Adjustment Disorders as a Stress-Related Disorder: A Longitudinal Study of the Associations among Stress,Resources, and Mental Health

Objective

Adjustment disorders are re-conceptualized in the DSM-5 as a stress-related disorder; however, besides the impact of an identifiable stressor, the specification of a stress concept, remains unclear. This study is the first to examine an existing stress-model from the general population, in patients diagnosed with adjustment disorders, using a longitudinal design.

Methods

The study sample consisted of 108 patients consecutively admitted for adjustment disorders. Associations of stress perception, emotional distress, resources, and mental health were measured at three time points: the outpatients’ presentation, admission for inpatient treatment, and discharge from the hospital. To evaluate a longitudinal stress model of ADs, we examined whether stress at admission predicted mental health at each of the three time points using multiple linear regressions and structural equation modeling. A series of repeated-measures one-way analyses of variance (rANOVAs) was performed to assess change over time.

Results

Significant within-participant changes from baseline were observed between hospital admission and discharge with regard to mental health, stress perception, and emotional distress (p<0.001). Stress perception explained nearly half of the total variance (44%) of mental health at baseline; the adjusted R² increased (0.48), taking emotional distress (i.e., depressive symptoms) into account. The best predictor of mental health at discharge was the level of emotional distress (i.e., anxiety level) at baseline (β = −0.23, R² _corr = 0.56, p<0.001). With a CFI of 0.86 and an NFI of 0.86, the fit indices did not allow for acceptance of the stress-model (C_min/df = 15.26; RMSEA = 0.21).

Conclusions

Stress perception is an important predictor in adjustment disorders, and mental health-related treatment goals are dependent on and significantly impacted by stress perception and emotional distress.     

Evolutionary conservation of the chromosomal configuration and regulation of amylase genes among eight species of the Drosophila melanogaster species subgroup

Nuclear DNA was extracted from each of the eight species comprising the Drosophila melanogaster species subgroup. Southern hybridization of this DNA by using a molecular probe specific for the alpha-amylase coding region showed that the duplicated structure of the amylase locus, first found in D. melanogaster, is conserved among all species of the melanogaster subgroup. Evidence is also presented for the concerted evolution of the duplicated genes within each species. In addition, it is shown that the glucose repression of amylase gene expression, which has been extensively studied in D. melanogaster, is not confined to this species but occurs in all eight members of the species subgroup. Thus, both the duplicated gene structure and the glucose repression of Drosophila amylase gene activity are stable over extended periods of evolutionary time.      

Transformation and mineralization of benzo[<Emphasis Type="Italic">a</Emphasis>]pyrene by microbial cultures enriched on mixtures of three- and four-ring polycyclic aromatic hydrocarbons

Microorganisms originating from a soil contaminated by low levels of polycyclic aromatic hydrocarbons (PAHs) were enriched with three- and four-ring PAHs as primary substrates in the presence of benzo[a]pyrene (BaP). Most enrichment cultures, isolated in the presence or absence of a sorptive matrix, significantly transformed BaP. Evidence of BaP mineralization was obtained with cultures enriched on phenanthrene and anthracene. Our findings supplement literature data suggesting the wide occurrence of microbial activity against BaP. Journal of Industrial Microbiology & Biotechnology (2002) 28, 70–73 DOI: 10.1038/sj/jim/7000211 Received 11 December 2000/ Accepted in revised form 04 September 2001     

Prenatal stress enhances susceptibility of murine adult offspring toward airway inflammation

Allergic asthma is one of the most prevalent and continuously increasing diseases in developed countries. Its clinical features include airway hyperresponsiveness and inflammation upon allergen contact. Furthermore, an emerging area of research subsumed as fetal programming evaluates the impact of environmental insults in utero on the incidence of diseases in later life. The aim of this study was to identify whether prenatal exposure to stress, which constitutes a severe environmental insult, perpetuates airway inflammation in later life. Our experiments were performed in mice and revealed that prenatally stressed adult offspring indeed show an increased vulnerability toward airway hyperresponsiveness and inflammation. Furthermore, we provide persuasive insights on dysregulated pathways of the cellular and humoral immune response upon Ag challenge in prenatally stressed adult offspring, reflected by a Th2 greater Th1 adaptive immune response and increased CCR3 and IgE levels in vivo. Additionally, APCs derived from prenatally stressed offspring trigger clonal expansion of Th2 cells in vitro. We also deliver experimental evidence for a reduced corticotrophin-releasing hormone expression in the paraventricular nucleus of adult offspring in response to prenatal stress. Furthermore, behavioral analyses indicate an increase in anxiety in these mice. In conclusion, our data will facilitate future research aiming to identify the individual impact, hierarchy, and redundancy of multiple key protagonists in airway inflammation in an interdisciplinary context. This will foster the substantiation of disease-prevention strategies, such as asthma, during the prenatal period.     

