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Biomedical subjects

J Yin

Publications and source records attributed to J Yin.

At least 163 records · Page 9Linked to original sources
PubMed1994

Fetal cocaine exposure and neonatal bilirubinemia.

To assess the effect of fetal exposure to cocaine on neonatal serum bilirubin values, we compared 17 infants whose cocaine exposure was confirmed by urine toxicology studies, with no evidence of other drug exposure by history or urinalysis, with 31 sequentially born healthy term infants without evidence of maternal drug use. The mean (+/- SD) bilirubin concentration in control infants was 110 +/- 32 mumol/L (6.5 +/- 1.9 mg/dl) at 30.5 +/- 5.4 hours of age, compared with 55 +/- 26 mumol/L (3.2 +/- 1.5 mg/dl) at 30.8 +/- 5.3 hours in cocaine-exposed infants (p < 0.001). We also compared the abilities of cocaine and clofibrate, a known inducer of bilirubin uridine diphosphate-glucuronosyl transferase (BGT), to induce drug and bilirubin metabolizing pathways in young male Sprague-Dawley rats. Animals received drugs or saline solution for 7 days, and livers were assayed for cytochrome P-450, peroxisomal beta-oxidase, delta 5-3-ketosteroid isomerase (KSI), glutathione-S-transferase (GST), and BGT. Cocaine was a weak inducer of GST but a strong inducer of KSI, a member of the GST family of enzymes that is closely associated with bilirubin transport (ligandin) in liver, and a moderately strong inducer of BGT. Neither drug increased cytochrome P-450 levels, and only clofibrate induced peroxisomal beta-oxidase. We conclude that cocaine appears to induce bilirubin metabolizing pathways, resulting in a lower risk of neonatal hyperbilirubinemia.

Animals↗
PubMed1994

A unique p53 intragenic deletion flanked by short direct repeats results in loss of mRNA expression in a human esophageal carcinoma.

A 45 base pair (bp) intragenic deletion of the p53 gene from a human esophageal cancer was analyzed in detail. This deletion contained all RNA splice consensus sequences at the 3' end of intron 7, including the RNA splice branch point, the pyrimidine-rich region and the 3' splice acceptor site. Northern blotting revealed a total lack of p53 mRNA expression in this tumor. Short direct repeats (TACTG) were found at the 5' and 3' breakpoints of the deletion and it removed one complete repeat as well as the entire region between the repeats. These results suggest that a 'slipped mispairing' mechanism occurring during DNA replication may generate p53 intragenic deletion in human esophageal cancer, leading to abolished p53 mRNA expression.

Base Sequence↗
PubMed1994

The MTS1 gene is frequently mutated in primary human esophageal tumors.

Homozygous and heterozygous deletions involving chromosome 9p21 have been reported in a variety of primary human tumors in vivo, and point mutations have been reported in melanoma cell lines in vitro within a probable tumor suppressor gene, MTS1, located at chromosome 9p21. We describe six sequence alterations occurring among twenty-four primary esophageal squamous carcinomas and nineteen primary esophageal adenocarcinomas analyzed by DNA sequencing of MTS1 exon 2. Nucleotide substitutions were observed in five squamous cell carcinomas and in one adenocarcinoma. Two occurred in the germline, while four were somatic alterations. All six nucleotide changes resulted in marked alterations in amino acid sequence. Four were nonsense mutations leading to premature termination codons; nucleotide substitutions identical to two of these stop codons were previously reported in other tumor types. Loss of heterozygosity occurred in all five informative (constitutionally heterozygous) cases in which a sequence alteration was present. Esophageal cancer is one primary human tumor in which MTS1 constitutes an apparent target of heterozygous or homozygous deletions occurring at chromosome 9p21.

Base Sequence↗
PubMed1993

Clonal ordering of 17p and 5q allelic losses in Barrett dysplasia and adenocarcinoma.

