Heat-induced Defects Research Articles

A comparative study for demonstrating the effect of the assist gas and E-field on hole generation characteristics induced by femtosecond laser layered ring hole-cutting of magnesium alloy AZ91D sheets

The widely-used magnesium alloy AZ91D is light-weight and energy-saving with good castability and mechanical performance. The traditional machining way for magnesium and its alloys is the high-speed mechanical contact cutting, which usually leads to uncontrollable intense ignition with some notable heat-induced machining defects. However, it has been rarely reported that the non-contact precision laser machining is used for cutting the magnesium and its alloys. The problems such as the local heat effect, the heat-induced defects and the local ignition as well as the vapor-plasma plume usually encountered during laser machining of magnesium and its alloys. Hence, in this study, a hybrid laser cutting way of femtosecond laser layered ring hole-cutting using the assist gas and E-field is reported to machine micro holes in the AZ91D material. The effect of the lateral E-field and assist gas on the hole formation characteristics was demonstrated for femtosecond laser cutting of the AZ91D sheets. It was indicated that the use of the lateral E-field and assist gas suppressed the ignition as well as the vapor-plasma plume. The hole depth was increased by the external assistance used especially the lateral nitrogen blowing. The hole wall formation quality was improved by using the lateral E-field and compressed air blowing, while it got poorer if using the lateral nitrogen blowing. The ignition-induced carbonization was effectively suppressed by the assist gas used. The hole depth, microstructure and micro hardness were improved by using the lateral E-field and assist gas.

Deuterium retention in cyclic transient heat loaded tungsten with increasing cycle numbers

Surface damage and microscopic defect evolution of tungsten (W) armor under transient heat loads are key factors for fuel retention in fusion reactors. In this work, experiments were conducted to investigate the effects of cyclic thermal shocks on deuterium (D) retention and surface blistering in W. Thermal shock experiments were conducted on recrystallized W using an electron beam with a power density of 0.15 GW m−2 across 100–1500 cycles, followed by D plasma exposure with high-fluence (∼1 × 1026 D m−2). The results demonstrate that samples subjected to 500 and 1500 cycles exhibit a significant presence of sub-grains within 90 μm. Notably, the inhibition of blistering induced by thermal shock leads to a substantial reduction in D retention (5.45 × 1019 D m−2) at lower cycle numbers (100 cycles) compared to the reference sample (2.35 × 1020 D m−2) which was only exposed to D plasma. When cycle numbers increase to 500 and 1500, D retention reaches 1.98 × 1020 D m−2 and 4.56 × 1020 D m−2, respectively. Based on the tritium migration analysis program, we propose that total D retention is a consequence of the competition between defects reduced by thermal shock-induced suppression of blistering and defects generated by plastic deformation induced by thermal stress. D retention initially decreases with the increase in cycle numbers, followed by a subsequent rise, with the inflection point slightly higher than 500 cycles. Additionally, due to the extensive scope of thermal stress, an escalated exposure period will result in substantial D captured by heat-induced defects, consequently intensifying the D retention. Whether there exists an upper limit to D retention induced by the increasing thermal shock cycles necessitates further experimental analysis. Nonetheless, it is evident that thermal shock significantly contributes to D retention within a profoundly deep bulk region under high cycles.

Friction stir incremental forming of polyoxymethylene: process outputs, force and temperature

ABSTRACT Despite good creep and fatigue durability, high resistance against chemicals and good surface finish, Polyoxymethylene (POM) has been sidelined in incremental sheet forming (ISF) literature due to its low formability at room temperature. This paper addresses the issue by deploying a cost-effective friction-induced heat at the tool-sheet interface. This work demonstrates a combined experimental, analytical, and numerical approach to investigate the effects of elevated temperature in ISF of POM. For this purpose, the formability of POM was first experimentally investigated under the interactive effects of the process parameters. Employing the membrane analysis approach, the stress state in the FSISF process was defined. The tool-sheet contact area was calculated as a function of toolpath and the relevant process parameters. The Johnson-Cook plasticity model was calibrated based on several universal mechanical tests at various temperatures and rates. Embedding the stress state, contact area, and the material model inside an algorithm developed by adopting the Finite Difference Method, force, friction-induced heat, and temperature at the tool-sheet interface were evaluated. Simulation results were validated by experimental outcomes. A threshold boundary for the maximum allowable tooltip temperature was established to avoid heat-induced defects while ensuring the sheet formability.

Maternal loading of a small heat shock protein increases embryo thermal tolerance in Drosophila melanogaster.

