Rod Fragments Research Articles

Temperature effect on the thermal-physical properties of fire-protective mineral wool cladding of steel structures under the conditions of fire resistance tests

The value of the thermal conductivity coefficient depending on the temperature of the samples of steel rod fragments with fire-retardant cladding has been determined in the present research. The thermal conductivity coefficient of mineral wool fire-retardant cladding was determined; special patterns of its dependence on temperature were revealed. This is explained by the thermal decomposition with the release of thermal energy of inclusions between the fibers of mineral wool and its fibers at a temperature of 750 °C. The apparent minimum of the thermal conductivity factor for fire-retardant mineral wool cladding with a thickness of more than 50 mm is observed at a temperature of about 100 °C. This happens due to the fact that at this temperature the free moisture contained between the fibers of the mineral wool evaporates. Generalized temperature dependence of the thermal conductivity coefficient of mineral wool fire-retardant cladding has also been derived, in a tabular form. It can be used for calculating the temperature in steel structures with such fire protection. The thickness range for application is up to 80 mm for the specific heat capacity of 1,000 J/(kg °C) and a density of 200 kg/m 3 . It is shown how the obtained dependence can be used for predicting heating in steel structures with fire-retardant mineral wool cladding. The relative error between the calculated and experimental data was calculated. The Cochrane, Student, and Fischer criteria for the results of temperature calculation in steel structures with fire-retardant mineral wool cladding between the calculated and experimental data accept values that do not exceed the tabular quantities. This means that the results of the calculation using the obtained temperature dependence of the thermal conductivity coefficient are adequate

Addressing the Molecular Mechanism of Longitudinal Lamin Assembly Using Chimeric Fusions.

The molecular architecture and assembly mechanism of intermediate filaments have been enigmatic for decades. Among those, lamin filaments are of particular interest due to their universal role in cell nucleus and numerous disease-related mutations. Filament assembly is driven by specific interactions of the elementary dimers, which consist of the central coiled-coil rod domain flanked by non-helical head and tail domains. We aimed to investigate the longitudinal ‘head-to-tail’ interaction of lamin dimers (the so-called ACN interaction), which is crucial for filament assembly. To this end, we prepared a series of recombinant fragments of human lamin A centred around the N- and C-termini of the rod. The fragments were stabilized by fusions to heterologous capping motifs which provide for a correct formation of parallel, in-register coiled-coil dimers. As a result, we established crystal structures of two N-terminal fragments one of which highlights the propensity of the coiled-coil to open up, and one C-terminal rod fragment. Additional studies highlighted the capacity of such N- and C-terminal fragments to form specific complexes in solution, which were further characterized using chemical cross-linking. These data yielded a molecular model of the ACN complex which features a 6.5 nm overlap of the rod ends.

Liquid Crystal Ordering in the Hexagonal Phase of Rod-Coil Diblock Copolymers.

Density functional theory of rod-coil diblock copolymers, developed recently by the authors, has been generalised and used to study the liquid crystal ordering and microphase separation effects in the hexagonal, lamellar and nematic phases. The translational order parameters of rod and coil monomers and the orientational order parameters of rod-like fragments of the copolymer chains have been determined numerically by direct minimization of the free energy. The phase diagram has been derived containing the isotropic, the lamellar and the hexagonal phases which is consistent with typical experimental data. The order parameter profiles as functions of temperature and the copolymer composition have also been determined in different anisotropic phases. Finally, the spatial distributions of the density of rigid rod fragments and of the corresponding orientational order parameter in the hexagonal phase have been calculated.

Force-Induced Calpain Cleavage of Talin Is Critical for Growth, Adhesion Development, and Rigidity Sensing.