Both 17p and 5q allelic losses appear to be involved in the pathogenesis or progression of many human solid tumors. In colon carcinogenesis, there is strong evidence that the targets of the 17p and 5q allelic losses are TP53, the gene encoding p53, and APC, respectively. It is widely accepted that 5q allelic losses precede 17p allelic losses in the progression to colonic carcinoma. The data, however, supporting this proposed order are largely based on the prevalence of 17p and 5q allelic losses in adenomas and unrelated adenocarcinomas from different patients. We investigated the order in which 17p and 5q allelic losses developed during neoplastic progression in Barrett esophagus by evaluating multiple aneuploid cell populations from the same patient. Using DNA content flow cytometric cell sorting and polymerase chain reaction, 38 aneuploid cell populations from 14 patients with Barrett esophagus who had high grade dysplasia, cancer or both were evaluated for 17p and 5q allelic losses. 17p allelic losses preceded 5q allelic losses in 7 patients, both 17p and 5q allelic losses were present in all aneuploid populations of 4 patients, and only 17p (without 5q) allelic losses were present in the aneuploid populations of 3 patients. In no patient did we find that a 5q allelic loss preceded a 17p allelic loss. Our data suggest that 17p allelic losses typically occur before 5q allelic losses during neoplastic progression in Barrett esophagus.

Adenocarcinoma↗
PubMed1993

Altered messenger RNA and unique mutational profiles of p53 and Rb in human esophageal carcinomas.

Seventy-nine esophageal carcinoma patients were studied for genetic abnormalities in the p53 and Rb tumor suppressor genes. Single-strand conformation polymorphism analysis and DNA sequencing were used to detect p53 point mutations, Northern blotting was used to examine abnormal expression of p53 and Rb, and polymerase chain reaction and Southern blotting were used to analyze allelic loss. Twenty-five cases were analyzed by DNA sequencing to detect mutations in p53. Fourteen samples contained mutations within exons 5 through 9 of p53; seven had missense mutations giving rise to single amino acid substitutions. The remaining seven (50%) contained nonsense mutations leading to premature termination, five due to single base pair substitutions, and two that were the result of frameshift mutations. In other human tumors, p53 mutations are predominantly missense mutations, but our data as well as those from other groups show that nonsense mutations are common in human esophageal cancer. All but one of the constitutionally heterozygous samples containing mutations also manifested loss of the normal p53 allele; the one exception without allelic loss contained a silent mutation, which should not have had any affect on the p53 protein product. In addition, Northern blotting analysis revealed abnormalities (altered transcript size or mRNA levels) in 5 of 7 cases involving p53 and in 2 of 7 cases analyzed for Rb. Thirty-four cases were informative for allelic loss studies of both p53 and Rb; of these, 25 (74%) lost heterozygosity of p53, Rb, or both. When point mutations and mRNA expression abnormalities were also considered, 33 of 45 (73%) tumors informative for allelic loss assays of both genes as well as for mRNA or point mutation studies showed one or more abnormalities in p53 or Rb. Our results strongly suggest that a unique profile of molecular alterations involving p53 and Rb characterizes human esophageal cancer and that these specific genetic lesions are important in the development and/or progression of most human esophageal carcinomas.

Adenocarcinoma↗
PubMed1993

Loss of heterozygosity of p53 in oral cancers demonstrated by the polymerase chain reaction.

BACKGROUND: Alterations in the tumor suppressor gene p53 are the most frequently detected genetic abnormalities in human cancers. Inactivated tumor suppressor genes, including p53, often are suggested by loss of heterozygosity (LOH) studies. p53 gene inactivation has been reported in esophageal cancers. Because the etiologic factors for esophageal and intraoral carcinomas often are the same, corresponding molecular events may occur in oral squamous cell carcinoma (SCC) development. METHODS: The authors investigated LOH of the p53 gene in DNA from 27 primary oral cancers using a polymerase chain reaction (PCR)-based restriction fragment length polymorphism assay. DNA from fixed specimens of SCC and normal tissues was isolated and amplified at two p53 gene polymorphic restriction sites. RESULTS: In heterozygous individuals, 10 of 14 (71%) intraoral SCC demonstrated loss of p53 heterozygosity at one polymorphic restriction site. Two of five carcinomas showed LOH at a second site. CONCLUSIONS: These results suggest that inactivation of p53 is involved in the development or progression of SCC of the oral cavity.

Base Sequence↗
PubMed1993

p53 point mutations in dysplastic and cancerous ulcerative colitis lesions.

