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Biomedical subjects

Y Olsson

Publications and source records attributed to Y Olsson.

At least 73 records · Page 4Linked to original sources
PubMed1996

Monozygotic twins with MELAS-like syndrome lacking ragged red fibers and lactacidaemia.

Typical cases of MELAS present a combination of clinical and neuroradiological features, lactacidaemia, and ragged red fibers (RRFs) in striated muscle. We have observed a MELAS-like syndrome in monozygotic twins. They developed seizures typically in conjunction with physical exertion, sleep deprivation or febrile episodes. Stroke-like episodes occurred usually during seizures. In twin 2 the course was fatal at age 20 years. Neuroradiological findings were typical of MELAS. Plasma lactate was normal in both. CSF lactate was normal in twin 1 and normal/elevated in twin 2. RRFs were not seen in muscle biopsies of the twins. Complex I activity was reduced in muscle in twin 1. Brain tissue removed at epilepsy surgery in twin 2 showed the presence of mitochondrial angiopathy. The commonest mitochondrial DNA mutation in MELAS, at base pair 3243, was absent. Lactacidaemia and mitochondrial myopathy with RRFs constitute part of the diagnostic criteria of MELAS. However, the absence of these features does not exclude mitochondrial disorder with the serious manifestations of MELAS (seizures and stroke-like episodes) as seen in these twins.

Acidosis, Lactic↗
PubMed1996

Paraganglioma of the cauda equina. A case report and review of the literature.

A 59-year-old man presented with clinical evidence of a primary tumor of the cauda equina region. It was well circumscribed and was completely removed by neurosurgery. Routine staining showed that it had structural similarities to an ependymoma, but immunohistochemistry with antisera to synaptophysin, NSE, chromogranin-A and PGP 9.5 proved it to be a neuroendocrine tumor, i.e. a paraganglioma. We propose the use of endocrine markers in cases with tumors of the cauda equina to differentiate a paraganglioma from an ependymoma. Paragangliomas appear to have a better clinical outcome than ependymomas. Recurrence after surgery for a paraganglioma in the cauda equina region, especially if it is encapsulated, is rarely encountered.

Biomarkers, Tumor↗
PubMed1996

Vascular expression of glucose transporter in and around hematogenous metastases of the human brain. Immunohistochemical observations.

The expression of the glucose transporter protein, GLUT 1, in endothelial cells of microvessels within and around hematogenous metastases of the human brain was investigated by immunohistochemistry using a polyclonal antibody raised against the carboxyl terminus of the transporter molecule. The metastases were obtained from 18 autopsy cases with pulmonary carcinomas. Endothelial cells of controls without evidence of brain pathology showed a strong immunoreactivity, indicating that the antigenic sites of the glucose transporter remained in the postmortem material. The endothelial cells of microvessels around the metastases did not show any changes with regard to expression of the glucose transporter. However, in 14 of the 18 tumor cases, microvessels located in the metastases did not express the transporter. Our results indicate that in human cases of brain metastases functional changes with regard to glucose transport occur within the metastases rather than in the peritumoral region.

Adult↗
PubMed1995

Traumatic brain injury in rat produces changes of beta-amyloid precursor protein immunoreactivity.

beta-Amyloid precursor protein immunoreactivity (APP) was studied after a mild compression contusion trauma to rat parietal cortex. Neurones in the periphery of the cortical lesion, i.e. tissue subjected to shear stress, showed markedly reduced immunoreactivity 1 and 3 days after injury. Numerous axons in the ipsilateral subcortical white matter and thalamus became immunoreactive. At 21 days, small rounded profiles appeared in the neuropil of the damaged cortex and in the thalamus. Thus, traumatic brain injury appears to induce several types of APP changes. The accumulation in neuronal processes is probably caused by disturbed axonal transport induced by trauma. Since APP is assumed to be excitoprotective, modulating intracellular Ca2+ responses, the decreased immunoreactivity noticed in the periphery of the lesion may render the neurones in this region more vulnerable to secondary injury mechanisms.

