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Biomedical subjects

P Sourander

Publications and source records attributed to P Sourander.

At least 19 recordsLinked to original sources
PubMed1992

Atypical pyramidal cells in epileptic human cortex: CFLS and 3-D reconstructions.

Epileptic temporal cortices, removed from 3 patients with intractable partial epilepsy (IPE) during neurosurgery, were studied. Pyramidal neurons (40-50 per slice) in laminae III, V and white matter, were injected with lucifer yellow. Samples were examined in a confocal laser scanning microscope (Biorad 600) and individual cells scanned at 0.1-1 microns incremental levels. 2-D maximal linear projection was used for overview. Frames (50-60) of scanned neurons were transformed into 3-D volumes, using VoxelView software on a Silicone Graphics workstation and rotated. All samples contained neurons with duplicated apical dendrites, additional basal dendrites or were misplaced in a horizontal position in the white matter. The relation between these preliminary observations and the disease is discussed.

Epilepsies, Partial↗
PubMed1991

Neurobiorheology. A new branch of biorheology. Historical background and current ideas.

The application of principles of biorheology, hemorheology and perihemorheology on problems of the nervous system in health and disease was suggested by Alfred L. Copley (1982, 1987). Late in 1988 Copley and Sourander considered neurobiorheology to be an appropriate term for a new branch of biorheology bridging the gap between biorheology and neurobiology. Neurobiorheology can be defined as a research field concerned with deformation behaviour of matter including flow and transportation in context with the structure and function of the nervous system at macroscopic, cellular, subcellular and molecular levels. It may be considered a basic life science with important clinical applications. Its "raison d'être" should be to apply various ways of thinking, calculations and techniques used in biorheology to treat and if possible to solve neurobiological problems. Many regionally different chemical, structural and functional properties characterize the developing and adult nervous system and those parts of the circulatory system ("vessel-blood organ") which penetrate the nervous system at all levels. Considering the close metabolic and functional relations between neurons and surrounding non-neuronal ectodermal cells, neuroglial and Schwann cells deriving from common precursor cells in the wall of the neural tube and neural crest respectively, the term neuroectodermal organ appears suitable. The almost parallel ontogenetic evolution of vessel-blood organ and neuroectodermal organ and their interaction during the entire individual life cycle constitutes a challenging stimulus for integrated research. The main purpose of this review is to give some examples of importance concerning still insufficiently elucidated neurobiological problems suitable for biorheological approaches. Particular attention will be paid to the microenvironment at central and peripheral levels of the neuroectodermal organ.

Animals↗
PubMed1990

Pathology of the central nervous system with special reference to the lipids.

The historical background of lipid research with particular reference to the nervous system is outlined. Attention is called to the early studies of Swedish investigators on the morphology and physical properties of the lipid rich myelin sheath. The pioneering research of the late Gunnar Brante on quantitative topical lipid chemistry of the human nervous system in health and disease is pointed out. A selection of lipid histochemical methods for various spingolipids is presented. Results are reported of their application to cases of four genetically determined sphingolipidoses. The morphological changes characterizing these diseases are interpreted in terms of histochemistry and biochemistry. The recently developed method by Dowson for the characterization of autofluorescence emission spectra from neuronal lipopigment in various ceroidoses (ceroid-lipofuscinosis) has been applied to cases of Sanfilippo's syndrome and Salla disease. The results are briefly commented upon.

Brain Diseases, Metabolic↗
PubMed1989

Distribution of lead in the cerebellum of suckling rats following low and high dose lead exposure. A micro-PIXE analysis.

