Search PubMed⌕ Search

Biomedical subjects

S J Martin

Publications and source records attributed to S J Martin.

At least 163 records · Page 9Linked to original sources
PubMed1970

Malpractice.

Explore the source record for details and available documents.

Humans↗
PubMed1968

A study of the heterogeneous 37S ribonucleic acid induced by foot-and-mouth-disease virus.

1. The 37s RNA induced in baby-hamster kidney cells by infection with foot-and-mouth-disease virus was examined on sucrose gradients and by filtration through Sepharose 4B. 2. The RNA sedimented faster (37s) and as a broader band than the 35s RNA from purified virus. 3. Treatment with deoxyribonuclease, Pronase or amylase did not alter the sedimentation profile of the 37s RNA. 4. Treatment of individual fractions of the RNA with phenol, dimethyl sulphoxide or methylCellosolve did not decrease the sedimentation rate of the faster-sedimenting molecules. 5. Sedimentation in sucrose gradients of different ionic strengths or containing EDTA had no effect on the heterogeneous nature of the profile. 6. On filtration through Sepharose 4B columns, the 37s virus-induced RNA was eluted before viral RNA. 7. Only 20% of the rapidly sedimenting RNA was incorporated into complete virus particles.

Animals↗
PubMed1967

Synthesis of ribonucleic acid in baby-hamster kidney cells in the presence of actinomycin D.

1. RNA molecules with sedimentation values in sucrose gradients of 12-20s are synthesized in baby-hamster kidney cells even after prolonged incubation in medium containing 1mug. of actinomycin D/ml. 2. The rate of formation of this RNA is dependent on the age of the cultures and is greatest during the exponential phase of growth. 3. Growth of cells on nutritionally poor medium causes degradation and inhibits the synthesis of these RNA fractions. 4. Replacement of the nutritionally poor medium with a rich medium stimulates the synthesis of actinomycin-resistant RNA. This stimulation is blocked by cycloheximide. 5. The base composition of this RNA is characterized by low cytidine and high guanosine values.

Journal Article↗
PubMed1967

Effect of virus infection on the stability and synthesis of actinomycin-resistant ribonucleic acid in baby-hamster kidney cells.

1. The sucrose-gradient pattern of (32)P-labelled RNA synthesized in actinomycintreated baby-hamster kidney cells infected with foot-and-mouth-disease virus depends greatly on the period of labelling. 2. Fractions are formed in infected cells that sediment at 12-20s and have the same base composition as similar fractions found in non-infected cells that have been treated with actinomycin. 3. In the presence of guanidine, which completely inhibits viral RNA synthesis, these fractions are labelled to a greater extent than in non-infected cells.

Journal Article↗
PubMed1966

Thermal stability of ribosomal ribonucleic acid from baby hamster kidney cells.

1. RNA has been prepared from baby hamster kidney cells by extraction with a phenol-EDTA mixture and further purified by passing through a column of Sephadex G-25 that had been equilibrated with water. 2. Aging of the total RNA extracts at 4 degrees or heating at 95 degrees followed by rapid cooling caused a conversion of 28s RNA into material sedimenting in sucrose gradients at approx. 18s. 3. When heated RNA was re-extracted with phenol the sedimentation profile was not returned to that of the unheated RNA. 4. The 28s and 18s RNA fractions were collected separately from sucrose gradients by precipitation with 2vol. of ethanol and passed through a Sephadex G-25 column equilibrated with water. 5. Heat treatment of purified 28s RNA at 95 degrees caused the sedimentation coefficient to increase to approx. 40s, whereas similar treatment of 18s RNA caused no significant increase. If the RNA was heated before the Sephadex G-25 treatment the sedimentation coefficient of the 28s and 18s RNA decreased to approx. 12s and 8s. 6. Heating mixtures of purified 28s and 18s RNA at 95 degrees caused some aggregation of 18s material with the 28s fraction.

Journal Article↗
PubMedDate not supplied

A learning deficit related to age and beta-amyloid plaques in a mouse model of Alzheimer's disease.

Mice that overexpress the human mutant amyloid precursor protein (hAPP) show learning deficits, but the apparent lack of a relationship between these deficits and the progressive beta-amyloid plaque formation that the hAPP mice display is puzzling. In the water maze, hAPP mice are impaired before and after amyloid plaque deposition. Here we show, using a new water-maze training protocol, that PDAPP mice also exhibit a separate age-related deficit in learning a series of spatial locations. This impairment correlates with beta-amyloid plaque burden and is shown in both cross-sectional and longitudinal experimental designs. Cued navigation and object-recognition memory are normal. These findings indicate that A beta overexpression and/or A beta plaques are associated with disturbed cognitive function and, importantly, suggest that some but not all forms of learning and memory are suitable behavioural assays of the progressive cognitive deficits associated with Alzheimer's-disease-type pathologies.

Aging↗
PubMedDate not supplied

Neuropathology and neurovirulence of canine distemper virus plaque isolates in the hamster.

The relationship between neuropathological abnormalities, antibody response and neurovirulence of plaque isolates has been studied in an experimental model of canine distemper in the hamster. Genetic virus variance influenced neurovirulence and the experimental evidence supports the hypothesis that the mechanism of this effect may be through the modulating effect of circulating antibody. Large plaque virus (LPV) produced severe encephalitis with little early antibody response and a high degree of pathological abnormality. Small plaque virus (SPV) produced mild chronic encephalitis and early antibody response. Microscopically, histological abnormalities in this group were qualitatively similar to those seen with LPV but generally of lesser degree. Immunosuppression in SPV infected animals increased the severity of the encephalitis, reflected by the increase in inflammation and inclusion formation. Combined SPV and LPV infection produced high antibody levels and less severe disease than LPV infection alone with an intermediate pattern of histological abnormality.

Animals↗
PubMedDate not supplied

Cell death via apoptosis and its relationship to growth, development and differentiation of both tumour and normal cells.

Cell death can occur by two possible mechanisms, necrosis or apoptosis. Necrosis is the classically recognised form of cell death and is characterised by high amplitude swelling of the mitochondria, nuclear flocculation and uncontrolled cell lysis. Tissue necrosis is normally seen following severe trauma to cells. The alternative form of cell death is via a programmed sequence of events and is termed apoptosis. Apoptosis occurs under a variety of physiological conditions and cells dying by this process undergo cytoplasmic and nuclear condensation, coupled with cleavage of the cell's DNA into nucleosome size fragments. DNA cleavage is due to the activation of a specific endogenous endonuclease. The cell finally fragments into apoptotic bodies which are engulfed by neighbouring cells and degraded. Apoptosis is an energy requiring process requiring intact energy generating systems, unlike that of necrosis. In relation to malignant disease, apoptosis is the mechanism by which cytotoxic T cells kill tumour target cells; it may also be the mechanism which accounts for the high loss of cells in growing tumour masses. Extensive apoptosis is seen in regressing tumours and also in those treated with chemotherapeutic agents. This form of death may require the activation of specific death genes, although in view of work carried out in this and other laboratories, demonstrating that inhibitors of both protein and RNA synthesis will readily induce apoptosis, this may not be universal. Finally, apoptosis has far reaching implications for the treatment of malignant disease, since only by understanding how cells die will be able to develop more effective means of killing them.

Animals↗