Cell growth depends upon formation of cell-matrix adhesions, but mechanisms detailing the transmission of signals from adhesions to control proliferation are still lacking. Here, we find that the scaffold protein talin undergoes force-induced cleavage in early adhesions to produce the talin rod fragment that is needed for cell cycle progression. Expression of noncleavable talin blocks cell growth, adhesion maturation, proper mechanosensing, and the related property of EGF activation of motility. Further, the expression of talin rod in the presence of noncleavable full-length talin rescues cell growth and other functions. The cleavage of talin is found in early adhesions where there is also rapid turnover of talin that depends upon calpain and TRPM4 activity as well as the generation of force on talin. Thus, we suggest that an important function of talin is its control over cell cycle progression through its cleavage in early adhesions.

Design considerations in coiled-coil fusion constructs for the structural determination of a problematic region of the human cardiac myosin rod.

X-ray structural determination of segments of the myosin rod has proved difficult because of the strong salt-dependent aggregation properties and repeating pattern of charges on the surface of the coiled-coil that lead to the formation of paracrystals. This problem has been resolved in part through the use of globular assembly domains that improve protein folding and prevent aggregation. The primary consideration now in designing coiled-coil fusion constructs for myosin is deciding where to truncate the coiled-coil and which amino acid residues to include from the folding domain. This is especially important for myosin that contains numerous regions of low predicted coiled-coil propensity. Here we describe the strategy adopted to determine the structure of the region that extends from Arg1677 - Leu1797 that included two areas that do not show a strong sequence signature of a conventional left-handed coiled coil or canonical heptad repeat. This demonstrates again that, with careful choice of fusion constructs, overlapping structures exhibit very similar conformations for the myosin rod fragments in the canonical regions. However, conformational variability is seen around Leu1706 which is a hot spot for cardiomyopathy mutations suggesting that this might be important for function.

Study on Scattering Process of Preformed Rod Fragment

By theoretical analysis and simulation on the scattering process and characteristic parameter of preformed rod fragment, dynamitic and static dispersion angle of preformed rod fragment is derivate. The theoretical research shows: the velocity of warhead is a important influence factor in analysis the scattering process of preformed rod fragment. The results of theoretical model are validated by numerical simulation, which can be provided theoretical assessment to target damage.

Removal analyses of chip and rod in rotary ultrasonic-assisted drilling of carbon fiber-reinforced plastics using core drill

Carbon fiber-reinforced plastics (CFRP) have been widely applied in aerospace industry as structural components due to their excellent mechanical and physical properties. Meanwhile, the drilling process is indispensable for machining the assembly holes of CFRP. However, in the conventional drilling process of CFRP, it is prone to produce the defects including delamination, spalling, fuzzing, and tool wear. In recent years, the rotary ultrasonic-assisted drilling (RUAD) with diamond core drill, as a novel machining method, has been employed to reduce the defects. But this is few reported investigations on chip adhesion of tool surface and machined rod jamming into core drill tool during RUAD of CFRP. Therefore, this paper detailedly reported a study on removal analyses of chip and rod in RUAD of CFRP using core drill under no cooling condition for the first time. To begin with, the principle analysis on RUAD of CFRP was presented to illustrate the removal process of chip and rod. And then, the experiment analysis on RUAD of CFRP was carried out to observe the removal effects of chip and rod. The experimental results indicated that compared with the common drilling of core drill, when the vibration amplitude reached 5.0 and 7.5 µm in RUAD, the cutting ability of core drill tool was greatly enhanced, excellent removal effects of chip and rod were obtained, which obviously reduced the chip adhesion, rod jamming, rod fragmentation, thrust force, cutting temperature, and surface roughness, improved the dimensional accuracy of machined hole and rod diameter, prolonged the tool life, as well as acquired superior surface integrity of machined hole and flat fibers fracture surfaces. Furthermore, the experimental results also validated the accuracy of the principle analysis.

