Association between temperature and maternal stress during pregnancy.
Relationship between Temperature and Stress of Ultraviolet-Curable Resin during Curing. E. Umezaki1a and H. Koyama2. 1Dept. of Mechanical Engineering. Download scientific diagram | The relationship between the surface stress and temperature, contrasting with the yield strength and ultimate tensile strength. from . This study was investigated what affect strength and temperature distribution by fiber orientation variation under tension test of GFRP.
These impacts can take the form of damage to human health, reductions in labor productivity and supply, and possible reductions in the rate of human capital accumulation—all of which may decrease gross domestic product GDP and overall social welfare in both the short and long run. In this Reflections, we review this emerging literature on the economics of extreme heat stress, focusing on several recent panel studies that permit causal identification of its consequences.
These findings make a compelling case for including labor-related impacts in integrated assessment models, which estimate the social cost of carbon, and highlights the possibility of climate change affecting poorer populations disproportionately. The recent economics literature offers two key methodological innovations, which we argue should be expanded. First, these studies provide causal estimation of the impacts of temperature in economically relevant contexts, shoring up weaknesses inherent in cross-sectional studies omitted variable bias and laboratory experiments limited contextual relevance.
Second, the new literature allows for more inclusive welfare analysis than the existing biomedical or policy simulation literature, analysis that accounts for behavioral responses of firms and individuals to temperature stress as well as for interactions with institutional settings. This orientation is especially relevant to the context of climate policy, since the realized welfare consequences of climate change will vary tremendously both across geographies due, for instance, to different institutional settings and across time given the prospect of adaptation.
We begin the next section with a brief overview of the biological basis for direct, temperature-driven welfare impacts. Then we present a stylized review of the emerging economics of temperature stress and human activity.
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We conclude with a discussion of potential policy implications, as well as directions for future research. The Biology of Temperature Stress Human beings are biological organisms, with clear biological constraints on the environments in which we can live and function comfortably.
A key feature of our environment is the combination of temperature and humidity that determines the heat balance of the human organism.
Anyone who has watched construction workers toil in midday heat or attended a class in a freezing lecture hall can readily attest to the clear link between temperature stress and human performance. Physiological Consequences of Exposure to Extreme Temperature As the body heats, it uses its stores of water and salt to create sweat, which dissipates heat.
If heat stress is prolonged and these stores are not adequately replenished, heat begins to cause dizziness, muscle cramps, and fever. In the extreme, hot or cold temperatures can cause acute cardiovascular, respiratory, and cerebrovascular reactions.
A longstanding literature on industrial ecology and physiology, pioneered by experimental studies of British naval officers Mackworthdocuments a systematic relationship between temperature stress and reduced performance.
Numerous lab experiments have quantified this relationship by randomly assigning subjects to rooms of varying temperatures and asking them to perform cognitive and physical tasks such as guiding a steering wheel or deciphering Morse code Grether ; Froom et al. These findings are summarized in figure 1reproduced from Seppanen, Fisk, and Leiwhich shows how task performance normalized to one at its best falls off with departures from the optimal temperature.
Given the well-documented cross-sectional relationship between tropical climates and low standards of living, it may be tempting to extrapolate the impacts of climate change on economic productivity based on the experimental literature e.
However, several factors must be taken into account to perform welfare analysis aimed at informing economic policy. Economically Relevant Contexts First, we must account for the ways in which individuals respond to temperature stress, which requires estimation of heat-related impacts in economically relevant contexts rather than in the lab. Behavioral responses—and the incentive systems that may constrain them—are especially important in the context of extreme temperature shocks, because there are many possible margins of adjustment and the final welfare impact will depend in part on the incentives individuals face in choosing certain adjustments over others.
For example, a worker at a manufacturing plant may respond to an unusually hot day in a number of ways. She may choose to wear lighter clothing or to take a taxi rather than walk to work.
She may turn on a fan at her workstation or ask to turn up the air conditioning if it is available. If these options are not available, and the heat stress is severe, she may decide to work fewer hours that day, to petition to work a night shift, or to call in sick.
She may also decide to work less intensively, taking more frequent breaks. Whether or not she decides to adjust her hours or reduce her effort will depend in large part on how she is paid. Thus the optimal response for someone who is paid a piece rate contract—in which payment is directly proportional to how much output she produces—will differ from someone who is paid on a fixed annual contract or simply by the hour.
Curiously enough, the most affected mutants in P5 trx3 and ahp1 were the less affected mutants in P This result reinforces the correlation between low temperature and oxidative stress in the P24 strain because the deletion of genes involved in response to this latter stress also affected its growth capacity at low temperature.
However, this correlation was not confirmed in the P5 strain, in which most mutants were not affected when grown at a low temperature. The only gene whose deletion in both heterozygosity and homozygosity provoked growth impairment in the P5 strain was AHP1, which encodes a thiol-specific peroxiredoxin that reduces hydroperoxides to protect against oxidative damage Trivelli et al. Relative growth rate of the mutants constructed in the background of a wine strain.
The selected genes of the BY collection were deleted in strains P5 and P24 and their fitness was tested under different conditions. It was noteworthy that mutants' growth capacity was not so widely affected in SM as in YPD at low temperature. This is striking because SM is a much more stressful medium because of high sugar and low nitrogen concentrations, low pH, etc. Together with growth capacity, we were also interested in these mutants' fermentation capacity because they were constructed in two strains used industrially for wine fermentations.
