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Stress-buffering factors related to adolescent coping: a path analysis.

To uncover those factors that buffer the impact of stressful negative experiences on adolescent adjustment, a theoretical model of adolescent stress and coping, with social support and social problem solving proposed as moderators, was investigated using path analysis. The study was conducted with 122 ninth-and tenth-grade nonreferred high school students. Using the LISREL statistical package (Jöreskog & Sörbom, 1986), it was found that a recursive loop leading from stress outcomes back to negative stressors did not allow for a successful solution to the model. However, the effects of stressful events on adjustment were mediated by coping resources, which included a combination of problem-solving abilities and social support. Overall, the findings replicated previous investigations that have demonstrated direct relationships among stressful life events, social support, problem solving, and adolescent adjustment. While a successful fit to the theoretical model was not attained, it was concluded that a refined model may provide a more acceptable solution.

Adaptation, Psychological↗

Elevated pain thresholds correlate with dissociation and aversive arousal in patients with borderline personality disorder.

In addition to reduced pain perception, patients with borderline personality disorder (BPD) show higher pain thresholds under subjective stress conditions as compared with non-stress conditions. However, the correlation between symptoms of stress and pain thresholds has not been investigated so far. Using a new and convenient methodology, electric stimulation, we expected higher pain and detection thresholds in patients with BPD than in to healthy controls as well as a positive correlation between pain thresholds and symptoms of stress (aversive arousal and dissociation) in BPD patients. Twelve female patients with BPD and twelve healthy controls were included in the study. Electric stimulation was applied on the right index finger, and detection and pain thresholds were assessed by gradually intensifying the stimuli. We found significantly elevated pain thresholds in patients with BPD as compared with healthy controls, but no difference between patients and controls in detection thresholds. In patients, a significant positive correlation was revealed between pain thresholds and dissociation as well as between pain thresholds and aversive arousal. Besides demonstrating a close correlation between pain thresholds and symptoms of stress in patients with BPD, this study replicated earlier findings of reduced pain perception in patients with BPD. Measuring electric pain thresholds is a valid and reasonable method for larger studies.

Adult↗

Major depression and its association with long-term medical conditions.

OBJECTIVE: To replicate previously reported associations between major depressive episodes (MDEs) and long-term medical conditions in a Canadian community sample. METHODS: A sample of 2542 household residents was selected using random digit dialing (RDD). Data were collected by telephone interview. The Composite International Diagnostic Interview (CIDI)-Short Form for major depression (CIDI-SFMD) was used to identify MDEs occurring in the previous 12 months. Long-term medical conditions were identified by self-report. RESULTS: The prevalence of MDE was elevated in those subjects who reported 1 or more long-term medical conditions. The association was not due to confounding by age, sex, social support, or stressful recent life events. CONCLUSION: This study replicates a previously reported association between depressive disorders and long-term medical conditions. These cross-sectional associations suggest that medical conditions may increase the risk of major depression or that major depression may increase the risk of medical conditions. Alternatively, comorbid medical conditions may influence the duration of depressive episodes, or vice versa. These explanations are not mutually exclusive.

Adult↗

Thiosemicarbazide injection followed by electric shock increases resistance to stress in rats.

Adult rats that had been raised with a minimum of stimulation were injected with thiosemicarbazide, a drug that lowers y-aminobutyric acid concentrations. Fifteen minutes later the animals were given 30 mild electric shocks over a half-hour period. Two. weeks later they were tested for their resistance to gastric ulceration induced by immobilization. The experimental animals showed a much greater resistance to stress than did the appropriate control groups. A replication confirmed the results of the first study.

Aminobutyrates↗

Effects of vitamin E and C supplementation on performance, in vitro lymphocyte proliferation, and antioxidant status of laying hens during heat stress.

