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PubMed1995

Rapid changes in oxidative metabolism as a consequence of elicitor treatment of suspension-cultured cells of French bean (Phaseolus vulgaris L.).

Stressed plant cells often show increased oxygen uptake which can manifest itself in the transient production of active oxygen species, the oxidative burst. There is a lack of information on the redox status of cells during the early stages of biotic stress. In this paper we measure oxygen uptake and the levels of redox intermediates NAD/NADH and ATP and show the transient induction of the marker enzyme for redox stress, alcohol dehydrogenase. Rapid changes in the redox potential of elicitor-treated suspension cultures of French bean cells indicate that, paradoxically, during the period of maximum oxygen uptake the levels of ATP and the NADH/NAD ratio fall in a way that indicates the occurrence of stress in oxidative metabolism. This period coincides with the maximum production of active oxygen species particularly H2O2. The cells recover and start producing ATP immediately of H2O2 production. This indicates that the increased O2 uptake is primarily incorporated into active O2 species. A second consequence of these changes is probably a transient compromising of the respiratory status of the cells as indicated in expression of alcohol dehydrogenase. Elicitor-induced bean ADH was purified to homogeneity and the M(r) 40,000 polypeptide was subjected to amino acid sequencing. 15% of the whole protein was sequenced from three peptides and was found to have nearly 100% sequence similarity to the amino acid sequence for pea ADH1 (PSADH1). The cDNA coding for the pea enzyme was used to demonstrate the transient induction of ADH mRNA in elicitor-treated bean cells. Enzyme activity levels also increased transiently subsequently. Increased oxygen uptake has previously been thought to be associated with provision of energy for the changes in biosynthesis that occur rapidly after perception of the stress signal. However the present work shows that this rapid increase in oxygen uptake as a consequence of elicitor action is not wholly associated with respiration.

Adenosine Triphosphate↗
PubMed1992

Tissue engineering science: consequences of cell traction force.

Blood and tissue cells mechanically interact with soft tissues and tissue-equivalent reconstituted collagen gels in a variety of situations relevant to biomedicine and biotechnology. A key phenomenon in these interactions is the exertion of traction force by cells on local collagen fibers which typically constitute the solid network of these tissues and gels and impart gross mechanical integrity. Two important consequences of cells exerting traction on such collagen networks are first, when the cells co-ordinate their traction, resulting in cell migration, and second, when their traction is sufficient to deform the network. Such cell-collagen network interactions are coupled in a number of ways. Network deformation, for example, can result in net alignment of collagen fibers, eliciting contact guidance, wherein cells move with bidirectional bias along an axis of fiber alignment, potentially leading to a nonuniform cell distribution. This may govern cell accumulation in wounds and be exploited to control cell infiltration of bioartificial tissues and organs. Another consequence of cell traction is the resultant stress and strain in the network which modulate cell protein and DNA synthesis and differentiation. We summarize, here, relevant mathematical theories which we have used to describe the inherent coupling of cell dynamics and tissue mechanics in cell-populated collagen gels via traction. The development of appropriate models based on these theories, in an effort to understand how events in wound healing govern the rate and extent of wound contraction, and to measure cell traction forces in vitro, are described. Relevant observations and speculation from cell biology and medicine that motivate or serve to critique the assumptions made in the theories and models are also summarized.

Biomechanical Phenomena↗
PubMed1988

Augmentation of the indirect sympathomimetic action of tyramine by cardioactive steroids is a consequence of elevated intracellular sodium.

