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At least 127 records · Page 7Linked to original sources

PubMed1982

Material thrombogenicity in central venous catheterization. I. A comparison between uncoated and heparin-coated, long antebrachial, polyethylene catheters.

In order to evaluate a new method of heparinization, uncoated (22) and heparin-coated (27) central venous polyethylene catheters were inserted in 49 patients via basilic and cephalic veins punctured at the fossa cubiti. The means duration of catheterization was 5.7 (1-11) days. One-third of the patients with heparin-coated catheters, and one sixth with uncoated catheters developed clinical thrombophlebitis, with a maximum incidence between 4 and 8 days after catheterization. A higher risk of developing thrombophlebitis in the first 4 days after catheterization was found in the patients with heparin-coated polyethylene catheters. After 8 days of catheterization, it seems that there is a lower risk of new cases of thrombophlebitis appearing both in patients with uncoated and those with heparin-coated polyethylene catheters. Radiological thrombosis, regardless of duration of catheterization and heparin-coating, was demonstrated in all 22 patients investigated by "pull-out" phlebography. The heparin-coating did not decrease the rate of thrombotic complications. Location of the catheter tip in subclavian veins was associated with a significantly higher incidence of large, parietal thrombi and catheter occlusion than when the tip was situated in anonymous veins, the superior vena cava, or the right atrium. Cannulation by heparin-coated, polyethylene tubing did not reduce the rate of catheter occlusion.

Adolescent↗

PubMed2005

The increased incidence of pure red cell aplasia with an Eprex formulation in uncoated rubber stopper syringes.

BACKGROUND: The incidence of pure red cell aplasia (PRCA) in chronic kidney disease patients treated with epoetins increased substantially in 1998, was shown to be antibody mediated, and was associated predominantly with subcutaneous administration of Eprex. A technical investigation identified organic compounds leached from uncoated rubber stoppers in prefilled syringes containing polysorbate 80 as the most probable cause of the increased immunogenicity. METHODS: This study investigated whether the incidence of PRCA was higher for exposure to the product form containing leachates than for leachate-free product forms. Antibody-mediated PRCA cases were classified according to indication, product form, and route of administration. Exposure estimates were obtained by country, indication, route of administration, and product form. RESULTS: For 2001 to 2003, the PRCA incidence rate for patients with subcutaneous exposure to Eprex in prefilled syringes with polysorbate 80 and uncoated rubber stoppers (leachates present) was 4.61/10,000 patient years (95% CI 3.88-5.43) versus 0.26/10,000 patient years (95% CI 0.007-1.44) for syringes with coated stoppers (leachates absent). The rate difference was 4.35/10,000 patient years (95% CI 3.44-5.26; P < 0.0001); the rate ratio was 17 (95% CI 3.14-707). A substantial rate difference remained in sensitivity analyses that adjusted for exposure to multiple product forms. CONCLUSION: The epidemiologic data, together with the chemical and immunologic data, support the hypothesis that leachates from uncoated rubber syringe stoppers caused the increased incidence of PRCA associated with Eprex. Currently, all Eprex prefilled syringes contain fluoro-resin coated stoppers, which has contributed to decreased incidence of PRCA with continued surveillance.

Chemistry, Pharmaceutical↗

PubMed1986

Prevention of rhinovirus and poliovirus uncoating by WIN 51711, a new antiviral drug.

WIN 51711, a potent new antipicornavirus drug, has been shown to inhibit an early event in the replication cycle of human poliovirus type 2 and human rhinovirus type 2. WIN 51711 was not virucidal and had no measurable effect on the adsorption of [3H]uridine-labeled virions to cells. When virion penetration of the plasma membrane was determined through loss of sensitivity to neutralizing antisera, WIN 51711 had no effect on poliovirus penetration, but inhibited rhinovirus penetration by 40%. In the presence of WIN 51711, exposure of neutral red-encapsidated virus-infected cells to light at 3 h postinfection resulted in a 3-log reduction in the number of infectious centers, indicating that WIN 51711 maintained the viral RNA in the encapsidated state after penetrating the cell membrane. The inhibition of uncoating by WIN 51711 in the neutral red assay was found to be concentration dependent, with a concentration of 0.03 micrograms/ml resulting in a 90% inhibition of uncoating. Sucrose gradient sedimentation of lysates from whole cells infected with [3H]uridine-labeled poliovirus showed that poliovirions remained intact in the presence of WIN 51711, but were uncoated in the absence of drug. WIN 51711 also prevented thermal inactivation of poliovirus infectivity, indicating a direct stabilizing effect of this compound on virion capsid conformation.

