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PubMedDate not supplied

Decreased cultured endothelial cell proliferation in high glucose medium is reversed by antioxidants: new insights on the pathophysiological mechanisms of diabetic vascular complications.

Exposure to hyperglycemia slows the rate of proliferation of cultured human endothelial cells. Recently, it has been reported that glucose may autoxidize generating free radicals which have been hypothesized to delay cell replication time. To test whether oxidative stress has an effect on delaying cell replication time in hyperglycemic conditions, human endothelial cells cultured from umbilical veins were incubated in 5 or 20 mM glucose, either alone or in the presence of one of three different antioxidants: superoxide dismutase (SOD), catalase and glutathione (GSH). Cells grown in medium with 5 mM glucose, with or without antioxidants, yielded similar population doubling times and cell cycle phase distributions. Significantly lower growth parameters were observed in cells grown in medium with 20 mM glucose, without antioxidants. The presence of the antioxidant reverted them to almost normal growth. These data show that high glucose levels may delay endothelial cells replication time through the generation of free radicals, suggesting a possible pathophysiological linkage between the high levels of glucose and the development of microvascular complications of diabetes, possibly suggesting a new therapeutic approach to prevent such complications.

Antioxidants↗
PubMed1987

Increased susceptibility and reduced phytoalexin accumulation in drought-stressed peanut kernels challenged with Aspergillus flavus.

Three genotypes of peanut (Arachis hypogaea L.), with ICG numbers 221, 1104, and 1326, were grown in three replicate plots and drought stressed during the last 58 days before harvest by withholding irrigation water. Within each plot there were eight levels of stress ranging from 1.1 to 25.9 cm of water. Kernels harvested from the plots were hydrated to 20% moisture and challenged with Aspergillus flavus. Fungal colonization, aflatoxin content, and phytoalexin accumulation were measured. Fungal colonization of non-drought-stressed kernels virtually ceased by 3 days after inoculation, when the phytoalexin concentration exceeded 50 micrograms/g (fresh weight) of kernels, but the aflatoxin concentration continued to rise exponentially for an additional day. When fungal colonization, aflatoxin production, and phytoalexin accumulation were measured 3 days after drought-stressed material was challenged, the following relationships were apparent. Fungal colonization was inversely related to water supply (r varied from -0.848 to -0.904, according to genotype), as was aflatoxin production (r varied from -0.876 to -0.912, according to genotype); the phytoalexin concentration was correlated with water supply when this exceeded 11 cm (r varied from 0.696 to 0.917, according to genotype). The results are discussed in terms of the critical role played by drought stress in predisposing peanuts to infection by A. flavus and the role of the impaired phytoalexin response in mediating this increased susceptibility.

Aflatoxins↗
PubMedDate not supplied

Measurement of 3-D hydraulic conductivity in aquifer cores at in situ effective stresses.

An innovative and nondestructive method to measure the hydraulic conductivity of drill core samples in horizontal and vertical directions within a triaxial cell has been developed. This has been applied to characterizing anisotropy and heterogeneity of a confined consolidated limestone aquifer. Most of the cores tested were isotropic, but hydraulic conductivity varied considerably and the core samples with lowest values were also the most anisotropic. Hydraulic conductivity decreased with increasing effective stress due to closure of microfractures caused by sampling for all core samples. This demonstrates the importance of replicating in situ effective stresses when measuring hydraulic conductivity of cores of deep aquifers in the laboratory.

Anisotropy↗
PubMed2004

Assessing stress in cancer patients: a second-order factor analysis model for the Perceived Stress Scale.

Using the Perceived Stress Scale (PSS), perceptions of global stress were assessed in 111 women following breast cancer surgery and at 12 and 24 months later This is the first study to factor analyze the PSS. The PSS data were factor analyzed each time using exploratory factor analysis with oblique direct quartimin rotation. Goodness-of-fit indices (root mean square error of approximation [RMSEA]), magnitude and pattern of factor loadings, and confidence interval data revealed a two-factor solution of positive versus negative stress items. The findings, replicated across time, also indicate factor stability. Hierarchical factor analyses supported a second-order factor of "perceived stress." This alternative factor model of the PSS is presented along with observations regarding the measure's use in cancer research.

