When Does Stress End? Evidence of a Prolonged Stress Reaction in Shiftworking Truck Drivers

This study aimed to analyze individual cortisol levels in relation to work conditions, sleep, and health parameters among truck drivers working day shifts (n?=?21) compared to those working irregular shifts (n?=?21). A total of 42 male truck drivers (39.8?±?6.2 yrs) completed questionnaires about sociodemographics, job content, work environment, health, and lifestyle. Rest-activity profiles were measured using actigraphy, and cardiovascular blood parameters were collected. Salivary cortisol samples were obtained: (i) at waking time, (ii) 30?min after waking, and (iii) at bedtime, during both one workday and one day off from work. Irregular-shift workers, compared to day-shift workers, showed significantly higher waist-hip ratio, very-low-density lipoprotein (VLDL) cholesterol, tiredness after work, years working as a driver, truck vibration, and less job demand (p?<?.05). High cortisol levels in irregular-shift workers were correlated with certain stressors, such as short sleep duration and low job satisfaction, and to metabolic parameters, such as total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), VLDL, and triglycerides. Day-shift workers had higher cortisol levels collected 30?min after waking (p?=?.03) and a higher cortisol awakening response (CAR; p?=?.02) during workdays compared to off days. Irregular-shift workers had higher cortisol levels on their off days compared to day-shift workers (p?=?.03). In conclusion, for the day-shift workers, a higher cortisol response was observed on workdays compared to off days. Although no direct comparisons could be made between groups for work days, on off days the irregular-shift workers had higher cortisol levels compared to day-shift workers, suggesting a prolonged stress response in the irregular-shift group. In addition, cortisol levels were correlated with stressors and metabolic parameters. Future studies are warranted to investigate further stress responses in the context of irregular work hours. (Author correspondence: crmoreno@usp.br)     

Stress “Deafness” Reveals Absence of Lexical Marking of Stress or Tone in the Adult Grammar

A Sequence Recall Task with disyllabic stimuli contrasting either for the location of prosodic prominence or for the medial consonant was administered to 150 subjects equally divided over five language groups. Scores showed a significant interaction between type of contrast and language group, such that groups did not differ on their performance on the consonant contrast, while two language groups, Dutch and Japanese, significantly outperformed the three other language groups (French, Indonesian and Persian) on the prosodic contrast. Since only Dutch and Japanese words have unpredictable stress or accent locations, the results are interpreted to mean that stress “deafness” is a property of speakers of languages without lexical stress or tone markings, as opposed to the presence of stress or accent contrasts in phrasal (post-lexical) constructions. Moreover, the degree of transparency between the locations of stress/tone and word boundaries did not appear to affect our results, despite earlier claims that this should have an effect. This finding is of significance for speech processing, language acquisition and phonological theory.     

How Cells Protect Themselves against Stress?

The current evidence on the mechanisms underlying cell response to heat shock is reviewed. The response dynamics, induction, and attenuation as well as heat shock proteins and the mechanisms through which they protect cells from stress are considered. The role of these proteins in regulating the signaling cascades, including apoptosis suppression, is shown.     

Stress et Spermatogénèse

Stress, which originates in the brain, can influence spermatogenesis hormonally or via the nervous system. The hormonal route commences with the central secretion of Corticotrophin-Releasing Factor, leading to a fall in LHRH production, a decrease in Leydig cell LH receptors and a decrease in 17 a hydroxylase activity. Thus, in the case of major, prolonged stress, testosterone secretion falls, which in turn affects spermatogenesis. However, given that the testosterone threshold required for normal seminiferous epithelium function is significantly less than the mean circulating level of this hormone, the importance of low intensity stress remains unknown. The nervous route involves catecholaminergic fibres which, in the testis, innervate the Highmore corpus, the vessels, the area adjacent to the Leydig cells, and the basement membrane of seminiferous tubules. The experimental destruction of these fibres leads a regression of the seminiferous epithelium. Moreover, the experimental ablation of the rat anterior neocortex leads to changes in spermatogenesis. Therefore, given that the endocrine system does not seem to be involved in these changes, these results indicate that the highest level of the nervous system may participate in the controlling the germinal epithelium which, all things considered, would tend to support psychosomatic influences. However, given that the number of spermatozoa varies significantly between ejaculate and independantly of the level of testosterone secretion necessary for normal spermatogenesis, it may be hypothesized that it is only when sperm production is low that temporary stress, in aggravating the situation, becomes deleterious to spermatogenesis. Since, under normal conditions, such periods are short, the role of the influence of stress on spermatogenesis can only be relative. Nevertheless, if variations occur during permanently low sperm production, the likelihood of negative effects is increased. Consequently, the impact of stress or psychological factors on spermatogenesis might well depend upon particular circumstances.     

