The results suggest that MBCT could work through some of the MBCT model's theoretically predicted mechanisms. However, there is a need for more rigorous designs that can assess greater levels of causal specificity.

Summary1. Thermal adaptation was investigated in the fruitfly Drosophila buzzatii Patterson and Wheeler. Two natural populations originating from a high-and a low-temperature environment, respectively, were compared with respect to Hsp70 (heat shock protein) expression, knock-down resistance and heat shock resistance. 2. Three main hypotheses were tested: (i) The expression level of Hsp70 in flies from the high-temperature habitat should be down-regulated relative to flies from the colder habitat. (ii) Flies having higher Hsp70 expression levels should be weakened most by a hardening treatment and go faster into coma, as Hsp70 level reflects stress intensity, and therefore display reduced heat knock-down resistance. (iii) Heat shock resistance should be increased in the population with highest Hsp70 expression because the level of Hsp70 is positively associated with this trait. 3. The results generally matched the hypotheses. Hsp70 expression was reduced in the high-temperature population. Knock-down resistance was higher in the hightemperature population and survival after heat shock was lower in the high-temperature population. 4. This study showed genetic differences in thermal tolerance between populations, indicating that high temperature in nature may be an important selective factor. Moreover, knock-down resistance in this study seems to be a more relevant trait than standard heat shock resistance for identifying thermal adaptation in natural populations.

1. Inducible heat‐shock proteins are synthesized when temperatures are increased to levels substantially above normal. The functional role of these proteins is well known at the cellular level. Today increasing interest has been directed towards the importance of heat‐shock proteins for resistance of whole organisms to high‐temperature stress and other environmental stressors. 2. Here the functional relationship between the heat‐shock protein, Hsp70, and thermal resistance in adult Drosophila melanogaster was examined by comparing thermal resistance, i.e. survival at 39 °C for 85 min, and levels of Hsp70 at various times elapsed (2, 4, 8, 16, 32 and 64 h) after thermotolerance was induced by short‐term acclimation/heat hardening at 37 °C for 55 min. 3. Levels of Hsp70 in both males and females were highest 2 h after heat hardening and declined with longer times elapsed. The rate of decrease initially was very fast but diminished with increasing time. After 32 h the level of Hsp70 approached the level in flies that were not hardened. Levels of Hsp70 in males exceeded that of females during the entire period. 4. Survival of both sexes increased with increasing time after heat hardening and reached an optimum between 8 and 32 h. Thereafter resistance decreased with longer times elapsed. Survival of females generally exceeded that of males except after 16 and 64 h. 5. Regression analysis applied to the data on Hsp70 levels revealed that the model describing these data could not explain the data for survival. Also, higher levels of Hsp70 in males compared with females were not associated with greater survival in males. However, statistical analysis on paired measurements of Hsp70 and survival revealed a positive association between Hsp70 level and survival at each time elapsed after induction of thermotolerance.

BackgroundInsomnia is two to three times more prevalent in cancer survivors than in the general population, where it is estimated to be 10% to 20%. Cognitive-behavioral therapy for insomnia (CBT-I) is the recommended treatment for chronic insomnia, but meeting survivor needs remains a challenge. Internet-delivered CBT-I (iCBT-I) has been shown efficacious in otherwise healthy adults. We tested the efficacy of iCBT-I in breast cancer survivors with clinically significant sleep disturbance.MethodsWomen from a national sample of Danish breast cancer survivors who experienced clinically significant sleep disturbance were randomly allocated to iCBT-I or waitlist control (55:45). The fully automated iCBT-I program consisted of six cores. Online measures of insomnia severity, sleep quality, and fatigue were collected at baseline, postintervention (nine weeks), and follow-up (15 weeks). Online sleep diaries were completed over two-week periods pre- and postintervention. Intention-to-treat analyses (time × group interactions) were conducted with mixed linear models and corrected for multiple outcomes. All statistical tests were two-sided.ResultsA total of 255 women were randomly allocated to iCBT-I (n = 133) or waitlist control (n = 122). Statistically significant (P ≤ .02) time × group interactions were found for all sleep-related outcomes from pre- to postintervention. Effect sizes (Cohen’s d) ranged from 0.33 (95% confidence interval [CI] = 0.06 to 0.61) for wake after sleep onset to 1.17 (95% CI = 0.87 to 1.47) for insomnia severity. Improvements were maintained for outcomes measured at follow-up (d = 0.66–1.10).ConclusionsiCBT-I appears to be effective in breast cancer survivors, with additional benefit in terms of reduced fatigue. This low-cost treatment could be incorporated in cancer rehabilitation programs.

Knockdown resistance to high temperature is an ecologically important trait in small insects. A composite interval mapping was performed on the two major autosomes of Drosophila melanogaster to search for quantitative trait loci (QTL) affecting knockdown resistance to high temperature (KRHT). Two dramatically divergent lines from geographically different thermal environments were artificially selected on KRHT. These lines were crossed to produce two backcross (BC) populations. Each BC was analysed for 200 males with 18 marker loci on chromosomes 2 and 3. Three X-linked markers were used to test for X-linked QTL in an exploratory way. The largest estimate of autosome additive effects was found in the pericentromeric region of chromosome 2, accounting for 19.26% (BC to the low line) and 29.15% (BC to the high line) of the phenotypic variance in BC populations, but it could represent multiple closely linked QTL. Complete dominance was apparent for three QTL on chromosome 3, where heat-shock genes are concentrated. Exploratory analysis of chromosome X indicated a substantial contribution of this chromosome to KRHT. The results show that a large-effect QTL with dominant gene action maps on the right arm of chromosome 3. Further, the results confirm that QTL for heat resistance are not limited to chromosome 3.