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H Kalimo

Publications and source records attributed to H Kalimo.

At least 199 records · Page 11Linked to original sources
PubMed1981

Brain lactic acidosis and ischemic cell damage: 2. Histopathology.

The influence of severe tissue lactic acidosis during incomplete brain ischemia (30 min) on cortex morphology was studied in fasted rats. Production of lactate in the ischemic tissue was varied by preischemic infusions (i.v.) of either a saline or a glucose solution. The brains were fixed by perfusion with glutaraldehyde at 0, 5, or 90 min of recirculation. In saline-infused animals (tissue lactate about 15 mumol g-1), changes observed at 0 and 5 min of recirculation were strikingly discrete: slight condensation of nuclear chromatin, mild to moderate mitochondrial swelling, and only slight astrocyte edema. These changes had virtually disappeared after 90 min recirculation and, at this time, only discrete ribosomal changes were observed. In contrast, glucose-infused rats (tissue lactate about 35 mumol g-1) showed severe changes: marked clumping of nuclear chromatin and cell sap in all cells was already evident at 0 and 5 min recirculation, while mitochondrial swelling was mild to moderate. Although tissue fixation was inadequate at 90 min, the ultrastructural appearance indicated extensive damage. It is concluded that excessive tissue lactic acidosis during brain ischemia exaggerates structural alterations and leads to irreversible cellular damage. A tentative explanation is offered for the paucity (less than 0.2%) of condensed neurons with grossly swollen mitochondria, previously considered a hallmark of ischemic cell injury.

Acidosis↗
PubMed1981

Hypoglycemic brain injury: metabolic and structural findings in rat cerebellar cortex during profound insulin-induced hypoglycemia and in the recovery period following glucose administration.

Previous results have shown that severe, prolonged hypoglycemia leads to neuronal cell damage in, among other structures, the cerebral cortex and the hippocampus but not the cerebellum. In order to study whether or not this sparing of cerebellar cells is due to preservation of cerebellar energy stores, hypoglycemia of sufficient severity to abolish spontaneous EEG activity was induced for 30 and 60 min. At the end of these periods of hypoglycemia, as well as after a 30 min recovery period, cerebellar tissue was sampled for biochemical analyses or for histopathological analyses or for histopathological analyses by means of light and electron microscopy. After 30 min of hypoglycemia. the cerebellar energy state, defined in terms of the phosphocreatine, ATP, ADP, and AMP concentrations, was better preserved than in the cerebral cortex. After 60 min, gross deterioration of cerebellar energy state was observed in the majority of animals, and analyses of carbohydrate metabolites and amino acids demonstrated extensive consumption of endogenous substrates. In spite of this metabolic disturbance, histopathologic alterations were surprisingly discrete. After 30 min, no clear structural changes were observed. After 60 min, only small neurons in the molecular layer (basket cells) were affected, while Purkinje cells and granule cells showed few signs of damage. The results support our previous conclusion that the pathogenesis of cell damage in hypoglycemia is different from that in hypoxia-ischemia and indicate that other mechanisms than energy failure must contribute to neuronal cell damage in the brain.

Adenosine Diphosphate↗
PubMed1980

Effects of severe hypoglycemia on the human brain. Neuropathological case reports.

The neuropathological findings in two cases of irreversible hypoglycemic brain injury are described. A 26-year-old diabetic man injected insulin without adequate food intake and died after 2 months in coma. An 84-year-old nondiabetic man accidentally received 10 mg of glibenclamide and died after 3 months in relatively superficial coma. In the first case, an extensive necrotizing injury with gliosis was present in the cerebral cortex with temporal preponderance, as well as in the amygdalae and hippocampus. Lesions were also present in the putamen and caudate nucleus whereas the globus pallidus and thalamus were less severely destroyed. The distribution of the lesions was therefore somewhat different from that commonly seen in hypoxic-ischemic brain injury, which, together with some previously published data, suggests some difference in the pathogenesis of hypoglycemic vs. hypoxic-ischemic brain injury. In the second case only a slight loss of cortical neurons with secondary gliosis could be attributed to the hypoglycemic insult. This case demonstrates the danger of accidental intake of sulfonylurea preparations, which can cause an irreversible brain injury due to their prolonged hypoglycemic effect.

Adult↗
PubMed1979

Late-onset malignant astrocytoma in a case of multiple sclerosis. Clinical, neuropathological, virological, and tissue culture studies.

