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PubMed1997

Comparisons of shear bond strength of precoated and uncoated brackets.

In an attempt to save chairside time during bonding, orthodontists are using ceramic and metal brackets that have been precoated with the adhesive material. The adhesive used on the precoated brackets is similar in composition to that used for bonding uncoated brackets; the difference is essentially in the percentages of the various ingredients incorporated in the material. The purpose of this study is to determine whether these changes in composition affect the shear bond strength and the site of bond failure when precoated and uncoated ceramic and metal brackets are used. Eighty-five recently extracted human molars were bonded according to the manufacturer's instructions and mounted in phenolic rings. An occlusogingival load was applied to the bracket, producing a shear force at the bracket-tooth interface with a Zwick Universal Test Machine. After debonding, all teeth and brackets were examined under 10x magnification. Any adhesive remaining after bracket removal was assessed with the Adhesive Remnant Index (ARI). The current findings indicated that: (1) Precoated ceramic brackets that used a slightly modified adhesive have similar shear bond strengths as that provided by Transbond XT adhesive on uncoated brackets; (2) precoated metal brackets that used the same adhesive have significantly lower shear bond strength than those obtained with Transbond XT on uncoated brackets. The differences in the bond strength between the ceramic and metal brackets were attributed to the combined effects of the changes in the composition of the adhesives used and in the retention mechanisms incorporated in the bracket bases of the different types of brackets; (3) all bracket/adhesive combinations tested provided clinically acceptable shear bond forces.

Acid Etching, Dental↗

PubMed1998

X-ray diffraction of bone at the interface with hydroxyapatite-coated versus uncoated metal implants.

The microstructural characteristics of the newly formed bone tissue at the interface with hydroxyapatite-coated and uncoated stainless steel pins used in an external fracture fixation system have been evaluated. The bone far from the interface was used as a control. Pins were transversally inserted into the diaphyses of sheep tibiae and were loaded in for six weeks. Three sheep received coated pins and two received uncoated pins. Crystallographic habit and mineralization of the implant-facing bone were evaluated. Moreover, lattice parameters of bone apatite were measured and hydroxyapatite (HA) coating degradation was investigated, by means of conventional and microbeam X-ray diffraction (XRD). In coated pins, six weeks after the implantation the newly formed bone tissue at the interface did not reach complete maturation, but the presence of the implant did not alter the apatite lattice structure; the lattice parameters did not show statistically significant variations with respect to those observed in the control bone. In uncoated pins, bone tissue rarely appeared totally mineralized and lattice parameters were significantly different with respect to those observed in the bone far from the implant. HA particles were observed spreading in the bone-facing coated pins; the XRD pattern of bone apatite surrounding HA particles was unmodified. It was concluded that HA coatings improved the bone remodelling process during pin fixation in comparison to uncoated pins and did not alter the crystallographic habit of apatite.

Journal Article↗

PubMed2000

A yeast DNA J protein required for uncoating of clathrin-coated vesicles in vivo.

Clathrin-coated vesicles mediate diverse processes such as nutrient uptake, downregulation of hormone receptors, formation of synaptic vesicles, virus entry, and transport of biosynthetic proteins to lysosomes. Cycles of coat assembly and disassembly are integral features of clathrin-mediated vesicular transport (Fig. 1a). Coat assembly involves recruitment of clathrin triskelia, adaptor complexes and other factors that influence coat assembly, cargo sequestration, membrane invagination and scission (Fig. 1a). Coat disassembly is thought to be essential for fusion of vesicles with target membranes and for recycling components of clathrin coats to the cytoplasm for further rounds of vesicle formation. In vitro, cytosolic heat-shock protein 70 (Hsp70) and the J-domain co-chaperone auxilin catalyse coat disassembly. However, a specific function of these factors in uncoating in vivo has not been demonstrated, leaving the physiological mechanism and significance of uncoating unclear. Here we report the identification and characterization of a Saccharomyces cerevisiae J-domain protein, Aux1. Inactivation of Aux1 results in accumulation of clathrin-coated vesicles, impaired cargo delivery, and an increased ratio of vesicle-associated to cytoplasmic clathrin. Our results demonstrate an in vivo uncoating function of a J domain co-chaperone and establish the physiological significance of uncoating in transport mediated by clathrin-coated vesicles.