The distribution of lead in the cerebellum of suckling Sprague-Dawley rats was examined using a nuclear microprobe for elemental mapping of tissue sections (particle-induced X-ray emission, 3-microns beam of 2.5 MeV protons; micro-PIXE). The rats were injected intraperitoneally with a lead-containing vehicle or vehicle only from ages 1 to 14 days. The calculated doses were 7.8 (low-dose) and 15.6 (high-dose) micrograms lead/g body weight. The rats were killed at 20 days of age. The vascular system was rinsed quickly with 0.15 M ammonium acetate to obtain determinations of intra-parenchymal lead with minimal influence of lead bound to erythrocytes and plasma proteins. Brains were frozen in propane/propylene in liquid nitrogen. Cryostat sections, 15 microns thick, were air dried on formvar coats that covered a hole, 15 mm in diameter, in a plastic disc, and were used for lead analysis by micro-PIXE. Very low concentrations of lead were found in the brain of controls. Lead levels in homogenates from cerebrum and cerebellum measured by atomic absorption spectrometry (AAS) were: low-dose 1.2-2.2 micrograms/g wet weight and high-dose 1.4-2.4 micrograms/g wet weight. The lead levels measured with the micro-PIXE method were in good agreement with the levels found with AAS. Lead was present in the cerebellar white matter in two to three times higher amounts than in the cortical grey (low-dose white matter 11-18 micrograms/g dry weight, grey matter 2.0-5.5 micrograms/g dry weight). This was true for both low and high dose exposed rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Autofluorescence emission spectra of neuronal lipopigment in mucopolysaccharidosis (Sanfilippo's syndrome).

Characteristics of intraneuronal lipopigment in two siblings with Sanfilippo's syndrome are reported. A lipopigment emission spectrum probably reflects its composition and the (uncorrected) autofluorescence emission spectra results are compared with spectra from non-diseased tissue and from previously reported childhood-onset neuronal ceroidlipofuscinoses (ceroidoses), adult-onset ceroidosis (Kufs' disease) and animal ceroidoses. Values derived from the emission spectra from Sanfilippo's syndrome could be distinguished from those obtained from equivalent regions of non-diseased brains and were within the range of abnormal values previously reported from accumulations of pigment in various types of neuronal ceroidosis. Some abnormal lipopigment in Sanfilippo tissue was indistinguishable from some lipopigment in childhood-onset ceroidosis and in Kufs' disease. These results indicate that the intraneuronal lipopigment which accumulates to an abnormal extent in Sanfilippo's syndrome should not be termed "lipofuscin", which is a normal cerebral constituent, but "ceroid" to denote lipopigment with abnormal characteristics.

Adult↗
PubMed1988

A syndrome of multiple congenital contractures: neuropathological analysis on five fetal cases.

We performed a neuropathological study on 5 fetuses with an autosomal recessive, lethal syndrome of congenital contractures diagnosed by fetal hydrops on ultrasonography. The fetuses showed a typical pattern of malpositioning of hips and knees with occasional pterygia of the neck and elbows. The muscles were hypoplastic and the spinal cords showed severe thinning, most markedly affecting the ventral half. A total loss of axons in the ventral and lateral funiculi, subtotal loss of anterior horn motor neurons with accompanying astrocytosis and astrogliosis, and similar but less severe changes at the brain stem level suggested a degenerative rather than a dysmorphogenetic mechanism. Sensory nuclei and pathways were distinctly less severely affected, if at all. The findings further delineate this condition as a genetically and pathoanatomically distinct autosomal recessive syndrome.

Abnormalities, Multiple↗
PubMed1988

Neuropathology of Salla disease.

A neuropathological study was performed on two patients with Salla disease, one male and one female, from different families. They both died at the age of 41 years. Both patients showed increased excretion of free sialic acid in the urine, psychomotor retardation starting in the 1st year of life, ataxia and spasticity. Several family members of both families were affected with the same disease indicating the hereditary character of the disorder. The neuropathological investigation revealed strikingly similar changes in the two cases. Macroscopically the cerebral white matter was severely reduced. Histologically marked loss of axons and myelin sheaths was accompanied by pronounced astrocytic proliferation. The remaining axons frequently showed ovoid swellings surrounded by a myelin sheath. The reduction of the number of myelin sheaths seemed proportional to the numerical reduction of axons. Many cortical nerve cells displayed in relation to age an abnormal amount of lipofuscin. Neurofibrillary tangles were observed in nerve cells of the neo-cortex, nucleus basalis of Meynert and locus ceruleus. Cerebellum showed moderate loss of Purkinje cells. In the spinal cord axonal degeneration was observed in both ascending and descending tracts.

