, and vice versa, pretreatment with thapsigargin prevented fendiline from releasing internal Ca2+. This indicates that the internal Ca2+ source for fendiline overlaps with that for thapsigargin. At a concentration of 50 microM, fendiline caused Mn2+ quench of fura-2 fluorescence at the 360 nm excitation wavelenghth, which was inhibited by 0.1 mM La3+ by 50%, implying that fendiline-induced Ca2+ influx has two components separable by La3+. Consistently, 0.1 mM La3+ pretreatment suppressed fendiline-induced [Ca2+]i rise, and adding La3+ during the rising phase immediately inhibited the signal. Addition of 3 mM Ca2+ increased [Ca2+]i after preincubation with 50-100 microM fendiline in Ca(2+)-free medium. However, 50-100 microM fendiline inhibited 1 microM thapsigargin-induced capacitative Ca2+ entry. Pretreatment with 40 microM aristolochic acid to inhibit phospholipase A2 inhibited 50 microM fendiline-induced internal Ca2+ release by 48%, but inhibition of phospholipase C with 2 microM U73122 or inhibition of phospholipase D with 0.1 mM propranolol had no effect. Collectively, we have found that fendiline increased [Ca2+]i in MDCK cells by releasing internal Ca2+ in a manner independent of inositol-1,4,5-trisphosphate (IP3), followed by external Ca2+ influx.

Animals↗

Improved cell adhesion by plasma-induced grafting of L-lactide onto polyurethane surface.

Lactide-grafted polyurethanes were prepared by exposing the polyurethane films to argon plasma discharge, followed by grafting L-lactide onto the plasma-treated surface. The modified surfaces were characterized by measuring the static contact angle and by electron spectroscopy for chemical analysis (ESCA). The water contact angle of polyurethanes was decreased by L-lactide grafting, indicating hydrophilicity of the modified surface. Grafting also increased the O/C atomic ratio and C(C=O)/Ctotal percentage on the surfaces as detected by ESCA. The grafted surfaces showed enhanced attachment and growth in both 3T3 fibroblast and human umbilical vein endothelial cell culture tests. Platelet adhesion to the modified surfaces was also reduced in vitro. L-Lactide monomers grafted onto polyurethane substrates could therefore be useful in facilitating endothelial cell seeding process in small vascular graft applications.

3T3 Cells↗

New jujubogenin glycosides from Colubrina asiatica.

Three new jujubogenin glycosides, namely, 3' '-O-acetylcolubrin (1); 3' ',2' "-O-diacetylcolubrin (2), and 3' '-O-acetyl-6' '-O-trans-crotonylcolubrin (3), were isolated from the leaves of Colubrina asiatica, in addition to the known colubrin, rutin, and kaempferol 3-O-rutinoside. Compounds 1-3 were isolated and purified via a combination of chromatographic procedures, and determined structurally using spectroscopic methods.

Acetylation↗

Lindane (gamma-hexachlorocyclohexane) induces internal Ca2+ release and capacitative Ca2+ entry in Madin-Darby canine kidney cells.

The effect of lindane (gamma-hexachlorocyclohexane), an organochlorine pesticide, on Ca2+ mobilization in Madin-Darby canine kidney cells was examined by fluorimetry using fura-2 as a Ca2+ indicator. Lindane (5-200 microM) increased [Ca2+]i concentration-dependently. The [Ca2+]i signal comprised an immediate initial rise followed by a persistent phase. Ca2+ removal inhibited the [Ca2+]i signal by reducing both the initial rise and the sustained phase. This implies lindane-triggered Ca2+ influx and Ca2+ release. In Ca2+ -free medium, 0.15 mM lindane increased [Ca2+]i after pretreatment with carbonylcyanide m-chlorophenylhydrazone (CCCP, 2 microM), a mitochondrial uncoupler, and two endoplasmic reticulum Ca2+ pump inhibitors, thapsigargin and cyclopiazonic acid. Conversely, pretreatment with lindane abolished CCCP- and thapsigargin-induced Ca2+ release. This suggests that 0.15 mM lindane released Ca2+ from the endoplasmic reticulum, mitochondria and other stores. La3+ (1 mM) partly inhibited 0.1 mM lindane-induced [Ca2+]i increase, confirming that lindane induced Ca2+ influx. Addition of 3 mM Ca2+ increased [Ca2+]i after pretreatment with 0.15 mM lindane for 750 sec. in Ca2+ -free medium, which indicates lindane-induced capacitative Ca2+ entry. Lindane (0.15 mM)-induced Ca2+ release was not reduced by inhibiting phospholipase C with 2 microM U73122, but was inhibited by 70% by the phospholipase A2 inhibitor aristolochic acid (40 microM).

