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[Evolution of the human brain].
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Dietary lipids and evolution of the human brain.
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Dietary lipids and evolution of the human brain.
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[The phosphopeptides of the brain and their evolution during growth].
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Oxygen deficiency and brain damage: localization, evolution in time, and mechanisms of damage.
Observations on some patients with CO intoxication have revealed a delayed type of brain injury, with symptoms appearing days after the initial insult. Possible mechanisms are discussed, with reference to recent experimental results on ischemic brain damage. These results have shown that brief periods of ischemia can cause necrosis of selectively vulnerable neurons, sometimes after a delay of 1-3 days. In at least one affected cell type (CAI pyramids in the hippocampus) delayed neuronal death was preceded by cellular hyperactivity. Recent neurochemical research offers tentative explanations. For example, several reactions triggered by increased calcium concentrations are long-lasting enough to cause sustained alteration of cell function and/or delayed neuronal death. These encompass physical interruption of the cytoskeleton by disassembly of microtubuli and degradation of neurofilaments, protein phosphorylation, and proteolytic degradation of dendritic structures. Reactions interrupting the cytoskeleton could cause cell death by impeding axonal transport, while phosphorylation-proteolysis could induce increased synaptic efficacy, with harmful overactivity.
Experimental brain abscess development in the chronically immunosuppressed host. Computerized tomographic and neuropathological correlations.
The neuropathological progression of brain abscess formation was studied experimentally in paired immunosuppressed and control dogs. The immunosuppressed animals received azathioprine and prednisone beginning 7 days prior to intracerebral inoculation with alpha streptococcus. Histological findings were correlated with computerized tomography (CT) brain scans. The evolution of brain abscess in the immunosuppressed animals could be divided into three stages based on histological evaluation: cerebritis stage (1 to 11 days), early-capsule stage (12 to 17 days), and late-capsule stage (18 days and later). There was a significant delay in the evolution of alpha streptococcus brain abscess compared to the authors' previous studies. Histologically, abscesses in immunosuppressed dogs were characterized by a decrease and delay in collagen formation, a reduction in polymorphonuclear leukocytes and macrophages, longer persistence of bacterial organisms, and an increase in gliosis. During the cerebritis stage, abscesses in control animals were consistently larger and more edematous than those in immunosuppressed animals and reached their maximum size by Day 8, whereas abscesses in immunocompromised animals reached their maximum size around Day 12. In the late-capsule stage, abscesses in immunosuppressed animals remained larger than those of control animals and continued to show signs of delayed development. This was evidenced by diffusion of contrast medium into the lucent center of ring-enhancing lesions on delayed CT scans. The results suggest that the decreased inflammatory response and edema formation in the immunosuppressed host resulted in less initial mass effect from brain abscess, but that the eventual size and area of the abscess may have become larger due to the less effective host response.
Conservative features of neocortical evolution in dolphin brain.
A Golgi survey of the convexity cortex in the brain of the dolphin, Tursiops truncatus, has revealed many cellular characteristics which may be indicative of conservative cortical evolution. These include a high degree of pyramidalization, and an accentuation of layer II. The presence of an accentuated layer II in convexity cortex is a protoneocortical characteristic found in more 'primitive' cortical arrangements. The growth ring concepts of cortical development outward in concentric waves from archicortical and paleocortical origins are discussed. In that context we have not been able to identify cores of hyperspecialization in the dolphin cortex corresponding to koniocortex and gigantopyramidal areas. This leads us to suggest that the cortex of the dolphin reflects a condition of the paralimbic-parinsular stage of evolutionary development. Thus, the dolphin brain may serve as a model of the theoretical mammalian archetype brain and its study may shed light on the organization of the brains of the initial ancestors of modern mammals.
Dietary lipids and evolution of the human brain.
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The role of dietary fatty acids in biology: their place in the evolution of the human brain.
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Alterations in the distribution of water, sodium, potassium, and chloride in brain during the evolution of ischemic cerebral edema.
