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Climate change is restructuring biodiversity on multiple scales and there is a pressing need to understand the downstream ecological and genomic consequences of this change. Recent advancements in the field of eco‐evolutionary genomics have sought to include evolutionary processes in forecasting species' responses to climate change (e.g., genomic offset), but to date, much of this work has focused on terrestrial species. Coastal and offshore species, and the fisheries they support, may be even more vulnerable to climate change than their terrestrial counterparts, warranting a critical appraisal of these approaches in marine systems. First, we synthesize knowledge about the genomic basis of adaptation in marine species, and then we discuss the few examples where genomic forecasting has been applied in marine systems. Next, we identify the key challenges in validating genomic offset estimates in marine species, and we advocate for the inclusion of historical sampling data and hindcasting in the validation phase. Lastly, we describe a workflow to guide marine managers in incorporating these predictions into the decision‐making process. [ABSTRACT FROM AUTHOR]

Objective: To determine whether the adducts formed when benzo(a)pyrene, a diol epoxide derivative, binds covalently to DNA (BPDE-DNA adducts) are detectable in the sperm of men who smoke cigarettes., Design: Prospective study., Setting: The Toronto Hospital IVF-ET program., Patient(s): Twenty-three patients with normal seminal parameters: 11 smokers (20.6 +/- 0.7 cigarettes per day) and 12 nonsmokers., Intervention(s): Semen samples obtained by masturbation., Main Outcome Measure(s): Seminal plasma samples were assessed for cotinine by RIA. Sperm were treated with dithiothreitol to release disulfide bonds and allow for DNA binding, then exposed to an anti-BPDE monoclonal antibody, a biotinylated antibody, and streptavidin-conjugated peroxidase. Staining intensity scores, determined in 100 cells per individual, were correlated with seminal plasma cotinine levels, a marker of smoking., Result(s): Cotinine levels correlated highly with the number of cigarettes smoked per day. Mean cotinine levels and mean staining intensity scores were higher in smokers than in nonsmokers. Staining intensity correlated highly with cotinine levels., Conclusion(s): We demonstrated, for the first time, that BPDE-DNA adducts in sperm cells are increased by smoking; we also detected comparatively high levels in nonsmokers, which indicates that environmental exposure also is substantial. The formation of adducts in spermatozoa is a potential source of transmissible prezygotic DNA damage.

Tobacco smoking is deleterious to reproduction. Benzo[a]pyrene (B[a]P) is a potent carcinogen in cigarette smoke. Its reactive metabolite induces DNA-adducts, which can cause mutations. We investigated whether B[a]P diol epoxide (BPDE) DNA adducts are detectable in preimplantation embryos in relation to parental smoking. A total of 17 couples were classified by their smoking habits: (i) both partners smoke; (ii) wife non-smoker, husband smokes; and (iii) both partners were non-smokers. Their 27 embryos were exposed to an anti-BPDE monoclonal antibody that recognizes BPDE-DNA adducts. Immunostaining was assessed in each embryo and an intensity score was calculated for embryos in each smoking group. The proportion of blastomeres which stained was higher for embryos of smokers than for non-smokers (0.723 versus 0.310). The mean intensity score was also higher for embryos of smokers (1.40+/-0.28) than for non-smokers (0.38+/-0.14; P = 0.015), but was similar for both types of smoking couples. The mean intensity score was positively correlated with the number of cigarettes smoked by fathers (P = 0.02). Increased mean immunostaining in embryos from smokers, relative to non-smokers, indicates a relationship with parental smoking. The similar levels of immunostaining in embryos from both types of smoking couples suggest that transmission of modified DNA is mainly through spermatozoa. We confirmed paternal transmission of modified DNA by detection of DNA adducts in spermatozoa of a smoker father and his embryo.

Purpose: Our purpose was to determine whether there is variation in levels of follicular fluid (FF) cotinine between the two ovaries of women undergoing IVF-ET who are exposed to cigarette smoke., Methods: In 61 women, there were two to four determinations of FF continine levels for each of two follicles, one from each ovary. For each woman a t test for significant difference between the means of both ovaries was done to test for interovarian variation., Results: Thirty-seven nonsmokers, 8 passive smokers, and 16 active smokers differed greatly (P < 0.0001) in mean FF cotinine levels: 13.0, 91.1, and 420.3 ng/ml, respectively. Fourteen women had significant differences, at the P = 0.025 level or below, between their two ovaries. Five of them had differences significant at the 0.001 level. Even so, the correlation between the cotinine levels of the two ovaries was high., Conclusions: Cotinine uptake between the two ovaries of a woman may differ approximately one-fourth of the time. In spite of these differences, the overall correlation between ovaries is high. The clear distinction in levels of FF cotinine among active, passive, and nonsmokers demonstrates the reliability of FF cotinine testing. Detection of cotinine in a large proportion of nonsmokers shows how pervasive nicotine is in the environment.

