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At least 343 records · Page 19Linked to original sources
PubMed1994

Cerebral blood flow and effects of cerebrospinal fluid on calcium transport in patients with cerebral infarction.

BACKGROUND AND PURPOSE: In this study we investigated whether cerebrospinal fluid in patients with brain infarction possesses an activity that contributes to the evolution of brain ischemia. As a test, the effect of cerebrospinal fluid on Ca2+ influx into the intracellular space was chosen because this process is a mechanism for vasospasm, platelet aggregation as thrombi, and neuron damage. METHODS: Effects of cerebrospinal fluid taken from 48 patients with cerebral hemispheric infarction on the concentration of cytosolic free Ca2+ in platelets were studied using the fluorescent probe quin-2. Hemispheric cerebral blood flow was measured using 133Xe intravenous injection. RESULTS: Cerebrospinal fluid in 19 of 48 patients with cerebral hemispheric infarction increased the level of cytosolic free Ca2+ in platelets. The course of the disease in the patients who showed a positive effect of cerebrospinal fluid on Ca2+, when compared with that of patients who showed a negative effect, was characterized by a more severe clinical manifestation and mortality. The decrease in hemispheric cerebral blood flow was more marked in both ischemic and contralateral hemispheres in patients with positive effects of cerebrospinal fluid on the level of Ca2+. CONCLUSIONS: These data suggest that the ability of cerebrospinal fluid to evoke Ca2+ influx into the intracellular space in patients with brain infarction is a factor that aggravates ischemic brain damage.

Biological Transport↗
PubMed1999

Biphasic edema after hypoxic-ischemic brain injury in neonatal rats reflects early neuronal and late glial damage.

Magnetic resonance imaging with diffusion- and T2-weighted imaging and 31P magnetic resonance spectroscopy was used to investigate the relationship between development of brain edema and alterations of the brain energy metabolism after hypoxia-ischemia (HI) brain injury in 7-d-old rats. The results were correlated with histologic examinations at various times during recovery up to 5 d. Moderate HI, induced by right common carotid artery ligation and subsequent exposure to 8% O2 for 90 min, produced a cytotoxic edema of 52+/-9% brain volume and depressed the ratio of phosphocreatine to inorganic phosphate from 1.43+/-0.21 to 0.11+/-0.09. Within 1 h of reoxygenation, the edema decreased to 4+/-2% of brain volume, demarcating the core of the lesion. At 5 h of recovery, a secondary cytotoxic edema together with a newly developing vasogenic edema expanded again, reaching its maximal extent of 45+/-10% brain volume at around 24 h. The ratio of phosphocreatine to inorganic phosphate recovered slowly, reaching 1.12+/-0.27 around 13 h. Thereafter it declined again in a manner analogous to the observations made in human newborns after severe perinatal asphyxia, reaching trough values of 0.48+/-0.22 around 24 h after HI. At the cellular level, the vast majority of neuronal death occurred before 15 h. Subsequently, strong glial activation lasted 2-3 d after HI. At 5 d, a cystic infarction of 35+/-12% brain volume was found. We conclude that the biphasic evolution of brain edema and energy metabolism reflects early neuronal and late glial damage in response to moderate HI injury. Therefore, the secondary energy breakdown reflects glial activation and subsequent glial death.

Animals↗
PubMed1985

[Acridine orange: a fluorochrome of nucleic acids for the study of muscle and nerve cells].

Acridine orange renders nucleic acids fluorescent when forming complexes with them: D.N.A. is coloured luminous yellow while R.N.A. is a brilliant orange. Its application to sections of muscle biopsies permits the identification of certain muscle fibres, recognized by their bright orange fluorescence which contrasts with the pale green of mature, normal myofibrils in three specific situations: denervation, regeneration following injury, and the rapid growth and maturation of fetal muscle. Moreover, myopathic nonregenerative atrophy, as well as histochemical type-specific atrophies, do not exhibit this same orange fluorescence. Because neurons, particularly motor neurons, contain large amounts of R.N.A. (by contrast with glial cells which have very little) the application of acridine orange in the central nervous system might help in understanding the development of the fetal brain, the evolution of some neurologic diseases, and the maturation of brain tumors. Since the technique does not require the exclusive use of frozen tissues, but also may be applied to formalin-fixed tissue in paraffin sections, it is well adapted to the study of tissue obtained at autopsy.

Acridine Orange↗
PubMed2000

Dynamics of regional brain metabolism and gene expression after middle cerebral artery occlusion in mice.

