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Results for “environmental variability”

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PubMed1986

Non relationship of climatologic factors and painful sickle cell anemia crisis.

Conflicting results have arisen from studies concerning the correlation (if any) between climatological changes and the frequency of painful episodes in the sickle cell population. During a 13 month period records of 71 patients with hemoglobin genotypes SS or SC were reviewed. Data analysis failed to reveal an association between the frequency of painful sickle cell crisis and a number of weather and environmental variables. We were unable to demonstrate relationships between the climatologic factors of temperature, humidity, carbon monoxide level and precipitation in the frequency of 362 pain crises in 71 sickle cell patients during a 13 month period.

Adolescent↗

PubMed1991

Regulation of the F plasmid traY promoter in Escherichia coli by host and plasmid factors.

F plasmid DNA transfer (tra) gene expression in Escherichia coli is regulated by chromosome- and F-encoded gene products. To study the relationship among these regulatory factors, we constructed low-copy plasmids containing a phi(traY'-'lacZ)hyb gene that couples beta-galactosidase and Lac permease synthesis to the F plasmid traY promoter. Wild-type transformants maintained high levels of beta-galactosidase over a broad range of culture densities. Primer extension analysis of tra mRNA from F'lac and phi(traY'-'lacZ)hyb strains indicated very similar, though not identical, transcription initiation sites. Moreover, phi(traY'-'lacZ)hyb gene expression required both TraJ and SfrA, as does tra gene expression in F+ strains. beta-Galactosidase activity was reduced approximately 30-fold in the absence of TraJ, which could be supplied in cis or in trans. In a two-plasmid system in which TraJ was supplied in trans by a lac-traJ operon fusion, phi(traY'-'lacZ)hyb expression was a linear, saturable function of traJ expression. Enzyme activity was reduced approximately tenfold in sfrA mutants. That reduction could not be attributed to an effect on the TraJ level. Several other cellular or environmental variables had only a modest effect on phi(traY'-'lacZ)hyb expression. Hyperexpression was observed at high cell density (twofold) and in anaerobic cultures (1.2- to 1.5-fold). In contrast, expression was reduced twofold in integration host factor mutants.

Aerobiosis↗

PubMed1992

Effects of environmental factors on maxillofacial elastomers: Part IV--Optical properties.

The optical properties of four currently used and two recently introduced maxillofacial prosthetic materials were evaluated after the materials were subjected to the following seven environmental variables: natural weathering; normal aging; two types of adhesives; two types of cleaning agents; and cosmetics. Optical density and color changes were evaluated. The currently used silicones Silastic 4-4210 and Silastic 4-4515, Medical Adhesive type A material, and polyurethane all showed more changes in color and optical density than the newly introduced silicone A-102 material.

Analysis of Variance↗

PubMed1990

Dam strain affects cardiovascular reactivity to acute stress in BHR.

The effect of maternal strain on reactivity to acute stress was studied in F1 reciprocals produced by crossing the spontaneously hypertensive rat (SHR) with its normotensive progenitor, the Wistar-Kyoto (WKY). This F1 generation, known as the borderline hypertensive rat (BHR), is genetically predisposed to develop hypertension in response to chronic stress or high dietary sodium. Reciprocals, considered to be genetically equivalent aside from sex-linked traits, differ in strain of dam during intrauterine and preweanling development. At 17 weeks of age, reciprocal F1 males did not differ in open-field behavior (squares crossed, rearings, and defecation measured over 3 days in 15-min sessions) or in home-cage measurements of mean arterial pressure (MAP) and heart rate (HR). However, different patterns of cardiovascular reactivity were displayed to transfer and footshock. While WKY-mothered rats reacted with graded pressor responses, SHR-mothered rats responded maximally to transfer, showed no additional increase to footshock, and maintained peak responding after footshock was terminated. Such reactivity differences may mediate the impact of environmental variables on the genetic disposition to hypertension.

Animals↗

PubMed1984

Risk spreading as an adaptive strategy in iteroparous life histories.

