Search

The goal of the present research is to introduce the Tungsten (W) nanoparticles as reinforcement into Al 6063 alloy to produce Al–W nanocomposites by the FSP technique. The vol% of the reinforcement was varied from 3 to 12 with a step of 3, besides the unreinforced Al matrix was considered as 0 vol% for comparison. The role of W nanoparticles in the Al 6063 matrix has been exhaustively investigated using advanced characterization techniques such as XRD analysis to observe the phases, FESEM to detect the distribution of reinforcements with their interparticle spacing and the average grain sizes, TEM analysis to study the strengthening factors, new phase formation at the interface between AA 6063 matrix and W particles, the morphology of the W nanoparticles. The achieved average matrix grains size was 42, 2, and 0.9 μm for 0, 6, and 12 vol% W nanocomposites, respectively. The obtained results disclosed the uniform dispersion of W nanoparticles, without any agglomeration, and with the absence of intermetallic compounds. The hardness and wear resistance of the fabricated nanocomposites were increased incommensurate with the incorporation of heavy metallic W element as reinforcement particle; which was due to the proper dispersion of W nanoparticles, refinement of matrix grains to ultrafine level, generation of dislocations, and clear interface between Al 6063 matrix and W nanoparticles. In a nutshell, AA 6063–12 vol% W nanocomposite has achieved the higher hardness (120 HV), lower wear rate (0.13 mm3/m), and friction coefficient (0.33) than other nanocomposites The goal of the present research is to introduce the Tungsten (W) nanoparticles as reinforcement into Al 6063 alloy to produce Al–W nanocomposites by the FSP technique. The vol% of the reinforcement was varied from 3 to 12 with a step of 3, besides the unreinforced Al matrix was considered as 0 vol% for comparison. The role of W nanoparticles in the Al 6063 matrix has been exhaustively investigated using advanced characterization techniques such as XRD analysis to observe the phases, FESEM to detect the distribution of reinforcements with their interparticle spacing and the average grain sizes, TEM analysis to study the strengthening factors, new phase formation at the interface between AA 6063 matrix and W particles, the morphology of the W nanoparticles. The achieved average matrix grains size was 42, 2, and 0.9 μm for 0, 6, and 12 vol% W nanocomposites, respectively. The obtained results disclosed the uniform dispersion of W nanoparticles, without any agglomeration, and with the absence of intermetallic compounds. The hardness and wear resistance of the fabricated nanocomposites were increased incommensurate with the incorporation of heavy metallic W element as reinforcement particle; which was due to the proper dispersion of W nanoparticles, refinement of matrix grains to ultrafine level, generation of dislocations, and clear interface between Al 6063 matrix and W nanoparticles. In a nutshell, AA 6063–12 vol% W nanocomposite has achieved the higher hardness (120 HV), lower wear rate (0.13 mm3/m), and friction coefficient (0.33) than other nanocomposites.The goal of the present research is to introduce the Tungsten (W) nanoparticles as reinforcement into Al 6063 alloy to produce Al–W nanocomposites by the FSP technique. The vol% of the reinforcement was varied from 3 to 12 with a step of 3, besides the unreinforced Al matrix was considered as 0 vol% for comparison. The role of W nanoparticles in the Al 6063 matrix has been exhaustively investigated using advanced characterization techniques such as XRD analysis to observe the phases, FESEM to detect the distribution of reinforcements with their interparticle spacing and the average grain sizes, TEM analysis to study the strengthening factors, new phase formation at the interface between AA 6063 matrix and W particles, the morphology of the W nanoparticles. The achieved average matrix grains size was 42, 2, and 0.9 μm for 0, 6, and 12 vol% W nanocomposites, respectively. The obtained results disclosed the uniform dispersion of W nanoparticles, without any agglomeration, and with the absence of intermetallic compounds. The hardness and wear resistance of the fabricated nanocomposites were increased incommensurate with the incorporation of heavy metallic W element as reinforcement particle; which was due to the proper dispersion of W nanoparticles, refinement of matrix grains to ultrafine level, generation of dislocations, and clear interface between Al 6063 matrix and W nanoparticles. In a nutshell, AA 6063–12 vol% W nanocomposite has achieved the higher hardness (120 HV), lower wear rate (0.13 mm3/m), and friction coefficient (0.33) than other nanocomposites.

