Esterase 6 and reproduction in Drosophila melanogaster.

A nonspecific carboxylesterase (esterase 6) of Drosophila melanogaster shows greater activity in adult males than in females and is highly concentrated in the anterior ejaculatory duct of the reproductive tract of the male. Esterase 6 is depleted in males by copulation and is transferred to females early during copulation as a component of the seminal fluid. That esterase 6 may be involved in a system controlling the timing of remating is suggested by differences in the activity of this enzyme in a strain of Drosophila selected for a decrease in time to remating and by differences in the timing of remating in females initially inseminated by males lacking or having active esterase 6.

Studies of esterase 6 in Drosophila melanogaster. VI. ejaculate competitive abilities of males having null or active alleles.

Recent studies of the function of the polymorphic seminal fluid enzyme, esterase 6, of Drosophila melanogaster suggested that it may act in the process of sperm displacement (Gilbert, Richmond and Sheehan, 1981a). This report examines the competitive ability of ejaculates from males homozygous for null or active alleles of esterase 6 under three experimental conditions that model aspects of sexual selection affecting males. The results demonstrate no significant difference in ejaculate competition between esterase 6 null or active male types, but marker males used for paternity identification had poorly competitive ejaculates. The proportion of second-male progeny, P2, used as an index of competition is primarily influenced by second-male genotype and uninfluenced by female genotype, P2 can change with time from remating and be unaffected by different intensities of competition, which suggests a complex ejaculate competition mechanism.

Does noise stress modulate effects of smoking/nicotine? Mood, vigilance, and EEG responses.

Effects of smoking multiple cigarettes on EEG, vigilance, and subjective state were assessed in a repeated measures design where noise level (high versus minimal) was crossed with nicotine dose (quasi-ad lib own versus 1.0 mg FTC nicotine machine-delivered dose versus 0.05 mg FTC nicotine machine-delivered dose). Vigilance was increased by nicotine, but not by noise and there was no noise by dose interaction. Effects of nicotine on EEG varied as a function of dose, noise, hemisphere, time, and eyes-open versus eyes-closed condition. Smoking normal nicotine delivery (0.9-1.1 mg FTC-estimated) cigarettes resulted in decreases in percentages of delta and theta EEG magnitude and increased percentage beta-1 EEG magnitude across conditions and time. Changes in alpha and theta magnitude were dependent on eyes being open versus closed. Hemispheric asymmetries varied as a function of noise and time. Consistent with inverted "U" models, effects of nicotine on EEG were clearly stimulant during the quiet conditions while there were minimal to no differences between nicotine doses during the high-noise conditions. The failure of nicotine to modify mood is interpreted in terms of bioinformational models of nicotine's subjective effects.

Flexible effects of quantified cigarette-smoke delivery on EEG dimensional complexity.

A quantified smoke delivery system (QSDS) was used to experimentally control the administration of inhaled cigarette smoke to 28 male smokers. One puff (2 s, 35 cc) was taken every 30 s on a cigarette (nicotine yield 1.0 mg) until the char line reached 3 mm from the filter wrap. The smoke was inhaled for 5 s. Resting eyes-closed and eyes-open EEG was recorded from F3, F4, P3, and P4 before and after quantified smoke delivery (QSD). EEG dimensional complexity (DCx, a measure derived from chaos theory) was computed using the Takens-Ellner method. QSD appeared to have a 'flexible' effect on EEG DCx, primarily lowering it in subjects whose pre-smoking level was high, not affecting it in subjects whose pre-smoking level was intermediate, and tending to raise it in subjects whose pre-smoking level was low. This replicates previous results obtained with ad libitum smoking, suggesting the hypothesis that smoking may have an "optimizing" effect on the complexity of brain dynamics.

Noise stress does not modulate effects of smoking/nicotine on beta-endorphin, cortisol, ACTH, glucose, and mood.

Noise-dependent effects of smoking multiple cigarettes on subjective state and blood concentrations of ACTH, beta-endorphin, cortisol, and glucose were assessed in a repeated measures design where noise level (high versus minimal) was crossed with nicotine dose (quasi-ad lib own brand versus 1.0 mg FTC nicotine machine-delivered dose versus 0.05 mg FTC nicotine machine-delivered dose). Cortisol and ACTH were increased by nicotine, but not by noise and there was no noise by dose interaction. In contrast, nicotine did not increase beta-endorphin in either noise condition and there was no dose by noise interaction for beta-endorphin. However, noise was associated with a modest increase in beta-endorphin. The effects of nicotine on blood glucose varied as a function of the number of cigarettes smoked. However, the effects of nicotine on glucose, hormones, and subjective state did not vary as a function of noise stress.