The augmentation by the cardioactive steroid acetylstrophanthidin of neurotransmitter release evoked by tyramine, and the dependence of the augmentation upon Na+, has been investigated in dog saphenous vein rings in which monoamine oxidase activity and uptake2 had been inhibited with pargyline and corticosterone respectively. High extracellular Na+ (Nao; 263 mmol/l) reduced basal efflux of 3H-compounds from the rings and also reduced tyramine-evoked efflux. Low Nao (25 mmol/l) increased basal efflux of 3H but reduced tyramine-evoked efflux. The increment in basal 3H-efflux caused by low Nao was cocaine-sensitive. A presumed increase in intracellular Na+ (Nai), produced by preincubating rings with acetylstrophanthidin in normal (143 mmol/l) or high Nao, augmented 3H-efflux evoked by subsequent incubation with tyramine in normal Nao. Pre-incubating rings with acetylstrophanthidin in low Nao, conditions which would not be expected to increase Nai, did not cause augmentation of the subsequent tyramine-evoked 3H-efflux. An increase in Nai, produced either as above or by pre-incubating rings in high Nao alone, reduced subsequent neuronal 14C-tyramine uptake. Low Nao present only during incubation reduced neuronal 14C-tyramine uptake, but high Nao present only during incubation did not increase neuronal 14C-tyramine uptake from that measured in normal Nao. The data are consistent with the following hypotheses: that tyramine uptake is dependent upon the prevailing inwardly directed Na+-gradient, that consequent noradrenaline efflux is Na+-gradient dependent and that the enhancement by acetylstrophanthidin of tyramine-evoked 3H-efflux is a consequence of the raised Nai caused by Na+,K+-ATPase inhibition.

Animals↗
PubMed1993

Morphological and functional consequences of chronic epilepsy in rat hippocampal slice cultures.

We have developed an in vitro model of chronic epilepsy in order to study the consequences of prolonged periods of epileptic activity. After applying the convulsants bicuculline and/or picrotoxin to mature rat hippocampal slice cultures for 3 days, large numbers of swollen and vacuolated cells were observed throughout all hippocampal subfields. The number of dendritic spines of pyramidal cells was massively reduced. These changes were similar to those observed previously in post-mortem studies of hippocampal tissue from human epilepsy patients. Intracellular recordings from CA3 pyramidal cells revealed that spontaneous synaptic activity was greatly reduced in treated cultures. gamma-Aminobutyric acid-mediated inhibition was apparently not affected by sustained convulsant activity, although synaptic excitation was markedly depressed. Acute re-application of bicuculline to treated cultures elicited, upon stimulation of the mossy fibre tract, a typical interictal burst lasting several hundred milliseconds, with a wave form similar to those occurring in untreated cultures, but of a shorter duration. In contrast, ictal bursts (lasting tens of seconds), which always occur spontaneously in control cultures during initial perfusion of bicuculline, were not observed in treated cultures. These pathological changes were reversible when treated cultures were returned to normal medium for 1 week. The surviving cells had a healthy morphology and a normal complement of dendritic spines. Spontaneous synaptic activity was normal, and ictal bursts occurred spontaneously upon perfusion of bicuculline. The findings suggest that the morphological and functional changes are a consequence, rather than a direct cause of epilepsy.

Animals↗
PubMed1989

Morphological consequences of early reperfusion following thrombotic or mechanical occlusion of the rat middle cerebral artery.

The early morphological consequences of recirculation following middle cerebral artery (MCA) occlusion were studied in two rat models. The proximal MCA was occluded for 1 h by either a surgical clip or platelet thrombus; subsequently, 1 h of recirculation was facilitated. Following clip occlusion and recirculation, mild astrocytic swelling, especially around blood vessels, was detected in reperfused cortical and striatal areas. Neuronal changes included slight chromatin clumping and dilation of the rough endoplasmic reticulum. In contrast, severe structural abnormalities were detected following recanalization of the thrombosed MCA segment. Marked astrocytic swelling of cell bodies and perivascular processes with neuropil vacuolation were commonly seen. A heterogeneous pattern of neuronal alterations, including a high frequency of dense shrunken neurons surrounded by swollen astrocytic processes was documented in cortical and striatal regions. Severe neuronal changes were documented in brain regions exhibiting a well-perfused microcirculation. Vascular endothelial cells contained large numbers of pinocytotic vesicles associated with luminal and abluminal surfaces. Pronounced and rapid morphological changes evolve with reperfusion when thrombotic and ischemic events occur simultaneously. The basis for these rapid parenchymal changes following vascular thrombosis may involve acute alterations in cerebral microvascular permeability which exacerbate ischemic consequences.

Animals↗
PubMed1993

Cardiovascular consequences of expressing, experiencing, and repressing anger.

