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PubMed1991

The dynamics of gene amplification described as a multitype compartmental model and as a branching process.

The present work is aimed at developing the mathematical tools by which the dynamics of gene amplification (GA) can be described in detail. Some discrete compartmental models of GA by disproportionate replication and a general model for other putative GA mechanisms are presented and analyzed. The dynamical distribution of gene copy number in the cell population is calculated with the loss of cells taken either as constant or as copy-number-dependent. Our analysis shows that for a one-copy GA process with constant loss of cells, the relative frequency of single-gene-copy cells (sensitive cells) converges to zero, with the rate of convergence depending on the amplification probability. In contrast, for a one-copy GA process with copy-number-dependent loss of cells, the relative frequency of single-copy cells is bounded, implying a bounded compartment of many-gene-copy cells. Using branching processes theory we calculate the dynamical distribution of the single-gene-copy compartment as well as its extinction probability. Our models are used for estimating treatment prognosis as affected by drug resistance due to GA, showing significant differences in prognosis resulting from small changes in drug dose.

Animals↗
PubMed2005

Modulation of biogenesis of the Francisella tularensis subsp. novicida-containing phagosome in quiescent human macrophages and its maturation into a phagolysosome upon activation by IFN-gamma.

Francisella tularensis is a highly virulent facultative intracellular pathogen that has been categorized as a class A bioterrorism agent, and is classified into four subsp, tularensis, holarctica, mediasiatica and novicida. Although the ability of F. tularensis subsp. novicida to cause tularemia in mice is similar to the virulent subsp. tularensis and holarctica, it is attenuated in humans. It is not known whether attenuation of F. tularensis subsp. novicida in humans is resulting from a different route of trafficking within human macrophages, compared with the tularensis or holarctica subsp. Here we show that in quiescent human monocytes-derived macrophages (hMDMs), the F. tularensis subsp. novicida containing phagosome (FCP) matures into a late endosome-like stage that acquires the late endosomal marker LAMP-2 but does not fuse to lysosomes. This modulation of phagosome biogenesis by F. tularensis is followed by disruption of the phagosome at 4-12 h and subsequent bacterial escape into cytoplasm where the organism replicates. In IFN-gamma-activated hMDMs, intracellular replication of F. tularensis is completely inhibited, and is associated with failure of the organism to escape from the phagosome into the cytoplasm for up to 24 h after infection. In IFN-gamma-activated hMDMs, the FCPs acquire the lysosomal enzymes Cathepsin D, which is excluded in quiescent hMDMs. When the lysosomes of IFN-gamma-activated hMDMs are preload with Texas Red Ovalbumin or BSA-gold, the FCPs acquire both lysosomal tracers. In contrast, both lysosomal tracers are excluded from the FCPs within quiescent hMDMs. We conclude that although F. tularensis subsp. novicida is attenuated in humans, it modulates biogenesis of its phagosome into a late endosome-like compartment followed by bacterial escape into the cytoplasm within quiescent hMDMs, similar to the virulent subsp. tularensis. In IFN-gamma-activated hMDMs, the organism fails to escape into the cytoplasm and its phagosome fuses to lysosomes, similar to inert particles.

Antigens, CD↗
PubMed1985

Enhanced alveolar macrophage-mediated antigen-induced T-lymphocyte proliferation in sarcoidosis.

Expansion of T-lymphocyte numbers is a characteristic feature of the alveolitis of pulmonary sarcoidosis. One mechanism that may influence the numbers of T-lymphocytes in the lung is the process of antigen presentation in which alveolar macrophages, in the presence of antigen, induce T-lymphocytes to replicate. To evaluate this process in sarcoidosis, alveolar macrophages were obtained by bronchoalveolar lavage, pulsed with tetanus toxoid, and co-cultured with purified autologous T cells. Strikingly, antigen-pulsed alveolar macrophages from sarcoid patients induced more than a twofold increase in autologous T-lymphocyte proliferation compared with the response seen using cells from normal or patients with idiopathic pulmonary fibrosis (P less than 0.001), all comparisons). In contrast, when monocytes were used as the antigen presenting cell, no significant differences were observed in T cell proliferation induced by antigen among the three groups. The enhanced T-lymphocyte proliferation induced by sarcoid alveolar macrophages was not dependent on the compartment from which the T cells were derived, and was independent of the specific antigen used. One possible explanation for augmented antigen presentation seen in sarcoid is that an increased percentage of sarcoid alveolar macrophages express HLA-DR or HLA-DS surface antigens. However, most normal and sarcoid alveolar macrophages express HLA-DR and HLA-DS surface antigens, and the percentage of macrophages expressing these antigens was not significantly different in the two groups. Thus, while the mechanisms of the enhanced antigen presentation in the sarcoid lung are unknown, the process of antigen-driven, alveolar macrophage-modulated lung T cell proliferation may explain, at least in part, the expansion of lung T-lymphocyte numbers that characterizes this disease.

