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Biomedical subjects

H Kalimo

Publications and source records attributed to H Kalimo.

At least 19 recordsLinked to original sources
PubMed1992

Adhesion in skeletal muscle during regeneration.

Adhesion molecules were studied in regenerating skeletal muscle immunohistochemically and ultrastructurally after a standardized trauma. In normal muscle, extracellular matrix (ECM) protein tenascin was restricted to myotendinous junctions (MTJ), while the integrin beta 1-subunit was present also on the sarcolemma. After injury, tenascin increased on the outer surface of regenerating myofibers, where cellular fibronectin also accumulated. Later, tenascin concentrated at the tips of regenerating myofibers, where new MTJs were formed. The beta 1-subunit disappeared on necrotized myofibers and reappeared on regenerating fibers in a thicker layer. The regenerating myofibers were invested by a basal lamina, except for the growth cones at the distal ends, which were laminin-negative until the formation of MTJs occurred. These results indicate that regenerating muscle cells are attached to the ECM in a way that allows both growth of the muscle cells across the scar and their use before the regeneration is completed.

Animals↗
PubMed1992

Muscle pathology in idiopathic cricopharyngeal dysphagia. Enzyme histochemical and electron microscopic findings.

The structural changes in the cricopharyngeal muscle (CM) were examined ultrastructurally and by enzyme histochemistry in five patients suffering from idiopathic cricopharyngeal dysphagia (ICD). Diagnosis was established by fiberoptic esophagoscopy, esophageal manometry and cineradiography. Cricopharyngeal myotomy was performed with marked improvement in all patients. Intraoperatively, a biopsy was taken from the CM. Additionally, all patients underwent neurological examination for possible generalized muscle disease, and a biopsy was taken from a limb muscle. CM from nine cadavers without known history of dysphagia served as control. The control samples disclosed structural changes which were considered to be pathological in other skeletal muscles, and required that the criteria for CM pathology we modified accordingly. In three patients changes in CM histology suggested specific pathogenesis: one patient had evidence for a generalized myositis but was only symptomatic for dysphagia. Another patient had muscle fiber atrophy and slight inflammation in her CM, possibly due to alcohol abuse. The third patient had loss of CM fibers with replacement by connective tissue enough to cause functional disturbances. In two patients no cause for dysphagia was found in either immunohistochemistry or electron microscopic studies. These results demonstrate the special structural features of the CM and indicate that ICD can have multiple etiologies.

Adenosine Triphosphatases↗
PubMed1992

Ultrastructural changes in the hippocampal CA1 region following transient cerebral ischemia: evidence against programmed cell death.

The ultrastructural changes in the pyramidal neurons of the CA1 region of the hippocampus were studied 6 h, 24 h, 48 h, and 72 h following a transient 10 min period of cerebral ischemia induced by common carotid occlusion combined with hypotension. The pyramidal neurons showed delayed neuronal death (DND), i.e. at 24 h and 48 h postischemia few structural alterations were noted in the light microscope, while at 72 h extensive neuronal degeneration was apparent. The most prominent early ultrastructural changes were polysome disaggregation, and the appearance of electron-dense fluffy dark material associated with tubular saccules. Mitochondria and nuclear elements appeared intact until frank neuronal degeneration. The dark material accumulated with extended periods of recirculation in soma and in the main trunks of proximal dendrites, often beneath the plasma membrane, less frequently in the distal dendrites and seldom in spines. Protein synthesis inhibitors (anisomycin, cycloheximide) and an RNA synthesis inhibitor (actinomycin D), administered by intrahippocampal injections or subcutaneously, did not mitigate neuronal damage. Therefore, DND is probably not apoptosis or a form of programmed cell death. We propose that the dark material accumulating in the postischemic period represents protein complexes, possibly aggregates of proteins or internalized plasma membrane fragments, which may disrupt vital cellular structure and functions, leading to cell death.

Animals↗
PubMed1992

Differential expression of two alpha 2-adrenergic receptor subtype mRNAs in human tissues.

