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Biomedical subjects

C Clarke

Publications and source records attributed to C Clarke.

At least 109 records · Page 6Linked to original sources
PubMed1988

The first seizure in adult life. Value of clinical features, electroencephalography, and computerised tomographic scanning in prediction of seizure recurrence.

408 adults (age 16 and over) were followed up after their initial seizure. The actuarial risk of recurrence was highest in the early weeks. For those seen within the first week, the risk of recurrence was 52% by the end of 3 years. In univariate analysis, the only clinical variable that was associated with recurrence was the time of day at which the initial seizure occurred. There was a tendency, that did not reach statistical significance, for younger age (less than 50 years) and a family history of seizures of any type, including febrile convulsions, to be associated with recurrence. Such risk factors appear to be additive, so that the risk of recurrence at 1 year for a subject with all three factors is about three times that of a subject with none of them. Sex, type of seizure, and features of the electroencephalogram were not of predictive value. Computerised tomographic scanning revealed tumours in 3% of subjects, and these individuals were particularly likely to have recurrent seizures.

Adolescent↗
PubMed1988

High altitude cerebral oedema.

High altitude cerebral oedema is a severe form of acute mountain sickness occurring at heights above 4500 metres. The clinical features are of headache, impairment of consciousness and a variety of neurological signs. The condition occurs during acclimatisation and also at extreme altitudes above 7500 metres when it is often fatal. Case histories of cerebral oedema patients, pathological findings and treatment are reviewed. Other forms of altitude-related illness are also reviewed, including stroke and retinal haemorrhage.

Acetazolamide↗
PubMed1987

N-terminal methylation of proteins: structure, function and specificity.

A common site for the posttranslational modification of proteins is at the N-terminal alpha-amino group. Here we consider the enzymatic addition of one or more methyl groups that has been found to occur in several proteins. Although the methylated proteins have different overall functions, they all appear to be involved in large macromolecular structures such as ribosomes, myofibrils, nucleosomes, pilins, or flagella. Structural features at the N-termini of these methylated proteins suggest that sequences in this region may serve as recognition sites for only a few different types of methylating enzymes. Thus, we propose that three enzymes could account for the N-methylated species so far identified in bacteria, the hypothetical MAK, QP, and pilin methyltransferases, and a single additional enzyme, the hypothetical PK methyltransferase, could account for all of the alpha-amino methylations observed in eukaryotic cells. Finally, we discuss criteria that could be used in conjunction with primary sequence data to predict proteins that might be subject to methylation at their amino termini.

Amino Acid Sequence↗
PubMed1987

Neuro-steroids: 3 beta-hydroxy-delta 5-derivatives in rat and monkey brain.

The rat brain accumulates pregnenolone (P) as the unconjugated steroid, the sulfate ester (S) and fatty acid esters (L). P + PS do not disappear from rat brain after combined adrenalectomy (adx) and castration (orx). PL does not serve a source of P after adx + orx. P is metabolized by several rat brain regions to progesterone and to PL. Brain microsomes contain the acyl-transferase which converts P to PL using endogenous substrates. Brain P and dehydroepiandrosterone (D) undergo a prominent circadian variation with their acrophases at the beginning of the dark span. The circadian variation of brain D persists after adx + orx. The monkey brain (Macaca fascicularis) also accumulates P and D. Adrenal suppression with dexamethasone for 4 days does not decrease the concentrations of brain P and 3rd ventricle CSFP and D. The concentrations of brain D are decreased to a much smaller extent than plasma D. D inhibits the aggressive behavior of castrated male mice exposed to lactating female intruders. This is not the case for DS or androst-5-ene-3 beta, 17 beta-diol. The D analog 3 beta-methyl-androst-5-en-17-one, which is not estrogenic and cannot be metabolized to testosterone or estradiol, is as active as D in inhibiting the aggressive behavior of castrated mice.