Amyloid beta-Protein Precursor↗
PubMed1995

Reactions of astrocytes and microglial cells around hematogenous metastases of the human brain. Expression of endothelin-like immunoreactivity in reactive astrocytes and activation of microglial cells.

An immunohistochemical study was made on the peritumoral gliosis which is produced around hematogenous metastases of the human brain. The material was derived from 73 autopsy cases with different primary malignancies and six control cases without evidence of brain disease. Reactive astrocytes of hypertrophic and gemistocytic types were present around and within all the metastases. Eighty-five percent of the cases with metastases showed expression of endothelin-like immunoreactivity in the peritumoral astrocytes. Such immunoreactive astrocytes were not present in the normal controls but have previously been found in reactive astrocytes around infarcts, lacunas, inflammatory and degenerative brain diseases. The endothelin-like immunoreactivity probably reflects an increased intracellular content of endothelin. If this peptide is released from the reactive astrocytes it may act as a mitogen and influence microcirculation by inducing vasoconstriction. Activation of microglial cells, detected by ferritin immunohistochemistry, was another frequent and widespread glial cell alteration around the metastases. In conclusion, the reactive gliosis, which is formed around metastases involves activated astrocytes as well as activated microglial cells. Both cell types can release numerous biologically active compounds which may influence the structure and function of the brain tissue around the metastases.

Adolescent↗
PubMed1995

A serotonin synthesis inhibitor, p-chlorophenylalanine reduces the heat shock protein response following trauma to the spinal cord: an immunohistochemical and ultrastructural study in the rat.

The influence of the serotonin synthesis inhibitor, p-CPA on the expression of the heat shock protein (70 kDa), which occurs around an injury to the rat spinal cord, was examined by immunohistochemistry. A longitudinal incision was made into the right dorsal horn at the T10-11 level. Five hours later samples were removed from the T9 and T12 segments. Samples from untreated traumatised animals showed signs of edema and many distorted neurons, particularly in the ipsilateral grey matter. Neurons of the same regions showed a profound increase in HSP-70 immunostaining compared with intact controls. At ultrastructural level, the immunoreactivity was detected in neuronal cytoplasm attached to the surface of organelles including endoplasmic reticulum, in the nucleus and in dendrites. Other groups of rats were given p-CPA before injury to reduce the synthesis of serotonin and to minimise its stores in the cord. The HSP-immunostaining in neurons of the T9 and T12 segments of the spinal cord was virtually lacking in the drug treated animals. The signs of edema and the structural changes of these segments were markedly reduced. The results show that inhibition of serotonin synthesis prior to the traumatic insult has an inhibitory influence on HSP response occurring in neurons around the site of injury to the spinal cord, not reported earlier.

Animals↗
PubMed1995

Vascular permeability to growth hormone in the rat central nervous system after focal spinal cord injury. Influence of a new anti-oxidant H 290/51 and age.

Vascular permeability to the growth hormone (GH) across the blood-brain barrier (BBB) is unknown. This investigation was undertaken to examine vascular permeability to 125I-labelled rat growth hormone (rGH) in the central nervous system (CNS) of normal animals. Since age and spinal cord injury influences the metabolism of GH, these factors were also included. No statistically significant difference was seen regarding rGH permeability between young (aged 19-21 weeks) and old (age 38-42 weeks) animals. A focal trauma to the cord, produced by an incision into the right dorsal horn of the T10-11 segments in young animals, increased rGH permeability in several spinal cord segments at 0.5-5.0 h after injury. This permeability increase progressed over time. Similar trauma to old rats resulted in a significantly less increase in rGH permeability in the spinal cord 5 h after the trauma. This indicates that trauma-induced increased permeability of rGH is age-dependent. Pretreatment of normal young animals with a new antioxidant (H 290/51) did not influence the rGH permeability. However the drug prevented the trauma-induced increase of rGH permeability at 5 h after injury. This indicates that inhibition of lipid peroxidation has some protective effect on trauma-induced increase in rGH permeability.

Aging↗
PubMed1995

Impairment of blood-brain barrier function by serotonin induces desynchronization of spontaneous cerebral cortical activity: experimental observations in the anaesthetized rat.