Genetic subtypes of alpha 2-adrenergic receptors (AR) may mediate distinct physiological functions, and undergo differential cell type-specific regulation. Thus, these distinct receptor subtypes are possible targets for the development of subtype-selective drugs. We have analyzed the tissue distribution of two human alpha 2-adrenoceptor subtype gene mRNAs, alpha 2-C4 and alpha 2-C10, in normal human fetal and adult tissues. Both receptor subtype mRNAs were abundantly expressed in fetal brain and choroid plexus. In non-neural fetal tissues, alpha 2-C10 mRNA was detected in spleen, kidney, adrenal gland, and skin, while alpha 2-C4 transcripts were observed only in kidney and skin. Most regions of the adult brain also expressed both subtypes, but with marked quantitative differences. For example, cerebral cortex contained predominantly alpha 2-C10 mRNA, whereas the caudate nucleus expressed mostly alpha 2-C4 mRNA. In adult peripheral tissues, alpha 2-C10 mRNA expression was most abundant in spleen and renal cortex, and expression of alpha 2-C4 mRNA was strongest in renal cortex and medulla. These different expression patterns provide evidence for the differential regulation of the two alpha 2-adrenergic receptor genes and warrant further investigation with techniques capable of improved anatomical resolution. Regional differences in receptor subtype expression may be valuable for the development of new, subtype-selective pharmacological agents with more targeted actions compared to currently used alpha 2-adrenoceptor agonists and antagonists.

Animals↗
PubMed1992

Activation of myogenic precursor cells after muscle injury.

The time and site of satellite cell activation in contusive myofiber rupture with segmental necrosis were studied in rat by labeling the cells in S phase of mitotic cycle with bromodeoxyuridine. The labeled satellite cell nuclei did not appear before phagocytosis of the necrotized debris had started, usually 1 d after the trauma. Most labeled satellite cell nuclei were found in the necrotized part of the ruptured myofibers, whereas very few of them were detected in the surviving part. The proliferation of satellite cells was extensive during the first 4 d in the regeneration zone; thereafter, it declined and only few labeled nuclei were observed on day 7. These results suggest that necrosis alone is not sufficient as a signal for the satellite cell activation, but it is speculated that (growth?) factors released by the macrophages are needed. A great majority of myoblasts derive from local precursor cells, and satellite cells recruited from the surviving part do not significantly contribute to the regeneration. Most myonuclei needed in regenerating myofibers are produced early within the preserved basal lamina cylinders to be later distributed into those parts of myofibers, which extend into connective tissue between the stumps.

Animals↗
PubMed1991

Inclusion body myositis and paramyxoviruses.

Inclusion body myositis (IBM) is a distinct type of muscle disease. The characteristic electron microscopic findings, intranuclear or intracytoplasmic inclusions composed of microtubular filaments, morphologically resemble paramyxovirus nucleocapsids. These findings and the reported immunoreactivity of the inclusions with mumps virus antibodies have suggested that inclusion body myositis is a chronic virus infection. We analyzed skeletal muscle specimens from three patients with characteristic light microscopic features and electron microscopically verified inclusions of IBM by immunocytochemistry using antibodies raised against members of the paramyxovirus group, and by in situ hybridization with a cRNA probe representing the mumps virus nucleocapsid gene. The specificity of the reactions was demonstrated with infected and uninfected cultured cells. No immunocytochemical staining or hybridization signal was observed in biopsy specimens from IBM patients. These findings speak against a paramyxovirus etiology of IBM.

Aged↗
PubMed1991

Electromyography and morphology during regeneration of muscle injury in rats.

Healing of the partially ruptured rat gastrocnemius muscle was studied correlating electromyographical findings with morphological changes. Fibrillation potentials and positive sharp waves were seen both proximal and distal to the injury 7 days after the injury and disappeared in the proximal part by day 14 and in the distal part by day 21. Late components of motor action potential were observed from day 14 onwards. Denervation was mainly myogenic, i.e. caused either by rupture of myofibres, whence the abjunctional stump lost its contact with the neuromuscular junction on the adjunctional stump, or by necrosis of the segment of the ruptured myofibre lying underneath the neuromuscular junction. Lesser extent of denervation was neurogenic, i.e. caused by damage to intramuscular nerve fibres. The reinnervation occurs either by regeneration of the necrotized myofibres, by regeneration of the severed nerves, or by collateral innervation of new neuromuscular junctions in the abjunctional stumps. The present study indicates that electromyography may be useful in the diagnosis and follow-up of skeletal muscle injuries.