Subjective correlates of cigarette-smoking-induced elevations of peripheral beta-endorphin and cortisol.

Two experiments assessed subjective and hormonal effects of smoking cigarettes with three different nicotine deliveries. In experiment 1, 12 males smoked two cigarettes on three different occasions: (1) nicotine-free; (2) their own brand (1.0 mg FTC-estimated nicotine delivery); or (3) 2.4 mg FTC nicotine cigarettes. In experiment 2, 12 males smoked cigarettes of comparable nicotine yield using a quantified smoke delivery system (QSDS). Blood was sampled 2 min after each cigarette completion. Relative to nicotine-free smoking, plasma beta-endorphin (BE) and serum cortisol concentrations increased after quasi-ad libitum smoking of 2.4 mg, but not after 1.0 mg nicotine cigarettes. Self-reported malaise (nausea, sickness, and unpleasantness) also increased after smoking 2.4 mg nicotine cigarettes; subjective distress was correlated with changes in blood BE and cortisol. Smoking 1.0 mg cigarettes did not increase BE or cortisol, or subjective distress. QSDS smoking produced hormonal and subjective effects similar to quasi-ad libitum smoking; however, correlations between neuromodulator concentrations and mood were non-significant. These findings suggest that the elevated levels of plasma BE and cortisol reported in some smoking studies may not be characteristic effects of normal smoking.

Hormonal and subjective effects of smoking the first five cigarettes of the day: a comparison in males and females.

The effects of smoking normal-nicotine-delivery cigarettes on serum cortisol, plasma beta-endorphin (BE), and mood were measured in 8 male and 8 female smokers; 8 male and 8 female nonsmokers served as sham-smoking controls. Smoking five cigarettes of the smokers' usual type after overnight deprivation, either ad lib or via a quantified smoke delivery system, produced small but reliable elevations in serum cortisol concentrations; BE was elevated somewhat after two, but not after four or five cigarettes. Smoking-induced elevations in serum cortisol were correlated with decreases in self-reported drowsiness after two and five cigarettes. Additionally, female smokers reported more drowsiness at baseline and after smoking nicotine-free cigarettes than did male smokers or female nonsmokers. Results suggest that smoking-induced elevations in serum cortisol, which persist for at least the first five cigarettes of the day, may modulate the arousing effects of smoking under conditions of low arousal. Also, nicotine-deprived female smokers may experience subnormal arousal compared to male smokers or female nonsmokers.

A system for administering quantified doses of tobacco smoke to human subjects: plasma nicotine and filter pad validation.

A new, automated system for administering quantified doses of cigarette smoke to human subjects is described and results of two studies demonstrating the reliability and validity of the system are presented. To overcome the large variability in nicotine and tar delivery associated with previous means of controlling smoke delivery, an automated quantified smoke delivery system was constructed. The system increases the precision and reliability of the smoke and nicotine dose delivered to human subjects. The quantified smoke delivery system was found to deliver doses of nicotine with a substantially greater degree of precision than procedures typically used in previous laboratory studies of smoking behavior.

Effects of monetary contingencies on smoking relapse: influences of trait depression, personality, and habitual nicotine intake.

Of 56 male smokers, 34 were randomly assigned (by 60% random odds) to quit smoking immediately, whereas the remaining 22 were assigned to quit after an additional 31 days. Compensation ($300) was contingent on abstinence for a minimum of 31 or 2 days (depending on random assignment) and completion of all experimental sessions. Contingencies for the immediate-quit group required 31 days of abstinence; those for the delayed-quit group required only 2 days of abstinence. Contingency duration (31 vs. 2 days) predicted days to relapse. All but 4 of the 31-day contingency participants maintained abstinence for at least 31 days, whereas only 3 of the 2-day contingency group abstained for 31+ days. However, 31-day contingencies did not result in longer postcontingency time to relapse. Higher trait neuroticism, depression, and psychopathic deviate scores predicted decreased time to relapse. Prequit cotinine concentrations and Fagerström Tolerance Questionnaire scores failed to predict time to relapse.

EEG, physiology, and task-related mood fail to resolve across 31 days of smoking abstinence: relations to depressive traits, nicotine exposure, and dependence.

