Abstract: Empirical evidence and theoretical considerations suggest that there are mechanisms protecting the germ line from untoward somatic influences. In the intraorganismal competition between cell lineages, evolution will give priority for protection to the germ line, which carriers the heritable genes. In embryogenesis, germ cells migrate along the midline as this is an area where developmental influences are lower; exposure to somatic factors may cause inception of teratomas. In order not to hinder the germ line, the female genital tract has a reduced level of cell determination, which results in the multifariousness of gynaecological proliferations, including mullerianosis. The external location of testes reduces somatic constraints on spermatogenesis.
Abstract: It is commonly assumed that sleep is secondary to the waking state. We consider that in evolution relational life, as represented by the waking state, was superimposed on vegetative life. Waking is periodic, and vegetation is manifest in the intervals. This vegetative phase takes the form of sleep. The model, which overturns the traditional view, offers new suggestions about the psychological and cultural conception of sleep, sleep and the brain, dreaming, mind and memory.
Abstract: The anteroposterior and the dorsoventral axes plus two semiaxes orthogonal to the median plane can give enantiomorphic positional information to the two halves of the embryo. This kind of positional information can both determine the development of bilateral symmetry and mark left and right. Left/right asymmetry may be caused by a generative programme that operates on the three orthogonal coordinates of one side. The chirality of the asymmetry will thus depend on which side the programme operates. Kartagener's syndrome can be explained by considering that a ciliation-or-division switch involved in gastrulation assigns the generative programme to one side by creating a difference in the growth rate between the two halves of the embryo: in the syndrome a defect of ciliation blocks the switch, and the generative programme is assigned randomly. The model may be of particular utility for cerebral L/R asymmetries, for which a distinction from truncal L/R asymmetries is proposed.
Abstract: The growth of lung neoplasias, meningiomas, basal cell carcinomas and large bowel neoplasias might be influenced by the fractal structure of their tissues of origin.
Abstract: Primary brain tumors invade and metastasize within the central nervous system (CNS), but rarely extraaxially. A model explaining this behavior is presented. In non-CNS tumors metastases occur since subpopulations of cells capable of invasion and metastases are selected by the tissular environment, and in particular by the connective stroma, which opposes invasion. The CNS lacks a connective stroma, therefore a primary tumor can grow easily in it, but subpopulations capable of metastasization are not selected. Implications of the explanation are: 1) metastasization is largely based on the ability to invade the connective stroma, 2) paradoxically, a less favourable host tissue environment can result in a more aggressive tumoral behavior.
Abstract: In the case of human brains significant functional connections and exchange of information exist not only within brains, but also between them (given language). Connected human brains constitute a physiological entity, which should be taken into account when modeling human brain functions.
Abstract: Cerebral and coronary arterial trees lack functional anastomoses and are 'non-redundant' in the number of arteries. These two morphological characteristics expose brain and myocardium to vascular pathologies. An elementary model common to the cerebral and myocardial blood supply permits an explanation of the two characteristics. On the ground of this model the brain and the myocardium are represented as dynamic systems--organ-systems--made up of units, these corresponding to neurons and to cardiac cells. A flow of information between the units determines variations of state of the units. The whole of the variations of state of the units gives the organ-system function. The artery tree is considered as an information channel--tree-channel--that conveys information to the units. This artery-transmitted information determines the way the units function. The tree-channel always emits the same message. Therefore the artery-transmitted information does not cause local or temporal variations in the functioning of the units. On the contrary, if the tree-channel is noised the ending branches will emit randomly varied messages. Such random emission--disorder--will cause random loco-temporal variations in the functioning of the units. Consequently the functioning of the organ-system will be disturbed. It is shown that a low number of branches lowers the quantity of disorder that a noised tree-channel can emit. The absence of anastomoses avoids combinatory phenomena between the diverse messages that would increase the disorder. Biological and pathological evidence supports the model and the explanation.
Abstract: Two characteristics of breast biology appear to constitute weak points in the fight against breast carcinoma. First, the epithelium from which breast carcinoma arises is of relatively easy accessibility, as it lines cavities which are in close communication with the outside. Second, the elimination of breast epithelium can be tolerated by the organism. Theoretically, breast carcinoma may be prevented by destroying breast epithelium through the injection of an agent into the ductal orifices at the nipple. This strategy appears relatively easy to perform in comparison with conventional strategies, which have not given reliable results. Therefore the possibility presented here should not be neglected.
Abstract: 1. Immunocytochemical evidence is presented of the ultrastructural localization of binding sites for S-100 protein in synaptosomal fractions and subfractions. Synaptosomes or isolated synaptosomal subfractions were first incubated with S-100, then centrifuged to remove unbound S-100, and finally fixed before treatment with anti-S-100 antiserum, using the unlabeled antibody peroxidase-antiperoxidase (PAP) method. 2. When intact synaptosomes were used, the immunoreaction product was localized to the postsynaptic density including the postsynaptic membrane. In some reactive synaptosomes, the presynaptic membrane was labeled as well, in the region of synaptic contact. No reaction deposit was found in the synaptic cleft or on intrasynaptosomal structures. Divalent cations (Ca2+ and Mg2+) were essential for S-100 to interact with synaptosomes. Of the synaptosomal subfractions tested, i.e., synaptic vesicles and intraterminal mitochondria, only synaptic vesicles showed immunoreactivity when treated with S-100 and anti-S-100 antiserum as described above. 3. The S-100 immunoreactivity in synaptic structures documented in this report parallels the distribution of the high-affinity binding sites for radiolabeled S-100 in synaptosomal fractions and subfractions.
