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Biomedical subjects

H Kalimo

Publications and source records attributed to H Kalimo.

At least 127 records · Page 7Linked to original sources
PubMed1988

Cerebral microangiopathy in stroke-prone spontaneously hypertensive rats. An immunohistochemical and ultrastructural study.

The morphology of cerebral microvessels was studied immunohistochemically and ultrastructurally in 6- to 9-month-old normotensive Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP) with a systolic blood pressure of 138 +/- 15 mm Hg, 189 +/- 9 mm Hg, and 258 +/- 30 mm Hg respectively. Regions with major opening of the blood-brain barrier (BBB) were revealed by an i.v. injection of Evans Blue. Multifocal BBB opening with massive leakage of plasma constituents rich in fibrinogen-fibrin-related antigen occurred in SHRSP with a blood pressure above 210-220 mm Hg. BBB-leakage sites were found in the cerebral cortex and the basal ganglia, most frequently in the arterial border zones. The perivascular tissue spaces were dilated within the BBB-leakage sites, in particular around arterioles. Damaged endothelial and smooth muscle cells were replaced by fibrin-like material, multiple layers of basement membranes and bundles of collagen fibrils surrounded by proliferated fibroblasts. The degenerative-infiltrative-proliferative disease process transformed short segments of single arterioles into severely thickened, tortuous and stenotic vessels. Fibrinoid degeneration, formation of microaneurysms and fibrin-rich vascular occlusions were observed. In contrast, only minor or no vascular alterations were seen in regions with preserved BBB in SHRSP and SHR. A severely increased intraluminal pressure load appears to be of major pathogenetic importance for breakdown of the BBB and initiation of the vascular disease process in SHRSP. However, since only short segments of a limited number of widely separated vessels are severely affected, and the number of affected vessels increase towards arterial end and border zones, additional predisposing and aggravating factors may play significant roles in the development of fibrinoid vascular lesions in arterial hypertension.

Animals↗
PubMed1988

Intraspinal pigmented schwannoma with malignant progression.

A case with recurrent pigmented intraspinal tumour with malignant progression is presented. The primary tumour grew around the nerve roots T9 and T10, was attached to dura and infiltrated the vertebral bone tissue. On light microscopy it was comprised of monomorphic cells with large amount of cytoplasmic pigment and many large pigmented globoid bodies. Mitoses were not observed. On electron microscopy, in addition to cytoplasmic melanosomes of regular size, macromelanosomes were numerous. The tumour cells were surrounded partially by basement membrane like material. On these bases a histological diagnosis of benign pigmented tumour of neural crest origin was suggested (a possible pigmented meningioma or pigmented schwannoma). The patient got a recurrence one year after the primary operation. Biopsy from the re-operation showed histologically the same type of tumour with more pleomorphic cells. Subsequently, the tumour grew progressively and metastases were observed in the lungs and in the skin. The patient died two years after the primary operation. The malignant progression of the tumour and other reports on similar tumours was most consistent with a diagnosis of malignant pigmented schwannoma and this was confirmed later on with immunohistochemical staining showing positive staining for basement membrane components, collagen type IV and laminin as well as a positive staining for S-100 protein. The present findings show that despite benign histological features these tumours can behave very aggressively and stress the need of more information on this type of tumour.

Female↗
PubMed1988

Identification of fibroblasts responsible for increased collagen production in localized scleroderma by in situ hybridization.

