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Y Ning

Publications and source records attributed to Y Ning.

71 records · Page 4Linked to original sources
PubMed1993

Highly polymorphic tetramer repeat (GATA)n on human chromosome 11p15.3.

A tetrameric repeat sequence (GATA)n was identified by random DNA sequencing of chromosome 11-specific cosmid clones and located at 11p15.3 by fluorescence in situ hybridization. Oligonucleotide primers flanking the repetitive unit were used to amplify the DNA using the polymerase chain reaction (PCR) and this repetitive element was shown to be highly polymorphic and inherited in typical Mendelian fashion. Analysis of amplification products containing the repetitive element from 45 unrelated Caucasian individuals and five families showed at least five alleles at this locus, ranging from 227 to 249 bases in length. This polymorphism may serve as a useful PCR-detectable genetic marker for 11p15.3, a landmark for disease gene isolation, and a locus for identity testing.

Alleles↗
PubMed1992

Heterozygote detection through bleomycin-induced G2 chromatid breakage in dyskeratosis congenita families.

We determined the mean number of chromatid breaks per cell (b/c) in the bleomycin-treated lymphocytes of 10 patients with dyskeratosis congenita (DC) and 26 of their relatives to ascertain whether bleomycin sensitivity would distinguish DC heterozygotes from normal individuals. We observed a significantly higher mean number of chromatid b/c in DC patients and obligate heterozygotes (patients versus controls, p less than 0.0001; heterozygotes versus controls, p = 0.0076, Mann-Whitney rank-sum test). Unequivocal heterozygote detection was not possible owing to overlap of the b/c values of patients, heterozygotes, and controls, but our findings provided strong evidence of a link between autosomal recessive as well as X-linked recessive DC mutations and bleomycin sensitivity in homozygous, hemizygous, and heterozygous individuals.

Adolescent↗
PubMed1992

Why are transformed cells immortal? Is the process reversible?

Normal cells have finite proliferative potential in culture. In contrast, cells derived from tumors immortalized by chemical carcinogens or viruses are able to divide indefinitely. A question of major importance is the mechanism that limits the proliferative potential of normal cells, and conversely, the process by which immortal cells have escaped irreversible growth cessation. To address this question we fused a number of different normal human fibroblast cell lines with various immortal human cell lines and determined the proliferative behavior of the resulting hybrids. In all cases the hybrids had a limited ability to proliferate in culture. These results suggested that the finite proliferative capacity of normal human cells was dominant and that immortal cells had acquired recessive changes in their genetic program, which allowed them to escape senescence. We were also able to assign approximately 30 immortal human cell lines to four complementation groups for indefinite division.

Animals↗
PubMed1992

Isolation of monochromosomal hybrids following fusion of human diploid fibroblast-derived microcells with mouse A9 cells.

Rodent x human hybrids containing single human chromosomes are valuable tools in the study of human genetics. Using a retrovirus carrying the neomycin gene, we generated a neomycin-resistant (neor) pool of human diploid fibroblasts. Following fusion of microcells prepared from this pool to mouse A9 cells, we obtained four neor hybrids containing a single human chromosome 2, 3, 5, or 15.

Animals↗
PubMed1991

Genetic analysis of indefinite division in human cells: evidence for a cell senescence-related gene(s) on human chromosome 4.

Earlier studies had demonstrated that fusion of normal with immortal human cells yielded hybrids having limited division potential. This indicated that the phenotype of limited proliferation (cellular senescence) is dominant and that immortal cells result from recessive changes in normal growth-regulatory genes. In additional studies, we exploited the fact that the immortal phenotype is recessive and, by fusing various immortal human cell lines with each other, identified four complementation groups for indefinite division. Assignment of cell lines to specific groups allowed us to take a focused approach to identify the chromosomes and genes involved in growth regulation that have been modified in immortal cells. We report here that introduction of a normal human chromosome 4 into three immortal cell lines (HeLa, J82, T98G) assigned to complementation group B resulted in loss of proliferation and reversal of the immortal phenotype. No effect on the proliferation potential of cell lines representative of the other complementation groups was observed. This result suggests that a gene(s) involved in cellular senescence and normal growth regulation resides on chromosome 4.

Base Sequence↗
PubMed1991

Tumor suppression by chromosome 11 is not due to cellular senescence.

Previous hybrid studies involving fusion of normal with immortal human cells indicated that the phenotype of cellular senescence is dominant and that immortality results from recessive changes in normal growth regulatory genes. We have further assigned 28 different immortal human cell lines to at least four complementation groups for indefinite division. In order to identify the chromosomes involved in regulating cell proliferation, we have introduced single human chromosomes by microcell fusion into immortal human cells representative of the different complementation groups. Our results demonstrate that the introduction of chromosome 11, implicated in tumor suppression, does not cause cellular senescence in three different immortal human cell lines tested.

Animals↗
PubMed1991

Prenatal diagnosis of mucopolysaccharidosis by continuous, monodimensional electrophoresis of amniotic fluid glycosaminoglycans.

A continuous dimensional electrophoretic method was used in 15 urine samples of clinically diagnosed mucopolysaccharidoses I or IV. Twelve of the 15 were glycosaminoglycans band positive. Of the 12 one was KS band positive but methyl toluidine blue test was negative. The other 11 were positive with both methods. Prenatal diagnosis was done in 10 cases during their next pregnancy with the same method on the amniotic fluid. Two affected fetuses were diagnosed and proved, one after induced abortion and the other after full-term delivery.

