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PubMedDate not supplied

Crystalloid inclusions in brain macrophages and hemopoietic tissue in GFAP-IL3 mice resemble inclusions identified in multiple sclerosis.

Crystalloid inclusions or "pole bodies" observed in brain macrophages in human demyelinating disease represent a morphological enigma. Similar inclusions were detected in brain macrophages from the GFAP-IL3 mouse, a transgenic murine model for macrophage mediated demyelination. Mice also showed inclusions in hematopoietic tissue. They appear to be related to phagocytosis and secretion, respectively, as evidenced by the fact that in phagocytosing cells they often merged with lysozomes and that affected cells showed empty channels open to the interstitium. Based on ultrastructural and immunolocalization studies using chaperonin-10, lysozyme, and cathepsin the authors suggest that these inclusions are consistent with phagocytosis-related secretory products. This study may provide insight into the nature and significance of similar macrophage inclusions recently identified in multiple sclerosis.

Animals↗
PubMed1980

An unusual degenerative disorder of neurons associated with a novel intranuclear hyaline inclusion (neuronal intranuclear hyaline inclusion disease). A clinicopathological study of a case.

A 21-year-old woman with an unusual, progressive, degenerative neurological disorder is described. The disorder is characterized clinically by behavioral abnormality, peculiar involuntary movements, and ataxia starting in early childhood and subsequent development of dementia, choreoathetosis, rectal and bladder incontinence, bulbar and spinal muscular weakness, pes cavus, kyphoscoliosis, and generalized seizures. The clinical manifestations are correlated, with widespread pathological changes affecting almost all neuronal systems. The pathological changes are discussed in relation to the wide spectrum of "multisystem atrophies." Particular attention is directed to the ubiquitous occurrence of a novel intranuclear, eosinophilic, hyaline inclusion in almost all types of central, peripheral, and autonomic neurons. The ubiquitous neuronal involvement seems to explain the diffuse multiple system degeneration. The pathogenesis of the neuronal inclusions is unknown, but it is speculated that the disorder may represent a metabolic abnormality affecting the nuclear protein of neurons, rather than a viral infection. The pathological features, consisting of the neuronal intranuclear hyaline inclusions associated with multiple system atrophy, have not hitherto been described, and "neuronal intranuclear hyaline inclusion disease" is proposed as a name for the disorder. Rectal biopsy demonstrating the intranuclear hyaline inclusions in ganglion cells of the hyenteric plexuses may serve as a diagnostic procedure for the disorder.

Adult↗
PubMed2006

Heterogeneous inclusions in neurofilament inclusion disease.

Neurofilament inclusion disease (NFID) is a rare disease, whose pathogenesis remains to be elucidated. Immunoreactivity of ubiquitin-binding protein p62 has been reported in various neurodegenerative diseases, but it has not been studied in NFID. In this report we show p62 immunoreactivity in neuronal perikaryon of three cases of NFID. We found inclusions in NFID to be heterogenous based on immunoreactivity for alpha-internexin, phosphorylated neurofilament-H, p62 and ubiquitin. Moreover, we showed both p62- and alpha-internexin-immunoreactive inclusions within the perikarya of the same neuron. Electron microscopy findings support the notion that inclusions in NFID are heterogenous. The present study extends the list of proteins that have been identified as components of neuronal inclusions in NFID, and may help account for the pathogenesis of NFID.

Adaptor Proteins, Signal Transducing↗
PubMed1991

Morphological studies of the association of mitochondria with chlamydial inclusions and the fusion of chlamydial inclusions.

The association of mitochondria with the inclusions of five strains of Chlamydia psittaci, two strains of C. trachomatis and one strain of C. pneumoniae was examined by electron microscopy. The results demonstrated that mitochondrial association occurred only with the C. psittaci inclusions, but not with the C. trachomatis and C. pneumoniae inclusions. Multiple inclusions formed by infection with a single strain could fuse with each other during their expansion, but fusion never occurred between the C. trachomatis and C. psittaci inclusions as a result of dual infection with these different species.

Cell Nucleus↗
PubMed1995

Ubiquitinated inclusions in inclusion-body myositis patients are immunoreactive for cathepsin D but not beta-amyloid.