Skin biopsies from seven patients with localized scleroderma (morphea) and from two healthy individuals were studied by in situ hybridization to localize the cells responsible for increased procollagen production. In scleroderma lesions, high levels of pro alpha 1 (I) and pro alpha 1 (III) collagen mRNAs were detected in some but not all fibroblasts, suggesting the presence of a subpopulation responsible for the increased collagen production. The levels of pro alpha 1 (I) and pro alpha 1 (III) collagen mRNAs in these fibroblasts were clearly elevated compared to control skin specimens hybridized at the same time under identical conditions. Most of the scleroderma samples represented intermediate stages where the fibroblasts containing elevated levels of type I and type III procollagen mRNAs were located in the papillary and upper reticular layer of the dermis. One of the scleroderma samples from an early inflammatory stage of the disease was found to contain activated fibroblasts in all dermal layers and also in aggregates adjacent to inflammatory cell infiltrates. In situ analyses were also performed on cell cultures from affected and unaffected skin of one scleroderma patient. These experiments revealed a homogeneous population of activated fibroblasts in cultures producing high levels of collagen. The results suggest that development of fibrosis in scleroderma could evolve through activation of a certain fibroblast subpopulation. During cell culturing, however, cell selection or uncharacterized regulatory mechanisms appear to modulate the behavior of these cells with respect to collagen production.

Autoradiography↗
PubMed1988

Mast cells and IgE in intestinal mucosa in adult atopic dermatitis patients.

Duodenal biopsies from 29 adult atopic dermatitis (AD) patients with multiple positive skin prick test reactions were examined and the results compared with biopsies from 13 non-atopic controls. The duodenal mucosa showed mild inflammatory changes in six out of the 29 patients, but was normal in all the controls. Numerous anti-IgE positive cells, increasing with the severity of AD, were found in the duodenal mucosa in 25 of the 29 AD patients compared with few sporadic positive cells seen in only two out of 13 controls (P less than 0.001). The total serum IgE level showed a significant positive correlation with the number of anti-IgE stained cells in the mucosa (P less than 0.05). No significant differences were found in the total number of toluidine blue stained cells or cells immunoreactive for histamine between patients and controls. However, AD patients who had high numbers of anti-IgE positive cells often had decreased numbers of histamine immunoreactive cells in the mucosa suggesting mast cell degranulation. These findings provide further evidence that also in adult AD patients the gastrointestinal tract may serve as a portal of entry for allergens which may lead to exacerbation of AD.

Adult↗
PubMed1988

Adrenaline-induced hypertension: morphological consequences of the blood-brain barrier disturbance.

Acute hypertension may transiently open the blood-brain barrier (BBB). To determine whether such temporary exposure of the brain parenchyma to plasma constituents may lead to permanent morphological alterations, acute hypertension was induced by i.v. adrenaline in conscious rates given Evan's blue and horseradish peroxidase as tracers. The brain were perfused in situ 24 h later: 17 of 21 brains showed multifocal sites of extravasation of the tracers and of endogenous plasma albumin, fibrinogen and fibronectin identified by immunohistochemistry. The proteins spread locally in the parenchyma and were taken up by neurons. Within the leaking sites in the cortex, hippocampus, thalamus and basal ganglia some shrunken and grossly distorted acidophilic neurons were present. Focal areas of sponginess were observed in the subpial and subependymal zones. Thus, a transient opening of the BBB may lead to neuronal damage.

Animals↗
PubMed1988

Linkage studies in a new X-linked myopathy, suggesting exclusion of DMD locus and tentative assignment to distal Xq.

We here report linkage studies in a family suffering from a recently described hereditary muscle disease named X-linked myopathy with excessive autophagy (XMEA). Significant lod scores excluding linkage to the Duchenne-Becker muscular dystrophy locus were found. Several other loci on the short and long arms of the X chromosome produced negative lod scores, whereas probe DX13-7 defining locus DXS15 showed no recombinants and a lod score of z = 0.903 at theta = .0. Further studies should be done to determine whether the gene for XMEA is (1) located at Xq and (2) caused by a mutation of the Emery-Dreifuss muscular dystrophy gene, which has been assigned to the same region.

Autophagy↗
PubMed1987

Extracellular edema and glial response to it in the cerebellum of suckling rats with low-dose lead encephalopathy. An electron microscopic and immunohistochemical study.