Animals↗
PubMed1991

Localization of type I and III collagen and fibronectin production in injured gastrocnemius muscle.

The healing of muscle rupture consists of two simultaneous processes, regeneration of disrupted muscle fibers and production of connective tissue scar. These two processes are at the same time supportive to and competitive with each other. Their balanced progression is necessary for optimal healing. Synthesis of three connective tissue proteins, collagen types I and III and fibronectin, was analyzed during the regeneration process from 2 days to 3 weeks by Northern blot and in situ hybridization and immunohistochemistry. For this purpose a partial standard rupture of the gastrocnemius muscle was induced in 56 rats by a strike with a blunt spring-loaded hammer. Northern blot analysis of the specific mRNAs during the healing process revealed distinctly different expression patterns for fibronection and type I and III collagens. During the early stages (days 2 and 3) fibronectin, derived mainly from plasma, was abundant in the traumatized area, but local production of fibronectin mRNA by fibroblasts had also already started by day 2, closely followed by that of type III collagen. This early active synthesis of type III collagen and fibronectin was followed by a decrease after 1 week. The production of type I collagen mRNAs was activated somewhat later and remained elevated for at least 3 weeks. The muscle cells did not contain procollagen mRNAs. The observed sequence of connective tissue proteins reflects the particular function that each carries out during muscle wound healing (e.g., fibronectin in fibroblast trapping, type III collagen in plasticity/flexibility, and type I collagen in tensile strength).

Animals↗
PubMed1991

Healing of skeletal muscle injury: an ultrastructural and immunohistochemical study.

The healing of gastrocnemius muscle injury induced with a spring-loaded hammer in rats was analysed ultrastructurally and immunohistochemically. The ends of the ruptured myofibers retracted, which resulted in a central blood filled cavity. Central zone (CZ) later becomes occupied by granulation tissue scar. CZ is surrounded by a zone where myofibers are necrotized and phagocytosed by days 2-3. Complete regeneration within the preserved basal lamina (BL) cylinders takes place in 5-7 days. The regeneration of myofibers across the scar follows a pattern different from that within BL cylinders. Thin, often branched, myotubes grow out of the BL cylinders into the granulation tissue, where they extend between fibroblasts and collagen fibrils, in general oriented parallel to the preserved myofibers. The extension of the regenerating myotube seems to take place primarily by local synthesis in the growth cone. Fusing myoblasts provide nuclei, mostly along the sides but also occasionally at the tip of myotubes. Some myoblasts seem to derive from undifferentiated cells in the granulation tissue. By three weeks only a few thin myotubes had extended across the gap between the stumps of the ruptured myofibers. Growing myotubes appear to attach to the surrounding connective tissue by specialized structures, an attachment which evidently transmits contraction force across the gap, allowing use of the injured limb before the healing is complete.

Animals↗
PubMed1990

Lymphocyte migration into the skin: the role of lymphocyte homing receptor (CD44) and endothelial cell antigen (HECA-452).

Lymphocyte migration into the lymphoid organs and sites of inflammation is controlled by lymphocyte-endothelial cell interaction at sites where lymphocytes exit from the blood. Expression of Hermes-defined CD44 class of lymphocyte homing receptor and HECA-452 antigen specific for high-endothelium-mediating physiologic lymphocyte extravasation was studied in dermatitis herpetiformis, celiac disease, psoriasis, mycosis fungoides, lymphocytosis cutis, atopic dermatitis, and allergic contact dermatitis. Also, duodenal biopsies of patients suffering from dermatitis herpetiformis or celiac disease were studied for existence of these antigens. Infiltrating lymphocytes in the skin and in the duodenal area expressed homing receptor molecules when studied with monoclonal antibodies, Hermes-1 and Hermes-3, that recognize the CD44 class of molecules involved in lymphocyte binding to high endothelial venules in peripheral lymph nodes, mucosa-associated lymphatic tissues, and inflamed synovium. However, the HECA-452 antigen was not detected on the venules, neither in the skin nor in the duodenum. Even the venules possessing high endothelium morphologically were HECA-452 negative. These findings suggest the CD44 class of lymphocyte homing receptor(s) is also involved in lymphocyte homing to inflamed skin and the duodenal area of the gut. However, on the basis of HECA-452 staining, high endothelial venules in inflamed skin and duodenum are not antigenically identical with high endothelial venules in organized lymphoid tissues. This finding indirectly supports the idea that molecules and/or mechanisms mediating lymphocyte extravasation might be distinct in these organs.

