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Schwann cells forming peri-insular glial sheath of the pancreatic islets in some mammals can be involved in the pathogenesis of diabetes mellitus. Human pancreatic cells contain small elongated or oval cells of unknown origin with S100-immunopositive processes. We found that cells with processes located in pancreatic islets of human fetuses and children are similar to Schwann cells by their morphological and ultrastructural characteristics, immunopositive reaction for S100, and integration with nerve endings. In the pancreas of fetuses and children, Schwann cells are often seen in forming pancreatic islets and around the pancreatic ducts. The data suggests that Schwann cells can participate in the morphogenesis of human pancreatic islets.

Using gas chromatography a comparative study of the range and content of individual non-esterified fatty acids in serum of patients with diabetes mellitus type 1 in the third trimester of pregnancy, and healthy pregnant and non-pregnant women has been carried out. In groups of pregnant women there was activation of lipid metabolism, confirmed by corresponding changes in serum biochemical parameters, as well as in the content of non-esterified fatty acids. Intergroup differences in the non-esterified fatty acids were not found. However, there were significant differences between the examined groups in the quantitative content of non-esterified fatty acids.

Immunohistochemical study of distribution of chromogranin A (neuroendocrine cell marker) in the developing human pancreas was carried out. Immunopositive reaction to chromogranin A was detected in the primordial pancreas from the early period of development (8 weeks). The count of chromogranin A-positive cells in early fetuses significantly surpassed that of insulin- and glucagon-containing cells. Chromogranin A immunoreactive cells, but not cells reacting with antibodies to insulin and glucagon were detected in the pancreatic islets and pancreatic ducts during all periods of gestation. These results suggested that hormone synthesis by pancreatic endocrine cells was preceded by the expression of chromogranin A and hence, this marker could be used for studies of the mechanisms of development of the endocrine part of the pancreas.

Ciliated cells were found in the epithelium of the oral cavity of human embryos and fetuses starting from the seventh week of prenatal development. At the early stages of prenatal development (until the 13th week), cells with cilia cover most of the dorsal surface of the tongue and the soft palate, whereas they are found only near the gland ducts in the circumvallate and foliate lingual papillae after 17 weeks of development. The ultrastructure of the axoneme of cilia corresponds to the structure of motile cilia and is represented by nine microtubule doublets that surround the central pair of microtubule singlets. An immunohistochemical study performed on weeks 10-12 of development identified nerve endings associated with the ciliated cells. Until the 14th week of development, the cytoplasm of ciliated cells is immunopositive for NSE. The spatial distribution of ciliated cells in the tongue epithelium until the 13th week of development is not related to the morphogenesis of lingual papillae, and their role in the human oral cavity during the first trimester of pregnancy is unclear and requires further study.

Proinsulin content was measured in the serum of 82 children (aged from 3 to 14 years) with type 1 diabetes mellitus of various duration. Three groups of patients characterized by low (54%), normal (42%) and high (4%) levels of this prohormone were recognized. No dependence the proinsulin level on the disease term was found. The serum proinsulin level may be used as a parameter specifying the pathogenesis of type 1 diabetes mellitus.

The appearance of autoantibodies to neuronal proteins (S100, GFAP, MBP, and NGF) in rat serum was analyzed by ELISA on days 5, 10, 17, 25, and 32 after streptozotocin injection. Simultaneously, blood glucose and insulin autoantibodies were assayed. Serum glucose level increased on the next day after streptozotocin injection and the level of autoantibodies to insulin significantly increased on day 5 indicating the development of diabetes. The levels of antibodies to specific neuronal proteins (S100, GFAP, MBP, and NGF) also increased at this term. It is concluded that diabetes with streptozotocin is associated with damage to the blood-brain barrier.

An experiment was carried out to validate and select feed to be supplied to Pachydactylus turneri in a 30-day orbital flight of robotic spacecraft BION-M1. Larvae of two Tenebrionidae species, i.e., Tenebrio molitor and Zophobas were tested for survivability, tolerance of hunger and cold, ability to stick to and move along different surfaces. Tenebrio molitor was shown to be best suited. A special feeder that will sustain the beetle over 30 days was designed. The experiment provided new data about Tenebrionidae biology and suggested the feeding technology for a 2-month space experiment with Pachydactylus turneri.