Adolescent↗
PubMed1991

Cytotoxic effect of adriamycin and agarose-coupled adriamycin on glomerular epithelial cells: role of free radicals.

It has been suggested that the generation of toxic radicals plays an important role in toxicity by Adriamycin (ADR) on cancer cell lines and in vivo. We have examined the role of free radicals in determining toxicity and resistance to ADR of rat glomerular epithelial cells in culture; this method provides a good model for analyzing the mechanisms responsible for ADR experimental nephrosis in rats. Three points were established: a) the intra- or extracellular site of ADR toxicity; b) the role of the superoxide anion and of the hydroxyl radical in determining intra- and -extracellular cytotoxicity; and c) the implication of oxido-reduction cycling as a potential route for ADR semiquinone transformation. Free ADR was found to induce the same inhibition of [3H]thymidine incorporation into DNA as ADR bound to an agarose macroporous bed which prevents the intracellular incorporation of the drug. Specific scavenging of free radical activity by the enzymes catalase and superoxide dismutase, the hydroxyl radical inhibitors dimethyl sulfoxide and dimethylthiourea (DMTU) and by chelation of intracellular free iron with deferoxamine produced only a partial restoration of [3H]thymidine incorporation into DNA, which was maximal for DMTU (30% of normal incorporation). DMTU treatment was unsuccessful in preventing the extracellular cytostatic effect of ADR. Finally, glomerular epithelial cell killing (51Cr-release method) by 5-iminodaunorubicin, an ADR analogue with a modified quinone function that prohibits oxido-reduction cycling, was higher than unmodified ADR. These results indicate that ADR may exert its cytotoxic effects on glomerular epithelial cells by interaction at the cell surface, whereas the intracellular compartment, principally DNA, does not seen to be the target of ADR effects. They also suggest that the free radicals are in part responsible for ADR intracellular cytotoxicity, but other mechanisms should also be hypothesized. Finally, the participation of the ADR semiquinone radical in oxido-reduction cycling seems not important for the induction of the cellular damage.

Allopurinol↗
PubMed2001

Morphology and immunology of the human palatine tonsil.

At the surface of the respiratory and digestive organs the organism first comes into contact nasally and orally with various foreign agents and substances in the air and in food. The palatine tonsils are located at the centre of this strategic region. Immunological processes, both humoral and cellular, are initiated in the different specialised compartments of the palatine tonsils, such as the crypt epithelium, lymphoid follicles and extrafollicular region. Each compartment has a typical composition of lymphocytes and dendritic cell subsets. This review summarises current data on the anatomy, histology, and pathology of the human palatine tonsils, describes their fundamental immunological functions, and provides insight into the various interactions involved in the initiation of immune responses. The palatine tonsil is the only easily accessible human lymphoid organ and is often taken as an example for lymphoid organs. Although affections of the palatine tonsils constitutes an essential part in the clinical routine, it is still controversial whether tonsillectomy is of general benefit. This is of increasing importance since it has been discovered in the last few years that the palatine tonsils are reservoir and replication sites of HIV.

Humans↗
PubMed2002

Ultrastructural element localization by EDXS in Empetrum nigrum.