Adult↗
PubMed1988

Reactions of vessel walls and brain parenchyma to the accumulation of Gaucher cells in the Norrbottnian type (type III) of Gaucher disease.

Splenectomy in children with the Norrbottnian type of Gaucher disease is followed by increased blood levels of glucosylceramide and impaired neurological and mental status. High blood levels are associated with an increased accumulation of glucosylceramide in perivascular Gaucher cells in the brain compared to non-splenectomised cases. Surrounding the Gaucher cell infiltrates there is loss of neurons and slight demyelination in the brain parenchyma. The brains of four cases with the Norrbottnian type of Gaucher disease were examined by immunohistochemical stains in an attempt to further characterize the perivascular Gaucher cells and to examine the reactions of the vessel walls and brain parenchyma to the accumulation of Gaucher cells. The perivascular storage cells showed granular staining with antibodies to muramidase and alpha 1-anti-chymotrypsin confirming that they are blood-derived macrophages belonging to the monocyte-macrophage system. The Gaucher cells contained material positive for antisera to plasma proteins strongly suggesting that large molecules (including glucosylceramide) can escape from the blood and be taken up by the macrophages in Gaucher disease. The storage cells were surrounded by a reticulin network stained by antisera to collagen type III, type IV and laminin. The infiltrates were bounded from the brain parenchyma by a membrane strongly positive with antiserum for the basal lamina protein collagen type IV and laminin. The formation of a basal lamina around the Gaucher cell cuffs probably constitutes a protective phenomenon governing the brain parenchyma against the foreign cells. A focal loss of neurons but only minor loss of axons could be demonstrated with the antiserum to neurofilament.(ABSTRACT TRUNCATED AT 250 WORDS)

Astrocytes↗
PubMed1988

Changes in brain temperature and free amino acids in normal and protein deprived suckling rats exposed to room temperature.

Previous reports on early-induced protein-calorie malnutrition (PCM) in rats have indicated alterations in the concentration of free amino acids and of protein synthesis in the brain. Recently it was shown that early-induced protein deprivation (PD) retards the development of thermoregulation. This resulted in a failure to maintain a normal rectal temperature after short exposure to room temperature (+22 degrees C) still at the age of 20-25 days corresponding to changes seen in normal rats at an age of 10-15 days. In the present study, 20-day old PD and normal rats where examined with regard to the effect of exposure to room temperature on brain temperature and on brain free amino acids. The results show a similar reduction in brain and rectal temperature of the PD rats occurring within 30 minutes after exposure to room temperature. The reduction was in the range of 5 degrees C. PD rats kept in room temperature for 5 hours and then allowed to recover at 32.5 degrees C showed a slow increase in brain and rectal temperature but normal temperatures were not reached even after 1 hour. The concentration of free amino acids in the brain was examined in rats kept for 1 hour at room temperature or at 32.5 degrees C. In the PD rats kept at 32.5 degrees C, free aspartate and glutamate were reduced whereas taurine, GABA and glycine were increased as compared to their corresponding control rats. As a result of the reduced brain temperature in PD rats exposed to room temperature there was a reduction in free asparagine.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1986

Nutritional rehabilitation of skeletal muscle in protein-deprived young rats.

The effect of severe protein deprivation and subsequent nutritional rehabilitation on the fibre size and mitochondrial enzyme activity of the extensor digitorum longus (EDL) and soleus muscles of the young rat has been examined. Protein deprived rats showed atrophy of type 2 fibres predominantly, reduced histochemical activity of succinic dehydrogenase (SDH) and reduced biochemical activity of citrate synthase. Nutritional rehabilitation indicated by resumption of the original body weight resulted in complete restitution of the weight of the muscles and the size of type 1 and type 2 fibres, but not of the activity of SDH and citrate synthase. The results indicate that regarding size, type 2 fibres tend to be more influenced than type 1 fibres by the nutritional supply. The mitochondrial enzyme activity which is decreased by protein deprivation does not regain the normal levels as quickly as the muscle fibres resume their normal size.