Biodiesel from waste cooking oil (WCO) can be used successfully in raising the cost of raw materials and in addressing the waste oil disposal issue. Biodiesel can be produced from WCO using ionic acid as a catalyst. Alkaline-based catalysts are commonly used to catalyze transesterification reactions. Still, direct use of WCO is not possible practically because WCO containing high free fatty acids due to layer isolation and saponification issues. The WCO may be used as a raw material for biodiesel processing, explaining their various fatty acids. The catalyst reused with high-yield output and their physicochemical properties is correlated with existing standards. This transesterification reaction's kinetic study is evaluated and followed the first-order reaction mechanism. The usage of biodiesel from WCO utilizing ionic liquids as a catalyst is discussed here.

Metal-organic frameworks (MOFs) are a type of materials that, because of their high contact area, controllable structures, and porous tone dimensions, have been attracted enormous attention over the past two decades. MOFs range from conventional gas separation and storage, drug distribution, sensors, and catalysis to modern technologies for energy storage, such as high-energy rechargeable battery power, and supercapacitors. High-energy batteries and high-power supercapacitors are critical for potential mobile devices, electric vehicles, unmanned aircraft, and so on. However, in particular, in electric fields, the insulating aspect of MOFs is often recognized as a limiting factor in the expansion of their applications. Specific functional or conducting materials were intercalated with MOFs because of these limitations, in order to improve their ability for such applications. In this context the uses of MOF-based materials for batteries and supercapacitors are discussed in this chapter.

An increase in tensile strength without compromising the ductility is an uphill task in the fabrication of MMCs. This issue can be overwhelmed by the addition of high temperature withstanding metallic nano-particles limiting solubility at elevated temperatures. The present research work concentrates on (a) the development of AA 6063 alloy reinforced with Tungsten nanoparticles (0, 3, 6, 9, and 12 vol%) via FSP, (b) examining the phase analysis using XRD technique, and microstructural evolutions through TEM and EBSD, (c) the improvement in mechanical properties (hardness and tensile strength) and investigate the contribution of strengthening mechanisms, and (d) the work hardening rate, intercept (k) and strain hardening exponents (n) through True stress-strain curves. The results revealed that the uniform dispersion of W nanoparticles is consistent across the stir zone (SZ) of the AA 6063 matrix. Tensile results were witnessed as improvement in UTS with the function of W nanoparticles addition and by elucidating the major loss in ductility. The dispersion strengthening has influenced more to the total strength of the fabricated MMCs due to the pinning effect produced by nano W particles. AA 6063 alloy reinforced with 12 vol% nano W particle specimen has produced superior mechanical properties (Vickers hardness strength of 1.23 GPa, UTS of 432.58 MPa and, elongation of 18.5%.

Large steam turbines used for electrical power generation demand governing systems of very high integrity (safety) and availability. The latest generation of electronic governors uses microprocessors in a distributed, two level architecture to achieve the required integrity and availability and in addition provides greater configuration flexibilities and wider facilities than earlier governors. Rolling element bearings are one of the major machinery components used in industries like power plants, chemical plants and automotive industries that require precise and efficient performance. Vibration monitoring and analysis is useful tool in the field of predictive maintenance in small hydro electric power plants. Health of rolling element bearings can be easily identified using vibration monitoring because vibration signature reveals important information about the fault development within them. Numbers of vibration analysis techniques are being used to diagnosis of rolling element bearings faults. This paper proposes a new signal feature extraction and fault diagnosis method for fault diagnosis of low-speed machinery. Initially, the proposed work explores the Continuous Wavelet Transform (CWT) to adaptively remove the exact noises from vibration analysis and then feature extraction is performed by exploiting the noise removed pre-processed data. Statistic filter (SF) and Hilbert transform (HT) are combined with moving-peak-hold method (M-PH) to extract features of a fault signal, and Special bearing diagnostic symptom parameters (SSPs) in a frequency domain that are sensitive to bearing fault diagnosis are defined to recognize fault types. The SF is first used to adaptively cancel noises, and then fault detection is performed by exploiting the optimum symptom parameters in a time domain to identify a normal or fault state. For precise diagnosis, the SSPs are calculated after the signals are processed by M-PH and HT.

