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PubMed1992

Inclusion bodies containing adenovirus-like particles in the intestine of a psittacine bird affected by inclusion body hepatitis.

This paper reports a case of inclusion body hepatitis with intranuclear inclusion bodies in the liver and the intestine of a Yellow-naped Amazon parrot (Amazona ochrocephala). Structurally, basophilic intranuclear inclusion bodies were found in hepatic cells and enterocytes. Ultrastructurally, icosahedral adenovirus-like particles, 60-75 nm in diameter, were found in the same cells.

Adenoviridae Infections↗
PubMedDate not supplied

Intranuclear inclusion bodies in an elderly demented woman: a form of intranuclear inclusion body disease.

Intranuclear inclusion body disease (INIBD) is a rare neuropathological entity characterized by eosinophilic intranuclear bodies in neurons and/or glia. While this disease generally occurs in children, in whom it presents as a multiple systems degeneration, a few adult cases are also described. Only 4 previously reported adult cases have had an associated dementia and all of these patients had additional significant neurological abnormalities. We report a 72-year-old woman with primary degenerative dementia in whom intranuclear inclusion bodies (INIB) were a major neuropathologic finding. The INIB were most easily found in astrocytes of Alzheimer II type, which had proliferated in the cortex and white matter. Occasional neurons were affected. The inclusions consisted of 13 nm diameter filaments associated with amorphous electron-dense material, arranged in a random pattern without lattice formation. They did not stain with antibodies against all 3 neurofilament subunits, glial fibrillary acidic protein, tau-1 protein, vimentin, keratin or actin. We conclude that INIBD is a rare substrate of primary degenerative dementia in elderly patients.

Aged↗
PubMed2002

Metal ion-dependent molecular inclusion chemistry: inclusion of aromatic anions by coordinated 1,4,7,10-tetrakis((S)-2-hydroxy-3-phenoxypropyl)-1,4,7,10-tetraazacyclododecane.

The ability of the pendant donor macrocyclic ligand 1,4,7,10-tetrakis((S)-2-hydroxy-3-phenoxypropyl)-1,4,7,10-tetraaza- cyclododecane((S)-thphpc12) (or [Cd((S)-thphpc12)](2+)) to act as a metal ion-dependent receptor for aromatic anions has been investigated in solution and in the solid state. [Cd((S)-thphpc12)](2+) adopts a stable conical conformation with a large hydrophobic cavity, which has been shown to contain, via complementary multiple hydrogen bonding, p-nitrophenolate, aromatic carboxylates, p-toluenesulfonate, certain aromatic amino acid anions, phenoxyacetate, and acetate. In the case of p-nitrophenolate only, one or two anions can be contained within the receptor cavity. The crystal structure of [Cd((S)-thphpc12)(p-nitrophenolate)(2)] shows a coplanar arrangement of the p-nitrophenolates, where each is retained in the cavity by a pair of hydrogen bonds to cis hydroxyl groups. The crystal structure of the p-aminobenzoate inclusion complex indicates retention of the guest via a pair of hydrogen bonds to each oxygen atom of the carboxylate moiety. The crystal structure of the (L)-phenylalaninate inclusion complex indicates that the amino acid is retained by five hydrogen bonds, two involving the nitrogen atom and three to the oxygen atoms of the carboxylate moiety. Binding constants (10(3)-10(5) M(-1)) for the inclusion of some of the aforementioned anions in [Cd((S)-thphpc12)](2+) and related receptors were measured by (1)H NMR titration in DMSO-d(6) at 298 K.

Amino Acids↗
PubMed1999

Metal Ion Dependent Molecular Inclusion Chemistry: Inclusion of p-Toluenesulfonate and p-Nitrophenolate within the Structure of Coordinated 1,4,7,10-Tetrakis((S)-2-hydroxy-3-phenoxypropyl)-1,4,7,10-tetraazacyclododecane.