Adult↗
PubMed2000

Relationships among trauma exposure, chronic posttraumatic stress disorder symptoms, and self-reported health in women: replication and extension.

Fifty-two women who served during the Vietnam era were assessed for war-zone exposure, traumatic life events, post-traumatic stress disorder (PTSD), and self-reported health status. Symptoms of PTSD were examined as mediators in the relationship between traumatic exposure and subsequent reports of health problems. Results showed that PTSD symptoms accounted significantly for variance in health problems reported by women with prior traumatic stressor exposure. When the cardinal symptom domains of PTSD (re-experiencing, numbing, avoidance, hyper-arousal) were analyzed separately, the symptom cluster representing hyper-arousal accounted uniquely for the variance associated with health complaints, beyond that contributed by other symptom clusters. Discussion of the results focuses on mechanisms underlying the relationship between specific symptoms of PTSD and self-reported health. Implications for intervention within the medical system are also considered.

Adult↗
PubMed2000

Rhinovirus-induced oxidative stress and interleukin-8 elaboration involves p47-phox but is independent of attachment to intercellular adhesion molecule-1 and viral replication.

Virus-induced elaboration of proinflammatory cytokines is mediated by virus-induced oxidative stress. The purpose of these studies was to determine the source of the virus-induced oxidative stress. Inhibition of viral replication with antibody to intercellular adhesion molecule-1 had no effect on virus-induced oxidative stress or interleukin-8 (IL-8) response (597+/-88 vs. 668+/-78 pg/mL in control cells). Treatment of cells with diphenylene iodonium inhibited virus-induced oxidative stress and IL-8 elaboration, but allopurinol, ibuprofen, and rotenone had no effect. Studies in cell lines produced from a patient with gp91-phox deficiency revealed normal responses. In contrast, the oxidative response was decreased and the IL-8 concentration was 227+/-36 pg/mL in cells from a patient with p47-phox deficiency, compared with 664+/-48 pg/mL in control cells. These studies suggest that the stimulation of reactive oxygen species by viral challenge occurs at the cell surface even in the absence of viral replication and involves a flavoprotein that may act in concert with p47-phox.

Allopurinol↗
PubMed2005

Telomeres as biomarkers for ageing and age-related diseases.

Telomeres in telomerase-negative cells shorten during DNA replication in vitro due to numerous causes including the inability of DNA polymerases to fully copy the lagging strand, DNA end processing and random damage, often caused by oxidative stress. Short telomeres activate replicative senescence, an irreversible cell cycle arrest. Thus, telomere length is an indicator of replicative history, of the probability of cell senescence, and of the cumulative history of oxidative stress. Telomeres in most human cells shorten during ageing in vivo as well, suggesting that telomere length could be a biomarker of ageing and age-related morbidity. There are two distinct possibilities: First, in a tissue-specific fashion, short telomeres might indicate senescence of (stem) cells, and this might contribute to age-related functional attenuation in this tissue. Second, short telomeres in one tissue might cause systemic effects or might simply indicate a history of high stress and damage in the individual and could thus act as risk markers for age-related disease residing in a completely different tissue. In recent years, data have been published to support both approaches, and we will review these. While they together paint a fairly promising picture, it needs to be pointed out that until now most of the evidence is correlative, that much of it comes from underpowered studies, and that causal evidence for essential pathways, for instance for the impact of cell senescence on tissue ageing in vivo, is still very weak.

Aging↗
PubMed1987

Type A personality and discrepancies between self-report and heart-rate responses to stress.

The present study was done to replicate previous findings on the discrepancy between Type A persons' self-reports of stress and their physiological arousal. An attempt was made to clarify whether this discrepancy was due to Type A persons' denial of their arousal or an inability to discriminate physiological change. The students' version of the Jenkins Activity Survey was administered to 30 female students, aged 19 to 43 yr., who then performed a digit recall. A Multiple Affect Adjective Check List and a self-report questionnaire were used to measure affective reactions. Analysis showed that Type A individuals had higher heart-rate responses to stress but did not report greater subjective arousal. These results replicated the previously reported discrepancy. The current findings are somewhat consistent with an explanation based on discrimination.