Amniotic Fluid↗
PubMed1990

Hybrids from fusion of normal human T lymphocytes with immortal human cells exhibit limited life span.

A number of normal human cell types have been shown to exhibit cellular senescence in vitro. We and others had found that fusion of normal human fibroblasts with immortal human cells yielded hybrids having limited lifespan. This indicated that the phenotype of cellular senescence is dominant and that immortality results from recessive changes in genes involved in growth control. They also supported the hypothesis that senescence results from genetic mechanisms rather than random damage. Since T lymphocytes are a highly differentiated cell type, in contrast to fibroblasts, it was of interest to determine whether similar mechanisms caused senescence in the T cells. We therefore fused normal human T lymphocytes with an immortal human cell line to determine whether they could restore the senescent, nondividing phenotype in hybrids, as do normal human fibroblasts. Eleven of fifteen hybrid clones studied exhibited limited proliferative potential after achieving a range of population doubling similar to that observed in the cell fusion studies involving normal fibroblasts. These results provide evidence that cellular senescence in T lymphocytes occurs via genetic mechanisms.

Adult↗
PubMed1990

Study on BcII/St14 RFLPs in Chinese for DNA diagnosis for hemophilia A.

The BcII polymorphism within DXS52 (St14) was reported. It was composed of 4 allelic fragments, 4.0 kb, 3.3 kb, 3.0 kb and 2.3 kb. The frequency of these fragment were 0.09, 0.12, 0.44 and 0.35 respectively in the Chinese. The polymorphism provided the PIC of 0.66. DNA analysis of families with hemophilia A showed that the confidence of the RFLPs was the same as the TaqI/St14 RFLPs and for carrier detection the former is much better than that of the TaqI/St14 RFLPs.

China↗
PubMedDate not supplied

Molecular genetic studies of cellular senescence.

The limited doubling potential of normal cells in culture was first proposed as a model for cellular aging by Hayflick in 1961. This phenomenon of in vitro cellular senescence is now well documented for a number of different normal human cell types. In an attempt to determine whether random events or programmed genetic processes were responsible for cellular aging, we performed a series of cell fusion studies. We determined that hybrids from fusion of normal with immortal human cells had limited proliferative potential, indicating that senescence is a dominant phenotype. We exploited the fact that immortality was recessive to assign a large number of different immortal human cell lines to four complementation groups for indefinite division. More recently, we have determined that the introduction of a single normal human chromosome 4 into HeLa (cervical carcinoma) cells by microcell fusion induced senescence in this immortal line. The results of these whole cell and microcell fusion studies support the hypotheses that propose senescence results from active, genetic mechanisms.

Cell Division↗
PubMedDate not supplied

Molecular genetic approaches to the study of cellular senescence.

Normal cells in culture exhibit limited division potential, which is used as a model for cellular aging. In contrast, tumor-derived, carcinogen- or virus-transformed cells are capable of dividing indefinitely (immortal). Fusion of normal with immortal human cells yielded hybrids having limited life span, indicating that cellular senescence is a dominant phenotype and that immortality is recessive. Fusions of various immortal human cell lines with each other led to the identification of four complementation groups for indefinite division. In order to identify the chromosomes and genes involved in growth regulation, that had been modified in immortal cells, we used the technique of microcell fusion to introduce either a normal human chromosome 11 or 4 into cell lines representative of the different complementation groups. Chromosome 11 had no effect on the in vitro life span of the different immortal human tumor lines. However, when a normal human chromosome 4 was introduced into cell lines assigned to complementation group B, the cells lost the immortal phenotype. No effect on the proliferation potential of cell lines representative of the other complementation groups was observed. These results suggest that a gene(s) on human chromosome 4 has been modified in immortal cell lines assigned to complementation group B, to allow escape from senescence. They also provide evidence for a genetic basis for cellular aging.

Animals↗
PubMedDate not supplied

An epidemiological analysis of leprosy from 1951-1996 in Sichuan.

Through the leprosy surveillance system established in 1990s the authors analysed the epidemiology of leprosy in Sichuan province from 1951 to 1996. By the end of 1996, the total number of registered cases was 32,772, the peak incidence rate (2.44/100,000) was in 1958. The annual average progressively decreasing speed (AAPDS) of the number of new cases, incidence rate, incidence rate among children, number of newly detected patients, detection rate, number of registered cases and registered prevalence rates were 4.7% (xg = 0.9534), 5.9% (xg = 0.9407), 7.4% (xg = 0.9263), 6.7% (xg = 0.9326), 8.1% (xg = 0.9195), 10.9% (xg = 0.8913) and 11.7% (xg = 0.8828) respectively. Among newly detected cases, the proportion of children gradually declined with an AAPDS of 2.9% (xg = 0.9712), but that of household contacts gradually increased, showing a gradual decline of source of infection. The multibacillary (MB) rate among new cases, newly registered cases and active cases also increased gradually. The MB rate among child cases was much lower than that among adults. The disability rates among newly registered cases tended to decline. The peak incidence was in the 20 to 35 years age group, the average age at onset being 31.92 years. Average age at onset gradually increased to 34.19 during 1991-1995. The average interval between onset of symptoms and diagnosis was 4.89 years and that had reduced gradually to 3.24 years during 1991-1995. The authors conclude that: (1) the epidemiological trend of leprosy in Sichuan province shows decline; (2) the case-finding activities have improved and intensified; but (3) the disability rate among newly detected cases is still high (> 20%) and the average delay in diagnosis is still too long, showing that early case finding is still not satisfactory.

Adolescent↗