Adaptor Proteins, Vesicular Transport↗

PubMed2006

Sirolimus-eluting versus uncoated stents in acute myocardial infarction.

BACKGROUND: Sirolimus-eluting stents reduce rates of restenosis and reintervention, as compared with uncoated stents. Data are limited regarding the safety and efficacy of such stents in primary percutaneous coronary intervention (PCI) for acute myocardial infarction with ST-segment elevation. METHODS: We performed a single-blind, multicenter, prospectively randomized trial to compare sirolimus-eluting stents with uncoated stents in primary PCI for acute myocardial infarction with ST-segment elevation. The trial included 712 patients at 48 medical centers. The primary end point was target-vessel failure at 1 year after the procedure, defined as target-vessel-related death, recurrent myocardial infarction, or target-vessel revascularization. A follow-up angiographic substudy was performed at 8 months among 174 patients from selected centers. RESULTS: The rate of the primary end point was significantly lower in the sirolimus-stent group than in the uncoated-stent group (7.3% vs. 14.3%, P=0.004). This reduction was driven by a decrease in the rate of target-vessel revascularization (5.6% and 13.4%, respectively; P<0.001). There was no significant difference between the two groups in the rate of death (2.3% and 2.2%, respectively; P=1.00), reinfarction (1.1% and 1.4%, respectively; P=1.00), or stent thrombosis (3.4% and 3.6%, respectively; P=1.00). The degree of neointimal proliferation, as assessed by the mean (+/-SD) in-stent late luminal loss, was significantly lower in the sirolimus-stent group (0.14+/-0.49 mm, vs. 0.83+/-0.52 mm in the uncoated stent group; P<0.001). CONCLUSIONS: Among selected patients with acute myocardial infarction, the use of sirolimus-eluting stents significantly reduced the rate of target-vessel revascularization at 1 year. (ClinicalTrials.gov number, NCT00232830 [ClinicalTrials.gov].).

Angioplasty, Balloon, Coronary↗

PubMed2006

Paclitaxel-eluting versus uncoated stents in primary percutaneous coronary intervention.

BACKGROUND: Drug-eluting coronary-artery stents have been shown to decrease restenosis and therefore the likelihood that additional procedures will be required after percutaneous coronary intervention (PCI). We evaluated the use of a drug-eluting stent in patients undergoing PCI for acute myocardial infarction with ST-segment elevation. METHODS: We randomly assigned 619 patients presenting with an acute myocardial infarction with ST-segment elevation to receive either a paclitaxel-eluting stent or an uncoated stent. The primary end point was a composite of death from cardiac causes, recurrent myocardial infarction, or target-lesion revascularization at 1 year. RESULTS: Baseline clinical and angiographic characteristics in both groups were well matched. There was a trend toward a lower rate of serious adverse events in the paclitaxel-stent group than in the uncoated-stent group (8.8% vs. 12.8%; adjusted relative risk, 0.63; 95% confidence interval, 0.37 to 1.07; P=0.09). A nonsignificant trend was also detected in favor of the paclitaxel-stent group, as compared with the uncoated-stent group, in the rate of death from cardiac causes or recurrent myocardial infarction (5.5% vs. 7.2%, P=0.40) and in the rate of target-lesion revascularization (5.3% vs. 7.8%, P=0.23). The incidence of stent thrombosis during 1 year of follow-up was the same in both groups (1.0%). CONCLUSIONS: Although the use of paclitaxel-eluting stents in acute myocardial infarction with ST-segment elevation reduced the incidence of serious adverse cardiac events at 1 year by 4.0 percentage points, as compared with uncoated stents, the difference was not statistically significant. (Current Controlled Trials number, ISRCTN65027270 [controlled-trials.com].).

Angioplasty, Balloon, Coronary↗

PubMed2002

Identification of domain required for catalytic activity of auxilin in supporting clathrin uncoating by Hsc70.