Newborn rats were exposed to daily intraperitoneal injections of 10 mg lead nitrate per kg body weight for the first 15 postnatal days. The growth and mortality of the lead-exposed animals did not differ from their control litter-mates, injected with vehicle only. In our previous studies, focal hemorrhages and spongy areas as well as breakdown of blood-brain barrier to plasma proteins were shown by light microscopy in the cerebellar parenchyma of 15-day-old rats exposed to this dose. In spite of these signs of edema, measurements of brain tissue specific gravity did not show increased water content. In the present investigation we examined the ultrastructure of the brain lesions in these rats with low-dose lead encephalopathy, focusing on signs of edema, and evaluated astroglial reaction by immunocytochemical staining for glial fibrillary acidic protein (GFAP). The electron microscopic findings were compatible with extracellular edema in the cerebellum of 15-day-old lead exposed rats. The number of GFAP-positive cell bodies in the gray substance of the cerebellar cortex was increased in the 15-day-old lead-exposed rats as compared with the controls of the same age, a finding which is presumably related to the leakage of plasma proteins. Both these findings were lacking at 20 days of age, suggesting reversibility of the lead-induced changes.

Animals↗
PubMed1987

Protective effect of lesion to the glutamatergic cortico-striatal projections on the hypoglycemic nerve cell injury in rat striatum.

In rat striatum severe hypoglycemia causes an irreversible nerve cell injury, which does not become manifest until during the post-insult recovery period. This injury can be ameliorated by lesions of the glutamatergic cortico-striatal pathway, which suggests that an "excitotoxic" effect mediated by the glutamatergic input is the likely cause of the post-hypoglycemic nerve cell destruction. In this paper we further characterize the protective effect of abolishing the glutamatergic innervation to striatum at the ultrastructural level. Two weeks after a unilateral cortical ablation rats were subjected to 30 min of severe hypoglycemia with isoelectric EEG and killed either immediately after the insult or following 60 min of recovery induced by restoring the blood glucose levels. Immediately after the hypoglycemic insult the structure of striatum was similar on both sides (except for the changes attributable to the ablation); i.e., the neurons and their dendrites had pale cytoplasm with condensed mitochondria, sparse RER and pinpoint ribosomes. After 60 min restitution numerous striatal neurons on the non-protected, non-ablated side had turned variably dark and condensed, whereas underneath the ablation they remained similar as immediately after hypoglycemia. This sequence indicates that the most likely cause of nerve cell destruction on the non-protected side is the "excitotoxic" effect mediated by the glutamatergic innervation, which is superimposed on the action of the hypoglycemic insult per se. Furthermore, the primary condensation of neurons and their dendrites indicate existence of another type of acute "excitotoxic" nerve cell injury which differs from the previously described injury characterized by neuronal swelling.

Animals↗
PubMed1987

Blood-brain barrier leakage and brain edema in stroke-prone spontaneously hypertensive rats. Effect of chronic sympathectomy and low protein/high salt diet.

Brain edema associated with severe chronic hypertension was studied in stroke-prone spontaneously hypertensive rats (SHRSP), 5 to 9 months of age. Blood-brain barrier (BBB) leakage sites and intracerebral spreading pathways for plasma proteins were delineated by an intravenously (i.v.) injected exogenous dye tracer (Evans blue), known to form a complex with albumin in blood, and by immunohistochemical visualization of extravasated endogenous plasma proteins. The tissue content of edema fluid was estimated by measuring the specific gravity of selected brain regions, stained or unstained by the tracer dye, on a bromobenzene-kerosene gradient column. Multifocal BBB leakage sites were macroscopically detected within the cerebral cortex and the deep gray matter after i.v. circulation of Evans blue-albumin for 30 min. After 24 h of i.v. circulation the dye tracer had spread not only locally in the gray matter but also into the adjacent white matter, where it was widely distributed. Immunohistochemically visualized plasma proteins showed similar distribution. Unilateral superior cervical ganglionectomy performed at 4 weeks of age neither increased the incidence of major BBB opening to Evans blue-albumin nor altered the specific gravity of the ipsilateral cerebral hemisphere in grown-up SHRSP, furthermore, the blood pressure remained unchanged. The lack of significant effect on BBB function may possibly be attributed to the extensive reinnervation of the cerebral arteries, verified in the grown-up SHRSP using the Falck-Hillarp fluorescence method for visualization of catecholaminergic nerve fibers. In SHRSP raised on a low-protein and high-salt diet the mean arterial blood pressure was 212 mm Hg compared to 195 mm Hg in controls (P less than 0.05) and the incidence of BBB opening was 72% compared to 25% in controls (P less than 0.05). After 24 h of i.v. circulation of Evans blue-albumin, brain regions stained by the dye tracer showed significantly reduced specific gravity (P less than 0.001), while unstained regions had normal values. Thus the brain edema fluid spread, as revealed by specific gravity measurements, corresponded to the intracerebral distribution of extravasated plasma proteins.

