Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cytoplasmic Structures”

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 829 records · Page 46Linked to original sources
PubMed1983

[Quantitative and qualitative analysis of the effects of various doses of beta-irradiation (50-5000 rads) on epidermal cells of embryos and larvae of Pleurodeles waltlii Mich. (Amphibia, Urodela)].

Embryos of Pleurodeles waltlii at the hatching stage were irradiated with doses of 50 to 5 000 rad. From 70 to 500 rad chromosomal aberrations appear; they are studied respectively 24,48 hours and 3 weeks after the treatment. Breakages are observed, that may be followed by rearrangements, i.e. acentric, telocentric and dicentric fragments, chromatid translocations and chromosome translocations. With time, the cells showing the most severe abnormalities are eliminated by the developing larvae. From 1 000 rad cytoplasmic structures (membrane systems and mitochondria) are alterated .

Animals↗
PubMed1980

Lymphadenopathy associated with dysgammaglobulinemia.

Conditions in which lymphadenopathy is associated with dysgammaglobulinemia may be divided into two groups: those in which etiologic factors and pathogenesis are well established, and those which are still a medical dilemma. Only a few belong to the former group: infections, immunizations, and drug-induced conditions being the best examples. Unfortunately, the great majority belong to the latter group. Interestingly enough, many conditions with lymphadenopathy and dysgammaglobulinemia share similar histologic features, such as infiltration with lymphocytes, immunoblasts, plasma cells, and histiocytes. This pleomorphic infiltration may appear together with prominent vascular proliferation. In animal experiments, angiogenesis was induced by administration of immunocompetent lymphocytes into the skin of unimmunized, irradiated mice. Therefore such lymphocyte-induced angiogenesis may be a manifestation of the graft-versus-host reaction. Recent developments in immunology, such as the discovery of many membranous markers and receptors on the lymphocyte membrane, the study of cytoplasmic structure and synthetic products, detection of enzymatic aberrations and chromosomal abnormalities, and refinement in histochemical techniques, have led to attempt to reclassify lymphoplasmacytic and leukemic disorders. Indeed, several classifications coming from different coutries and from various centers in the same country have been proposed, leading to a typical "Tower of Babel" phenomenon. It is obvious that more knowledge of etiologic factors and pathogenetic mechanisms is necessary to classify, cure, and eventually prevent the diseases described in this paper.

Adolescent↗
PubMed1981

Some functional aspects of the ultrastructure of rat pinealocytes.

An analysis of more than 75000 electron micrographs from 84 intact control and 167 experimental male rats divided into 11 groups subjected to various treatments, was performed in the present study, a special attention being paid to the relation of cytoplasmic organelles to the processes of synthesis and secretion of pinealocytes. From these observations the following conclusions have been drawn: 1. specific pineal cells - the pinealocytes - show several attributes of metabolically active endocrine cells; 2. at least two probably intimately related secretory processes are present in the rat pinealocytes; 3. several cytoplasmic structures may be involved in the secretory mechanism of the rat pinealocytes.

Animals↗
PubMed1981

Lysis of growing yeast-form cells of Candida albicans by echinocandin: a cytological study.

Yeast form cells of Candida albicans 6406 were treated with echinocandin, a new antifungal agent, which, in the absence of osmotic protection, provoked the lysis of exponentially growing cells. Lysis did not occur in stationary-phase cells and when protein synthesis was blocked. In intact cells, the synthesis of glucan, but not other important wall components, was partially inhibited. A cytological study of the effects of echinocandin at lytic doses (3.0 microgram ml-1) on osmotically protected yeast cells revealed a substantial thinning of the bud cell wall and derangement of its constitutive layers within 5-10 min, showing that the balance of wall growth was quickly and critically affected by the drug. Associated with this effect, a number of membranous bodies of myelin-like appearance were often seen in close proximity to the plasmamembrane of the emerging bud. Later during treatment (15 min onwards) membranous, convoluted bodies were detected in the nuclear and other intracytoplasmic membranes. Subsequent lytic events, unevenly distributed in cell population, eventually brought about complete lysis of the cell cytoplasmic structure. These results suggest that echinocandin may block a biosynthetic step during wall construction, or that it could alter wall metabolism as a result of a primary interaction with membranes.

