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Biomedical subjects

J Eyer

Publications and source records attributed to J Eyer.

At least 37 records · Page 2Linked to original sources
PubMed1990

Continuous arteriovenous hemofiltration in the patient with hepatorenal syndrome. A case study.

CAVH has gained increasing medical acceptance, as favorable outcomes in the critically ill have proven its worth. Unfortunately, CAVH is often used as a "last ditch" effort for the patient with multisystem organ failure and septicemia. Performing the procedure in such a setting sometimes seems little more than an exercise in futility. However, as more patients such as the patient described in this case study are shown to benefit from CAVH, the nursing role needs to be examined both in performing the procedure and in caring for the critically ill patients. The nursing literature has kept abreast of the procedural aspects of CAVH. Now, critical care nurses must move on to the patient-oriented approach, share case studies, and work together to formulate nursing diagnoses, develop specialized care plans, and identify areas for nursing research.

Adult↗
PubMed1989

Effect of a single dose of beta,beta'-iminodipropionitrile in vivo on the properties of neurofilaments in vitro: comparison with the effect of iminodipropionitrile added directly to neurofilaments in vitro.

The biochemical properties of neurofilaments isolated from control and iminodipropionitrile-treated rats were compared with regard to autophosphorylation capacity, hydrolysis of ATP, and the formation of a viscous gel between filaments. Both preparations exhibited a similar polypeptide composition, and no covalent cross-linking between neurofilament subunits was induced by iminodipropionitrile in vivo. An ATPase activity, systematically present in all preparations, was unaffected by the administration of iminodipropionitrile to the rats. Conversely, the autophosphorylation of neurofilament subunits in vitro was significantly higher in preparations from iminodipropionitrile-treated rats than from control animals, with a marked increase of the phosphorylation of a high molecular weight neurofilament-associated protein. Iminodipropionitrile provoked a higher gelation capacity of neurofilaments as measured in vitro, with a lower critical concentration for the preparation from treated animals. A similar increased interaction was obtained with millimolar concentrations of iminodipropionitrile added to bovine neurofilaments in vitro, involving likely neurofilament-associated molecules, because the effect of the drug was lost after their extraction by 0.8 M KCl. These results support the hypothesis that iminodipropionitrile interferes with the neurofilament networks through a preferential interaction with the neurofilament-associated proteins, resulting in a change in their properties and consequently in an increased capacity of interaction between the polymers.

Adenosine Triphosphatases↗
PubMed1988

Influence of the phosphorylation state of neurofilament proteins on the interactions between purified filaments in vitro.

The extensive enzymic dephosphorylation of neurofilaments determined the progressive loss of their capacity to interconnect in vitro into a reticulated network, measured by the formation of highly viscous gels in purified preparations of neurofilaments [Leterrier & Eyer (1987) Biochem. J. 245, 93-101]. Conversely, a cyclic AMP-dependent activation of the gelation process was obtained by phosphorylation of the neurofilament proteins by the cyclic-nucleotide-dependent protein kinase added to the preparation. These findings argue for a direct relationship between the high phosphorylation level of the neurofilament subunits and the cross-bridging of the polymers in vitro. However, a transient stimulation of the neurofilament viscosity kinetics was also observed during the early steps of dephosphorylation with acid phosphatase, which, moreover, disappeared with longer incubation times before the net inhibition was obtained. In the same way, the calmodulin-dependent brain phosphatase, calcineurin, induced a permanent activation of the phenomenon, correlated with a low dephosphorylation capacity of the neurofilament molecules. Taken together, these results suggest a functional heterogeneity of the numerous phosphate groups of the neurofilament subunits and raise the hypothesis of a highly controlled regulation of the neurofilament cross-bridging by selective phosphorylation-dephosphorylation mechanisms.

Acid Phosphatase↗
PubMed1987

Bull sperm 19S dynein polymerizes brain tubulin into microtubules.