Complete profiles of phospholipid and ceramide molecular species from erythrocyte lipid extracts of children without carbohydrate metabolism disorders, and children with type 1 diabetes were compared by means of high performance liquid chromatography/mass spectrometry. For the first time a statistically significant increase (p<0.05) of lysophosphatidylcholine content in two groups of diabetic children with different duration of the disease (less than one year and more than one year) was found. Statistically significant changes in other lipid classes were not observed. The dependence of the content of phosphatidylcholine and phosphatidylethanolamine molecular species containing arachidonic acid residue (20:4) on the duration of the disease was found. The observed shift in lipid metabolism suggests of phospholipase A2 and chronic inflammatory process at different stages of diabetes mellitus, in cells (erythrocytes), which aer not involved in the immune response.

To identify the association between distal peripheral neuropathy (DPN) and type 1 diabetes mellitus (T1D), 62 children and adolescents with different duration of T1D have been studied using electromyography (EMG). Subclinical symptoms of DPN occur with equal frequency in 74% of children with short duration of T1D (group 1) and in 72% of children with long duration of disease. In both groups, the highest frequency of disturbances of the neurophysiological parameters was found in the sural sensory nerve and the lowest frequency in the median motor nerve. Correlations between HbAlc levels and compound muscle action potential were revealed only in tibial and peroneal nerves and only in the early stages of T1D. However, this dependence disappears with increasing duration of the disease.

The functioning of Jacobson's or vomeronasal organ (VNO) in man is the subject-matter of discussion today. It is generally taken that VNO as an anatomic structure also remains in the adult; however, its receptor apparatus still degenerates in the fetal stage of ontogenesis. Nevertheless, the data available in the literature on the time and specific features of degenerative changes in the human fetal VNO are conflicting and ambiguous. The authors examined the human fetal nasal septum from the 8th week of development to birth, by applying the traditional histological procedures and neuron-specific beta3-tubulin antibodies. An immunohistochemical study could first show the receptor apparatus of the human fetal VNO at weeks 8-26 of development. The immunohistochemical study on a series of sections could reveal the regularities of spatial receptor distribution depending on the time of fetal development. In addition, the developed human fetal vomeronasal nerve and ganglion at weeks 8-26 were described, in human fetuses at weeks 8-26. The neuron-specific marker test has shown the nerve fibers departing directly from the VNO wall, which is inconsistent with the data available in the literature on vomeronasal nerve degeneration in this sign just after the 18th week of development.

A modified RP-HPLC-MS approach has been proposed for a single run separation and identification of the molecular species of different phospholipid classes in a complex extract. This approach has been applied to the analysis of glycero- and sphingolipid composition of human erythrocytes and a number of ceramide fractions have been identified; these fractions was missed in previous studies employing similar methods. The fine experimental design leads to the decrease in the number of procedures needed for a complete phospholipid profiling of the sample.

Principle trends in the evolution of brain associative centers are discussed. It is demonstrated that in various taxonomic groups the possibilities of adaptive changes, as far as the brain is concerned, go beyond the scope of biological, topographical, and dynamic coordinations, typical for other scopes and systems. The reason for such peculiarity of brain evolution is the multifunctional nature of nerve tissue. This property of nerve tissue allows vertebrates to implement the integrity principle and still preserve the flexibility of the brain, which is highly specialized morphologically and functionally.

An immunohistochemical study of the olfactory bulb (OB) in human fetuses was performed. Immunohistochemical markers for nervous system-specific protein complexes S-100 and SNAP-25 were used. At 20-22 weeks of development, the development of cells expressing protein S-100 was greater in the OB than in the neocortex (the areas of the gyrus rectus and the gyrus orbitalis longitudinalis internus). These quantitative differences indicate heterochronicity in glial differentiation in the OB and cerebral cortex. Immunopositive reactions for SNAP-25 were for the first time detected at the periphery of the OB and in glomeruli in human fetuses at 15-16 and 20-22 weeks of development. Immunohistochemical staining of the OB with antibodies to SNAP-25 indicated that the human olfactory system cannot function prior to 20-22 weeks of development. In the OB of fetuses at 28-29 weeks of development, the intensity of the immunohistochemical reaction showed topological differences. The reaction with antibodies to SNAP-25 in the OB of full-term fetuses was similar to the reaction in the OB of adult humans. The results of these immunohistochemical studies using the reaction for the protein complex SNAP-25 in fetuses of different ages suggest the that the primary olfactory center in humans starts to function no earlier than the 30th week of development.