Antiviral Agents↗

PubMed1967

Intracellular uncoating of type 5 adenovirus deoxyribonucleic acid.

Highly purified, (32)P-labeled type 5 adenovirus was employed to study "uncoating" of viral deoxyribonucleic acid (DNA)-defined as the development of sensitivity to deoxyribonuclease. Viral infectivity and radioactivity adsorbed to KB cells at the same rate, and significant amounts of (32)P did not elute from cells throughout the eclipse period. Kinetic studies of viral penetration, eclipse of infectivity, and uncoating of viral DNA indicated that the three events were closely related temporally, that the rates of each were similar, and that they were completed within 60 to 90 min after infection. Viral penetration, eclipse, and uncoating proceeded normally under conditions which blocked protein synthesis, but they did not occur at 0 to 4 C. Neither viral DNA nor viral protein was degraded to acid-soluble material during the eclipse period. The nature of adenovirus DNA was studied after it was converted intracellularly from deoxyribonuclease-resistant to deoxyribonuclease-susceptible. Intact virions centrifuged in sucrose gradients had a sedimentation coefficient of approximately 800, and viral DNA sedimented as a particle of about 30S. Infection of KB cells with purified (32)P-labeled virus yielded deoxyribonuclease-susceptible viral nucleic acid which was in particles with sedimentation coefficients of 350 to 450S, i.e., greater than 10 times faster than DNA obtained from purified virions which had been disrupted by exposure to pH 10.5. When the DNA from disrupted virions was mixed with cell lysates, its sedimentation characteristics were essentially unchanged by the presence of cellular material.

Adenoviridae↗

PubMed1991

Inhibitors of poliovirus uncoating efficiently block the early membrane permeabilization induced by virus particles.

The entry of animal viruses into cells is associated with permeabilization of the infected cells to protein toxins such as alpha-sarcin (C. Fernández-Puentes and L. Carrasco, Cell 20:769-775, 1980). This phenomenon has been referred to as "the early permeabilization by animal viruses" (L. Carrasco, Virology 113:623-629, 1981). A number of inhibitors of poliovirus growth such as WIN 51711 6-(3,4-dichlorophenoxy)-3-(ethylthio)-2-pyridincarbonitrile (DEPC) and Ro 09-0410 specifically block the uncoating step of poliovirus but have no effect on attachment or entry of poliovirus particles into cells. These agents are potent inhibitors of the early permeabilization induced by poliovirus to the toxin alpha-sarcin. Thus, the uncoating of poliovirus is required for the permeabilization of cell membranes to proteins. The increased entry of labeled heparin promoted by virus entry is not blocked by these agents, indicating that poliovirus binds to its receptor and is internalized along with heparin in endosomes in the presence of WIN 51711, DEPC, or Ro 09-0410. We conclude that the delivery to the cytoplasm of some molecules that coenter with virion particles does not take place if the uncoating process is hindered.

Antiviral Agents↗

PubMed2000

Uncoating kinetics of hepatitis A virus virions and provirions.

When the growth kinetics of immature hepatitis A virus provirions and mature virions were monitored, distinct eclipse phases were noted for both types of particles. Strikingly, uncoating of virions occurred around 4 h postinfection, while uncoating of provirions occurred predominantly between 8 and 10 h postinfection. It is proposed that the heterogeneous mixture of infectious hepatitis A virus particles (virions and provirions) typically present in inocula is responsible for the normally asynchronous nature of hepatitis A virus uncoating kinetics.

Hepatovirus↗

PubMed2003

Structural analysis of human rhinovirus complexed with ICAM-1 reveals the dynamics of receptor-mediated virus uncoating.