Vitamin E (dl-alpha-tocopheryl acetate) was evaluated for its effects on performance, lymphocyte proliferation, and antioxidation in layers during heat stress. In Trial 1, 25, 45, or 65 IU of vitamin E/kg were fed to four replicated pens (five hens/cage) of DeKalb Delta or Hy-Line W-36 per treatment starting at 20 wk of age. At 34 wk of age, hens were heat-stressed at diurnal temperature ranging from 21 C to 35 C for 3 wk. The performances of hens not exposed to heat stress were not influenced by supplemental vitamin E. Supplemental vitamin E did not affect egg production; however, egg mass was greater (P < 0.05) with supplementation of 65 IU of vitamin E/ kg during heat stress. Egg yolk was significantly increased (P < 0.04) when hens were fed 45 and 65 lU/kg compared with the control vitamin E level (25 lU/kg). Haugh units were higher (P < 0.01) for hens fed 65 IU of vitamin E/kg compared to 25 and 45 lU/kg. Lymphocyte proliferative responses to concanavalin A (Con A) and Salmonella typhimurium lipopolysaccharide (LPS) were greater (P < 0.0001) in hens fed 45 and 65 IU of vitamin E/kg during heat stress. Strain had no effect on any of the parameters measured. In Trial 2, a 2 x 2 factorial was designed to test effects of vitamin C in drinking water (0 and 1,000 ppm) and dietary vitamin E (25 and 65 IU/kg). Eight replications per treatment with four hens per replication cage were heat-stressed at constant temperature of 35 C for 3 wk. Egg production and egg mass were higher when hens were fed 65 IU of vitamin E/kg than when hens were fed 25 lU/kg (81.5 vs. 75.9%, P < 0.03 and 48.2 vs. 44.6 g, P < 0.03, respectively). Yolk solids weight for the 65 IU vitamin E/kg group was higher (P < 0.01) compared to the 25 IU/kg group. ConA and LPS mitogenic responses were greater in hens fed 65 IU of vitamin E (P < 0.001 or P < 0.003, respectively) or 1,000 ppm of vitamin C (P < 0.001 or P < 0.002, respectively). The combination of 65 IU vitamin E/kg and 1,000 ppm vitamin C showed the highest ConA and LPS mitogenic responses among the treatments. No interaction effects of the two vitamins on production measurements or lymphocyte proliferative responses were observed. TBA values in egg yolk and plasma of hens fed 65 IU of vitamin E/kg were lower (P < 0.0001) than those of hens that received 25 IU of vitamin E/kg. These results suggest that vitamin E supplementation at 65 IU/kg diet may enhance production, induction of in vitro lymphocyte proliferation by ConA and LPS, and antioxidant properties of egg yolks and plasma of White Leghorn hens during heat stress and that supplementation of 1,000 ppm vitamin C may further enhance in vitro lymphocyte proliferative responses of hens during heat stress.

Animals↗

Stress and the intensive care patient: perceptions of patients and nurses.

This study was a replication of an earlier Cochran & Ganong study that investigated the perception of nurses and patients regarding the stressors faced by patients in the intensive care unit environment. As the original study was American in origin, one of the aims of the present study was to discover if the results would be replicated in a United Kingdom (UK) intensive care unit. Data collection was by the use of an environmental stress questionnaire that was an adaptation of the original data collection tool modified for use in a UK intensive care unit. The study was undertaken in two intensive care units producing a sample size of 71 patients and 71 nurses. There appears to be a wide variation in the perception of nurses and patients regarding the stress faced by patients in the intensive care unit. Similarities were noted between subject groups as to the nature of the stressors, although nurses tended to rate items over which they believed they had control as being more stressful than did the patients. Patients tended to rate items related to their illness and physical comfort as being most stressful. The results are in keeping with those from the Cochran & Ganong study.

Adolescent↗

A new animal model of binge eating: key synergistic role of past caloric restriction and stress.

