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Biomedical subjects

A Chen

Publications and source records attributed to A Chen.

At least 253 records · Page 14Linked to original sources
PubMed1997

Predictive factors for early menarche in Taiwan.

The rapid increase of breast cancer in Taiwan has prompted the authors to evaluate the predictive factors of early menarche among contemporary Taiwanese girls. A total of 895 four-grade girls from eight elementary schools in Taipei City and County were identified as a closed cohort from the first semester of 1993. Data were collected from self-administered questionnaires and school records. A total of 799 girls who had not menstruated in the first year remained in the group through 1994. The effects of potential predictive factors were assessed by logistic regression. Among the 799 girls followed, 69 (8.6%) had first menstruation between the fourth and fifth grades. Height, weight, body mass index and maternal early onset of menarche were positively related to the onset of menarche within the preceding year. Energy consumption during exercise showed only moderate association after being adjusted for age and weight. Calorie intake from junk food was not associated with early menarche within the preceding year. Poor interpersonal family relationships and stressful life events also showed a moderate association with early menarche. The data obtained supported the hypothesis that height, weight, body mass index and maternal early menarche are positive predictive factors of early menarche. The effects of exercise and childhood stress are less prominent.

Age of Onset↗
PubMed1997

Percutaneous transluminal coronary angioplasty for acute myocardial infarction: initial experience in 43 cases.

OBJECTIVE: To evaluate the initial experience with the use of percutaneous transluminal coronary angioplasty (PTCA) in the set of acute myocardial infarction (AMI). METHODS: Between October 1993 and April 1996, PTCA was performed in 43 patients (34 male, 9 female) with initial onset of AMI. These patients ranged in age from 40 to 74 years (mean +/- SD, 60.3 3 +/- 9.2). Primary PTCA was performed in 16, rescue PTCA in 8, and semi-elective PTCA in 19 patients. RESULTS: The initial success was achieved in 95.3% (41/ 43). Failed angioplasty occurred in 2 patients, with acute reocclusion after rescue PTCA (this patient died of cerebral stroke 3 days later) in one patient, and small local intimal dissection during semi-elective PTCA in another patient. CONCLUSION: PTCA was a safe and effective approach in the treatment of AMI in the present study patients, with a high primary success and low acute complication rate.

Adult↗
PubMed1997

[In vitro experimental study of adriamycin-loaded chitosan drug delivery system].

Chitosan is a kind of biological material with good histocompatibility and gradual biodegradability in vivo. It has no toxicity or side-effect. For its gradual degradation, chitosan and adriamycin were mixed and formed drug delivery system (DDS). The release test of DDS and exudant of DDS in inhibiting OS-116 were examined in vitro. The results were as following: the DDS could release adriamycin in slow and stable way. The SO-116 inhidition rate of the exudant of the DDS on the 1st, 20th, 40th and 60th day was 58.11%, 36.48%, 24.32% and 21.62% respectively. It was concluded that the drug delivery system was a slow release system. It could maintain the concentration of adriamycin in a certain level. It was also suggested that the chitosan was a good carrier for slow release of chemotherapeutic drug in local therapy for postoperative treatment of bone tumor.

Antibiotics, Antineoplastic↗
PubMed1996

L-selectin binds to P-selectin glycoprotein ligand-1 on leukocytes: interactions between the lectin, epidermal growth factor, and consensus repeat domains of the selectins determine ligand binding specificity.

The selectins mediate cellular interactions by binding carbohydrate determinants present on a limited number of glycoprotein ligands. L-selectin binds multiple ligands expressed on endothelial cells, while P-selectin interacts exclusively with P-selectin glycoprotein ligand-1 (PSGL-1) on leukocytes. In this study, L-selectin was shown to bind leukocytes through the P-selectin ligand, PSGL-1, although at lower levels than P-selectin. L-selectin binding to PSGL-1 is specific since it was blocked by Abs to L-selectin or PSGL-1, required appropriate glycosylation of PSGL-1, and was Ca2+ dependent. The contributions of the extracellular domains of the selectins to ligand binding was assessed using a panel of chimeric selectins created by exchange of domains between L-selectin and P- or E-selectin. The lectin and epidermal growth factor domains of L- and P-selectin contributed significantly to binding through similar, if not identical, regions of PSGL-1. The different chimeric selectins revealed that the lectin domain was the dominant determinant for ligand binding, while cooperative interactions between the lectin, epidermal growth factor, and short consensus repeat domains of the selectins also modified ligand binding specificity. L-selectin binding to PSGL-1 expressed by leukocytes may mediate neutrophil rolling on stationary leukocytes bound to cytokine-induced endothelial cells, which was previously reported to be a L-selectin-dependent process.

