The consequences of facultative sex in a prey adapting to predation.

A species reproductive mode, along with its associated costs and benefits, can play a significant role in its evolution and survival. Facultative sexuality, being able to reproduce both sexually and asexually, has been deemed evolutionary favourable as the benefits of either mode may be fully realized. In fact, many studies have focused on identifying the benefits of sex and/or the forces selecting for increased rates of sex using facultative sexual species. The costs of either mode, however, can also have a profound impact on a population's evolutionary trajectory. Here, we used experimental evolution and fitness assays to investigate the consequences of facultative sexuality in prey adapting to predation. Specifically, we compared the adaptive response of algal prey populations exposed to constant rotifer predation and which had alternating cycles of asexual and sexual reproduction where sexual episodes were either facultative (sexual and asexual progeny simultaneously propagated) or obligate (only sexual progeny propagated). We found that prey populations with facultative sexual episodes reached a lower final relative fitness and suffered a greater trade-off in traits under selection, that is defence and competitive ability, as compared to prey populations with obligate sexual episodes. Our results suggest that costs associated with sexual reproduction (germination time) and asexual reproduction (selection interference) were amplified in the facultative sexual prey populations, leading to a reduction in the net advantage of sexuality. Additionally, we found evidence that the cost of sex was reduced in the obligate sexual prey populations because increased selection for sex was observed via the spontaneous production of sexual cells. These results show that certain costs associated with facultative sexuality can affect an organism's evolutionary trajectory.

Higher rates of sex evolve under K-selection.

The geographical distribution of sexual and related asexual species has been suggested to correlate with habitat stability; sexual species tend to be in stable habitats (K-selection), whereas related asexual taxa tend to be in unstable habitats (r-selection). We test whether this broad-scale pattern can be re-created at a microevolutionary scale by experimentally evolving populations of facultatively sexual rotifers under different ecological conditions. Consistent with the pattern in nature, we find that the rate of sex evolves to lower levels in the r-selected than in K-selection environments. We consider several different explanations for these results.

The effect of sex on the mean and variance of fitness in facultatively sexual rotifers.

The evolution of sex is a classic problem in evolutionary biology. While this topic has been the focus of much theoretical work, there is a serious dearth of empirical data. A simple yet fundamental question is how sex affects the mean and variance in fitness. Despite its importance to the theory, this type of data is available for only a handful of taxa. Here, we report two experiments in which we measure the effect of sex on the mean and variance in fitness in the monogonont rotifer, Brachionus calyciflorus. Compared to asexually derived offspring, we find that sexual offspring have lower mean fitness and less genetic variance in fitness. These results indicate that, at least in the laboratory, there are both short- and long-term disadvantages associated with sexual reproduction. We briefly review the other available data and highlight the need for future work.

Nicotine withdrawal and psychiatric symptoms in cigarette smokers with schizophrenia.

The prevalence of smoking is markedly elevated in schizophrenia. Low smoking cessation rates and reports that some smokers with schizophrenia experience an acute increase in symptoms during attempts to quit smoking, suggest a self-medication model. Alternatively, smoking may modulate medication side effects. The effects of treated and untreated smoking abstinence on psychotic symptoms and medication side effects were examined in this study. Nineteen outpatients with schizophrenia or schizoaffective disorder participated in a randomized, double-blind, balanced crossover study: 1 day of ad libitum smoking followed by 3 days of acute smoking abstinence while wearing 22 mg/day active or placebo transdermal nicotine patches, with a return to 3 days of smoking between patch conditions. Daily symptom and side-effect ratings, nicotine and cotinine blood levels were collected. Twelve subjects completed the study. Neither positive symptoms nor mood symptoms changed. An increase in negative symptoms during the first abstinent day occurred in both placebo and active patch conditions, but was not sustained over subsequent abstinent days. Despite physiological signs of withdrawal, completers did not endorse increased nicotine withdrawal symptoms. Dropouts reported higher withdrawal symptoms, but also had no increase in psychiatric symptoms in either phase of the study. Of note, dyskinesias decreased during abstinence and placebo patch treatment, but increased during abstinence and the active patch conditions. Acute exacerbation of psychiatric symptoms is an unlikely explanation for any difficulty smokers with schizophrenia have in early abstinence.

ATP converts necrosis to apoptosis in oxidant-injured endothelial cells.

