Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Inclusion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed2006

Mean time-of-flight of photons in transillumination measurements of optically anisotropic tissue with an inclusion.

We study the effect of optical anisotropy on the mean time-of-flight of photons in a slab of turbid medium containing an inclusion whose optical properties differ from those of the bulk. For this analysis the difference in the mean time for a photon introduced into the slab to reach a specified target point with and without the inclusion is calculated. This difference is defined to be a measure of the contrast. The theoretical model is based on a continuous-time random walk on a lattice, which can be solved exactly and furnishes an exact expression for the contrast. Qualitative and quantitative characteristics of the contrast are analysed as functions of the geometric configuration of the system components (locations of the source, the inclusion and the detector), parameters that specify the optical anisotropy of the medium, and either the scattering properties of the inclusion or the lifetime of the small fluorophore in the case of the time-resolved fluorescence experimental configuration.

Algorithms↗
PubMed2005

A support vector machine-based method for predicting the propensity of a protein to be soluble or to form inclusion body on overexpression in Escherichia coli.

MOTIVATION: Inclusion body formation has been a major deterrent for overexpression studies since a large number of proteins form insoluble inclusion bodies when overexpressed in Escherichia coli. The formation of inclusion bodies is known to be an outcome of improper protein folding; thus the composition and arrangement of amino acids in the proteins would be a major influencing factor in deciding its aggregation propensity. There is a significant need for a prediction algorithm that would enable the rational identification of both mutants and also the ideal protein candidates for mutations that would confer higher solubility-on-overexpression instead of the presently used trial-and-error procedures. RESULTS: Six physicochemical properties together with residue and dipeptide-compositions have been used to develop a support vector machine-based classifier to predict the overexpression status in E.coli. The prediction accuracy is approximately 72% suggesting that it performs reasonably well in predicting the propensity of a protein to be soluble or to form inclusion bodies. The algorithm could also correctly predict the change in solubility for most of the point mutations reported in literature. This algorithm can be a useful tool in screening protein libraries to identify soluble variants of proteins.

Algorithms↗
PubMed1994

The distribution of oligodendroglial inclusions in multiple system atrophy and its relevance to clinical symptomatology.

In this study a semiquantitative mapping of oligodendroglial cytoplasmic inclusions (GCIs), a feature of oligodendroglial degeneration in multiple system atrophy (MSA), was undertaken by means of a sensitive silver technique in 14 brains and 11 spinal cords of patients with various combinations of striatonigral degeneration, olivopontocerebellar atrophy and autonomic failure. The results show a system-bound extensive degeneration of interfascicular, perineuronal and perivascular oligodendrocytes. Oligodendroglial cytoplasmic inclusion-rich structures occur in the supra-segmental motor systems (primary motor and higher motor areas of cerebral cortex, 'pyramidal', 'extrapyramidal' and cortico-cerebellar systems), in the supraspinal autonomic systems and in their targets. In contrast, the visual and auditory pathways, olfactory structures, somatosensory systems, association and limbic cortical areas and subcortical limbic structures contain no or only a few GCIs. Comparison of the severity of oligodendroglial degeneration (GCI-density) with that of the neuronal alterations (neuronal cytoplasmic and nuclear inclusions, degenerated neuronal processes and loss of nerve cells) indicates a striking preponderance of oligodendroglial degeneration and that degeneration neither of axons, nor of neuronal cell bodies is a prerequisite of the development of GCIs. It also suggests that inclusion-bearing oligodendroglial degeneration may cause or contribute to the manifestation of clinical symptomatology in structures with GCI accumulation but without convincing neuronal alterations, i.e. cerebral motor cortical areas and reticular formation of the lower brainstem, both previously thought to be spared in MSA.

Aged↗
PubMed2000

Semantic dementia with ubiquitin-positive tau-negative inclusion bodies.