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Allometry in primates, with emphasis on scaling and the evolution of the brain.
Allometry should be defined broadly as the study of size and its consequences, not narrowly as the application of power functions to the data of growth. Variation in size may be ontogenetic, static or phyletic. Errors of omission and treatment have plagued the study of allometry in primates. Standard texts often treat brain size as an independent measure, ignoring its allometric relation with body size - on this basis, gracile australopithecines have been accorded the mental status of gorillas. Intrinsic allometries of the brain/body are likewise neglected: many authors cite cerebral folding as evidence of man's mental superiority, but folding is a mechanical correlate of brain size itself. Confusion among types of scaling heads errors of treatment in both historical primacy [Dubois' ontogenetic inferences from interspecific curves] and current frequency. The predicted parameters of brain-body plots differ greatly for ontogenetic, intrapopulational, interspecific and phyletic allometries. I then discuss basic trends in bivariate allometry at the ordinal level for internal organ weights, skeletal dimensions, lifespan and fetal weight. In considering the causes of basic bivariate allometries, I examine the reason for differences among types of scaling in brain-body relationships. The interspecific exponent of 0.66 strongly suggests a relationship to body surfaces, but we have no satisfactory explanation for why this should be so. The tripartite ontogenetic plot is a consequence of patterns in neuronal differentiation. We do not know why intraspecific exponents fall between 0.2 and 0.4; several partial explanations have been offered. Multivariate techniques have transcended the pictorial representation of transformed coordinates and offer new, powerful approaches to total allometric patterns. Allometry is most often used as a 'criterion for subtraction'. In order to assess the nature and purpose of an adaptation, we must be able to identify and isolate the aspect of its form that depends both upon its size and the size of the body within which it resides. Cranial indices and limb lengths are misinterpreted when authors apply no correction for body size. The search for a criterion of subtraction has been most diligently pursued in studies of the brain. Clearly, brain size must be assessed by comparison with a 'standard' animal of the same body size. But how shall size be measured, especially in fossils; and how shall a standard animal be construed. I discuss and criticize three methods recently used: RADINSKY'S foramen magnum criterion; Jerison's minimum convex polygons and cephalization quotients; and the indices of progression in comparison with 'basal' insectivores' of BAUCHOT, Stephan and their colleagues.
[Recapitulation law and its significance in the morphofunctional evolution of the vetebrate brain].
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The temporal evolution of hypoglycemic brain damage. III. Light and electron microscopic findings in the rat caudoputamen.
The caudate nucleus and putamen belong to the selectively vulnerable brain regions which incur neuronal damage in clinical and experimental settings of both hypoglycemia and ischemia. We have previously documented the density and distribution of the hypoglycemic damage in rat caudoputamen, but the evolution of the injury, i.e., the sequence of structural changes, has not been assessed. Therefore, in the present study we analyze the light and electron microscopic alterations in the caudoputamen of rats exposed to standardized, pure insults of severe hypoglycemia with isoelectric EEG for 10-60 min, or in rats which, following insults of 30 or 60 min, were allowed to recover for periods from 5 min to 6 months. The hypoglycemic insult produced severe nerve cell injury in the dorsolateral caudoputamen. Immediately after the insult abnormal light neurons with clearing of the peripheral cytoplasm were present. These cells disappeared early in the recovery period, as they do in the cerebral cortex. Dark neurons were also present, but unlike those in the cerebral cortex they did not appear until recovery was instituted. Their number increased for a couple of hours and they became acidophilic within 4-6 h. At this stage, electron microscopy revealed severe clumping of the nuclear chromatin and cytoplasm as well as incipient fragmentation of cell membranes, all these changes indicating an irreversible injury. Within 24 h flocculent densities appeared in the mitochondria and by day 2-3 of recovery the great majority of the medium-sized neurons had undergone karyorrhexis and cytorrhexis, their remnants being subsequently removed by macrophages. After some weeks only large and a few medium-sized neurons remained amidst reactive astrocytes and numerous macrophages. The delay in the appearance of dark, lethally injured medium-sized neurons until the recovery was instituted suggests an effect that does not become apparent until the substrate supply and energy production are restored. Furthermore, it points out again the selectivity of the hypoglycemic nerve cell injury with respect to the type (metabolic characteristics?) and topographic location of the neurons.