The authors made a clinicoanatomic analysis of fetal death in a 32-year-old diabetic gravida at 34-35 weeks gestational age. Fetal autopsy identified the characteristic signs of fetopathy: macrosomy, cardiomegaly, hepatomegaly, and brain weight reduction. Histological analysis revealed minute foci of leukomalacia with glial proliferation in the cerebral hemispheres; adipose and hyaline drop degeneration of cardiomyocytes in the heart, that of hepatocytes in the liver, the proximal renal tubular epithelial cells; hemorrhages in the respiratory portions of the lung. The pancreas displayed inflammation foci, hypertrophy and hyperplasia of the islets of Langerhans. Immunohistochemical studies identified cells with enlarged nuclei among the beta and alpha-cells. The placenta showed a large mass with pronounced changes. It has been demonstrated that steroid diabetes may lead to the development of diabetic fetopathy and placental changes, which are typical of maternal diabetes.

To determine the endogenous alloxane content in blood of healthy donors we stabilized it by rapid lowering of pH in the sample to 2.0. Alloxane was then allowed to form a colored product in a reaction with o-phenylenediamine and its content was measured by spectrophotometry using an internal calibration curve. The experiment showed that the concentration of alloxane in blood of most of the healthy donors varied from 41 to 265 micromol/l. However, a small group of healthy people was had their blood alloxane level greatly exceeding the above-mentioned values.

Principal events in the early embryonic development of the nervous system, from neurulation to primary differentiation, are considered in different amphibian species. Attention is paid to numerous interspecific differences in the structure of neuroepithelium and the patterns of neurulation and embryonic brain segmentation. The data presented indicate that similarity in brain developmental patterns is apparently explained by universality of morphogenetic mechanisms rather than by the common origin of particular species. A hypothesis is proposed that similarity in the shape of the developing amphibian brain is determined by mechanisms of coding positional information necessary for histogenetic differentiation.

With the application of a double immunohistochemical labeling method, several types of neuroendocrine interactions were demonstrated in the pancreas of nutria. Two types of neuroinsular complexes were detected that have the organization typical to the mammals. It was found to be typical of nutria that several pancreatic islets were integrated with nerve cells and nerve fibers. The complexes detected that reflect the interactions between nervous elements and single endocrine cells or their small groups, are species-specific. The data obtained demonstrate the diversity of neuroendocrine interactions in the pancreas and possible influence of the nervous system on B-cell differentiation.

Immunohistochemical (tests for insulin, glucagons, periferin, SNAP-25, GFAP, NGF-R, RMR-22, MBP) and morphological studies were performed to examine the pancreatic nervous apparatus of human adults and fetuses in late phases of development. A role of the morphogenetic activity of the pancreatic nervous apparatus was investigated in type 1 diabetes mellitus (DM-1). The neurons and gliocytes located in the pancreas are suggested to have a morphogenetic activity and form a glial capsule throughout their life. The insular endocrine cells are shown to synthesize the proteins (SNAP-25, GFAP) characteristic of nerve cells and their synaptic terminals. A neurobiological model of DM-1 'development has been stated. The onset of the disease is characterized by the development of autoimmune processes directed to the nervous system. In nerve tissue protein autoimmunization, the fine insular neuroglial membrane is rapidly disrupted. This leads to the transfer of autoimmune aggression to the insulin-producing cells of the islets of Langerhans, which carry specific nerve tissue proteins onto their surface. Recovery of the islets becomes impossible without forming a protective neuroglial membrane, which makes the development of DM-1 irreversible.