Animals↗
PubMed1987

Mitochondrial encephalomyopathy. A variant with heart failure and liver steatosis.

We report the clinical and autopsy findings in a young man of 18 with a chronic progressive disorder comprised of lactic acidosis, mental deterioration, and epileptic seizures which were sometimes accompanied by stroke-like episodes with transient hemiparesis and cortical blindness. He died of congestive heart failure. The autopsy showed lesions of the gray matter of the brain. Both the putamen and parieto-occipital cortex showed loss of neurons and proliferation of macrophages, astrocytes and vessels. There was marked loss of neurons in the inferior olives, and slight reduction of the number of Purkinje cells. Skeletal muscle studies revealed ragged-red fibers and structurally abnormal mitochondria. The heart was enlarged: accumulations of mitochondria occurred in the muscle fibers. The liver exhibited marked fatty degeneration. Biochemical analyses showed normal activities of pyruvate dehydrogenase in thrombocytes, pyruvate carboxylase in lymphocytes, biotinidase in serum as well as succinate dehydrogenase and cytochrome c oxidase. The features of this disorder differ in many respects from cases of mitochondrial encephalomyopathy previously reported and cannot be assigned to any specific disease entity.

Acidosis, Lactic↗
PubMed1987

Minicore myopathy with dominant inheritance.

Minicore disease (multicore disease) is a benign myopathy characterized by segmental muscle fibre degeneration with disruption of myofibrils and loss of mitochondria. The disease is generally thought to occur either sporadically or follow an autosomal recessive mode of inheritance. We describe 2 patients, a mother and her son, with essentially non-progressive weakness of both proximal and distal muscles. Biopsies from both patients showed focal defects of oxidative enzyme activity as well as focal disturbances of cross-striation typical of minicore myopathy. Normal fibre type differentiation was lacking. Three other families reported in the literature suggest dominant inheritance of minicore myopathy or closely related disease.

Adolescent↗
PubMed1987

Pigmented primitive neuroectodermal tumor with multipotential differentiation in cerebellum (pigmented medullomyoblastoma). A case with light- and electron-microscopic, and immunohistochemical analysis.

A 5-year-old girl had a midline cerebellar primitive neuroectodermal tumor (PNET) with neuronal, astrocytic, rhabdomyoblastic and melanocytic differentiation (a variant of pigmented medullomyoblastoma). The tumor recurred following surgery and radiation therapy and the child died within 6 months. Autopsy revealed spread into cerebellar hemispheres, subarachnoidal space and brain stem. Neuronal differentiation was verified by electron microscopy and antiserum against neurofilament protein. Neoplastic astrocytes were identified by use of antisera to glial fibrillary acidic and S-100 proteins. Rhabdomyoblasts were identified by the use of antisera against skeletal muscle type 2 myosin and myoglobin, as well as by electron microscopy. This tumor is compared with 20 previously reported cases of cerebellar PNETs containing muscle, 2 of which showed a similar pattern of multipotential differentiation. The oncogenesis of these tumors is in dispute although origin of both the neuroectodermal and mesenchymal components from the neural crest (mesectodermal differentiation) is most widely accepted.

Cerebellar Neoplasms↗
PubMed1986

Structural aspects of ischemic brain damage.