Amino Acid Sequence↗
PubMed1996

Identification of a sequence within the integrin beta6 subunit cytoplasmic domain that is required to support the specific effect of alphavbeta6 on proliferation in three-dimensional culture.

The integrin alphavbeta6 augments the proliferation of epithelial cells in collagen gels and in vivo. This effect depends on the presence of a unique carboxyl-terminal region of the beta6 subunit cytoplasmic domain. In the present study, we have utilized deletional and alanine substitution mutagenesis within this region to map the amino acids responsible for alphavbeta6-mediated proliferation in more detail. Replacement or deletion of any of 6 amino acids (glutamic acid 778, lysine 779, lysine 781, valine 782, aspartic acid 783, and leucine 784) largely abolished the proliferative effects of alphavbeta6, but none of the mutants examined interfered with alphavbeta6-mediated cell adhesion or with localization of alphavbeta6 to focal adhesions. These findings suggest that residues contained within the sequence EKXKVDL are critical for the effects of alphavbeta6 on proliferation in collagen gels and that pathways initiated by interaction with this sequence are distinct from those required for integrin-mediated cell attachment or focal adhesion formation.

Alanine↗
PubMed1996

Suppression of stellate cell type I collagen gene expression involves AP-2 transmodulation of nuclear factor-1-dependent gene transcription.

The regulation of collagen gene expression was studied in culture-activated rat hepatic stellate cells, the fibrogenic effector cell involved in hepatic fibrogenesis. Treatment of cells with a 5-lipoxygenase-specific inhibitor caused a reduction in alphaI(I) collagen mRNA transcript abundance, which suggested that leukotriene production was involved in maintaining the activated cell's high level of collagen mRNA production. The underlying mechanism involved a decrease in collagen gene transcription. Suppression of gene transcription was localized to an nuclear factor-1 (NF-1) binding domain in the proximal promoter and an AP-2 binding domain adjacent to it. Gel retardation assays demonstrated that an increase in AP-2 binding adjacent to the NF-1 site was likely to be the transmodulator responsible for the suppression of the NF-1-dependent gene expression. The data suggest that post-translational alterations in AP-2 activity are responsible for this unappreciated mechanism of regulating the collagen gene.

Animals↗
PubMed1996

Raf and mitogen-activated protein kinase regulate stellate cell collagen gene expression.

Hepatic stellate cells become activated into myofibroblast-like cells during the early stages of hepatic injury associated with fibrogenesis. The subsequent dysregulation of hepatic stellate cell collagen gene expression is a central pathogenetic step during the development of cirrhosis. The cytoplasmic Raf and mitogen-activated protein (MAPK) kinases were found to differentially regulate alpha I(I) collagen gene expression in activated stellate cells. This suggests an unappreciated branch point exists between Raf and MAPK. A MAPK-stimulatory signal was mapped to the most proximal NF-1 and Sp-1 binding domains of the 5'-untranslated region of the collagen gene. A Raf-inhibitory signal was mapped to a further upstream binding domain involving a novel 60-kDa DNA-binding protein (p60). The cell-specific expression and induction of p60 in stellate cells during the early stages of hepatic fibrogenesis in vivo suggest a central role for this pathway during liver injury and stellate cell activation.

Animals↗
PubMed1996

Identification of the gltX gene encoding glutamyl-tRNA synthetase from Methanobacterium thermoautotrophicum.

The gltX gene encoding glutamyl-tRNA synthetase from Methanobacterium thermoautotrophicum has been cloned, sequenced, and identified. The gene is located immediately downstream of idsA in an operon containing at least three additional ORFs. The deduced protein sequence from gltX contains conserved regions (HIGH and KMSKS) indicative of a class I aminoacyl-tRNA synthetase.

Amino Acid Sequence↗
PubMed1996

Flutamide-induced liver toxicity including fatal hepatic necrosis.

PURPOSE: To describe hepatic injuries in three patients who received flutamide prior to and during radiation treatment to make radiation oncologists aware of the need for careful monitoring of liver function during use of this drug. METHODS AND MATERIALS: The records of three patients who developed abnormal liver function tests while undergoing total androgen suppression (TAS), as well as the literature concerning flutamide toxicity were reviewed and summarized. RESULTS: Three of 34 patients treated with a TAS regimen incorporating flutamide developed significant hepatic abnormalities: elevated transaminases [2] and fatal hepatic necrosis [1]. Following the discontinuation of flutamide, two patients recovered fully. Unfortunately, the third patient's hepatic function continued to deteriorate, which culminated in his death. Transient elevations in serum transaminases, which do not exceed four times the upper limits of normal, are common and apparently without clinical significance. Unfortunately, idiosyncratic serious and/or fatal liver damage can occur. Significant liver toxicity may be obviated by monitoring of liver function tests (LFT) early in the course of flutamide therapy. CONCLUSION: The incidence of hepatic toxicity associated with flutamide may be higher than previously suggested. To prevent the development of serious hepatic dysfunction, all patients receiving flutamide should be monitored clinically for signs and symptoms referable to hepatic injury and with serial LFT. We recommend baseline LFT followed by serial LFT at weeks 2, 4, 6, and 8 from the start of treatment with flutamide. Flutamide should be stopped promptly if significant liver abnormalities are detected.