BACKGROUND: The molecular basis of colorectal dysplasia and carcinoma arising in ulcerative colitis is poorly understood. Loss of heterozygosity involving the tumor suppressor gene p53 occurs frequently in neoplastic ulcerative colitis lesions. Point mutation affecting p53 is associated with loss of heterozygosity in other cancers. Therefore, it was determined whether p53 point mutation occurs in ulcerative colitis-associated neoplasia. METHODS: Single-strand conformation polymorphism analysis, DNA sequencing, and loss of heterozygosity studies were performed on 45 patients with ulcerative colitis-associated dysplasia and carcinoma. RESULTS: Point mutations were detected in 26 lesions from 20 patients, including 18 carcinomas, 6 dysplasia-associated masses, 1 flat dysplasia, and 1 lymph node metastasis. In two cases, identical p53 mutations were observed in both carcinoma and adjacent dysplasia. Missense mutations causing amino acid substitutions as well as nonsense mutations resulting in premature stop codons were seen. Tandem mutations, in which more than 1 sequence alteration occurred on the same allele of p53, were also detected. Point mutation was accompanied by loss of the other p53 allele in 8 of 10 patients informative for both loss of heterozygosity and mutation assays. CONCLUSIONS: These findings suggest that inactivation of p53 by mutation and loss of heterozygosity is a common mechanism of malignant transformation in ulcerative colitis. They also imply that in contrast to sporadic colorectal carcinoma, ulcerative colitis-associated neoplastic progression may involve p53 inactivation at relatively early, noninvasive stages.

Chromosome Deletion↗
PubMed1993

Evolution of bacteriophage T7 in a growing plaque.

The emergence of mutants during the 10(9)-fold amplification of a bacteriophage was spatially resolved in a growing plaque. When wild-type phage T7 was grown on an Escherichia coli host which expressed an essential early enzyme of the phage infection cycle, the T7 RNA polymerase, mutant phage relying on this enzyme appeared in 10(8) phage replications and outgrew the wild type. Spatial resolution of the selection process was achieved by analyzing stab samples taken along a plaque radius. Different mutants were selected at different rates along different radii of the plaque, based on host range and restriction patterns of the isolates. The mutants deleted up to 11% of their genomes, including the gene for their own RNA polymerase. They gained an advantage over the wild type by replicating more efficiently, as determined by one-step growth cultures.

Bacteriophage T7↗
PubMed1993

Treatment of respiratory syncytial virus infection with recombinant interferon alfa-2a.

A prospective randomised, double blind, controlled trial was conducted in 52 infants to determine whether recombinant interferon alfa-2a (INF-alpha-2a) would reduce the morbidity of acute bronchiolitis and the respiratory syncytial virus shedding time. All infants had a positive direct antigen immunofluorescence test for respiratory syncytial virus. INF-alpha-2a (50,000 IU/kg/day) or placebo was administered by daily intramuscular injection for three consecutive days. Sixteen infants received INF-alpha-2a and 36 received placebo treatment. The two groups were similar in demographic characteristics and initial oxygenation. The treatment group, however, had a significantly higher overall score for severity of illness at the start of treatment. More rapid drop of the clinical score was observed in the INF-alpha-2a group after treatment in the first three days and the two groups had similar clinical severity by day 3. There was no significant difference of the duration of viral shedding in the two groups. In conclusion, the overall clinical improvement was greater in the treatment group over the first three days, but the duration of viral shedding was not altered.

Double-Blind Method↗
PubMed1993

Induction of hepatic bilirubin and drug metabolizing enzymes by individual herbs present in the traditional Chinese medicine, yin zhi huang.

Yin Zhi Huang (YZH) is a decoction of four plants which is widely used in Asia to treat neonatal jaundice. This study compares the ability of phenobarbital and the individual herbs comprising YZH, Artemisia, Gardenia, Rheum, and Scutellaria baicalensis, to induce hepatic drug and bilirubin metabolizing enzymes in rats. Herbal decoctions (30 ml/kg/day) or phenobarbital (60 mg/kg/day) were administered for 5 days. Only phenobarbital increased cytochrome P-450 levels whereas Gardenia slightly decreased levels. Artemisia, Rheum and phenobarbital increased bilirubin glucuronyl transferase activity. Glucuronidation of alpha-naphthol was increased by Gardenia and phenobarbital, whereas Artemisia and Rheum were ineffective inducers. Phenobarbital was the most effective inducer of glutathione-S-transferase (GSHT) activity. Phenobarbital and Gardenia both induced delta 5-3-ketosteroid isomerase activity, a marker for the Ya subunit of GSHT responsible for intracellular bilirubin transport in liver. The selective patterns of enzyme induction suggest potential value for using specific plant decoctions to modify drug and bilirubin metabolic pathways.

