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 901 records · Page 50Linked to original sources
PubMed2006

An autopsy case of frontotemporal dementia with severe dysarthria and motor neuron disease showing numerous basophilic inclusions.

We report a clinicopathological study of a patient suffering from frontotemporal dementia (FLD) with severe dysarthria and concomitant motor neuron disease (MND). The patient was a 52-year-old woman with almost simultaneous emergence of severe dysarthria and FTD. The severe dysarthria subsequently evolved into anterior opercular syndrome. Motor neuron signs then emerged, and the patient developed akinetic mutism approximately 2 years after the onset of the disease. The patient died of pneumonia after a 7-year clinical illness. Pathologically, severe and widespread degeneration in the frontal and temporal lobes, including the anterior opercular area, limbic system, basal ganglia, spinal cord and cerebellum, and frequent ubiquitin- and tau-negative basophilic inclusions were observed. The pyramidal tracts and anterior horns of the cervical cord also showed marked degeneration. Cases showing basophilic inclusions reported so far have been divided into two groups: early onset FTD and MND with basophilic inclusions. Our case presented clinicopathological features of both FTD and MND, which suggests that cases showing basophilic inclusions may constitute a clinicopathological entity of FTD/MND.

Autopsy↗
PubMed2004

Increased expression of p62 in expanded polyglutamine-expressing cells and its association with polyglutamine inclusions.

Huntington's disease is a progressive neurodegenerative disorder that is associated with a CAG repeat expansion in the gene encoding huntingtin. We found that a 60-kDa protein was increased in Neuro2a cells expressing the N-terminal portion of huntingtin with expanded polyglutamine. We purified this protein, and, using mass spectrometry, identified it as p62, an ubiquitin-associated domain-containing protein. A specific p62 antibody stained the ubiquitylated polyQ inclusions in expanded polyglutamine-expressing cells, as well as in the brain of the huntingtin exon 1 transgenic mice. Furthermore, the level of p62 protein and mRNA was increased in expanded polyglutamine-expressing cells. We also found that p62 formed aggresome-like inclusions when p62 was increased in normal Neuro2a cells by a proteasome inhibitor. Knock-down of p62 does not affect the formation of aggresomes or polyglutamine inclusions, suggesting that p62 is recruited to the aggresome or inclusions secondary to their formation. These results suggest that p62 may play important roles as a responsive protein to a polyglutamine-induced stress rather than as a cross-linker between ubiquitylated proteins.

Animals↗
PubMedDate not supplied

Dendritic inclusions in the cerebellar granular layer after long term alcohol consumption in adult rats.

Whorled multiplanal inclusions up to 1.5 micron in diameter were observed in dendrites of the cerebellar Golgi cells after 6 months of alcohol treatment, increasing in number with time. Inclusions are formed by apposed cytomembranes stacked parallel or in a twisted arrangement. The paired membranes merged into a dense, finely textured material. A close relationship with dendritic smooth endoplasmic reticulum is apparent. A correlation between chronic alcohol intake and the development of these inclusions is shown although, in common with many other types of neuronal cytoplasmic inclusions, their genesis and function remains to be determined.

Alcoholism↗
PubMed1988

Inclusion body myositis in post-poliomyelitis muscular atrophy.

A 38-year-old male developed a new muscle weakness in his left thigh 35 years after having acute paralytic poliomyelitis with residual right distal leg weakness and atrophy. EMG studies showed widespread denervation in proximal and distal muscles regardless the clinical involvement. Muscle biopsy from an affected muscle showed the findings of inclusion-body myositis consisting of perivascular and interstitial mononuclear infiltration, sarcoplasmic granular inclusions with membranous whorls and typical filamentous inclusions in several myonuclei. This raises the possibility of inclusion body myositis in other cases of progressive post-poliomyelitis muscular atrophy, especially those with perivascular infiltration of mononuclear cells in the muscle biopsy.

Adult↗
PubMed1990

Mitochondrial inclusions in keratinocytes of hairless mouse skin exposed to UVB radiation.

Mitochondrial inclusions were observed in keratinocytes during an ultrastructural investigation of the skin of hairless mice exposed to UVB radiation. Mice were irradiated 3 times a week for 5-6 months with sunlamps at individual doses seldom exceeding 0.06 J/cm2. Strips of dorsal skin were processed for electron microscopic examination; blocks were sectioned to include both epidermis and dermis. Mitochondrial inclusions were observed in keratinocytes of the basal, spinous and granular layers. They were spherical in shape and of moderate and homogeneous electron density. Mitochondria toward the upper regions of the epidermis were swollen and had fragmented cristae; mitochondria in the lower areas of the epidermis usually contained smaller and less dense inclusions and intact or partially disrupted cristae. Because mitochondria are essential in providing the energy for cellular function, keratinocyte mitochondrial damage induced by UVB radiation may have serious pathological consequences. Possible mechanisms involved in mitochondrial inclusion formation are suggested.