Cell death due to necrosis results in acute inflammation, while death by apoptosis generally does not. The effect of adenosine triphosphate (ATP) on the pattern of cell death induced by oxidants was examined in bovine endothelial cells. ATP levels were altered by hydrogen peroxide (H2O2), glutamine (Gln), and metabolic inhibition (MI), to determine if necrosis can be shifted to apoptosis during oxidant injury. The form of cell death was determined by fluorescence microscopic techniques and the pattern of DNA degradation on agarose gels. ATP levels were measured using the luciferase-luciferin assay. Apoptosis occurred with 100 microM H2O2 without an alteration in ATP levels. ATP was significantly lowered with 5 mM H2O2, and necrosis occurred. MI, in combination with 100 microM H2O2, decreased ATP and resulted in necrosis. MI alone, however, did not cause cell death. Gln partially restored ATP levels in cells injured with 5 mM H2O2 and resulted in a significant increase in apoptosis. DNA laddering on agarose gels confirmed the apoptotic changes seen by fluorescence microscopy. In summary, a threshold level of ATP 25% of basal levels is required for apoptosis to proceed after oxidant stress, otherwise necrosis occurs. Agents like glutamine that enhance ATP levels in oxidant-stressed cells may be potent means of shifting cell death during inflammation to the noninflammatory form of death--apoptosis.

Tardive dyskinesia, clozapine, and treatment response.

1. Tardive Dyskinesia (TD) can be a serious consequence of the use of antipsychotic medications to treat psychotic illness. There is evidence to suggest that the atypical antipsychotic, clozapine, is less likely to cause, and may even ameliorate TD. 2. The authors reviewed their experience regarding clozapine and TD among patients in their Clozapine Clinic, and summarize some of the recent clinical literature in this area. 3. Retrospective review of chart records for 13 patients was carried out. Comparisons of TD and symptom rating scales were made: 1) between groups (with and without TD) at baseline; 2) between individuals (self as own control) in the TD group at baseline and at the end of the follow-up period. 4. Subjects with and without TD at baseline had a significant decrease in psychiatric symptoms over the course of treatment. 5. In those with TD at baseline, mean Abnormal Involuntary Movement Scale (AIMS) score decreased by 85% over 10.3 +/- 5.5 (mean +/- S.D.) months at a dose of 358 +/- 196 mg/day of clozapine. 6. The data, and the recently published clinical literature on clozapine and TD, continue to support the striking utility of clozapine for chronically psychotic patients, and particularly those with TD.

Relationship of seizure duration to antidepressant efficacy in electroconvulsive therapy.

BACKGROUND: A relationship between the anticonvulsant and antidepressant properties of electroconvulsive therapy (ECT) has been hypothesized. The goal of this study was to see whether the anticonvulsant effects of ECT could be measured in a clinical setting and whether there was any relationship between the anticonvulsant effects of ECT and the antidepressant response to it. METHODS: We examined the temporal relationship between change in seizure duration (as an index of anticonvulsant activity) and improvement in Hamilton Rating Scale for Depression scores in a retrospective sample of 114 depressed patients who received 145 courses of ECT. A linear mixed effects model was utilized for analysis so that the repeated measures nature of the data could be taken into account. RESULTS: Both seizure duration and depression scores decreased significantly through the course of ECT. However, no evidence was found for a relationship between decrease in seizure duration and clinical improvement as measured by Hamilton ratings. CONCLUSIONS: The process underlying the reduction in seizure duration through a course of ECT may not be related to antidepressant efficacy.

Sulfur mustard induces apoptosis and necrosis in endothelial cells.

Sulfur Mustard (SM) is a vesicant or blistering chemical warfare agent, for which there still is no effective therapy. Endothelial cells are one of the major cellular targets for SM. The mechanism of endothelial cell death during SM injury is poorly understood. We studied the effect of exposure of endothelial cells to 0-1000 microM SM over the time course of 2-24 hr to determine the role of apoptotic and necrotic patterns of cell death in endothelial injury induced by SM. SM concentrations < or = 250 microM induced exclusively apoptosis which was observed after 5 hr in 30% of endothelial cells. Exposure to SM concentrations > or = 500 microM caused apoptosis and necrosis to the same extent in 60-85% of all cells after 5 to 6 hr. Necrosis was accompanied by a significant (approximately 50%) depletion of intracellular ATP, while in apoptotic cells ATP remained at the level similar to healthy cells. Interestingly, disruption of the long actin filament stress fibers and rounding of cells preceded other features of apoptosis--DNA fragmentation, membrane budding, and apoptotic body formation. In apoptotic cells, microfilaments formed constricted perinuclear bands, which were not observed in necrotic cells. Pretreatment with 50 mM N-acetyl-L-cysteine (NAC), a sulfhydryl donor and antioxidant, nearly eliminated the apoptotic features of cell death but did not prevent necrosis in response to SM. NAC pretreatment alone induced reorganization of actin filaments into an enhanced network of long stress fibers instead of a dominant cortical band of actin. NAC pretreatment prevented loss of cell adherence and cell rounding following exposure to 250 microM SM. The effect of NAC on cytoskeletal organization and its ability to eliminate SM-induced apoptosis suggests that actin filament organization may be an important element in cellular susceptibility to apoptotic stimuli.