Congenital Dyserythropoietic Anemia

Reading the excellent article by Drs. Murphy and Oski, "Congenital Dyserythropoietic Anemia (CDA)",1 which further defines type II, produced a sense of deja vu. In the 1950s, nonspherocytic, hemolytic anemias (HNHA) were categorized as type I and II based on the in vitro autohemolysis test.2 This group of anemias has subsequently been demonstrated to be due to a series of enzymatic abnormalities in carbohydrate metabolism.3 In CDA, the morphological characteristics which define types I, II, and III probably reflect nuclear rather than cytoplasmic abnormalities.

Download Full-text

Modeling Endoleaks and Collateral Reperfusion following Endovascular AAA Exclusion

Journal of Endovascular Therapy ◽

10.1177/152660280301000305 ◽

2003 ◽

Vol 10 (3) ◽

pp. 424-432 ◽

Cited By ~ 10

Author(s):

Chuh K. Chong ◽

Thien V. How ◽

Geoffrey L. Gilling-Smith ◽

Peter L. Harris

Keyword(s):

Stent Graft ◽

Aortic Pressure ◽

Type I ◽

Type Ii ◽

Pump System ◽

Type Ii Endoleak ◽

Type I Endoleak ◽

The Impact ◽

Mean Aortic Pressure

Purpose: To investigate the effect on intrasac pressure of stent-graft deployment within a life-size silicone rubber model of an abdominal aortic aneurysm (AAA) maintained under physiological conditions of pressure and flow. Methods: A commercial bifurcated device with the polyester fabric preclotted with gelatin was deployed in the AAA model. A pump system generated physiological flow. Mean and pulse aortic and intrasac pressures were measured simultaneously using pressure transducers. To simulate a type I endoleak, plastic tubing was placed between the aortic wall and the stent-graft at the proximal anchoring site. Type II endoleak was simulated by means of side branches with set inflow and outflow pressures and perfusion rates. Type IV endoleak was replicated by removal of gelatin from the graft fabric. Results: With no endoleak, the coated graft reduced the mean and pulse sac pressures to negligible values. When a type I endoleak was present, mean sac pressure reached a value similar to mean aortic pressure. When net flow through the sac due to a type II endoleak was present, mean sac pressure was a function of the inlet pressure, while pulse pressure in the sac was dependent on both inlet and outlet pressures. As perfusion rates increased, both mean and pulse sac pressures decreased. When there was no outflow, mean sac pressure was similar to mean aortic pressure. In the presence of both type I and type II endoleaks, mean sac pressure reached mean aortic pressure when the net perfusion rate was low. Conclusions: In vitro studies are useful in gaining an understanding of the impact of different types of endoleaks, in isolation and in combination, on intrasac pressure after aortic stent-graft deployment.

Download Full-text

Type VI collagen expression is upregulated in the early events of chondrocyte differentiation

Development ◽

10.1242/dev.117.1.245 ◽

1993 ◽

Vol 117 (1) ◽

pp. 245-251

Author(s):

R. Quarto ◽

B. Dozin ◽

P. Bonaldo ◽

R. Cancedda ◽

A. Colombatti

Keyword(s):

Suspension Culture ◽

Type I Collagen ◽

Type Ii Collagen ◽

Type I ◽

Type Ii ◽

Type Vi Collagen ◽

Full Spectrum ◽

Collagen Expression ◽

Hypertrophic Chondrocyte

Dedifferentiated chondrocytes cultured adherent to the substratum proliferate and synthesize large amounts of type I collagen but when transferred to suspension culture they decrease proliferation, resume the chondrogenic phenotype and the synthesis of type II collagen, and continue their maturation to hypertrophic chondrocyte (Castagnola et al., 1986, J. Cell Biol. 102, 2310–2317). In this report, we describe the developmentally regulated expression of type VI collagen in vitro in differentiating avian chondrocytes. Type VI collagen mRNA is barely detectable in dedifferentiated chondrocytes as long as the attachment to the substratum is maintained, but increases very rapidly upon passage of the cells into suspension culture reaching a peak after 48 hours and declining after 5–6 days of suspension culture. The first evidence of a rise in the mRNA steady-state levels is obtained already at 6 hours for the alpha 3(VI) chain. Immunoprecipitation of metabolically labeled cells with type VI collagen antibodies reveals that the early mRNA rise is paralleled by an increased secretion of type VI collagen in cell media. Induction of type VI collagen is not the consequence of trypsin treatment of dedifferentiated cells since exposure to the actin-disrupting drug cytochalasin or detachment of the cells by mechanical procedures has similar effects. In 13-day-old chicken embryo tibiae, where the full spectrum of the chondrogenic differentiation process is represented, expression of type VI collagen is restricted to the articular cartilage where chondrocytes developmental stage is comparable to stage I (high levels of type II collagen expression).(ABSTRACT TRUNCATED AT 250 WORDS)