SummaryTissue factor pathway inhibitor (TFPI) plays an important role in regulating tissue factor (TF)-initiated blood coagulation. Since serum stimulation of fibroblasts, vascular smooth muscle cells and cardiac myocytes in culture increases the expression of TF mRNA and antigen (Ag) in these cells, we hypothesized that serum may also induce increased synthesis of TFPI in these cells to regulate the TF-induced extravascular clotting at an injury site. To test this concept, we used primary isolates of the following human cell types – fetal and adult lung fibroblasts, pulmonary and aortic smooth muscle cells, and cardiac myocytes. Serum-stimulation of these cells resulted in an increased expression of TF mRNA and Ag (8 to10-fold). Upon serum stimulation, expression of TFPI mRNA and Ag was also increased in these cells. However, the increase in TFPI-Ag (6 to 8-fold) was significantly greater than the TFPI mRNA (2 to 3-fold). Notably, increased expression of TFPI persisted after the TF expression had declined. Further, increased synthesis of TFPI initially led to the saturation of heparin-releasable binding sites. TFPI-Ag was detected by Western blotting, 35S-metabolic labeling and activity assays on the conditioned media, heparin-released material from cells, and in cell lysates. TFPI-Ag was also detected by immunofluorescence staining of cells. Actinomycin D partially whereas cycloheximide completely prevented the serum-induced increased expression of TFPI synthesis by these cells, suggesting control primarily at the translational but some at the transcriptional level as well. The Mr of undegraded TFPI in all cases was ~45 kDa and was of full length. TFPI synthesized locally by fibroblasts, vascular smooth muscle cells and cardiac myocytes could play a significant role in regulating TF-initiated extravascular clotting especially since plasma TFPI that may be available at the injury site lacks a portion of the carboxyl segment and is a less efficient inhibitor.

SummaryUnder normal physiologic conditions, tissue factor pathway inhibitor (TFPI) is synthesized primarily by the microvascular endothelium. Using Northern blotting, we studied its transcriptional expression in different organs and compared it with the expression of two other endothelial specific proteins, namely thrombomodulin (TM) and von Willebrand factor (vWF). The order of mRNA expression for each protein was: TFPI–placenta>lung>liver>kidney>heart>skeletal muscle≥pancreas>brain; TM–heart>pancreas>lung>skeletal muscle>kidney≥liver>placenta>brain; and vWF–heart>skeletal muscle>pancreas>lung≥kidney>placenta>brain>liver. Notably, heart expressed TM and vWF mRNA in large amounts and only small amounts of TFPI whereas lung expressed all three mRNAs in significant amounts. Placenta, on the contrary, expressed large amounts of TFPI but only small amounts of TM and vWF mRNAs. Brain by this technique was found to express undetectable amounts of TFPI and TM mRNAs but small amounts of vWF mRNA. The expression of TFPI mRNA in the brain was however detected by RT/PCR and the antigen was localized to the endothelium of microvessels as well as to the astrocytes and oligodendrocytes. Since ultimate expression of proteins is linked to the expression of their mRNAs, our data support a concept that vascular endothelium is made up of phenotypically diverse groups of cells and that endothelial cells of different vascular beds express specific sets of genes that enable them to carry out tissue-specific functions. Importantly, since astrocytes are known to express tissue factor, the TFPI expression by these cells may control coagulation in their microenvironment and their response to injury and inflammation.

The increasing demand for nanopowders (particles size

Recent advancements in technology, design and manufacture of equipment for small power generating sets have facilitated harnessing the resources of small hydro potential in India. Large number of firms are now manufacturing standard turbo-generating units to suit different head, discharge and other parameter requirements. Cavitation in water systems is due to the formation of cavitation bubbles, which results from local pressure falling below the vapour pressure of the flowing water. Cavitation occurs in areas of accelerated flow such as the gap between turbine blade tips and the turbine housing or on the suction side of runner blades. Cavitation can also occur in the gap between the blade roots and hub and in the hub vortex behind the turbine runner. In hydraulic machines, efficiency is reduced considerably due to cavitation and this alters the flow pattern. Loss of energy is caused due to vibration and noise. Pitting of the surface causes loss of material. In hydraulic turbines, the power output is reduced due to cavitation, since the force exerted by water on the turbine blades decreases.

In the traditional mobile ad hoc network (MANET) systems route rediscovery approaches; there exists route failure in all route discovery methods resulting in information loss and communication overheads. Thus, the routing must be completed inaccordance with mobility persona of the community. On this manuscript, an Improved Lion optimization algorithm (ILOA)-centered lifetime prediction algorithm for route healing in MANET has been proposed. This manner predicts the lifetime of link and node within the to be had bandwidth headquartered on the parameters like relative mobility of nodes and power drainfee, and so on. Utilizing predictions, the parameters are fuzzified and fuzzy ideas were shaped to select the nodefame. This expertise is made to alternate among the entire nodes. Accordingly, the repute of every node is verified earlier than knowledge transmission. Even for a weak node, the efficiency of a route recuperation mechanism is made in this type of means that corresponding routes are diverted to the robust nodes. With the aid of the simulated results, the minimization of information loss and communication overhead making use of ILOA prediction has been mentioned in element.