Three cases are reported with dementia and ubiquitin-positive but tau-negative inclusion bodies. All patients had a semantic dementia and the clinical details of two of these have been published as the first description of a selective semantic memory impairment. The original diagnosis had been of Pick's disease based on frontotemporal atrophy, but re-examination has revealed ubiquitin-positive but tau-negative inclusions as well as neurites in the frontotemporal cortices and ubiquitin-positive, intracytoplasmic inclusions in the granule cells of the dentate fascia. These inclusions are identical to those reported in association with amyotrophic lateral sclerosis (motor neuron disease), but none were seen in brainstem or spinal cord motor neurons.

Dementia↗
PubMed2000

Alpha-synuclein inclusions in amygdala in the brains of patients with the parkinsonism-dementia complex of Guam.

We investigated by immunohistochemistry the deposition of alpha-synuclein in the brains of deceased patients with the parkinsonism-dementia complex (PDC) of Guam. Five of 13 PDC brains showed numerous alpha-synuclein positive neuronal inclusions and abnormal neurites, chiefly in the amygdala. Similar alpha-synuclein positive lesions were observed, although to a lesser extent, in the entorhinal cortex and the dorsal vagal nucleus. No alpha-synuclein positive inclusions were observed in motor cortex or locus coeruleus, and only a small number of positive inclusions were found in the Sommer's sector, temporal cortex, or substantia nigra. Some of the alpha-synuclein positive inclusions were reminiscent of cortical Lewy bodies (LB), but many of those in the amygdala coexisted with tau-positive pretangles and/or neurofibrillary tangles (NFT) within the same neurons. In these neurons, tau-positive shells encapsulated alpha-synuclein positive central cores or irregularly shaped alpha-synuclein-positive deposition intermingled with pretangles/NFT. Thus, the present study suggests that a common mechanism may govern aggregation of alpha-synuclein and tau in the amygdala, and that aggregation of alpha-synuclein may play some role in the neurodegenerative process of a tauopathy (i.e. PDC) in which Abeta deposition is virtually absent.

Adult↗
PubMed2002

Promyelocytic leukemia protein is redistributed during the formation of intranuclear inclusions independent of polyglutamine expansion: an immunohistochemical study on Marinesco bodies.

Marinesco bodies (MBs) are ubiquitinated intranuclear inclusions observed in nigral pigmented neurons. They increase in number during aging, and their formation is considered to represent a cellular reaction to stress, but is not always associated with neuronal degeneration. We conducted immunohistochemical studies on MBs abundant in myotonic dystrophy brains and compared their nature with that of neuronal intranuclear inclusions (NIIs) in polyglutamine diseases. First, we examined the relationship between MBs and polyglutamine proteins and demonstrated that one of the polyglutamine proteins, ataxin-3, as well as a 19S proteasomal protein, was preferentially recruited into MBs even in the absence of expanded polyglutamine. This indicates that an alternative mechanism during the formation of MBs that is not related to polyglutamine expansion or neuronal degeneration may recruit ataxin-3 into nuclear inclusions in a protein-specific manner. Secondly, we investigated the relationship between MBs and promyelocytic leukemia protein (PML), a nuclear matrix-associated protein that is normally localized to intranuclear punctate structures (PML nuclear bodies) and is known to reorganize itself in association with polyglutamine aggregation. In nigral pigmented neurons in myotonic dystrophy, spherical, hemispherical or rod-like PML-immunoreactive structures, in addition to punctate structures, were observed in their nuclei. Similar PML redistribution was also observed in nigral pigmented neurons in aged controls and cases of hepatic encephalopathy, 2 other conditions in which abundant MBs are formed. Double immunofluorescence study revealed that these PML-positive structures undergo morphological changes in association with ubiquitin accumulation during MB formation. It is therefore indicated that PML reorganization does not represent a specific nuclear event involved in the pathogenesis of polyglutamine diseases, but may commonly occur during the formation of intranuclear inclusions as a reaction against various stresses that involve the ubiquitin-proteasome pathway.

Adult↗
PubMed2000

Convenient and efficient in vitro folding of disulfide-containing globular protein from crude bacterial inclusion bodies.