It has long been conjectured, though without satisfactory proof, that life tables with a long reproductive span are advantageous in an environment where fecundity or immature survival rates fluctuate randomly. In the present analysis we recast the nonlinear Leslie matrix problem as an autoregressive time series model for the birth rate, with random addition and removal of newborn. This transformation renders the model linear with respect to the environmental variation, allowing ready solution for the ultimate population size and for the conditions resulting in stationarity of the population distribution. We show that for life tables where the fecundities of all adult age classes are the same (no restrictions are put on the survivorship schedule, or on the age at first reproduction), and where density dependence operates via total adult density, the realized growth rate is less than the growth rate calculated from the mean Leslie matrix associated with the population's growth history. The degree of the discrepancy increases with the environmental variability, and decreases with iteroparity, thus completing a proof which confirms the correctness of the initial conjecture for a class of biologically reasonable life-table models.

Birth Rate↗

PubMed1987

Evolutionarily [corrected] stable strategies: a review of basic theory.

Widely successful in applied population biology, the Evolutionarily Stable Strategy concept remains controversial because of the severe restrictions present in its original formulation. We review theory which explores and relaxes these restrictions, finding the concept to be quite robust and adaptable, incorporating considerations such as genetics, population diversity, environmental variability, and mutation.

Animals↗

PubMed1994

Surfactant bioconcentration--a critical review.

Bioconcentration data for surfactants have been collected and critically reviewed. Twenty-two references report whole body bioconcentration data. Most of these data are inappropriate to quantitatively describe the bioconcentration of surfactants because the most frequently used analytical method, LSC without prior chromatographic separation of radiolabelled compounds, does not allow to distinguish between parent compound and metabolites. Hence, the measured concentrations very likely are overestimates of the concentration of the parent surfactant. In order to compare data we defined a comparability criterion. Data which fulfil this criterion consistently overestimate the true extent of bioconcentration. Fifty-four out of 100 whole body concentration ratios (CRs) were selected employing the above criterion, with 33, 11, and 10 Crs reported for anionic, cationic and nonionic surfactants, respectively. Further findings are: 1. Selected CRs range between 2.4 for octyltrimethylammonium chloride and 1960 for tallowtrimethylammonium chloride. In general, CRs increased with increasing alkyl chain length. 2. Surfactants of all classes are readily taken up across the gills. Hexadecylpyridinium and dialkyl dimethyl ammonium surfactants appear to be taken up rather slow. 3. Nonionic and anionic surfactants were demonstrated to be biotransformed. Tissue specific data demonstrated that elimination via the gall bladder is an important excretion route. 4. Environmental variables appeared to influence bioconcentration of ionic surfactants.

Animals↗

PubMed1990

Longitudinal Gompertzian analysis of adult mortality in the U.S., 1900-1986.

Analysis of mortality data for the United States from 1900 through 1986 demonstrates near perfect Gompertzian mortality rate distributions for adult American men and women. In the U.S. between 1900 and 1986, annual age-adjusted mortality rate distributions were determined by a fixed common intersect point (for men, the mortality rate at age 87.41 years was 18,810/100,000; for women, the extrapolated mortality rate at age 108.69 years was 75,365/100,000) and a variable environmental factor. Despite living in the same environment, the environmental factor contributing to adult mortality is at present significantly less for women than men. However, analysis predicts that in an environment less conducive to human survival than has existed in the United States during this century, the environmental factor contributing to adult mortality was less for men than women. The study further implies that as the environment becomes more favorable for human survival, men will experience an effective lowering of their theoretical maximal life span toward a limit of 87.4 years. The calculated maximal life span for men has already decreased 7 years during this century. This negative effect of a more favorable environment also occurs in women, although the theoretical maximal life span in women is lowered only toward a limit of 108.7 years.

Adult↗

PubMed1990

Longitudinal Gompertzian analysis of Parkinson's disease mortality in the U.S., 1955-1986: the dramatic increase in overall mortality since 1980 is the natural consequence of deterministic mortality dynamics.

Age-adjusted mortality rates for Parkinson's disease (PD) for men and women in the United States, from 1955 to 1986, were calculated and subjected to longitudinal Gompertzian analysis. Annual age-adjusted PD mortality rate distributions were determined by a common intersect point and a variable environmental factor. For men, the death rate at age 73.75 years was 19.15/100,000; for women, the death rate at age 78.99 years was 28.64/100,000 for each year from 1955 to 1986. The environmental factor declined (improved) 360.7-fold for men and 319.6-fold for women in 1986 compared to 1955. Despite this dramatic environmental improvement favoring survival in PD, there has been a 57.6% increase since 1980 in the annual crude PD mortality rate for men compared to the stable annual crude mortality rate from 1955 to 1979. A corresponding 37.9% increase in the annual crude PD mortality rate for women has also occurred since 1980. The increase in overall mortality is due entirely to rapidly increasing age-adjusted mortality rates at ages greater than the intersect points for men and women. The results suggest that overall mortality due to common 'degenerative' diseases may increase dramatically as has occurred in PD.

