[Parameters of thermohomeostasis and psychophysiological monitoring in the evaluation of the phasic structure of adaptation during 240-day isolation].
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Genomic imprinting, by which maternal and paternal alleles of some genes have different levels of activity, has profound effects on growth and development of the mammalian fetus. The action of imprinted genes after birth, in particular while the infant is dependent on maternal provision of nutrients, is far less well understood. We disrupted a paternally expressed transcript at the Gnas locus, Gnasxl, which encodes the unusual Gs alpha isoform XL alpha s. Mice with mutations in Gnasxl have poor postnatal growth and survival and a spectrum of phenotypic effects that indicate that XL alpha s controls a number of key postnatal physiological adaptations, including suckling, blood glucose and energy homeostasis. Increased cAMP levels in brown adipose tissue of Gnasxl mutants and phenotypic comparison with Gnas mutants suggest that XL alpha s can antagonize Gs alpha-dependent signaling pathways. The opposing effects of maternally and paternally expressed products of the Gnas locus provide tangible molecular support for the parental-conflict hypothesis of imprinting.
Symbiotic associations have arisen independently in several groups of the largely free-living turbellarians. Morphological adaptations of turbellarians to a symbiotic way of life include suckers and adhesive glands for attachment, elaborate systems of microvilli and other epidermal structures for absorption of food, glands for the formation of cysts, cocoons and cement material, and lack of a pharynx and intestine in some species. However, many species closely resemble their free-living relatives. Egg production is greatly increased at least in some species, and life cycles are always direct. Food of symbiotic turbellarians consists of host food and/or host tissue. Ectosymbiotes show fewer physiological adaptations than entosymbiotes. The major groups of parasitic Platyhelminthes (Trematoda Aspidogastrea, Trematoda Digenea, Monogenea, Udonellidea, Cestoda including Gyrocotylidea, Amphilinidea and Eucestoda), form one monophylum, the Neodermata, characterized by a neodermis (tegument) replacing the larval epidermis, epidermal cilia with a single horizontal rootlet, sensory receptors with electron-dense collars, spermatozoa with axonemes incorporated in the sperm body by proximodistal fusion, and protonephridial flame bulbs formed by two cells each contributing a row of longitudinal ribs to the filtration apparatus. The sister group of the Neodermata is unknown but is likely to be a large taxon including the Proseriata and some other turbellarian groups. Among the Neodermata, the Aspidogastrea is likely to be the most archaic group, as indicated by DNA studies, morphology, life cycles and physiology. Aspidogastreans can survive for many days or even weeks outside a host in simple media, they show little host specificity, and have an astonishingly complex nervous system and many types of sensory receptors, both in the larva and the adult. It is suggested that Aspidogastrea were originally parasites of molluscs (and possibly arthropods and other invertebrates) and that they are archaic forms which have remained at a stage where vertebrates represent facultative hosts or obligatory final hosts into which only the very last stages of the life cycle (maturation of the gonads) have been transferred. The complex life cycles of Digenea have evolved from the simple aspidogastrean ones by intercalation of multiplicative larval stages (sporocysts, rediae) in the mollusc host, and of cercarial stages ensuring dispersal to the now obligatory final host. Monogenea may have lost the molluscan host or evolved before the early neodermatans had acquired it. Cestoda either replaced the original molluscan with an arthropod host, retained an original arthropod host or evolved from an early neodermatan before molluscan hosts had been acquired, newly acquiring an arthropod host.(ABSTRACT TRUNCATED AT 400 WORDS)
Olive-mill wastewater (OMW) has a high organic and polyphenol content and is resistant to biodegradation. Its disposal leads to a major environmental pollution problem in the Mediterranean basin. The detoxification of OMW following inoculation with Azotobacter vinelandii (strain A) was performed for two successive 5-day-period cycles in an aerobic, biowheel-type reactor, under non-sterile conditions. The phytotoxicity of the processed product was reduced by over 90% at the end of both cycles. To exclusively monitor the A. vinelandii population in the reactor a most probable number-PCR approach was employed and applied daily to serial dilutions of total DNA extracted from reactor samples. PCR sensitivity was independent of the presence of OMW or non-target DNA. The A. vinelandii population dynamics were successfully monitored, showing an initial adaptation period, followed by a sharp population maximum on the fourth day of both cycles (1.6x10(8) and 9.6x10(7) cells ml(-1) respectively), after a major phytotoxicity decline. N(2) fixation rates were estimated using the acetylene reduction assay and reached a peak during the first 1-2 days of each cycle (36 and 29 nmol C(2)H(2) ml(-1) h(-1) respectively). The data are consistent with an initial physiological adaptation phase, where the presence of phenolic compounds limits A. vinelandii growth but stimulates N(2) fixation, followed by a rapid growth phase as phytotoxicity declines.