Integral cytophotometry was used to measure lactate dehydrogenase (LDH) and its H-and M-isoforms in neurons and satellite gliocytes in tissue sections from the cranial cervical sympathetic ganglion of the rabbit in normal conditions and after experimental partial and complete pharmacological blockade of nicotinic cholinoreceptors (n-CR). In normal conditions, both cell types showed both the H-and M-type isoforms, though the isoenzyme profiles differed--neurons showed a dominance of H-isoform activity while the M-isoform was more active in satellite gliocytes. In partial and complete blockade, the activity of LDH and its H-and M-isoforms decreased significantly in proportion to the number of blocked n-CR. In satellite gliocytes, increases in the extent of blockade were associated with decreases in the activity only of the M-isoform, while the activity of the H-isoform did not change. In partial blockade, the LDH isoenzyme profile of satellite gliocytes shifted towards the neuronal isoform, while in complete blockade there was no difference from the LDH isoenzyme profile of intact neurons. These data led to the suggestion that the formation of lactate in satellite gliocytes is induced by nicotinic cholinergic synapses directly involved in neuron-glial interactions and in controlling the activity of the LDH enzyme system in sympathetic neurons.

Some trends in the phylogenetic changes of the vertebrate neural system in the course of their transition from aquatic to terrestrial mode of life are analyzed. Wide multifunctionality of the neural centers and heterotopic substitution of the brain functions are supposed to be prerequisites of transition of archaic amphibians to the land via a stable transitional environment. The latter include underground or vegetation aquatic-air labyrinths in which conditions of gradual acquisition of adaptations to the terrestrial mode of life occurred. The principal neurological adaptations to such mode of life and less dependence on aquatic environment developed during the long-term evolution in that environment. The neurobiological model of evolutionn of the archaic amphibians in the transitional environment of aquatic-air labyrinths suggested herewith is compared to other hypotheses of the tetrapod origin.

RNA contents in the cytoplasm of neurons and satellite gliocytes in the cranial cervical ganglion of rabbits were determined by photographic cytophotometry during pharmacological blockade of N-cholinergic (N-Ch) synapses with the N-cholinolytic dimecoline (s.c. doses of 10, 30, and 50 mg/kg) and during the gradual decrease and elimination of blockade (1-11 h after dosage). Partial blockade and blockade of intermediate intensity induced concordant variations in RNA contents in the two cell types. This concordance in changes was impaired in conditions of complete blockade. Analysis of these results suggests that N-Ch synaptic processes in the sympathetic ganglion directly modulate quantitative changes in RNA levels in the neuron cytoplasm and represent a factor synchronizing the metabolism of neuronal and glial RNA.

Immunohistochemical study revealed three types of neuroendocrine contacts in nutria pancreas. In most cases, the pancreatic islets and individual endocrine cells were associated with a diffuse neural network. Integration of neural ganglia with the islets and innervation of endocrine cells by projections of ganglionic cells were detected. It is hypothesized that the structure of neuroendocrine interactions plays different roles in the regulation of endocrine secretion.

Activity of LDH isoenzymes and the level of ATP, ADP, and AMP were determined in the rabbit superior cervical sympathetic ganglion under conditions of experimentally induced partial or total blockade of N-cholinergic (N-CE) synapses. This blockade changed the spectrum of LDH isoenzymes: partial blockade was accompanied by disappearance of LDH-4 and LDH-5; total blockade also caused disappearance of LDH-3. LDH-1 and LDH-2 that remained in the isoenzyme spectrum as well as total LDH activity decreased significantly. Under conditions of total N-CE blockade total activity of LDH represented 9% of control, whereas activity of LDH-1 and LDH-2 represented 16% of control. ATP content decreased by 53 and 93% under conditions of partial and total N-CE blockade, respectively. The levels of ADP and AMP decreased by 33 and 65 and 80 and 56%, respectively. Results of the present study suggest that activity of N-CE synapses is a crucial factor involved into the energy homeostasis of the sympathetic ganglion.