Animals↗
PubMed1982

Cytoplasmic blood plasma inclusions in human hepatocytes.

Hepatocellular blood plasma inclusions were demonstrated in conventional formalin-fixed paraffin-embedded liver tissue by the immunoperoxidase technique in 114 out of 197 liver specimens. They were usually round or elliptical in shape, their size varying from a few microns to about 30 microns in diameter. Albumin, fibrinogen, alpha 1-antitrypsin, IgG, IgM, IgA, ceruloplasmin and transferrin were demonstrated in the inclusions, in that order of frequency. A majority were negative with the periodic acid Schiff stain after amylase digestion, but a few were positive. Many of them seemed to correspond to vacuoles in the hepatocytes but some were not seen in HE-stained sections. The inclusions were frequently seen in autopsy liver specimens, but were rare in surgical ones. Most of the inclusions might develop at an agonal stage, probably as a result of hypoxia or circulatory disturbances in the livers.

Adult↗
PubMed1972

Lead poisoning: rapid formation of intranuclear inclusions.

A single dose of lead (0.05 milligram per gram of body weight) induced characteristic intranuclear inclusions in the epithelium of proximal tubules in rat kidney within 1 to 6 days. The development of the intranuclear inclusions is thus an acute manifestation of lead poisoning, not a delayed one, as has been thought hitherto. Cytoplasmic structures resembling the intranuclear inclusions and situated in the vicinity of endoplasmic reticulum were regularly found in cells bearing the pathognomonic intranuclear inclusions. The latter and the cytoplasmic structures may be derived from a common precursor, perhaps a soluble protein-lead complex.

Animals↗
PubMed1972

Quantitative assay of paravaccinia virus based on enumeration of inclusion-containing cells.

Bovine paravaccinia virus produces cytoplasmic inclusion bodies on infection of bovine embryonic kidney cells; these were easily recognized when stained with acridine orange or May-Grünwald-Giemsa stain. The inclusions could be shown to contain newly synthesized deoxyribonucleic acid by autoradiography. Counts of inclusion-containing cells decreased when virus suspensions were treated with immune serum before being used to inoculate cell cultures. At 24 hr after infection, the number of cells containing inclusions was directly proportional to the concentration of infectious virus inoculated. These observations provide the basis for a virus assay which is simpler, faster, and more sensitive than the plaque assay.

Acridines↗
PubMed2006

The hypothetical protein CT813 is localized in the Chlamydia trachomatis inclusion membrane and is immunogenic in women urogenitally infected with C. trachomatis.

Using antibodies raised with chlamydial fusion proteins, we have localized a protein encoded by hypothetical open reading frame CT813 in the inclusion membrane of Chlamydia trachomatis. The detection of the C. trachomatis inclusion membrane by an anti-CT813 antibody was blocked by the CT813 protein but not unrelated fusion proteins. The CT813 protein was detected as early as 12 h after chlamydial infection and was present in the inclusion membrane during the entire growth cycle. All tested serovars from C. trachomatis but not other chlamydial species expressed the CT813 protein. Exogenously expressed CT813 protein in HeLa cells displayed a cytoskeleton-like structure similar to but not overlapping with host cell intermediate filaments, suggesting that the CT813 protein is able to either polymerize or associate with host cell cytoskeletal structures. Finally, women with C. trachomatis urogenital infection developed high titers of antibodies to the CT813 protein, demonstrating that the CT813 protein is not only expressed but also immunogenic during chlamydial infection in humans. In all, the CT813 protein is an inclusion membrane protein unique to C. trachomatis species and has the potential to interact with host cells and induce host immune responses during natural infection. Thus, the CT813 protein may represent an important candidate for understanding C. trachomatis pathogenesis and developing intervention and prevention strategies for controlling C. trachomatis infection.

Antibodies, Bacterial↗
PubMed1995

Cytochemical localization of glycogen in Chlamydia trachomatis inclusions.

The origin and distribution of glycogen in inclusions of Chlamydia trachomatis were demonstrated with silver proteinate stain for electron microscopy. Glycogen particles were detected in all developmental stages of C. trachomatis, as well as free in the inclusions. Intrachlamydial glycogen was most common in elementary bodies but was also detected in intermediate forms and reticulate bodies (RBs). Abnormal divisions and breakdown of cytoplasmic membranes were common in RBs. Cytoplasmic contents, including glycogen particles, were released into the inclusions after rupture of the outer membranes of abnormal RBs and intermediate forms. From these observations, we conclude that glycogen in inclusions of C. trachomatis originates in the organisms themselves.