Animals↗
PubMed1992

Loss of heterozygosity involves multiple tumor suppressor genes in human esophageal cancers.

Loss of heterozygosity occurring on various chromosomes has been described in the majority of human tumors. The targets of frequent or consistent subchromosomal deletions are believed to be tumor suppressor genes. We examined 72 esophageal tumors (46 squamous cell carcinomas and 26 adenocarcinomas) for loss of heterozygosity at the p53, Rb, APC, MCC, and DCC loci. Inclusion of these tumor suppressor genes in the allelic deletions was directly ascertained by performing polymerase chain reaction at polymorphic sites within the genes. Loss of heterozygosity occurred in 55% of informative cases at p53, in 48% of informative cases at Rb, in 66% at APC, in 63% at MCC, and in 24% at DCC. Ninety-three % of tumors informative at all loci (fully informative) lost heterozygosity of at least one locus. A high percentage of fully informative tumors (71%) also lost heterozygosity at more than one locus. There were no significant differences among histological types in the prevalence of loss of heterozygosity at any locus. There were correlations of losses involving MCC versus DCC, Rb, and p53. These data suggest that (a) allelic deletions including these tumor suppressor genes are important in the formation and/or progression of most esophageal cancers; (b) allelic deletions involving MCC may not occur independently of deletions involving other tumor suppressor genes; and (c) the accumulation of multiple allelic deletions involving specific tumor suppressor genes may be important in most esophageal tumorigenesis or tumor evolution.

Adenocarcinoma↗
PubMed1992

Loss of heterozygosity involving the APC and MCC genetic loci occurs in the majority of human esophageal cancers.

The tumor suppressor gene APC was recently identified, and the cDNA was cloned from chromosome 5q21. Point mutations affecting APC are seen in the hereditary syndrome familial adenomatous polyposis, and point mutations in APC and a closely linked gene, MCC, as well as loss of heterozygosity involving chromosome 5q have been reported in sporadic colon cancer. To our knowledge, loss of heterozygosity involving APC or MCC or both has not yet been described in any other human cancer besides lung cancer. We used the polymerase chain reaction and DNA content flow cytometric nuclear sorting to examine 30 primary human esophageal cancers for loss of heterozygosity of APC or MCC or both. Loss of one allele was detected in 77% of 26 informative cases. These data suggest that loss of heterozygosity of regions on 5q including the APC and MCC genetic loci is involved in the development and/or progression of most human esophageal cancers. They imply that inactivation of APC, MCC, and/or a linked gene on chromosome 5q plays a role in the pathogenesis of some cancers of the upper gastrointestinal tract, as well as in colon cancer and familial adenomatous polyposis.

Adenocarcinoma↗
PubMed1992

Loss of heterozygosity affecting the p53, Rb, and mcc/apc tumor suppressor gene loci in dysplastic and cancerous ulcerative colitis.

Allelic deletions of tumor suppressor genes have been observed frequently in a variety of human tumors. These losses are believed to contribute to the development of human cancer. Three of the most frequently deleted chromosomal loci contain the tumor suppressor genes p53, retinoblastoma (Rb), and mcc/apc. In order to detect loss of heterozygosity (LOH) within these genes in dysplastic and cancerous ulcerative colitis, we used an application of the polymerase chain reaction. LOH affecting p53 was observed in 8 of 17 (47%) of heterozygous patients, while LOH of Rb and the mcc/apc locus was observed in 9 of 27 (33%) and 13 of 39 (33%) of heterozygotes, respectively. Among 35 patients heterozygous at 2 or more loci, LOH of p53, Rb, and/or mcc/apc was observed in 18 (51%). LOH was more common in left-sided neoplasms. These data suggest that allelic deletion of p53, Rb, mcc, and/or apc is involved in the pathogenesis and/or progression of at least a subset of colonic dysplasias and carcinomas occurring in the setting of ulcerative colitis.

