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Y K Fung

Publications and source records attributed to Y K Fung.

87 records · Page 5Linked to original sources
PubMed1981

On the mechanism of retrovirus-induced avian lymphoid leukosis: deletion and integration of the proviruses.

There is considerable evidence that infection by avian lymphoid leukosis viruses can led to tumor development in the target organ of the host. The mechanism by which virus-induced oncogenic transformation occurs, however, is not clearly understood. As a first step toward deciphering this process, we have characterized the proviruses of the lymphoid leukosis viruses in DNAs extracted from the leukotic and metastatic tumors by using restriction enzyme digestion and filter hybridization analysis with radioactive probes specific for the infecting genome. Our results indicate (i) that lymphoid leukosis tumors are clonal in origin; (ii) that there are multiple sites in the cellular genome of the target tissue where the virus DNA can integrate and that, in the majority of the tumors, at least one such site of each tumor is adjacent to a cellular sequence related to the oncogene of MC-29 virus; and (iii) that deletions and other structural alterations in the proviral DNA may facilitate tumorigenesis.

Animals↗
PubMed1981

Synthesis of plus strands of retroviral DNA in cells infected with avian sarcoma virus and mouse mammary tumor virus.

The vast majority of plus strands synthesized in quail cells acutely infected with avian sarcoma virus were subgenomic in size, generally less than 3 kilobases (kb). A series of discrete species could be identified after agarose gel electrophoresis by annealing with various complementary DNAs, indicating specificity in the initiation and termination of plus strands. The first plus strand to appear (within 2 h postinfection) was similar in length to the long redundancy at the ends of linear DNA (0.35 kb), and it annealed with complementary DNAs specific for the 3' and 5' termini of viral RNA (Varmus et al., J. Mol. Biol. 120:50-82, 1978). Several subgenomic plus-strand fragments (0.94, 1.38, 2.3, and 3.4 kb) annealed with these reagents. At least the 0.94- and 1.38-kb strands were located at the same end of linear DNA as the 0.35-kb strand, indicating that multiple specific sites for initiation were employed to generate strands which overlapped on the structural map. We were unable to detect RNA liked to plus strands isolated as early as 2.5 h postinfection; thus, the primers must be short (fewer than 50 to 100 nucleotides), rapidly removed, or not composed of RNA. To determine whether multiple priming events are a general property of retroviral DNA synthesis in vivo, we also examined plus strands of mouse mammary tumor virus DNA in chronically infected rat cells after induction of RNA and subsequent DNA synthesis with dexamethasone. In this case, multiple, discrete subgenomic DNA plus strands were not found when the same methods applied to avian sarcoma virus DNA were used; instead, the plus strands present in the linear DNA of mouse mammary tumor virus fell mainly into two classes: (i) strands of ca. 1.3 kb which appeared early in synthesis and were similar in size and genetic content to the terminally repeated sequence in linear DNA; and (ii) plus strands of the same length as linear DNA. A heterogeneous population of other strands diminished with time, was not found in completed molecules, and was probably composed of strands undergoing elongation. These two retroviruses thus appear to differ with respect to both the number of priming sites used for the synthesis of plus strands and the abundance of full-length plus strands. On the other hand the major subgenomic plus strand of mouse mammary tumor virus DNA (1.3 kb) is probably the functional homolog of a major subgenomic plus strand of avian sarcoma virus DNA (0.35 kb). The significance of this plus strand species is discussed in the context of current models which hold that it is used as a template for the completion of the minus strand, thereby generating the long terminal redundancy.

Animals↗
PubMed1980

Effect of calcium on locomotor activity of mice.

Intracerebroventricular administration of calcium severely depressed the locomotor activity of unanesthetized mice, producing ataxic gait and motor incoordination. Pretreatment with pentobarbital (30 mg/kg, IP) twice daily for 2 and 6 days partially reversed this effect of calcium, suggesting that calcium and pentobarbital may in part exert their depressant effect by a similar mechanism.

Animals↗
PubMed1980

The effect of dopamine uptake blocking agents on the amphetamine-induced circling behavior in mice with unilateral nigro-striatal lesions.