Intercellular adhesion molecule 1 (ICAM-1) functions as the cellular receptor for the major group of human rhinoviruses, being not only the target of viral attachment but also the mediator of viral uncoating. The configurations of HRV3-ICAM-1 complexes prepared both at 4 degrees C and physiological temperature (37 degrees C) were analyzed by cryoelectron microscopy and image reconstruction. The particle diameters of two complexes (with and without RNA) representing uncoating intermediates generated at 37 degrees C were each 4% larger than that of those prepared at 4 degrees C. The larger virus particle arose by an expansive movement of the capsid pentamers along the fivefold axis, which loosens interprotomer contacts, particularly at the canyon region where the ICAM-1 receptor bound. Particle expansion required receptor binding and preceded the egress of the viral RNA. These observations suggest that receptor-mediated uncoating could be a consequence of restrained capsid motion, where the bound receptors maintain the viral capsid in an expanded open state for subsequent genome release.

Binding Sites↗

PubMed2004

Cryoelectron microscopy analysis of the structural changes associated with human rhinovirus type 14 uncoating.

Release of the human rhinovirus (HRV) genome into the cytoplasm of the cell involves a concerted structural modification of the viral capsid. The intracellular adhesion molecule 1 (ICAM-1) cellular receptor of the major-group HRVs and the low-density lipoprotein (LDL) receptor of the minor-group HRVs have different nonoverlapping binding sites. While ICAM-1 binding catalyzes uncoating, LDL receptor binding does not. Uncoating of minor-group HRVs is initiated by the low pH of late endosomes. We have studied the conformational changes concomitant with uncoating in the major-group HRV14 and compared them with previous results for the minor-group HRV2. The structure of empty HRV14 was determined by cryoelectron microscopy, and the atomic structure of native HRV14 was used to examine the conformational changes of the capsid and its constituent viral proteins. For both HRV2 and HRV14, the transformation from full to empty capsid involves an overall 4% expansion and an iris type of movement of viral protein VP1 to open up a 10-A-diameter channel on the fivefold axis to allow exit of the RNA genome. The beta-cylinders formed by the N termini of the VP3 molecules inside the capsid on the fivefold axis all open up in HRV2, but we propose that only one opens up in HRV14. The release of VP4 is less efficient in HRV14 than in HRV2, and the N termini of VP1 may exit at different points. The N-terminal loop of VP2 is modified in both viruses, probably to detach the RNA, but it bends only inwards in HRV2.

Capsid↗

PubMed2006

Evidence for a functional link between uncoating of the human immunodeficiency virus type 1 core and nuclear import of the viral preintegration complex.

Human immunodeficiency virus type 1 (HIV-1) particles begin their replication upon fusion with the plasma membrane of target cells and release of the viral core into the host cell cytoplasm. Soon thereafter, the viral capsid, which is composed of a polymer of the CA protein, disassociates from the internal ribonucleoprotein complex. While this disassembly process remains poorly understood, the available evidence indicates that proper uncoating of the core is a key step in infection. Defects in uncoating most often lead to a failure of the virus to undergo reverse transcription, resulting in an inability to form a functional viral preintegration complex (PIC). In a previous study, we reported that an HIV-1 mutant containing two substitutions in CA (Q63A/67A) was unusual in that it was poorly infectious yet synthesized normal levels of viral DNA. Here we report that this mutant is impaired for nuclear entry. Quantitative analysis of viral DNA synthesis from infected cells by Southern blotting and real-time PCR revealed that the Q63A/Q67A mutant is impaired in the synthesis of one-long terminal repeat (1-LTR) and 2-LTR circles. Isolation of PICs from acutely infected cells revealed that the Q63A/Q67A mutant produces protein-DNA complexes similar to wild-type in yield and overall composition, but these PICs contained elevated levels of CA and were impaired for integration in vitro. These results demonstrate that mutations in CA can have deleterious effects on both nuclear targeting and integration, suggesting that these steps in the HIV-1 life cycle are dependent on proper uncoating of the viral core.

Active Transport, Cell Nucleus↗

PubMed1980

Concentrations and dimensions of coated and uncoated asbestos fibres in the human lung.

Concentrations and length distributions of uncoated and coated amphibole-type fibres in samples of human lung taken at necropsy were measured by optical microscopy using the membrane filter technique that enables fibres with diameters down to about 0.2 micron to be detected. The subjects included 10 who died with mesothelial tumours, three with lung cancer, and eight of other causes. Measurements of fibre concentrations are compared with those of other workers. It can be deduced from the length distributions that fibres less than 5 microns long are cleared from the lung more efficiently than longer ones. The clearance of short fibres appears to be inhibited in subjects with asbestosis, however. The length distributions of uncoated and coated fibres were dissimilar. In general, few fibres less than 10 microns in length were coated and few greater than 40 microns in length were uncoated. The probability of a fibre of given length, however, becoming coated varied considerably from subject to subject. Possible reasons for this are discussed.