During clathrin-mediated endocytosis Hsc70, supported by the J-domain protein auxilin, uncoats clathrin-coated vesicles. Auxilin contains both a clathrin-binding domain and a J-domain that binds Hsc70, and it has been suggested that these two domains are both necessary and sufficient for auxilin activity. To test this hypothesis, we created a chimeric protein consisting of the J-domain of auxilin linked to the clathrin-binding domain of the assembly protein AP180. This chimera supported uncoating, but unlike auxilin it acted stoichiometrically rather than catalytically because, like Hsc70, it remained associated with the uncoated clathrin. This observation supports our proposal that Hsc70 chaperones uncoated clathrin by inducing formation of a stable Hsc70-clathrin-AP complex. It also shows that Hsc70 acts by dissociating individual clathrin triskelions rather than cooperatively destabilizing clathrin-coated vesicles. Because the chimera lacks the C-terminal subdomain of the auxilin clathrin-binding domain, it seemed possible that this subdomain is required for auxilin to act catalytically, and indeed its deletion caused auxilin to act stoichiometrically. In contrast, deletion of the N-terminal subdomain weakened auxilin-clathrin binding and prevented auxilin from polymerizing clathrin. Therefore the C-terminal subdomain of the clathrin-binding domain of auxilin is required for auxilin to act catalytically, whereas the N-terminal subdomain strengthens auxilin-clathrin binding.

Animals↗

PubMed1984

An enzyme that removes clathrin coats: purification of an uncoating ATPase.

Uncoating ATPase, an abundant 70,000-mol-wt polypeptide mediating the ATP-dependent dissociation of clathrin from coated vesicles and empty clathrin cages, has been purified to virtual homogeneity from calf brain cytosol. Uncoating protein is present in cells in amounts roughly stoichiometric with clathrin. This enzyme is isolated as a mixture of monomers and dimers, both forms being active. ATP can support protein-facilitated dissociation of clathrin at micromolar levels; all other ribotriphosphates as well as deoxy-ATP are inactive. The clathrin that is released from cages consists of trimers (triskelions) in a stoichiometric complex with uncoating ATPase. These complexes with clathrin have little tendency to self-associate at neutral pH, and at acidic pH they interfere with the assembly of free clathrin. The possible existence and function of these complexes as clathrin carriers in cells would explain why uncoating protein is made in quantities equivalent to clathrin.

Adenosine Triphosphatases↗

PubMed1980

An effect of interferon on the uncoating of murine leukaemia virus not related to the antiviral state.

Adsorption of murine leukaemia virus (MLV) to NIH/3T3 cells, as determined by analysing its reverse transcriptase activity in the cell membrane, was found to be unaffected by interferon (IFN). Virus penetration and uncoating were followed by quantifying intracellular virions in terms of sedimentable reverse transcriptase activity in the cytoplasmic fraction. The penetrating virions were found to accumulate to a higher level in IFN-treated cells than in untreated controls. Intracellular virions were uncoated in untreated cells shortly after their penetration, whereas their uncoating was delayed in the IFN-treated cells for 2 to 3 h. Neither virus uncoating nor the effect of IFN on this process appeared to require new protein synthesis, since both were unaffected by cycloheximide (CH).

Animals↗

PubMed1980

Effect of human fibroblast interferon on uncoating and release of murine leukaemia virus in NIH/3T3 mouse cells.

The effect of human fibroblast interferon (IFN), a heterologous IFN, on the uncoating of murine leukaemia virus (MLV) was investigated in exogenously infected NIH/3T3 mouse cells. Virus uncoating was determined by following the disappearance of the penetrating virus particles from the cytoplasm of the infected cells. Intracellular virus particles were estimated by sedimenting them at high speed from the cytoplasmic fraction of the infected cells and assaying their reverse transcriptase activity. In untreated control cells, uncoating started immediately after penetration, but in cells treated with human IFN, uncoating was delayed for 2 to 3 h. This delay led to prolongation of the infectious cycle, with delayed release of progeny virus. The delay in release did not result from inhibition by IFN of the process of release, since in NIH/3T3 cells chronically infected with MLV, treatment with IFN had no effect on virus release.

Animals↗

PubMed1982

Uncoating of a rimantadine-resistant variant of influenza virus in the presence of rimantadine.