The pendant donor macrocyclic ligand 1,4,7,10-tetrakis((S)-2-hydroxy-3-phenoxypropyl)-1,4,7,10-tetraazacyclododecane ((S)-thphpc12) has been synthesized in quantitative yield from cyclen (1,4,7,10-tetraazacyclododecane) and (2S)-(+)-3-phenoxy-1,2-epoxypropane. An X-ray diffraction study supports the result of molecular orbital calculations in showing that complexation with hydrated cadmium(II) diperchlorate produces an approximately square-antiprismatic complex in which the metal ion is located between a plane containing the four nitrogen atoms and a plane containing the four oxygen atoms. As a consequence of this the four phenoxymethyl moieties, each attached to one of the four N-O chelate rings, juxtapose to form a substantial empty cavity allowing the complex to act as a molecular receptor. Inclusion complexes have been formed from this complex in which either a p-toluenesulfonate or p-nitrophenolate anion has entered the cavity. An X-ray crystallographic study of [Cd((S)-thphpc12)(p-toluenesulfonate)]ClO(4) shows that the guest anion is retained within the cavity by four hydrogen bonds to the group of hydroxyl moieties associated with the ligand. (13)C NMR and conductivity studies indicate that this inclusion complex retains its integrity in DMSO or DMF solution. Parallel studies have been conducted with [Pb((S)-thphpc12)](ClO(4))(2) indicating that the corresponding inclusion complexes are of lower stability.

Journal Article↗
PubMed2004

Mental health, social inclusion and the green agenda: an evaluation of a land based rehabilitation project designed to promote occupational access and inclusion of service users in North Somerset, UK.

The current debate about social inclusion in the field of mental health reveals a tension between the political and economic objectives of social policy. The former utilises the language of citizen empowerment and rights, whilst the latter is concerned with reducing welfare dependency through labour market activation. A central question here is whether a suitable programme of therapeutic work, training and support will produce better outcomes than those predicted by either a clinical diagnostic assessment or indeed open employment in the labour market. This article evaluates a research project with mental health users designed to develop pathways towards inclusion. The principal means for achieving this was a programme of 'green' land-based activities, training and social support. The researchers employed a mixed method approach, utilising a quasi-experimental design with a hypothetical control and standardised testing. This was followed by interviews with users, staff and focus group discussion. The evaluation produced some unexpected findings; for example, it was found that no strong correlation existed between diagnosis and performance. Many users performed better than had been predicted by their diagnostic assessment. However, the reasons for this remained unclear until the qualitative interviews enabled users to give accounts of the problems they faced, explain what inclusion meant for them, and outline how the project had brought gains in confidence, motivation and self belief. The data gathered during the research derived from different epistemological positions. This can be seen as representing two ways of 'slicing the reality cake' rather than producing one complete view of mental health users reality. One construction related to how 'the system' diagnosed, processed, and 'objectively' managed them. The other was about how users' responded to their situation, utilised the opportunities available, and made 'subjective' sense of their experience.

Agriculture↗
PubMed1960

Virus isolated from inclusion conjunctivitis of newborn (inclusion blennorrhea).

An infant developed acute conjunctivitis 7 days after birth. Smears of the mucopurulent discharge contained many typical elementary-body inclusions. From conjunctival scrapings a virus resembling trachoma was grown in eggs. When instilled into monkey eyes, it produced an acute conjuctivitis resembling the human disease. Nine other patients with inclusion conjunctivitis of similar intensity failed to yield viruses.

Child↗
PubMed1992

Immunocytochemical and ultrastructural studies of neuronal and oligodendroglial cytoplasmic inclusions in multiple system atrophy. 2. Oligodendroglial cytoplasmic inclusions.

Oligodendroglial cytoplasmic inclusions (OCI) in multiple system atrophy were investigated immunocytochemically and ultrastructurally. Among the 17 cases examined, 16 had OCIs. Almost all OCIs were positive for both alpha B-crystallin and ubiquitin. The antibodies against tubulin, paired helical filament and tau stained OCIs to various extents. Ultrastructurally OCIs consisted of meshworks of granule-associated filaments about 25 nm in diameter that sometimes formed flame-shaped tangle-like structures. Immunoelectron microscopy showed that an epitope of alpha B-crystallin was located on the granule-associated filaments composing OCIs. Our studies further support a cooperative role of alpha B-crystallin, ubiquitin and cytoskeletal protein in the formation of some types of intracytoplasmic inclusions.

Adolescent↗
PubMed2002

Influences of intranuclear inclusion on nuclear size - morphometric study on pontine neurons of neuronal intranuclear inclusion disease cases.