Age Factors↗

PubMed1990

Longitudinal Gompertzian analysis of stroke mortality in the U.S., 1951-1986: declining stroke mortality is the natural consequence of competitive deterministic mortality dynamics.

Age-adjusted mortality rates for stroke in the United States from 1951 to 1986 were subjected to longitudinal Gompertzian analysis. Age-adjusted stroke mortality rate distributions were determined by a variable environmental factor and a constant Gompertz slope. Compared to 1951 values, the environmental factor in 1986 had declined (improved) 49.8% for men and 59.1% for women. This was associated with a 51.9% and 31.4% decrease in the annual crude mortality rate from stroke for men and women respectively. However, the Gompertz slope remained remarkably constant from 1951 to 1986; 0.050152 for men and 0.048341 for women. The constant Gompertz slope for age-adjusted mortality rate distributions for stroke is in sharp contrast to the increasing Gompertz slope which occurs with an improving environment in 'degenerative' diseases and aging in general. These findings suggest that the recent dramatic decline in overall stroke mortality is the natural consequence of competitive deterministic mortality dynamics. As the overall environment becomes more conducive to human survival, Gompertzian diseases with converging mortality rate distributions must increase as causes of human mortality at the expense of diseases with constant Gompertz slopes.

Adult↗

PubMed1991

Longitudinal Gompertzian analysis of ischemic heart disease mortality in the U.S., 1962-1986: a method of demonstrating the deterministic dynamics describing its decline.

Age-adjusted mortality rates for ischemic heart disease (IHD) in the United States from 1962 to 1986 were subjected to longitudinal Gompertzian analysis. Age-adjusted IHD mortality rate distributions between age 40 and 85 years were determined by a variable environmental factor and an extrapolated common intersect point. The environmental factor declined (improved) 3.73-fold for men and 2.07-fold for women in 1986 as compared to 1962. However, the environmental factor in 1986 remained 15.34 fold more conductive to IHD mortality among men than women. The age at the extrapolated common intersect point was 126.7 years for men and 267.4 years for women. Longitudinal Gompertzian analysis of IHD mortality data suggests that IHD will remain a significant cause of mortality for men despite advances in risk factor reduction and medical therapy.

Adult↗

PubMed1991

Longitudinal Gompertzian analysis of primary malignant brain tumor mortality in the U.S., 1962-1987: rising mortality in the elderly is the natural consequence of competitive deterministic dynamics.

Age-adjusted mortality rates for primary malignant brain tumors (PMBT) in the United States from 1962 to 1987 were subjected to longitudinal Gompertzian analysis. Age-adjusted PMBT mortality rate distributions between age 25 and 65 years were determined by a variable environmental factor and a common intersect point. The environmental factor declined (improved) 1.58-fold for men and 2.34-fold for women in 1987 as compared to 1962. The age at the common intersect point was 68.4 years for men and 64.1 years for women. Between 1962 and 1987, non-age-standardized annual crude PMBT mortality rates increased 14.5% for men and 37.8% for women. However, PMBT mortality rates at age 77.5 years rose 259% for men and 409% for women between 1962 and 1987. Longitudinal Gompertzian analysis of PMBT mortality data suggests that rapidly rising PMBT mortality rates in the elderly are the natural consequence of competitive deterministic mortality dynamics and should not be attributed to environmental factors, past or present, that are directly contributing to PMBT mortality. Furthermore, longitudinal Gompertzian analysis demonstrates that PMBT mortality should not be studied in isolation, but rather should be examined in relation to other causes of death. When viewed from this perspective, the basis for the dramatic rise in PMBT mortality in the elderly becomes quite evident.

Adult↗

PubMed1991

Longitudinal Gompertzian analysis of lung cancer mortality in the U.S., 1968-1986. Rising lung cancer mortality is the natural consequence of competitive deterministic mortality dynamics.