Anti-Bacterial Agents↗
PubMed1982

Cytochemical investigations of phagocytes in thyroid gland cysts.

Certain similarities in the cytoplasmic structure could indicate a histogenetic affinity between thyrocytes and pigmented macrophages in thyroid glands. On the other hand, the monocytogenic origin of macrophages in other organs in the body contradicts this assumption. We investigated these cells in smears of thyroid aspirates as well as in imprints, frozen sections and paraffin-embedded sections of freshly removed thyroid glands, using several cytochemical reactions and the usual panoptic stains. With the sodium-fluoride-inhibited alpha-naphthyl acetate esterase and tartrate-inhibited acid phosphatase reactions, the pigmented macrophages exhibited enzyme cytochemical patterns corresponding to those of blood monocytes or monocytogenic histiocytes but differing definitely from those of thyrocytes. Furthermore, we observed macrophages that exhibited a clearly monocytoid nuclear form and chromatin pattern in the interstitial space of the thyroid gland. These findings practically exclude a derivation of thyroidal pigmented macrophages from follicular epithelial cells and positively underline their derivation from blood monocytes.

Acid Phosphatase↗
PubMed1980

[Ultrastructural changes in plague microbes of vaccinal strain EB and alveolar macrophages of guinea pigs during their interaction in vitro].

Aerosol immunization with plague vaccine EB was found to stimulate an increase in the number of free alveolar macrophages and to enhance their ingesting activity which correlated with an increase in specific antibody titers. Immunological transformation was accompanied by ultrastructural changes in the cytoplasm and the nuclei of alveolar macrophages. The phagocytosis of microbes occurred by their adsorption onto the microphage surface, invagination and enclosing into the endocytic bubble having the function of the digestive vacuole. The growth of the number of macrophages and an increase in their ingesting activity, progressive changes in the cytoplasmic structures may be used as indicators of immunological transformation resulting from the administration of plague vaccine by the inhalation method.

Aerosols↗
PubMed1980

[Tactile (Merkel) cells of the sinuous hairs of cats following colchicine application to nerves].

The state of the tactile cells (Merkel's cells) in epithelium of the internal follicle in the cat sinuous hairs is controlled by sensitive neurons. This statement, derived from the experiments on denervation, was analysed in the investigation when colchicine (an agent blocking axoplasmic transport) was applied on the nerve. Thirty and 60 days after colchicine effect a statistically important decrease in the number of the tactile cells with certain changes in their structure (cytoplasmic consolidation, changes in density of specific granules, increasing number and size of vacuoles) was registered. In epithelium of the internal hairy follicle a contact of the tactile cells with tactile menisci was followed. As in myelin neural fibres of the internal hairy follicle connective tissue, certain signs of destruction, resulting from blockade of colchicine-induced axoplasmic transport, were noted. Participation of the axoplasmic transport in the neurosensory control for the state of the tactile cells is discussed together with the changes described.

Animals↗
PubMed1995

Ultrastructural localization of alkaline phosphatase activity in the proximal convoluted tubule cells of the gerbil Meriones crassus using a cerium-based method.

