scholarly journals Acclimation, duration and intensity of cold exposure determine the rate of cold stress accumulation and mortality in Drosophila suzukii

2021 ◽  
pp. 104323
Author(s):  
Pénélope Tarapacki ◽  
Lisa Bjerregaard Jørgensen ◽  
Jesper Givskov Sørensen ◽  
Mads Kuhlmann Andersen ◽  
Herve Colinet ◽  
...  
1959 ◽  
Vol 37 (1) ◽  
pp. 671-677
Author(s):  
Doris Nicholls ◽  
Rosemary Molloy ◽  
Kathleen Stavraky ◽  
R. J. Rossiter

The incorporation of inorganic phosphorus labelled with P32 into the inorganic phosphorus of the adrenal gland was measured in rats acclimatized to cold for 4 weeks. Previously it was reported that the immediate pituitary–adrenal response to brief cold exposure (2 hours at −5 °C), as judged by the increased P32 incorporation is considerably decreased in rats that have been acclimatized. Some observations are now reported on the mechanism of this reduced immediate response.The administration of ACTH, pitressin, or adrenaline caused similar increases in the adrenal phosphorus metabolism in acclimatized and non-acclimatized control rats. Acclimatization could still be demonstrated in rats after the fur had been removed by clipping.From these results it is concluded that the decreased immediate pituitary–adrenal response to an exposure to more severe cold, observed in acclimatized rats, is not the result of an increased fur thickness, nor is it the result of a decreased sensitivity of the adrenal tissue to ACTH, or to a decreased sensitivity of the pituitary or hypothalamus to a given stimulus. It is suggested that the reduction in the immediate pituitary–adrenal response to a more severe cold stress in acclimatized rats might be due to an alteration in the sensitivity of the peripheral nerve receptors, or in the mechanism, nervous or otherwise, whereby the pituitary is stimulated.


1959 ◽  
Vol 14 (1) ◽  
pp. 43-45 ◽  
Author(s):  
M. B. Kreider ◽  
P. F. Iampietro ◽  
E. R. Buskirk ◽  
David E. Bass

Effects of continuous cold stress on 24-hour patterns of body temperature were studied in five men. Cold stress consisted in living at 15.6℃ (60℉) for 14 days wearing only shorts. The cold period was preceded and followed by 2 weeks at 26.7℃ (80℉). Activity (minimal) and diet were the same for all periods. One blanket was used at night. Rectal temperature (Tr) and skin temperature (Ts) were measured. Tr during sleep fell more rapidly and to lower values during cold exposure (35.6℃) than during the control period (36.1℃). Ts during sleep was slightly lower in the cold than in the control period; also, Ts did not exhibit the gradual drop characteristic of sleep in the control period. Comparison of Tr and Ts between early and later cold days revealed the following differences: a) nocturnal Tr fell to lower levels on the later cold days; b) nocturnal toe temperatures were 15℃ (27℉) higher on the later cold days. The arch temperatures followed the same pattern as the toes. No significant differences were found in daytime temperatures between early and later cold days. The data suggest that evidence for acclimatization to cold in terms of altered body temperature responses may be fruitfully sought in responses during rewarming and/or sleep. Submitted on September 19, 1958


1964 ◽  
Vol 19 (1) ◽  
pp. 9-12 ◽  
Author(s):  
Jacques Leblanc ◽  
M. Pouliot ◽  
S. Rheaume

Previous studies have shown a decreased response in fishermen to cold applied locally. In the present study, the same subjects, when exposed naked for 1 hr at 60 F maintained a higher skin temperature than a control group. If these findings indicate a decreased vasoconstriction, all results obtained to date on these fishermen would indicate a decreased adrenergic response. Evidence of gross shivering was much more pronounced in the fishermen but this was not reflected by greater heat production. Both groups excreted more hydroxycortisone in the cold, and the excretion was higher in the control subjects. Cold exposure did not increase the catecholamine excretion in either group. Note: (With the Technical Assistance of P. Tousignant) acclimatization; body temperature; skin temperature; vasomotor adaptation; shivering; adrenergic response in cold habituation; hydroxycortisone excretion in cold stress Submitted on June 17, 1963


Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 612 ◽  
Author(s):  
Bin Xu ◽  
Li-min Lang ◽  
Shi-Ze Li ◽  
Jing-Ru Guo ◽  
Jian-Fa Wang ◽  
...  

