A series of laboratory tests were conducted to evaluate whether denitrification would be a suitable alternative for biorestoration of an aquifer contaminated with JP-4 jet fuel. Microcosms were prepared from both uncontaminated and contaminated aquifer material from the site, in an anaerobic glovebox, amended with nitrate, nutrients, and aromatic hydrocarbons, and incubated under a nitrogen atmosphere at 12 °C. With uncontaminated core material, there was no observable lag period prior to removal of toluene whereas 30 days was required before biodegradation commenced for xylenes, ethylbenzene, and 1,2,4-trimethylbenzene. An identical test with contaminated aquifer material exhibited not only much longer lag periods but decreased rates of biodegradation; benzene, ethylbenzene, and o-xylene were not significantly degraded within the 6-month time period even though active denitrification occurred at this time. First-order biodegradation rate constants ranged from 0.016 to 0.38 day™1 for uncontaminated core material and from 0.022 to 0.067 day™1 for contaminated core material. Tests with individual compounds in uncontaminated core indicated that benzene and m-xylene inhibited the basal rate of denitrification. These data demonstrate that several aromatic compounds can be degraded under denitrifying conditions, but rates of biodegradation may be lower in material contaminated with JP-4 jet fuel.

A spill of JP‐4 jet fuel at the U.S. Coast Guard Air Station in Traverse City, Michigan, contaminated a water‐table aquifer. An infiltration gallery (30 ft × 30 ft) was installed above a section of the aquifer containing 700 gal JP‐4. Purge wells recirculated three million gallons of ground water per week through the infiltration gallery at a rate designed to raise the water table above the contaminated interval. Ground water containing ambient concentrations of oxygen and nitrate was first recirculated for 40 days. Concentrations of benzene in monitoring wells beneath the infiltration gallery were reduced from 760 to <1μ/1. Concentrations of toluene, ethylbenzene, m,p‐xylene, and o‐xylene were reduced from 4500 to 17, 840 to 44, 2600 to 490, and 1400 to 260 μ/1, respectively. Average core concentrations of benzene, toluene, ethylbenzene, m,p‐xylene, and o‐xylene were reduced from 0.84 to 0.032, 33 to 0.13, 18 to 0.36, 58 to 7.4, and 26 to 3.2 mg/kg, respectively. Ground water amended with nitrate (10 mg/1 nitrate‐nitrogen) and nutrients was then recirculated for 76 days. Final core concentrations of benzene, toluene, ethylbenzene, m,p‐xylene, and o‐xylene were 0.017,0.036,0.019,0.059, and 0.27 mg/kg, respectively. Final aqueous concentrations were <1 μ/1 for benzene and toluene, 6 μ/1 for ethylbenzene, and 20 to 40 μ/1 for the xylene isomers, in good agreement with predicted values based on residual fuel content and partitioning theory. Although alkylbenzene concentrations have been substantially reduced, the test plot is still contaminated with the weatheredfuel. Based on stoichiometry, approximately 10 times more nitrate was consumed than could be accounted for by BTX degradation alone, indicating that other compounds were also degraded under denitrifying conditions.

Interleukin-1β is one of the main mediators in the cross-talk between the immune system and the central nervous system. Higher interleukin-1β levels are found in mood spectrum disorders, and the stress-induced expression rate of the interleukin-1β gene (IL1B) is altered by polymorphisms in the region. Therefore we examined the effects of rs16944 and rs1143643 single nucleotide polymorphisms (SNPs) within the IL1B gene on depressive and anxiety symptoms, as measured by the Brief Symptom Inventory, in a Hungarian population sample of 1053 persons. Distal and proximal environmental stress factors were also included in our analysis, namely childhood adversity and recent negative life-events. We found that rs16944 minor (A) allele specifically interacted with childhood adversity increasing depressive and anxiety symptoms, while rs1143643's minor (A) allele showed protective effect against depressive symptoms after recent life stress. The genetic main effects of the two SNPs were not significant in the main analysis, but the interaction effects remained significant after correction for multiple testing. In addition, the effect of rs16944 A allele was reversed in a subsample with low-exposure to life stress, suggesting a protective effect against depressive symptoms, in the post hoc analysis. In summary, both of the two IL1B SNPs showed specific environmental stressor-dependent effects on mood disorder symptoms. We also demonstrated that the presence of exposure to childhood adversity changed the direction of the rs16944 effect on depression phenotype. Therefore our results suggest that it is advisable to include environmental factors in genetic association studies when examining the effect of the IL1B gene.

With very few exceptions, no coherent model of representing the self exists for nonhuman species. According to our hypothesis, understanding of the Self as an object' can also be found in a wide range of animals including the dog, a fast-moving terrestrial predator/scavenger, with highly developed senses and complex cognitive capacity. We tested companion dogs in three experiments in which they faced three different variations of the same physical challenge: passing through an opening in a wall. We predicted that if dogs are capable of representing their own body size, they will react differently when faced with adequate or too small openings. We found that dogs started to move towards and approached the too small openings with significantly longer latencies than the suitable ones; and upon reaching it, they did not try to get through the too small openings. In another experiment, the medium-size (still large enough) opening was approached with latencies that fell between the latencies measured in the cases of the very large or the too small openings. Having discussed the potential underlying mechanisms, we concluded that our results convincingly assume that dogs can represent their own body size in novel contexts.