In looking for a possible influence of nuclear inclusions (NIs) on neurodegeneration in human brains, we quantified morphological features of pontine neurons of three unrelated cases of neuronal intranuclear inclusion disease (NIID) and five control cases. Cross-sectional area of each neuronal nucleus and the indices for its deformity (long axis/short axis and circularity index defined as deviation from the perfect circle) were measured on pontine sections and their relation to NIs was statistically analyzed. Cross-sectional area of neuronal nuclei harboring ubiquitin-immunopositive NIs was significantly larger (110.6+/-1.6 micro m(2), mean +/- SE), while that of nuclei not harboring NIs was smaller (77.8+/-1.5 micro m(2)) than that in controls (90.5+/-0.7 micro m(2)). This difference remained significant even when the cross-sectional area occupied by NIs was subtracted from that of the nucleus harboring the NI (97.4+/-1.5 micro m(2)). This could hardly be explained if nuclear shrinkage is accelerated in the presence of NI. On the contrary, NI formation in pontine neurons of NIID might be linked, either directly or indirectly, to a mechanism, which counteracts rather than accelerates nuclear shrinkage. Because nuclear deformity was apparent even in neurons with NIs, whose nuclei were significantly larger than controls, the nuclear deformity is not secondary to its shrinkage and represents another aspect of neurodegeneration independent of nuclear shrinkage. Association of NIs to neurons of larger nuclear size in NIID brain indicates that NIs are not necessarily toxic to neurons.

Adult↗
PubMed2004

Spatial correlations between the neuronal inclusions, swollen achromatic neurons, and glial cells in neuronal intermediate filament inclusion disease (NIFID).

Neuronal intermediate filament (IF) inclusion disease (NIFID) is characterized by neuronal loss, neuronal cytoplasmic IF-positive inclusions (NI), swollen neurons (SN), and a glial cell reaction. We studied the spatial correlations between the clusters of NI, SN, and glial cells in four gyri of the temporal lobe (superior temporal gyrus, inferior temporal gyrus, lateral occipitotemporal gyrus, and parahippocampal gyrus) in four cases of NIFID. The densities of histological features (per 50 x 250 microm sample field) were as follows: NI (mean = 0.41, range 0.28-0.68), SN (mean = 1.41, range 0.47-2.65), glial cell nuclei (mean = 5.21, range 3.63-8.17). The NI and the SN were positively correlated in half of the brain regions examined, the correlations being present at the smallest field size (50 x 250 microm). The NI were also positively or negatively correlated with the glial cell nuclei in different areas, the negative correlations being present at the smallest field size. Glial cell nuclei were positively or negatively correlated with the SN in different brain areas, mainly at the larger field sizes (400 x 250 and 800 x 250 microm). The spatial correlation between the clusters of NI and SN in the cortex suggests their development within the same columns of cells. At first, the glial cell reaction is also confined to these columns but later becomes more generally distributed across the cortex.

Adult↗
PubMed2000

Association of active extracellular signal-regulated protein kinase with paired helical filaments of inclusion-body myositis muscle suggests its role in inclusion-body myositis tau phosphorylation.

The possible role of extracellular signal-regulated kinase (ERK) in the pathogenesis of inclusion-body myositis (IBM) was investigated by immunostaining the active phosphorylated form of ERK in muscle biopsies of six IBM and 14 control patients. Between 80% and 90% of IBM vacuolated muscle fibers contained well-defined ERK-immunoreactive inclusions, which were co-localized by light microscopy, with phosphorylated tau in 70 to 80% of those fibers. Immunoelectronmicroscopy colocalized ERK to small amorphous tufts adjacent to the muscle fiber paired-helical filaments. Strong ERK immunoreactivity was also present at the postsynaptic domain of all human neuromuscular junctions. Our study suggests 1) that ERK, a signal transducer, might play a role in IBM pathogenesis, including participation in the pathological phosphorylation of IBM tau; and 2) that signal transduction abnormalities may be a component of the IBM pathogenic cascade. Our novel immunolocalization of ERK at the postsynaptic domain of human neuromuscular junctions supports a role in transcription of junctional-protein genes. The ERK localized in nonjunctional regions of IBM fibers may underlie the known pathological up-regulation of junctional proteins there.

Humans↗
PubMed1998

Familial neuronal intranuclear inclusion disease with ubiquitin positive inclusions.

Female monozygotic twins developed upper and lower limb neurogenic weakness in their thirties, followed by cerebellar ataxia, dysarthria and death after an illness duration of about 20 years. Autopsy revealed pathological features typical of neuronal intranuclear inclusion disease (NIID) and positive ubiquitin immunostaining of the inclusions. Two adult sons of one of the twins have now developed an identical illness. This family provides strong evidence of an hereditary form of NIID.