More singular? Self-similar dynamics of damage localization and instability in dynamic fracture

Dynamic fracture instability is studied for three characteristic statements: dynamic crack propagation, dynamic fragmentation and failure wave initiation to combine theoretical interpretation and “in-situ” high resolution experimental data for dynamically loaded quasi-brittle materials (PMMA, glasses, ceramics and fused quartz). Specific type of criticality (the structural-scaling transitions) was established in solid with defects in terms of two structural variables: defect density tensor (defect induced strain) and structural scaling parameter. Two critical values for structural scaling parameter were found that separate characteristic nonlinearity of free energy release in damage kinetic equation that allowed one to establish specific self-similar solution (blow-up dissipative structures) responsible for final stage of damage localization and crack initiation. The set of spatial scales of damage localization (that has the image of mirror zones) and corresponding “incubation” time follow from the self-similar solution as the “eigen-values” of non-linear problem. Different scenario of instability of dynamic fracture in mentioned experiments were analyzed as nonlinear dynamic problem in the presence of two self-similar solutions (two attractors): intermediate asymptotical solution for stress field in crack process zone (as the basement for stress intensity factor) and the set of blow-up self-similar solutions for damage localization kinetics playing the role of collective modes of damage localization. Theoretically predicted flicker noise temporal-spatial statistics was found in dynamic experiments for fused quartz and ceramic rod fragmentation combined with fracto-luminescence recording and analysis of fragment statistics. Resonance excitation of blow-up modes allowed explanation of self-similar pattern of multiple spall kinetics (“dynamic branch” under spall) due to “resonance” excitation of blow-up damage localization kinetics.

Fractal statistics of brittle fragmentation

The study of fragmentation statistics of brittle materials that includes four types of experiments is presented. Data processing of the fragmentation of glass plates under quasi-static loading and the fragmentation of quartz cylindrical rods under dynamic loading shows that the size distribution of fragments (spatial quantity) is fractal and can be described by a power law. The original experimental technique allows us to measure, apart from the spatial quantity, the temporal quantity - the size of time interval between the impulses of the light reflected from the newly created surfaces. The analysis of distributions of spatial (fragment size) and temporal (time interval) quantities provides evidence of obeying scaling laws, which suggests the possibility of selforganized criticality in fragmentation.&nbsp

Nuclear fuel rod fragmentation under accidental conditions

This paper deals with fuel rod fragmentation during a core meltdown accident in a Nuclear Power Plant. If water is injected on the degraded core to stop the degradation, embrittled fuel rods may crumble to form a reactor debris bed. The size and the morphology of the debris are two key parameters which determine in particular heat transfer and flow friction in the debris bed and as a consequence its coolability. To address this question, a bibliographic survey is performed with the aim of evaluating the size and the surface area of the fragments resulting from fuel rod fragmentation. On this basis, a model to estimate the mean particle diameter obtained in a reflooded degraded core is proposed. Modelling results show that the particle size distribution is very narrow if we only take into account fuel cracking resulting from normal operating conditions. It leads to minimum mean diameters of 2.5mm (for fuel particles), 1.35mm (for cladding particles) and 2mm (for the mixing of cladding and fuel fragments). These results are obtained with fuel rods of 9.5mm outer diameter and cladding thickness of 570μm. The particle size distribution is larger if fine fragmentation of the highly irradiated fuel rods during temperature rise is accounted for. This is illustrated with the computation by the severe accident code ASTEC, codeveloped by IRSN abd GRS, of the size of the debris expected to form in case of reflooding of a French 900MW reactor core during a core meltdown accident.

Precursor and Oxygen Dependence of the Unidirectional, Seeded Growth of CdSe Nanorods

It was recently shown that, by controlling the O(2) concentration, the seeded-growth of CdSe nanocrystals (NC) can be manipulated to proceed either unidirectionally (from the (0001) facet) or three-dimensionally. In this contribution, we investigate two new Se precursors (i.e. SeO(2) and NaHSe) and compare them with Se obtained from etching of smaller NC seeds. Under anaerobic conditions, both precursors led to successful 3-dimensional (3D) NC growth. At high O(2) concentrations, the seeded growth of rods was enhanced by the NaHSe precursor, while impeded by the use of SeO(2). Mechanistic studies showed that the reduction of SeO(2) to Se(2-) produces an excessive amount of O(2). This leads to rod fragmentation due to etching as well as the production of deep traps that quench their luminescence. These new precursors, along with a heightened understanding of oxygen's role, expand the synthetic repertoire of the redox-assisted, seeded-growth of CdSe and better position this low temperature (125 °C) methodology towards realizing advanced NC heterostructures.