Empetrum nigrum L. is one of the few species growing on highly polluted areas in the northern boreal forests and it accumulates considerable amounts of heavy metals especially in its older stems. Previous-year stems of Empetrum nigrum were collected from two different sites located at distances of 0.5km (highly contaminated) and 8km (low contaminated) from a Cu--Ni smelter at Harjavalta, SW Finland. The element (Al, As, Cu, Fe, Mn, Zn, Ca, K, P, S, Mg, Na) localization was performed by energy-dispersive X-ray spectroscopy (EDXS) after cryofixation, freeze-drying and pressure infiltration of the material. The results showed higher levels of Cu, As and Fe in cell compartments of E. nigrum close to the smelter than at further distance. The Al and Zn levels, in contrast, showed no clear differences between the sites. Cu was distributed homogeneously in the tissue and occurred in vacuoles, cytoplasm, cell walls as well as in lumens of the vascular tissue. The higher amounts of As were localized in the outer regions of the stem cross-section and the amounts were higher in the primary cell walls of living (ray cells, phloem) than dead cells (xylem, sclereids). Ray cells, phloem and sclereids had elevated Fe amounts compared to the other tissues in the contaminated stem samples but owing to the high variation between the replicates, no significant differences were found. Based on the rather homogeneous localization of Cu, As and Fe in the living tissue and increased levels of Cu, As and Fe in vacuoles, cell walls and cytoplasm near the smelter, it seems that more than one specific mechanism contribute to the heavy metal tolerance of E. nigrum. Macronutrients did not show clear differences between the two distances or connection to heavy metal localization. Neither the role of complexing agents in heavy metal tolerance in the cytoplasm or vacuoles could be shown by this study. Because of the more frequent localization of electron dense phenolic material in the polluted samples, it might also have a function in the heavy metal tolerance of E. nigrum.

Asteraceae↗
PubMed2005

Detection of hepatitis C virus (HCV) in serum and peripheral-blood mononuclear cells from HCV-monoinfected and HIV/HCV-coinfected persons.

It has been speculated that hepatitis C virus (HCV) replicates in peripheral-blood mononuclear cells (PBMCs), which, therefore, may be a site for interaction with human immunodeficiency virus (HIV). We used strand-specific real-time polymerase chain reaction to detect HCV RNA in 28 HCV-monoinfected and 20 HIV/HCV-coinfected women. At the first visit, positive-strand HCV RNA was detected in serum samples from 89% of the women, whereas positive-strand HCV RNA was detected in PBMC samples from 32% and 55% of the HCV-monoinfected and HIV/HCV-coinfected women, respectively. After initiation of antiretroviral therapy, the HIV/HCV-coinfected women were significantly more likely to have detectable positive- and negative-strand HCV RNA in the PBMC compartment than were the HCV-monoinfected women. HIV and HCV RNA levels were not correlated. Serum HCV RNA levels were correlated over time; HCV RNA levels in the serum and PBMC compartments were not. These data suggest differential regulation of HCV RNA in the serum and PBMC compartments and may partially explain the limited HCV antiviral response rates observed in coinfected persons.

Adult↗
PubMed1999

Reconstitution of human thymic implants is limited by human immunodeficiency virus breakthrough during antiretroviral therapy.

Human immunodeficiency virus type 1 (HIV-1)-infected SCID-hu thymic implants depleted of CD4(+) cells can support renewed thymopoiesis derived from both endogenous and exogenous T-cell progenitors after combination antiretroviral therapy. However, successful production of new thymocytes occurs transiently. Possible explanations for the temporary nature of this thymic reconstitution include cessation of the thymic stromal support function, exhaustion of T-cell progenitors, and viral resurgence. Distinguishing between these processes is important for the development of therapeutic strategies aimed at reconstituting the CD4(+) T-cell compartment in HIV-1 infection. Using an HIV-1 strain engineered to express the murine HSA heat-stable antigen surface marker, we explored the relationship between HIV-1 expression and CD4(+) cell resurgence kinetics in HIV-1-depleted SCID-hu implants following drug therapy. Antiviral therapy significantly suppressed HIV-1 expression in double-positive (DP) CD4/CD8 thymocytes, and the eventual secondary decline of DP thymocytes following therapy was associated with renewed viral expression in this cell subset. Thymocytes derived from exogenous T-cell progenitors induced to differentiate in HIV-1-depleted, drug-treated thymic implants also became infected. These results indicate that in this model, suppression of viral replication occurs transiently and that, in spite of drug therapy, virus resurgence contributes to the transient nature of the renewed thymic function.

Animals↗
PubMed1993

Regulation of megakaryocytopoiesis.