Adult↗
PubMed1991

The effect of restraint stress on the kinetics, magnitude, and isotype of the humoral immune response to influenza virus infection.

The stress of physical restraint has been shown to modulate the cellular immune response during a viral infection. We have studied the effects of stress on the humoral immune response during infection by influenza virus. Restraint stress altered the kinetics of the antibody response; seroconversion in the IgG and IgA isotypes was delayed in virus-infected C57BL/6 mice subjected to repeated cycles of physical restraint. However, the magnitude and isotype of the mature antibody response were unaffected during the plateau phase; no significant differences were observed between restrained/infected and nonrestrained/infected mice. Thus, the time during infection at which the antibody response was measured was a significant variable in the study of stress-induced alterations of the host's response to a replicating viral antigen. While restraint stress did not significantly affect the magnitude or class of the humoral response, it did alter the kinetics of response.

Animals↗
PubMed2004

Physiological responsiveness of motor vehicle accident survivors with chronic posttraumatic stress disorder.

This study sought to replicate past research that has shown differences in physiological responsiveness among survivors of motor vehicle accidents (MVAs) with posttraumatic stress disorder (PTSD) and those survivors who do not develop this disorder. Such physiological differences have been found specifically with heart rate (HR) reactivity. This study also attempts to account for differences among those survivors with PTSD who do respond physiologically in laboratory situations and those who do not show a physiological response when presented with audiotaped descriptions of their accidents. Results replicated the significant differences in HR reactivity between diagnostic groups with chronic PTSD versus those with subsyndromal PTSD and non-PTSD. Variables related to the severity of the diagnosis and trauma were found to discriminate between physiological responders and nonresponders with chronic PTSD.

Accidents, Traffic↗
PubMed1993

Stress and exercise among the Japanese elderly.

This study seeks to replicate and extend research on the stress process by examining the relationships among stress, social support, physical exercise, and depressive symptoms with data provided by a recent nationwide survey of older adults in Japan. The findings reveal that more frequent physical exercise is associated with less psychological distress. Moreover, the data suggest that some (but not all) types of stressors tend to diminish the frequency of physical activity. Finally, and perhaps most important, the results reveal that social support tends to promote more frequent exercise. This can occur in two ways. First, more emotional support was related to better exercise habits. In addition, negative interaction was also associated with more frequent exercise, suggesting that informal social sanctions can foster positive health behaviors.

Aged↗
PubMed2005

Human Rad9 is required for the activation of S-phase checkpoint and the maintenance of chromosomal stability.

In response to DNA damage or replication block, cells activate a battery of checkpoint signaling cascades to control cell cycle progression and elicit DNA repair in order to maintain genomic stability and integrity. Identified as a homolog of its fission yeast counterpart, human Rad9 was proposed to form a Rad9-Hus1-Rad1 protein complex to mediate checkpoint signals. However, the precise function of Rad9 in the process of checkpoint activation is not fully understood. Using the RNA interference technique, we investigated the role of Rad9 in the genotoxic stress-induced activation of S-phase checkpoint and the maintenance of chromosomal stability. We found that Rad9 knockdown reduced the phosphorylation of Rad17, Chk1 and Smc1 in response to DNA replication block and certain types of DNA damage. Immunofluorescence studies showed that the removal of Rad9 disrupted the foci formation of phosphorylated Chk1, but not ATR. Moreover, Rad9 knockdown resulted in radioresistant DNA synthesis and reduced cell viability under replication stress. Finally, removal of Rad9 by RNAi led to increased accumulation of spontaneous chromosomal aberrations. Taken together, these results suggest a critical and specific role of Rad9 in the activation of S-phase checkpoint and the maintenance of chromosome stability.