The nature of the inclusions in the human muscle disease inclusion-body myositis (IBM) has been the subject of debate. Parallels with Alzheimer's disease have been drawn after these inclusions were found to be ubiquitinated, and immunoreactive with antibodies to beta-amyloid (A beta) and certain amyloid-associated proteins. We have used a battery of antibodies against A beta and associated proteins to immunostain muscle biopsies from patients with IBM. Although the inclusions are ubiquitinated, we could not show immunoreactivity for A beta or the associated proteins investigated. We did, however, find that the ubiquitinated inclusions colocalised with the lysosomal marker, cathepsin D.

Alzheimer Disease↗
PubMed2004

alpha-internexin is present in the pathological inclusions of neuronal intermediate filament inclusion disease.

Neuronal intermediate filament (IF) inclusion disease (NIFID) is a novel neurological disease of early onset with a variable clinical phenotype including frontotemporal dementia, pyramidal, and extrapyramidal signs. Pathologically, in affected areas, there is neuronal loss, astrocytosis, and neuronal intracytoplasmic aggregates of abnormal neuronal IFs that contain neither tau nor alpha-synuclein. Thus, to characterize the neuronal IF protein profile of inclusions in NIFID, immunohistochemistry (IHC) was performed on 10 cases of NIFID, four normal aged controls (NL), and two cases of Alzheimer's disease (AD) using a panel of anti-neuronal IF proteins. Immunoelectron microscopy was performed on selected cases and frozen tissue from the frontal lobe of four cases was used for biochemical studies including sequential extractions and Western blotting. Based on these studies, we report here for the first time that alpha-internexin, a neuronal IF protein, is present within the inclusions of NIFID as are all three neurofilament subunits: heavy, medium, and light. Thus, all class IV neuronal IF proteins are present within the pathological inclusions of this disease. Biochemistry revealed that IF aggregates were soluble in sodium dodecyl sulfate (SDS) and no post-translational modification was detected when compared with Alzheimer's disease or aged control brains. Hence, we conclude that NIFID is characterized by the pathological cytoplasmic aggregation of all class IV neuronal IF proteins in brain. The discovery of alpha-internexin in the cytoplasmic inclusions implicates novel mechanisms of pathogenesis in NIFID and other neurological diseases with pathological accumulations of IFs.

Adult↗
PubMed2006

Kinetics and mechanism of cyclodextrin inclusion complexation incorporating bidirectional inclusion and formation of orientational isomers.

The kinetics of cyclodextrin (CD) inclusion complexation has been usually analyzed in terms of a one-step reaction or a consecutive two-step reaction involving intracomplex structural transformation as a second step. These schemes presume the inclusion of guest molecules through only one side of the CD cavity and the formation of unidirectional CD complexes. However, there has been increasing experimental evidence for the inclusion of guests through both sides of the CD cavity and the formation of orientational isomers for noncentrosymmetric guest molecules. This article presents a novel parallel reaction scheme for CD inclusion complexation, incorporating bidirectional inclusion and the formation of orientational isomers into the scheme. It is shown that the parallel reaction scheme gives the same concentration versus reaction time relationship as the consecutive two-step reaction scheme. The experimental methods for determining the microscopic directional rate constants are presented. The kinetic parameters of the two-step reaction scheme are expressed as functions of the directional rate constants. The ratios of orientational isomers of alpha-CD-based [2]-pseudorotaxanes and the microscopic directional rate constants of the threading and dethreading reactions are estimated from the reported thermodynamic and kinetics data obtained by using either the one-step or two-step reaction scheme. It is shown that the thermodynamic preference of an isomer over the other is mainly due to the slow dethreading rate of the isomer.

Journal Article↗
PubMed2006

[Influence of inclusive child day-care on nursery school teachers: a questionnaire survey of teachers with experience in inclusive child day-care in K City].

The purpose of this survey questionnaire is to investigate the factors influencing how nursery school teachers perceive inclusive child day-care in K City in order to qualify what support we can provide. The questionnaire was sent to nursery school teachers with experience in inclusive child day-care in K City. Three hundred seventeen teachers provided sufficient data for analysis. The results of this survey suggest that teachers perceive inclusive child day-care to lead up to self-development and the pleasure of child-caring. On the other hand, they feel a burden of inclusive child day-care, with teachers in their 40 s feeling a stronger burden than teachers in their 20 s. And teachers with experience in taking care of emotionally disturbed children or teachers with experience in taking care of hearing-impaired children feel a stronger burden than teachers without experience in taking care of them. The results of our survey also suggest that it is necessary for support systems to have special knowledge about disabled children and special ways of caring, and to decrease teachers' burden or dissatisfaction with inclusive child day-care.