Animals↗
PubMed1986

Changes in specific gravity as a sign of disturbed brain maturation in protein-deprived rats.

The specific gravity of the cerebral cortex of normal and protein-deprived rats aged 15, 21 and 25 days was determined. The increase in specific gravity seen in control rats in the course of their development was reduced in protein-deprived rats in the course of the period between 15 and 21 days of age. The results are in agreement with previous reports on delayed maturation of the brain in protein-deprived rats and indicate that determination of brain specific gravity may serve as a suitable screening method in situations when a disturbed brain maturation is suspected.

Animals↗
PubMed1986

The influence of maternal protein deprivation on the developmental pattern of serum immunoreactive insulin-like growth factor 1 (IGF-1) levels.

The influence of maternal protein deprivation on body and brain growth and on serum immunoreactive insulin-like growth factor I (IGF-I) levels was examined in rats during development. The offspring of protein-deprived mothers were significantly growth-retarded postnatally and showed an altered developmental pattern of serum immunoreactive IGF-I levels. In contrast to control animals, between days 5 and 20 postnatally, a significant elevation in serum immunoreactive IGF-I levels which peaked at day 15 was found. However, in adult growth-retarded rats a significant reduction in serum immunoreactive IGF-I levels was found. These findings suggested the preweaning period to be critical for the development of the mature somatomedin system.

Animals↗
PubMed1985

Changes in the integrity of the blood-brain barrier in suckling rats with low dose lead encephalopathy.

Previous studies on the toxic effects of lead on the brains of young animals have shown damage to the blood-brain barrier (BBB) which in severe forms appears as hemorrhagic encephalopathy. In those studies the doses of lead have been of such magnitude that lead-induced anorexia resulting in growth retardation has contributed to the extent of the injury (Sundström et al. 1984). The growth retardation can be prevented by using low lead doses (Sundström et al. 1983). Consequently, we have examined to which extent the BBB is injured in suckling rats with low dose lead encephalopathy. This was done by testing the permeability of the BBB to plasma proteins and assessing the possible occurrence of vasogenic edema by measuring the specific gravity of brain tissue. Low dose lead encephalopathy was induced by daily i.p. injections of lead nitrate 10 mg/kg body weight (b.wt.) for the first 15 days. The lead contents of the blood and homogenates of the cerebrum and cerebellum were assayed by atomic absorption spectrophotometry. The brains were examined at 15, 20, or 30 days of age. When Evans blue-albumin (EBA) was injected i.v. 2 h before killing, most 15-day-old rats exposed to lead displayed a bluish discoloration in their cerebellum. Microscopically, red fluorescence of EBA was seen in the blue-stained regions. Immunohistochemically, extravasation of albumin, fibrinogen, and fibronectin was demonstrated as positive staining in the cerebellar cortex, with diffuse spread to the white matter of the corresponding folium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Functional development of the visual system in normal and protein deprived rats. II. Morphometric and biochemical studies on adult optic nerve.

The optic nerve of normal (C) and protein deprived (PD) adult rats was examined by morphometry and biochemistry. The mean cross-sectional area of the optic nerve was reduced by 15% and the number of axons per unit area increased by 17% in the PD rats. Calibre spectrum analysis of axons revealed a reduction in median diameter from 0.49 micron in controls to 0.45 micron in PD rats. The number of axons with a diameter larger than 1 micron was reduced by 35% in PD rats. These reductions were probably due to a general reduction in size, since the calculated total number of axons in the optic nerve was almost identical in C and PD rats (126 X 10(3) and 124 X 10(3), respectively). The increased packing density of axons in the nerve was not only due to thinner axons. The biochemical measurements showed a marked reduction in myelin basic protein in the optic nerves of PD rats, without an alteration in the composition of the total protein. This confirms the persistent hypomyelination which has been reported previously in other malnutrition models. The possible relations between the structural and biochemical changes affecting optic nerve fibres and physiological findings on cortical visual evoked response and on optic nerve in vitro in PD rats are discussed.

Animals↗