Crude dynein extracted from bull sperm flagella polymerized pure phosphocellulose tubulin isolated from brain tissues into microtubules. This effect was predominantly due to the 19S dynein particle in the extract. ATP stimulated up to five fold the polymerization of brain tubulin by bull sperm dynein. Hydrolysis of ATP was not required since vanadate at a concentration sufficient to block dynein ATPase activity did not interfere with ATP stimulation and because the non hydrolyzable ATP analogue adenylyl (beta-gamma-methylene) diphosphate (AMPPCP) had effects similar to those of ATP. These results suggest that, in addition to hydrolyzing ATP to generate the driving force necessary for microtubule sliding within the axoneme, dynein may also interact with ATP to polymerize tubulin into microtubules.

Adenosine Triphosphatases↗
PubMed1987

Properties of highly viscous gels formed by neurofilaments in vitro. A possible consequence of a specific inter-filament cross-bridging.

Neurofilaments freshly isolated from bovine spinal cord form a reversible gel in vitro, consisting of nearly parallel and interlinked filaments organized in bundles. This phenomenon is obtained above a critical neurofilament concentration and is highly sensitive to denaturation. No gelation occurs with neurofilaments reconstituted from urea-solubilized subunits. The velocity of the gelation kinetics, optimum at a slightly acidic pH, is inhibited by low and high ionic strength and activated by millimolar concentrations of Mg2+ and other bivalent cations. No protein other than the purified neurofilament preparation itself (80-95% neurofilament triplet) is necessary for the formation of a gel. However, purified cytoskeletal proteins from microtubules and neurofilaments influence the viscosity of the native preparation. These observations suggest a reticulation in vitro between neurofilaments, dependent upon a fragile conformation of the polymers and possibly mediated through the high-Mr neurofilament subunits (200 kDa and 150 kDa). The significance of these results is discussed with regard to the inter-neurofilament cross-bridging in situ involving the 200 kDa subunit described by Hirokawa, Glicksman & Willard [(1984) J. Cell Biol. 98, 1523-1536].

Animals↗
PubMed1980

Social causes of coronary heart disease.

By combining the results of prospective and other studies with cross-national and time series analyses of death rates, it is possible to roughly quantify the relative contribution of various causal factors to excess mortality. When coronary heart disease is treated in this way, it is apparent that broad social forces are its main causal factors. Primary among these forces are overwork and various kinds of social disruption. These in turn are at the center of the typical social transformation which accompanies modern economic growth (capitalism).

Adolescent↗
PubMed1977

Does unemployment cause the death rate peak in each business cycle? A multifactor model of death rate change.

Natural time series and prospective studies are combined to determine the contribution of many causal factors to the business cycle variation of the death rate. The variation of housing and nutrition together accounts for roughly a tenth of the death rate fluctuation. Drug consumption accounts for about one-sixth, with 11 percent of the total variation due to alcohol and 6 percent due to cigarette smoking. Social relationship changes, both as sources of stress and as means of relief, account for the greatest part (72 percent) of the business cycle variation of the death rate.

Adult↗
PubMed1977

Prosperity as a cause of death.

The general death rate rises during business booms and falls during depressions. The causes of death involved in this variation range from infectious diseases through accidents to heart disease, cancer, and cirrhosis of the liver, and include the great majority of all causes of death. Less than 2 percent of the death rate-that for suicide and homicide-varies directly with unemployment. In the older historical data, deterioration of housing and rise of alcohol consumption on the boom may account for part of this variation. In twentieth-century cycles, the role of social stress is probably predominant. Overwork and fragmentation of community through migration are two important sources of stress which rise with the boom, and they are demonstrably related to the causes of death which show this variation.

Accidents↗
PubMed1975

Hypertension as a disease of modern society.

About 50 per cent of people in modern societies have blood pressure sufficiently elevated to result in increased mortality. This proportion is much smaller in undisrupted societies of hunter-gatherers. In most cases the elevated blood pressure in modern societies is associated with physiological changes characteristic of chronic stress. The difference between blood pressure in modern populations and that in undisrupted hunter-gatherer societies cannot be accounted for by genetic differences or differences in salt consumption. Two primary features of modern society which contribute to the elevation of blood pressure are community disruption and increased work pressure. Drug therapy and relaxation therapies for hypertension attempt to counteract the physiological effects of social stress. However, it is more appropriate to use the occurrence of hypertension as an indicator of fundamental social problems which need to be solved.

Adaptation, Psychological↗