Talin Contains A C-Terminal Calpain2 Cleavage Site Important In Focal Adhesion Dynamics

Talin is a large (∼2540 residues) dimeric adaptor protein that associates with the integrin family of cell adhesion molecules in cell-extracellular matrix junctions (focal adhesions; FAs), where it both activates integrins and couples them to the actin cytoskeleton. Calpain2-mediated cleavage of talin between the head and rod domains has previously been shown to be important in FA turnover. Here we identify an additional calpain2-cleavage site that removes the dimerisation domain from the C-terminus of the talin rod, and show that an E2492G mutation inhibits calpain cleavage at this site in vitro, and increases the steady state levels of talin1 in vivo. Expression of a GFP-tagged talin1 E2492G mutant in CHO.K1 cells inhibited FA turnover and the persistence of cell protrusion just as effectively as a L432G mutation that inhibits calpain cleavage between the talin head and rod domains. Moreover, incorporation of both mutations into a single talin molecule had an additive effect clearly demonstrating that calpain cleavage at both the N- and C-terminal regions of talin contribute to the regulation of FA dynamics. However, the N-terminal site was more sensitive to calpain cleavage suggesting that lower levels of calpain are required to liberate the talin head and rod fragments than are needed to clip off the C-terminal dimerisation domain. The talin head and rod liberated by calpain2 cleavage have recently been shown to play roles in an integrin activation cycle important in FA turnover and in FAK-dependent cell cycle progression respectively. The half-life of the talin head is tightly regulated by ubiquitination and we suggest that removal of the C-terminal dimerisation domain from the talin rod may provide a mechanism both for terminating the signalling function of the talin rod and indeed for inactivating full-length talin thereby promoting FA turnover at the rear of the cell.

Asymmetric Mode of Ca2+-S100A4 Interaction with Nonmuscle Myosin IIA Generates Nanomolar Affinity Required for Filament Remodeling

SummaryFilament assembly of nonmuscle myosin IIA (NMIIA) is selectively regulated by the small Ca2+-binding protein, S100A4, which causes enhanced cell migration and metastasis in certain cancers. Our NMR structure shows that an S100A4 dimer binds to a single myosin heavy chain in an asymmetrical configuration. NMIIA in the complex forms a continuous helix that stretches across the surface of S100A4 and engages the Ca2+-dependent binding sites of each subunit in the dimer. Synergy between these sites leads to a very tight association (KD ∼1 nM) that is unique in the S100 family. Single-residue mutations that remove this synergy weaken binding and ameliorate the effects of S100A4 on NMIIA filament assembly and cell spreading in A431 human epithelial carcinoma cells. We propose a model for NMIIA filament disassembly by S100A4 in which initial binding to the unstructured NMIIA tail initiates unzipping of the coiled coil and disruption of filament packing.