The role that Na,K-ATPase plays in Na+ and K+ antiport through the sarcolemma, in cation-homeostasis in cardiomyocytes as well as in excitation-contraction coupling and cell signalling in the myocardium is now widely recognized. It was its key importance for the cell membrane function that kept this enzyme intensively studied during the last three decades and finally brought to its discoverer the deserved Nobel Prize. Almost weekly are appearing new data concerning structure, function, regulation and role of the Na,K-ATPase in different physiological and pathological conditions. The special importance of the enzyme for heart function as well as the great amount of data that is concerned specifically with the heart Na,K-ATPase and accumulated since yet, started to call for setting them in order. The present paper updates basically important data on the cardiac Na,K-ATPase in relation to its specific properties, molecular mechanisms of function, mode of action, humoral and pharmacological modulation, adaptability, physiological role and clinical aspects.
Adaptations to survive periods of limited access to oxygen should have been favored along the evolution of vertebrates. Paradigmatic examples of this adaptation are the diving animals, which can sustain prolonged and repetitive periods of anoxia. These animals support what would be considered a severe gas imbalance in their internal environment thanks to three main strategies: increased oxygen stores, resistance to asphyxia, and reduced metabolic expenditure during the apneic intervals. However, diving animals developed their abilities from very old life-sustaining responses that should have been used on many other occasions. Humans with sleep apneas perhaps share many physiological adaptations with diving animals. We review here the extent of such similarities and offer clear evidence of its existence and suggest possible research lines that could improve the clinical knowledge about this condition.
Febrile responses to bacterial pathogens are attenuated near term of pregnancy in several mammalian species. It is unknown, however, whether this reflects a fundamental physiological adaptation of female rats or whether it is specific to pregnancy. The aims of this study therefore were 1) to determine whether febrile responses to the bacterial endotoxin lipopolysaccharide (LPS) are attenuated in female vs. male rats and, if so, to identify possible mechanisms involved in modulating this and 2) to assess whether plasma concentrations of the anti-inflammatory cytokine, interleukin-1 receptor antagonist (IL-1ra), an important regulator of fever, are dependent on the physiological state of the female and could therefore be involved in modulating febrile responses. We found febrile responses were attenuated in cycling female vs. male rats and also in near-term pregnant dams vs. cycling females after intraperitoneal injection of LPS (0.05 mg/kg). Plasma levels of IL-1ra were significantly greater in female rats after injection of LPS, particularly during pregnancy, than in males. This was accompanied by attenuated levels of hypothalamic IL-1beta and cyclooxygenase-2 mRNA, two key mediators of the febrile response, in female rats. Furthermore, increasing plasma levels of IL-1ra in male rats by intraperitoneal administration of the recombinant antagonist attenuated hypothalamic mRNA levels of these mediators after LPS. These data suggest that there is a fundamental difference in febrile response to LPS between the genders that is likely regulated by IL-1ra. This may be an important mechanism that protects the developing fetus from potentially deleterious consequences of maternal fever during pregnancy.
The characteristics of intercellular connection have been observed during the dormancy development of garlic by the transmission electron microscope (TEM). The results indicated that the appearances of the different states of intercellular connection were physiological adaptation to the development of garlic clove during storage. Ectodesmata-like existed at the wall boundary between the declining tissue and the living cells in the garlic during germination period. By Confocal Laser Scanning Microscopy (CLSM) combined with fluorescence probe, 457Da Lucifer Yellow (LYCH) which was impermeable to the membrane, could enter the living parenchyma cell through symplastic route. The result proved that ectodesmata-like structure, which may be recognized as the modified plasmodesata, still retained physiological activity during a certain time and function as the channels of the symplastic transport of nutrient.