Download Full-text

Disparate cytokine regulation of ICAM-1 in rat alveolar epithelial cells and pulmonary endothelial cells in vitro

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1995.269.1.l127 ◽

1995 ◽

Vol 269 (1) ◽

pp. L127-L135 ◽

Cited By ~ 5

Author(s):

W. W. Barton ◽

S. Wilcoxen ◽

P. J. Christensen ◽

R. Paine

Keyword(s):

Endothelial Cells ◽

Epithelial Cells ◽

Inflammatory Cytokines ◽

Alveolar Epithelial Cells ◽

Normal Lung ◽

Type I ◽

Type Ii Cells ◽

Type Ii ◽

Alveolar Epithelial

Intercellular adhesion molecule-1 (ICAM-1) is expressed at high levels on type I alveolar epithelial cells in the normal lung and is induced in vitro as type II cells spread in primary culture. In contrast, in most nonhematopoetic cells ICAM-1 expression is induced in response to inflammatory cytokines. We have formed the hypothesis that the signals that control ICAM-1 expression in alveolar epithelial cells are fundamentally different from those controlling expression in most other cells. To test this hypothesis, we have investigated the influence of inflammatory cytokines on ICAM-1 expression in isolated type II cells that have spread in culture and compared this response to that of rat pulmonary artery endothelial cells (RPAEC). ICAM-1 protein, determined both by a cell-based enzyme-linked immunosorbent assay and by Western blot analysis, and mRNA were minimally expressed in unstimulated RPAEC but were significantly induced in a time- and dose-dependent manner by treatment with tumor necrosis factor-alpha, interleukin-1 beta, or interferon-gamma. In contrast, these cytokines did not influence the constitutive high level ICAM-1 protein expression in alveolar epithelial cells and only minimally affected steady-state mRNA levels. ICAM-1 mRNA half-life, measured in the presence of actinomycin D, was relatively long at 7 h in alveolar epithelial cells and 4 h in RPAEC. The striking lack of response of ICAM-1 expression by alveolar epithelial cells to inflammatory cytokines is in contrast to virtually all other epithelial cells studied to date and supports the hypothesis that ICAM-1 expression by these cells is a function of cellular differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

Download Full-text

Biological Relevance of Colony Morphology and Phenotypic Switching by Burkholderia pseudomallei

Journal of Bacteriology ◽

10.1128/jb.01258-06 ◽

2006 ◽

Vol 189 (3) ◽

pp. 807-817 ◽

Cited By ~ 93

Author(s):

Narisara Chantratita ◽

Vanaporn Wuthiekanun ◽

Khaemaporn Boonbumrung ◽

Rachaneeporn Tiyawisutsri ◽

Mongkol Vesaratchavest ◽

...

Keyword(s):