Age-adjusted mortality rates for lung cancer (LC) in the United States from 1968 to 1986 were subjected to longitudinal Gompertzian analysis. Age-adjusted LC mortality rate distributions between age 20 and 50 years were determined by a variable environmental factor and a common intersect point. The environmental factor declined (improved) 1.89-fold for men and 3.11-fold for women in 1986 as compared to 1968. The age at the common intersect point was 47.2 years for men and 39.1 years for women. Between 1968 and 1986, the non-age-standardized annual crude LC mortality rate increased 44.8% for men and 217.6% for women. Longitudinal Gompertzian analysis of LC mortality data suggests that the rising LC mortality rates in the United States are the natural consequence of competitive deterministic mortality dynamics and not a reflection of an environment that is directly more conductive to LC mortality. That is, more people are dying of LC because they are not dying from other diseases such as ischemic heart disease and stroke. Longitudinal Gompertzian analysis demonstrates that single disease mortality should not be studied in isolation, but rather examined in relation to other causes of death. When viewed from this perspective, the basis for the more dramatic rise in LC mortality in women becomes immediately evident.

Adult↗

PubMed1984

Cardiovascular responsiveness to physiological agonists of male rats made hypertensive by long-term exposure to cadmium.

The mechanisms by which cadmium may affect cardiovascular regulation are controversial. In this study, we investigated haemodynamics and cardiovascular reactivity to various physiological agonists in anaesthetized male Sprague-Dawley rats which received, for 190 days, deionized drinking water containing 0 (control), 10 and 20 micrograms/ml of cadmium (as acetate). Systolic and diastolic blood pressure, as well as cardiac inotropism, were increased in a similar manner in the two groups of treated rats. Heart rate was reduced in the rats exposed to the higher dose of cadmium, while no electrocardiographic alteration was demonstrated. Cadmium exposure reduced the pressor responses following intravenous norepinephrine (0.25-1 microgram/kg), angiotensin I (0.25-1 microgram/kg) and higher doses of epinephrine (0.50 and 1 microgram/kg) as well as the depressor responses to bradykinin (0.40-1.6 microgram/kg). On the other hand, the exposed rats showed an increased vascular responsiveness to the beta-adrenoceptor stimulating effects of lower doses of epinephrine (0.125 and 0.25 microgram/kg). Moreover, the effects on blood pressure, heart rate and cardiac inotropism of graduated doses of intravenous acetylcholine, angiotensin II, histamine and serotonin were unchanged. Cadmium was accumulated in the kidney of the treated rats at levels similar to those found in exposed humans. Renal copper and zinc were also augmented, possibly in relation to the cadmium-induced synthesis of metallothionein, a protein able to bind different metals. On the whole, this study suggests that cadmium affects several neurohumoral mechanisms that regulate cardiovascular function. It is likely that the changes in these mechanisms have additive effects, under a possible influence of genetic and/or environmental variables, in determining cardiovascular alterations.

Acetylcholine↗

PubMed1993

Transgenic mice that express a myelin basic protein-specific T cell receptor develop spontaneous autoimmunity.

We constructed a transgenic mouse model that mimics the human autoimmune disease multiple sclerosis in its spontaneous induction and pathology. Transgenic mice were constructed expressing genes encoding a rearranged T cell receptor specific for myelin basic protein (MBP). T cell tolerance was not induced in the periphery, and functional, autoreactive T cells were found in the spleen and lymph nodes of these mice. Transgenic mice developed experimental allergic encephalomyelitis (EAE) following immunization with MBP and adjuvant plus pertussis toxin as well as with administration of pertussis toxin alone. Spontaneous EAE can develop in transgenic mice housed in a non-sterile facility but not in those maintained in a sterile, specific pathogen-free facility. This model system affords a unique opportunity to dissect the genetic and environmental variables that may contribute to the development of spontaneous autoimmune disease.

Animals↗

PubMed1990

The role of alterations in membrane lipid composition in enabling physiological adaptation of organisms to their physical environment.