Adult↗
PubMed1998

Intranuclear neuronal inclusions in Huntington's disease and dentatorubral and pallidoluysian atrophy: correlation between the density of inclusions and IT15 CAG triplet repeat length.

Huntington's disease (HD) is caused by CAG triplet repeat expansion in IT15 which leads to polyglutamine stretches in the HD protein product, huntingtin. The pathological hallmark of HD is the degeneration of subsets of neurons, primarily those in the striatum and neocortex. Specific morphological markers of affected cells have not been identified in patients with HD, although a unique itranuclear inclusion was recently reported in neurons of transgenic animals expressing a construct encoding the N-terminal part (including the glutamine repeat) of huntingtin (Davies et al., 1997). In order to understand the importance of this finding, we sought for comparable nuclear abnormalities in autopsy material from patients with HD. In all 20 HD cases examined, anti-ubiquitin and N-terminal huntingtin antibodies identified itranuclear inclusions in neurons and the frequency of these lesions correlated with the length of the CAG repeat in IT15. In addition, examination of material from the related HD-like triplet repeat disorder, dentatorubral and pallidoluysian atrophy, also revealed intranuclear neuronal inclusions. These findings suggest that intranuclear inclusions containing protein aggregates may be common feature of the pathogenesis of glutamine repeat neurodegenerative disorders.

Adolescent↗
PubMed1975

Organized inclusions in astrocytic and amorphous inclusions in neuronal mitochondria of human frontal brain tissue.

Brain tissue specimens were obtained early post mortem from the frontal lobe of seven unselected elderly subjects known to have been free of neurologic disease. Electron microscopically, two types of intramitochondrial inclusions were seen in four of seven cases. In two cases a few astrocyte mitochondria of the gyral white matter showed dense, elongated inclusions with an ordered linear substructure. These inclusions were, as a rule, accompanied by a row of prismatic cristae. In three cases some nerve cell mitochondria contained amorphous material of medium density and compact appearance. The globular masses often occupied the whole width of the mitochondrion. A relationship between the observed finding and a particular disease or morbid condition was not apparent. The inclusions are regarded as the morphologic substrate of a nonspecific metabolic change or degenerative process of the mitochondrion.

Astrocytes↗
PubMed2000

Neuronal intranuclear hyaline inclusion disease with polyglutamine-immunoreactive inclusions.

Neuronal intranuclear hyaline inclusion disease (NIHID) is a group of neurodegenerative disorders characterized by the presence of intranuclear inclusions in neurons (NIs). We report here clinicopathological findings of a 25-year-old female patient who died after 13 years of a clinical course characterized by progressive gait disturbance and movement disorders. Histological examination revealed widespread NIs with neuronal loss in restricted regions; neuronal loss was severe in the subthalamic nucleus, internal pallidum, substantia nigra, Edinger-Westphal nucleus and Purkinje cell layer. Quantification of the NIs combined with a graded evaluation of neuronal loss revealed an overall tendency for more severe neuronal loss to be accompanied by a lower frequency of NIs. A morphological similarity to the nuclear inclusions recently identified in several CAG repeat diseases prompted us to examine the immunolocalization of ubiquitin and expanded polyglutamine stretches, which demonstrated the presence of ubiquitin at the periphery of most NIs. An expanded polyglutamine stretch was seen in the center of limited number of NIs. These findings indicate that abnormal fragments such as expanded polyglutamine regions are incorporated into the inclusion, aggregated in its center, and thereby metabolized by a ubiquitin-dependent proteolytic pathway. Although it remains to be elucidated how the formation of NIs is related to neuronal degeneration, our findings suggest that NIs are formed in the process of sequestering or degrading abnormal protein fragments and formation of NIs may not be immediately toxic to neurons.

Adult↗
PubMed1991

Cardiomyopathy and myocyte intranuclear inclusions in neuronal intranuclear inclusion disease: a case report.