Bombesin, but not amylin, blocks the orexigenic effect of peripheral ghrelin

The interaction between ghrelin and bombesin or amylin administered intraperitoneally on food intake and brain neuronal activity was assessed by Fos-like immunoreactivity (FLI) in nonfasted rats. Ghrelin (13 microg/kg ip) increased food intake compared with the vehicle group when measured at 30 min (g/kg: 3.66 +/- 0.80 vs. 1.68 +/- 0.42, P < 0.0087). Bombesin (8 microg/kg) injected intraperitoneally with ghrelin (13 microg/kg) blocked the orexigenic effect of ghrelin (1.18 +/- 0.41 g/kg, P < 0.0002). Bombesin alone (4 and 8 microg/kg ip) exerted a dose-related nonsignificant reduction of food intake (g/kg: 1.08 +/- 0.44, P > 0.45 and 0.55 +/- 0.34, P > 0.16, respectively). By contrast, ghrelin-induced stimulation of food intake (g/kg: 3.96 +/- 0.56 g/kg vs. vehicle 0.82 +/- 0.59, P < 0.004) was not altered by amylin (1 and 5 microg/kg ip) (g/kg: 4.37 +/- 1.12, P > 0.69, and 3.01 +/- 0.78, respectively, P > 0.37). Ghrelin increased the number of FLI-positive neurons/section in the arcuate nucleus (ARC) compared with vehicle (median: 42 vs. 19, P < 0.008). Bombesin alone (4 and 8 microg/kg ip) did not induce FLI neurons in the paraventricular nucleus of the hypothalamus (PVN) and coadministered with ghrelin did not alter ghrelin-induced FLI in the ARC. However, bombesin (8 microg/kg) with ghrelin significantly increased neuronal activity in the PVN approximately threefold compared with vehicle and approximately 1.5-fold compared with the ghrelin group. Bombesin (8 microg/kg) with ghrelin injected intraperitoneally induced Fos expression in 22.4 +/- 0.8% of CRF-immunoreactive neurons in the PVN. These results suggest that peripheral bombesin, unlike amylin, inhibits peripheral ghrelin induced food intake and enhances activation of CRF neurons in the PVN.     

Either or neither, but not both: locating the effects of masked primes

Execution of a response that has been primed by a backward-masked stimulus is inhibited (negative compatibility effect; NCE). Three experiments investigated the locus of this inhibition. Masked primes (left- or right-pointing arrows) were followed either by an arrow or a circle target. Arrow targets always required a left- or right-hand response, but the experiments differed in the response required to circles: press neither, either or both response keys (i.e. nogo, free choice and bimanual, respectively). Arrow targets showed the usual NCEs. Circle targets showed NCEs in the form of a response bias away from the primed response in the nogo and free-choice tasks; primes and targets differed on these trials, ruling out a perceptual explanation of the NCE. The bimanual task showed no such bias, suggesting that the NCE is located at a level of abstract response codes rather than specific muscle commands.     

Adenine nucleotide translocation in cauliflower mitochondria.

The exchange of adenine nucleotides in cauliflower mitochondria was studied. Although these mitochondria translocate ADP and ATP at high rates and possess high affinity binding for the nucleotides, they differ from mammalian mitochondria with respect to the action of atractyloside. It was observed that (i) atractyloside at a concentration of 100 μm does not inhibit State 3 respiration significantly; (ii) atractyloside inhibits the 2,4-dinitrophenol-stimulated ATPase activity; (iii) atractyloside inhibits the exchange of low concentrations of ADP; on the other hand, atractyloside inhibits the exchange of ATP at all concentrations of ATP employed; (iv) ATP inhibits ADP exchange through a process that is abolished by atractyloside.     