Objective: To assess cotinine, a metabolite of nicotine, in follicular fluids (FF) of women who smoke either actively or passively or not all., Design: Controlled clinical study., Setting: Infertile patients in a hospital IVF-ET program., Patients: One hundred eleven women classified by smoking habits: active smokers (n = 44), passive smokers (n = 17), or nonsmokers (n = 50)., Interventions: Ovarian hyperstimulation., Main Outcome Measure: Cotinine levels in FF., Results: A strong correlation between number of cigarettes smoked and levels of FF cotinine was found. The levels of FF cotinine were: active smokers 710.4 +/- 128.2, passive smokers 76.3 +/- 56.5, and nonsmokers 4.2 +/- 2.0 ng/mL (mean +/- SEM). The level in active smokers was significantly greater than in other groups. The levels of FF cotinine in passive smokers differed significantly from nonsmokers. Eighty-four percent of nonsmokers actually were exposed to nicotine, with a mean value of 5.0 ng/mL., Conclusions: Cotinine was detectable in a dose-dependent manner in active and passive smokers. It was detected in all active smokers and in a majority of passive smokers and self-reported nonsmokers. A strong interindividual variation suggests differences in metabolism and smoking habits. Follicular fluid cotinine assessments are useful for infertility studies.

The present study examined the contribution of genetic factors to Digit Symbol performance and its decline in 23 monozygotic twin pairs (mean age at examination 1, 57.1 years) and 21 dizygotic twin pairs (mean age at examination 1, 56.3 years). These men were assessed twice during a 5-year interval as part of the National Heart, Lung, and Blood Institute Twin Study. The prevalence of decline (a change, greater than 1 SD) during the 5-year interval was 35% and 39% for monozygotic and dizygotic twins, respectively. The pairwise concordance for decline was 45% in monozygotic and 8% in dizygotic twin pairs, suggesting a possible role for genetic factors in the decline in Digit Symbol performance in this sample. A comparison of baseline biologic and behavioral characteristics within monozygotic twin pairs discordant for decline in Digit Symbol performance revealed that decliners had higher initial systolic blood pressures, lower serum cholesterol levels, and lower heart rates than nondecliners.

Earlier reports indicated that sperm from 25% of patients from infertile couples, but not from normal or fertile donors, show deviations from the theoretical Poisson distribution of the number of sperm penetrating zona-free hamster ova. Using semen samples from 15 grandfathers (aged 60 to 84 years) and 24 young fathers (aged 25 to 36 years), this study analyzed whether age also has an effect on the distribution. It was found that the overall fit to the Poisson distribution of the samples from grandfathers was very poor; in contrast, the samples from young fathers fit well. The observed deviations from the Poisson distribution among grandfathers may be a consequence of their long periods of sexual abstinence. Decrease in sexual activity produces age-different populations of sperm that probably differ in penetrating ability. Samples from older fathers also show a worse fit to the Poisson distribution than do those from younger fathers. These results suggest that the duration of sperm storage in the genital tract after maturation has an effect on sperm function.

The effects in vivo of acute doses of ethanol on impulse transmission in the region of the neuromuscular junction are poorly known. These effects were studied with a new procedure, using mouse tails in a constant temperature chamber to study the delay in nerve-to-muscle impulse transmission. A saline control and five ethanol doses (0.5, 1.0, 1.4, 2.0, 4.24 g/kg) were used with 96 mice. The interval ("residual latency", RL), between (a) the peak of the compound nerve action potential and (b) the first peak of the associated compound muscle action potential, was measured. Ethanol was given IP and tail nerve stimulations were done at 4 min intervals to 16 min post-ethanol. The mean pre-ethanol RL was 0.93 +/- 0.01 (SE) msec; about 25% of this time should be synaptic delay and the remainder is nerve and muscle fiber conduction time. Individual post-ethanol relative RL (RRL) values were calculated for each moue, based on its pre-ethanol value. With doses of 1.0 g/kg and higher there was a mean increase in RRL; at 16 min this increase was 0.8 to 4.4% (all p less than 0.01). At 0.5 g/kg, and also at higher doses, there was a significantly (p less than 0.01) increased variance in RRL 8 to 16 min post-ethanol. A marked correspondence between mean RRL and ataxia is apparent. This appears to be the first in vivo demonstration of acute effects of ethanol on neuromuscular transmission. The methods and mice used may comprise a useful animal model for detecting acute effects of low doses of ethanol on synaptic function.