An unusual case of concurrent MS and anaplastic astrocytoma is presented. MS was diagnosed in a female patient at the age of 22 years. A left side thalamotomy was performed for relief of severe intention tremor at age 28 and at age 32 she received immunosuppressive therapy for 1 year. At the age of 36 after a severe exacerbation of her symptoms a left side fronto-temporal tumor was diagnosed and a subtotal neurosurgical extirpation was performed. Histopathologically, the tumor was an anaplastic astrocytoma, which was further substantiated by electron microscopy and establishment of a permanent cell line in vitro. The cultured tumor cells were negative for measles virus by immunofluorescence. The relationship between the reactive astrocytes in MS plaques and astrocytic neoplasia is discussed.

Adult↗
PubMed1979

Alveolar soft part sarcoma: a report of two cases with some histochemical and ultrastructural observations.

In a survey of all malignant soft tissue tumors in the extremities and limb girdles in Finland between 1960 and 1969, only one alveolar soft part sarcoma was found among 246 tumors (0.4%). Another alveolar soft part sarcoma, diagnosed in 1976, was more thoroughly studied. There was evidence that the characteristic crystals of alveolar soft part sarcoma are formed from the dense granules. Both were PASM-positive at ultrastructural level. No monoamines were detected in the cells by formaldehyde-induced fluorescence. This is a further fact to nullify the theory of the paraganglionic origin of alveolar soft part sarcoma, but the question of the histogenesis of the tumor still remains open.

Adult↗
PubMed1979

Familial subacute necrotizing encephalomyelopathy of the adult form (adult Leigh syndrome).

A family--mother and 2 sons--with a heredodegenerative neurological disease is described. The disease started with bilateral optic atrophy, central scotoma, and color blindness during the second decade. This was followed by a quiescent period until additional neurological symptoms appeared, around the age of 50 years in the case of the mother and 40 and 30 years, respectively, in the sons. The additional symptoms were ataxia, spastic paresis, clonic jerks, grand mal seizures, psychia lability, and slight dementia. The disease was progressive, resulting in permanent hospitalization within a few years. The mother died at the age of 63 years and the sons at 46 and 43 years of age. Neuropathological examination revealed lesions histopathologically characteristic of subacute necrotizing encephalomyelopathy (SNE, Leigh disease), and their distribution in the brain and brainstem also conformed to this disease. On the basis of the clinical course and neuropathological findings, we consider that these 3 patients represent the first reported familial cases of the adult form of SNE.

Adult↗
PubMed1979

The efficiency of aldehyde fixation for electron microscopy: stabilization of rat brain tissue to withstand osmotic stress.

Rat brains were fixed either with glutaraldehyde (GA) or formaldehyde (FA). After 20 min or 24 h fixation the osmotic sensitivity of the tissue was tested by immersion in (a) distilled water (b) 0.15 M or (c) 0.3 M cacodylate buffer. GA-fixed material retained some sensitivity to osmotic stress after 20 min fixation but was entirely resistant after 24 h fixation. Ultrastructural preservation was good after only 20 min GA-fixation, provided that the subsequent treatment was with isotonic solutions. The fixation with FA was less efficient and slower. Dark neurons and other artifacts were commonly seen after the 20 min fixation with FA. Prolongation of the FA-fixation overnight gave markedly better preservation, but however, never equivalent to that with GA.

Aldehydes↗
PubMed1979

Myelocystocele with cerebellar heterotopia. Case report.

The authors describe a case with well differentiated cerebellar tissue contained in a hydromyelic dilation of the spinal cord, that is, myelocystocele, in connection with a cervicothoracic meningocele. The embryology is discussed.

Adult↗
PubMed1978

Scanning electron microscopic appearance of viral-antigen-coated polystyrene balls.

A radioimmunoassay (RIA) was recently developed for the detection of antiviral IgG and IgM class-specific antibodies using antigen-coated polystyrene balls as the RIA solid-phase. In this communication the attachment and distribution of herpes simplex virus (HSV) capsid and envelope antigens and rubella viruses on the surface of the balls was examined by scanning electron microscopy (SEM). In SEM the surface of the untreated 'clear frosted' polystyrene balls appeared very uneven with innumerable pits and grooves. The viral particles were haphazardly distributed both in the grooves and on the exposed surface of the balls. The strength of adsorption of the viral antigens onto the balls seemed to be remarkably resistant to outside mechanical forces. HSV antigens frequently appeared in clusters, whereas rubella viruses were mostly found as single particles.