We investigated how the folding yield of disulfide-containing globular proteins having positive net charges from crude bacterial inclusion bodies was affected by additives in the folding buffer. In screening folding conditions for human ribonucleases and its derivative, we found that addition of salt (about 0.4 M) to a folding buffer increased the folding yield. This suggested that electrostatic interaction between polyanionic impurities such as nucleic acids and cationic unfolded protein led to the formation of aggregates under the low-salt conditions. Since inclusion bodies were found to contain nucleic acids regardless of the electrostatic nature of the expressed protein, the electrostatic interaction between phosphate moieties of nucleic acids and basic amino acid residues of a denatured protein may be large enough to cause aggregation, and therefore the addition of salt in a folding buffer may generally be useful for promotion of protein folding from crude inclusion bodies. We further systematically investigated additives such as glycerol, guanidium chloride, and urea that are known to act as chemical chaperons, and found that these additives, together with salt, synergistically improved folding yield. This study, suggesting that the addition of salt into the folding buffer is one of the crucial points to be considered, may pave the way for a systematic investigation of the folding conditions of disulfide-containing foreign proteins from crude bacterial inclusion bodies.

Bacterial Proteins↗
PubMed1994

Fibroepithelial tumor of the breast with digital fibroma-like inclusions in the stromal component. Case report with immunocytochemical and ultrastructural analysis.

A case of fibroepithelial tumor of the breast in a 34-year-old woman, showing digital fibroma-like inclusions in the stromal component is presented. Morphological, immunocytochemical, and ultrastructural findings indicate that the peculiar eosinophilic intracytoplasmic inclusions observed may represent tightly packed actin filaments. Although they are more frequently detected within digital fibrous proliferations of infancy, their rare occurrence at either unusual site or in adulthood has been reported. Similar inclusions have also been rarely observed in intranodal myofibroblastoma and in benign leiomyomas. These findings suggest that these inclusions may be the result of some metabolic or organisational abnormality shared by neoplastic actin-rich cells. Myofibroblastic and smooth muscle lesions are probably the commonest to show this defect.

Actins↗
PubMed1998

Hereditary inclusion body myopathies.

Hereditary inclusion body myopathies comprise autosomal recessive and autosomal dominant muscle disorders that have a variable clinical phenotype but share similar morphological features. These include rimmed vacuoles within muscle fibres and collections of intrasarcoplasmic and intranuclear tubulofilamentous inclusions, 16-18 nm in external diameter. The resemblances and the differences between the sporadic and the hereditary inclusion body myopathies are discussed. Recent advances in the identification of various proteins involved in these diseases are mentioned because they have provided better insight into their underlying pathophysiological mechanisms. Linkage studies have allowed the localization of the genetic defect of some hereditary inclusion body myopathies and related disorders, contributing to their individualization.

Genes, Dominant↗
PubMed2002

Inclusion-body myositis and myopathies: different etiologies, possibly similar pathogenic mechanisms.

PURPOSE OF REVIEW: Sporadic inclusion-body myositis (s-IBM) and hereditary inclusion body myopathies are progressive muscle diseases that lead to severe disability. We discuss recent advances in illuminating their pathogenic mechanism(s). RECENT FINDINGS: We emphasize how different etiologies might lead to the strikingly similar pathology and possibly similar pathogenic cascade. Our basic hypothesis is that over-expression of amyloid-beta precursor protein within aging muscle fibers is an early upstream event causing the subsequent pathogenic cascade. On the basis of our research, several processes seem to be important in relation to the still speculative pathogenesis: (a) increased transcription and accumulation of amyloid-beta precursor protein, and accumulation of its proteolytic fragment Abeta; (b) accumulations of phosphorylated tau and other Alzheimer-related proteins; (c) accumulation of cholesterol and low-density lipoprotein receptors, the cholesterol accumulation possibly due to its abnormal trafficking; (d) oxidative stress; and (e) a milieu of muscle cellular aging in which these changes occur. We discuss unfolded and/or misfolded proteins as a possible mechanism in formation of the inclusion bodies and their consequences. The remarkable pathologic similarities between s-IBM muscle and Alzheimer disease brain are discussed. SUMMARY: Unfolding knowledge of the various pathogenetic aspects of the s-IBMs and hereditary inclusion body myopathies may lead to new therapeutic avenues.