T values below 1 indicated faster sugar consumption, while T values over 1 implied a delayed fermentation end compared with control strains P5 and P In this case, only the homozygous mutants were analyzed because we expected a higher impact on fermentation activity as a result of the deletion of both copies of a gene. Figure 5A shows the relative T of the P5 deletant strains. Conversely to growth data, a delay in the fermentation process at low temperature took place with most strains, except for genes TSA1 and GLR1.
The mutants with the most affected phenotypes were MUP1, and specially AHP1, whose deletion rendered this mutant incapable of ending fermentation at both temperatures. Generally speaking, end of fermentation was delayed longer for the mutants constructed in P24 than for the P5 mutants. T is the time needed to consume the total amount of sugars present in the must. The T value was compared with the control normalized as value 1.
Indicates a stuck fermentation before T Discussion In a previous study we selected two wine strains P5 and P24 based on their divergent phenotype at a low, but not at optimum, temperature.
The transcriptomics analysis revealed key changes in the sulfur assimilation pathway and in other genes involved in oxidative stress defense at low temperature.
So we hypothesized that low temperature adaptation and oxidative stress can share common protective mechanisms. Hence the present work aimed to investigate the relationship between low-temperature adaptation and recovery after oxidative stress shock.
For this purpose, we analyzed the growth of 40 S. Our results revealed that low-temperature growth correlated highly with the behavior of cells against most of the assayed oxidants, but particularly with hydrogen peroxide.
Thus our results clearly correlated low temperature and the oxidative stress produced by some strong oxidant molecules. However, one question remains: Previous studies have demonstrated that a downward shift in the growth temperature of S. Recently, two independent studies Paget et al. In both strategies, the S. In order to assess a direct implication of the cellular mechanisms involved in the oxidative stress response during adaptation at low temperature, different homozygous mutants of the BY strain were tested for their fitness to grow at low temperature.
Although most of these genes showed impaired growth for any of the conditions tested at low temperature, we only selected 10 genes, those that showed a severe growth defect, to construct heterozygous and homozygous mutants in both wine strains with different competitiveness at low temperature.
One striking result was that the growth of practically all the heterozygous mutants deletion of one copy was strongly affected after oxidative shock, and exhibited a haploinsufficient growth defect. Haploinsufficiency is defined as a dominant phenotype in diploid organisms that are heterozygous for a loss-of-function allele.
However, in this set of genes related with oxidative stress, the retention of a single copy, which implies reduced gene dosage, was not enough to fight against and recover after an oxidative stress response.
This denotes the importance of proper protein production on these oxidative response pathways. Conversely, few heterozygous or homozygous mutants of P5 displayed impaired growth at low temperature, which correlates with its better fitness for this condition and denotes a lower dependency of the oxidative stress protection.
It is also interesting the different response obtained in both media, wherein growth capacity was less affected in SM. The deletion of some genes that relaxed these strict controls might be beneficial in a stressful and complex medium as SM.
As P5 and P24 have a wine origin, we also tested the fermentation capacity of the homozygous mutants constructed in these strains.
Regarding the P5 mutants, most of the genes also impacted fermentation activity at low temperature, but deletion of MUP1 was quite remarkable as it increased the fermentation time by more than 2. MUP1 is a high-affinity methionine permease that is also involved in cysteine uptake Kosugi et al. As explained above, this strain showed a very active up-regulated sulfur assimilation pathway at low temperature, and the phenotype observed for mup1 also evidenced the need for sulfur amino acid uptake during wine fermentation at low temperature.
Another gene to consider was AHP1, a thiol-specific peroxiredoxin that reduces hydroperoxides Trivelli et al. The deletion of this gene in P5 strongly impaired the growth rate and produced a stuck fermentation in the strain P5 at both temperatures. However, this phenotype was temperature-independent and strain-dependent because the deletion of AHP1 in P24 did not lead to the greatest reduction in growth and fermentation fitness.
Strangely enough, the deletion with the strongest impact on the fermentation activity of P24 was URM1, a gene which encodes an ubiquitin-related protein that serves as a post-translational modification of other proteins. The Urm1p conjugation has been implicated in the budding process and in nutrient sensing. Nevertheless, if the Ahp1p-Urm1p conjugate was necessary for a proper antioxidant response, why did the disruption of one of these genes strongly affect the fitness in P5, but not in P24, and vice versa?
Further future studies will be necessary to answer this question. In conclusion, we clearly established herein a strong correlation between low temperature fitness and oxidative stress resistance in S. Our hypothesis is that growing this yeast at a suboptimal temperature raises the intracellular levels of ROS and induces an antioxidant response. The fitter strains to fight against this oxidative stress are also the strains that display better growth and fermentation performance at low temperature.
This correlation is also very interesting from an applied point of view because it could be a trait for future selections of industrial cryotolerant strains or for the genetic improvement of them. An alternative strategy could be the long-term culture of these strains in the presence of oxidants to obtain fitter genetic variants to cope with the oxidative stress and to better adapt to low temperature.
In order to assess this correlation at the molecular level, we constructed mutants of the genes involved on the main antioxidant response pathways in two wine strains with a divergent phenotype at low temperature. The growth and fermentation fitness of P24 was seen to strongly depend on an optimal oxidative stress response. With P5, this being the strain that displayed better competitiveness at low temperature, the deletion of key oxidative stress defense genes did not lead to a general reduction in its fitness.
- Association between temperature and maternal stress during pregnancy.
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As low temperature adaptation is a trait that is regulated by many complex mechanisms at different levels in the cell, P5 must cope with this stress by other alternative mechanisms of stress response.