Changes in task-related mood and physiology associated with 31 days of smoking abstinence were assessed in smokers, 34 of whom were randomly assigned to a quit group and 22 to a continuing-to-smoke control group. A large financial incentive for smoking abstinence resulted in very low participant attrition. Individuals were tested during prequit baselines and at 3, 10, 17, and 31 days of abstinence. Abstinence was associated with decreases in heart rate and serum cortisol, a slowing of electroencephalogram (EEG) activity, and task-dependent and trait-depression-dependent hemispheric EEG asymmetries. Differences between the quit group and the smoking group showed no tendency to resolve across the 31 days of abstinence. Trait depression and neuroticism correlated with increases in left-relative-to-right frontal EEG slow-wave (low alpha) activity at both 3 and 31 days of abstinence. In contrast, prequit nicotine intake and Fagerström Tolerance scores correlated with alpha asymmetry and with greater EEG slowing only at Day 3. Thus, the effects of smoking abstinence appear to last for at least several months.

The effects of cigarette smoking on human sexual potency.

Forty-two male cigarette smokers, age 18 to 44, were randomly assigned to high-nicotine, low-nicotine, or control groups in a study relating cigarette smoking to sexual response. Subjects watched erotic film segments while their penile diameters, heart rates, and finger pulse amplitudes were continuously recorded by a polygraph. Subjects in the smoking groups smoked relatively high-nicotine (.9 mg) or very low-nicotine (.002 mg) cigarettes prior to watching the last two films, while control subjects ate candy. Smoking two high-nicotine cigarettes in immediate succession significantly decreased the rate of penile diameter change relative to the other conditions. These effects were not seen after a single cigarette was smoked. High-nicotine cigarettes caused significantly more vasoconstriction and heart rate increase than did low-nicotine cigarettes, which did not differ from control conditions.

Two Hypercard calculators for molecular biology.

Two calculators built in Macintosh Hypercard are described. GelFragSizer estimates and plots DNA restriction fragment sizes, using the local reciprocal or cubic spline methods. Enzyme Kinetics estimates the Michaelis-Menton rate parameters for enzyme-catalyzed reactions, and plots data versus estimated curve in a variety of formats. These stacks help to demonstrate the ease and sophistication of calculation tools that scientists can develop with Hypercard.

Estimating single gene effects on quantitative traits 1. A diallel method applied to Est 6 in D. melanogaster.

A modified diallel cross is used to estimate effects of alleles at the esterase 6 locus, relative to strain and environmental variance, in Drosophila melanogaster. Three strains homozygous for Est 6 (s) and three homozygous for Est 6 (F) were crossed in all 36 combinations. Male progeny were scored for mating speed, copula duration and esterase 6 enzyme activity, and all progeny for developmental time. These alleles show a significant additive effect on mating speed, but not on the other traits. Copula duration, developmental time and enzyme activity show additive strain genetic variance. Enzyme activity and developmental time also have maternal or X-chromosome strain variance, and these two traits are significantly correlated. This modified diallel method is generally useful because it permits the partition of trait variance into additive and dominant locus, background genetic and environmental components.

Estimating single gene effects on quantitative traits : 2. Statistical properties of five experimental methods.

Experimental designs for measuring the effects of single loci on quantitative traits are compared for statistical properties. The designs tested are single population, combined strains, multiple strains, diallel of strains, and co-isogenic strains. Testing was done by simulating population genotypic and phenotypic arrays. Statistical properties measured are type I error, power, bias and efficiency. The relative ranking of designs is consistent for all properties and over eight conditions examined. The co-isogenic design is superior, followed closely by the single population method. The other three designs are similar in ability, with the diallel design somewhat superior. Based on its good statistical performance and wide feasibility, the single population method is recommended. The diallel method provides the most information on genetic components of variation.

Personality, psychopathology, and nicotine response as mediators of the genetics of smoking.

Individual differences in psychopathology, personality, and nicotine responsivity and their biological bases are evaluated as mechanisms potentially mediating smoking heritability. Smokers are more likely to be high in neurotic traits (e.g., depression, anxiety, anger) and in social alienation (psychoticism, impulsivity, unsocialized sensation-seeking, low conscientiousness, low agreeableness) and low in achievement/socioeconomic status. Psychological and biological mechanisms putatively mediating these associations are reviewed. It is concluded that a number of relatively indirect and complex processes, as well as more direct (e.g., self-medication for psychopathology, nicotine sensitivity), mediate the inheritance of smoking behavior.