Aging↗
PubMed1979

Morphogenesis of nuclear inclusions and virus capsids in HEL cells infected with temperature-sensitive mutants of human cytomegalovirus.

The morphogenesis of nuclear inclusions and virus capsids in human embryonic lung cells infected with ts mutants of human cytomegalovirus at permissive (34 degrees C) and non-permissive (39 degrees C) temperatures was studied by indirect immunofluorescence (IF) and electron microscopic analyses and compared with the morphogenesis of these structures in wild-type virus infection with or without phosphonoacetate. Mutants tested belonged to five different complementation groups: two groups were DNA- (those unable to synthesize virus DNA at 39 degrees C) and the others were dna+. Based on the previous finding that the electron-dense, reticular nuclear inclusions (EM-NI) observed by the thin-section analysis correspond with nuclear inclusions (IF-NI) detected by the indirect IF staining (i.e. they occupy the same space in the nucleus), the following conclusions were obtained in ts mutant infection at 39 degrees C: (i) the formation of EM-NI, IF-NI and virus capsids requires replication of virus DNA. (II) The formation of EM-NI is not necessarily accompanied by the formation of IF-NI; EM-NI itself is not IF-positive unless it acquires virus-specific late antigens. (iii) The assembly of virus capsids occurs only in those cells in which EM-NI is formed; however, it can occur without the formation of IF-NI. (iv) Virus capsids assembled are not the major antigens responsible for the fluorescence of nuclear inclusions.

Capsid↗
PubMed1993

Association of the non-structural P3 viral protein with cylindrical inclusions in potyvirus-infected cells.

Antibodies raised against the 42K non-structural P3 protein encoded by the RNA genome of a potyvirus (tobacco vein mottling virus, TVMV) have been used with immunogold labelling procedures to determine the subcellular location of P3 in infected Nicotiana tabacum cells. P3-specific gold label was found almost exclusively associated with the cylindrical inclusions typically formed in the cytoplasm of potyvirus-infected cells by another non-structural viral protein, the cylindrical inclusion protein. The P3 antibodies reacted with inclusions in both the transverse (pinwheel-like) and longitudinal (bundle-like) orientations of these structures. Immunocytological examination of TVMV-infected protoplasts showed the association of P3 with cylindrical inclusions during the early stages of formation of these structures and suggests that the P3 may be involved in the replication of potyviral RNA.

Genome, Viral↗
PubMed1982

Unusual intracytoplasmic immunoglobulin inclusions in chronic lymphocytic leukaemia.

Unusual intracytoplasmic immunoglobulin inclusions were found by immunofluorescence in three patients with chronic lymphocytic leukaemia. The inclusions contained the same immunoglobulin chains as those detected on the plasma membrane, except for delta chains which were expressed on the cell surface and not in the cytoplasmic inclusions. The cytoplasmic staining persisted throughout culture for 8 or more days. An initial study of patients 1's cells showed that the inclusions contained only mu chains, and kappa chains gradually became apparent after in vitro culture. In a second study, the fresh lymphocytes contained both mu and and kappa chains. Initially, biosynthetic experiments showed production of mu chains which polymerized in the cytoplasm and were not secreted. Subsequently there was synthesis of heavy and light chains which assembled into monomeric subunits that were retained and secretion of free light chains. The apparent molecular weight of these immunoglobulin chains was larger than that of their secretory counterparts. Immunoelectronmicroscopy revealed cytoplasmic mu chains in strands of endoplasmic reticulum. In the two other patients, immunofluorescence displayed unusual staining patterns of bright networks in perinuclear areas.

Cytoplasm↗
PubMed1990

Fibrillary cytoplasmic inclusions in neoplastic Paneth cells.

Paneth cell differentiation was investigated in two colorectal carcinomas. Ultrastructural study showed a range of granules and, in one case, fibrillary cytoplasmic inclusions. Similar inclusions in normal Paneth cells have been associated with zinc deficiency. However, there was no clinical evidence of abnormal zinc metabolism in this patient, nor were inclusions seen in adjacent non-neoplastic Paneth cells. It is speculated that these fibrillary inclusions might reflect an intrinsic zinc-related metabolic defect in the tumour cells.