Maternal investment is likely to have direct effects on offspring survival. In oviparous animals whose embryos are exposed to the external environment, maternal provisioning of molecular factors like mRNAs and proteins may help embryos cope with sudden changes in the environment. Here, we sought to modify the maternal mRNA contribution to offspring embryos and test for maternal effects on acute thermal tolerance in early embryos of Drosophila melanogaster We drove in vivo overexpression of a small heat shock protein gene (Hsp23) in female ovaries and measured the effects of acute thermal stress on offspring embryonic survival and larval development. We report that overexpression of the Hsp23 gene in female ovaries produced offspring embryos with increased thermal tolerance. We also found that brief heat stress in the early embryonic stage (0-1 h old) caused decreased larval performance later in life (5-10 days old), as indexed by pupation height. Maternal overexpression of Hsp23 protected embryos against this heat-induced defect in larval performance. Our data demonstrate that transient products of single genes have large and lasting effects on whole-organism environmental tolerance. Further, our results suggest that maternal effects have a profound impact on offspring survival in the context of thermal variability.

Direct calorimetric verification of thermodynamic instability of lead halide hybrid perovskites

Hybrid perovskites, especially methylammonium lead iodide (MAPbI3), exhibit excellent solar power conversion efficiencies. However, their application is plagued by poor chemical and structural stability. Using direct calorimetric measurement of heats of formation, MAPbI3 is shown to be thermodynamically unstable with respect to decomposition to lead iodide and methylammonium iodide, even in the absence of ambient air or light or heat-induced defects, thus limiting its long-term use in devices. The formation enthalpy from binary halide components becomes less favorable in the order MAPbCl3, MAPbBr3, MAPbI3, with only the chloride having a negative heat of formation. Optimizing the geometric match of constituents as measured by the Goldschmidt tolerance factor provides a potentially quantifiable thermodynamic guide for seeking chemical substitutions to enhance stability.

Inverse determination of heat input during the friction stir welding process

Determining the input heat required to achieve a satisfactory standard during the friction stir welding (FSW) process is a novel study. This study proposes a computational method for predicting an appropriate heat input during the FSW process to reduce the effect of heat-induced defects caused by heat response. The method was deduced from a finite element method based on an inverse algorithm. No preselected functional form for an unknown function and no sensitivity analysis are required in the algorithm. One example was used to demonstrate the characteristics of the proposed method. The numerical results indicated that the predicted heat input is adequate for the welding process.

Microstructure, strength and structural integrity of heat-treated beech and spruce wood

Heat treatment of wood is an effective method by which to improve the dimensional stability and biological durability, but the mechanical strength is decreased at the same time. Besides chemical modification of cell-wall constituents, physical weakening of the microstructure owing to heat-induced defects may also contribute to strength loss. Therefore, anatomical properties of heat-treated beech (Fagus sylvatica L.) and spruce (Picea abies Karst.), studied by light microscopic and scanning electron microscopic analysis, and their interrelation with strength properties and structural integrity were investigated. For determination of structural integrity, the high-energy–multiple-impact (HEMI) test was applied. Microscopic analyses showed frequent formation of radial cracks in heat-treated beech close to the rays as well as tangential cracks in the latewood of spruce. In addition, the modulus of rupture was more affected by the heat treatments than the resistance to impact milling (RIM) determined by the HEMI test, because RIM is based on multiple fractures on the microlevel that are not affected by the formation of intercellular cracks or other defects due to the heat treatment. It was concluded that heat-induced defects in the wood microstructure contribute to the substantial strength loss of thermally modified timber.

Apoptosis, the heat shock response, hyperthermia, birth defects, disease and cancer. Where are the common links?

Many cells die during normal prenatal development. Throughout postnatal life, production of new cells is balanced by death of older cells to maintain the normal mass of organs and tissues. In these situations, cell death is usually in the form of apoptosis, characterized morphologically by shrinkage of cellular contents within their membranes, condensation and margination of chromatin against the nuclear membrane and phagocytic removal by macrophages or adjacent cells of the organ. It is initiated and controlled by a complex set of gene-directed activities. The process is tidy and avoids the inflammatory effects of degenerating cellular contents on other tissues. The capacity to undergo this form of cell death is lost in neoplastic cell lines. In embryos the normal process of apoptosis has been termed programmed cell death, and in prenatal and mature animals a number of toxic agents can also cause morphologically typical forms of apoptosis. The heat shock (HS) response occurs in a wide range of plants and animals as a basic reaction that assists survival and recovery from the effects of heat and other toxic agents. It appears to be an extension of the cellular mechanism by which newly synthesized proteins are received by other ('chaperone') proteins to be transported within cells and folded into their functional configurations. Chaperone proteins adhere to hydrophobic sites on newly synthesized proteins, preventing the formation of functionless aggregates by random adhesion to hydrophobic sites on other proteins. After disengagement, the new protein can assume its proper configuration. Chaperone proteins are normally present in embryos, the genes encoding for their synthesis becoming activated particularly at inductive and rapid growth stages of organ formation. Hyperthermia and some other toxic agents also activate a set of inducible heat shock genes to synthesize induced HS proteins that adhere to uncovered hydrophobic sites on the heat denatured proteins, preventing random associations and allowing reconstitution or assisting degradation of irreparably damaged proteins. Irreparable damage usually results in a morphologically typical form of apoptotic cell death. Knowledge of signals initiating the response is incomplete but includes prostaglandin release, amplification by kinase cascades of mitogen and stress-activated protein signals, binding of the HS factor to the HS element on the HS gene. Maternal hyperthermia is a proven teratogen in all species studied. The HS response is inducible in early embryonic life but it fails to protect embryos against damage at certain stages of development. An embryo must absorb a threshold 'dose' of heat if defects are to be caused, the dose being the product of the level and the duration of elevation above the normal maternal temperature. The lowest elevation causing damage is 2-2.5 degrees C. Low elevations require longer durations and as the elevation increases, the time required is reduced logarithmically. Heat-induced defects are most common in the central nervous system (CNS) and include open neural tube, microencephaly, microphthalmia and neurogenic contractures. Apoptotic cells are found in these organs soon after threshold doses of heat. The periods of high susceptibility are brief, occurring at the time of organ induction and, paradoxically, at this stage, chaperone protein synthesis is at high levels, presumably to protect this process. Susceptibility might be due to gene activity being concentrated into organ induction with chaperone proteins being unavailable for repair of heat-denatured proteins. With activation of the HS response, normal protein synthesis is suspended (perhaps including those controlling induction of organs) and protective HS proteins are produced which rescue the embryo, but survival is achieved at the expense of normal development.