Psychoanalytic theory's pathogenic view of repression gave rise to the widely held belief that the expression of anger is beneficial to mental and physical health. The present paper reviews a number of experimental and correlational studies which demonstrate that the full expression of anger, with its vocal manifestations, is associated with significant cardiovascular hyperreactivity. Furthermore, epidemiological studies indicate that such expression of anger are also related to coronary heart disease (CHD) and to some physiological and hormonal changes that have been implicated in the pathophysiology of CHD. On the other hand, neither the mere experience of anger nor its repression has any of the above negative cardiovascular consequences, although the repression of anger seems to have other untoward health consequences.

Adult↗
PubMed1991

Home environmental consequences of commute travel impedance.

The physical and perceptual dimensions of commuting travel impedance were again found to have stressful consequences in a study of 99 employees of two companies. This quasi-experimental replication study, which focuses here on home environment consequences, investigated the effects of physical impedance and subjective impedance on multivariate measures of residential satisfaction and personal affect in the home. Both sets of residential outcome measures were significantly related to the two impedance dimensions. As predicted, gender was a significant moderator of physical impedance effects. Women commuting on high physical impedance routes were most negatively affected. Previously found subjective impedance effects on negative home mood, regardless of gender, were strongly replicated with several methods and were buttressed by convergent results with objective indices. The theoretical conjecture that subjective impedance mediates the stress effects of physical impedance was supported by the personal affect cluster but only for one variable in the residential satisfaction cluster. Traffic congestion has increased in metropolitan areas nationwide, and commuters, families, and organizations are absorbing associated hidden costs. The results are reviewed in terms of our ecological model, and the moderating effects of gender are discussed in terms of choice and role constraints.

Adult↗
PubMed1989

PHysical exercise: evidence for differential consequences of tryptophan on 5-HT synthesis and metabolism in central serotonergic cell bodies and terminals.

The aim of the present study was to investigate the effects of physical exercise (running) on serotonin (5-hydroxytryptamine, 5-HT) synthesis and metabolism in midbrain on the one hand, and in striatum and hippocampus on the other hand. To address such a question, tryptophan (TRP) and 5-hydroxytryptophan (5-HTP) were measured in running rats pretreated with an inhibitor of aromatic amino acid decarboxylase, namely NSD 1015. In another series of experiments, the consequences of a TRP load on TRP, 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels were compared in resting and running rats. Although running triggered a 30% increase in TRP levels in the three brain regions examined, inhibition of 5-HT synthesis by NSD 1015 was found to promote increased (midbrain), unchanged (striatum) or decreased (hippocampus) 5-HTP accumulation in the running situation, respectively compared to that measured in the resting situation. Inasmuch as running-induced elevation in TRP was not associated with an increased 5-HTP accumulation in the striatum and the hippocampus, the consequences of running on regional TRP, 5-HT and 5-HIAA levels were analyzed in saline- and TRP-injected rats. Indeed, running, per se, was found to increase central TRP, 5-HT and 5-HIAA levels. On the other hand, a TRP load that promoted identical increases in central TRP levels in running and resting rats revealed that running, according to the region examined, differentially affected TRP utilization in the 5-HT synthesis pathway. Thus, in the midbrains of the resting and running rats, respective 210-250% increases in TRP led to identical 25% increases in 5-HT and 90% increases in 5-HIAA levels. Conversely, in hippocampus, TRP loads triggered marked increases in TRP levels that were similar in the controls and the runners, but the rise in 5-HIAA promoted by such a precursor load was found to be significantly minored in the runners, compared to the resting rats. Moreover, such a running-induced impairment in 5-HT synthesis and metabolism was even more observable in the striatum; thus, TRP loads which promoted identical increases in striatal TRP levels in the resting and the running rats respectively triggered a 50% and a 32% increase in 5-HT levels and a 76% and a 47% increase in 5-HIAA levels. The results presented herein indicate that under certain pharmacological conditions, TRP utilization into the 5-HT synthesis pathway is altered in serotonergic nerve terminals, but not in the cell bodies of the running rat.

Animals↗
PubMed1977

Chemical and biological consequences of beta-decay. Part 1.

