Porosity and Microcrack Effects on Thermal Stress and Shock Fracture and Properties at Elevated Temperatures

2017 ◽  
pp. 429-474
Author(s):  
Roy W. Rice
Keyword(s):  
Thermal Stress ◽  
Elevated Temperatures

173 HINDERING OF CLEAVAGE TIMING IN BOVINE PARTHENOTES DURING THE HOT SEASON

2007 ◽  
Vol 19 (1) ◽  
pp. 203 ◽  
Author(s):  
A. Aroyo ◽  
S. Yavin ◽  
Z. Roth ◽  
A. Arav
Keyword(s):  
Thermal Stress ◽  
Embryonic Development ◽  
Elevated Temperatures ◽  
Time Lapse ◽  
Cold Season ◽  
Seasonal Effects ◽  
Cell Stage ◽  
Developmental Potential ◽  
Hot Season

Heat stress is a major contributing factor to low fertility among dairy cattle, as reflected by the dramatic reduction in conception rate during the hot months. The effects of thermal stress on oocyte competence and embryonic development have been well documented. However, timing of embryonic cleavage, which may be considered a parameter for the identification of good-quality embryos, and its association with elevated temperatures have not been studied. Two experiments were performed to examine and characterize seasonal effects (i.e. thermal stress) on cleavage timing of bovine parthenogenetic embryos. Oocytes were aspirated from ovaries collected at the local abattoir in 2 seasons: cold (Dec–Apr) and hot (May–Nov). Matured oocytes were chemically activated (ionomycin followed by 6-DMAP) and cultured in vitro; cleavage timing to the 2- and 4-cell stages was observed and documented. The one-way ANOVA procedure was used for statistical analysis. In the first experiment (n = 5416 oocytes), cleavage was documented at specific time points during development post-activation. The peak in embryonic development to the 2-cell stage was earlier (22 to 27 vs. 27 to 40 h after activation) and the cleavage rate higher (39 vs. 21%; P < 0.0001) during the cold season relative to the hot season, respectively. Similarly, the peak in 4-cell-stage development was also observed earlier (46–52 vs. 52–70 h after activation) and corresponded with a higher proportion of developing embryos (33 vs. 21%; P < 0.0001) during the cold season as compared to the hot season, respectively. These results indicate that embryonic development is delayed and a lower proportion of embryos cleaved during the hot season. To better understand the delay in cleavage timing, a second experiment (n = 308 oocytes) was performed through two consecutive hot seasons. A time-lapse system (EmbryoGuard; IMT, Ltd., Ness-Ziona, Israel) was employed to collect accurate data on the first cleavage division, known to be indicative of embryo quality. The time-lapse system was pre-programmed to take photos at 1-h intervals such that culture dishes did not need to be removed from the incubator. Similar to the pattern noted for the hot season in the first experiment, a wide distribution of cleavage timing (18-40 h after activation) was observed. Further analysis revealed that embryos cleaved in 2 distinct waves: cleavage timing of the first wave (18 to 25 h after activation) was characterized by a time frame similar to that in the cold season, suggesting good-quality embryos; however, the second wave, from 27 to 40 h after activation, presented a delay in cleavage timing, suggesting that these late-cleaving embryos are of inferior quality. Taken together, the results of the 2 experiments lead to the assumption that oocytes harvested from lactating cows during the hot season are of reduced developmental potential, which may be explained, in part, by the pattern of 2 cleavage waves. Furthermore, cleavage timing appears to be a good indicator of embryo potential and may increase the chances of selecting better in vitro-derived embryos during the hot season for embryo transfer.

scholarly journals Symbiodinium functional diversity and clade specificity under global change stressors

2017 ◽  
Author(s):  
S.W. Davies ◽  
J.B. Ries ◽  
A Marchetti ◽  
Rafaela Granzotti ◽  
K.D. Castillo
Keyword(s):  
Thermal Stress ◽  
Elevated Temperatures ◽  
Transcriptome Profiling ◽  
Photosynthetic Performance ◽  
Molecular Response ◽  
Functional Variation ◽  
Conserved Genes ◽  
Clade C ◽  
Highly Correlated ◽  
Photosynthetic Efficiencies