Antigens, Viral↗
PubMed1978

Natural history of juvenile rheumatoid arthritis. A follow-up study of a case with special reference to clinical, electroencephalographic and neuropathological findings.

A detailed comparison between the clinical and EEG findings is made in a case of a boy with juvenile rheumatoid arthritis (JRA) who died at 15 years, 6.5 years after the beginning of the follow-up period. In the course of the disease, seven EEG recordings were made, showing a progressive diffuse slowing and disorganization with some improvement during short remissions. In relapses, diffuse slowing was associated with grave asymmetries in the EEG which, however, fluctuated and later disappeared without accompanying clinical or neuroradiological abnormalities. An abundancy of different residual findings, however, remained in the EEG after relapses. There were spike-and-wave paroxysms in every record except at the terminal stage. A stepwise slowing and disorganization was also seen in these paroxysms as background activity. The final cause of death was an intraventricular haemorrhage. No cerebral amyloidosis was found at autopsy. In conclusion, it is suggested that JRA is also a brain disease manifested as a cerebral vasculitis.

Adolescent↗
PubMed1977

Cellular events during partial cerebral ischemia. I. Electron microscopy of feline cerebral cortex after middle-cerebral-artery occlusion.

The feline right cerebral hemisphere was subjected to regional (incomplete) ischemia after clipping the middle cerebral artery for 5, 10, 15, 30 or 60 min, respectively. After each ischemic episode, a 10-min recirculation period was allowed, following which the brain was fixed and processed for electron microscopy. The earliest alterations, detected in the cerebral cortex after 15 min, increased in severity with longer ischemic episodes and were distributed multifocally. There was: (a) marked neuronal mitochondrial matrical swelling and progressive condensation of cytoplasm and nucleoplasm; (b) cytoplasmic swelling of astrocytes with preservation of glial mitochondrial volume; (c) capillaries, oligodendrocytes, myelin sheaths and axis cylinders did not change significantly, even after the longest interval studied: 60 min. This type of tissue reaction appears to be common for those forms of cerebral ischemia, in which circulation is either sustained partially (via collateral arteries) or restored after a period of absolute ischemia. Under these conditions, as yet undefined permeability changes in cell membranes lead to pronounced volumetric alterations of cellular compartments. Although no softening is detectable by digital examination, we suggest that such a set of structural abnormalities constitutes encephalomalacia, or the earliest stage of a lesion which is designated infarction, once it reaches irreversibility.

Animals↗
PubMed1977

The ultrastructure of "brain death". II. Electron microscopy of feline cortex after complete ischemia.

Permanent, complete global cerebral ischemia was induced in cats by filling the cardiovascular system with a plasma substitute (37 degrees C). At variable intervals and up to 120 min thereafter, these feline brains were perfused with aldehydes and processed for electron microscopy. The resulting cellular alterations were homogeneous and uniform throughout the entire brain; they included early chromatin clumping, gradually increasing electron lucency of the cell sap, distention of endoplasmic reticulum and Golgi cisternae, transient mitochondrial condensation followed by swelling and appearance of flocculent densities, and dispersion of ribosomal rosettes. The marked contrast between the structural alterations in permanent, complete ischemia and incomplete cerebral ischemia, suggest differences in their pathogenesis. A basic determinant factor of the structural changes appears to be the volume of flow (serum, plasma, other) which is available at the time of the injury. This analysis of global cerebral ischemia provides some insight on the nature of cellular changes occurring shortly after somatic death.

Animals↗
PubMed1977

Differentiating intracerebral neuroblastoma: report of a case and review of the literature.

A case of the rare primary intracerebral neuroblastoma is reported. The patient, a 13-year-old girl, was subjected to craniotomy because of a right frontal tumor. The removed tumor tissue was composed of immature, highly cellular areas with numerous mitotic figures, adjacent to fields with Homer-Wright rosettes, and areas consisting of neuroblasts and mature neurons. There was no evidence of a primary tumor elsewhere in the body and 25 months after the operation and postoperative irradiation, the patient is without any signs of recurrence. Determination of catecholamines and their metabolites in the urine and cerebrospinal fluid gave normal results. Dense-corded vesicles could not be detected in the tumor cells by electron microscopy. A review of previously reported cases of primary intracerebral neuroblastomas is included. The cell of origin and the possibility of transition of a differentiating intracerebral neuroblastoma to ganglioneuroma are discussed.

Adolescent↗