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PubMed1999

Otx genes and the genetic control of brain morphogenesis.

Understanding the genetic mechanisms that control brain patterning in vertebrates represents a major challenge for developmental neurobiology. The cloning of genes likely to be involved in the organization of the brain and an analysis of their roles have revealed insights into the molecular pathways leading to neural induction, tissue specification, and regionalization of the brain. Among these genes, both Otx1 and Otx2, two murine homologs of the Drosophila orthodenticle (otd) gene, contribute to several steps in brain morphogenesis. Recent findings have demonstrated that Otx2 plays a major role in gastrulation and in the early specification of the anterior neural plate while Otx1 is mainly involved in corticogenesis, and Otx1 and Otx2 genes cooperate in such a way that a minimal level of OTX proteins are required for proper regionalization and subsequent patterning of the developing brain. Finally, experiments have shown functional equivalence between Drosophila otd and vertebrate Otx genes, suggesting a surprising conservation of function required in brain development throughout evolution.

Animals↗
PubMed1987

Evolution of criteria for determination of brain death in Japan.

In 1974, the Japanese EEG Society's Ad Hoc Committee on Brain Death published criteria for determining brain death only in cases of acute gross primary brain lesions. In 1983, a new brain death study group was organized to re-evaluate these criteria. During a 6-month period from March 1, 1984, 217 neurosurgical and neurological clinics and emergency services throughout Japan reported 718 brain deaths caused not only by primary lesions but also by secondary brain lesions and diagnosed as such on the basis of the 1974 criteria excluding the condition of "abrupt fall of blood pressure followed by persistent hypotension". The data derived from the 718 cases in this collaborative study were pooled and analyzed, and it became known that the 1974 criteria still are generally reliable. Some changes have been made, however, and new criteria for determination of brain death adopted.

Advisory Committees↗
PubMed2004

Feather brained.

Explore the source record for details and available documents.

Animals↗
PubMedDate not supplied

[The evolution of the incidence of glial brain tumors in Moldova in 1981-1991: the effect of excessive accidental hyper-radioactivity].

The authors discussed the effects of nuclear accident from Chernobyl (1986) upon the histotypes of cerebral glial tumors, first diagnosed during 1981-1991 at the Department of Pathology, Neurosurgical Hospital, Iaşi. It's microscopic diagnosis was determined according to the World Health Organization criterion (1979). The investigations established a tendency to diminish the incidence of astrocytomas and to increase the oligo-astrocytic tumors number, after 1986. Malignant astrocytomas did not presented any modifications with statistical significance during the eleven studied years.

Brain Neoplasms↗
PubMed2004

Reconstructing the evolutionary history of microcephalin, a gene controlling human brain size.

The defining process in the evolution of primates and particularly humans is the dramatic expansion of the brain. While many types of genes could potentially contribute to this process, genes that specifically regulate brain size during development may be especially relevant. Here, we examine the evolution of the microcephalin gene, whose null mutation in humans causes primary microcephaly, a congenital defect characterized by severe reductions in brain size without other gross abnormalities. We show that the evolution of microcephalin's protein sequence is highly accelerated throughout the lineage from simian ancestors to humans and chimpanzees, with the most pronounced acceleration seen in the early periods of this lineage. We further demonstrate that this accelerated evolution is coupled with signatures of positive selection. Statistical analysis suggests that about 45 advantageous amino acid changes in microcephalin might have fixed during the 25-30 million years of evolution from early simian progenitors to modern humans. These observations support the notion that the molecular evolution of microcephalin may have contributed to brain expansion in the simian lineage leading to humans. We have recently shown that ASPM, another gene linked to primary microcephaly, experienced strong positive selection in the ape lineage leading to humans. We therefore propose that genes regulating brain size during development may have the general propensity to contribute to brain evolution in primates and particularly humans.

Animals↗
PubMedDate not supplied

Otx genes in evolution: are they involved in instructing the vertebrate brain morphology?