Histochemical activity of alkaline phosphatase in the proximal convoluted tubule of the gerbil Meriones crassus has been detected. The reaction product was strongly marked at both the apical surface and the basal part of the cells comprising the basal infoldings with their extended tips and the profiles of the membrane-bound bodies that were easily recognisable by their rounded shape. The reaction product was in the form of fine, uniform deposits in response to cerium chloride as a capture agent. Other cytoplasmic structures did not display these deposits. In addition, the study provided the application of levamisole which caused remarkable reduction of the enzyme activity. Using lead nitrate as a capture agent, the sections showed dense coarse, irregular clusters nearly at the same sites. Control experiments, processed in the absence of the substrate sodium beta-glycerophosphate did not demonstrate the presence of any deposits. The present study, which demonstrates for the first time the presence of alkaline phosphatase activity in the proximal convoluted tubule cells of such desert rodents, does not consider the relationship of the enzyme localization and the basal components of the cells including the nature of the membrane-bound bodies which are still under investigation.

Alkaline Phosphatase↗
PubMedDate not supplied

Development of lymphopoiesis as a function of the thymic microenvironment. Use of CD8+ cytotoxic T lymphocytes for cellular immunotherapy of human cancer.

The mammalian thymic histogenesis can be immunomorphological divided into three consecutive states: 1) Epithelial: 2) Lymphopoietic or lympho-epithelial and 3) Differentiated cellular microenvironment with formation of Hassall's bodies. The embryonic, epithelial pharynx serves as the origin of the mammalian thymus. The epithelial cell layer of endodermic origin expands into pharyngeal pouches and the thymic anlagen are formed from the dorsolateral portions of the third pharyngeal pouch. In absence of humoral and cell to cell interactions with the ectomesenchyme, the primary epithelial anlagen are unable to proliferate. Experimental or spontaneous neural crest ablation early in ontogenesis also results in non-physiologic thymic organogenesis. Earlier thymic studies detected a subcapsular A2B5+ and Thy-11+, TE4+, Vimentin+, Cytokeratin+ endocrine reticulo-epithelial cell or nurse cell subpopulation within the cortical reticulo-epithelial cell network. Secretion of multiple in situ active, autocrine growth factors and a humoral chemotactic factor by the cells of ectomesenchymal origin allows the commencement of immigration of hemopoietic stem cells. The thymic lymphopoiesis is initiated by the immigration of pluripotent (with cellular immunophenotype TdT+, Ki67+, CD3-, CD7+, CD34+, CD38+, CD44+, CD45+ or T200+), but already to T lymphocyte cell lineage committed hemopoietic stem cells during the 6-7th week of ontogenesis. CD2, a 50-55 kD glycoprotein is the first intrathymic, early differentiation antigen expressed during the 8-9th ontogenetic weeks. This antigen also serves as a cell surface component of the alternative or antigen independent pathway of thymocyte activation. The 10th week is defined as the first expression of CD4 and CD8 antigens which determine the basic, characteristic dichotomy of the T lymphocytes. The induction of the initial proliferative wave of immature cortical thymocytes is carried out by the LFA-3 (CD58) adherence molecules, the receptors of CD2 antigens located on reticulo-epithelial cells. As a result of the extremely high proliferation rate the thymic mass markedly expands in all dimensions and numerous microlobules are formed. Between the 13th to 16th week the typical thymic cell environment is formed and the first Hassall's bodies are developed. The outer layer of the bodies contain hypertrophized TE8+, TE16+ and TE19+ reticulo-epithelial cells, with an active secreting cytoplasmic structure. Cytotoxic cells express special receptors by which they are capable to distinguish altered or foreign cells from autologous cells of the host. Solid human tumors are characterized with a marked poly- and mononuclear cell infiltrate containing phagocytes, various subtypes and clones of lymphocytes and granulocytes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1975

Intranuclear inclusions in Bence Jones lambda plasma cell myeloma.

A patient with plasma cell myeloma producing only Bence Jones lambda protein was found to have pale intranuclear inclusions in the majority of the bone marrow plasma cells. These inclusions, previously undescribed in myeloma patients producing only Bence Jones protein, contained Bence Jones lambda protein, were non-electron dense, bound by a single membrane, and contained no cytoplasmic structures. Intracytoplasmic inclusions were not present, and the perinuclear cistern was not dilated. Thus, the inclusions may represent intranuclear protein synthesis with anomalous release in the abnormal cells.