The evolution of brain infarcts during permanent occlusion of the middle cerebral artery (MCA) was studied in mice using multiparametric imaging techniques. Regional protein synthesis and the regional tissue content of ATP were measured on adjacent cryostat sections at increasing intervals after vascular occlusion ranging from 1 hour to 3 days. The observed changes were correlated with the expression of the mRNA of hsp70, c-fos, c-jun, and junB, as well as the distribution of DNA double-strand breaks visualized by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling (TUNEL). One hour after MCA occlusion, the tissue volume with suppressed protein synthesis was distinctly larger than that in which ATP was depleted. With ongoing ischemia time, the ATP-depleted area gradually expanded and, within 1 day, merged with the region of suppressed protein synthesis. Expression of hsp70 mRNA occurred mainly in the penumbra (defined as the region of suppressed protein synthesis but preserved ATP), peaking at 3 hours after vascular occlusion. Expression of the immediate-early genes c-jun, c-fos, and junB increased both in the penumbra and the periinfarct normal tissue already at 1 hour after vascular occlusion, with slightly different regional and temporal patterns for each of these genes. DNA fragmentations were clearly confined to neurons; they appeared after 1 day in the infarct core (defined as the region of suppressed ATP) and never were detected in the penumbra. The late appearance of TUNEL after infarcts had reached their final size and the absence in the penumbra points against a major pathogenetic role of apoptosis. Permanent MCA occlusion in mice thus produces a gradually expanding infarct, the final size of which is heralded by the early inhibition of protein synthesis.

Adenosine Triphosphate↗
PubMed1994

Phylogeny through brain traits: more characters for the analysis of mammalian evolution.

We have assembled data on nine brain traits, in addition to the fifteen we have previously described, which provide new evidence for assessing mammalian relationships. States of these characters are tabulated as they occur in each of 152 mammalian species, providing data in numerically ordered form, useful for multiple analyses of phylogenetic relationships in programs which take into account variations in several different characters simultaneously. Derived states of each of the nine traits are characteristic of certain restricted groups of mammals; (1) mirroring of the complete SI body representation in isocortex (anthropoid primates); (2) loss of the accessory olfactory bulbs (sirenians, cetaceans, most bats, catarrhine primates); (3) Rindenkerne, clumps of cell bodies in layer 6 of cerebral cortex (sirenians); (4) posteriorly-pointing digits in the SI body representation (bats, both mega- and micro-); (5) equivalent tectopetal connections to the anterior colliculus of one side from both retinas, rather than predominantly from the contralateral retina (primates and megabats); (6) loss of lamination in dorsal cochlear nuclei (anthropoid primates, bats, seals, sirenians, cetaceans); (7) separation of claustrum from cerebral cortex (diprotodont marsupials, carnivores, artiodactyls, perissodactyls, hyracoids, cetaceans and primates), (8) presence of a complete secondary (SII) somatic sensory region of cerebral cortex (therians-all extant mammals other than monotremes), and (9) presence of a distinct external cuneate nucleus among the nuclei of the dorsal columns (all mammalian groups except monotremes and sirenians). Two examples of phylogenetic trees derived from these data are presented. These sample trees maintain the segregation of the monotremes and the marsupials, and the basic dichotomy of placentals seen in our earlier trees based entirely on brain data. They also show: an orderly sequence of bifurcations (rather than the commonly seen multifurcation near the base of the radiation) in the reconstruction of placental relationships; extremes of derivation for the Cetacea, the Chiroptera, and the Sirenia (in concordance with trees based on other data); a ferungulate association of Carnivora, Perissodactyla, Artiodactyla, Hyracoidea and Sirenia; and an assemblage of related Dermoptera, Primates, Scandentia, and Chiroptera which in this model also includes Insectivora and Macroscelidea. Analyses based on brain characters can reinforce conclusions based on other data, while at the same time introducing new ideas about relationships. Neural traits provide a source of data independent of those commonly used in phylogenetic analysis, and are extremely valuable for testing old hypotheses and for introducing new ones.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Plasticity of the central nervous system--a neurosurgeon's experience of cerebral compensation and decompensation.

Cerebral plasticity constitutes one of the most decisive factors in recovery and readaptation after cerebral lesions. In contrast to the considerable progress in current studies on normal neuronal plasticity including the idea of "l'homme neuronal", the concept of plasticity postulated by Albrecht Bethe in 1929 received little attention. The author, as a neurosurgeon, has tried to describe cranial morphological plasticity, morphological and functional plasticity in infantile encephalopathies and especially in hemiatrophic lesions. It is supposed that a true morphological substrate exists due to compensatory hyperplasia of the uninvolved hemisphere. Modern neurosurgical techniques have demonstrated that the functional plastic capacity is much larger than has been supposed, even in the elderly. Some aspects of the mechanisms of compensation and decompensation of cortical and subcortical structures as well as of the central regulation systems are discussed. The full extent of the amazing recovery and functional reorganization is reached by plastic capacity, personal motivation, adequate training and sufficient time. The contribution ends with an exposition of a personal philosophy concerning psycho-somatic dualism, the body-mind problem, the future of the human brain and the ethical outlook, based on the progressive biological evolution of the basal neocortex and the immanent functional development (H. Spatz).

Adaptation, Physiological↗
PubMed2001

Anthropoid cranial base architecture and scaling relationships.