The structural changes during cerebal ischemia are reviewed. In the acute phase the neurons may show either pale or dark type of ischemic injury. The former is usually associated with complete ischemia and the structural alterations are fairly inconspicious, while the latter is seen in incomplete ischemia or ischemia with recirculation and is characterized by shrinkage of neurons with extensive mitochondrial swelling and astrocytic edema. Both types of injury may be irreversible, but long post-ischemic period is usually necessary to see the final outcome of the insult, all the more since the neurons may not die until after a free postischemic interval (even with resumed function) of several hours to days. The delayed death is preceded by peculiar proliferation of cytoplasmic membranes before the doomed neurons become shrunken and disintegrate. This "maturation phenomenon" or "delayed neuronal death" is understandably important since it suggests that a longer postischemic interval for therapeutic interventions may exist. Several factors both during and after the ischemic insult can modify the changes and affect the severity of the damager among the most important ones are the degree of lactic acidosis during the ischemic period, as well as the characteristics of the neurons, since excitoxic damage by transmitter substances released by the ischemic insult has been suggested to be responsible for the delayed neuronal death.

Acidosis, Lactic↗
PubMed1986

The multifidus muscle in patients with lumbar disc herniation. A histochemical and morphometric analysis of intraoperative biopsies.

Structural changes in the multifidus muscle were analyzed in 41 patients operated on for herniated intervertebral disc. Twelve cadavers served as controls. The two main findings follow: Both in the patients and in the controls the Type 2 muscle fibers were markedly and selectively smaller than the Type 1 fibers, which were of normal size for striated muscles, and the internal structure of Type 1 fibers showed so-called core-targetoid and/or moth-eaten change. Group atrophy or fiber-type grouping (indicators of denervation and reinnervation) were observed only in a few patients. The selective small size of the Type 2 fibers may indicate atrophy due to relative inactivity of the multifidus muscle both in the patients and in the controls, ie, it does not need to be related to the herniated disc. Definite proof for denervation of the multifidus muscle was not observed, but neither the possibility be excluded. The cause of the core-targetoid and/or moth-eaten changes cannot yet be determined with certainty, because these changes are not specific for any single entity but may be due, for example, to denervation, ischemia, or altered use of the muscles because of pain. In any case, because the changes were significantly more common in the patients than in the controls, they signal for a pathologic condition, the character of which remains to be elucidated.

Adult↗
PubMed1986

Familial olivopontocerebellar atrophy with macular degeneration: a separate entity among the olivopontocerebellar atrophies.

A family with hereditary, neuropathologically confirmed olivopontocerebellar atrophy (OPCA) associated with macular degeneration is described. The mode of inheritance was autosomal dominant. The first symptom was insidious, progressive visual loss caused by macular degeneration. Another early sign was slow saccades. Some years after the visual symptoms, gradually progressing cerebellar dysfunction and pyramidal signs developed. Computed tomography of the brain indicated cerebellar and pontine atrophy. Finally the patients were blind, due to a severe chorioretinal atrophy, and disabled because af motor dysfunction. The present study, together with a review of other reported families with OPCA associated with macular degeneration, suggests that this disorder is a specific and clinically recognizable subtype of OPCA.

Adult↗
PubMed1986

Clinical and muscle biopsy findings in malignant hyperthermia susceptibility.

Patients (155) were investigated for malignant hyperthermia susceptibility (MHS), by in vitro testing of muscle taken from the vastus medialis muscle. Histopathological and histochemical investigation of muscle was also performed. Ultrastructural investigation was performed in 13 MHS patients; 90% of the patients replied to a questionnaire concerning present or previous neuromuscular symptoms. The majority of MHS and MH negative (MHN) patients had no or only minor histopathological and histochemical abnormalities. Core-targetoid fibres were the only potentially important abnormalities found in MHS patients. There were no differences in neuromuscular symptoms between MHS, MHN and control patients, and most patients in both the MHS and MHN group were normal on clinical examination.

Adolescent↗