It is clear from the literature reviewed that modifications in membrane lipid composition play a major role in the adaptation of diverse organisms to specific environments and physiological circumstances. Acyl chain and molecular species restructuring in phospholipids are the most ubiquitous adaptations to environmental insult, being implicated in membrane adjustments to temperature, pressure, water activity, pH and salinity. In contrast, other adaptations (e.g. modulation of anionic phospholipids (salinity adaptation), trehalose content (dehydration) and the PC/PE ratio (temperature acclimation] appear to be more context specific. Although the volume of correlative data relating membrane composition to environmental state is impressive, several questions must be explicitly addressed in future research if a mechanistic understanding of the role of lipids in fine tuning membrane function is to be achieved. These include: (1) Adaptation thresholds--How much environmental variation is required before an acclimatory response is initiated, and is the extent of membrane perturbation induced by such minimally effective stimuli similar for different stress vectors? Interspecific comparisons of the Na+/K(+)-ATPase of fish collected at different depths indicate that species must be separated in depth by a distance corresponding to a pressure difference of 20 MPa before pressure adaptation is evident. Assuming a dT/dP value of 0.23 (Table 1), a 20 MPa change in pressure corresponds to ca. a 5 degrees C change in temperature, which agrees well with the minimal temperature change required to elicit changes in the lipid composition of plasma membranes in kidney tissue of thermally-acclimating trout. A pressure of 20 MPa also corresponds approximately to the maximum depth from which deep sea animals survive being brought to the surface. Collectively, these observations suggest that the minimally effective stimuli for both temperature and pressure adaptation are similar. Comparable data are not available for other environmental variables. (2) Signal transduction--What signals are being sensed and how are they transduced into an adaptational response? In some cases, it is clear that the enzymes of lipid metabolism respond directly (either by a variation in catalytic rate or substrate preference) to variations in the physical environment in an apparently adaptive manner (e.g. refer Sections VI.A.1 and VI.B.2). It seems unlikely, however, that such direct effects can explain the totality of the adaptive capacity of organisms, especially given the evidence for the induction of desaturase synthesis in cold adaptation (refer to Section VI.A.2).(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗

PubMed1980

Primary care multidimensional model: a framework for formulating health problems in a primary care setting.

There is a need to develop a systematic method for integrating organic, emotional, personal, and environmental data of a patient's lifestyle into the management of health problems. The Primary Care Multidimensional Model (PCMM) was developed to assist in the formulation of an individual's health problem, whether categorized as biological, psychological or social. The PCMM was applied to 276 health problems attended in a consecutive sample of 84 adult patients cared for in an inner city primary care setting. Seventy-five percent of the problems were categorized as primarily biological, 14% as psychological, and 9% as social. Sixty-seven percent of the "biological" problems were found to have emotional, personal, or environmental variables from the patient's lifestyle considered relevant at the time of the study visit. All psychological and social problems were likewise multidimensional. In the population studied, over 75% of the health problems attended in a primary care practice fulfilled the biopsychosocial model of illness as defined by the PCMM. The heuristic value of this study is discussed.

Adaptation, Psychological↗

PubMed1987

Melatonin: a principal neuroimmunoregulatory and anti-stress hormone: its anti-aging effects.

Major environmental variables such as daily and seasonal changes of light and temperature regulate the daily circadian variations of synthesis and release of the pineal neurohormone N-acetyl-5-methoxytryptamine (melatonin). Melatonin has now been shown to be a potent immunoregulatory agent, and to be able to antagonize the immunosuppressive effects of acute anxiety stress in mice, as measured by antibody production, by thymus weight, and by the capacity of stressed- and evening-melatonin-treated mice to react against a lethal virus. Both psychogenic factors and infectious agents such as viruses can act as "stressors" and induce an immunosuppression. Their combination is a determinant for the course of infectious diseases and, perhaps, cancer. Circadian (evening) melatonin possesses thus the singular ability to up-regulate the immunosuppression of stressed mice. This effect of melatonin is not exerted directly on immunocompetent cells, but mediated via the endogenous opioid system upon antigen-activation of T cells. Melatonin being a short-lived hormone with negligible side-effects which is rapidly degraded and eliminated by the body, the use of melatonin offers a new approach to the physiological control of stress and stress-related infectious diseases. In addition, melatonin could be used for the potentiation of primary immunization (vaccination) against antigens of the most varied nature which do not evoke a robust or longlasting secondary (memory) response. The regulatory function of pineal melatonin is discussed also in relation to hematopoiesis, to its oncostatic effects, and to its possible dual role in reproduction physiology and generation of immunocompetence and tolerance during ontogeny.

Aging↗