Radioactive decay in a labelled molecule leads to specific chemical and biological consequences which are due to local transmutation effects such as recoil, electronic excitation, build-up of charge states and change of chemical identity, as well as to internal radiolytic effects. In the present paper these effects are reviewed emphasizing the relation of the chemical alterations on a molecular level to the biological manifestation. Potential importance of this type of research for biomedical applications is pointed out. In part 1 we review the underlying physical and chemical principles and consequences of beta-decay of 3H, 14C, 32P, 33P, 35S and 125I for gaseous and simple condensed organic systems. Part 2 which will appear in the next issue will include the discussion of biological effects associated with beta-decay.

Bromodeoxyuridine↗
PubMed1991

[Prevalence, circumstances and consequences of falls in institutionalized elderly; a pilot study].

Falls are frequent among elderly people, and are a still-underestimated medical problem with respect to causes and consequences. The present epidemiological study describes the experience from a 79-bed nursing home in the city of Zürich, regarding frequency, circumstances and consequences of falls. Over half of residents of the studied nursing home fell at least once during the study period of one year, and one third even suffered 3 or more falls. Dizziness, tripping and slipping were among the reasons given for falling. However, in one third of the cases the person involved was not able to specify the cause of the fall. Every fifth fall to injury or fracture, and every tenth fall to fall-related pain. The fall-related overall morbidity therefore amounted to 35.3%.

Accidental Falls↗
PubMed1987

Family characteristics and long-term consequences associated with sexual abuse.

As opposed to father-daughter incest, little attention has been paid to the long-term consequences and family dynamics associated with child sexual abuse of females perpetrated by extended family members or extrafamilial contacts. Female undergraduates (n = 586) completed questionnaires on family history, sexual experiences, and current functioning. Results confirmed other research suggesting that father-daughter incest is associated with a traditional patriarchal family structure. However, sexual abuse overall, regardless of perpetrator, was associated with certain uniform family characteristics. Moreover, sexual abuse had certain long-term consequences, regardless of perpetrator. These results suggest the importance of attention to family characteristics in all cases of child sexual abuse.

Adolescent↗
PubMed1981

[Social consequences of psychic disturbances in the population: a field study on young adults (author's transl)].

In epidemiological surveys about neurotic and psychosomatic disturbances there is the question of how relevant the reported syndromes are. An important criterion to evaluate the relevance of a syndrome is its individual and social consequences. In a general population sample of 600 young adults in the Canton of Zurich (Switzerland), subjects answered a structured interview (SPIKE) about 25 different neurotic and psychosomatic syndromes and their consequences: personal suffering, imparied role performance, tendency to become chronic, and medical treatment. A number of neurotic syndromes (especially depression, anxiety, and exhaustion) ranked highest with regard to individual suffering and impaired role performance, but they rarely led to medical treatment. Psychosomatic syndromes, on the other hand, while treated more often, only caused minor personal suffering and did not impair role performance very much.

Adult↗
PubMed1995

Behavioural consequences of maternal exposure to natural cannabinoids in rats.

Cannabis sativa preparations (hashish, marijuana) are the most widely used illicit drugs during pregnancy in Western countries. The possible long-term consequences for the child of in utero exposure to cannabis derivatives are still poorly understood. Animal models of perinatal cannabinoid exposure provide a useful tool for examining the developmental effects of cannabinoids. Behavioral consequences of maternal exposure to either cannabis preparations or to its main psychoactive component, delta 9-tetrahydrocannabinol (THC) in rat models are reviewed in this paper. Maternal exposure to cannabinoids resulted in alteration in the pattern of ontogeny of spontaneous locomotor and exploratory behavior in the offspring. Adult animals exposed during gestational and lactational periods exhibited persistent alterations in the behavioral response to novelty, social interactions, sexual orientation and sexual behavior. They also showed a lack of habituation and reactivity to different illumination conditions. Adult offspring of both sexes also displayed a characteristic increase in spontaneous and water-induced grooming behavior. Some of the effects were dependent on the sex of the animals being studied, and the dose of cannabinoid administered to the mother during gestational and lactational periods. Maternal exposure to low doses of THC sensitized the adult offspring of both sexes to the reinforcing effects of morphine, as measured in a conditioned place preference paradigm. The existence of sexual dimorphisms on the developmental effects of cannabinoids, the role of sex steroids, glucocorticoids, and pituitary hormones, the possible participation of cortical projecting monoaminergic systems, and the mediation of the recently described cannabinoid receptors are also analyzed. The information obtained in animal studies is compared to the few data available on the long-term behavioral and cognitive effects on in utero exposure to cannabis in humans.