The possibility that elevation of serotonin in the circulation, which is found in various pathological states, influences the spontaneous cerebral cortical activity was examined in a rat model. The electroencephalogram was recorded using bipolar epidural electrodes placed over the frontal and parietal cerebral cortex. Intravenous infusion of serotonin (10 micrograms/kg per min for 10 min) decreased the electroencephalogram amplitude in both frontal and parietal recordings within 4 min of infusion. This decrease in amplitude was reversible, Pretreatment with cyproheptadine (a potent serotonin2 receptor antagonist) prevented the serotonin-induced decrease of the electroencephalogram amplitude. The blood-brain barrier permeability to Evans Blue and [131I]sodium was increased in frontal and parietal cortex. This increase in blood-brain barrier permeability was absent in animals pretreated with cyproheptadine. These results provide direct evidence that an elevated level of serotonin in blood has the capacity to influence spontaneous cortical electrical activity. This effect of serotonin on electroencephalogram appears to be due to its ability to enter into the brain parenchyma by inducing a short-term breakdown of the blood-brain barrier, probably via serotonin2 receptors.

Anesthesia↗
PubMed1995

Changes of beta-amyloid precursor protein after compression trauma to the spinal cord: an experimental study in the rat using immunohistochemistry.

We evaluated by immunohistochemistry the changes of beta-amyloid precursor protein (beta APP) and beta-amyloid peptide (beta A) in the spinal cord of rats with compression injury at Th8-9 of mild, moderate, and severe degrees. The spinal cord of normal rats and animals with laminectomy revealed immunoreactivity to beta APP in nerve cell bodies, the initial part of a few axons of the gray matter, and in scattered glial cells. At 4 h after compression, beta APP-immunoreactivity occurred in a few swollen axons of the longitudinal tracts; such beta APP-immunoreactive axons remained throughout the experimental period of 9 days. The number of immunoreactive axons and the intensity of their immunoreactivity were increased in rats with moderate and severe compression. The caudal Th10 segment exhibited more pronounced accumulation of beta APP immunoreactivity than the cranial Th segment. There was no evidence of beta A accumulation after compression injury. In conclusion, there is a rapidly occurring, long-lasting accumulation of immunoreactive beta-amyloid precursor protein after compression injury of rat spinal cord. This accumulation is related to the degree of impact to the cord.

Amyloid beta-Peptides↗
PubMed1995

Astrocytic reaction after graded spinal cord compression in rats: immunohistochemical studies on glial fibrillary acidic protein and vimentin.

The relation between the degree of spinal cord compression and the extent of early posttraumatic reaction of astrocytes was investigated in rats using the blocking-weight technique to induce a spinal cord compression at the level of the Th8-9. Immunohistochemistry was used to detect changes in the expression of glial fibrillary acidic protein (GFAP) and vimentin up to 24 h after injury. A mild compression, which did not cause any measurable neurological deterioration, induced a mild increase of GFAP immunoreactivity at 4 h and a more marked and widespread immunoreactivity at 24 h. The greatest increase of GFAP immunoreactive astrocytes occurred in rats with moderate compression of the cord causing reversible paraparesis and in animals with severe compression leading to paraplegia. The increase of GFAP immunoreactivity was present already 4 h after injury in virtually all the segments investigated (Th5-6-Th11-12) and was most marked at 24 h. Vimentin immunoreactivity of control rats was present in the ependymal cells of the central canal, the leptomeninges, and walls of a few intramedullary vessels. Occasional astrocytes were stained. In rats surviving 24 h after moderate and severe compression vimentin immunoreactivity was increased in the walls of intramedullary blood vessels including capillaries of one rostral and one caudal segment. Many macrophages with immunoreactivity appeared and occasional glial cells with astrocyte shape were stained. This investigation shows that within 24 h after compression of the spinal cord a widespread astrocyte reaction occurs. Even a mild compression that does not produce any signs of motor dysfunction can induce widespread astrocyte alterations in the spinal cord. This astrocyte response is more marked in rats with more severe compression leading to more pronounced neurological deterioration. The increase in vimentin immunoreactivity of blood vessels is more localized and occurs in moderate and severe compression of the cord.