Adult↗
PubMed1998

HLA allele distribution distinguishes sporadic inclusion body myositis from hereditary inclusion body myopathies.

We studied the HLA class II associations in patients with sporadic inclusion body myositis (s-IBM) and hereditary inclusion body myopathies (h-IBM) and attempted to distinguish these myopathies on the basis of HLA allele assignments. Forty-five patients, 30 with s-IBM and 15 with h-IBM, underwent HLA class II allele-specific typing using polymerase chain reaction sequence-specific primers for 71 alleles contained in the DRbeta1, DRbeta3-5, and DQbeta1 loci. In s-IBM, we found a high (up to 77%) frequency of DRbeta1*0301, DRbeta3*0101 (or DRbeta3*0202) and DQbeta1*0201 alleles. No significant association with alleles in the DR and DQ haplotypes was found among the 15 h-IBM patients. The strong association of prominent alleles with s-IBM, but not h-IBM, suggests that s-IBM is a distinct disorder with an immunogenetic background that differs from h-IBM.

Aged↗
PubMed2005

Neuronal intranuclear inclusion disease without polyglutamine inclusions in a child.

Neuronal intranuclear inclusion disease (NIID) is a rare and heterogeneous group of slowly progressive neurodegenerative disorders characterized by the widespread presence of eosinophilic neuronal intranuclear inclusions (NII) accompanied by a more restricted pattern of neuronal loss. We report here the pathologic findings in a 13-year-old boy who died after a 6-year clinical history of progressive ataxia, extrapyramidal manifestations, and lower motor neuron abnormalities. Histological evaluation of the brain revealed widespread NII in most neurons. Marked loss of cerebellar Purkinje cells and neurons in the dentate nucleus, red nucleus, and spinal cord anterior horns was accompanied by a modest astrocytosis. Because of the abundance of NII and the absence of a relationship between NII and neuronal loss or microglial activation, we conclude that loss of cerebellar, brainstem, and spinal cord neurons reflects selective neuronal vulnerability. NII were immunoreactive for ubiquitin, glucocorticoid receptor, and SUMO-1, a small, ubiquitin-like protein purportedly involved in protein transport and gene transcription. NII were non-reactive for polyglutamine (1C2), TATA binding protein, promyelocytic leukemia protein, heat shock protein 90, tau, alpha-synuclein, neurofilament, and beta amyloid. The moderate ubiquitin and strong SUMO-1 staining of NII in juvenile cases is the reverse of the pattern noted in adult diseases, suggesting the two age groups are pathogenically distinct. We suggest that juvenile NIID is a spinocerebellar brainstem ataxic disease possibly related to an abnormality in SUMOylation.

Adolescent↗
PubMed1998

Sporadic inclusion-body myositis and hereditary inclusion-body myopathies: current concepts of diagnosis and pathogenesis.

We discuss the pathologic diagnostic criteria and review the major new advances related to seeking the pathogenic mechanism of sporadic inclusion-body myositis (s-IBM) and hereditary inclusion-body myopathy (h-IBM). A classification of the various h-IBM syndromes is also presented. The several forms of the h-IBMs have different genetic transmissions and probably different genetic defects. In neither s-IBM nor the h-IBMs are the sequential steps of the pathogenic cascade understood. Because s-IBM and the h-IBMs have a number of characteristic pathologic features in common, we postulate that their different causes trigger the same upstream aberration leading to a similar downstream cascade of pathologic events, which are ultimately responsible for the characteristic muscle-fiber degeneration. Muscle-biopsy and experimental evidence is given supporting our hypothesis that overexpression of beta-amyloid precursor protein within abnormal muscle fibers is an early upstream event causing the pathogenic cascade. We also present evidence supporting our concept that muscle aging and oxidative stress are important factors contributing to the s-IBM-specific muscle fiber destruction. Additionally, the intriguing parallels between the pathologic phenotype of IBM muscle fibers and Alzheimer's disease brain are summarized.

Aging↗
PubMed1994

New types of human papillomaviruses and intracytoplasmic inclusion bodies: a classification of inclusion warts according to clinical features, histology and associated HPV types.