Adenocarcinoma↗
PubMed1996

Splenic blood flow and fluid efflux from the intravascular space in the rat.

1. Previous evidence has suggested that fluid is extracted from the blood during its passage through the splenic circulation. In order to further investigate this phenomenon, flow probes were placed around the splenic artery and vein of rats. Splenic blood flow and mean arterial blood pressure were measured immediately after surgery, while the rats were still anaesthetized. Five days later, the measurements were repeated first in conscious rats, and then after administering sodium pentobarbitone. Final measurements were made in the conscious animals at day 10 post surgery. 2. Splenic arterial blood flow was lowest at the time of surgery. It had doubled by day 5, and remained stable thereafter at about 8 ml min-1. Splenic venous blood flow also increased after surgery, but less so than the arterial flow, so that the arteriovenous difference had increased to 2.0 +/- 0.4 ml min-1 by day 5. 3. In response to sodium pentobarbitone (20 mg I.V.), there was a transient fall in splenic arterial blood flow from 6.7 +/- 0.9 to 4.9 +/- 0.7 ml min-1. There was no significant change in the arteriovenous difference of blood flow. 4. In conclusion, we have shown that splenic blood flow is considerably higher than previously reported. We have also revealed a significant new path for fluid efflux from the intravascular space; at least 25% of fluid volume flowing into the splen is removed from the circulating blood. 5. Although anaesthesia modulates splenic blood flow, the changes are not as pronounced as those observed in the acute surgically prepared animal.

Adjuvants, Anesthesia↗
PubMed1996

Enhanced malignant progression of nasopharyngeal carcinoma cells mediated by the expression of Epstein-Barr nuclear antigen 1 in vivo.

Nasopharyngeal carcinoma (NPC) is consistently associated with Epstein-Barr virus (EBV) and mostly classified as poorly differentiated squamous cell carcinoma or undifferentiated carcinoma with early metastasis and a rapidly progressive clinical course. The EBV-encoded latent proteins, Epstein-Barr nuclear antigen 1 (EBNA 1) and latent membrane proteins (LMPs), may be expressed in NPC, but their biological effects are poorly understood. EBNA 1 may predispose B lymphocytes to lymphomagenesis in transgenic mice, but its biological effects in NPC are still unknown. This study investigated the biological effects of EBNA 1 by expressing it in an EBV-negative NPC cell line (HONE-1), which was then inoculated into both nude and severe combined immunodeficiency mice. The EBNA 1 caused HONE-1 cells to grow in a less differentiated pattern and to progress more rapidly, as well as increasing their tumourigenicity and metastatic capability. These data suggest that EBNA 1 may play a critical role in the progressive evolution of NPC.

Animals↗
PubMed1996

Ki-ras and p53 mutations are early and late events, respectively, in urethane-induced pulmonary carcinogenesis in A/J mice.

In the A/J strain of mice, urethane (ethyl carbamate) induces lung hyperplasia, adenoma, and adenocarcinoma in a time-dependent manner. These distinct morphological stages may correlate with sequential molecular genetic changes in this mouse model. To test this hypothesis, we investigated the presence of mutations involving Ki-ras and p53 in urethane-induced lung lesions in A/J mice at early and late stages of tumorigenesis. We precisely microdissected 40 lung lesions from paraffin-embedded sections. Ki-ras mutations around codon 61 and p53 mutations in exons 5-8 were identified by polymerase chain reaction-single-strand conformation polymorphism and DNA sequencing techniques. In 29 early-stage lung lesions classified as hyperplasias (seven) or adenomas (22), we observed 19 Ki-ras mutations (66%), including three silent mutations and one double mutation at different codons, and one silent p53 mutation (3.5%). In 11 late-stage adenomas, we identified nine activating Ki-ras mutations (82%) and four missense p53 mutations (36%). These results indicate that Ki-ras mutations arise early, whereas p53 mutations occur relatively late during the benign stages of urethane-induced lung carcinogenesis in A/J mice.

Adenocarcinoma↗
PubMed1996

Methylprednisolone administration improves axonal regeneration into Schwann cell grafts in transected adult rat thoracic spinal cord.