This paper examines how various measures of basicranial length and cranial base angulation affect the relationship between basicranial flexion and relative brain size in anthropoids, including Homo sapiens. Most recent studies support the "spatial packing" hypothesis, that basicranial flexion in haplorhines maximizes braincase volume relative to basicranial length. However, a few studies find the basicranium is less flexed in H. sapiens than expected for other anthropoids, suggesting that other factors contribute to variation in hominin basicranial flexion. The measure of relative brain size used to test the spatial packing hypothesis, the Index of Relative Encephalization (IRE), is calculated with basicranial length (BL) in its denominator, so that shorter BL and larger brain size potentially inflate H. sapiens IREs. To investigate this problem, the lengths of midline cranial floor sections were scaled relative to the cube root of endocranial volume in 157 specimens from 18 anthropoid species. Results indicate that the posterior cranial base and planum sphenoideum are significantly shorter in H. sapiens than in other anthropoids, accounting for higher IREs. Including the cribriform plate in BL, advisable in studies using anthropoids, affects whether H. sapiens differs from other anthropoids for basicranial flexion vs. IRE. However, despite a shorter BL and elevated IRE, H. sapiens does not deviate significantly from the anthropoid relationship between basicranial flexion and relative brain size for two cranial base angles. Because different measures of cranial base angulation change how H. sapiens falls along the anthropoid regression line, it remains equivocal whether the basicranium is less flexed in H. sapiens than in other anthropoids when compared to relative brain size.

Animals↗
PubMed1986

Studies on L-arginase in developing rat small intestine, brain, and kidney. I. Ontogenic evolution of arginase isoenzymes.

The adult patterns of arginase isoenzymes in rat intestine, kidney, and brain are nearly identical and consist of two forms, cationic A1 and anionic A4. In this paper, the organ-specific maturation of the enzyme equipment in these tissues is reported. The activity of arginase in all tissues studied could be detected on the 13th to 16th days of gestation. In fetal intestine and kidney the arginase activity is low, and persists up to the weaning time when the rapid, 10-fold rise of the enzyme activity occurs. However, the adult pattern of arginase isoenzymes in these tissues is accomplished in different ways. In the intestine, arginase A1 appears in fetal life and is the only form of the enzyme till the 19th to 21st days of postnatal life when the second form of arginase, A4, appears and rapidly accumulates, being exclusively responsible for the rise of the total enzyme activity at the time of weaning. In kidney, arginase A1 alone is present in the early fetal period. Arginase A4 appears 3-4 days before birth and its activity persists unchanged within the first 2 weeks of postnatal life. The intensive rise in total specific activity of kidney arginase at weaning is due to the accumulation of preexisting arginase A4. In brain, the adult pattern of arginase isoenzymes is achieved earlier than in other tissues. Both forms, A1 and A4, occur on Days 13-14 of gestation.

Aging↗
PubMed2003

Induced gene expression in human brain after the split from chimpanzee.

Despite only approximately 1% difference in genomic DNA sequence, humans and chimpanzees differ considerably in mental and linguistic capabilities, and in susceptibility to some diseases. A recent comparison of gene expression in human and great apes cast some light on the genetic basis of these differences, but more rigorous study is required. Our statistical reanalysis of these microarray data shows that there have indeed been dramatic alterations in the expression of genes in the human brain since the split from chimpanzees, mainly caused by a set of genes with increased (rather than decreased) expression in the human brain.

Animals↗
PubMed1983

Energy metabolism, brain size and longevity in mammals.

The mathematical relations between basal energy metabolism, brain size, and life span in mammals have been investigated. The evolutionary level of brain development, or encephalization (c), is a function both of brain weight (E) and of body weight (P) according to (formula; see text) Brain weight was found to be a linear function of the product of encephalization and basal metabolic rate. The oxygen consumption of the brain (Mbrain) is proportional to both encephalization and body weight according to (formula; see text) The ratio of metabolic rate in the cerebral cortex to that in the brain as a whole depends solely upon the degree of encephalization and is independent of the size of the animal. The maximum potential life span of a mammal was found to be proportional to the product of its degree of encephalization and the reciprocal of its metabolic rate per unit weight. Life span may be regarded as the algebraic sum of two components: (1) a deduced somatic component (Lb) inversely related to the basal metabolic rate per unit weight, and (2) an encephalization component (Le) related directly to the evolutionary increase of relative brain size.

Animals↗
PubMed1977

The theory of encephalization.

The theory of encephalization is developed from elementary dimensional requirements for the construction of a brain of given size. The basic assumption in the theory is that most of the brain in vertebrates is constructed as a series of mappings repeated at various levels. Encephalization is seen as a composite of an amplification factor for the repeated mappings (identical with the encephalization quotient EQ) and a factor associated with "added" tissue. The latter may be viewed as tissue that corresponds to new functions. The relation of the theory to allometric analysis is a relationship of theory to empirical estimation of "expected" brain size at a given body size. But body size is not fundamental to the theory. It is merely one of several possible sources of a measure of the area of a basic mapping, as it were, which is then subject to the amplification factor. Issues in the use of encephalization to assess behavioral capacities are reviewed briefly, as are the neurobiological correlates of encephalization and brain size.

Animals↗