ABSTRACTCoral bleaching episodes are increasing in frequency, demanding examination of the physiological and molecular responses of corals and their Symbiodinium to climate change. Here we quantify bleaching and Symbiodinium photosynthetic performance of Siderastrea siderea from two reef zones after long-term exposure to thermal and CO2-acidification stress. Molecular response of in hospite Symbiodinium to these stressors was interrogated with RNAseq. Elevated temperatures reduced photosynthetic efficiency, which was highly correlated with bleaching status. However, photosynthetic efficiencies of forereef symbionts were more negatively affected by thermal stress than nearshore symbionts, indicating greater thermal tolerance in nearshore corals. At control temperatures, CO2-acidification had little effect on symbiont physiology, although forereef symbionts exhibited greater photosynthetic efficiencies than nearshore symbionts. Transcriptome profiling revealed that S. siderea were dominated by clade C Symbiodinium, except under thermal stress, which caused shifts to thermotolerant clade D. Comparative transcriptomics of conserved genes across symbiotic partners revealed few differentially expressed Symbiodinium genes when compared to corals. Instead of responding to stress, clade C transcriptomes varied by reef zone, with forereef Symbiodinium exhibiting enrichment of genes associated with photosynthesis. Our findings suggest that functional variation in photosynthetic architecture exists between forereef and nearshore Symbiodinium populations.

scholarly journals Thermal Stress and Bleaching in the Cnidarian-Dinoflagellate Symbiosis: The Application of Metabolomics

2021 ◽  
Author(s):  
◽  
Katie E. Hillyer
Keyword(s):  
Thermal Stress ◽  
Coral Reefs ◽  
Metabolite Profiling ◽  
Alternative Energy ◽  
Metabolic Networks ◽  
Elevated Temperatures ◽  
Central Metabolism ◽  
Diverse Range ◽  
Thermally Induced ◽  
Profiling Techniques

<p>Reef-building corals form critical ecosystems, which provide a diverse range of goods and services. Their success is based on a complex symbiosis between cnidarian host, dinoflagellate algae (genus Symbiodinium) and associated microorganisms (together termed the holobiont). Under functional conditions nutrients are efficiently recycled within the holobiont; however, under conditions of thermal stress, this dynamic relationship can dysfunction, resulting in the loss of symbionts (bleaching). Mass coral bleaching associated with elevated temperatures is a major threat to the long-term persistence of coral reefs. Further study is therefore necessary in order to elucidate the cellular and metabolic networks associated with function in the symbiosis and to determine change elicited by exposure to thermal stress. Metabolomics is the study of small compounds (metabolites) in a cell, tissue or whole organism. The metabolome comprises thousands of components, which will respond rapidly to change, reflecting a combination of genotype, phenotype and the environment. As a result, the study of these metabolic networks serves as a sensitive tool for the detection and elucidation of cellular responses to abiotic stress in complex systems.  This thesis presents outputs of gas chromatography-mass spectrometry-based metabolite profiling techniques, which have been applied to the study of thermal stress and bleaching in the cnidarian-dinoflagellate symbiosis. In Chapter 2 these techniques were developed and applied to the model symbiotic cnidarian Aiptasia sp., and its homologous symbiont (Symbiodinium ITS 2 type B1), to characterise both ambient and thermally-induced metabolite profiles (amino and non-amino organic acids) in both partners. Thermal stress, symbiont photodamage and associated bleaching, resulted in characteristic modifications to the free metabolite pools of both partners. These changes differed between partners and were associated with modifications to central metabolism, biosynthesis, catabolism of stores and homeostatic responses to thermal and oxidative stress.  In Chapter 3 metabolite profiling techniques (focussing this time on carbohydrate pools) were once again applied to the study of thermally-induced changes to the free pools of the coral Acropora aspera and its symbionts (dominant Symbiodinium ITS 2 type C3) at differing stages of symbiont photodamage and thermal stress. Additionally, targeted analysis was employed to quantify these changes in terms of absolute amounts. Once again exposure to elevated temperatures resulted in symbiont photodamage, bleaching and characteristic modifications to the free metabolite pools of symbiont and host, which differed between partners and with the duration of thermal stress. These changes were associated with increased turnover of a number of networks including: energy-generating pathways, antioxidant networks, ROS-associated damage and damage signalling, and were also indicative of potential alterations to the composition of the associated microbial holobiont.  Finally in Chapter 4, metabolite profiling techniques optimized in Chapter 2 and 3 were coupled to 13C labelling in both Aiptasia sp. and A. aspera, in order to further investigate the questions raised in these preceding studies. Once again changes were observed to central metabolism, biosynthesis and alternative energy-generation modes in symbiont and host, in both symbioses. Interestingly however, in all cases there was continued fixation of carbon, production- and translocation of mobile products by the remaining symbionts in hospite. This suggests that even during the later stages of bleaching, symbionts are, at least in part, metabolically functional in terms of photosynthate provision.  This study therefore serves as an important first step in developing the application of metabolomics-based techniques to the study of thermal stress in the cnidarian-dinoflagellate symbiosis. The power of these techniques lies in the capacity to simultaneously assess rapid and often post-translational change in a highly repeatable and quantitative manner. With the use of these methods, this study has shown how metabolic, homeostatic and acclimatory networks interact to elicit change in each partner of the symbiosis during thermal stress and how these responses vary between symbiotic partners. Further understanding of these networks, individual sensitivities- and enhanced resistance to thermal stress are essential if we are to better understand the capacity of coral reefs to acclimate and persist in the face of climate change.</p>