Adult↗

PubMed1998

Examination of potential inhibitors of hepatitis A virus uncoating.

Hepatitis A virus (HAV) replication in BS-C-1 cells was studied in the presence of ten potential uncoating inhibitors. Strong inhibition of HAV replication was only observed in the presence of the phenothiazine compound chlorpromazine and the lysosomotropic agent chloroquine, but not by other lysosomotropic agents. Chlorpromazine and chloroquine were found to prevent virus uncoating. Chlorpromazine is known to inhibit endocytosis of non- clathrin-coated vesicles. Chloroquine is a weak base amine, and thought to inhibit virus replication by preventing endosomal acidification. These results therefore suggest that entry of HAV in BS-C-1 cells does not depend on the low pH encountered in the clathrin-coated endocytic entry pathway. A possible role of calcium ions in mediating viral uncoating is discussed, as calcium ions were found to destabilize HAV particles in vitro.

Animals↗

PubMed1983

Biological and structural studies with an adenovirus type 2 temperature-sensitive mutant defective for uncoating.

We compared some of the biological and structural features of an adenovirus type 2 temperature-sensitive mutant (ts1) defective for maturation cleavages and uncoating with wild-type (WT) virus. The cleavage defect caused ts1 to produce virions at 39 degrees that contained five precursor proteins (pTP, 11K, PVI, PVII, PVIII). Coinfection of cells with such ts1 virions and a variety of mutants or WT virus not only failed to complement ts1 but actually depressed the infection by the second virus. The uncoating defect could only be overcome by multiplicity-dependent leakiness. The structure of the ts1 virion was compared with that of WT virus by iodination with chloramine-T, chloroglycoluril and lactoperoxidase, by cross-linking, and by digestion with proteases. Aside from the presence of precursor proteins and the greater stability of ts1 virions, no other differences were found that could account for the uncoating defect. Therefore, we postulate that this defect was caused by the greater stability imparted to the virion by precursor proteins PVI, PVII and PVIII.

Adenoviruses, Human↗

PubMed1999

The biologic tissue responses to uncoated and coated implanted biomaterials.

Ultrastructural examination of the morphology and morphometry of the bone supporting uncoated titanium and ceramic implants was assessed in an experimental animal model involving 120 implants placed into the mandibles of 30 adult mongrel dogs. Further, preliminary morphologic and morphometric observations of the bone supporting uncoated and hydroxylapatite-coated endosteal titanium implants was evaluated in a second investigation involving 72 implants placed into the mandibles and maxillae of 6 additional dogs. A densely mineralized collagen fiber matrix was observed directly interfacing with uncoated implants. The only material interposed between the implant and bone matrix was a 20- to 50-nm electron-dense material suggestive of a proteoglycan. Also seen in these same osseointegrated implants were narrow unmineralized zones interposed between the implant and bone matrix. In these zones of remodeling bone, numerous osteoblasts were observed interacting with the collagen fiber matrix. It was shown that a normal homeostasis of anabolic osteoblastic activity and catabolic osteoclastic activity resulted in bone remodeling and the resultant osseointegration of the implants. Hydroxylapatite-coated implants intimately interfaced with healthy bone. The mineralized matrix extended into the microporosity of the HA coating. This matrix contained viable osteocytes.

Alloys↗

PubMed1995

The effect of warfarin on the attachment of bone to hydroxyapatite-coated and uncoated porous implants.

The attachment of bone to hydroxyapatite-coated and uncoated porous implants made of cobalt-chromium-molybdenum alloy was investigated with and without postoperative administration of warfarin sodium. The implants were placed transcortically in the femoral diaphysis of adult female goats and were evaluated after three, six, and twelve weeks in situ. Mechanical push-out testing and histological evaluation revealed that the attachment strength and the ingrowth of bone at the bone-implant interface increased with time in situ for both the hydroxyapatite-coated and the uncoated implants. The administration of warfarin significantly impaired both the attachment strength and the ingrowth of bone at twelve weeks. At twelve weeks, the attachment strength and bone ingrowth of the hydroxyapatite-coated implants in the animals that had received warfarin were statistically equal to those of the uncoated implants in the control animals.