Amylases↗
PubMed1999

Polyhydroxyalkanoate inclusion body-associated proteins and coding region in Bacillus megaterium.

Polyhydroxyalkanoic acids (PHA) are carbon and energy storage polymers that accumulate in inclusion bodies in many bacteria and archaea in response to environmental conditions. This work presents the results of a study of PHA inclusion body-associated proteins and an analysis of their coding region in Bacillus megaterium 11561. A 7, 917-bp fragment of DNA was cloned and shown to carry a 4,104-bp cluster of 5 pha genes, phaP, -Q, -R, -B, and -C. The phaP and -Q genes were shown to be transcribed in one orientation, each from a separate promoter, while immediately upstream, phaR, -B, and -C were divergently transcribed as a tricistronic operon. Transfer of this gene cluster to Escherichia coli and to a PhaC- mutant of Pseudomonas putida gave a Pha+ phenotype in both strains. Translational fusions to the green fluorescent protein localized PhaP and PhaC to the PHA inclusion bodies in living cells. The data presented are consistent with the hypothesis that the extremely hydrophilic protein PhaP is a storage protein and suggests that PHA inclusion bodies are not only a source of carbon, energy, and reducing equivalents but are also a source of amino acids.

Acyltransferases↗
PubMed2004

Reovirus nonstructural protein mu NS recruits viral core surface proteins and entering core particles to factory-like inclusions.

Mammalian reoviruses are thought to assemble and replicate within cytoplasmic, nonmembranous structures called viral factories. The viral nonstructural protein mu NS forms factory-like globular inclusions when expressed in the absence of other viral proteins and binds to the surfaces of the viral core particles in vitro. Given these previous observations, we hypothesized that one or more of the core surface proteins may be recruited to viral factories through specific associations with mu NS. We found that all three of these proteins--lambda 1, lambda 2, and sigma 2--localized to factories in infected cells but were diffusely distributed through the cytoplasm and nucleus when each was separately expressed in the absence of other viral proteins. When separately coexpressed with mu NS, on the other hand, each core surface protein colocalized with mu NS in globular inclusions, supporting the initial hypothesis. We also found that lambda 1, lambda 2, and sigma 2 each localized to filamentous inclusions formed upon the coexpression of mu NS and mu 2, a structurally minor core protein that associates with microtubules. The first 40 residues of mu NS, which are required for association with mu 2 and the RNA-binding nonstructural protein sigma NS, were not required for association with any of the three core surface proteins. When coexpressed with mu 2 in the absence of mu NS, each of the core surface proteins was diffusely distributed and displayed only sporadic, weak associations with mu 2 on filaments. Many of the core particles that entered the cytoplasm of cycloheximide-treated cells following entry and partial uncoating were recruited to inclusions of mu NS that had been preformed in those cells, providing evidence that mu NS can bind to the surfaces of cores in vivo. These findings expand a model for how viral and cellular components are recruited to the viral factories in infected cells and provide further evidence for the central but distinct roles of viral proteins mu NS and mu 2 in this process.

Animals↗
PubMed1993

Inclusion body myositis: an underdiagnosed condition?

Inclusion body myositis is an increasingly recognised form of inflammatory myopathy with characteristic clinical and histopathological features which has seldom been reported in the United Kingdom. This paper presents the clinicopathological features of a series of patients diagnosed in Nottingham from 1986 to 1990. During this period, 1319 muscle biopsy samples were processed by this laboratory and rimmed vacuoles were seen in 17 patients. Eleven patients had definite or probable inclusion body myositis according to published criteria. The mean age of the group was 69.4 years with a male to female ratio of 8:3. Typical clinical features were a slowly progressive painless, proximal lower limb weakness, with muscle wasting and early loss of reflexes. The median duration of illness from first symptom to presentation was five years (range 2-18 years). Falls were a prominent symptom in six patients and distal weakness occurred in nine patients. Creatine kinase was increased in 10 patients but only one had a level > 1000 IU/l; the erythrocyte sedimentation rate was normal in five patients. Treatment with steroids or cytotoxic drugs, or both, did not prevent disease progression. It is confirmed that inclusion body myositis is a distinct cause of inflammatory myopathy which is probably underdiagnosed in the United Kingdom. Clinically, it should be suspected in older patients presenting with muscle weakness of insidious onset. Pathologically, a careful search should be made for rimmed vacuoles and inflammation; ultrastructurally, the presence of inclusions will confirm the diagnosis.

Aged↗
PubMed1977

Ultrastructure of abnormal membrane inclusions in nuclei of human myocardial cells.