Cold stress can induce neuronal apoptosis in the hippocampus, but the internal mechanism involving neuronal loss induced by cold stress is not clear. In vivo, male and female C57BL/6 mice were exposed to 4 °C, 3 h per day for 1 week. In vitro, HT22 cells were treated with different concentrations of cortisol (CORT) for 3 h. In vivo, CORT levels in the hippocampus were measured using ELISA, western blotting, and immunohistochemistry to assess the neuronal population and oxidation of the hippocampus. In vitro, western blotting, immunofluorescence, flow cytometry, transmission electron microscopy, and other methods were used to characterize the mechanism of mitochondrial damage induced by CORT. The phenomena of excessive CORT-mediated oxidation stress and neuronal apoptosis were shown in mouse hippocampus tissue following cold exposure, involving mitochondrial oxidative stress and endogenous apoptotic pathway activation. These processes were mediated by acetylation of lysine 9 of histone 3, resulting in upregulation involving Adenosine 5‘-monophosphate (AMP)-activated protein kinase (APMK) phosphorylation and translocation of Nrf2 to the nucleus. In addition, oxidation in male mice was more severe. These findings provide a new understanding of the underlying mechanisms of the cold stress response and explain the apoptosis process induced by CORT, which may influence the selection of animal models in future stress-related studies.


2006 ◽  
Vol 31 (4) ◽  
pp. 480-481
Author(s):  
Carla L.M. Geurts

The research in this thesis investigated the effects of cold stress on neuromuscular function with the main focus on cold acclimation. In total, 6 studies, 1 field study and 5 experiments, were conducted. The field study showed that during manual work in cold weather, finger and hand temperature can drop to levels that may impair manual function. The first 2 experiments were conducted to investigate the effect of acute local cold stress on force control and to investigate the effect of cold-induced vasodilatation (CIVD) on neuromuscular function. In experiment 1, it was found that cooling of the hand in 10 °C cold water for 10 min did not improve force control, although neuromuscular function was significantly impaired after cooling. In experiment 2, cold-induced vasodilatation, occurring after 20 min of 8 °C cold-water immersion of the hand, was confined to the finger tip and had no effect on the temperature of the first dorsal interosseus (FDI) muscle or its neuromuscular function. A series of cold acclimation studies was conducted to investigate the effect of repeated cold-water hand immersions on neuromuscular function. In these experiments, neuromuscular function was tested before and after 2–3 weeks of daily hand immersion in 8 °C cold water for 30 min. In experiment 3, it was found that 3 weeks of cold-water immersion resulted in a decrease in minimum and mean index finger temperature and CIVD was attenuated. Neuromuscular function was not affected by this change in temperature response. In experiment 4, one hand was exposed daily to cold water and compared with the opposite control hand. Blood plasma catecholamine concentrations were increased after 2 weeks in the cold-exposed hand, but no changes in temperature response or neuromuscular function were found after repeated cold exposure. Thermal comfort after 30 min of cold-water immersion significantly improved after repeated cold exposure causing a discrepancy between actual and perceived temperature and it was suggested that this may impose a greater risk of cold injury owing to a change in behavioural thermoregulation. In the last experiment, core temperature was elevated by bicycling at a submaximal level during the cold hand immersion. Exercise had a direct effect on the temperature response during cold-water immersion, decreasing the minimum FDI temperature and slowing down the deteriorating effect of cold on neuromuscular function; however, exercise showed was no effect on local cold acclimation. It is concluded that local repeated cold exposures may improve finger and hand temperature and subjective thermal ratings, but that these changes are too small to improve neuromuscular function. The best remedy to maintain manual function is to limit or avoid cold stress as much as possible. If sufficient protection of the hands is impossible, core heating through exercise or passive heating may be a solution.