We recently proposed that endothelium may represent the primary physiologic site of synthesis of the tissue factor pathway inhibitor (TFPI). In support of this conclusion, we have now found that the poly(A)+ RNAs obtained from rabbit and bovine lung tissues contain abundant amounts of TFPI messenger RNAs (mRNAs), whereas the poly(A)+ RNAs obtained from the liver of these animals contain less than 5% of that found in the lung tissues. Because inflammatory mediators are known to upregulate tissue factor (TF) expression by the endothelium, we have examined the effect of these agents on the TFPI expression by the cultured endothelial cells. When cultured human umbilical vein endothelial cells were stimulated (in 10% fetal bovine serum) with phorbol myristate acetate (PMA), endotoxin, interleukin-1, or tumor necrosis factor-alpha, the TF mRNA increased approximately 7- to 10- fold within 2 to 4 hours. Unstimulated cells constitutively expressed TFPI mRNA and its levels either did not change or increased slightly (up to 1.5-fold) upon stimulation with these inflammatory agents. TF mRNA abruptly declined to a negligible level and the TFPI mRNA returned essentially to the basal level at approximately 24 hours. The membrane- bound TF clotting activity of induced cells peaked between 4 and 8 hours, and finally declined. The cumulative TFPI activity secreted into the media was either unchanged or slightly higher in the induced cell cultures as compared with that present in the noninduced cultures. Endothelial cells were also cultured in 10% heat-inactivated human serum derived from plasma or whole blood. TFPI secreted into the media containing whole blood serum was consistently higher (approximately 1.5- fold at 8 hours) than that secreted into the media supplemented with serum obtained from plasma lacking the formed elements; these cells also expressed similarly increased levels of TFPI mRNA. Moreover, PMA- stimulated cells cultured in whole blood serum expressed modestly increased levels of TFPI mRNA (approximately 1.5-fold); supernatants from these cells also contained similarly increased TFPI activity. Cumulatively, our data indicate that, unlike thrombomodulin and fibrinolytic enzymes synthesized by the endothelial cells, TFPI synthesis is not downregulated and may be slightly upregulated during an inflammatory response. Inspection of the 5′ flanking region of the TFPI gene showed a conserved GATA-binding motif located approximately 400 bp upstream of the proposed transcription initiation site(s). This motif by binding to the GATA-2 transcriptional factor may keep the endothelium in an ‘on’ state for constitutive expression of TFPI.(ABSTRACT TRUNCATED AT 400 WORDS)

Factor IX is a multidomain protein essential for hemostasis. We describe a mutation in a patient affecting the first epidermal growth factor (EGF)-like domain of the protein. All exons and the promoter region of the gene were amplified by the polymerase chain reaction method, and sequenced. Only a single mutation (C----G), that predicts the substitution of Pro55 by Ala in the first EGF domain was found in the patient's gene. This mutation leads to new restriction sites for four enzymes. One new site (Nsi) was tested in the amplified exon IV fragment and was shown to provide a rapid and reliable marker for carrier detection and prenatal diagnosis in the affected family. The factor IX protein, termed factor IXHollywood (IXHW), was isolated to homogeneity from the patient's plasma. As compared with normal factor IX (IXN), IXHW contained the same amount of gamma-carboxy glutamic acid but twice the amount of beta-OH aspartic acid. Both IXHW and IXN contained no detectable free -SH groups. Further, IXHW could be readily cleaved to yield a factor IXa-like molecule by factor Xla/Ca2+. However, IXaHW (compared with IXaN) activated factor X approximately twofold slower in the presence of Ca2+ and phospholipid (PL), and 8- to 12-fold slower in the presence of Ca2+, PL, and factor VIIIa. Additionally, IXaHW had only approximately 10% of the activity of IXaN in an aPTT assay. In agreement with the nuclear magnetic resonance- derived structure of EGF, the Chou-Fasman algorithm strongly predicted a beta turn involving residues Asn-Pro55-Cys-Leu in IXN. Replacement of Pro55 by Ala gave a fourfold decrease in the beta turn probability for this peptide, suggesting a change(s) in the secondary structure in the EGF domain of IXHW. Since this domain of IXN is thought to have one high-affinity Ca2+ binding site and may be involved in PL and/or factor VIIIa binding, the localized secondary structural changes in IXHW could lead to distortion of the binding site(s) for the cofactor(s) and, thus, a dysfunctional molecule.