Megakaryocytopoiesis is the cellular developmental process prior to the release of platelets into the circulation. Regulation of megakaryocytopoiesis is a complex phenomenon that begins with commitment of hematopoietic stem cells to the replication and maturation of progenitor cells through endomitosis and megakaryocyte differentiation [1-4]. Platelet production is determined by the number and size of megakaryocytes in the marrow and may be regulated at two levels: at early stages of cell proliferation resulting in increased megakaryocyte numbers, and at later stages by endoreplication which increases DNA content and the size of megakaryocytes [5]. The mature megakaryocyte is a large polyploid cell with a highly defined invaginated membrane (demarcation membrane) and contains the membrane molecules necessary for platelet function [6-9]. Platelet shedding appears to occur by fragmentation of the cytoplasm of the megakaryocyte. Platelet release is thought to occur via transendothelial processes projecting into the vascular compartment [10, 11], although several studies indicate that megakaryocytes lodged in the lungs are capable of platelet formation [12-17]. The factors stimulating megakaryocytopoiesis in the lung have not been well characterized. In the past, the study of megakaryocyte development in vivo and in vitro was hampered by the rarity of megakaryocytes in the bone marrow, the poorly defined cell populations, and inadequate assays. These prior studies of megakaryocyte development have been discussed in the recent past by R. Hoffman [1], N. Williams [3], and M. W. Long [2]. An attempt will be made in this review to highlight and synthesize various new concepts of regulation of megakaryocytopoiesis.

Animals↗
PubMed1980

Perturbation of cell cycle progression in mouse epidermis prior to the regenerative response.

Cell kinetic perturbations that resulted in a wave of increased cell division during the 6-8 hr lag period prior to regenerative DNA replication in mouse epidermis were examined. The epidermis was stimulated to proliferate by adhesive tape stripping, and flow cytometric DNA measurements of isolated epidermal basal cells counting of mitoses, of Colcemid arrested metaphases and of labeled mitoses among basal cells in histologic sections were made. The results showed that mitotic peaks that occur in the prereplicative period subsequent to tape stripping can be explained by a delay in cell progression through the S phase, followed by subsequent release and partial synchrony in further cell cycle progression. Early peaks of mitoses in epidermis stimulated to proliferate should therefore not, without further evidence, be assumed to originate from cells triggered into division from a resting G2 compartment. The results also indicate an initial delayed cell progression through the G2 phase, whereas the mitotic duration seemed to be initially reduced, indicating that the DNA synthesis phase and the G2 phase are parts of the epidermal cell cycle that may be most vulnerable to various types of influences.

Animals↗
PubMed1985

Nuclear compartmentalization of the v-myb oncogene product.

Nuclei obtained from chicken leukemic myeloblasts transformed by avian myeloblastosis virus were fractionated into various subnuclear compartments, which were then analyzed by specific immunoprecipitation for the presence of the leukemogenic product, p48v-myb, of the viral oncogene. In cells labeled for 30 or 60 min with L-[35S]methionine and in unlabeled exponentially dividing leukemic cells analyzed by Western blotting, p48v-myb was detected within the nucleoplasm (29 +/- 9% [standard deviation] of the total), chromatin (7 +/- 4%), and lamina-nuclear matrix (64 +/- 9%). Also, in myeloblasts analyzed by immunofluorescence during mitosis, p48v-myb appeared to be dispersed through the cell like the lamina-nuclear matrix complex. Strong attachment to the nuclear matrix-lamina complex suggests that p48v-myb may be involved in DNA replication or transcription or both.

Animals↗
PubMed1990

Streaming pancreas: islet cell kinetics.

Thirty male young adult rats aged 7 weeks, weighing 200 g, were injected with 0.5 microCi/g body weight tritiated thymidine (specific activity 5.0 Ci/mM). The rats were then killed in groups of five, at the following times: 1 hour, and 14, 28, 42, 56, 90, and 120 days. The pancreata were dissected, embedded in paraffin, and cut into 5 microns thick sections which were then dipped into liquid emulsion. The labelling index of acini and islet cells was estimated in each autoradiogram, and their distance from intercalated duct was measured. Acini and islet cells streamed away from the intercalated duct at a daily velocity of 0.52 microns. Acinus labelling index which was initially 0.78% declined with time. Islet cell labelling index was initially 0.38%. In the following days it climbed upward reaching on the 42nd day its peak value of 0.78%. From then onward it declined to a low of 0.38%. Since cells were labelled only once, and labelling was instantaneous, it is concluded that labelled acinus cells entered the islet, and that acinus cells are actually islet cell precursors. The pancreas is structured kinetically like other exocrine glands, being a two compartment cell renewal system which continuously renews its cells. The pancreocyte is a descendant of an intercalated duct progenitor. After leaving the duct it turns into an acinus cell, gradually approaching the Langerhans islet. After crossing its border it becomes an islet cell, and proceeds toward the islet center. Its population size dwindles exponentially until at islet center all cells are eliminated.