Bence Jones Protein↗
PubMed1993

Lethal midline granuloma: a case of Ki-1 lymphoma.

Lethal midline granuloma syndrome (LMG) is the clinical term generally used to describe a rare clinical entity of unknown cause characterized by a progressive and often fatal ulceration and destruction of the upper airway involving the nose, the paranasal sinuses and the soft tissues of the face. The following histopathologic entities have always been grouped under the term LMG: Wegener granulomatosis (WG), non-Hodgkin lymphoma, polymorphic reticulosis (PR) and idiopathic midline destructive disease (IMDD). Today in order to begin an adequate therapy a differential diagnosis is necessary. The progresses in clinical immunology and immunohistochemistry and cytophotometric findings are useful to define the LMG syndrome better. First of all the LMG must be discriminated from localized WG occurring in the midface. Serologic examinations of patients with WG in its active form show a high percentage of autoantibodies against cytoplasmic structures in leucocytes and monocytes. Moreover a review of the literature allows us to suppose that cases described as IMDD and PR are indeed a large evolutionary spectrum from almost benign to fatal malignant lymphoma. We report a case of Ki 1-lymphoma presenting as LMG syndrome.

Adult↗
PubMed1993

Immunological evidence for the localization of a 110 kDa poly(A) binding protein from rat liver in nuclear envelopes and its phosphorylation by protein kinase C.

We have purified a 110 kDa poly(A) binding protein (P110) from rat liver which is thought to be involved in mRNA translocation through the nuclear pores and have demonstrated its localisation in the nuclear envelope using polyclonal antibodies and confocal laser scanning microscopy. Although P110 was prepared from highly purified nuclear envelopes, the polyclonal antibodies raised against them bind to nucleo- and cytoplasmic structures to a minor extent, but not to nucleolar structures. P110 decays spontaneously into several fragments which are also recognized by the polyclonal antibodies. The 110 kDa polypeptide and its fragments were phosphorylated by a nuclear envelope kinase and this phosphorylation was inhibited by a monoclonal antibody against protein kinase C and by a specific protein kinase C inhibitor obtained from bovine brain. Scatchard analysis was used to determine the influence of protein kinase C activators and inhibitors on nuclear envelope protein phosphorylation and RNA binding. The data indicate a close association between the RNA translocation machinery (the 110 kDa protein) and protein kinase C within the nuclear envelope. We suggest that the fragmentation of P110 is triggered before or during mRNA export and is not due to nonspecific proteolysis.

Animals↗
PubMed1993

Microvascular and cellular defects of the periosteum of osteogenesis imperfecta.

Periosteum stripped from fragments of diaphyseal long bones from osteogenesis imperfecta (OI) patients was examined both in vivo and in vitro. The OI periosteum was thickened and characteristic finding was a defective microvascular system. The vascular walls of arterioles and capillaries were thick and the lumina of many of these vessels were narrowed or occluded by hypertrophic endothelial cells and multiplication of smooth muscle cell layers. Circulatory deficiency in the OI periosteum might be regarded as one of the causes of the slender, osteopenic diaphyseal bone characteristic of the disorder. A higher proliferative activity was observed in cultured OI periosteal cells, but the cytoplasmic structure showed increased myelinoid bodies and smooth endoplasmic reticulum and decreased lysosomes and rough endoplasmic reticulum. These findings may be related to the abnormal metabolic activity of OI periosteal cells.

Adolescent↗
PubMed1996

The molecular nature of the F-actin binding activity of aldolase revealed with site-directed mutants.