Burkholderia Pseudomallei ◽

Vaccine Development ◽

Colony Morphology ◽

Phenotypic Switching ◽

Type I ◽

Type Ii ◽

Altered Expression ◽

Replication Fitness

ABSTRACT Melioidosis is a notoriously protracted illness and is difficult to cure. We hypothesize that the causative organism, Burkholderia pseudomallei, undergoes a process of adaptation involving altered expression of surface determinants which facilitates persistence in vivo and that this is reflected by changes in colony morphology. A colony morphotyping scheme and typing algorithm were developed using clinical B. pseudomallei isolates. Morphotypes were divided into seven types (denoted I to VII). Type I gave rise to other morphotypes (most commonly type II or III) by a process of switching in response to environmental stress, including starvation, iron limitation, and growth at 42°C. Switching was associated with complex shifts in phenotype, one of which (type I to type II) was associated with a marked increase in production of factors putatively associated with in vivo concealment. Isogenic types II and III, derived from type I, were examined using several experimental models. Switching between isogenic morphotypes occurred in a mouse model, where type II appeared to become adapted for persistence in a low-virulence state. Isogenic type II demonstrated a significant increase in intracellular replication fitness compared with parental type I after uptake by epithelial cells in vitro. Isogenic type III demonstrated a higher replication fitness following uptake by macrophages in vitro, which was associated with a switch to type II. Mixed B. pseudomallei morphologies were common in individual clinical specimens and were significantly more frequent in samples of blood, pus, and respiratory secretions than in urine and surface swabs. These findings have major implications for therapeutics and vaccine development.

Download Full-text

Role of collagenase in mediating in vitro alveolar epithelial wound repair

Journal of Cell Science ◽

10.1242/jcs.112.2.243 ◽

1999 ◽

Vol 112 (2) ◽

pp. 243-252

Author(s):

E. Planus ◽

S. Galiacy ◽

M. Matthay ◽

V. Laurent ◽

J. Gavrilovic ◽

...

Keyword(s):

Cell Migration ◽

Cell Adhesion ◽

Epithelial Cell ◽

Type I Collagen ◽

Alveolar Epithelial Cell ◽

Cell Monolayer ◽

Type I ◽

Type Ii ◽

Alveolar Epithelial

Type II pneumocytes are essential for repair of the injured alveolar epithelium. The effect of two MMP collagenases, MMP-1 and MMP-13 on alveolar epithelial repair was studied in vitro. The A549 alveolar epithelial cell line and primary rat alveolar epithelial cell cultures were used. Cell adhesion and cell migration were measured with and without exogenous MMP-1. Wound healing of a cell monolayer of rat alveolar epithelial cell after a mechanical injury was evaluated by time lapse video analysis. Cell adhesion on type I collagen, as well as cytoskeleton stiffness, was decreased in the presence of exogenous collagenases. A similar decrease was observed when cell adhesion was tested on collagen that was first incubated with MMP-1 (versus control on intact collagen). Cell migration on type I collagen was promoted by collagenases. Wound healing of an alveolar epithelial cell monolayer was enhanced in the presence of exogenous collagenases. Our results suggest that collagenases could modulate the repair process by decreasing cell adhesion and cell stiffness, and by increasing cell migration on type I collagen. Collagen degradation could modify cell adhesion sites and collagen degradation peptides could induce alveolar type II pneumocyte migration. New insights regarding alveolar epithelial cell migration are particularly relevant to investigate early events during alveolar epithelial repair following lung injury.

Download Full-text

LeuRS can leucylate type I and type II tRNALeus in Streptomyces coelicolor

Nucleic Acids Research ◽

10.1093/nar/gkz443 ◽

2019 ◽

Vol 47 (12) ◽

pp. 6369-6385

Author(s):

Jia-Yi Fan ◽

Qian Huang ◽

Quan-Quan Ji ◽

En-Duo Wang

Keyword(s):

Tertiary Structure ◽

Streptomyces Coelicolor ◽

Catalytic Efficiency ◽

Type I ◽

Type Ii ◽

Specific Domain ◽

Recognition Mechanism ◽

Variable Loop

Abstract Transfer RNAs (tRNAs) are divided into two types, type I with a short variable loop and type II with a long variable loop. Aminoacylation of type I or type II tRNALeu is catalyzed by their cognate leucyl-tRNA synthetases (LeuRSs). However, in Streptomyces coelicolor, there are two types of tRNALeu and only one LeuRS (ScoLeuRS). We found that the enzyme could leucylate both types of ScotRNALeu, and had a higher catalytic efficiency for type II ScotRNALeu(UAA) than for type I ScotRNALeu(CAA). The results from tRNA and enzyme mutagenesis showed that ScoLeuRS did not interact with the canonical discriminator A73. The number of nucleotides, rather than the type of base of the variable loop in the two types of ScotRNALeus, was determined as important for aminoacylation. In vitro and in vivo assays showed that the tertiary structure formed by the D-loop and TψC-loop is more important for ScotRNALeu(UAA). We showed that the leucine-specific domain (LSD) of ScoLeuRS could help LeuRS, which originally only leucylates type II tRNALeu, to aminoacylate type I ScotRNALeu(CAA) and identified the crucial amino acid residues at the C-terminus of the LSD to recognize type I ScotRNALeu(CAA). Overall, our findings identified a rare recognition mechanism of LeuRS to tRNALeu.