A rimantadine-resistant variant of the Texas strain of influenza virus (Tr) was obtained by serial passages in eggs in MDCK cells in the presence of the drug, and its uncoating in MDCK cells was compared to that of the sensitive variant (Ts). First and second steps of uncoating were defined respectively by the appearance of subviral particles (SVP) in nuclear-associated cytoplasm (NAC) and ribonucleoproteins (RNPs) in nucleoplasm. In cells infected with Ts, SVP and RNPs were revealed in NAC, while in the presence of rimantadine RNPs were neither found in NAC nor in the nucleoplasm. In cells infected with Tr, SVP but not RNPs were observed in NAC. The amount of RNPs in the nucleoplasm was almost unchanged in rimantadine-treated cells, demonstrating that rimantadine did not interfere with uncoating of the resistant variant. These findings confirm the suggestion that rimantadine blocks the second step of uncoating of sensitive influenza viruses, and are consistent with the idea that this event does account for the prevention of influenza virus infection by the drug.

Adamantane↗

PubMed2003

Hyperfine polarization and its normal gradient coefficient of (87)Rb atoms in the vicinity (approximately 10(-5) cm) of coated and uncoated Pyrex glass surfaces.

We have made regionally specific measurement of the hyperfine polarization of 87Rb atoms in the vicinity ( approximately 10(-5) cm) of coated and uncoated Pyrex glass surfaces. We find that the polarization near an uncoated surface decreases rapidly with decreasing distance from the surface whereas for a silicone-coated surface the polarization is independent of the distance from the surface. We have also determined the normal gradient coefficient micro (S.I) of the hyperfine polarization in uncoated cells. In a representative uncoated cell, at a Rb density 7.35 x 10(13) cm(-3) and a pump beam intensity 1.3 W/cm(2), we find micro(S.I)=24+/-7 microm(-1).

Journal Article↗

PubMed1995

WIN51711-resistant mutants of poliovirus type 3: capsid residues important in uncoating functions.

Capsid-binding drugs that inhibit the first stage of picornaviral uncoating were used to select drug-resistant mutants of the Sabin strain of poliovirus type 3. Such mutants provide information about parts of the capsid that are important for functions blocked by the drugs, and also about pathways to drug resistance. Amino-acid substitutions allowing virus to produce progeny in the presence of drug were mapped to 13 different residues occupying three distinct locations: (I) the canyon base; (II) the lining of the drug-binding pocket; and (III) the base of the protomer. These loci might be thought of as action points for transmitting the uncoating signal from receptor, through the pocket, and to the base of the protomer. All of the mutations in a special class of drug-dependent mutants were clustered at site (III) and all were hyperlabile, i.e., uncoated spontaneously (without receptor) at growth temperature unless prevented from doing so by the presence of drug in the pocket. Thus, site (III) seems to represent a kind of thermostat which regulates the temperature at which the uncoating transition (release of VP4 to form A particles) is triggered.

Journal Article↗

PubMed1992

Role of ribosomes in Semliki Forest virus nucleocapsid uncoating.

The mechanism by which Semliki Forest virus nucleocapsids are uncoated was analyzed in living cells and in vitro. In BHK-21 cells, uncoating occurred with virtually complete efficiency within 1 to 2 min after the nucleocapsids entered the cytoplasm. It was inhibited by monensin, which blocks nucleocapsid penetration from endosomes. As previously shown for Sindbis virus (G. Wengler and G. Wengler, Virology 134:435-442, 1984), the capsid proteins from incoming nucleocapsids became associated with ribosomes. The ribosome-bound capsid proteins were distributed throughout the cytoplasm, while the viral RNA remained associated with vacuolar membranes. Using purified nucleocapsids and ribosomes in vitro, we established that ribosomes alone were sufficient for uncoating. Their role was to release the capsid proteins from nucleocapsids and irreversibly sequester them, in a process independent of energy and translation. The process was stoichiometric rather than catalytic, with a maximum of three to six capsid proteins bound to each ribosome. More than 80% of the capsid proteins could thus be removed from the viral RNA, resulting in the formation of nucleocapsid remnants whose sedimentation coefficients progressively decreased from 140S to 80S as uncoating proceeded.

Animals↗

PubMed1998

Effect of bafilomycin A1 and nocodazole on endocytic transport in HeLa cells: implications for viral uncoating and infection.