We used site-directed mutagenesis of rabbit muscle aldolase, falling ball viscometry, co-sedimentation binding assays, and negative stain electron microscopy, to identify specific residues involved in the aldolase-actin interaction. Three mutants, R42A (Arg --> Ala), K107A (Lys --> Ala), and R148A (Arg --> Ala), had minimal actin binding activity relative to wild type (wt) aldolase, and one mutant, K229A (Lys --> Ala), had intermediate actin binding activity. A mutant with approximately 4,000-fold reduced catalytic activity, D33S (Asp --> Ser), had normal actin binding activity. The aldolase substrates and product, fructose 1,6-bisphosphate, fructose 1-phosphate, and dihydroxyacetone phosphate, reversed the gelling of wt aldolase and F-actin, consistent with at least partial overlap of catalytic and actin-binding sites on aldolase. Molecular modeling reveals that the actin-binding residues we have identified are clustered in or around the catalytic pocket of the molecule. These data confirm that the aldolase-actin interaction is due to specific binding, and they suggest that electrostatic interactions between specific residues, rather than net charge, mediate this interaction. Low concentration of wt and D33S aldolase caused formation of high viscosity actin gel networks, while high concentrations of wt and D33S aldolase resulted in solation of the gel by bundling actin filaments, consistent with a potential role for this enzyme in the regulation of cytoplasmic structure.

Actins↗
PubMedDate not supplied

A novel PNET cell line with melanotic differentiation.

The primitive neuroectodermal tumor (PNET) cell line, ONS-99, was established from a human melanotic neuroectodermal tumor of infancy (MNTI). ONS-99 cells were polygonal adherent cells and transplantable to BALB/c-nu/nu mouse. ONS-99 cells were positive for NSE, HMB-45 (melanoma-associated antigen) and N-myc, but lacked the antigenic features of terminally differentiated neurons or glias. ONS-99 cells had many intermediate filaments in the cytoplasm and tight intercellular junctions with scant cytoplasmic structures by electron microscopy. To date, ONS-99 is the only example of an established PNET cell line with melanotic differentiation.

Animals↗
PubMed1996

[Peroxisomal diseases--a survey].

Peroxisomes are ubiquitous cytoplasmic structures in mammalian tissues. The metabolic functions of these organelles include synthesis of plasmalogens and other ether lipids, beta-oxidation, especially of very long-chain fatty acids (VLCFAs, > C22) and their derivatives, inactivation of hydrogen peroxide by peroxisomal catalase and involvement in several other metabolic pathways, e.g. gluconeogenesis, catabolism of purines and polyamines and detoxification of ethanol. Peroxisomal diseases which may arise from genetic faults in the biogenesis of the organelle or aberrant targeting of one or more proteins to the peroxisome, are divided into three groups based on the extent of loss of peroxisomal functions. Prototype of the first group is the cerebro-hepato-renal syndrome of Zellweger (ZS) which shows generalised loss of peroxisomal functions and absence of demonstrable mature peroxisomes in the liver. Other syndromes which are briefly discussed include neonatal adrenoleukodystrophy (NALD) and infantile Refsum syndrome (IRS) which may be regarded as milder variants of ZS, and diseases caused by loss of a limited number of peroxisomal functions (rhizomelic chondrodysplasia punctate). However, the group of peroxisomal diseases with the highest incidence are those syndromes where only a single peroxisomal function is impaired. The most common peroxisomal disease, X-linked adrenoleukodystrophy (XALD) belongs to this group. XALD develops as a result of an isolated defect of peroxisomal acyl-CoA synthetase with resultant accumulation of VLCFAs, especially C26:0. Primary hyperoxaluria type 1 is caused by deficient activity of peroxisomal alanine: glyoxylate aminotransferase due to aberrant targeting of this enzyme to mitochondria and not peroxisomes, a unique example of a genetic enzyme trafficking defect. The primary diagnosis of these syndromes is usually based on clinical findings and measurement of accumulated or depleted metabolites in the body e.g. VLCFAs, bile acid intermediates, phytanic acid, pipecolic acid and plasmalogens. Therapy includes dietary adjustments e.g. supplementation with oleic acid derivatives to normalise elevated VLCFAs in XALD. Treatment with hypolipidaemic drugs and certain peroxisomal substrates which induce proliferation of mature peroxisomes offers promise in the therapy of these debilitating and often fatal diseases.