Mutations in Drosophila Myosin Rod Cause Defects in Myofibril Assembly

The roles of myosin during muscle contraction are well studied, but how different domains of this protein are involved in myofibril assembly in vivo is far less understood. The indirect flight muscles (IFMs) of Drosophila melanogaster provide a good model for understanding muscle development and function in vivo. We show that two missense mutations in the rod region of the myosin heavy-chain gene, Mhc, give rise to IFM defects and abnormal myofibrils. These defects likely result from thick filament abnormalities that manifest during early sarcomere development or later by hypercontraction. The thick filament defects are accompanied by marked reduction in accumulation of flightin, a myosin binding protein, and its phosphorylated forms, which are required to stabilise thick filaments. We investigated with purified rod fragments whether the mutations affect the coiled-coil structure, rod aggregate size or rod stability. No significant changes in these parameters were detected, except for rod thermodynamic stability in one mutation. Molecular dynamics simulations suggest that these mutations may produce localised rod instabilities. We conclude that the aberrant myofibrils are a result of thick filament defects, but that these in vivo effects cannot be detected in vitro using the biophysical techniques employed. The in vivo investigation of these mutant phenotypes in IFM development and function provides a useful platform for studying myosin rod and thick filament formation generically, with application to the aetiology of human myosin rod myopathies.

Enucleation of human erythroblasts involves non-muscle myosin IIB

AbstractMammalian erythroblasts undergo enucleation, a process thought to be similar to cytokinesis. Although an assemblage of actin, non-muscle myosin II, and several other proteins is crucial for proper cytokinesis, the role of non-muscle myosin II in enucleation remains unclear. In this study, we investigated the effect of various cell-division inhibitors on cytokinesis and enucleation. For this purpose, we used human colony-forming unit-erythroid (CFU-E) and mature erythroblasts generated from purified CD34+ cells as target cells for cytokinesis and enucleation assay, respectively. Here we show that the inhibition of myosin by blebbistatin, an inhibitor of non-muscle myosin II ATPase, blocks both cell division and enucleation, which suggests that non-muscle myosin II plays an essential role not only in cytokinesis but also in enucleation. When the function of non-muscle myosin heavy chain (NMHC) IIA or IIB was inhibited by an exogenous expression of myosin rod fragment, myosin IIA or IIB, each rod fragment blocked the proliferation of CFU-E but only the rod fragment for IIB inhibited the enucleation of mature erythroblasts. These data indicate that NMHC IIB among the isoforms is involved in the enucleation of human erythroblasts.

Dynamic assembly properties of nonmuscle myosin II isoforms revealed by combination of fluorescence correlation spectroscopy and fluorescence cross-correlation spectroscopy

Myosin II molecules assemble into filaments through their C-terminal rod region, and are responsible for several cellular motile activities. Three isoforms of nonmuscle myosin II (IIA, IIB and IIC) are expressed in mammalian cells. However, little is known regarding the isoform composition in filaments. To obtain new insight into the assembly properties of myosin II isoforms, especially regarding the isoform composition in filaments, we performed a combination analysis of fluorescence correlation spectroscopy (FCS) and fluorescence cross-correlation spectroscopy (FCCS), which enables us to acquire information on both the interaction and the size of each molecule simultaneously. Using C-terminal rod fragments of IIA and IIB (ARF296 and BRF305) labelled with different fluorescent probes, we demonstrated that hetero-assemblies were formed from a mixture of ARF296 and BRF305, and that dynamic exchange of rod fragments occurred between preformed homo-assemblies of each isoform in an isoform-independent manner. We also showed that Mts1 (S100A4) specifically stripped ARF296 away from the hetero-assemblies, and consequently, homo-assemblies of BRF305 were formed. These results suggest that IIA and IIB can form hetero-filaments in an isoform-independent manner, and that a factor like Mts1 can remove one isoform from the hetero-filament, resulting in a formation of homo-filaments consisting of another isoform.