Abnormalities, Drug-Induced↗
PubMed1996

N-acetyltransferases: pharmacogenetics and clinical consequences of polymorphic drug metabolism.

Since the discovery of polymorphic N-acetylation of drugs nearly 40 years ago, great progress has been made in understanding the molecular genetics of acetylation as well as the clinical consequences of being a rapid or slow acetylator. Inborn errors (several different alleles) at the NAT2 locus are responsible for the traditional acetylator polymorphism. Studies have revealed variant alleles at the NAT1 locus as well. The consequences of pharmacogenetic variation in these enzymes include (i) altered kinetics of specific drug substrates; (ii) drug-drug interactions resulting from altered kinetics; (iii) idiosyncratic adverse drug reactions. The latter have been extensively investigated for the arylamine-containing sulfonamide antimicrobial drugs. Individual differences in multiple metabolic pathways can increase the likelihood of covalent binding of reactive metabolites of the drugs to cell macromolecules with resultant cytotoxicity and immune response to neoantigens. This can result clinically in an idiosyncratic hypersensitivity reaction, manifested by fever, skin rash, and variable toxicity to organs including liver, bone marrow, kidney, lung, heart, and thyroid. Slow acetylation by NAT2 is a risk factor for such reactions to sulfonamides. Given the incidence of these severe adverse drug reactions (much less than 1/1000), slow acetylation cannot be the sole mechanism of predisposition in the population. Differences in rates of production of hydroxylamine metabolites of the drugs by cytochrome P450 (CYP2C9), myeloperoxidase, and thyroid, roxidase, along with an inherited abnormality in detoxification of the hydroxylamines are critically important in determining individual differences in adverse reaction risk. Both NATs, particularly NAT1, also can further metabolize hydroxylamine metabolites to N-acetoxy derivatives. Intensive investigation of patients with these rare adverse reactions using a variety of tools from in vitro cell toxicity assays through molecular genetic analysis will help elucidate mechanisms of predisposition and ultimately lead to diagnostic tools to characterize individual risk and prevent idiosyncratic drug toxicity.

Alleles↗
PubMedDate not supplied

Stochasticity in membrane-localized "ligand-receptor-G protein" binding: consequences for leukocyte movement behavior.

The signal that governs the chemotactic response of mammalian white blood cells and tissue cells arises from membrane-localized binding events involving chemotactic factor ligands and receptors and G proteins. Fluctuations in this signal have been traditionally attributed to significant "noise" in receptor-ligand binding owing to a limited number of receptors. This paper examines the validity and consequences of a new hypothesis which states that the noise could be associated with a limited number of G proteins as well as receptors. This work characterizes via stochastic analysis and simulation the effects of the relative sizes of G protein and receptor populations on the variance of fluctuations of receptor states and consequently on the directional persistence behavior of cells in uniform chemotactic factor concentrations under the assumptions of the model used to link a G protein-mediated receptor signal to cell turning. Our results suggest that there may exist an optimal number of G proteins through which chemotactic receptors can signal that maximizes cell orientation accuracy in a chemotactic factor gradient.

Animals↗
PubMed1990

Consequences of copper deficiency are not differentially influenced by carbohydrate source in young pigs fed a dried skim milk-based diet.