Animals↗
PubMed1994

Naloxone reduces alterations in evoked potentials and edema in trauma to the rat spinal cord.

The influence of naloxone (an opioid receptor antagonist) on spinal cord conduction and edema formation as a result of trauma to the cord was investigated in a rat model. The spinal cord injury (SCI) was inflicted in urethane anesthetized animals by a longitudinal incision into the right dorsal horn of the T10-11 segments, about 2 mm deep and 5 mm long. Spinal cord evoked potentials (SCEP) were recorded epidurally from the T9 (rostral) and T12 (caudal) segments after stimulation of the ipsilateral tibial and sural nerves at the ankle. The edema was measured by determining water content of the cord at s h after injury. In rats not given naloxone SCI resulted in an immediate long-lasting depression of the rostral maximal negative peak (MNP) amplitude (about 60%) and a significant increase in the latency of the rostral maximal positive peak (MPP). Pretreatment with naloxone inhibited the immediate post-injury decrease of the rostral MNP and some of the increase of MPP latency. The water content in the traumatized spinal cord was reduced by 3% in naloxone treated animals compared with untreated injured controls. Our results indicate that endogenous opioid peptides participate in changes of spinal cord conduction after trauma and influence edema formation probably via multiple opioid receptors.

Afferent Pathways↗
PubMed1994

The microvascular changes in cases of hereditary multi-infarct disease of the brain.

A report on a cerebro-vascular disease with autosomal dominant inheritance, characterised by stroke-like episodes beginning in early adulthood and progressive dementia, afflicting one family living in Sweden was presented in 1977. Another afflicted member showing gait and coordination disturbances and impaired cognitive functions is now introduced. Magnetic resonance imaging revealed multiple brain lesions indicating ischaemic injuries. Previous autopsy studies of other cases revealed white matter atrophy, multiple infarcts and lacunes. In one patient who had died from a cerebral haemorrhage, obliteration of intracerebral arteries, occasionally with organised thrombi was present. Autopsy material has now been reinvestigated with special attention to changes of intracerebral arterioles. Cases with long duration of the disease presented pronounced fibrous thickening of the wall of numerous intracerebral arterioles, degeneration of smooth muscle cells of the media and obliteration of the lumen. Immunohistochemistry showed marked expression of fibrillary collagen types I, III and V and of the basal lamina components collagen type IV and laminin. These depositions are probably induced by some primary dysfunction of smooth muscle cells or endothelial cells. Perivascular reactive astrocytes with endothelin-1-like immunoreactivity were present in some brain regions. Endothelin-1 is the most powerful vasoconstrictor peptide known to date. Structural remodelling of intracerebral arterial vessels, actions of different vasoactive factors and rheological disturbances may all interfere with local blood flow in this disease and cause the parenchymal changes of the brain.

Adult↗
PubMed1994

Astrocytes in Alzheimer's disease express immunoreactivity to the vaso-constrictor endothelin-1.

The avidin-biotin peroxidase complex method and a polyclonal antiserum were used to investigate the distribution of endothelin-1-like immunoreactivity of cerebral astrocytes in autopsy cases of Alzheimer's disease compared with controls. The cases of Alzheimer's disease presented numerous astrocytes with intense endothelin-1-like immunoreactivity of the cell body often extending into the finest ramifications of the cell processes. Absorption of the antiserum by the corresponding antigen eliminated this immunostaining. The immunoreactive astrocytes were most consistently present in the subcortical white matter of the cerebral hemispheres and the folia of the cerebellum. The immunoreactive cells were often located in small clusters close to blood vessels. Five of the seven cases showed immunoreactive astrocytes in the molecular layer of the cerebral cortex and three of the seven cases presented regions in which immunoreactive astrocytes appeared to be located in the periphery of plaques. The pons contained small groups of immunoreactive astrocytes in five of the cases. The cerebellum had such cells in six of the seven investigated patients. Immunoreactive astrocytes were very rare in control cases without cerebral disease. Many nerve cells in the cerebral neocortex, hippocampus, cerebellum and pons of Alzheimer cases and controls exhibited endothelin-1-like immunoreactivity. Oligodendrocytes and endothelial cells of blood vessels of controls and Alzheimer cases did not show such immunoreactivity. The expression of endothelin-1-like immunoreactivity in astrocytes of Alzheimer's disease probably reflects an increased content of endothelin-1. If endothelin-1 is released from such astrocytes it may reach smooth muscle cells of the intracerebral blood vessels and disturb micro-circulation since this compound is a most powerful vasoconstrictor peptide.