Myosin II Tailpiece Determines Its Paracrystal Structure, Filament Assembly Properties, and Cellular Localization

Non muscle myosin II (NMII) is a major motor protein present in all cell types. The three known vertebrate NMII isoforms share high sequence homology but play different cellular roles. The main difference in sequence resides in the C-terminal non-helical tailpiece (tailpiece). In this study we demonstrate that the tailpiece is crucial for proper filament size, overcoming the intrinsic properties of the coiled-coil rod. Furthermore, we show that the tailpiece by itself determines the NMII filament structure in an isoform-specific manner, thus providing a possible mechanism by which each NMII isoform carries out its unique cellular functions. We further show that the tailpiece determines the cellular localization of NMII-A and NMII-B and is important for NMII-C role in focal adhesion complexes. We mapped NMII-C sites phosphorylated by protein kinase C and casein kinase II and showed that these phosphorylations affect its solubility properties and cellular localization. Thus phosphorylation fine-tunes the tailpiece effects on the coiled-coil rod, enabling dynamic regulation of NMII-C assembly. We thus show that the small tailpiece of NMII is a distinct domain playing a role in isoform-specific filament assembly and cellular functions.

Structural Determinants of Integrin Binding to the Talin Rod

The adaptor protein talin serves both to activate the integrin family of cell adhesion molecules and to couple integrins to the actin cytoskeleton. Integrin activation has been shown to involve binding of the talin FERM domain to membrane proximal sequences in the cytoplasmic domain of the integrin β-subunit. However, a second integrin-binding site (IBS2) has been identified near the C-terminal end of the talin rod. Here we report the crystal structure of IBS2 (residues 1974-2293), which comprises two five-helix bundles, “IBS2-A” (1974-2139) and “IBS2-B” (2140-2293), connected by a continuous helix with a distinct kink at its center that is stabilized by side-chain H-bonding. Solution studies using small angle x-ray scattering and NMR point to a fairly flexible quaternary organization. Using pull-down and enzyme-linked immunosorbent assays, we demonstrate that integrin binding requires both IBS2 domains, as does binding to acidic phospholipids and robust targeting to focal adhesions. We have defined the membrane proximal region of the integrin cytoplasmic domain as the major binding region, although more membrane distal regions are also required for strong binding. Alanine-scanning mutagenesis points to an important electrostatic component to binding. Thermal unfolding experiments show that integrin binding induces conformational changes in the IBS2 module, which we speculate are linked to vinculin and membrane binding.

Anterior scoliosis rod migration to the lower extremity

Background context Scoliosis rod migration has been reported rarely in the literature. We present a case study on three patients with distant migration of anterior scoliosis rod implants. Purpose To report an unusual complication of rod migration of anterior retroperitoneally implanted scoliosis rods in three patients. Study design/setting A retrospective case report. Methods Radiographic analysis. Results Asymptomatic rod migration occurred from the anterior spine to the lower extremity in two cases and to the retroperitoneal space in the third case. The rod fragment appeared in the lower extremity in two cases and was removed through a small skin incision in the extremity. The average time from scoliosis surgery until the rods were found at a distant site was 9 years. Conclusions The scoliosis surgery was effective in preventing further deformity; however, in two cases there was nonunion at one or two levels. Patients are asymptomatic at the present time and followed at regular intervals to see if further surgery is necessary to correct areas of nonunion.

How Force Might Activate Talin's Vinculin Binding Sites: SMD Reveals a Structural Mechanism

Upon cell adhesion, talin physically couples the cytoskeleton via integrins to the extracellular matrix, and subsequent vinculin recruitment is enhanced by locally applied tensile force. Since the vinculin binding (VB) sites are buried in the talin rod under equilibrium conditions, the structural mechanism of how vinculin binding to talin is force-activated remains unknown. Taken together with experimental data, a biphasic vinculin binding model, as derived from steered molecular dynamics, provides high resolution structural insights how tensile mechanical force applied to the talin rod fragment (residues 486–889 constituting helices H1–H12) might activate the VB sites. Fragmentation of the rod into three helix subbundles is prerequisite to the sequential exposure of VB helices to water. Finally, unfolding of a VB helix into a completely stretched polypeptide might inhibit further binding of vinculin. The first events in fracturing the H1–H12 rods of talin1 and talin2 in subbundles are similar. The proposed force-activated α-helix swapping mechanism by which vinculin binding sites in talin rods are exposed works distinctly different from that of other force-activated bonds, including catch bonds.