1982 ◽  
Vol 52 (4) ◽  
pp. 1024-1029 ◽  
Author(s):  
I. R. Oddershede ◽  
R. S. Elizondo

The purpose of this study was to examine body fluid adjustments during prolonged cold exposure in primates. Six male rhesus monkeys were acclimated for 35 days and 6 degrees C and 80% rh. Red cell mass, extracellular fluid volume, and total body water (TBW) were determined with 51Cr, 35SO4, and 3H2O, respectively, prior to and at various intervals during the cold stress. TBW was increased throughout the exposure, whereas changes in extravascular compartments had occurred within the 1st wk of cold exposure, after which they returned to control values. An increased concentration of blood constituents on day 1 was not accompanied by a decrease in cardiovascular volume. Blood volume and plasma volume in relation to TBW were significantly increased on day 3 and remained increased during the remainder of the exposure. These cardiovascular volume changes were accompanied by a significant hemodilution on day 3 and a gradual return to control values. An increased plasma osmolality and expansion of the erythrocytes (decrease in mean corpuscular hemoglobin concentration) were observed throughout the cold stress. These data suggest that the rhesus monkey may be an adequate primate model for studies of body fluid adjustments, especially during prolonged cold exposure, in primates in general, including the human.


2021 ◽  
Author(s):  
Jiaying Hu ◽  
Heng Wei Cheng

Abstract Background: Cold temperature is a common environmental stressor that has a great impact on the poultry industries, inducing pathophysiological stress in birds with profound economic losses. Current methods used for preventing cold stress, such as reducing ventilation and using gas heaters, are facing challenges due to poor indoor air quality and its deleterious effects on bird and caretaker health. The aim of this study was to examine if the novelly designed warmed perch system, as a thermal device, can reduce cold stress-associated adverse effects on laying hens. Methods: Seventy-two 32-week-old DeKalb hens were randomly assigned to 36 cages arranged to 3 banks. The banks were assigned to 1 of 3 treatments: cages with warmed perches (WP; perches with circulating water at 30 oC), air perches (AP, regular perches only) or no perches (NP) for a 21- day trial. The room temperature was set at 10 oC during the entire experimental period. Rectal temperature and body weight were measured from the same bird of each cage at day 1, 8, 15, and 21 during the cold exposure. Egg production was recorded daily. Feed intake, egg and eggshell quality were determined during the 1st and 3rd week of cold stress. Plasma levels of corticosterone, thyroid hormones (3, 3’, 5-triiodothyronine and thyroxine), interleukin (IL)-6 and IL-10, were determined at day 1 and 21 post initiation of cold exposure. Results: Compared to both AP and NP hens, WP hens were able to maintain their body temperature without increasing feed intake and losing body weight. The eggs laid by WP hens had thicker eggshell during the 3rd week of cold exposure. Warmed perch hens also had a lower thyroxine conversion rate (3, 3’, 5-triiodothyronine/thyroxine) at day 1, while higher plasma concentrations of IL-6 at day 21. Plasma levels of corticosterone, 3, 3’, 5-triiodothyronine, and IL-10 were not different among treatments. Conclusions: Our results indicate that the warmed perch system can be used as a novel thermal device for preventing cold stress-induced negative effects on hen health and welfare through regulating innate immunity and metabolic hormonal homeostasis.


Author(s):  
Андрей Одиреев ◽  
Andrey Odireev ◽  
Ксения Килимченко ◽  
Kseniya Kilimchenko ◽  
Николай Безруков ◽  
...  