Carbohydrates (CHO) such as fructose (FR) or sucrose, but not starch (ST), aggravate the consequences of dietary copper (Cu) deficiency in rats. To evaluate whether this Cu X CHO interaction is pertinent to human health, the pig was used as an animal model. In two studies, 66 weanling pigs were fed dried skim milk (DSM)-based diets for 10 wk with 20% of the total calories provided as either FR, glucose, or ST and containing either deficient (1.0-1.3 micrograms/g diet) or adequate (7.1 micrograms/g) levels of Cu. Plasma and tissue levels of Cu, the activities of plasma ceruloplasmin ferroxidase and erythrocyte Cu, Zn-superoxide dismutase, and hematocrits were lower (p less than 0.05) in animals fed Cu-deficient diets. The relative cardiac mass of all Cu-deficient groups was greater (p less than 0.05) than that of animals fed Cu-adequate diets. These effects were in general unaffected by type of CHO. For comparison, weaned male rats were also fed DSM-based containing diets ST or FR with adequate or deficient Cu for as long as 10 wk. Rats consuming the Cu-deficient diets were characterized by significantly lower hematocrits, decreased tissue Cu levels, and enlarged hearts, regardless of the CHO source. Together, these data demonstrate that DSM-based diets are not suitable for delineation of potential Cu X CHO interactions, and one or more components of DSM may exacerbate the consequences of dietary Cu deficiency.

Animal Feed↗
PubMed2001

Effects of prenatal exposure to cocaine on the developing brain: anatomical, chemical, physiological and behavioral consequences.

Earlier studies of human infants and studies employing animal models had indicated that prenatal exposure to cocaine produced developmental changes in the behavior of the offspring. The present paper reports on the results obtained in a rabbit model of in utero exposure to cocaine using intravenous injections (4 mg/kg, twice daily) that mimic the pharmacokinetics of crack cocaine in humans. At this dose, cocaine had no effect on the body weight gain of dams, time to delivery, litter size and body weight or other physical characteristics of the offspring. In spite of an otherwise normal appearance, cocaine-exposed neonates displayed a permanent impairment in signal transduction via the D1 dopamine receptor in caudate nucleus, frontal cortex and cingulate cortex due to an uncoupling of the receptor from its associated Gs protein. This uncoupling in the caudate nucleus was shown to have behavioral consequences in that young or adult rabbits, exposed to cocaine in utero, failed to demonstrate amphetamine-elicited motor responses normally seen after activation of D1 receptors in the caudate. The cocaine progeny also demonstrated permanent morphological abnormalities in the anterior cingulate cortex due to uncoupling of the D1 receptor and the consequent inability of dopamine to regulate neurite outgrowth during neuronal development. Consistent with the known functions of the anterior cingulate cortex, adult cocaine progeny demonstrated deficits in attentional processes. This was reflected by impairment in discrimination learning during classical conditioning that was due to an inability to ignore salient stimuli even when these were not relevant to the task. The impairment in discrimination learning also occurred in an instrumental avoidance task and could be shown to be due to an impairment of cingulothalamic learning-related neuronal coding. It was proposed that the selective loss of D1-related neurotransmission in the anterior cingulate cortex prevented an appropriate activation of GABA neurons and thus a loss of inhibitory regulation that is necessary for processes involved in associative attention. Taken together, these findings suggest that the uncoupling of the D1 receptor from its G protein may be the fundamental source of the anatomic, cognitive and motor disturbances seen in rabbits exposed to cocaine in utero. Moreover, the long-term cognitive and motor deficits observed in the rabbit model are in agreement with the recent reports indicating that persistent attentional and other behavioral deficits may be evident in cocaine-exposed children as they grow older and are challenged to master more complex cognitive tasks.

Journal Article↗
PubMed1998

[Consequences of the latest Euratom directive 96/29 ("basic standard") regarding radiotherapy].

AIM: The Council Directive 96/26 will be brought into force by the Member States of the EC until the year 2000. What practical consequences on both mounting and holding radiotherapeutical facilities should be considered? METHODS: Regarding the Council Directive, facts on workers' actual occupational exposure in medicine and representative calculations on structural shielding the consequences will be evaluated. RESULTS: Increasing both total number of occupationally exposed workers and number of Category A workers but also enforced structural shielding should be expected. Working in any protected area during pregnancy will be strictly prohibited now. CONCLUSIONS: With respect to the generally sufficient structural shielding no restrictions for existing radiotherapeutical facilities are to be expected. But it is emphasized to carry out further mountings on base of the latest Council Directive 96/26 Euratom.

Environmental Monitoring↗