Interleukin-6 (IL-6) has emerged as a potent biomarker for depression as its elevated plasma levels in patients with clinical depression have been confirmed by meta-analyses. Increased plasma IL-6 concentration was associated with various psychological stress factors and physical disorders accompanied by pain. Another modulator of the IL-6 level is rs1800795, a promoter polymorphism in the IL-6 gene which is able to influence its expression rate. Therefore, we examined in a Hungarian population sample of 1053 volunteers with European origins if rs1800795 polymorphism can affect depression symptoms measured by Zung Self-rating Depression Scale (ZSDS), and Brief Symptom Inventory (BSI). We also investigated the interactions of the polymorphism with reported painful physical conditions and Recent Negative Life Events (RLE) measured by the List of Life Threatening Experiences. Rs1800795 significantly interacted with both RLE and painful condition on depressive symptoms measured by ZSDS and BSI using different heritability models, while no main effects of the polymorphism were identified. After correction for multiple testing only the rs1800795 × RLE interaction effect (recessive model) remained significant on the BSI score, while both RLE and painful conditions significantly interacted on the ZSDS. In conclusion, the functional IL-6 rs1800795 polymorphism in interaction with various stress factors increases the risk of depression and has a greater impact on symptoms measured by the ZSDS. Thus, IL-6 and other cytokines may be more relevant in the development of somatic symptoms compared to affective signs of depression, delineating a specific genotype–phenotype relationship in this heterogeneous disorder.

BackgroundAlthough 5-HTTLPR has been shown to influence the risk of life stress-induced depression in the majority of studies, others have produced contradictory results, possibly due to weak effects and/or sample heterogeneity.MethodsIn the present study we investigated how age, type and intensity of life-stressors modulate the effect of 5-HTTLPR on depression and anxiety in a European population cohort of over 2300 subjects. Recent negative life events (RLE), childhood adversity (CHA), lifetime depression, Brief Symptoms Inventory (BSI) depression and anxiety scores were determined in each subject. Besides traditional statistical analysis we calculated Bayesian effect strength and relevance of 5-HTTLPR genotypes in specified models.ResultsThe short (s) low expressing allele showed association with increased risk of depression related phenotypes, but all nominally significant effects would turn to non-significant after correction for multiple testing in the traditional analysis. Bayesian effect strength and relevance analysis, however, confirmed the role of 5-HTTLPR. Regarding current (BSI) and lifetime depression 5-HTTLPR-by-RLE interactions were confirmed. Main effect, with other words direct association, was supported with BSI anxiety. With more frequent RLE the prevalence or symptoms of depression increased in ss carriers. Although CHA failed to show an interaction with 5-HTTLPR, in young subjects CHA sensitized towards the depression promoting effect of even mild RLE. Furthermore, the direct association of anxiety with the s allele was driven by young (≤30) individuals.LimitationsOur study is cross-sectional and applies self-report questionnaires.ConclusionsAlbeit 5-HTTLPR has only weak/moderate effects, the s allele is directly associated with anxiety and modulates development of depression in homogeneous subgroups.

Immunotherapies revolutionised the treatment of several disorders but show specific side-effect profiles which frequently involve psychological symptoms. Long term interferon-alpha (IFN-alpha) therapy can cause wide-ranging psychiatric side-effects from fatigue, insomnia, anxiety to full-blown depression. This treatment-emergent depression shares several symptoms with major depressive disorder (MDD) with a predominance of somatic/neurovegetative symptoms, and can be treated with antidepressants. However, this experience directed research to inflammatory mechanisms in MDD. MDD has been confirmed as a heterogeneous disorder with a subgroup of patients suffering from low-grade chronic inflammation and frequently resistant to traditional antidepressant treatment. Thus future research should develop strategies to identify those MDD patients who could benefit from drugs acting through inflammatory pathways.

Several studies indicate that 5-HTTLPR mediates the effect of childhood adversity in the development of depression, while results are contradictory for recent negative life events. For childhood adversity the interaction with genotype is strongest for sexual abuse, but not for other types of childhood maltreatment; however, possible interactions with specific recent life events have not been investigated separately. The aim of our study was to investigate the effect of four distinct types of recent life events in the development of depressive symptoms in a large community sample. Interaction between different types of recent life events measured by the List of Threatening Experiences and the 5-HTTLPR genotype on current depression measured by the depression subscale and additional items of the Brief Symptom Inventory was investigated in 2588 subjects in Manchester and Budapest. Only a nominal interaction was found between life events overall and 5-HTTLPR on depression, which failed to survive correction for multiple testing. However, subcategorising life events into four categories showed a robust interaction between financial difficulties and the 5-HTTLPR genotype, and a weaker interaction in the case of illness/injury. No interaction effect for the other two life event categories was present. We investigated a general non-representative sample in a cross-sectional approach. Depressive symptoms and life event evaluations were self-reported. The 5-HTTLPR polymorphism showed a differential interaction pattern with different types of recent life events, with the strongest interaction effects of financial difficulties on depressive symptoms. This specificity of interaction with only particular types of life events may help to explain previous contradictory findings.