To date, the role of dysfunction of the bronchial ciliated epithelium (BCE) in the formation of mucociliary disorders during cold exposure has not been fully established. The aim of the study was to investigate the nature and severity of changes in the ciliary motility of the BCE under the influence of a cold stimulus in vitro. Ten volunteers with asthma underwent a bronchoscopy with biopsy of the lobar bronchus mucosa. The biopsy specimens were placed in a Hank’s balanced salt solution (HBSS) on a slide, located on the thermal stage, used to simulate the effect of various temperature on the BCE. Ciliary beat frequency (CBF, Hz) was recorded using a microscope, high-sensitivity digital camera and computer with specially developed software. The initial recording of CBF was performed at 24ºC, after which the temperature of HBSS was gradually increased to physiological level and repeated recording was made at the control points (28ºC and 36ºC). Then, the temperature of the solution was lowered and CBF was registered again at 28ºC, 21ºC and 17ºC. The initial CBF of the BCE varied from 6.74 to 3.77 Hz with average of 5.25±1.48 Hz (M±m). There was a statistically significant increase in CBF when the solution was heated: at 28ºC it was 6.33±1.36 Hz (p=0.004) and remained at this level up to 36ºC – 7.14±1.33 Hz (p=0.002). A gradual decrease in the solution temperature produced a reduction in CBF in comparison with the physiological conditions: 28ºC – 6.12±1.31 Hz (p=0.121), 21ºC – 5.27±1.32 Hz (p=0.001) and 17ºC – 3.95±1.18 Hz (p=0.0001). By the end of the experiment, CBF of the BCE decreased almost 2-fold in comparison with the physiological conditions. A mathematical model that characterizes the behavior of BCE cilia under cold stress was developed. Thus, the results of the study demonstrate a marked decrease in the motor activity of the BCE cilia under cold stress, which underlines a significant contribution of the functional disturbance of BCE to the pathophysiological mechanisms of hypersecretory disorders induced by inhalation of cold air.


1979 ◽  
Vol 59 (4) ◽  
pp. 721-726 ◽  
Author(s):  
P. E. V. WILLIAMS ◽  
R. O. PARKER ◽  
B. A. YOUNG ◽  
F. X. AHERNE

Radioactive ruthenium labelled microspheres 15 ± 3 μm in diameter were used to determine distribution of cardiac output in unfed control (35 °C) and unfed cold stressed (5 °C) piglets 3.5 h of age. The cold stress produced an average 7.1 °C drop in rectal temperature and a redistribution of blood flow. In cold exposed piglets the adrenal fraction of cardiac output was significantly (P < 0.05) lower: 0.56% in the control compared with 0.29% in the cold exposed piglets; however, the relative blood flow to the adrenals was higher than for other tissues. The fractions of cardiac output reaching the psoas and biceps muscles increased (P < 0.05) by 148 and 260%, respectively, during cold exposure, while that reaching the heart, brain, alimentary tract, skin and fat was not significantly (P > 0.05) affected by cold exposure.


2019 ◽  
Vol 20 (10) ◽  
pp. 2456 ◽  
Author(s):  
Huanyu Lu ◽  
Shan Tang ◽  
Chong Xue ◽  
Ying Liu ◽  
Jiye Wang ◽  
...  

Cold exposure stress causes hypothermia, cognitive impairment, liver injury, and cardiovascular diseases, thereby increasing morbidity and mortality. Paradoxically, cold acclimation is believed to confer metabolic improvement to allow individuals to adapt to cold, harsh conditions and to protect them from cold stress-induced diseases. However, the therapeutic strategy to enhance cold acclimation remains less studied. Here, we demonstrate that the mitochondrial-derived peptide MOTS-c efficiently promotes cold adaptation. Following cold exposure, the improvement of adipose non-shivering thermogenesis facilitated cold adaptation. MOTS-c, a newly identified peptide, is secreted by mitochondria. In this study, we observed that the level of MOTS-c in serum decreased after cold stress. MOTS-c treatment enhanced cold tolerance and reduced lipid trafficking to the liver. In addition, MOTS-c dramatically upregulated brown adipose tissue (BAT) thermogenic gene expression and increased white fat “browning”. This effect might have been mediated by MOTS-c-activated phosphorylation of the ERK signaling pathway. The inhibition of ERK signaling disturbed the up-regulatory effect of MOTS-c on thermogenesis. In summary, our results indicate that MOTS-c treatment is a potential therapeutic strategy for defending against cold stress by increasing the adipose thermogenesis via the ERK pathway.


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