Thermal Stress Effects of Thin Superconducting Films

1968 ◽  
Vol 26 ◽  
pp. 386-387
Author(s):  
M. Connella ◽  
R. J. Deck ◽  
R. H. Morriss
Keyword(s):  
Thermal Stress ◽  
Structural Changes ◽  
Elevated Temperatures ◽  
Superconducting Films ◽  
Temperature Cycle ◽  
Superconducting Properties ◽  
Replication Method ◽  
Thermal Expansion Coefficients ◽  
Before And After ◽  
The Difference

In order to completely understand the role of microstructural defects in superconductivity, it is very desirable to have quantitative correlations between superconducting properties and structural properties. This research is part of a study to correlate grain-sizes with “flux creep phenomena” which occur in the mixed state of Type II superconducting films. Since the superconducting properties in our study must be observed at liquid helium temperatures, whereas the films are evaporated at elevated temperatures, the structural changes produced in some films by cycling to 4.2°K have been investigated.As the temperature of a film is lowered, the difference in thermal expansion coefficients of a film and its substrate results in thermal stress. This stress can produce structural changes. Films have been examined by electron microscopy techniques before and after a temperature cycle down to 4.2°K and back to room temperature. All temperature cycles were carried out in approximately 20 minutes. Both transmission and replication techniques have been employed. The direct replication method was employed using carbon. The carbon replica was separated from the film and post-shadowed with Pt-C.

scholarly journals Differential Regulation by Heat Stress of Novel Cytochrome P450 Genes from the Dinoflagellate Symbionts of Reef-Building Corals

2010 ◽  
Vol 76 (9) ◽  
pp. 2823-2829 ◽  
Author(s):  
Nedeljka N. Rosic ◽  
Mathieu Pernice ◽  
Simon Dunn ◽  
Sophie Dove ◽  
Ove Hoegh-Guldberg
Keyword(s):  
Cytochrome P450 ◽  
Heat Stress ◽  
Thermal Stress ◽  
Elevated Temperatures ◽  
Fold Increase ◽  
Transcript Abundance ◽  
Stress Conditions ◽  
Cytochrome P450 Monooxygenases ◽  
Gene Transcript ◽  
Mrna Pool

ABSTRACT Exposure to heat stress has been recognized as one of the major factors leading to the breakdown of the coral-alga symbiosis and coral bleaching. Here, we describe the presence of three new cytochrome P450 (CYP) genes from the reef-building coral endosymbiont Symbiodinium (type C3) and changes in their expression during exposure to severe and moderate heat stress conditions. Sequence analysis of the CYP C-terminal region and two conserved domains, the “PERF” and “heme-binding” domains, confirmed the separate identities of the CYP genes analyzed. In order to explore the effects of different heat stress scenarios, samples of the scleractinian coral Acropora millepora were exposed to elevated temperatures incrementally over an 18-h period (rapid thermal stress) and over a 120-h period (gradual thermal stress). After 18 h of gradual heating and incubation at 26°C, the Symbiodinium CYP mRNA pool was approximately 30% larger, while a further 6°C increase to a temperature above the average sea temperature (29°C after 72 h) resulted in a 2- to 4-fold increase in CYP expression. Both rapid heat stress and gradual heat stress at 32°C resulted in 50% to 90% decreases in CYP gene transcript abundance. Consequently, the initial upregulation of expression of CYP genes at moderately elevated temperatures (26°C and 29°C) was followed by a decrease in expression under the greater thermal stress conditions at 32°C. These findings indicate that in the coral-alga symbiosis under heat stress conditions there is production of chemical stressors and/or transcriptional factors that regulate the expression of genes, such as the genes encoding cytochrome P450 monooxygenases, that are involved in the first line of an organism's chemical defense.

scholarly journals HSP78 encodes a yeast mitochondrial heat shock protein in the Clp family of ATP-dependent proteases.