Animals↗
PubMed2004

Selective pressure for a decreased rate of asymmetrical divisions within stem cell niches may contribute to age-related alterations in stem cell function.

Most mammalian continuously renewing tissues are maintained by stem cells located within stem cell niches. Each niche contains a number of stem cells that replicate asymmetrically to give differentiated cells and also undergo periodic deletion and compensatory replacement by symmetrical "self-renewal" divisions of stem cells remaining within the niche. It has been recognized that there is selective pressure for an increased rate of self-renewal divisions and that the increasingly likely consequence is neoplasia. However, to date it has not been appreciated that there is also an independent selective pressure for a decreased rate of asymmetrical divisions. In this article, the origin of this second type of selective pressure is explained and its consequences explored through the use of computer modeling. It is shown that age-related changes in a range of mammalian stem cell compartments can be understood in the context of a decreased rate of asymmetrical stem cell divisions with an increased propensity for self-renewal divisions. It is proposed that a decreased rate of asymmetrical divisions impairs the ability of old stem cell compartments to respond effectively to stress.

Aging↗
PubMed1983

Mutant Chinese hamster ovary cells pleiotropically defective in receptor-mediated endocytosis.

Populations of Chinese hamster ovary cells selected for resistance to diphtheria toxin were found to be highly enriched for mutants deficient in the uptake of lysosomal hydrolases via the mannose 6-phosphate receptor. One doubly defective mutant, DTF 1-5-1, exhibited increased resistance to Sindbis virus, although it was able to bind and internalize virus normally. Normal production of virus was obtained when, subsequent to virus binding, the mutant was exposed for 2 min to acidic pH. Similarly, a shift to acidic pH increased the sensitivity of DTF 1-5-1 to diphtheria toxin 12-fold. Decreased uptake of lysosomal hydrolases by the mutant correlated with decreased mannose 6-phosphate receptor activity at the cell surface; results of lactoperoxidase-catalyzed iodination indicated that the surface-associated receptor was present but inactive on DTF 1-5-1. Total mannose 6-phosphate receptor activity was also decreased in the mutant and this decrease was reflected by increased secretion of lysosomal hydrolases. The phenotype of DTF 1-5-1 resembles in many ways that of cells treated with ammonia. We suggest that the defect in DTF 1-5-1 stems from an inability to deliver virus, diphtheria toxin, and lysosomal hydrolases to an acidic compartment. Other ligands may be endocytosed through a different pathway since the defect of DTF 1-5-1 did not decrease the endocytosis of ricin, modeccin, or Pseudomonas toxin and had minimal effects on uptake and degradation of low density lipoprotein.

Animals↗
PubMed2004

Budding events in herpesvirus morphogenesis.

Herpes virions are complex particles that consist of more than 30 different virally encoded proteins. The molecular basis of how this complicated structure is assembled is only recently beginning to emerge. After replication in the host cell nucleus viral DNA is incorporated into preformed capsids, which leave the nucleus by a first budding event at the inner nuclear membrane resulting in the formation of primary enveloped virions in the perinuclear space. The primary envelope then fuses with the outer leaflet of the nuclear membrane thereby releasing nucleocapsids into the cytoplasm. Final envelopment, including the acquisition of more than 15 tegument and more than 10 envelope (glyco) proteins occurs by budding into Golgi-derived vesicles. Mature virions are released after fusion of the vesicle membrane with the plasma membrane of the cell. Thus, herpesvirus morphogenesis requires two different budding steps, which are distinct not only in the subcellular compartments in which they occur but also by the viral proteins involved. This review summarizes recent advances in our understanding of the two herpesvirus budding events.

Animals↗
PubMed2003

Relative risk of injury and death in ambulances and other emergency vehicles.