Analysis of Variance↗

PubMed1998

Comparison of osseointegration between hydroxyapatite-coated and uncoated threaded titanium dental implants placed into surgically-created bone defect in rabbit tibia.

The purpose of this study was to compare the degree of osseointegration between hydroxyapatite (HA)-coated and uncoated threaded titanium dental implants placed into a surgically created bone defect with or without an expanded polytetrafluorethylene (ePTFE) membrane. A conventional implant site was prepared and either a HA-coated or an uncoated implant was placed in each tibia of 12 rabbits (conventional group). A bone defect approximately 3 mm in width was created on the distal end of the conventional site and either a HA-coated or an uncoated implant was placed there (bone defect group). For another group, the same procedure was performed as in the bone defect group, except the implant sites were covered with ePTFE membranes (ePTFE group). After 4 months, the rabbits were sacrificed. Specimens were prepared and examined histometrically. The results demonstrated that HA-coated threaded titanium dental implants consistently showed a greater amount of osseointegrated surface either in the conventional site or defect region with and without ePTFE membranes in this animal model. In conclusion, a HA-coated threaded titanium implant may be the choice of dental implants to establish greater osseointegration with the defect or conventional site.

Animals↗

PubMed1979

Effect of hemoperfusion with coated and uncoated charcoal on human blood in vitro.

During 4 hours, in-vitro hemoperfusion of human blood was performed in 4 series of experiments: control, cellulose coated charcoal, polyacrylohydrogel coated charcoal and uncoated charcoal. In the control series little change on corpuscular elements and electrolytes was observed. In all hemoperfusion series there was little change of RBC and uniformly a marked fall of the granulocyte count. Platelet- and lymphocyte counts were significantly less affected by cellulose coated charcoal than by the other preparations. Coated and uncoated charcoal absorbed avidly calcium and glucose from the blood. By contrast the potassium level decreased moderately with polyacrylohydrogel coated and uncoated charcoal, whereas the opposite was observed with cellulose coated charcoal.

Blood Cell Count↗

PubMed1990

Immunosorbents based on uncoated synthetic charcoals: preparation, properties, applications.

By means of water-soluble carbodiimide coupling technique various bioligands were covalently attached to the surface of uncoated synthetic active carbons and a number of sorbents with certain biological functions were thus designed. Carbonaceous sorbents with immobilized ligands demonstrate increased affinity towards specific sorbates compared to that of starting matrix. As soon as SCN and SCS synthetic carbons are used uncoated they can be highly loaded with protein molecules - up to 80 mg serum albumin, 6-10 mg IgG rabbit etc. per gram of sorbent. Carbonaceous immunosorbents retain biocompatibility and substantial non-specific adsorptive capacity of initial hemosorbents. A conclusion is drawn that uncoated synthetic charcoals can serve a basis for design of selective hemosorbents intended for solving complicated problems of immunocorrection.

Biocompatible Materials↗

PubMed1994

Pin tract infections: silver vs uncoated pins.

To test the hypothesis that coating external fixation pins with a silver-containing compound (Spi-Argent, Spire Corp, Bedford, Mass) will reduce bacterial colonization and/or pin tract infection, 36 silver-coated and 12 conventional stainless steel pins were placed in the iliac crest of six sheep and inoculated with Staphylococcus aureus. After 2 1/2 weeks the pin sites were examined for motion and inflammation, and the pin tips were quantitatively cultured and examined with scanning electron microscopy (SEM). We found that 84% of the uncoated pins were infected, while 62% of the silver-coated pins were infected. Silver-coated pins were less frequently infected than uncoated pins (confidence interval [CI] > 85%). Also, silver-coated pins were loose less frequently than uncoated pins. Pin motion was closely correlated with infection: 28 of 32 infected pins (88%) had motion, while only 9 of 16 uninfected pins (56%) had motion (CI > 80%). SEM study of the pin tips showed a decreased level of glycocalyx-protected colonization on the surface of the silver-coated pins. Clinically, these results suggest that silver-coated pins will result in less infection and motion at the pin site, the most significant problems in external fixation.

Animals↗