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Biomedical subjects

I Robinson

Publications and source records attributed to I Robinson.

At least 37 records · Page 2Linked to original sources
PubMed1995

Leucocyte interleukin-1-like activity in the common seal (Phoca vitulina) and grey seal (Halichoerus grypus).

Interleukin-1 (IL-1) is an important cytokine with predominantly proinflammatory activities, which have been characterized in many mammals. This study showed the production of IL-1-like bioactivity by cultured seal leucocytes. Increasing concentrations of lipopolysaccharide (LPS) (0-1 micrograms/ml) stimulated an increase in measurable IL-1-like activity in cell culture supernates. This activity increased for the first 24 h after LPS stimulation and the substance responsible had an apparent molecular weight of 17 kDa on gel filtration, similar to that described for other species. Specificity of the bioassay used was confirmed by blocking the bioactivity with an IL-1 receptor antagonist (IL-1 ra).

Animals↗
PubMed1994

Rising amyotrophic lateral sclerosis mortality in France 1968-1990: increased life expectancy and inter-disease competition as an explanation.

Gompertzian analysis is a statistical technique which has been successfully applied to the analysis of amyotrophic lateral sclerosis (ALS) mortality in England and Wales, Japan and the United States. This paper analyses the consistent trend of rising ALS mortality in France over the years 1968-1990, a period during which crude mortality rose from 400 deaths in 1968 to 950 deaths in 1990. The findings indicate that age-specific mortality rates have risen at ages older than 54 years for men and 53 years for women and decreased slightly at younger ages. The evolving ALS mortality pattern is attributable to changing inter-disease competition resulting from the increased life expectancy of the French population, rather than to changing environmental aetiopathogenic factors or to substantial artefact effects.

Adolescent↗
PubMed1994

Longitudinal analysis of amyotrophic lateral sclerosis mortality in Norway, 1966-1989: evidence for a susceptible subpopulation.

Mortality from amyotrophic lateral sclerosis (ALS) in Norway has increased substantially over the last two or three decades, as it has in other Western nations. The reasons for this general increase are not clear, but the rise has been attributed to increasing exposure to a broad range of environmental agents. Our previous research has indicated that another explanation for the substantial rise in ALS mortality is more likely to be valid. In particular, the mortality rate curve for ALS is consistent with deaths being confined to an inherently susceptible subpopulation. The size of susceptible subpopulations and mortality rates within them have been shown to be consistent in England and Wales, Japan and the United States. The same methods have been used to analyse Norwegian mortality data. The analysis demonstrates that the rise in ALS mortality is real and that the cause of the increase is almost entirely attributable to the increasing life expectancy of the Norwegian population. Increased life expectancy, a consequence of decreasing general mortality, allows ALS susceptible individuals to survive to the ages at which ALS is expressed. As in other national populations, it is expected that mortality from the disease will continue to increase with continuing increases in life expectancy.

Adolescent↗
PubMed1994

Rising mortality from motor neurone disease in Sweden 1961-1990: the relative role of increased population life expectancy and environmental factors.

Recent studies of mortality from motor neurone disease (MND) in Sweden have demonstrated rising levels of mortality from the disease, especially amongst older age groups. Case-control investigations have suggested that certain environmental factors are significantly related to variations in mortality from the disease, and are associated with a probable individual susceptibility to MND. This study applies an innovative epidemiological technique to longitudinal and cohort analysis of Swedish mortality from MND during the period 1961 to 1990. Survival modelling shows that a subpopulation susceptible to MND exists in Sweden, as has been demonstrated in other countries. The increased life expectancy of the Swedish population since 1961 has resulted in more of that susceptible population living to the ages at which MND is expressed, explaining the majority of the increase in mortality from the disease. However, environmental factors may play a role in accelerating the course of MND and may affect the timing of death within the susceptible sub-population.

Adolescent↗
PubMed1994

Closet hypoglycemia.

An elderly nondiabetic woman was found stuporous and unresponsive at home. In the emergency department, testing revealed that she had a serum glucose of 40 mg/dL (2.2 mmol/L). No underlying metabolic cause could be determined. An inspection of her medications disclosed a professional medication sample bottle labeled as containing a nonsteroidal anti-inflammatory drug (NSAID) that actually contained chlorpropamide tablets. Drugs, notably sulfonylureas, must be considered as a possible cause of unexplained severe hypoglycemia.