Previous mouse models have indicated that Otx1 and Otx2 play an important role in brain and sense organ development and, together with the Drosophila orthodenticle (otd) gene, they share a high degree of reciprocal functional equivalence. Interestingly, mouse models replacing the same region of the Otx2 locus with Otx1, otd or lacZ genes have revealed the existence of a differential post-transcriptional control between the visceral endoderm (VE) and epiblast cells. Indeed Otx1, otd or lacZ mRNA were transcribed in both tissues but translated only in the VE. Embryos lacking OTX1 or OTD proteins in the epiblast and derived tissues, such as the neuroectoderm and axial mesendoderm (AME), fail to maintain the anterior identity and result in a headless phenotype. This finding leads us to hypothesise that, during evolution, the specification of the vertebrate-type brain may have required epiblast cells to translate Otx2 mRNA in order to establish maintenance properties. The establishment of this regulatory control might have been reflected into a remarkable reorganisation of the rostral CNS architecture and might have represented an important event in the evolution of the vertebrate head. Current data suggest that the Otx2 replaced region and in particular the 3' untranslated region (UTR), may contain regulatory element(s) necessary to translate and/or stabilise Otx2 mRNA in epiblast and its derivatives.

3' Untranslated Regions↗
PubMed1994

Identification of cholecystokinin from frog and turtle. Divergence of cholecystokinin and gastrin occurred before the evolution of amphibia.

Cholecystokinins from brain and small intestine of the bullfrog (Rana catesbeiana) and red-eared slider turtle (Pseudomys scripta) were isolated. The purifications were monitored by an antiserum specific for the common C-terminus of mammalian cholecystokinin and gastrin. The peptide structures were identified by sequence analysis of the intact peptides and proteolytic fragments, mass spectrometry, and amino acid analysis. Brain and small intestine of both species contained cholecystokinin-8 and substantial amounts of cholecystokinin-7. Furthermore, the small intestine of both frog and turtle contained a major fraction of the immunoreactive material as large peptides consisting of 69 residues and 70 residues, respectively. The structure for frog cholecystokinin-69 is ASSSAQLKPFQRIDGTSDQKAVIGAMLAKYLQTRKAGSSTGRYAVLPNRPVIDPTHRINDRDYMGWMDF .NH2 and the structure for turtle cholecystokinin-70 is VPSSAGQLKPIQRLDGNVDQKANIGALLAKYLQQARKGPTGRISMMGNRVQNIDPTHRINDRDYMGWMD F.NH2. All the isolated peptides were tyrosine sulfated at the seventh last residue. The peptides are highly similar to each other and to mammalian cholecystokinins (70% mutual identity and more than 50% identity with human cholecystokinin). Thus, they are clearly related to the known mammalian cholecystokinins. Both peptides include the monobasic and dibasic cleavage sites giving rise to cholecystokinins-33, -39, and -58 in mammals. However, only a small amount of turtle cholecystokinin-40 (corresponding to mammalian cholecystokinin-39) was isolated. This confirms that post-translational processing is highly species dependent. Recently, we isolated peptides from frog and turtle antrum. Following their origin they were named gastrins in spite of their C-terminal cholecystokinin-like structure. Thus, two different cholecystokinin/gastrin peptides exist in frog and turtle justifying the choice of two names. This finding of two members of the cholecystokinin/gastrin family in frog shows that the divergence of cholecystokinin and gastrin occurred simultaneously with or earlier than the appearance of amphibia during phylogenesis. Frog cholecystokinin and gastrin show sufficient similarity along the whole sequence to support the notion of a gene duplication of a common ancestor.

Amino Acid Sequence↗
PubMed1984

Are the limits of the mind expandable?