CCK inhibits the orexigenic effect of peripheral ghrelin

CCK and ghrelin exert antagonistic effects on ingestive behavior. The aim of the present study was to investigate the interaction between ghrelin and CCK administered peripherally on food intake and neuronal activity in specific hypothalamic and brain stem nuclei, as assessed by c-Fos-like immunoreactivity (c-FLI) in nonfasted rats. Ghrelin (13 microg/kg body wt) injected intraperitoneally significantly increased the cumulative food intake when measured at 30 min and 1 h after injection, compared with the vehicle group (2.9 +/- 1.0 g/kg body wt vs. 1.2 +/- 0.5 g/kg body wt, P < 0.028). Sulfated CCK octapeptide (CCK-8S) (2 or 25 microg/kg body wt) injected simultaneously blocked the orexigenic effect of ghrelin (0.22 +/- 0.13 g/kg body wt, P < 0.001 and 0.33 +/- 0.23 g/kg body wt, P < 0.0008), while injected alone, both doses of CCK-8S exerted a nonsignificant trend to reduce food intake. Ghrelin (13 microg/kg body wt ip) markedly increased the number of c-FLI-positive neurons per section in the arcuate nucleus (ARC) compared with vehicle (median: 31.35 vs. 9.86, P < 0.0001). CCK-8S (2 or 25 microg/kg body wt ip) had no effect on neuronal activity in the ARC, as assessed by c-FLI (median: 5.33 and 11.21 cells per section), but blocked the ghrelin-induced increase of c-fos expression in this area when both peptides were administered simultaneously (median: 13.33 and 12.86 cells per section, respectively). Ghrelin at this dose had no effect on CCK-induced stimulation of c-fos expression in the paraventricular nucleus of the hypothalamus and the nucleus of the solitary tract. These results suggest that CCK abolishes ghrelin-induced food intake through dampening increased ARC neuronal activity.     

Expression of substance P and nitric oxide synthase in vagal sensory neurons innervating the mouse airways

INTRODUCTION: Airway sensory nerves have the capacity to release neuromediators such as substance P and nitric oxide to control airway functions. The aim of the present study was to investigate substance P and neuronal nitric oxide synthase (NOS-1) expression in airway-specific sensory neurons. METHODS: Airway-projecting neurons in the jugular-nodose ganglia were investigated for NOS-1 and substance P expression by neuronal tracing and double-labelling immunoreactivity. RESULTS: Of the Fast blue labelled neurons, 14.6+/-1.8% (mean+/-S.E.M.) were immunoreactive only for NOS-1, 3.0+/-0.3% for NOS-1 and substance P, 2.7+/-0.3% only for substance P, and 79.7+/-1.7% of the labelled neurons were nonimmunoreactive for substance P or NOS-1 but were partly positive for I-B4-lectin-binding. Fast blue labelled NOS and/or substance P-positive neurons were small to medium sized (<20 microm). CONCLUSION: Based on the expression of substance P and nitric oxide synthase in airway neurons, the present study suggests that there may be substance P and NO biosynthesis and release following a peripheral activation of the afferents, there could be a triggering of substance P and NO-mediated phenomena, including those related to airway inflammation, such as plasma extravasation and vasodilatation.     

Evidence for an interaction between leptin, T cell costimulatory antigens CD28, CTLA-4 and CD26 (dipeptidyl peptidase IV) in BCG-induced immune responses of leptin- and leptin receptor-deficient mice

We assessed changes of the enzyme dipeptidyl peptidase IV (DPP IV, CD26) in the context of leptin or leptin receptor deficiency. C57BL/6 mice, Leptin-deficient mice (ob/ob mice, B6.V-Lep) and Leptin-receptor-deficient mice (db/db mice, B6.Cg-m+/+Lepr) were infected with B. Calmette-Guerin (BCG) and sacrificed three days later. DPP IV activity in serum was higher in ob/ob mice and in db/db mice than in wild-type mice. The expression of DPP IV/CD26 on splenocytes was higher in ob/ob mice than in wild-type animals, and lower in db/db mice, and decreased upon stimulation with BCG in ob/ob mice only. Several T cell antigens including CTLA-4 were expressed aberrantly in ob/ob and in db/db mice. Our observations provide evidence for a relationship between DPP IV and leptin.