1993 ◽  
Vol 13 (10) ◽  
pp. 6304-6313 ◽  
Author(s):  
S A Leonhardt ◽  
K Fearson ◽  
P N Danese ◽  
T L Mason
Keyword(s):  
Thermal Stress ◽  
Heat Shock ◽  
Carbon Source ◽  
Heat Shock Protein ◽  
Elevated Temperatures ◽  
Regulatory Element ◽  
Nuclear Gene ◽  
Sequence Comparisons ◽  
Atpase Subunit ◽  
Mitochondrial Heat Shock Protein

The Saccharomyces cerevisiae nuclear gene for a 78-kDa mitochondrial heat shock protein (hsp78) was identified in a lambda gt11 expression library through immunological screening with an hsp78-specific monoclonal antibody. Sequencing of HSP78 revealed a long open reading frame capable of encoding an 811-amino-acid, 91.3-kDa basic protein with a putative mitochondrial leader sequence and two potential nucleotide-binding sites. Sequence comparisons revealed that hsp78 is a member of the highly conserved family of Clp proteins and is most closely related to the Escherichia coli ClpB protein, which is thought to be an ATPase subunit of an intracellular ATP-dependent protease. The steady-state levels of HSP78 transcripts and protein varied in response to both thermal stress and carbon source with an approximately 30-fold difference between repressed levels in cells growing fermentatively on glucose at 30 degrees C and derepressed levels in heat-shocked cells growing on a nonfermentable carbon source. The response to heat shock is consistent with the presence of a characteristic heat shock regulatory element in the 5'-flanking DNA. Submitochondrial fractionation showed that hsp78 is a soluble protein located in the mitochondrial matrix. Cells carrying disrupted copies of HSP78 lacked hsp78 but were not impaired in respiratory growth at normal and elevated temperatures or in the ability to survive and retain mitochondrial function after thermal stress. The absence of a strong mitochondrial phenotype in hsp78 mutants is comparable to the nonlethal phenotypes of mutations in other Clp genes in bacteria and yeast. HSP78 is the third gene, with SSC1 and HSP60, known to encode a yeast mitochondrial heat shock protein and the second gene, with HSP104, for a yeast ClpB homolog.

HSP78 encodes a yeast mitochondrial heat shock protein in the Clp family of ATP-dependent proteases

1993 ◽  
Vol 13 (10) ◽  
pp. 6304-6313
Author(s):  
S A Leonhardt ◽  
K Fearson ◽  
P N Danese ◽  
T L Mason
Keyword(s):  
Thermal Stress ◽  
Heat Shock ◽  
Carbon Source ◽  
Heat Shock Protein ◽  
Elevated Temperatures ◽  
Regulatory Element ◽  
Nuclear Gene ◽  
Sequence Comparisons ◽  
Atpase Subunit ◽  
Mitochondrial Heat Shock Protein

The Saccharomyces cerevisiae nuclear gene for a 78-kDa mitochondrial heat shock protein (hsp78) was identified in a lambda gt11 expression library through immunological screening with an hsp78-specific monoclonal antibody. Sequencing of HSP78 revealed a long open reading frame capable of encoding an 811-amino-acid, 91.3-kDa basic protein with a putative mitochondrial leader sequence and two potential nucleotide-binding sites. Sequence comparisons revealed that hsp78 is a member of the highly conserved family of Clp proteins and is most closely related to the Escherichia coli ClpB protein, which is thought to be an ATPase subunit of an intracellular ATP-dependent protease. The steady-state levels of HSP78 transcripts and protein varied in response to both thermal stress and carbon source with an approximately 30-fold difference between repressed levels in cells growing fermentatively on glucose at 30 degrees C and derepressed levels in heat-shocked cells growing on a nonfermentable carbon source. The response to heat shock is consistent with the presence of a characteristic heat shock regulatory element in the 5'-flanking DNA. Submitochondrial fractionation showed that hsp78 is a soluble protein located in the mitochondrial matrix. Cells carrying disrupted copies of HSP78 lacked hsp78 but were not impaired in respiratory growth at normal and elevated temperatures or in the ability to survive and retain mitochondrial function after thermal stress. The absence of a strong mitochondrial phenotype in hsp78 mutants is comparable to the nonlethal phenotypes of mutations in other Clp genes in bacteria and yeast. HSP78 is the third gene, with SSC1 and HSP60, known to encode a yeast mitochondrial heat shock protein and the second gene, with HSP104, for a yeast ClpB homolog.

