4,807 research outputs found
Human papillomavirus type 18 is associated with less apoptosis in fibroblast tumours than human papillomavirus type 16.
In human cervical neoplasia human papillomavirus (HPV) type 18 has a higher cancer/cervical intraepithelial neoplasia (CIN) prevalence ratio than HPV 16. Fibrosarcomas derived from rat fibroblasts transfected with HPV 16 or 18 genomes showed increased apoptosis compared with controls. However, HPV 18 was associated with significantly less apoptosis than HPV 16, affording one possible explanation for the more rapidly progressive cervical neoplasia associated with HPV 18
Apoptosis: A Basic Biological Phenomenon with Wide-ranging Implications in Tissue Kinetics
The term apoptosis is proposed for a hitherto little recognized mechanism of controlled cell deletion, which appears to play a complementary but opposite role to mitosis in the regulation of animal cell populations. Its morphological features suggest that it is an active, inherently programmed phenomenon, and it has been shown that it can be initiated or inhibited by a variety of environmental stimuli, both physiological and pathological
Magnetocardiography with a modular spin-exchange relaxation free atomic magnetometer array
We present a portable four-channel atomic magnetometer array operating in the
spin exchange relaxation-free regime. The magnetometer array has several design
features intended to maximize its suitability for biomagnetic measurement,
specifically foetal magnetocardiography, such as a compact modular design, and
fibre coupled lasers. The modular design allows the independent positioning and
orientation of each magnetometer, in principle allowing for non-planar array
geometries. Using this array in a magnetically shielded room, we acquire adult
magnetocadiograms. These measurements were taken with a 6-11 fT Hz^(-1/2)
single-channel baseline sensitivity that is consistent with the independently
measured noise level of the magnetically shielded room.Comment: 15 pages, 5 figure
Susceptibility to apoptosis is differentially regulated by c-myc and mutated Ha-ras oncogenes and is associated with endonuclease availability.
Oncogenes and oncosuppressors can deregulate cell replication in tumours, and recently have been shown to influence the probability of apoptosis. The effects of human c-myc and mutated (T24) Ha-ras oncogenes on susceptibility to apoptosis were investigated by introducing them into immortalised rat fibroblasts. The resulting family of transfectants showed closely similar measures of proliferation, but widely divergent rates of apoptosis, differing by up to fifteen-fold, that correlated inversely with population expansion rates in vitro. T24-ras transfectants with moderate or high p21ras expression showed reduced apoptosis, and this was reversed by pharmacological inhibition of membrane localisation of p21ras by mevinolin. In contrast, c-myc stimulated apoptosis, and this was further enhanced by serum deprivation. Inducibility of effector proteins represents one possible mechanism of genetic control of the susceptibility to apoptosis, and its investigation showed that c-myc was associated with expression by viable cells of latent calcium/magnesium sensitive endonuclease activity characteristic of apoptosis. In contrast, endonuclease activity was not detected in viable cells of a T24-ras transfectant expressing high levels of p21ras. Thus, there appeared to be differential regulation of susceptibility to apoptosis, positively by c-myc and negatively by activated ras, and this was associated with availability of endonuclease activity. Genetic modulation of apoptosis in human neoplasms is likely to influence net growth rate, retention of cells acquiring new mutations and response to certain chemotherapeutic agents
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