This study addresses of the impacts of emergency vehicle (ambulances, police cars and fire trucks) occupant seating position, restraint use and vehicle response status on injuries and fatalities. Multi-way frequency and ordinal logistic regression analyses were performed on two large national databases, the National Highway Traffic Safety Administration's Fatality Analysis Reporting System (FARS) and the General Estimates System (GES). One model estimated the relative risk ratios for different levels of injury severity to occupants traveling in ambulances. Restrained ambulance occupants involved in a crash were significantly less likely to be killed or seriously injured than unrestrained occupants. Ambulance rear occupants were significantly more likely to be killed than front-seat occupants. Ambulance occupants traveling non-emergency were more likely than occupants traveling emergency to be killed or severely injured. Unrestrained ambulance occupants, occupants riding in the patient compartment and especially unrestrained occupants riding in the patient compartment were at substantially increased risk of injury and death when involved in a crash. A second model incorporated police cars and fire trucks. In the combined ambulance-fire truck-police car model, the likelihood of an occupant fatality for those involved in a crash was higher for routine responses. Relative to police cars and fire trucks, ambulances experienced the highest percentage of fatal crashes where occupants are killed and the highest percentage of crashes where occupants are injured. Lack of restraint use and/or responding with 'lights and siren' characterized the vast majority of fatalities among fire truck occupants. A third model incorporated non-special use van and passenger car occupants, which otherwise replicated the second model. Our findings suggest that ambulance crewmembers riding in the back and firefighters in any seating position, should be restrained whenever feasible. Family members accompanying ambulance patients should ride in the front-seat of the ambulance.

Accidents, Traffic↗
PubMed1999

Do plastid envelope membranes play a role in the expression of the plastid genome?

A unique biochemical machinery is present within the two envelope membranes surrounding plastids (Joyard et al., Plant Physiol. 118 (1998) 715-723) that reflects the stage of development of the plastid and the specific metabolic requirements of the various tissues. Envelope membranes are the site for the synthesis and metabolism of specific lipids. They are also the site of transport of metabolites, proteins and information between plastids and surrounding cellular compartments. For instance, a complex machinery for the import of nuclear-encoded plastid proteins is rapidly being elucidated. The functional studies of plastid envelope membranes result in the characterization of an increasing number of envelope proteins with unexpected functions. For instance, recent experiments have demonstrated that envelope membranes bind specifically to plastid genetic systems, the nucleoids surrounded by plastid ribosomes. At early stages of plastid differentiation, the inner envelope membrane contains a unique protein (named PEND protein) that binds specifically to plastid DNA. This tight connection suggests that the PEND protein is at least involved in partitioning the plastid DNA to daughter plastids during division. The PEND protein can also provide a physical support for replication and transcription. In addition, factors involved in the control of plastid protein synthesis can become associated to envelope membranes. This was shown for a protein homologous to the E. coli ribosome recycling factor and for the stabilizing factors of some specific chloroplast mRNAs encoding thylakoid membrane proteins. In fact, the envelope membranes together with the plastid DNA are the two essential constituents of plastids that confer identity to plastids and their interactions are becoming uncovered through molecular as well as cytological studies. In this review, we will focus on these recent observations (which are consistent with the endosymbiotic origin of plastids) and we discuss possible roles for the plastid envelope in the expression of plastid genome.

Animals↗
PubMed1994

Induced gene expression of the hypusine-containing protein eukaryotic initiation factor 5A in activated human T lymphocytes.

The hypusine-containing protein eukaryotic initiation factor 5A (eIF-5A) is a cellular cofactor critically required for the function of the Rev transactivator protein of human immunodeficiency virus type 1 (HIV-1). eIF-5A localizes in the nuclear and cytoplasmic compartments of mammalian cells, suggesting possible activities on the level of regulated mRNA transport and/or protein translation. In this report we show that eIF-5A gene expression is constitutively low but inducible with T-lymphocyte-specific stimuli in human peripheral blood mononuclear cells (PBMCs) of healthy individuals. In contrast, eIF-5A is constitutively expressed at high levels in human cell lines as well as in various human organs. Comparison of eIF-5A levels in the PBMCs of uninfected and HIV-1-infected donors shows a significant upregulation of eIF-5A gene expression in the PBMCs of HIV-1 patients, compatible with a possible role of eIF-5A in HIV-1 replication during T-cell activation.

Base Sequence↗