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Adaptation of biological membranes to temperature. The lack of homeoviscous adaptation in the sarcoplasmic reticulum.

Temperature adaptation of biological membranes was examined by comparing the fragmented sarcoplasmic reticulum preparation of goldfish acclimated to different temperatures. Membrane fluidity was estimated using the fluorescence polarization technique. There was considerable variation between preparations, but no consistent differences in fluidity were observed between 5- and 25 degrees C-acclimated goldfish, fish species adapted over an evolutionary period to arctic or desert temperatures, and rat. The fatty acid composition of the sarcoplamic reticulum preparations of differently acclimated goldfish showed differences in the proportion of mono- and polyunsaturated fatty acids while the proportion of saturated fatty acids remained relatively constant. However, the fatty acid composition of sarcoplasmic reticulum phosphoglycerides became more unsaturated in the order rat, desert pupfish, arctic sculpin, which correlates with their respective environmental or body temperature. It is concluded that differences in membrane components other than fatty acids are important in determining membrane dynamic structure. The inability to demonstrate homeoviscous adaptation in sarcoplasmic reticulum is supported by other evidence suggesting that functions of the sarcoplasmic reticulum that are measured in vitro are not affected by such modifications of their phosphoglyceride fatty acid composition as occur during thermal acclimation.

Adaptation, Biological↗

Modern concepts of beauty.

Since the beginning of humanity, man has sought to define beauty. Whether by philosophy, mathematical constructs, social studies, or biology, the fascination with and the study of beauty has consumed our emotions and intellect. Many myths about this powerful force in our daily lives have been created, and some continue to be believed. Recent studies are shaping a new reality of beauty, one founded on evolutionary and biologic findings that link our fascination with beauty to our reproductive success. Cosmetic surgery, itself, may be an ongoing part of our biologic adaptation.

Adaptation, Biological↗

Earliest phases in the evolution of sickness and healing.

Sickness and healing constitute the root concepts that center medical anthropological inquiry and give the field its identity. Here, they are held to manifest a biological adaptation designed by evolution that requires culture for its final realization. Sickness and healing thus provide anthropology with a biocultural form that has changed in content and expression during cultural evolution. The early phases of this evolution, those bearing the most apparent influences of the environment of evolutionary adaptedness, are reviewed and analyzed in the article. Some of the implications of this for medical anthropology are discussed.

Adaptation, Biological↗

Ethanol-induced injury and adaptation in biological membranes.

Ethanol intoxication, both acute and chronic, exerts profound effects on the protein and lipid constituents of biological membranes, which reflect damage and adaptation. Changes in mitochondrial structure are accompanied by specific decreases in components of the electron transport chain, an effect probably related to decreased mitochondrial protein synthesis. Ethanol in vitro reduces the transition temperatures of membrane-bound enzyme activities and decreases the order parameter, as measured by electron paramagnetic resonance. By contrast, both are increased after chronic ethanol administration, and membranes from rats chronically treated with ethanol are highly resistant to disordering by ethanol. This adaptation to the acute fluidizing effect of ethanol may be attributed to an increased saturation of mitochondrial phospholipids, particularly cardiolipin. The increased rigidity of mitochondrial and synaptosomal membranes leads to conspicuously reduced binding of ethanol and of the general anesthetic halothane in preparations from chronically treated animals, a finding that may explain tolerance to ethanol and cross-tolerance to anesthetics. Ethanol also affects the plasma membrane, as demonstrated by a decrease in amino acid transport by hepatocytes. Moreover, the addition of physiological concentrations of ethanol to nonlethal concentrations of membrane-active hepatotoxins produces necrosis of hepatocytes, apparently by augmenting the permeability of the plasma membrane to calcium. Inasmuch as the human liver es exposed to numerous membrane-active agents, e.g., viruses, products of intestinal bacteria, and xenobiotics, this finding may explain the sudden onset of hepatic necrosis in individuals who have abused alcohol for many years. The data suggest that initially ethanol increases the fluidity of all biological membranes. This effect, if continued chronically, is balanced by a change in the lipid composition of the membranes, which increases their rigidity and makes them resistant to disordering by ethanol (homeoviscous adaptation). The increased rigidity reduces the binding of ethanol and other compounds, but also impairs a variety of membrane-bound functions. The combination of ethanol and membrane-active toxins can lead to cell necrosis, a mechanism that may explain cell death not only in the liver, but also in organs that do not metabolize ethanol, such as the heart, pancreas, and brain.

