Spectrophotometric Determination of Dissociation Constants of 3-Mercuri-5-sulphosalicylic Acid & Stability Constant of Its Fe(III) Complex

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Joining of carbon fibre reinforced polymer (CFRP) composites and aluminium alloys – A review

This paper investigates comprehensive knowledge regarding joining CFRP and aluminium alloys in available literature in terms of available methods, bonding processing and mechanism and properties. The methods employed comprise the use of adhesive, self-piercing rivet, bolt, clinching and welding to join only CFRP and aluminium alloys. The non-thermal joining methods received great attention though the welding process has high potential in joining these materials. Except adhesive bonding and welding, other joining methods require the penetration of metallic pins through joining parts and therefore, surface preparation is unimportant. No model is found to predict the properties of jointed structures, which makes it difficult to select one over another in applications. The choice of bonding methods depends primarily on the specific applications. The load-bearing mechanism of bolted joints is predominantly the friction that is the first stage resistance. Hybrid joints performance is enhanced by combining rivets, clinch or bolts with adhesives

A Dynamic Model of Interactions of Ca^(2+), Calmodulin, and Catalytic Subunits of Ca^(2+)/Calmodulin-Dependent Protein Kinase II

During the acquisition of memories, influx of Ca^(2+) into the postsynaptic spine through the pores of activated N-methyl-D-aspartate-type glutamate receptors triggers processes that change the strength of excitatory synapses. The pattern of Ca^(2+) influx during the first few seconds of activity is interpreted within the Ca^(2+)-dependent signaling network such that synaptic strength is eventually either potentiated or depressed. Many of the critical signaling enzymes that control synaptic plasticity, including Ca^(2+)/calmodulin-dependent protein kinase II (CaMKII), are regulated by calmodulin, a small protein that can bind up to 4 Ca^(2+) ions. As a first step toward clarifying how the Ca^(2+)-signaling network decides between potentiation or depression, we have created a kinetic model of the interactions of Ca^(2+), calmodulin, and CaMKII that represents our best understanding of the dynamics of these interactions under conditions that resemble those in a postsynaptic spine. We constrained parameters of the model from data in the literature, or from our own measurements, and then predicted time courses of activation and autophosphorylation of CaMKII under a variety of conditions. Simulations showed that species of calmodulin with fewer than four bound Ca^(2+) play a significant role in activation of CaMKII in the physiological regime, supporting the notion that processing ofCa^(2+) signals in a spine involves competition among target enzymes for binding to unsaturated species of CaM in an environment in which the concentration of Ca^(2+) is fluctuating rapidly. Indeed, we showed that dependence of activation on the frequency of Ca^(2+) transients arises from the kinetics of interaction of fluctuating Ca^(2+) with calmodulin/CaMKII complexes. We used parameter sensitivity analysis to identify which parameters will be most beneficial to measure more carefully to improve the accuracy of predictions. This model provides a quantitative base from which to build more complex dynamic models of postsynaptic signal transduction during learning

Effect of Pulsation in Microstructure and Mechanical Properties of Titanium Alloy-Annealed Welded Joints at Different Temperatures

Thin sheets of Ti-6Al-4V alloy of thickness 1 mm were butt welded using a pulsed Nd-YAG low-power laser setup. The goal of this research is to explore the influence of pulsation on the microstructure and mechanical properties. In addition to that, annealing at different temperatures has been performed to compare the results of pulsation and heat treatment. The results indicate that after annealing at 980 °C, the structure completely transformed into an equiaxed structure. When annealed at 1010 °C, almost the total area is composed of an equiaxed α phase, and the grains are coarse as compared to the previous. This suggests that the grain size becomes thicker when the annealing temperature is raised above 980 °C. The volume fraction of the equiaxed structure is maximum. It can be deduced that the volume–fraction is dependent on the annealing temperature. The volume fraction of the equiaxed structure increases as the annealing temperature increases. A higher tensile strength value of the sample annealed at 980 °C was found as compared with the overlapped sample (A-2). The fusion zone overlapped sample (A-2) shows high hardness with a value of 397 HV1. In the FZ sample, annealing at 980 °C has a hardness of 386 HV1. The (A-2) sample indicates higher (3–4%) hardness as compared to the annealed sample at the FZ. The β phase is increased by 16% in the XRD analysis of the overlapped samples. Hence, it is evident that the amount of β phase has increased during heating, and a complete transformation has taken place at a temperature of 958 °C. © 2023 by the authors.This research was funded by the Researchers Supporting Project number RSP2023R373