Relationship between diffusion-weighted MR images, cerebral blood flow, and energy state in experimental brain infarction.
The regional evolution of brain infarction was studied in Wistar rats submitted to remotely controlled thread occlusion of the middle cerebral artery. Occlusion was performed in the magnet of an NMR tomography system to allow continuous recording of diffusion-weighted images. After 30 min (n = 6) or 2 h (n = 9), cerebral blood flow was measured by [14C] iodoantipyrine autoradiography while the regional distribution of ATP, glucose, lactate, and pH was imaged using pictorial bioluminescence and fluoroscopic methods. In diffusion-weighted images, the hemispheric lesion area (HLA) at the level of caudate-putamen amounted to 54.2 +/- 10.9% after 30 min and to 67.0 +/- 5.9% after 2 h vascular occlusion. These areas corresponded to the regions exhibiting tissue acidosis (60.8 +/- 9.3% and 70.4 +/- 4.5%), but were clearly larger than those in which ATP was depleted (22.3 +/- 20.8% and 49.6 +/- 12.9% after 30 min and 2 h, respectively). The threshold of blood flow for the increase of signal intensity in diffusion-weighted images increased between 30 min and 2 h occlusion from 34 to 41 ml/100 g per minute, the threshold of acidosis from 40 to 47 ml/100 g per minute, and the threshold for ATP depletion from 13 to 19 ml/100 g per minute. Our study demonstrates that diffusion-weighted imaging detects both the core and the penumbra of the evolving infarction but is not able to differentiate between the two parts. It further shows that the ischemic lesion grows during the initial 2 h of vascular occlusion, and that the size of the infarct core increases more rapidly than that of the penumbra.
[The human brain as a higher stage of the evolution of living matter: social matter].
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Newborn: adult brain ratios in hominid evolution.
The ratio of newborn to adult brain size varies widely in primates. These variations provide an index of the different degrees of postnatal brain growth in the different members of the primate order. The uniquely low figure for Homo sapiens indicates a greater degree of postnatal brain growth and therefore postnatal dependence and also a greater need and opportunity for social organisation. An attempt is made to determine the newborn adult brain ratio in a proto-human population, Australopithecus africanus. Two possible causes of the reduction of the ratio in hominid evolution are discussed. The first is the limiting confines of the maternal pelvis adapted primarily for orthograde progression rather than parturition. The second concerns the resultant of a set of three paired variables between the members of each pair of which there exists an allometric relationship. These are the relation between brain and body size in the adult, feto-maternal weight allometry and the relation between newborn brain-size and birth weight.
A progressive deposition of paired helical filaments (PHF) in the brain characterizes the evolution of dementia in Alzheimer's disease. An immunocytochemical study with a monoclonal antibody against the PHF core.
Using the monoclonal antibody (mAb) 6.423 which recognizes epitopes of the pronase-resistant core of paired helical filaments (PHF), we studied postmortem frontal cortex from Alzheimer's disease (AD) patients with short (Group II) and long (Group III) histories of clinical dementia. Four cases with clinically unconfirmed dementia and a postmortem diagnosis of AD (Group I) were also studied. In Group I, the 6,423 mAb was negative whereas in Group II, the antibody recognized primarily neurofibrillary tangles (NFT). In contrast, brains in Group III contained a dense network of 6,423-immunoreactive (IR) thread-like structures ("ghost" neurites) and plaque-like structures with granular appearance, in addition to NFT. The number of 6,423-IR structures appeared to be related to the duration of clinical dementia and the age of onset. Furthermore, "ghost" neurites were more abundant in young AD cases. The possible significance of the 6,423-IR pattern in the pathogenesis of AD is discussed.