Two new types of intracytoplasmic inclusion bodies (ICBs) associated with distinct clinical features, and the presence of DNA of distinct types of human papillomaviruses (HPVs) are reported. One hundred and seven cutaneous warts containing ICBs were grouped into three categories according to distinct clinicopathological features: 67 were wart lesions with well-known granular (Gr)-ICB, 13 were punctate keratotic lesions with filamentous (Fl)-ICB and 31 were pigmented warts with homogeneous (Hg)-ICB. Molecular biological studies were performed in order to assess a specific association of each group of warts with distinct types of HPV. HPV-1 DNA sequences were detected in all the lesions with a Gr-ICB. Punctate keratotic lesions with Fl-ICB were associated with HPV-63, which was newly cloned from such a lesion. One of the samples also contained HPV-1 DNA. Pigmented warts with Hg-ICBs contained one of the related HPVs, i.e. HPV-4, HPV-60 or a novel type of HPV, HPV-65. Based on these associations, a classification of inclusion warts is proposed.

Adolescent↗
PubMed1994

Abnormal accumulation of prion protein mRNA in muscle fibers of patients with sporadic inclusion-body myositis and hereditary inclusion-body myopathy.

Sporadic inclusion-body myositis is the most common progressive muscle disease of older patients. The muscle biopsy demonstrates mononuclear cell inflammation and vacuolated muscle fibers containing paired helical filaments and 6 to 10-nm fibrils, both resembling those of Alzheimer brain, and Congo-red positivity. Hereditary inclusion-body myopathy designates patients cytopathologically similar but without inflammation. In both muscle diseases, prion, and several proteins characteristic of Alzheimer brain--eg, beta-amyloid protein and hyperphosphorylated tau (which normally are expressed mainly in neurons), and apolipoprotein E--are abnormally accumulated in vacuolated muscle fibers, by unknown mechanisms. We now demonstrate in both muscle diseases that prion mRNA is strongly expressed in the vacuolated muscle fibers, which suggests that their accumulated prion protein results, at least partly, from increased gene expression. This, to our knowledge, is the first demonstration of abnormally increased prion mRNA in human disease. Another novel finding is the increased prion mRNA in human muscle macrophages, and both increased prion protein and prion mRNA in regenerating muscle fibers. The latter indicates that prion may play a role in human muscle development.

Adult↗
PubMed2000

Enantioselective inclusion of methyl phenyl sulfoxides and benzyl methyl sulfoxides by (R)-phenylglycyl-(R)-phenylglycine and the crystal structures of the inclusion cavities

Crystalline (R)-phenylglycyl-(R)-phenylglycine [(R,R)-1] includes methyl phenyl sulfoxides (2 and 3) and benzyl methyl sulfoxides (4) with high enantioselectivity. The dipeptide exhibited different stereoselectivity depending on four structural isomers of methyl tolyl sulfoxide (C(8)H(10)OS): R for methyl 2-tolyl sulfoxide, S for methyl 3-tolyl sulfoxide, and racemic for methyl 4-tolyl sulfoxide. A structural isomer, benzyl methyl sulfoxide, was included in racemic form. Chlorophenyl methyl sulfoxides 3 (C(7)H(7)ClOS) with a similar volume showed the same enantioselectivity for their recognition. By single-crystal X-ray analyses of these inclusion compounds, it was elucidated that (R,R)-1 molecules self-assembled to form layer structures and included the sulfoxides between these layers and that the origin of the enantioselectivity based on chiral cavities was induced by conformation of the C-terminal phenyl group of the dipeptide. The relative position between the ammonio proton and the C-terminal phenyl group in one molecule of the dipeptide determined the stereochemistry of the methyl sulfinyl groups to be recognized. Various positional isomers of methyl xylyl sulfoxide having the formula of C(9)H(12)OS were subjected to the enantioselective inclusion by (R,R)-1 crystals and these results are also discussed.

Journal Article↗
PubMed1976

Glycogenous hepatonuclear inclusions in the aged mouse--an electron microscopical study of the histogenesis of nuclear inclusions.

Fifty-three and 84 week old mice have been investigated for liver nuclear inclusions. Light microscopical investigations revealed a significantly higher incidence of intranuclear PAS-positive material in the 84 week old mice. Electron microscopical studies showed a continuous development of nuclear inclusions from invagination of the double nuclear membrane containing all cytoplasmic organelles in various conditions via isolation of the invaginated portion to intranuclear free glycogen as a visible final stage. During the whole process alpha-glycogen is degraded to beta- and gamma-particles. These nuclear changes are not accompanied by other pathological changes either in the cells concerned or in the surrounding liver parenchyma. These nuclear findings are attributed to specific metabolic conditions in the ageing mouse.

Aging↗