Contribution of machining to the fatigue behaviour of metal matrix composites (MMCs) of varying reinforcement size

The high cycle constant stress amplitude fatigue performance of metal matrix composite (MMC) components machined by a milling process was investigated in this study as a function of machining speed, feed rate and reinforcement particle size. The presence of reinforcement and particle size were found to be the most influential factors that affected the fatigue life. In contrast to this, the effect of feed and speed on tool-particle interaction, strain hardening and heat generation during milling of MMCs were balanced in such a way that the contributions of feed and speed on fatigue life were negligible. The interactions of different parameters contributed significantly to the fatigue life which indicated that the modelling of fatigue life based on these three parameters was relatively complex. The fatigue life of the machined MMC samples increased with decreasing particle size and increasing feed. However, the fatigue life was not influenced by speed variation. The presence of smaller or no particles induced a complete separation of failed samples, in contrast to that of specimens containing larger reinforcing particles where crack growth was arrested or deflected by the reinforcing particles

Glutamate May Be an Efferent Transmitter That Elicits Inhibition in Mouse Taste Buds

Recent studies suggest that l-glutamate may be an efferent transmitter released from axons innervating taste buds. In this report, we determined the types of ionotropic synaptic glutamate receptors present on taste cells and that underlie this postulated efferent transmission. We also studied what effect glutamate exerts on taste bud function. We isolated mouse taste buds and taste cells, conducted functional imaging using Fura 2, and used cellular biosensors to monitor taste-evoked transmitter release. The findings show that a large fraction of Presynaptic (Type III) taste bud cells (∼50%) respond to 100 µM glutamate, NMDA, or kainic acid (KA) with an increase in intracellular Ca2+. In contrast, Receptor (Type II) taste cells rarely (4%) responded to 100 µM glutamate. At this concentration and with these compounds, these agonists activate glutamatergic synaptic receptors, not glutamate taste (umami) receptors. Moreover, applying glutamate, NMDA, or KA caused taste buds to secrete 5-HT, a Presynaptic taste cell transmitter, but not ATP, a Receptor cell transmitter. Indeed, glutamate-evoked 5-HT release inhibited taste-evoked ATP secretion. The findings are consistent with a role for glutamate in taste buds as an inhibitory efferent transmitter that acts via ionotropic synaptic glutamate receptors

Maturation of GABAergic Inhibition Promotes Strengthening of Temporally Coherent Inputs among Convergent Pathways

Spike-timing-dependent plasticity (STDP), a form of Hebbian plasticity, is inherently stabilizing. Whether and how GABAergic inhibition influences STDP is not well understood. Using a model neuron driven by converging inputs modifiable by STDP, we determined that a sufficient level of inhibition was critical to ensure that temporal coherence (correlation among presynaptic spike times) of synaptic inputs, rather than initial strength or number of inputs within a pathway, controlled postsynaptic spike timing. Inhibition exerted this effect by preferentially reducing synaptic efficacy, the ability of inputs to evoke postsynaptic action potentials, of the less coherent inputs. In visual cortical slices, inhibition potently reduced synaptic efficacy at ages during but not before the critical period of ocular dominance (OD) plasticity. Whole-cell recordings revealed that the amplitude of unitary IPSCs from parvalbumin positive (Pv+) interneurons to pyramidal neurons increased during the critical period, while the synaptic decay time-constant decreased. In addition, intrinsic properties of Pv+ interneurons matured, resulting in an increase in instantaneous firing rate. Our results suggest that maturation of inhibition in visual cortex ensures that the temporally coherent inputs (e.g. those from the open eye during monocular deprivation) control postsynaptic spike times of binocular neurons, a prerequisite for Hebbian mechanisms to induce OD plasticity