Mechanisms of Stress-Induced and Electromigration-Induced Damage in Passivated Narrow Metallizations on Rigid Substrates

MRS Bulletin ◽  
1992 ◽  
Vol 17 (7) ◽  
pp. 61-69 ◽  
Author(s):  
M.A. Korhonen ◽  
P. Børgesen ◽  
Che-Yu Li
Keyword(s):  
Thermal Stress ◽  
Thermal Stresses ◽  
Elevated Temperatures ◽  
Semiconductor Industry ◽  
Pure Aluminum ◽  
Void Formation ◽  
Silicon Substrates ◽  
Thermal Expansion Coefficients ◽  
Hillock Formation ◽  
Current Densities

Narrow, passivated metal lines are generally used as interconnects in VLSI microcircuits at the chip level. In most metals, high electric current densities lead to a mass flow of constituent atoms accompanying the current of electrons. Electromigration (EM) has long been considered an important reliability concern in the semiconductor industry because the current-induced atomic fluxes can give rise to void formation and open circuits, or hillock formation and short circuits between nearby interconnects. The problem is exacerbated because of the continued trend of increasing the density of the devices on the chip. This means that the line widths of the interconnects have been reduced and are now in the submicron range; correspondingly, the current densities have increased and may be as high as 106 A/cm2. Recently, thermal-stress-induced damage in metallizations has also been recognized as an important reliability concern, perhaps of the same gravity as EM. Thermal stresses in the metallizations are caused by the different thermal expansion coefficients of the metal and the substrate. Stress-induced void and hillock formation are the main causes of in terconnect failures before service. More recently, concern has been growing that thermal stresses or thermal-stress-induced voids may enhance the subsequent electromigration damage during the service life of the microchips.For simplicity, this article addresses the case of pure aluminum metallizations on oxidized silicon substrates. However, much of what is said applies to other metal-rigid substrate systems as well, most notably to various aluminum and copper-based metallizations on ceramic substrates. The present treatment emphasizes void formation and growth in the metallizations during nd after cooldown from elevated temperatures, or those due to electromigration in service or testing conditions. Many of the mechanisms we explain are also applicable to hillock formation under compressive stresses, whether due to EM or thermal cycles during manufacturing.

scholarly journals Coral larvae suppress the heat stress response during the onset of symbiosis thereby decreasing their odds of survival

2021 ◽  
Author(s):  
Sheila A Kitchen ◽  
Duo Jiang ◽  
Saki Harii ◽  
Noriyuki Satoh ◽  
Virginia M Weis ◽  
...  
Keyword(s):  
Heat Stress ◽  
Thermal Stress ◽  
Stress Response ◽  
Elevated Temperatures ◽  
Expression Profiles ◽  
Combined Treatment ◽  
Larval Survival ◽  
Coral Larvae ◽  
Heat Stress Response ◽  
Trade Offs

The endosymbiosis between most corals and their photosynthetic dinoflagellate partners begins early in the host life history, when corals are larvae or juvenile polyps. The capacity of coral larvae to buffer climate-induced stress while in the process of symbiont acquisition could come with physiological trade-offs that alter larval behavior, development, settlement and survivorship. Here we examined the joint effects of thermal stress and symbiosis onset on colonization dynamics, survival, metamorphosis and host gene expression of Acropora digitifera larvae. We found that thermal stress decreased symbiont colonization of hosts by 50% and symbiont density by 98.5% over two weeks. Temperature and colonization also influenced larval survival and metamorphosis in an additive manner, where colonized larvae fared worse or prematurely metamorphosed more often than non-colonized larvae under thermal stress. Transcriptomic responses to colonization and thermal stress treatments were largely independent, while the interaction of these treatments revealed contrasting expression profiles of genes that function in the stress response, immunity, inflammation and cell cycle regulation. The combined treatment either canceled or lowered the magnitude of expression of heat-stress responsive genes in the presence of symbionts, revealing a physiological cost to acquiring symbionts at the larval stage with elevated temperatures. In addition, host immune suppression, a hallmark of symbiosis onset under ambient temperature, turned to immune activation under heat stress. Thus, by integrating the physical environment and biotic pressures that mediate pre-settlement event in corals, our results suggest that colonization may hinder larval survival and recruitment creating isolated, genetically similar populations under projected climate scenarios.

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