Humans↗
PubMed1996

Automated monitoring of apoptosis in suspension cell cultures.

Cell death by apoptosis is often accompanied by extensive DNA cleavage at internucleosomal linker sites. Thus, the foremost techniques for estimating apoptosis are based on biochemical, electrophoretic, or flow cytometry analysis of nuclear DNA. However, apoptosis is also associated with a chain of morphologic changes in the nuclear and cytoplasmic structures that are easily recognizable using light microscopy. We suggest that changes in morphology of cells undergoing apoptosis might cause characteristic changes in their optical properties. It follows that continuous measuring of the OD of cells undergoing apoptosis would enable the study of the kinetics of cell death. We recently described an automated microculture kinetic (MiCK) assay that provides multiple OD measurements in nondisrupted cell cultures. In the present study the MiCK assay was employed to follow OD changes in HL-60 and OCI/AML-3 myelogenous leukemia cells and murine thymocytes exposed to ethanol, hydrogen peroxide, etoposide, cisplatin, doxorubicin, or hyperthermia; i.e., divers stimuli known to induce cell death via apoptosis or necrosis. The MiCK assay revealed prominent differences between the optical properties of the cells undergoing the two different modes of death. Plotting the OD data accumulated during the assay period against time betrayed characteristic patterns of either "apoptotic" or "necrotic" OD curves. The best fit slope of the indicative of apoptosis steep rising component of the apoptotic curve, correlated directly with the percentage of morphologically apoptotic cells in the culture. Criteria for graphical estimate of apoptosis were suggested and used to study apoptosis induced in HL-60 cells by the chemotherapy compounds etoposide and cisplatin. The MiCK assay demonstrated markedly varying time courses of the cell apoptotic response to these two drugs. In both cases, however, the time of graphically predicted peaks of apoptosis correlated with the time of morphologically and electrophoretically recognized peaks of apoptosis. Adaptability of the MiCK assay to a 96-well microplate format opens the way for large-scale studying of cell apoptotic response to various stimuli. An important technical advantage of the automated MiCK assay of apoptosis is that it does not require additional laboratory procedures after microcultures are initiated.

Animals↗
PubMed1996

Coupling of the IL2 receptor complex with non-receptor protein tyrosine kinases.

IL2 induces the proliferation of T lymphocytes through the IL2 receptor (IL2R) following T lymphocyte activation. The IL2R consists of at least three subunits, IL2R alpha, beta and gamma chains. The cytoplasmic regions of the IL2R beta and gamma chains are critical for transduction of the IL2 signal to the cell interior. Although IL2R beta and gamma chains lack an intrinsic protein tyrosine kinase (PTK) domain, these chains recruit various non-receptor type PTKs, such as p56lck (and other Src family PTKs), Jak PTKs and Syk PTKs. The recruited PTKs are then activated following ligand stimulation to invoke intracellular signalling for the cell proliferation. Furthermore, it has been demonstrated that the IL2R is linked to at least three distinct signalling pathways leading to the induction of the c-fos/c-jun genes, c-myc gene induction and bcl-2 gene induction. All these pathways are essential for IL2 mediated proliferative signalling and co-operate with each other to ensure a full scale signal transduction. These signalling pathways, except that for bcl-2 pathway, appear to be mediated by multiple PTKs: p56lck is critical for the induction of the c-fos/c-jun genes, the activation of Syk PTKs results in the induction of the c-myc gene and Jak3 PTK is required for the induction of both c-fos and c-myc genes. Finally, the IL2 system may serve as a prototype in understanding the pleiotropic function of cytokine receptors that lack intrinsic PTK domains; the cytoplasmic structures of these cytokine receptors have evolved to allow the combined action of different PTK family members (and other signalling molecules) expressed in different cell types, which may determine the activity of cytokines.

Humans↗