Schwann cell (SC) grafts support the regeneration of axons of numerous spinal cord neurons when placed into transected adult rat midthoracic spinal cord. Clinically, methylprednisolone (MP) has been shown to be neuroprotective if administered within 8 h after spinal cord injury. We investigated whether axonal regrowth into SC grafts is enhanced when MP is administered at the time of spinal cord transection and SC implantation. SCs from adult rat sciatic nerves were purified in culture, suspended in Matrigel, and drawn into semipermeable polymeric channels. MP (30 mg/kg) or vehicle (control) was administered intravenously at 5 min, 2 h, and 4 h to adult Fischer rats after transection at T8 and removal of the next three caudal segments. The rostral cord stump was inserted 1 mm into the channel; the distal end of the channel was capped. Thirty to forty-five days later, the SC/MP group showed large tissue cables in the channels and host cord tissue retained in the rostral end of the channels. Significantly more myelinated axons (1159 +/- 308) were present at the 5-mm level in SC/MP grafts (n = 6) than in SC/vehicle cables (355 +/- 108, n = 5). More unmyelinated than myelinated axons (approximately 4:1, n = 3) were resolved in the cables by electron microscopy. In the SC/MP group, unlike the SC/vehicle group, serotonergic and noradrenergic fibers were detected immunocytochemically 2.5 and 2.0 mm respectively, into the graft; astrocytes were also identified at similar distances from the interface. Fast Blue retrograde tracing (SC/MP, n = 4; SC/vehicle, n = 3) showed that more spinal cord neurons (1116 +/- 113 vs 284 +/- 88, respectively) and spinal cord neurons more distant from the graft (C8 vs C5) responded by extending axons into the graft in the presence of MP. Also, very significantly, supraspinal brain stem neurons extended axons into the graft only when MP was administered (mean 46 vs 0, n = 3). These results indicate that MP improves axonal regenerationn from both spinal cord and brain stem neurons into thoracic SC grafts, possibly by reducing secondary host tissue loss adjacent to the graft.

Animals↗
PubMed1996

Pharmacology of L-744,453, a novel nonpeptidyl endothelin antagonist.

L-744,453 ((+/-)3-[4-(1-carboxy-1-(3,4-methylenedioxyphenyl)methoxy)-3,5-diprop ylphenyl methyl]-3H-imidazo[4,5-c]pyridine) is an endothelin (ET) receptor antagonist from a new structural class, the dipropyl-alpha-phenoxyphenylacetic acid derivatives. L-744,453 competitively and reversibly inhibits [125I]-ET-1 binding to Chinese Hamster Ovary cells expressing cloned human ET receptors (K(i)s: hET(A)=4.3 nM; hET(B)=232 nM), and is selective for endothelin receptors compared to other peptide receptors. It is an antagonist of ET-1 stimulated phosphatidyl inositol hydrolysis in rat uterine slices (IC50=220 nM) and exhibits no agonist activity. This compound also inhibits ET-1 stimulated contraction of rat aortic rings with a K(b) value of 50 nM. L-744,453 protects against ET-1 induced lethality in mice after i.v. (AD50=13 mg/kg i.v.) or oral administration. This compound also antagonizes ET-1 induced increases in diastolic blood pressure in conscious normotensive rats (AD50=0.67 mg/kg i.v.) and anesthetized ferrets (AD50=1.6 mg/kg i.v.). L-744,453 is a potent, selective, orally active endothelin antagonist which may be useful in elucidating the role of endothelin in normal and pathophysiological states.

Animals↗
PubMed1996

Direct 99mTc-labeling of antibodies by sodium dithionite reduction, and role of ascorbate as a stabilizer in cysteine challenge.

A method for the direct 99mTc-labeling of antibodies by dithionite reduction was developed. Among three murine monoclonal IgG1 and one human polyclonal IgG (hIgG) antibodies tested, hIgG was the most quickly reduced by dithionite. These differences may reflect the reactivities of antibody disulfide bonds toward the oxidation products of dithionite. By optimizing reduction conditions to generate enough free sulfhydryl groups, it was possible to radiolabel human IgG and monoclonal antibody 170 with 99mTc with a 90% monomeric antibody efficiency. The process avoided colloid formation. In contrast, about 0.1 sulfhydryl groups per antibody molecule, less than 1% of the possible 36, were detected after treatment with ascorbate (up to 35,000:1 molar ratio) at room temperature for 1 h for the antibodies tested. Sulfhydryl groups generated in antibodies were estimated using a new method: 5-iodoacetamidofluorescein-labeled antibodies quantitated by size exclusion HPLC. Ascorbate was found to prevent antibody aggregate formation in cysteine-challenged samples.

Animals↗