This paper describes how laser welding is increasingly applied in the automotive industry in order to assemble sheet structures because of its efficiency and reliability. However, the numerous material and gauge combinations pose a major challenge in characterizing and understanding the crash behavior of the welded joints. Body-in-white (BIW) structures normally have numerous laser welded joints along with other kinds of joints like adhesive bonding, spot welds etc. Owing to limitations in computing time, the structures with all these kinds of joints have to be modeled with coarse finite element meshes. Simplified or substitute joint models with just one or few elements but with correct representation of geometry and stiffness of the joint are largely desired in practice. This paper discusses such modeling techniques, including element selection, choice of material models for the weld etc. The type and dimension of the weld model is fixed and validated on experimental crash test results. An empirical relationship is then developed which covers the numerous physical effects like sheet thickness, static and dynamic strength and failure behavior of the joint. A general description of the model and some recommendations for application of the model where coarse meshes are involved for both welds and flanges are given as well.

Tissue factor pathway inhibitor (TFPI) plays an important role in regulating tissue factor (TF)-initiated blood coagulation. Since serum stimulation of fibroblasts, vascular smooth muscle cells and cardiac myocytes in culture increases the expression of TF mRNA and antigen (Ag) in these cells, we hypothesized that serum may also induce increased synthesis of TFPI in these cells to regulate the TF-induced extravascular clotting at an injury site. To test this concept, we used primary isolates of the following human cell types - fetal and adult lung fibroblasts, pulmonary and aortic smooth muscle cells, and cardiac myocytes. Serum-stimulation of these cells resulted in an increased expression of TF mRNA and Ag (8 to 10-fold). Upon serum stimulation, expression of TFPI mRNA and Ag was also increased in these cells. However, the increase in TFPI-Ag (6 to 8-fold) was significantly greater than the TFPI mRNA (2 to 3-fold). Notably, increased expression of TFPI persisted after the TF expression had declined. Further, increased synthesis of TFPI initially led to the saturation of heparin-releasable binding sites. TFPI-Ag was detected by Western blotting, 35S-metabolic labeling and activity assays on the conditioned media, heparin-released material from cells, and in cell lysates. TFPI-Ag was also detected by immunofluorescence staining of cells. Actinomycin D partially whereas cycloheximide completely prevented the serum-induced increased expression of TFPI synthesis by these cells, suggesting control primarily at the translational but some at the transcriptional level as well. The Mr of undegraded TFPI in all cases was approximately 45 kDa and was of full length. TFPI synthesized locally by fibroblasts, vascular smooth muscle cells and cardiac myocytes could play a significant role in regulating TF-initiated extravascular clotting especially since plasma TFPI that may be available at the injury site lacks a portion of the carboxyl segment and is a less efficient inhibitor.

Under normal physiologic conditions, tissue factor pathway inhibitor (TFPI) is synthesized primarily by the microvascular endothelium. Using Northern blotting, we studied its transcriptional expression in different organs and compared it with the expression of two other endothelial specific proteins, namely thrombomodulin (TM) and von Willebrand factor (vWF). The order of mRNA expression for each protein was: TFPI-placentalungliverkidneyheartskeletal muscleor =pancreasbrain; TM-heartpancreaslungskeletal musclekidneyor =liverplacentabrain; and vWF-heartskeletal musclepancreaslungor =kidneyplacentabrainliver. Notably, heart expressed TM and vWF mRNA in large amounts and only small amounts of TFPI whereas lung expressed all three mRNAs in significant amounts. Placenta, on the contrary, expressed large amounts of TFPI but only small amounts of TM and vWF mRNAs. Brain by this technique was found to express undetectable amounts of TFPI and TM mRNAs but small amounts of vWF mRNA. The expression of TFPI mRNA in the brain was however detected by RT/PCR and the antigen was localized to the endothelium of microvessels as well as to the astrocytes and oligodendrocytes. Since ultimate expression of proteins is linked to the expression of their mRNAs, our data support a concept that vascular endothelium is made up of phenotypically diverse groups of cells and that endothelial cells of different vascular beds express specific sets of genes that enable them to carry out tissue-specific functions. Importantly, since astrocytes are known to express tissue factor, the TFPI expression by these cells may control coagulation in their microenvironment and their response to injury and inflammation.