Dieting and stress are important in the etiology and maintenance of eating disorders, and dieting strongly predicts stress-induced overeating in humans. We hypothesized that caloric restriction and stress interact in a unique manner to promote binge eating. To test this hypothesis, a group of young female rats were cycled through a restriction period (4 days of 66% of control food intake) followed by 6 days of free feeding prior to being stressed by acute foot shock. After three of these cycles, the food intake of rats exposed only to restriction (R), or only to stress (S), did not differ from controls. However, R+S rats that were restricted and refed, despite normal body weight and food intake after free feeding, engaged in a powerful bout of hyperphagia when stressed (Experiment 1). The R + S effect was replicated in an older group of rats (Experiment 2). The hyperphagia was characteristically binge-like, it constituted a 40% selective increase in highly palatable (HP) food (P < .001) over a discrete period of time (within 24 h post-stress), and reflected feeding for reward (higher HP:chow ratio) over metabolic need as occurred after restriction (higher chow:HP ratio). Subsequent experiments revealed that binge eating did not occur if only chow was available (Experiment 3) or if restriction-refeeding (R-R) did not proximally precede stress (Experiment 4). Experiment 5 revealed that a history of R-R cycles followed by only one stress episode was sufficient to increase intake to 53% above controls as early as 2 h after stress (P < .001). This animal model of binge eating should facilitate investigations into the neurochemical changes induced by dieting and environmental stress to produce disordered eating and provide a preclinical tool to test preventive strategies and treatments more relevant to bulimia nervosa, multiple cases of binge eating disorder (BED) and binge-purge type anorexia nervosa.

Animals↗

Anxiolytic effects of smoking associated with four stressors.

There is a widespread belief that cigarette smoking alleviates stress. The literature reveals conflicting results on the anxiolytic effects of smoking. This study was designed to replicate a report that smoking (a) reduced subjective anxiety induced by stressful anagrams and (b) increased pain threshold for a cold pain task. This study (N = 15) included two other stressors: white noise and an auditory vigilance task. A significant Time x Condition (smoking vs. deprived) interaction was found for Spielberger State Anxiety Inventory scores in the anagram task. A borderline significant interaction effect was found for the cold pain task. No significant effects were found with the two other tasks. These results provide partial support for the popular notion that smoking mitigates stress-induced anxiety. No difference was found between the smoking and deprived conditions for either pain threshold or pain endurance.

Adaptation, Psychological↗

Influence of metabolic stress on the inheritance of cell determination in the moss, Pottia intermedia.

Epigenetically-determined apogamy in aposporous regenerants of the moss Pottia intermedia persists during vegetative propagation, the capacity of apogamy being inherited by individual aposporous protonemal cells. To test Bauer-Lazarenko's proposal that stable apogamy in mosses may be due to some self-replicating cytoplasmic factor, the effects of different metabolic stress treatments on the expression of apogamy have been tested. Chronic metabolic stress caused by long-term growth of autotrophic aposporous protonema on mineral medium with 0.25% of casamino acids and on Murashiga-Skoog (MS) medium with sucrose and phytohormones, as well as by transitory action of high kinetin concentration, have a much stronger influence on the expression of apogamy, than short-term stress treatments with RNase and Pb(2+). Apogamy has been found to be lost stably, after prolonged growth on MS medium containing kinetin and ABA. The proposal that the capacity for apogamy is related to the release of aposporous protonemal cells from a putative factor for apogamy is discussed.

Abscisic Acid↗

Stress-induced premature senescence in BJ and hTERT-BJ1 human foreskin fibroblasts.

To test the involvement of the telomeres in the senescent phenotype, we used telomerase-immortalized human foreskin fibroblasts (hTERT-BJ1). We exposed hTERT-BJ1 and parental BJ cells to either UVB or H(2)O(2) subcytotoxic stress(es). Both cell lines developed biomarkers of replicative senescence: loss of replicative potential, increase in senescence-associated beta-galactosidase activity, typical senescence-like morphology, overexpression of p21(WAF-1) and p16(INK-4a), and decreased level of the hyperphosphorylated form of pRb. Telomere shortening was slightly higher under stress for both BJ and hTERT-BJ1 but still much lower than that reported for other cell lines. We conclude that pathways alternative to telomere shortening must cause the appearance of the senescence phenotype.

Cell Line↗

Hormonal modulation of Epstein-Barr virus replication.