Bafilomycin A1 (baf), a specific inhibitor of vacuolar proton ATPases, is commonly employed to demonstrate the requirement of low endosomal pH for viral uncoating. However, in certain cell types baf also affects the transport of endocytosed material from early to late endocytic compartments. To characterize the endocytic route in HeLa cells that are frequently used to study early events in viral infection, we used 35S-labeled human rhinovirus serotype 2 (HRV2) together with various fluid-phase markers. These virions are taken up via receptor-mediated endocytosis and undergo a conformational change to C-antigenic particles at a pH of <5.6, resulting in release of the genomic RNA and ultimately in infection (E. Prchla, E. Kuechler, D. Blaas, and R. Fuchs, J. Virol. 68:3713-3723, 1994). As revealed by fluorescence microscopy and subcellular fractionation of microsomes by free-flow electrophoresis (FFE), baf arrests the transport of all markers in early endosomes. In contrast, the microtubule-disrupting agent nocodazole was found to inhibit transport by accumulating marker in endosomal carrier vesicles (ECV), a compartment intermediate between early and late endosomes. Accordingly, lysosomal degradation of HRV2 was suppressed, whereas its conformational change and infectivity remained unaffected by this drug. Analysis of the subcellular distribution of HRV2 and fluid-phase markers in the presence of nocodazole by FFE revealed no difference from the control incubation in the absence of nocodazole. ECV and late endosomes thus have identical electrophoretic mobilities, and intraluminal pHs of <5.6 and allow uncoating of HRV2. As bafilomycin not only dissipates the low endosomal pH but also blocks transport from early to late endosomes in HeLa cells, its inhibitory effect on viral infection could in part also be attributed to trapping of virus in early endosomes which might lack components essential for uncoating. Consequently, inhibition of viral uncoating by bafilomycin cannot be taken to indicate a low pH requirement only.

Anti-Bacterial Agents↗

PubMed1985

A comparison of the ferruginous body and uncoated fiber content in the lungs of former asbestos workers.

Tissue samples from 12 former asbestos workers were digested and analyzed for ferruginous body and uncoated fiber populations. It was noted that there were large numbers of nonasbestos fibers in each of the samples. In some samples, these fibers constituted over 80% of the total uncoated fibers, and they could greatly influence the data as to asbestos content of the tissue unless differentiated by light and electron microscopic techniques, such as X-ray energy-dispersive analysis. There were great variations in the numbers of uncoated fibers per ferruginous body between the individual workers. The digested samples from lungs of 2 workers yielded no ferruginous bodies by light microscopy, even though these samples by electron microscopy contained respective loads of 780,000 and 1.2 million uncoated amphibole fibers per gram. Light microscopy examination of adjacent tissues confirmed mild fibrosis in both workers. Ferruginous bodies serve as a general marker for asbestos exposure. However, our data suggest that their absence in tissue with interstitial fibrosis from a worker with previous occupational exposure may not be sufficiently conclusive to rule out asbestos-induced disease. Rather, as shown by our data, individual exceptions may require correlated analysis by analytical electron microscopy in order to define particulate load and support the diagnosis of the disease.

Asbestos↗

PubMed1995

Selective action of uncoating ATPase towards clathrin-coated vesicles from brain.

Clathrin-coated vesicles from brain are primarily involved in synaptic vesicle recycling and are substrates for the constitutively expressed heat shock cognate hsc70 protein (uncoating ATPase). To investigate the regulation of clathrin coat turnover in other tissues the activity of hsc70 towards coated vesicles from other sources was examined. Concentrations of hsc70 which caused near-complete removal of clathrin from brain coated vesicles effected only partial uncoating of vesicles prepared from other tissues. The selective action of hsc70 could not be accounted for by tissue or species specificities of hsc70, but rather reflected differences in coat structure. Selective action was associated with two differences in the hsc70-dependent ATPase cycle. Firstly, uncoating of brain, but not placental vesicles, could occur under circumstances where ATP hydrolysis was prevented. Secondly, only brain coated vesicles could support multiple rounds of hsc70-dependent ATP hydrolysis. Implications of these findings for the mechanism of hsc70-dependent vesicle uncoating in non-neuronal cells and the organisation of the endocytic pathway in the axon are discussed.