Adult↗
PubMed1990

Severe degeneration of rabbit vastus intermedius muscle immobilized in shortened position.

The authors have previously shown that passive daily mobilization of the rabbit hind limb immobilized with the knee in extension leads to necrosis of the deep thigh muscles and myositis ossificans-like periosteal bone formation. In this study the effect of immobilization alone on the rabbit hind limb muscles was examined similarly to that of immobilized limbs. Serum creatine kinase activities increased significantly and intravenously administered Evans blue albumin showed increased vascular permeability in the deep vastus intermedius muscle even on day 1. Necrotic fibers were clearly present in the deep part of the vastus intermedius muscle on day 5 in light and electron microscopy and in enzyme histochemistry. Fibrosis and atrophy were found later. The superficial portion of the vastus intermedius and the deep contralateral nonimmobilized vastus intermedius showed degenerative changes. Bone formation was not noted. The conclusion was that the deep vastus intermedius muscle composed almost exclusively of type I fibers is exceptionally prone to damage when immobilized in a shortened position. Contact of the necrotic muscle with the underlying periosteum is not alone sufficient to induce heterotopic ossification. The additional trauma caused by daily mobilization is needed for the myositis ossificans-like bone formation.

Animals↗
PubMed1990

In situ detection of enterovirus genomes in mouse myocardial tissue by ribonucleic acid probes.

We have applied a sensitive in situ hybridization method for the detection of coxsackievirus RNA in myocardial tissue. Two radioactive cRNA probes were used: an RNA transcript representing the 5' end of poliovirus 3 which recognizes a highly conserved region among enteroviruses and an RNA transcript of a 1.1 kb fragment from the polymerase gene region of coxsackievirus B3. The reactivity of these probes was tested by dot-blot hybridization against a panel of enteroviruses. Formaldehyde-fixed and paraffin-embedded tissue of experimentally coxsackievirus B3 infected mice was analyzed for the localization of virus RNA. Both the probes gave signals in mouse myocardial cells, disseminated evenly in the heart tissue 7 days postinfection. At this time point, hybridization-positive cells and inflammatory reaction were mainly found in different areas that may be due to the inability of the immune system to recognize the infected cells before cytolysis. The samples were still positive when fixed 52 hours postmortem indicating that virus RNA is in a relatively stable form in the cells.

Animals↗
PubMed1990

Expression of the myc proto-oncogenes in developing human fetal brain.

We have analysed c-myc, N-myc and L-myc gene expression in developing human fetal brain by Northern hybridization, RNAase protection and in situ hybridization. The unique zonal organization of the developing fetal brain allows a particularly good assessment of the coupling of myc gene expression to cell proliferation and differentiation in vivo. By Northern and in situ hybridization, L-myc as well as c-myc and N-myc transcripts in the brain were found in the post-mitotic cortical and intermediate layers, as well as in the mitotically active layers containing the neuroepithelial precursor cells. Consistent results were also obtained for L-myc using RNAase protection analysis. Both the 3.6 and 3.8kb forms of the L-myc mRNA, resulting from alternative splicing of intron I, were detected in layers of neuroectodermal origin, but not in the meninges or choroid plexus. We also extended L-myc expression and splicing analyses to other developing human fetal tissues. L-myc mRNA was expressed in several other fetal tissues, particularly in fetal skin. Predominantly intron I containing L-myc mRNA was observed in fetal striated and cardiac muscle. Thus, L-myc is expressed in a wider spectrum of developing tissues than previously known. Our findings also, show that L-myc as well as N-myc and c-myc expression is uncoupled from cell division in developing brain.

Blotting, Northern↗