Using the method of integral cytophotometry, lactate dehydrogenase (LDH) N- and M-isoform activity was determined in neurons and satellite glial cells in tissue sections of rabbit cervical cranial sympathetic ganglion under normal conditions and after experimentally induced total and partial pharmacological blockade of nicotinic acetylcholine receptors (N-CR). In normal animals, activity of N- and M-isoforms was demonstrated in both cellular types, however, their LDH isoenzyme profile was different: N-isoforms prevailed in neurons, while M-isoforms were more active in glial cells. After partial and total blockade, activity of LDH, N- and M-isoforms was significantly reduced in neurons in proportion to the number of N-CR blocked. In satellite glial cells, the increase of blockade intensity was accompanied by the reduction of only M-isoform activity, while that of N-isoforms remained unchanged. After partial N-CR blockade, satellite glial cell LDH isoenzyme profile was shifted in the direction of a neuronal one, and after total blockade became indistinguishable from LDH isoenzyme profile of intact neurons. It is suggested that lactate formation in satellite glial cells is induced by N-cholinergic synapse activity, which directly mediates the neuron-glial interaction and participates in control of LDH enzyme system activity in sympathetic neurons.

Cytoplasmic rRNA content in neuronal and in satellite glial cells of cervical sympathetic ganglion was defined using photographic cytophotometry during the pharmacological blockade of N-cholinergic (N-CE) synapses, induced by the injection of N-cholinolytic drug dimecoline (10, 30 and 50 mg/kg subcutaneously), as well as during the period of blockade gradual resolution and termination (1-11 hours after treatment with cholinolytic drug). The partial blockade and average intensity blockade induced coordinated oscillations of rRNA content in both types of cells. The coordination of these changes was violated during the complete blockade. Analysis of the results obtained suggested that N-CE synaptic processes directly modulated quantitative changes of rRNA in neuronal cytoplasm could be a factor synchronizing the metabolism of neuronal and glial rRNA in a sympathetic ganglion.

X-ray microtomography using a wavelength of 0.7 A was used to detect elevated calcium concentration areas that integrate all types of human epiphyseal concretions. They consisted of both concretions and extracellular calcium, which could not be attributed to any particular tissue. There were no concretions outside of these zones. The center of concretion formation was found to be a single source that may be an individual pinealocyte. Comparison of postmortem human epiphyses in normalcy (natural aging), in chronic alcoholism, Alzheimer's disease, and schizophrenia revealed that there were differences in both the number of concretions and their formation topology. In normalcy, the field of elevated calcium concentration was continuous whereas in patients with the study mental diseases, it was divided into separate areas. There is evidence that in mental diseases, the amount of acervulus and its density decrease, which may a marker of the development of these diseases.

The epiphysis is a gland containing firm extracellular bodies (brain sand) the number of which increases with age. Microscopy and roentgen microtomography showed that in some cases of schizophrenia the amount of brain sand decreases. In parallel, cytoplasm of pinealocytes appears to contain concrements of a new type--irregular hollow spheres of 0.1-1.5 microm in size. They may contain fluoride. Typical hydroxyapatite retaining organic stroma may dissolve starting from the center both in health and schizophrenia.

Aim: To examine relationships between genital prolapse and joint hypermobility (JHM), between GP severity and degree of JHM, to reveal causes of GP in JHM patients., Material and Methods: A total of 208 females with GP (mean age 38.9 years) entered the trial. They were divided into three groups by severity of connective tissue dysplasia (CTD): with mild CTD--16.3%, moderate CTD--35.6% and severe CTD--48.1%. The following methods of investigation were used: podometric Freedland's technique, ultrasonic investigation of the gall bladder, kidneys, echocardiography, morphological study of platelets, morphological and immunohistochemical study of the ligaments., Results: In GP patients JHM occurred in 41.8% patients. Hypermobility of large joints reaches 38.9%, large--20.7%. Such associated manifestations of CTD as flatfoot, JHM, deformation of the spine, varicosity, predisposition to vegetovascular dysfunctions, mitral prolapse, arrhythmia, impaired conduction, refraction, gastroptosis, nephroptosis, hernias were observed in 69.2, 46.1, 38, 53.8, 49, 43.3, 38, 19.2, 12, 6.7, 14.4%, respectively. The morphological changes are explained by 40 +/- 15% type 1-3 collagen loss in the interstitial substance. Severe forms of GP in patients with JHM were observed in 84%. 52.4% females with JHM developed severe GP within 3 years after delivery of a child. Most of the examinees carried undifferentiated congenital dysplasias., Conclusion: JHM is a criterion of CTD diagnosis.