Adenocarcinoma↗
PubMed1992

Glucocorticoid-mediated down regulation of c-fos mRNA in C6 glioma cells: lack of correlation with proenkephalin mRNA.

We investigate the linkage between the transcriptional factor, c-fos, and expression of proenkephalin in rat C6 glioma cells. C6 cells contained abundant levels of c-fos mRNA. Treatment of cells with dexamethasone resulted in a 10-fold decline in c-fos transcripts and a small increase in proenkephalin mRNA. Combined exposure to dexamethasone and isoproterenol also induced a decrease in c-fos mRNA while proenkephalin mRNA increased 8-fold. Treatment of the C6 cells with phorbol 12-myristate 13-acetate caused a 13-fold increase in c-fos expression 0.5 h after administration and a decrease in proenkephalin mRNA. These data indicate that c-fos and proenkephalin mRNA are not regulated in a sequential, parallel manner, that newly synthesized c-fos is not the determining factor controlling proenkephalin gene regulation, and that c-fos expression is under negative control by glucocorticoids.

Animals↗
PubMed1992

Stimulation of c-fos and c-jun gene expression and down-regulation of proenkephalin gene expression in C6 glioma cells by endothelin-1.

The linkage between the transmembrane signal transduction system utilized by endothelin and alterations in gene expression has been investigated in C6 glioma cells. Treatment of C6 cells with endothelin-1 caused a rapid and transient 5-fold increase in c-fos and c-jun mRNA levels, followed by a decrease at 4 h. Dose-response studies indicated that 1 nM endothelin-1 caused half-maximal induction of c-fos mRNA 0.5 h after treatment and that maximal induction was elicited with a concentration of 10 nM. Actinomycin D totally abolished the rapid increase in c-fos mRNA caused by endothelin, indicating that the effect is at the transcriptional level. Endothelin-1 caused a decrease in proenkephalin mRNA to 50% of control levels at 4 h after treatment and had no effect on histone H4 mRNA over a 24 h period that was examined. These data indicate that receptor binding of endothelin-1 leads to rapid changes in the expression of immediate-early response genes which may cause more prolonged changes in the expression of AP-1 and/or CREB target genes in the nervous system.

Animals↗
PubMed1992

Replication of viruses in a growing plaque: a reaction-diffusion model.

An understanding of the viral replication process commonly referred to as "plaque growth" is developed in the context of a reaction-diffusion model. The interactions among three components: the virus, the healthy host, and the infected host are represented using rates of viral adsorption and desorption to the cell surface, replication and release by host lysis, and diffusion. The solution to the full model reveals a maximum in the dependence of the velocity of viral propagation on its equilibrium adsorption constant, suggesting that conditions can be chosen where viruses which adsorb poorly to their hosts will replicate faster in plaques than those which adsorb well. Analytic expressions for the propagation velocity as a function of the kinetic and diffusion parameters are presented for the limiting cases of equilibrated adsorption, slow adsorption, fast adsorption, and large virus yields. Hindered diffusion at high host concentrations must be included for quantitative agreement with experimental data.

Bacterial Physiological Phenomena↗
PubMed1992

[Successful intrauterine digoxin therapy for fetal complete atrioventricular block with endocardial cushion defect: a case report].

We report herein a case of fetal complete atrioventricular block accompanied with endocardial cushion defect, successfully diagnosed and treated, in utero, with transplacental digitalization. A 23-year-old Japanese woman, at 20 weeks of gestation, was referred to the Maternity and Perinatal Care Unit of Kyushu University Hospital because of fetal continuous bradycardia. B-mode scanning and dual M-mode echocardiography revealed that the fetus had complete atrioventricular block with endocardial cushion defect with a ventricular rate of 60 beats per minute. At 23 weeks of gestation, it was found that the fractional shortenings (FSs) in both ventricles and the ventricular rate had decreased, with an increase in pericardial effusion. Thus, we diagnosed the fetus as having cardiac failure. Transplacental digoxin treatment was started and continued for 10 weeks, after which fetal pericardial effusion, as well as FSs ameliorated. The pregnancy was interrupted by cesarean section at 33 weeks of gestation due to a decrease in FSs with an accumulation of fetal ascites. A 1780g female infant was delivered and a pacemaker was implanted surgically, immediately after birth. She is alive and well at the time of writing.

Adult↗