Adult↗
PubMed1995

Intracytoplasmic lumina and mucinous inclusions in ovarian carcinomas.

Intracytoplasmic mucinous inclusions and lumina have been previously described in non-glandular neoplasms such as urothelial carcinoma. We describe their presence in 93% of non-mucinous ovarian carcinomas. They were found in abundance in all 25 cases (100%) of clear cell carcinoma, in 48 of 50 cases (96%) of serous carcinoma and 20 of 25 cases (80%) of endometrioid carcinoma. The degree of the differentiation of the tumour did not influence the number of inclusions or lumina observed. These results suggest that the presence of intracytoplasmic lumina and mucinous inclusions is more widespread than hitherto appreciated. Their presence in an otherwise poorly differentiated metastatic carcinoma might, at the very last, prompt one to consider the ovary as a possible primary site. In addition, an abundance of intracytoplasmic mucinous inclusion and lumina with microcyst formation, in an otherwise poorly differentiated malignant primary ovarian epithelial tumour, might suggest the possibility of a clear cell carcinoma.

Adenocarcinoma, Clear Cell↗
PubMedDate not supplied

Nuclear inclusions in Alzheimer's disease.

Biopsy samples of parietal cortex from seven patients undergoing atrio-ventricular shunt operations have been examined electron microscopically. Five were suffering from Alzheimer's disease, while two were subjects with normotensive hydrocephalus following previous head injuries. Intranuclear neuronal, inclusions of three types were found. Most frequent was the intranuclear rodlet, which was commonly observed in four of the patients with Alzheimer's disease, but in one block only from one of the hydrocephalus cases. The other two types, namely the spherical inclusion body and the vermicellar-like inclusion, were found less commonly and in only two cases. No inclusions were seen in glial nuclei.

Aged↗
PubMedDate not supplied

Intracytoplasmic rod-like inclusions in caudate nucleus.

A number of intraneuronal inclusion bodies have been described as incidental findings, but the intracytoplasmic rod-like inclusions in the caudate nucleus are not widely known. They are called 'alcoholic hyaline-like bodies', because they were first reported in two patients with chronic alcoholism and the inclusions were likened to Mallory bodies of alcoholic liver. However, we have found that their prevalence was not significantly different in alcoholics with or without liver damage, in individuals with miscellaneous neurological disorders and in a control group of patients without neurological or hepatic disease. It was therefore concluded that these inclusions represent a non-specific finding.

Adolescent↗
PubMed1993

In borna disease virus infected rabbit neurons 100 nm particle structures accumulate at areas of Joest-Degen inclusion bodies.

Borna disease virus infected rabbits were chosen to search for electronmicroscopic structures. Intensively investigated hippocampal neurons showed intranuclear inclusions; 100 nm particle-like structures surrounded by 20 nm granular forms were prominent. In connection with elsewhere reported in situ hybridization studies of virus-specific RNA to areas of the Joest-Degen inclusions we suggest that these particle structures may represent Borna virus. Jost-Degen (8) found intranuclear inclusion bodies in neurons to be pathognomonic for Borna disease (BD) in the horse. Half a century later these structures were suggested to represent BD virus (BDV)-specific antigen aggregates (15). A century later we characterized the virus to contain a single and negative stranded RNA of 8.5 kb, which transcribes in the nucleus (5) and could show that virus complementary RNA seems to hybridize spot-like to nuclear areas, probably representing the Jost-Degen inclusions (7). Electron microscopic (EM) findings on structures in BDV infected brain cells and about particle-like structures obtained from infected tissue culture cells have been reported by different groups (1, 2, 3, 4, 5, 6, 9, 11, 12, 13). The demonstration of crystalline aggregates and filament bundles in the cytoplasma and karyospheridia (nuclear bodies) were prominent. Such structures were seen in infected rabbits, hamsters, rats mice and naturally infected horses. The phenotypic description of filamentous structures, crystalline aggregates in the cytoplasma and large karyospheridia were prominent. Based on our experience with BDV infections in rabbits we selected this species for ultrastructural studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