12 human embryos (stages 14-18) with different form of holoprosencephaly were studied. Spatial organization of the brain was reproduced with graphic reconstructions. It is demonstrated that the cause of different forms of holoprosencephaly is disturbed or delayed movement of the neurulation wave coming through the hemispheres of the forebrain. The cause of the defect may be an unspecific teratogenic factor or some cytogenetic damage. Severity and type of holoprosencephaly are associated not with the etiological factor but with the time of the action on the neurulation wave. Alobar holoprosencephaly results from the impact on neuralation for 22 days, semilobar--for 23 days and lobar--for 24 days.

Urinary incontinence (UI) in patients with genital prolapse is not always related to stress. It may result from dyslocation of the vesicourethral segment. While genital prolapse in young patients after a single normal delivery is common manifestation of connective tissue dysplasia (CTD) at the level of the reproductive system, 51.8% cases of UI may be of neurogenic origin and present as dysfunction of the vesicourethral segment and pelvic diaphragm. Unstability of the bladder and urethra in these cases may represent CTD at the level of the pelvic organs.

The mechanisms of early embryonal shaping of the brain in man and animals were studied. Analysis of the biomechanical properties of development of nervous tissue and embryological experiments demonstrated that tangential neuroepithelial intention is the major source of positional information. Experimental changes in the neuroepithelial intention system resulted in various types of embryonal anomalies of the nervous system. Mechanism-dependent ion channels that have marked periods of sensitivity and determine the histogenetic direction of neuroblast cell differentiation were found to underlie the mechanosensitivity of the neuroepithelium. Experimental findings were compared with unique autopsy data on early development of the human brain. Human embryos were examined from neurulation to week 6 of development. Different types of human embryonal brain anomalies were shown to occur with 3 types of neurulation disorders: 1) an open preneuropore is responsible for anomalies of the forebrain and ethmoidal area; 2) arrested neurulation in the postneuropore leads to anomalies of the diencephalon, midbrain, and occipital region; 3) impaired neurulation in the caudal region is a cause of spinal cord anomalies. The above anomalies resulted from local compensatory responses of the neuroepithelium due to the lack of intentions that are characteristic of normal development of the neural tube.

The effect of some developmental abnormalities on the morphogenesis of human brain asymmetry during early embryonic stages was studied. Insignificant predominance of the left hemisphere (1-3%) was revealed in human embryos.

Histological and morphometrical analysis of the brain and peripheral analyzers revealed proliferative migration abnormalities of brain development and neuron differentiation in mammals during a space flight, which can limit space exploration.

In experiments with rats effects of hypokinesia on the course of pregnancy and the mother-fetus system were investigated. Immobilization in penal-type cages of female rats on days 8 through to 19 of pregnancy gave rise to significant shifts in mother's organism, i.e. retarded body mass gain, mass reductions in thymus, spleen, liver, some other organs, and adipose tissue. Rates of prenatal fatality in the experimental group were not changed; yet, fetuses were behind the control by the values of body mass, ossification ranges, development of analyzers and other parameters. Quantities of liquid, sodium, magnesium and calcium per one gram of dry tissue were equal in the experimental and control fetuses. Comparison of the data with results of the embryological experiment with rats aboard the space "shuttle" suggests that immobilization is more baneful for the mother-fetus system than microgravity of the same length.

47 human embryos aged from 22 days to 6 weeks with various brain anomalies were studied. Space reconstruction of the brain organization is performed in 6 embryos. Neurulation anomalies analysis allowed to establish that human nervous system development is highly unstable between days 21 and 27 after fecundation when active change of the brain shape takes place and non-specific disturbance or delay of nervous cylinders closing results in the development of the nervous system embryonal pathologies. Various forms of the brain embryonal anomalies result from the three following variants of the neurulation disturbances; neurulation halt in the postneuropore zone leads to anomalies of the intermediate and median brain and occipital region of the head; neurulation disturbance in the caudal area of the nervous tube is the cause of spinal cord anomalies. The above anomalies are formed as a result of local neurulation disturbances which are the primary cause of the morphogenetic pathologies in the nervous system development. Therefore, it is justifiable to classify early embryonal anomalies of the nervous system according to their morphological origin and not by the final state of the fetus.