Adenosine Triphosphate↗

PubMedDate not supplied

The treatment of uncoated and titanium nitride-coated abutments with different instruments.

PURPOSE: The aim of this in vitro study of titanium abutments was to investigate the extent of treatment traces, the roughness depth, and the quantity of titanium or, in the case of coated abutments, titanium nitride (TiN) removed from the surface after treatment with various instruments. MATERIALS AND METHODS: Eleven uncoated, mechanically smoothed abutments and 11 TiN-coated abutments were used. The abutments were treated with titanium, steel, and plastic curettes; a rubber cup; an ultrasonic scaler with a steel tip; and an air scaler and cleaning powder. There were two 2 x 2-mm test fields on each abutment; each was subjected to standardized treatment with an instrument. The untreated surfaces of each abutment served as controls. The roughness depth (Rz) and profile height of treated and untreated surfaces were measured with a profilometer; profile height served as a basis for determining the amount of substance removed by treatment. The treatment traces were analyzed by scanning electron microscopy and light microscopy. RESULTS: Both the ultrasonic scaler and the steel and titanium curettes left pronounced traces on the uncoated abutments and increased Rz. Substantial substance removal was recorded following the use of the ultrasonic scaler (17.57 +/- 2.87 microm) and the steel curettes (8.48 +/- 2.81 microm) on the uncoated abutments. In tests of the coated abutments, measurable substance removal (4.80 +/- 0.99 microm) and increased roughness depth were noted only with use of the steel curettes. The treatment traces left by the other instruments were distinctly less pronounced than on the uncoated abutments. Light microscopy revealed detachment of the TiN coating after use of the ultrasonic scaler, titanium curettes, and steel curettes. Slight to moderate treatment traces were recorded after use of the rubber cup; no substance removal was observed. On the TiN-coated abutments, only slight treatment traces, if any, were recorded, and there was no substance removal. A planing effect (ie, an Rz decrease of 66.4%) was observed. The plastic curette and the air scaler caused no damage to the titanium or TiN surfaces. DISCUSSION AND CONCLUSION: The TiN-coated abutments displayed fewer treatment traces, less roughness depth, and less substance removal after being treated with various instruments. Two concerns, however, are the detachment of the coating after only few actions with steel and titanium curettes or with an ultrasonic scaler with steel tip, and the greater initial roughness depth of coated implants.

Air↗

PubMed2005

Haemocompatibility of polymer-coated stainless steel stents as compared to uncoated stents.

Acute and subacute stent thrombosis still represent an unsolved problem in connection with endovascular stents. For this reason coatings are tested now with the intention to reduce thrombogenicity of stainless steel surfaces. This comparative study examined whether a polymeric stent coating affected the haemocompatibility of a stainless steel stent. For compatibility testing, coated and non-coated stents were implanted in a low-grade thrombogenic closed-loop system perfused with platelet rich plasma at shear rates far below the threshold value at which shear-rate-induced activation of thrombocytes occurs. After 21 circulations of the filling volume (exposure time: 6.2 min), the number of single circulating platelets in the perfusion system with uncoated stainless steel stents decreased almost twice as much as was the case with polymer-coated stents. This is thought to indicate that more thrombocytes had adhered to the uncoated stainless steel stent, or that the thrombocytes were clustered in circulating aggregates. Parallel to the platelet aggregation/adherence, a release reaction took place, as was evident from the TAT complexes indicating the generation of thrombin. In the case of the implantation of uncoated stainless steel stents, both the number of activated circulating thrombocytes and the level of platelet reactivity (number of thrombocytes circulating in the plasma as aggregates) were notably higher than in the system with polymer-coated stents. At the same time it should be noted that the activation or aggregation is almost wholly attributable to the exogenic surface of the implanted stent, since activation due to the tube system or to shear rate can be excluded (as shown by measurements of the system without a stent). In addition to activation of the thrombocytes, a notable increase in the number of receptors per platelet (significant only in the system with the uncoated stent) took place. This supports both the adherence of the thrombocytes and their readiness to aggregate, since more receptors (docking places for ligands) are available. The better haemocompatibility of the polymer-coated stents, as verified in the laboratory, was also evident under microscopic examination of the explanted stents following the perfusion tests.

Blood Platelets↗