Functional defect of heat-inactivated human lymphocytes in mixed-lymphocyte culture

Possible causes were examined for the inability of heat-inactivated lymphocytes to induce proliferative responses in mixed-lymphocyte cultures (MLC). Cells heated at 45 °C for 60 min lost >90% of their capacity to stimulate in primary (1 °c) or secondary (2 °c) MLC. This was not due to accelerated or delayed proliferation, nor to a simple quantitative loss of antigen since a 10-fold increase in stimulators or sequential addition of heated stimulators at 4-hr intervals was ineffective. Heated B lymphocytes had approximately 80% expression of HLA-DR and DQ antigens compared to unheated B cells when measured by flow cytometry using monoclonal antibodies detecting both monomorphic and polymorphic antigens. Contrary to some reports, there was no evidence of direct suppression or induction of suppression by heated stimulators or their supernatants. Reconstitution of 1 °c and 2 °c MLC with crude MLC supernatants or more purified interleukin 1 (Il-1) or interleukin 2 (Il-2) was unsuccessful. The results indicate the heatinduced defect occurs immediately and is not due to direct or indirect suppression, insufficient amounts of Il-1 or Il-2, nor loss of polymorphic Class II HLA determinants. Heat inactivation of stimulator function may result from failure to present an “immunogenic grid” or loss of accessory molecules required in lymphocyte interactions.

Effect of Heating on the Functional Properties of Ovotransferrin

The effect of heating on the functional properties of ovotransferrin greatly varied with both the pH and ionic strength of the solution. When small amounts of inorganic salts (μ<0.1) were present in the ovotransferrin solution of which the pH was between 6.0 and 8.5, both the solubility and foaminess greatly decreased upon heating at a temperature above 60°C for 5 min. However, when the amounts of inorganic salts were larger μ≥0.3), no decrease in either property was observed. These phenomena were assumed to be caused by either cation binding (at a low concentration of salts) or anion binding (at a high concentration of salts) of ovotransferrin. Among the anions tested, both phosphate and citrate which are assumed to have a rather high affinity for ovotransferrin did not cause any heat-induced defect at any of the salt concentrations tested.

Effect of heating on the functional properties of ovotransferrin.

The effect of heating on the functional properties of ovotransferrin greatly varied with both the pH and ionic strength of the solution. When small amounts of inorganic salts (μ<0.1) were present in the ovotransferrin solution of which the pH was between 6.0 and 8.5, both the solubility and foaminess greatly decreased upon heating at a temperature above 60°C for 5 min. However, when the amounts of inorganic salts were larger μ≥0.3), no decrease in either property was observed. These phenomena were assumed to be caused by either cation binding (at a low concentration of salts) or anion binding (at a high concentration of salts) of ovotransferrin. Among the anions tested, both phosphate and citrate which are assumed to have a rather high affinity for ovotransferrin did not cause any heat-induced defect at any of the salt concentrations tested.

Heat treatment-induced effects in metallic Si(P): photoluminescence and electron paramagnetic resonance

Heat treatment of silicon doped with phosphorus is found to produce marked changes in the photoluminescence and the electron paramagnetic resonance for samples containing impurity concentrations above the critical concentration [Formula: see text] for the semiconductor–metal transition. A possible explanation is suggested in terms of a heat-induced defect which is populated only when the phosphorus-doped electrons are delocalized. Clusters of Si-interstitials are considered. At concentrations greater than about 2.0 × 1019 P/cm3 the heat-induced changes are exceedingly small.