Ataxia Telangiectasia Mutated Proteins↗
PubMed2001

The UV-inducible RNA-binding protein A18 (A18 hnRNP) plays a protective role in the genotoxic stress response.

We have previously shown that specific RNA-binding proteins (RBP) are activated by genotoxic stress. The role and function of these stress-activated RBP are, however, poorly understood. The data presented here indicate that the RBP A18 heterogeneous ribonucleoprotein (hnRNP) is induced and translocated from the nuclei to the cytoplasm after exposure to UV radiation. Using a new in vitro system we identified potential cellular targets for A18 hnRNP. Forty-six mRNA transcripts were identified, most of which are stress- or UV-responsive genes. Two important stress-responsive transcripts, the replication protein A (RPA2) and thioredoxin, were studied in more detail. Northwestern analyses indicate that A18 hnRNP binds specifically to the 3'-untranslated region of RPA2 transcript independently of its poly(A) tail, whereas the poly(A) tail of thioredoxin mRNA reinforces binding. Overexpression of A18 hnRNP increases the mRNAs stability and consequently enhances translation in a dose-dependent manner. Moreover, cell lines expressing reduced levels of A18 hnRNP are more sensitive to UV radiation. These data suggest that A18 hnRNP plays a protective role against genotoxic stresses by translocating to the cytosol and stabilizing specific transcripts involved in cell survival.

3' Untranslated Regions↗
PubMed2005

Oxidative stress and antioxidant capacity in smoking and nonsmoking men with HIV/acquired immunodeficiency syndrome.

BACKGROUND: Past studies document decreased levels of antioxidants and selenium and increased levels of oxidative stress in people living with HIV/acquired immunodeficiency syndrome (AIDS). Cigarette smoking is another source of oxidative stress. Excessive oxidative stress can induce HIV replication, resulting in disease progression. The purpose of this study was to determine whether subjects with HIV/AIDS who smoke cigarettes have increased oxidative stress and decreased antioxidant status compared with nonsmokers with HIV/AIDS. METHODS: Thirty-one men with HIV/AIDS (adhering to highly active antiretroviral therapy for the previous 3 months) were recruited during regular visits to a Veterans Affairs Medical Center Infectious Disease Clinic in a southeastern US city. Plasma was obtained from a 1-time blood draw for this comparison study. Plasma lipid peroxide (LPO) was used as a marker of oxidative stress. Indicators of antioxidant capacity included plasma glutathione peroxidase (GPx, the functional indicator of selenium status), vitamin C, and antioxidant potential (AOP). RESULTS: Fifteen smokers and 10 nonsmokers with HIV/AIDS were enrolled. Median plasma LPO level was above the normal range of 0-1.3 micromol/L in both nonsmokers (2.5 [0-23.4] micromol/L, median [range]) and smokers (4.0 [0-47.5] micromol/L), but there was no difference between groups. Plasma GPx concentration was significantly lower in smokers (169 [118-295] mumol/min/L) compared with nonsmokers (197 [149-414] micromol/min/L). Vitamin C and AOP levels were not different between groups. CONCLUSIONS: This pilot study suggests that effects of smoking on oxidative stress are not additive, as no striking differences were observed in oxidative stress or antioxidant capacity between clinically stable smoking and nonsmoking men with HIV/AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Heat shock enhances the susceptibility of BHK cells to rotavirus infection through the facilitation of entry and post-entry virus replication steps.

Rotavirus infection is known to induce several cellular stress proteins, although their possible involvement in the replication cycle of the virus has not been studied. In addition, the heat shock cognate protein hsc70 has been shown to function as a post-attachment receptor during virus entry. In this work we have studied the effect of heat shock on the susceptibility of cells to rotavirus infection. BHK cells, which are largely refractory to the virus, became about 100-fold more susceptible when heat-treated, while the rotavirus highly susceptible MA104 cells did not significantly modified their susceptibility upon heat stress, suggesting that heat shock induces factors that are rate-limiting the replication of rotaviruses in BHK but not in MA104 cells. The heat treatment was shown to facilitate the rotavirus infection of BHK cells at the penetration and post-penetration levels, and each of these stages seems to contribute comparably to the overall observed 100-fold increase in infectivity. Since the binding of the virus to the cell surface was not affected, the caloric stress probably facilitates the penetration and/or uncoating of the virus. The pathway of virus entry into heat-shocked BHK cells seems to be similar to that used in MA104 cells, since treatments that affect MA104 cell infection also affected rotavirus infectivity in heat-treated BHK cells.