Considering the faculty for learning as a primary human characteristic and means to adaptation, any influence that may reduce this faculty becomes a hazard. Sensory and cognitive stimulation of inappropriate strength, both underload and overload, appears to be one such hazard. The central theme of this paper is overload, in contrast to writings in the 1950s and 1960s which dealt mainly with the ill effects of sensory and cognitive deprivation. The presentation consists of four parts: An account of the author's investigation in which the learning performance of students was correlated with varying input loads; critiques of overload by commentators of different backgrounds; the effects of input on man in the perspective of evolution and of brain-mind identity; a recommendation of physiological and biochemical testing of students exposed to varying input loads in correlation with their learning performance. The physical testing is either to ratify or to invalidate two conclusions reached in observations on the behavioral level. These conclusions are (1) that overload, quantitative or qualitative, obstructs the human capacity for learning, and that such interference may to some extent be a reflection of undesirable changes in autonomic conditions; and (2) that preventive measures can be taken by the structure of an input that reduces it in the perception of its receivers.

Biological Evolution↗
PubMedDate not supplied

[Stereotaxic technics in expanding lesions of the brain stem].

Stereotactic biopsies, according to the Talairach's system, define the histopathological data (nature, grading, spatial delimitation, evolutive potential) of brain stem lesions, precisely localized by computerized tomography scanner and magnetic resonance imaging. They are the more valued complement of the modern neuro-imaging and they prove the extreme polymorphism of theses lesions. According to this histological analysis and the volume of the lesions, it's possible to choose the best therapeutic procedure.

Adult↗
PubMed1985

The brain of the planarian as the ancestor of the human brain.

The planarian is the simplest living animal having a body plan of bilateral symmetry and cephalization. The brain of these free-living flatworms is a bilobed structure with a cortex of nerve cells and a core of nerve fibres including some that decussate to form commissures. Special sensory input from chemoreceptors, photoreceptor cells of primitive eyes, and tactile receptors are integrated to provide motor responses of the entire body, and local reflexes. Many morphological, electrophysiological, and pharmacological features of planarian neurons, as well as synaptic organization, are reminiscent of the vertebrate brain. Multipolar neurons and dendritic spines are rare in higher invertebrates, but are found in the planarian. Several neurotransmitter substances identified in the human brain also occur in the planarian nervous system. The planarian evolved before the divergence of the phylogenetic line leading to vertebrates. This simple worm therefore is suggested as a living example of the early evolution of the vertebrate brain. An extraordinary plasticity and regenerative capacity, and sensitivity to neurotoxins, provide unique opportunities for studying the reorganization of the nervous system after injury. Study of this simple organism may also contribute to a better understanding of the evolution of the human nervous system.

Animals↗
PubMed1997

Progressive impairment of brain oxidative metabolism reversed by reperfusion following middle cerebral artery occlusion in anaesthetized baboons.

A better understanding of the temporospatial evolution of ischaemic brain tissue towards necrosis would be of crucial value to establish and validate therapeutic strategies for stroke in man. By means of sequential positron emission tomographic (PET) studies performed through the acute to the chronic stages of infarction, we addressed the question of the effect of 6 h temporary occlusion of the middle cerebral artery (MCAO) on the evolution of the volume of severely hypometabolic tissue in anaesthetized baboons and compared it to that reported previously in permanently occluded baboons. Thirteen anaesthetized baboons underwent serial PET (15O steady-state technique) examinations before and 1, 4, 7, 24-48 h and 15-62 days following transorbital MCAO. Reperfusion, at 6 h post-occlusion, was assessed by Doppler sonography and cerebral blood flow (CBF) values after clip removal. In each baboon, the infarct volume was calculated by standard histological procedures 20-91 days after MCAO. The severely hypometabolic tissue volume, as defined by a threshold of oxidative metabolism, showed a progressive increase for up to 24-48 h in a not dissimilar manner to that found in baboons with permanent occlusion. However, these hypometabolic volumes regressed in the chronic stage (p < 0.05). Permanent and temporary occluded baboons, when taken together, showed a highly significant relationship between histological and chronic hypometabolic volumes (r = 0.84; p < 0.001). Moreover, the final hypometabolic volume where cerebral metabolic rate of oxygen (CMRO2) was below 40% of contralateral metabolism corresponded well to that of histological infarction volume. We conclude that, in anaesthetized baboons, restoration of blood flow will reverse (even if not immediately) the progressive derangement of metabolism after MCAO and markedly limit the final volume of consolidated infarction.)

Analysis of Variance↗