Amphibian embryos (Triturus vulgaris, Pleurodeles waltl, Hynobius keyserlingii, Ambystoma mexicanum, Rana temporaria, Bufo bufo, and Xenopus laevis) were investigated. We ascertained the morphological right-side asymmetry of the brain, which appears at the neurula stage and is preserved during the postembryonic (larval) development. In T. vulgaris, P. waltl, H. keyserlingii, and X. laevis, we observed right-side asymmetry of peripheral analyzers, such as the retina, ganglia of nerve VIII, and olfactory placodes. Structural analysis of the forebrain in A. mexicanum has shown that in the larvae, the pallium prevails on the left side of the cerebral hemisphere. During metamorphosis, left-side asymmetry is replaced by right-side, which is then preserved. We propose that the brain asymmetry arose at the early stages of evolution as a result of embryonic formation of the nervous system.

The histological structure of the brain and spinal cord, visual, olfactory, auditory and vestibular analysers, and endocrine organs (epiphysis, hypophysis, thyroid and parathyroid glands) were investigated in newborn rats delivered by females who had been exposed to weightlessness a half of the pregnancy period. Analysers of the flight animals did not have any marked deviations from the norm. Loci of neurone degeneration resembling porencephaly but less massive were revealed in various brain portions (cortex, hypocampus, metencephalon, spinal cord) of the infant rats developed in space flight. Endocrine studies showed accelerated differentiation of the thyroid cells secreting thyroid hormones, C-cells, and parathyroid cells in most of the infant rats of the flight group. The test animals reduced the size of epiphysis and the number of pinealocytes. Adenohypophysis was found to be smaller with altered spatial distribution of the trabecular system. The changes look quite impressive but do not threaten viability of the animals.

Age-related changes in the organon vomeronasalis (VO) and related structures have been described in normal human embryos of 19, 25, 28 and 40 mm in crown-rump length and in the embryo of 19 mm in crown-rump length during abnormal development in the uterine tube. The fourth branch of the VO nerve appeared in the 25 mm embryo. Signs of asymmetry and degenerative VO changes were analyzed in the 25 and 40 mm embryos. A supposed vomeronasal ganglion has been described. The possibility of fetuses at the late stages of prenatal development using the VO system is discussed.

Four patients with Stage III-IV Parkinson's disease were operated on. Stereotactic cryodestruction of the ventrolateral nucleus was made, followed 10 minutes later by implantation of mixed fetal and xenogenic nerve tissue cells. The nerve cells-the fetal part-are obtained from human fetuses in the age range of 14-18 weeks of development. Tissues from the ventral portion of the midbrain and basal ganglia of the forebrain were used. Neurogenic layings of Notch Drosophila melanogaster mutants serve as a xenograft. The mixture of nerve cells were prepared in ratios of 1000:20 and 1000:12. The follow-up of the patients lasted a year. Relapses were absent. The effect occurred on the operating table (in the combination of nuclear destruction and nerve cell transplantation) and only 6 months later only during transplantation of nerve cells (without destruction). An attempt of transplanting the above fetal xenogenic mixture of nerve cells to patients previously undergone 2 ineffective stereotactic operations provided no significant clinical effect. The concurrent destruction of ventrolateral nuclei in combination with fetal xenogenic tissue grafting is considered to be promising.

We studied the origin and development of the vomeronasal system in early human embryos of 10-18 mm crown-rump length under normal and pathological conditions. The formation of the vomeronasal organ from the vomeronasal groove and placode in a 10-mm embryo is described. We propose that the vomeronasal cavity originates in the schizocoel way. We studied the development of the vomeronasal and olfactory nerves. Attention is paid to the development of the nasolacrimal duct and the epithelial plug. The possible use of the vomeronasal system by embryos during the first seven weeks of development is discussed.