Neuronal intranuclear inclusion disease (NIID) is a progressive, usually fatal degenerative neurologic condition characterized by eosinophilic, intranuclear inclusions in neurons of the central and peripheral nervous system. We report a boy with onset of disease manifestations at age 3 and death at age 9, who showed clinical and pathologic findings characteristic of NIID. The case is unique because of cardiomyopathy manifested 1 year prior to death. Postmortem findings confirmed the presence of cardiomyopathy and revealed intranuclear inclusions in myocytes. Neither nuclear inclusions in the myocardium nor cardiac involvement have previously been reported in NIID.

Cardiomyopathies↗
PubMed2003

Congenital myopathy with abundant ring fibres, rimmed vacuoles and inclusion body myositis-type inclusions.

We report a 17-year-old girl with an unusual neuromuscular disorder characterised by slowly progressive proximal muscle weakness whose muscle biopsy showed multiple ring fibres and numerous rimmed vacuoles as well as intracytoplasmic and intranuclear inclusions of the inclusion body myositis-type. The clinical features of the presented case, manifested by the onset of the disease in early childhood, delayed motor development, short stature, lordosis and joint contractures were suggestive of congenital myopathy. The coexistence of ring fibres, rimmed vacuoles and inclusion-body myositis-type inclusions in a child with congenital myopathy has not been previously reported.

Adolescent↗
PubMed1991

A temporal study of the expression of the capsid, cytoplasmic inclusion and nuclear inclusion proteins of tobacco etch potyvirus in infected plants.

Young leaves of tobacco, systemically infected by tobacco etch potyvirus (TEV), were examined for the presence and distribution of four virus encoded proteins [capsid, cytoplasmic inclusion (CI) and two nuclear inclusion (NI) proteins] at various time periods after inoculation of expanded leaves of the plants. The analyses were carried out by ELISA and by immunogold electron microscopy of thin sections of the leaves. All four proteins were detected simultaneously in the systemic leaves for the first time on the fifth day after inoculation of the expanded leaves. All four proteins increased in concentration until the seventh day and then showed no further increase with the exception of the capsid protein which continued to accumulate. The CI protein was first detected in association with the plasmalemma/cell wall and was subsequently found mostly in the form of pinwheels in the cytoplasm. The two NI proteins were found at all times after infection within the nucleus, although small concentrations were detected in the cytoplasm. These experiments suggest that both the NIa and NIb proteins are transported into the nucleus immediately after synthesis. At the earliest time periods after infection, high concentrations of these proteins (NIa and NIb) were found in their non-inclusion form in the nucleolus. At 14 days after infection, both proteins were found only as inclusions in the nucleus. The capsid protein was found at all stages of infection only in the cytoplasm.

Capsid↗
PubMed1996

Difference in expression of phosphorylated tau epitopes between sporadic inclusion-body myositis and hereditary inclusion-body myopathies.

Sporadic inclusion-body myositis (s-IBM) and the hereditary inclusion-body myopathies (h-IBMs) are severe and progressive muscle diseases, characterized pathologically by vacuolated muscle fibers containing paired-helical filaments (PHFs). An interesting feature of the s- and h-IBM muscle phenotype is its striking similarity to Alzheimer-disease (AD) brain. We immunostained muscle biopsies of 9 s-IBM patients, 9 autosomal-recessive h-IBM patients, 1 autosomal-dominant h-IBM patients, and 18 normal and disease-controls with several antibodies known to react with the hyperphosphorylated tau of AD-PHFs. Those included SMI-31, SMI-310, PHF-1, and AT8. In both s- and h-IBM, virtually all vacuolated muscle fibers had strongly immunoreactive inclusions with SMI-31, and by immuno-electronmicroscopy SMI-31 was exclusively localized to PHFs. Approximately 40 to 50% of both s- and h-IBM vacuolated muscle fibers were also immunoreactive with AT8 antibody. To the contrary, in h-IBM, there was no immunoreactivity with SMI-310 and PHF-1 antibodies, whereas in s-IBM the vacuolated muscle fibers had strong immunoreactivity with those two antibodies. By immunoelectronmicorscopy, SMI-310 and PHF-1 also were localized to PHFs. Within s-IBM muscle fibers, the structures immunoreactive with SMI-310 were congophilic, whereas h-IBM muscle fibers did not have congophilia. Our studies: (a) demonstrate a distinct difference between s-IBM and the h-IBMs in regard to expression of immunoreactive phosphorylated tau and congophilia; (b) demonstrate a new "diagnostic duo" combination of SMI-31 and SMI-310 antibodies for identifying and distinguishing s-IBM and the h-IBMs; and (c) provide another close similarity of pathologic phenotypes between s-IBM muscle and AD brain, suggesting that similar cellular pathogenic mechanisms may be active in both diseases.