The ultrastructure of the nuclear envelope was studied in cardiac muscle cells of 12 patients undergoing cardiopulmonary bypass surgery. Two main types of membrane inclusions, globular and tubular, were observed in the nuclei. The globular type was found in 6 patients. The globular inclusions were about 0-5mu to 1-5mu in diameter and lined by two unit membranes equal in structure to that of the nuclear envelope. The lining was probably always in continuity with the nuclear membranes. Such inclusions contained a granular matrix in which no cytoplasmic organelles could be seen, with the exception of a limited number of ribosomes. The tubular type of nuclear inclusion was observed in the cardiac tissue of 3 patients. These tubules ran in straight or slightly bent segments of about 0-2 mu to 1-6 mu length, interrupted by bendings at obtuse or right angles. The diameter of their lumina measured about 300 A to 800 A. Such tubules were nearly always found in areas of the nucleoplasm rich in heterochromatin. Nuclear pore-like structures were occasionally found in the tubular wall. The tubular wall consisted of a single unit membrane shown to be in continuity with the inner membrane of the nuclear envelope. Since these nuclear aberrances have been observed at all of the stages examined, the possibility is considered that they may represent a specific nuclear response to the process of cardiac hypertrophy.

Cardiomegaly↗
PubMed1980

Adult pulmonary cytomegalic inclusion disease: report of a case.

A case is presented of pulmonary cytomegalic inclusion disease in adult. The condition was only diagnosed post mortem. A detailed description of the inclusions and inclusion-bearing cells is given. Histochemical observations which reveal an outer and inner zone to the intranuclear inclusion body are confirmed. Electron microscopy shows the viral basis of the infection. The morphology of the virus particles is compatible with a herpesvirus infection.

Cytomegalovirus↗
PubMed1984

Intracellular inclusion bodies in 14 patients with B cell lymphoproliferative disorders.

Two types of intracytoplasmic inclusion were detected by immunofluorescence microscopy in 12 patients with chronic lymphocytic leukaemia and two patients with a leukaemic phase of well differentiated lymphocytic lymphoma. Further analysis with light- and electron microscopy, showed that most inclusion bodies were rod-like crystalline structures. However, in three patients they consisted of amorphous vesicular precipitates. Immunological studies revealed the presence of immunoglobulins of the same class and type at the cell surface as well as in the inclusion bodies. The monoclonal immunoglobulins were all of lambda type except in two cases. The origin of immunoglobulin inclusion bodies in B cell malignancies is discussed in relation to published data and our own observation in one patient followed during treatment.

Aged↗
PubMed2004

Spinocerebellar ataxia type 2 with glial cell cytoplasmic inclusions.

Glial cell cytoplasmic inclusions were identified in a case of spinocerebellar ataxia type 2. These have not been reported before. The inclusions were found in low frequency in the dentate nucleus, cerebellar white matter, pontine transverse fibres, and the inferior olivary nucleus. They were of variable size and shape and expressed ubiquitin, thus resembling glial cytoplasmic inclusions in multiple system atrophy. However, their immunohistochemical profile was different as they did not show immunoreactivity for either tau protein or alpha-synuclein. There was no evidence of expanded polyglutamine tracts in these inclusions, which also failed to label with silver stains. As in many other neurodegenerative diseases, in spinocerebellar ataxia type 2 there may be pathogenic contributions of glial cells other than the common astrogliotic response to neuronal damage.

Adolescent↗
PubMed1997

The role of quantitative electromyography in inclusion body myositis.

OBJECTIVE AND METHODS: Inclusion body myositis is said to have both myopathic and neurogenic features on electrophysiological tests. Twenty one studies from 20 patients with biopsy defined inclusion body myosis, 13 of whom had quantitative electromyography (qEMG), were reviewed to determine if this technique added diagnostic specificity (one patient had both needle EMG and a later study with qEMG before muscle biopsy). RESULTS: Excessive numbers of polyphasic motor unit potentials (MUPs) (> 12% per muscle) were seen in 11 of the 13 patients. In 10 of 13 patients, mean MUP duration was abnormally reduced (26% to 48%). In three patients, mean MUP duration was abnormally reduced only after polyphasic MUPs were excluded. In all 13 patients, the simple MUP duration was reduced. Myopathy was unequivocally diagnosed in all 13 studies that included qEMG; of the remaining eight patients, the conclusions of the electrophysiological studies without qEMG was myopathy (one), neurogenic (four) or non-diagnostic (three). CONCLUSIONS: There is no evidence of a neurogenic component in inclusion body myosis if qEMG is used. Quantitative EMG is often necessary to make an electrophysiological diagnosis of a myogenic disorder in patients with inclusion body myosis.

Adult↗