Animals↗
PubMed1995

It takes two to replicate: a mediational model for the impact of parents' stress on adolescent adjustment.

In this study of parental stress and adolescent adjustment, experiences of negative life events during the recent past were used to generate a measure of acute stress. In addition, multiple indicators based on reports from various informants were used to estimate latent constructs for parental depression, discipline practices, and adolescent adjustment. Employing 2 independent samples of families from 2 different regions of the country (rural Iowa and a medium-sized city in Oregon), structural equation models were used to test the hypothesis that in intact families acute stress experienced by parents is linked to boys' adjustment (average age equaled 11.8 years in the Oregon sample, 12.7 years in the Iowa sample) through 2 different causal mechanisms. The findings showed that parental stress was related to adjustment through stress-related parental depression that is, in turn, correlated with disrupted discipline practices. Poor discipline appears to provide the direct link with developmental outcomes. The structural equation model (SEM) used to test the proposed mediational process was consistent with the data for mothers and boys from both the Oregon and the Iowa samples. The similarity in results was less clear for fathers and boys. Implications of these results for future replication studies are discussed.

Adaptation, Psychological↗
PubMed2003

Heat-induced expression of a molecular chaperone decreases by selecting for long-lived individuals.

The 70 kDa heat-shock protein (Hsp70) exhibits a broad range of chaperone functions that respond both to internal and external stresses, and its heat-induced expression both declines with age and reduces age-specific mortality rates. Here we test for changes in both longevity and the level of Hsp70-induced expression as correlated responses to selection on both heat-stress resistance and longevity in D. melanogaster. Three replicated H lines were heat-stress selected and compared to their respective non-selected controls (C lines) in the 25th generation of heat-stress selection. The direct response in heat-stress resistance was 56% in males and 38% in females. Heat-stress selection improved longevity in males at normal temperatures. All lines were subsequently subjected to one generation of truncation selection on longevity (selection intensity, i=1.28 for H lines and 1.36 for C lines). The heat-induced Hsp70 expression seems to increase very weakly by heat-stress selection but shows a dramatic and persistent decline by selecting for long-lived flies. A mechanism of longevity selection, involving changes in Hsp70 regulation, is suggested.

Animals↗
PubMed1990

Further evidence for the implication of a kappa-opioid receptor mechanism in the production of psychological stress-induced analgesia.

The analgesic effect induced by exposure to psychological stress, using a communication box (psychological stress-induced analgesia, PSY-SIA), was completely antagonized by 10 min pretreatment with 0.5, 1 and 2 mg/kg of nor-binaltorphimine and with 0.5 and 1 mg/kg of Mr2266, selective kappa-opioid receptor antagonists, in the tail pinch method. Neither footshock (FS)- nor forced swimming (SW)-SIA was affected by these antagonists. The selective delta-opioid receptor antagonist naltrindole, at doses up to 20 mg/kg, had no appreciable effect on PSY-SIA. Daily morphine treatment, 10 mg/kg, s.c., resulted in tolerance to the analgesic effect, and concurrent exposure to PSY-stress suppressed the development of morphine tolerance. The substitution of treatment with U-50,488H for PSY-stress still resulted in analgesia on the initial day; and likewise, the suppression by U-50,488H of the development of morphine tolerance was replicated by PSY-stress. Pretreatment with nor-binaltorphimine antagonized the suppressive effect of PSY-stress on the development of morphine tolerance without affecting the analgesic effect of morphine per se. These results provide further evidence that PSY-SIA involves the mediation by kappa-opioid receptor mechanisms.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