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Biomedical subjects

H Kalimo

Publications and source records attributed to H Kalimo.

At least 217 records · Page 12Linked to original sources

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↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗

The role of the blood-brain barrier in perfusion fixation of the brain for electron microscopy.

Regions of the brain vascularized by capillaries of the blood-brain barrier (BBB) type require a different fixative from regions which have capillaries of the endocrine type. Fixative with isotonic buffer gives excellent ultrastructural preservation in the BBB regions, but cause severe shrinkage of cells in the endocrine regions. This is evidently due to the difference in the permeability of the capillary walls to solutes in the fixative. In the BBB regions in less permeable capillaries do not allow outflow of osmotically active particles to a harmful extent, whereas in the endocrine regions osomotic imbalances are created between the intra- and extracellular compartments. The diffusion rate of the fixative and the final volume of the fixed brain depend on the balance between the intravascular and intersitial hydrostatic and oncotic pressures across the capillary wall during the perfusion fixation, as those pressures regulate the amount of perfusate that will enter the parenchyma. Generally, as high a perfusion pressure as possible is recommended to obtain effective wash-out of blood and rapid diffusion of fixative into the tissue. Addition of macromolecules (2% PVP, mol. wt. 40,000) into the fixative slightly improved the ultrastructural preservation in the BBB regions of the central nervous system.

Animals↗

Human adenohypophysis in Nelson syndrome. Ultrastructural and clinical study.

The manifestations that comprise the disease known as Nelson syndrome are pituitary hyperplasia and cutaneous hyperpigmentation, which sometimes follow bilateral adrenalectomy, in patients with hypercortisolism. We present a comprehensive endocrinologic, structural study of a patient in whom the evidence obtained supports the hypotheses that: (a) the primary disorder in this form of hypercortisolism is probably hypothalamic; (b) the hyperplasia of the adenohypophysis, following adrenalectomy, is closely associated with lowered plasma cortisol levels; and (c) the cillular hyperplasia in the adenohypophysis involves primarily the corticotroph, a cell believed to be associated with the secretion of adrenocorticotrophic hormone and melanocyte-stimulating hormone.

17-Ketosteroids↗

Ultrastructural studies on the hypothalamic neurosecretory neurons of the rat. III. Paraventricular and supraoptic neurons during lactation and dehydration.

The ultrastructural features of paraventricular (PVN) and supraoptic (SON) neurons and of their axons were studied in lactating and dehydrated rats. Under both conditions of stimulation, the PVN and SON neurons and their axons enlarge. The protein synthesizing apparatus of the neurons becomes activated, but the number of neurosecretory granules (NSG) is decreased. No differences are seen between the PVN and SON neurons during lactation or dehydration. The similarity and simultaneity of the response of the PVN and SON neurons to these two different stimuli is discussed in the light of the theory of nuclear and neuronal specialization for the production of only one hormone. After prolonged lactation of over 2 1/2 weeks' duration, neurons with extreme vacuolation of the rough endoplasmic reticulum (RER) appear in the PVN and SON; the vacuolated neurons appear earlier and predominantly in the PVN involving a maximum of 10-15% of all PVN neurons. Vacuolated neurons were never seen in either nucleus during dehydration of up to 6 days' duration. The vacuolation is suggested to represent an exhaustion phenomenon due to an intense, long-lasting stimulus for oxytocin synthesis. The predominant location of the vacuolated neurons in the PVN supports the theory that oxytocin is produced predominantly in the PVN. The decrease in the number of NSGs during these states of enhanced hormone secretion is considered to corroborate the proposed existence of an extragranular fast axoplasmic transport mechanism in PVN and SON neurons. The possible existence of a reuptake mechanism into NSGs, similar to that in the vesicles of monoaminergic nerve endings is discussed.

Animals↗