Aged↗
PubMed1993

The use of monoclonal antibodies specific for seal immunoglobulins in an enzyme-linked immunosorbent assay to detect canine distemper virus-specific immunoglobulin in seal plasma samples.

A method is described for the measurement of antigen-specific immunoglobulin in seal pup plasmas. Four monoclonal antibodies (H1a, H13a, H24b and H49a) raised against grey seal (Halichoerus grypus) immunoglobulin were used in an ELISA procedure. Levels of canine distemper virus (CDV) specific macroglobulin (IgM like protein) were found to peak approximately 10 days after the first vaccination. Levels of other smaller CDV-specific immunoglobulins (IgG like protein) also increased after vaccination. Using immunoblotting the CDV specific IgG-like protein reacted with a CDV protein, having a molecular weight of approximately 75 kDa.

Animals↗
PubMed1993

A new analysis of mortality from motor neurone disease in Japan, 1950-1990: rise and fall in the postwar years.

Recent studies have demonstrated a worldwide rise in mortality from motor neurone disease (MND). However, in Japan mortality appears to have fallen significantly since the late 1960s, especially amongst women. Studies of the cause of both the worldwide rise, and the unique decline in MND mortality in Japan, have largely failed to substantiate the role of any single factor, or group of factors in these phenomena. Modelling the relationship between age and mortality using gompertzian analysis has already shown that the rise in MND mortality in England and Wales, and the United States, is mainly the result of increased longevity and decreasing competition from other causes of death amongst a susceptible subpopulation. Employing the same techniques on Japanese mortality data from 1950 to 1990 demonstrates that an unusual and accelerated increase of mortality occurred in the 1950s and 1960s, probably caused by an earlier unknown but extremely potent environmental agent or agents. This premature depletion of the susceptible subpopulation resulted subsequently in a lower than expected mortality rate. Mortality is now rising slowly to expected levels as the size of the susceptible subpopulation recovers to reach the ages at which MND is normally expressed. Further substantial rises in mortality are anticipated in future decades.

Adolescent↗
PubMed1993

Static and dynamic models of interdisease competition: past and projected mortality from amyotrophic lateral sclerosis and multiple sclerosis.

Longitudinal Gompertzian analysis is an effective method for determining both the pure probability of death for a given condition and the size of inherently susceptible subpopulations [1]. Gompertzian analysis has been used in this study to provide the parameters necessary to construct a stationary population lifetable (static model) of mortality for amyotrophic lateral sclerosis (ALS) and for multiple sclerosis (MS). The static model demonstrates the relative effect of changing general mortality upon the mortality from each specific disease in a situation where interdisease competition is continuously changing. In order to represent mortality in a real population more closely (where age structure is not the result of mortality rates alone) a dynamic model was constructed for both conditions using the age distributions of the population of England and Wales. The quality of the model was verified by comparison of estimated mortality with historical data from the last three decades. The dynamic model has then been used to estimate mortality from each condition over the next three decades on the basis of population projections made by the Central Statistical Office [2], assuming no major change in the factors which lead to either condition. This analysis demonstrates both the theoretical applicability and practical capabilities of Gompertz-derived mortality models for analysing changing mortality patterns.

Adult↗
PubMed1993

Cross-sectional Gompertzian analysis: the development of a Gompertz mortality ratio (GMR) and its applicability.

Many conventional epidemiological analyses of the distribution and aetiology of disease employ standardised mortality ratios (SMRs) as a basis upon which to evaluate comparative studies of disease in populations. However SMRs, whilst constructed to control for age and sex, are not capable of incorporating other variables such as life expectancy which has been demonstrated to be of crucial importance in understanding the changing relationships between mortality from different causes. The development of a Gompertz mortality ratio (GMR) and its application to recent mortality from amyotrophic lateral sclerosis (ALS) in the Counties of England and Wales illustrates the value of substituting GMRs for SMRs in the analysis of competitive relationships between conditions, especially those associated with enhanced life expectancy.

Adolescent↗
PubMed1993

Reinterpreting mortality statistics: some uses of Gompertzian analysis in epidemiological research.