The effects of the dopamine (DA) uptake blocking agents, benztropine, cocaine, nomifensine and mazindol, were studied on the amphetamine-induced circling behavior in mice that received a unilateral nigro-striatal lesion with 6-hydroxydopamine. When administered intrastriatally to these animals, none of the DA uptake inhibitors elicited net circling. However, they inhibited circling induced by amphetamine. In contrast, these agents had no effect on the circling produced by apomorphine in mice that received an electrolytic lesion destroying one striatum. In biochemical studies in vitro, all of the DA uptake blocking agents inhibited the stimulatory effects of amphetamine on [3H]DA synthesis and release in mouse striatal slices. In contrast to the DA uptake blocking agents, ethylene glycol bis(beta-aminoethyl ether)N,N'-tetraacetic acid (EGTA), which also inhibited amphetamine-induced circling, only inhibited the amphetamine-stimulated [3H]DA synthesis. EGTA did not inhibit the amphetamine-induced increase in the percentage of newly synthesized DA released into the medium. However, EGTA and the uptake blocking agents reduced the amount of [3H]DA found in the medium in the presence of amphetamine. If the amount of [3H]DA released into the medium in vitro reflects the amount of DA released from nerve terminals in the striatum in vivo then the inhibitory effect of the uptake blocking agents and EGTA on [3H]DA synthesis and/or release induced by amphetamine could account for their inhibitory effects on amphetamine-induced circling.

Animals↗
PubMedDate not supplied

Inhibition by bromoestrogens of the effects of estradiol on apomorphine-induced climbing behavior.

The chronic administration of estrogens to mice or rats will result in antidopaminergic effects. Apomorphine-induced climbing behavior in mice, the result of direct stimulation of dopamine receptors in the striatal and mesolimbic regions, is a simple animal model for examining these antidopaminergic effects of estrogens. Bromoestrogens, inhibitors of catechol estrogen formation, have been utilized in order to examine the role of estrogen metabolism in dopaminergic antagonism. Mice were pretreated for 3 days with 2-bromoestradiol, 4-bromoestradiol, or 2,4-dibromoestradiol dibenzoates alone or in combination with estradiol benzoate prior to apomorphine administration. The haloestrogens did not alter the climbing-induced responses elicited by apomorphine, whereas estradiol benzoate clearly attentuated the actions of apomorphine. Furthermore, the bromoestradiol dibenzoates were effective in reversing the effects of estradiol benzoate when the two steroids (estradiol benzoate and a bromoestrogen dibenzoate) were administered simultaneously during pretreatment. Thus, the bromoestrogens are able to inhibit the antidopaminergic effects of estradiol exhibited in the apomorphine-induced mouse climbing model.

Animals↗
PubMedDate not supplied

Mode of proviral activation of a putative mammary oncogene (int-1) on mouse chromosome 15.

Most mammary carcinomas induced in C3H mice by the mouse mammary tumour virus (MMTV) bear a new proviral insertion within a highly conserved locus on chromosome 15 called int-1. A transcriptional unit within this locus is inactive in all tested normal tissues but expressed at low levels in mammary tumours with proviral insertions positioned on either the 5' and 3' sides of the gene. Transcription of the proviruses proceeds away from int-1; thus an indirect mechanism appears to activate expression of this putative oncogene.

Animals↗
PubMedDate not supplied

Effects of nitrous oxide exposure on behavioral changes in mice.

This study was designed to examine the effects of continuous exposure to low levels of nitrous oxide on several behavioral paradigms and the occipital cortex cells of mice. Different groups of mice were exposed to air or two different levels of nitrous oxide (1000 ppm or 2000 ppm) 8 hr/day for eight consecutive days. The exposure to nitrous oxide was achieved by placing animals in a specially designed, enclosed chamber. At the end of the exposure period, all mice were tested for motor coordination, locomotor activity, stereotypic behavior and anxiety level. Cellular examination of the occipital cortex was conducted by counting both the larger neural cells and the smaller neuroglial cells in a specific region. Our results indicated that animals showed no deficit in motor coordination or anxiety level. Histological examination indicated no significant difference in the number of neural cells, neuroglial cells, or total cells counted in the control tissue, as compared to the neural tissue from mice exposed to nitrous oxide. Nitrous oxide-exposed mice showed reduced locomotor activity compared to control animals; however, with the exception of one time period, this decrease was not statistically significant. Animals exposed to nitrous oxide showed a dose-dependent reduction in stereotypic behavior. Our results suggest that short-term exposure to trace levels of nitrous oxide might alter central dopaminergic neuronal activities in striatal and mesolimbic regions. Further research in this area is needed to provide more information regarding the potential effects of repeated exposure to low levels of nitrous oxide. (Pediatr Dent 15:93-98, 1993).

Analysis of Variance↗
PubMedDate not supplied

Mercury determination in nursing home patients with Alzheimer's disease.

Trace-element neurotoxicity contributing to the development of Alzheimer's disease (AD) may be an important etiologic factor for this disorder. This clinical study was conducted to determine the urine concentrations of mercury (Hg) from patients with AD disorders. Within the confines of a nursing home, all subjects were exposed to the same environment and a diet that excluded seafood. The results of this study do not indicate that subjects with AD have a greater body burden of Hg, according to urinary excretion. This can be further evidence that Hg from amalgam restorations or diet is not related to etiology and pathogenesis of AD.

Aged↗