Among the various factors thought to be associated with the reactivation of latent herpesviruses is psychological stress. An increase in levels of 'stress hormones' such as glucocorticoids occurs in individuals who are stressed and previous studies have shown that glucocorticoid hormones can reactivate latent Epstein-Barr virus (EBV) in vitro. In this study, we confirm that the EBV genome in latently infected lymphoblastoid cells can be reactivated with two glucocorticoid hormones, hydrocortisone and dexamethasone. In addition to hydrocortisone and dexamethasone, we also found that other hormones of the hypothalamic-pituitary-axis (corticotropin-releasing factor and adrenocorticotropin hormone but not epinephrine and norepinephrine) as well as somatostatin can enhance the lytic replication of the HR-1 strain of EBV in superinfected cells. These results suggest that multiple endocrine interactions may be involved in stress-induced reactivation/replication of latent EBV.

Adrenocorticotropic Hormone↗

DNA damage, repair, and replication in selenite-induced cataract in rat lens.

DNA synthesis was evaluated in vitro by measuring incorporation of 3H-thymidine in rat lens following systemic delivery of a cataractogenic dose of selenite. Among early metabolic changes observed in the lenses of rats receiving a single dose of 30 nmol Na2SeO3/g body weight was a 30% decrease in DNA replication in lens epithelium occurring between 6 and 12 h after administration of the selenite. This change was followed by an 80% increase in replication by 24 h. Thymidine incorporation in DNA remained elevated compared to controls through 96 h. Unscheduled DNA synthesis was found to be approximately 10% of the total DNA formed, but there was a 30% and 70% increase of this putative DNA repair in the lenses from selenite-treated animals at 6 and 24 h after the injection. Using the alkaline unwinding assay, the proportion of single-strand DNA in lenses from selenite-treated animals increased after 24 h. This estimate of DNA damage was greater in lenses after 96 h. Each component of DNA metabolism: damage, repair, and replication, was affected by the occurrence of selenite stress in lens. These changes both preceded and accompanied nuclear cataract formation.

Animals↗

Dimerization of the ATRIP protein through the coiled-coil motif and its implication to the maintenance of stalled replication forks.

ATR (ATM and Rad3-related), a PI kinase-related kinase (PIKK), has been implicated in the DNA structure checkpoint in mammalian cells. ATR associates with its partner protein ATRIP to form a functional complex in the nucleus. In this study, we investigated the role of the ATRIP coiled-coil domain in ATR-mediated processes. The coiled-coil domain of human ATRIP contributes to self-dimerization in vivo, which is important for the stable translocation of the ATR-ATRIP complex to nuclear foci that are formed after exposure to genotoxic stress. The expression of dimerization-defective ATRIP diminishes the maintenance of replication forks during treatment with replication inhibitors. By contrast, it does not compromise the G2/M checkpoint after IR-induced DNA damage. These results show that there are two critical functions of ATR-ATRIP after the exposure to genotoxic stress: maintenance of the integrity of replication machinery and execution of cell cycle arrest, which are separable and are achieved via distinct mechanisms. The former function may involve the concentrated localization of ATR to damaged sites for which the ATRIP coiled-coil motif is critical.

Adaptor Proteins, Signal Transducing↗

Heme oxygenase-1 prevents superoxide anion-associated endothelial cell sloughing in diabetic rats.

Heme oxygenase-1 (HO-1) represents a key defense mechanism against oxidative injury. Hyperglycemia has been linked to increased oxidative stress, leading to endothelial dysfunction, delayed cell replication, and enhanced apoptosis. The effect of streptozotocin (STZ)-induced diabetes on HO activity, HO-1 promoter activity, superoxide anion (O*-2, and the number of circulating endothelial cells was measured. The expression of HO-1/HO-2 protein was unchanged, but HO activity was decreased in aortas of diabetic rats compared with control (p < 0.05). High glucose decreased HO-1 promoter activity (p < 0.05). Hyperglycemia increased O*-2 and this increase was augmented with HO-1 inhibition and diminished with HO-1 upregulation (p < 0.05). Circulating endothelial cells were significantly higher in diabetic rats and were decreased or increased with administration of the HO-1 inducer (CoPP) or inhibitor (SnMP), respectively (p<0.05). In conclusion, HO-1 upregulation in diabetic rats brings about an increase in serum bilirubin, a reduction in O*-2 production, and a decrease in endothelial cell sloughing.

Animals↗

The genetic covariance among clinal environments after adaptation to an environmental gradient in Drosophila serrata.