Adult↗
PubMed1994

Reactive astrocytes in viral infections of the human brain express endothelin-like immunoreactivity.

In order to investigate the expression of endothelin-like immunoreactivity in astrocytes of viral infections of the human brain the avidin-biotin peroxidase complex method and a polyclonal antiserum were used. Autopsy material was obtained from 5 cases of herpes simplex encephalitis, two of progressive multifocal leukoencephalopathy (PML) and two of subacute sclerosing panencephalitis (SSPE). All the 5 herpes simplex encephalitis cases presented groups of immunoreactive astrocytes around necrotic, inflammatory lesions. The PML cases exhibited a large number of immunoreactive astrocytes in and around lesions of the white matter. The cases of SSPE disclosed numerous, markedly stained fibrillary immunoreactive astrocytes; they were most abundant in degenerated regions of the white matter. The processes and peripheral cytoplasm of giant astrocytes in the PML cases contained immunoreactive material but the perinuclear region was devoid of such material. In the herpes simplex and the SSPE cases immunoreactivity was present throughout the cytoplasm and processes of reactive fibrillary astrocytes. Many nerve cells in the cerebral cortex, hippocampus, cerebellum and pons of control cases exhibited endothelin-like immunoreactivity but this occurred in only exceptional astrocytes of control cases. Endothelin-like immunoreactivity was not present in the oligodendrocytes and vascular endothelial cells of controls and cases of virus infection. The expression of endothelin-like immunoreactivity in astrocytes in human viral diseases reflects probably an increased intracellular content of endothelin. If this peptide is released from such astrocytes, it may act as a mitogen and by inducing constriction of arterioles it may influence the microcirculation.

Adolescent↗
PubMed1994

Opioid receptors influence spinal cord electrical activity and edema formation following spinal cord injury: experimental observations using naloxone in the rat.

The possibility that opioid peptides participate in alteration of spinal cord conduction following trauma to the cord was investigated in a rat model using a pharmacological approach. Spinal cord injury was produced in urethane anesthetized animals by a longitudinal incision into the right dorsal horn of T10-11 segments (2 mm deep and 5 mm long). Spinal cord evoked potentials (SCEP) were recorded epidurally from the T9 (rostral) and T12 (caudal) segments after stimulation of the ipsilateral tibial and sural nerves at the ankle. SCEP from both rostral and caudal segments consisted of a small positive peak followed by a high negative peak. Infliction of trauma in untreated rats resulted in an immediate depression of the rostral maximal negative peak (MNP) amplitude. This depression was long-lasting. Later, a significant increase in the latency of the rostral MNP amplitude occurred. Naloxone was administered in a high dosage (10 mg/kg, i.p.) to block mu-, delta- and kappa-opioid receptors 30 min before injury. This drug treatment inhibited the immediate post-injury decrease of the rostral MNP amplitude without any significant effect on latency changes. Measurement of water content in the traumatized spinal cord segment showed a significant reduction in the drug treated animals 5 h after trauma (71.46 +/- 0.54) as compared with untreated controls (74.65 +/- 0.76). However, 1 mg or 5 mg/kg dosages of the drug were not effective in reducing the SCEP changes or edema after injury. These results strongly suggest that blockade of kappa-opioid receptors with high doses of naloxone is important in reduction of trauma induced alteration of SCEP and edema formation in spinal cord injury.

Animals↗