Adrenal Glands↗
PubMed1987

Studies of gene transfer and reversion to mitomycin C resistance in Fanconi anemia cells.

As a first step to the cloning of the Fanconi anemia (FA) gene, we have attempted to correct the sensitivity of FA cells to DNA crosslinking agents by the introduction of wild-type DNA. The protocol involved the introduction of both genomic and pRSVneo DNA, selection for G418-resistant colonies and the subsequent selection of mitomycin C-resistant cells from the latter. Preliminary experiments indicated that untransformed FA cells were not suitable recipients for the introduction of foreign DNA, so all experiments were performed with an SV40-transformed FA cell line. Approximately 40,000 G418-resistant colonies were obtained in 5 separate experiments at an overall frequency of about 5 X 10(-4). These were then selected in mitomycin C and 15 colonies were recovered. Colonies were obtained with wild-type DNA (both human and rodent) and with FA DNA at about the same frequency of 2 X 10(-7). Colonies were isolated and shown to have a stable, partial (from 25 to 90% of wild-type) resistance to mitomycin C. One colony was also shown to be partially resistant to two other DNA crosslinking agents, diepoxybutane and nitrogen mustard. This clone also had an intermediate level of spontaneous and MMC-induced chromosome aberrations. pRSVneo, but not rodent, DNA could be demonstrated in the high molecular weight fraction of several colonies. Thus, it is likely that these colonies represent partial revertants rather than transfectants. These mitomycin C-resistant FA cells should be useful for the biochemical analysis of the FA mutation.

Anemia, Aplastic↗
PubMed1987

Variation in mortality from ischaemic heart disease between England and Scotland.

A comparison of mortality from ischaemic heart disease under the age of 60 for 1980 to 1981 between the Grampian Health Board and the North Staffordshire Health Authority has been made. A total of 993 deaths was notified by death certificate from the two areas of similar population of which 434 were from Grampian and 559 from North Staffordshire. After examination of general practitioner and hospital case notes, autopsy reports and death certificates, nearly all (532) of the North Staffordshire deaths were accepted as being due to ischaemic heart disease but only three-fifths (263) of the Grampian deaths could be substantiated as there was inadequate information for the remainder. Deaths from ischaemic heart disease seem apparently to be twofold greater in North Staffordshire than Grampian but much of this discrepancy could be attributed to a widely different autopsy rate and to unavailability of case notes. Experience of this survey suggests that the results of other epidemiological investigations may be equally or even more unreliable.

Autopsy↗
PubMed1986

Characterization of a simian virus 40-transformed Fanconi anemia fibroblast cell line.

We have characterized a SV40-transformed human fibroblast cell line (GM6914) derived from a patient with Fanconi anemia (FA) in order to establish its usefulness for biochemical and genetic experiments, including DNA-mediated gene transfer. GM6914 cells have a growth rate similar to that of SV40-transformed normal human fibroblasts and an indefinite lifespan in culture. As has been established for other FA cell types, GM6914 cells have an increased sensitivity to DNA-crosslinking agents such as mitomycin C (MMC). The D10 for GM6914 cells is 8 times lower than for equivalent controls. GM6914 cells also have an elevated frequency of spontaneous chromosome aberrations and this frequency can be increased by MMC concentrations which show no effect on control cells. Genetic complementation studies with lymphoblasts derived from two affected sibs of the donor of GM6914 cells show that GM6914 belongs to FA complementation group A. In DNA-transfection studies using plasmid pRSVneo, colonies of GM6914 cells resistant to the drug G-418 were observed at frequencies ranging from 1.7 to 16 X 10(-4), values similar to those observed with several other SV40-transformed human cell lines. GM6914 should be a useful recipient cell line in experiments using DNA-mediated gene transfer to clone the normal allele of the gene which is defective in FA complementation group A. GM6914 would also be an excellent cell line for studies on mutagenesis, recombination and repair using plasmid vectors.

Anemia, Aplastic↗