Animals↗

An endoscopic injection with N-butyl-2-cyanoacrylate used for colonic variceal bleeding: a case report and review of the literature.

We report a 64-yr-old patient with liver cirrhosis and bleeding esophageal varices that were obliterated by repeated endoscopic sclerotherapy. Eleven years later, he developed a massive, life-threatening rectosigmoid variceal hemorrhage. An endoscopic injection with N-butyl-2-cyanoacrylate (Histoacryl), performed over the rectosigmoid varices, achieved temporary hemostasis. The etiology, prevalence, relationship with portal hypertension, diagnosis, and treatment of colorectal varices are discussed.

Colon, Sigmoid↗

Four new terpenes from the pericarp of Platycladus orientalis.

A new monoterpene, platydiol (1), and three new diterpenes, platyclolactonic acid (2), 14,15-bisnor-8(17)-labdene-16,19-dioic acid (3), and 6,7-dehydrosandaracopimaric acid (4), were isolated from the pericarp of Platycladus orientalis. Their structures were elucidated by spectral and chemical methods.

Molecular Structure↗

Symptomatic esophageal stricture after endoscopic variceal ligation--success of endoscopic balloon dilation.

Endoscopic variceal ligation is a preferred endoscopic method to treat esophageal variceal bleeding. Esophageal stricture complicated by endoscopic ligation is very unusual. We report a case of symptomatic esophageal stricture after variceal ligation. Endoscopic balloon dilatation was used to treat the stricture successfully. The possible mechanism of stricture formation is discussed.

Aged↗

Transrectal ultrasonographic findings in patients with hemospermia.

BACKGROUND: Hemospermia causes anxiety in many men. Its etiology includes inflammatory disorders, vascular lesions, malignancies and congenital anomalies. With the advent of modern transrectal ultrasonography (TRUS) and magnetic resonance imaging technology, we can now visualize the internal structures of the seminal vesicles and prostate, and identify a more accurate etiology for hemospermia. This study was performed to assess the efficacy of TRUS in the evaluation of hemospermia. METHODS: TRUS was used to evaluate 40 patients with hemospermia. Patients' ages ranged from 20 to 72 years, with an average age of 41 years. The duration of symptoms was 3 days to 10 years, (average age 12.4 months). Apart from three patients with hepatitis, there was no major illness found in the medical histories. TRUS was performed with a B & K, type 3535 transrectal transducer device, with an 1850 multiplane probe. RESULTS: TRUS revealed abnormalities in 33 (83%) of 40 patients, which included ejaculatory duct cysts, müllerian duct cysts, asymmetric seminal vesicle dilatation, preprostatic vein engorgement and prostatic enlargement. There were stones in the ejaculatory ducts, ejaculatory duct cysts, müllerian duct cysts or prostate. Nine patients with prostatic stones were under 40 years-of-age. Other than the development of stones, there were no significant differences between patients less than 40 years-of-age and those more than 40 years old. CONCLUSIONS: The results suggest that TRUS is an effective method for examining the seminal vesicles, ejaculatory duct and prostate complex. Sonoguided aspiration, injection of contrast medium or biopsy can further help to differentiate the nature of hemospermia.