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The evidence that ETS increases risk of death from heart disease is similar to that which existed in 1986 when the US Surgeon General concluded that ETS caused lung cancer in healthy nonsmokers. There are 10 epidemiological studies, conducted in a variety of locations, that reflect about a 30% increase in risk of death from ischemic heart disease or myocardial infarction among nonsmokers living with smokers. The larger studies also demonstrate a significant dose-response effect, with greater exposure to ETS associated with greater risk of death from heart disease. These epidemiological studies are complemented by a variety of physiological and biochemical data that show that ETS adversely affects platelet function and damages arterial endothelium in a way that increases the risk of heart disease. Moreover, ETS, in realistic exposures, also exerts significant adverse effects on exercise capability of both healthy people and those with heart disease by reducing the body's ability to deliver and utilize oxygen. In animal experiments, ETS also depresses cellular respiration at the level of mitochondria. The polycyclic aromatic hydrocarbons in ETS also accelerate, and may initiate, the development of atherosclerotic plaque. Of note, the cardiovascular effects of ETS appear to be different in nonsmokers and smokers. Nonsmokers appear to be more sensitive to ETS than do smokers, perhaps because some of the affected physiological systems are sensitive to low doses of the compounds in ETS, then saturate, and also perhaps because of physiological adaptions smokers undergo as a result of long-term exposure to the toxins in cigarette smoke. In any event, these findings indicate that, for cardiovascular disease, it is incorrect to compute "cigarette equivalents" for passive exposure to ETS and then to extrapolate the effects of this exposure on nonsmokers from the effects of direct smoking on smokers. These results suggest that heart disease is an important consequence of exposure to ETS. The combination of epidemiological studies with demonstration of physiological changes with exposure to ETS, together with biochemical evidence that elements of ETS have significant adverse effects on the cardiovascular system, leads to the conclusion that ETS causes heart disease. This increase in risk translates into about 10 times as many deaths from ETS-induced heart disease as lung cancer; these deaths contribute greatly to the estimated 53,000 deaths annually from passive smoking. This toll makes passive smoking the third leading preventable cause of death in the United States today, behind active smoking and alcohol.
Stress is usually defined on the basis of the consequences observed after a threatening environmental change. This type of definition is mainly attributable to Seyle who conceived stress reaction as a final pathway, related to numerous aggressions against physical or psychological integrity, and threatening homeostasis. On the other hand, different authors showed that aggression does not systematically leads to retroactive undoing, as some types of environmental modifications can provoke an increase of knowledge, enriching both coping style and adaptative processes. Life events can be considered as a neurohormonal activation following action, the activation process being strictly dependent on the suddenness and unexpectedness of the event. "Normal" (at times necessary) stress, allowing the adaptative and sometimes survival processes, has thus to be distinguished from pathological stress, which provokes suffering. Stressful life event is modifying the environment, and the subject has to mobilize all his capacity, specificity and defense style in order to cope with the new situation. In this view, stressful life events may provoke enrichment and reinforcement for some and severe anxious disorders for others. Numerous factors are involved in the deleterious effect of a stressful life event, explaining why the modalities of the answer are so dramatically variable between different subjects.
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An overview of the main problems and misconceptions in the clinical application and theoretic evaluation of the stress concept reveals that the same 10 problems appear to cause the greatest difficulties in its application, irrespective of the specialty in which it is used: (1) the correct definition of stress, stressors and the general adaptation syndrome; (2) the concept of nonspecificity in biology and medicine; (3) the conditioning of stress responses by diverse endogenous (mainly genetically determined) and exogenous (environmental) factors; (4) the relation between the genral and the local adaptation syndromes; (5) the difference between direct and indirect pathogens; (6) the definition of the morbid lesions in whose pathogenesis stress plays a particularly prominent role--the so-called diseases of adaptation; (7) the role of genetics versus that of factors under voluntary self-control in mastering biologic stress; (8) the mode of action of syntoxic and catatoxic hormones, drugs and behavioural attitudes; (9) the so-called first mediator of the stress response, which carries the message that a state of stress exists from the directly affected area to the neurohormonal regulatory centres; and (10) the prophylaxis and treatment of stress-induced damage by pharmacologic and behavioural techniques.
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