Download Full-text

Adrenal steroid receptor binding in spleen and thymus after stress or dexamethasone.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1990.259.3.e405 ◽

1990 ◽

Vol 259 (3) ◽

pp. E405 ◽

Cited By ~ 3

Author(s):

A H Miller ◽

R L Spencer ◽

M Stein ◽

B S McEwen

Keyword(s):

Receptor Binding ◽

Steroid Receptor ◽

Receptor Activation ◽

Receptor Subtypes ◽

Type I ◽

Type Ii ◽

Adrenal Steroid ◽

Immune Tissues ◽

Intact Rats

Type I and II adrenal steroid receptor binding was measured in spleen and thymus of adrenalectomized (ADX) rats and intact rats at basal levels of corticosterone after 1 h of restraint stress or after exogenous administration of dexamethasone (DEX). Concurrent receptor determinations were made in the hippocampus and pituitary. Receptor binding measures in immune tissues and pituitary were less responsive to varying levels of endogenous hormones than binding measures in hippocampus. Compared with ADX rats, type I binding in spleen and pituitary of intact rats at basal levels of corticosterone was unchanged, whereas type I binding in the hippocampus was significantly decreased. Furthermore, despite peak levels of corticosterone, type II binding in spleen, thymus, and pituitary of stressed rats was also unchanged, whereas type II binding in the hippocampus of stressed animals was significantly lower. In contrast, DEX, a well-known immunosuppressant, reduced type II binding in immune tissues more than in the hippocampus. Because a decrease in receptor binding measured in vitro may reflect receptor activation in vivo, these results suggest that there may be considerable heterogeneity in the degree of activation of adrenal steroid receptor subtypes in immune, pituitary, and hippocampal tissue by endogenous and exogenous glucocorticoids.

Download Full-text

Mechanisms and regulation of ion transport in adult mammalian alveolar type II pneumocytes

AJP Cell Physiology ◽

10.1152/ajpcell.1991.261.5.c727 ◽

1991 ◽

Vol 261 (5) ◽

pp. C727-C738 ◽

Cited By ~ 72

Author(s):

S. Matalon

Keyword(s):

Epithelial Transport ◽

Cultured Cells ◽

Basolateral Membrane ◽

Alveolar Epithelium ◽

Alveolar Type ◽

Type I ◽

Type Ii ◽

Epithelial Lining ◽

Epithelial Lining Fluid

The adult alveolar epithelium consists of type I and type II (ATII) pneumocytes that form a tight barrier, which severely restricts the entry of lipid-insoluble molecules from the interstitial to the alveolar space. Current in vivo and in vitro evidence indicates that the alveolar epithelium is also an absorptive epithelium, capable of transporting Na+ from the alveolar lumen, which is bathed by a small amount of epithelial lining fluid, to the interstitial space. The in situ localization of Na(+)-K(+)-ATPase activity in ATII cells and the fact that these cells are involved in a number of crucial functions, such as surfactant secretion and alveolar remodeling after injury, led investigators to examine their transport characteristics. Radioactive flux studies, in both freshly isolated and cultured cells, and bioelectric measurements in ATII cells grown on porous supports indicate that they transport Na+ according to the Koefoed-Johnsen and Ussing model of epithelial transport. Na+ enters the apical membrane, because of the favorable electrochemical gradient, through Na+ cotransporters, a Na(+)-H+ antiport, and cation channels and is pumped across the basolateral membrane by a ouabain-sensitive Na(+)-K+ pump. Na+ transport is enhanced by substances that increase intracellular adenosine 3',5'-cyclic monophosphate. In addition to Na+ transporters, ATII cells contain several transporters that regulate their intracellular pH, including a H(+)-ATPase, which may explain the low pH of the epithelial lining fluid. The absorptive properties of ATII cells may play an important role in regulating the degree of alveolar fluid in health and disease.

Download Full-text