We examined the genetic basis of clinal adaptation by determining the evolutionary response of life-history traits to laboratory natural selection along a gradient of thermal stress in Drosophila serrata. A gradient of heat stress was created by exposing larvae to a heat stress of 36 degrees for 4 hr for 0, 1, 2, 3, 4, or 5 days of larval development, with the remainder of development taking place at 25 degrees. Replicated lines were exposed to each level of this stress every second generation for 30 generations. At the end of selection, we conducted a complete reciprocal transfer experiment where all populations were raised in all environments, to estimate the realized additive genetic covariance matrix among clinal environments in three life-history traits. Visualization of the genetic covariance functions of the life-history traits revealed that the genetic correlation between environments generally declined as environments became more different and even became negative between the most different environments in some cases. One exception to this general pattern was a life-history trait representing the classic trade-off between development time and body size, which responded to selection in a similar genetic fashion across all environments. Adaptation to clinal environments may involve a number of distinct genetic effects along the length of the cline, the complexity of which may not be fully revealed by focusing primarily on populations at the ends of the cline.

Adaptation, Biological↗

Social support, stress, and age in women undergoing breast biopsies.

The relationship among stress, age, and social support was explored in 30 women scheduled for a breast biopsy. Stress was determined using the State Trait Anxiety Inventory. Social support strength and network size were measured using the Norbeck Social Support Questionnaire in this correlational study. Findings demonstrated that women do experience stress before their biopsies. Stress was also found to have a negative correlation with social support strength. Moreover, although statistically insignificant, these women tended to have increased stress with aging until age 40, then stress decreased with increasing age. Additional research should replicate the natural age division of < or = 40 years and > 40 years in a larger sample of women. Advanced practitioners are ideally suited to affect patient outcomes by providing social support. This social support could consist of facilitated support groups or access to the information needed by women during this stressful diagnostic experience.

Adult↗

Macrophages inhibit Salmonella typhimurium replication through MEK/ERK kinase and phagocyte NADPH oxidase activities.

Host responses during the later stages of Salmonella-macrophage interactions are critical to controlling infection but have not been well characterized. After 24 h of infection, nearly half of interferon-gamma-primed murine RAW 264.7 macrophage-like cells infected by Salmonella enterica serovar Typhimurium contained filamentous bacteria. Bacterial filamentation indicates a defect in completing replication and has been previously observed in bacteria responding to a variety of stresses. To understand whether macrophage gene expression was responsible for this effect on Salmonella Typhimurium replication, we used gene arrays to profile interferon-gamma-primed RAW 264.7 cell gene expression following infection. We observed an increase in MEK1 kinase mRNA at 8 h, an increase in MEK protein at 24 h, and measured phosphorylation of MEK's downstream target kinase, ERK1/2, throughout the 24-h infection period. Treatment of cells with MEK kinase inhibitors significantly reduced numbers of filamentous bacteria observed within macrophages after 24 h and increased the number of intracellular colony-forming units. Phagocyte NADPH oxidase inhibitors and antioxidants also significantly reduced bacterial filamentation. Either MEK kinase or phagocyte oxidase inhibitors could be added 4-8 h after infection and still significantly decrease bacterial filamentation. Oxidase activity appears to mediate bacterial filamentation in parallel to MEK kinase signaling, while inducible nitric-oxide synthase inhibitors had no significant effect on bacterial morphology. In summary, Salmonella Typhimurium infection of interferon-gamma-primed macrophages triggers a MEK kinase cascade at later infection times, and both MEK kinase and phagocyte NADPH oxidase activity impair bacterial replication. These two signaling pathways mediate a host bacteriostatic pathway and may play an important role in innate host defense against intracellular pathogens.

Animals↗

Further research using a psychological diary technique to investigate psychosomatic relationships.

Reported further data using a pathological diary technique designed to monitor Ss' (N = 110) emotional states over time. Using aggregate measures obtained over a 10-day period, the basic factor structure of the dairy was replicated. The principal factors identified were interpersonal stress, depression-isolation and physical complaints. Items in both the interpersonal stress and depression-isolation factors tended to be related positively to the total number of physical complaints reported during the time period.

Adult↗