Gompertzian analyses of mortality data have recently been undertaken for a number of individual conditions (Riggs JE. Mech Ageing Dev 1990; 55: 207-220 [1]; Neilson S et al. Mech Ageing Dev 1992; 64: 201-216 [2]; Neilson S et al. Acta Neurol Scand 1993; 87: 184-191 [3]). Such analyses are in principle of particular epidemiological value in circumstances where demographic change is occurring and where the balance between mortality from different conditions is subject to change. However, the extent to which a Gompertzian relationship between age and mortality holds for particular conditions has been subject to debate. In this analysis it is demonstrated that even some conditions which do not superficially hold to a Gompertz relationship do in fact do so, if such conditions are considered to be restricted to small, inherently susceptible subpopulations. By analysing mortality from a range of neurological conditions within the context of general mortality in England and Wales, conditions with different aetiologies such as Huntington's chorea, amyotrophic lateral sclerosis and multiple sclerosis can be shown to have a Gompertzian mortality rate distribution. Such analyses are of substantial value in indicating how demographic change affects the balance of mortality between conditions, as well as directing interest to revised aetiological possibilities.

Age Distribution↗
PubMed1993

Rising mortality from motor neurone disease: an explanation.

There is considerable debate about the increasing mortality from motor neurone disease (MND). However, examination of the relationship between increased life expectancy (through decreased general mortality) and increased mortality in both England and Wales and the United States indicates a close association between the two variables. Using a statistical model, defined sub-populations susceptible to MND can be identified in both countries. The size of such a sub-population has been estimated from the 1989 mortality data to be approximately 160,000 people in England and Wales. The proportion of this sub-population dying from MND has increased over the last 30 years, rather than, as previously, dying at an earlier age from other conditions. On this basis, deaths from MND are expected to increase by a further 20% in this sub-population between 1991-2021 because of continuing changes in life expectancy. MND is a condition made increasingly visible in mortality statistics through decreased general mortality, rather than one in which the underlying population at risk has substantially changed. Aetiological extrapolations from the data indicate that susceptibility to the disease is acquired early in life, and that it is unlikely, given the relative stability of the underlying sub-population, that either changed environmental circumstances or artifactual factors can account in themselves for the rise in mortality.

Aged↗
PubMed1993

Exocytosis in adrenal chromaffin cells.

Recent advances have led to an increased understanding of the Ca(2+)-signalling pathway leading to exocytosis in bovine adrenal chromaffin cells. Video-imaging studies have allowed the temporal and spatial aspects of the Ca2+ signal to be investigated in detail. Ca2+ entry at the plasma membrane appears to be crucial for the activation of exocytosis. Ca2+ can enter through the nicotinic channel or characterised voltage-activated channels, or through other poorly defined pathways due to a variety of agonists. Emptying of internal Ca2+ stores is sufficient to activate a Ca2+ entry pathway. The elevation of cytosolic Ca2+ concentration leads to a reorganisation of the cortical actin network and to the triggering of exocytosis. Studies on permeabilised chromaffin cells have resulted in the identification of some of the proteins that control Ca(2+)-dependent exocytosis. These include the peripheral plasma membrane protein annexin II and the cytosolic proteins, protein kinase C and 14-3-3 proteins (Exo1).

Actins↗
PubMed1992

Hepatic steroid hydroxylating enzymes are controlled by the sexually dimorphic pattern of growth hormone secretion in normal and dwarf rats.

In rats, the onset of the sexually dimorphic pattern of growth hormone (GH) secretion and increased hepatic GH-binding capacity at puberty are temporally correlated with the sex-dependent expression of some hepatic cytochrome P450 enzymes involved in steroid metabolism. There are indications that the expression of the GH receptor gene itself is dependent on the sexually differentiated pattern of GH secretion. However, the molecular mechanisms by which a given pattern of GH secretion turns on a specific set of genes in the hepatocyte are not yet understood. Studies of the cytochrome P450 2C gene subfamily in hypophysectomized rats and isolated hepatocytes suggest that one major mechanism of GH action in the liver occurs through modulation of gene transcriptional initiation. The occurrence, in dwarf rats and in rats treated neonatally with monosodium glutamate, of sex differences in GH secretion and liver steroid metabolism typical of normal rats, in spite of a 95% reduction in pituitary GH levels, is compatible with the notion that extremely low levels of circulating GH are sufficient to regulate the expression of liver steroid-metabolizing enzymes. This, together with the fact that single daily subcutaneous injections of GH are sufficient to masculinize the liver of a hypophysectomized rat, indicates that neither the amplitude nor the frequency of the GH pulse is recognized as male or female by the hepatocyte, but rather the complete and prolonged suppression (in males) or the persistence (in females) of circulating GH during the trough period after a GH surge.

Animals↗