Adult↗
PubMed1993

Cytoplasmic inclusions of respiratory syncytial virus-infected cells: formation of inclusion bodies in transfected cells that coexpress the nucleoprotein, the phosphoprotein, and the 22K protein.

Immunofluorescence staining and immunoelectron microscopy of respiratory syncytial (RS) virus-infected cells revealed the presence of cytoplasmic inclusions that were specifically labeled with monoclonal antibodies directed against the nucleoprotein (NP), the phosphoprotein (P), or the 22K protein. Transient expression of these three proteins with the vaccinia-T7 system, either individually or in different combinations, demonstrated that coexpression of NP and P was sufficient to induce the formation of cytoplasmic inclusions similar to those found in RS virus-infected cells. In addition, the 22K protein was also incorporated to the inclusions when coexpressed with both NP and P proteins. Immunobinding assays revealed the presence of NP-P and NP-22K complexes in extracts of RS virus-infected cells. These complexes were also detected in extracts of transfected cells that coexpressed the corresponding proteins. The implications of these results for the RS virus replicative cycle are discussed.

Cell Line↗
PubMed1997

An inflammatory, familial, inclusion body myositis with autoimmune features and a phenotype identical to sporadic inclusion body myositis. Studies in three families.

We describe the occurrence of an inflammatory inclusion body myositis in siblings of a single generation in three separate families. The disease in this total of seven patients was characterized by selective and early involvement of forearm and finger flexors, confirmed by MRI, and weakness of the quadriceps, triceps and foot extensors. Muscle biopsies in at least two members from each family showed endomysial inflammation, red-rimmed vacuoles, intracellular amyloid deposition and 15-18-nm tubulo-filaments within the vacuolated muscle fibres. Immunocytochemistry on serial muscle biopsy sections demonstrated an abundance of CD8+ cells invading non-necrotic, MHC-1-expressing muscle fibres. Immunogenetic studies showed the presence of the DR3 allele (DRB1*0301/0302) in all seven patients. The combination of the clinical, histological, immunopathological and immunogenetic features indicate that these patients have a disease identical to sporadic inclusion body myositis (s-IBM). We conclude that the classic, inflammatory, s-IBM can also occur in families (familial inclusion body myositis), in a pattern analogous to the familial occurrence of other autoimmune neurological diseases such as myasthenia gravis and multiple sclerosis. These observations strengthen the view that s-IBM behaves like other autoimmune diseases and has disease susceptibility linked to the DR3 allele.

Aged↗
PubMed1995

New advances in the understanding of sporadic inclusion-body myositis and hereditary inclusion-body myopathies.

This review emphasizes new advances in seeking the pathogenic mechanisms of sporadic inclusion-body myositis and hereditary inclusion-body myopathy syndromes. Clinical and pathologic similarities and differences between sporadic and hereditary forms are described. Hypotheses are presented regarding the possible causes and consequences of abnormally accumulated intramyofiber beta-amyloid precursor protein (beta APP) (including beta-amyloid protein and C- and N-terminal epitopes), hyperphosphorylated tau, alpha 1-antichymotrypsin, apolipoprotein E, prion protein, ubiquitin, nicotinic acetylcholine receptor and its 43-kD associated protein, fibroblast growth factor, and transforming growth factor-beta. Also increased are beta APP mRNA and prion protein mRNA. Striking similarities between the pathology of muscle specimens from sporadic inclusion-body myositis and samples from the brains of patients with Alzheimer's disease in regard to Congo red positivity and accumulations of several proteins are discussed. Because most of the proteins that pathologically accumulate throughout the abnormal muscle fibers also accumulate focally at normal human neuromuscular junctions, the possible "junctionalization" of nonjunctional nuclei as a pathogenic mechanism in the muscle fiber is discussed.

Diagnosis, Differential↗