Adenosine Triphosphate↗

The adaptive value of dental crowding: a consideration of the biologic basis of malocclusion.

Malocclusion, an ambiguous concept that refers to structural disharmony of the teeth and jaws, can be defined only in reference to normal occlusion. If normal occlusion is synonymous only with ideal occlusion, then normal occlusion becomes a rare occurrence. A biologically valid concept of normal occlusion includes a range of variation in the relevant occlusal variables that is compatible with health and unimpaired function. The difficulty in defining malocclusion is the determination of the point at which normal variation becomes abnormal. A clearer concept of malocclusion is obtained if the occlusal variables that it comprises are considered. Dental crowding is endemic among technologically advanced populations and uncommon in primitive groups. The significant elements in the development of most dental crowding are mesial migration and the lack of interproximal attrition. Mesial migration of the posterior teeth provides the functional replacement for the tooth surface lost to attrition because of the rigors of a primitive diet. In modern man there is little attrition of the teeth because of a soft, processed diet; this can result in dental crowding and impaction of the third molars. It is postulated that the tooth-jaw size discrepancy apparent in modern man as dental crowding is, in primitive man, a crucial biologic adaptation imposed by the selection pressures of a demanding diet that maintains sufficient chewing surface area for long-term survival. Selection pressures for teeth large enough to withstand a rigorous diet have been relaxed only recently in advanced populations, and the slow pace of evolutionary change has not yet brought the teeth and jaws into harmonious relationship.

Adaptation, Biological↗

[Atherosclerosis as a problem of general biology: cell adaptation to deficiency of essential fatty acids].

It is suggested that intracellular deficiency of polyenic fatty acids (FA) is the biochemical basis of atherosclerosis. Its cause in the presence of abundant blood polyenic FA as cholesterol esters (cholesterol-esterified polyenic FA) is blockade of apoB-100-receptor endocytosis. The occurrence of polyenic FA deficiency in phylo- and ontogenesis and the cell adaptation reactions which accomplish the cell transfer and receptor absorption of polyenic FA are considered. The pathogenesis of atherosclerosis is a long-term adaptation to deficient cellular essential FA. At the same time the cells form a plasma membrane, synthesize thromboxanes, prostaglandins, and leukotrienes from omega-9-dihomo-Y-linolenic FA rather than from essential omega-6-arachidonic and omega-3-eicosapentaenic acids. This adaptation process determines all metabolic disturbances which are peculiar to atherosclerosis.

Adaptation, Physiological↗

Physical models of biological information and adaptation.

The bio-informational equivalence asserts that biological processes reduce to processes of information transfer. In this paper, that equivalence is treated as a metaphor with deeply anthropomorphic content of a sort that resists constitutive-analytical definition, including formulation within mathematical theories of information. It is argued that continuance of the metaphor, as a quasi-theoretical perspective in biology, must entail a methodological dislocation between biological and physical science. It is proposed that a general class of functions, drawn from classical physics, can serve to eliminate the anthropomorphism. Further considerations indicate that the concept of biological adaptation is central to the general applicability of the informational idea in biology; a non-anthropomorphic treatment of adaptive phenomena is suggested in terms of variational principles.

Adaptation, Biological↗

Transmembrane adapters: structure, biochemistry and biology.

Transmembrane adapter proteins (TRAPs) represent a relatively new and unique group of signalling molecules in hematopoetic cells. They differ from other signalling proteins as they lack any enzymatic or transcriptional activity, instead they possesses multiple tyrosine-based signalling motifs (TBSMs). Triggering of immunoreceptors induces tyrosine phosphorylation of these motifs by members of the Src-, Syk- or Tec-family of protein tyrosine kinases thus enabling the TRAPs to recruit cytosolic adapter and/or effector molecules via their SH2-domains into close proximity to the immunoreceptors, a position from which they can coordinate and modulate signal transduction pathways important for lymphocyte function.

Adaptor Proteins, Signal Transducing↗