Adult↗

Comparison of clinical behaviors and responses to radiation between squamous cell carcinomas and adenocarcinomas/adenosquamous carcinomas of the cervix.

BACKGROUND: Adenocarcinomas/adenosquamous carcinomas (AC/ASC) are relatively uncommon histological subtypes in cervical cancer. In this study, we retrospectively compared the clinical behaviors and responses to radiation of squamous cell carcinomas (SCC) and AC/ASC in patients with stage I-IVA cervical cancer primarily treated by radiotherapy (RT). METHODS: Nine hundred twenty-eight patients with cervical cancer primarily treated with RT were included in this study. Ninety-four percent of the patients had SCC and 6% had AC/ASC. The association of histological subtype to various clinical parameters was assessed. Tumor response and failure patterns were analyzed, and the prognostic significance of histological subtype and other clinical parameters were evaluated by univariate and multivariate analyses. RESULTS: (1) Patients with AC/ASC had a significantly higher percentage of bulky I-IIA disease, a younger age (< 45 years), and an elevated carcinoembryonic antigen (CEA) level, but a lower percentage of elevated squamous cell carcinoma antigen (SCC-Ag) level, than patients with SCC. Hemoglobin (Hb) levels and lymph node status were not significantly different between SCC and AC/ASC patients. (2) A higher percentage of AS/ASC patients had residual induration 2 to 3 months after RT than those with SCC (40% vs. 21.6%, p = 0.008). Higher local failure rates were found for AC/ASC patients compared to SCC patients (38% vs. 15%, p = 0.001). (3) The 5-year disease-specific survival rate was 66% and 50% for SCC and AC/ASC patients, respectively (p = 0.016). Advanced stages, Hb levels lower than 10 g/dl, positive lymph nodes, AC/ASC histological subtype, and SCC-Ag levels higher than 10 ng/ml were independent prognostic factors for worse survival for all patients. For patients with AC/ASC in particular, only stage and positive lymph nodes were significant prognostic factors. CONCLUSION: Cervical cancer patients with AC/ASC are relatively younger and have a higher incidence of elevated CEA and a lower incidence of elevated SCC-Ag levels than those with SCC. For AC/ASC patients, the tumor responses to RT were relatively slow and poor. This group of patients had a worse survival rate than patients with SCC, mainly because of the higher incidence of uncontrolled local disease for AC/ASC patients.

Adenocarcinoma↗

Does Ser364Pro mutation of connexin 43 exist in Taiwanese patients with Ivemark syndrome?

BACKGROUND: A previous study by Britz-Cunningham et al (N Engl J Med, 1995) indicated that a mutation of the connexin 43 (CX43) gap junction gene might be responsible for Ivemark syndrome. Ser364Pro substitution (TCA-->CCA) is the most common mutation located in the cytoplasmic tail domain of CX43. This domain may be an important part of the conductance channel of the gap junction. It may, therefore, result in heart anomalies and situs inversus during embryonic development, resulting in Ivemark syndrome. METHODS: We investigated 10 patients with Ivemark syndrome, 10 healthy individuals, one patient with Kartagener syndrome and one with polysplenia and situs inversus but without heart anomaly for this mutation. Seminested polymerase chain reaction (PCR) was performed using a DNA template from DNA extracted from peripheral blood cells. Direct sequencing was done after purification of the second round of PCR products. Then, the sequence was compared with the last 402 bp of the cDNA-coding region of CX43. RESULTS: No base changes were found in the patients with Ivemark syndrome or other patient groups at the previously reported CX43 residues of Thr326, Gln352, Ser364, Ser365 and Ser373. CONCLUSIONS: The results indicate that Ser364Pro mutation of CX43 did not exist in the 10 Taiwanese patients with Ivemark syndrome. Other genes responsible for the Ivemark syndrome should be further investigated.

Abnormalities, Multiple↗