Does Early Psychosocial Stress Affect Mate Choice?

Early psychosocial stress (e.g., parental divorce, abuse) is conjectured to place individuals on a developmental trajectory leading to earlier initiation of sexual activity, earlier reproduction, and having more sex partners than those with less early psychosocial stress. But does it also affect an individual’s mate choice? The present study examined whether early psychosocial stress affects preferences and dislikes for opposite-sex faces varying in masculinity/femininity, a putative indicator of mate quality, in premenopausal women (58 with a natural cycle, 53 pill-users) and 196 men. No significant three-way interactions were found when women selected the most or least preferred face with participant group (natural cycle, pill), conception risk (low, high), and early psychosocial stress (low, high) as between-subjects factors. Early psychosocial stress did not affect men’s face preferences when selecting the most preferred face. However, men with high early psychosocial stress disliked masculine faces significantly more so than men with low early psychosocial stress. Overall it was concluded that early psychosocial stress does not affect mate choice with the exception that men with high early psychosocial stress were more likely to dislike masculine female faces. It was suggested that men with high early psychosocial stress may dislike masculine female faces because they have nothing to gain from associating with women with such faces.     

The Stress Relaxation of Concentrated Poly γ-Benzyl-l-Glutamate

The effect of temperature and concentration on the relaxation of poly γ-benzyl-l-glutamate (PBLG-mol. wt. 394,000 to 397,000) was examined as a model of protein behavior under “stress” leading to the definition of intra- and inter-molecular forces involved. The relaxation of PBLG, unlike that of the random coil polymers, takes places in two stages. The lower the temperature and concentration of the polymer, the greater is the shift of the inflexion point towards the lower values.

The distribution spectrum of relaxation has a three zone characteristic. The possible significance of each of them is discussed.     

Stress responses in yeasts: what rules apply?

Living organisms have evolved a complex network of mechanisms to face the unforeseen nutritional and environmental circumstances imposed on their natural habitats, commonly termed “stress”. To learn more about these mechanisms, several challenges are usually applied in the laboratory, namely nutrient starvation, heat shock, dehydration, oxidative exposures, etc. Yeasts are chosen as convenient models for studying stress phenomena because of their simple cellular organization and the amenability to genetic analysis. A vast scientific literature has recently appeared on the defensive cellular responses to stress. However, this plethora of studies covers quite different experimental conditions, making any conclusions open to dispute. In fact, the term “yeast stress” is rather confusing, since the same treatment may be very stressful or irrelevant, depending on the yeast. Customary expressions such as “gentle stress” (non-lethal) or “severe stress” (potentially lethal) should be precisely clarified. In turn, although prototypic yeasts share a common repertoire of signalling responsive pathways to stress, these are adapted to the specific ecological niche and biological activity of each particular species. What does “stress” really mean? Before we go any deeper, we have to define this uncertain meaning along with a proper explanation concerning the terms and conditions used in research on yeast stress.     

Understanding Plant Development and Stress Responses through Integrative Approaches

正As the name reflects,integrative plant biology is the core topicof JIPB.In the past few years JIPB has been pursuing the development of this area     

Oxidative Stress,Redox Homeostasis and Cellular Stress Response in Ménière’s Disease: Role of Vitagenes

Ménière’s disease (MD) is characterized by the triad of fluctuating hearing loss, episodic vertigo and tinnitus, and by endolymphatic hydrops found on post-mortem examination. Increasing evidence suggests that oxidative stress is involved in the development of endolymphatic hydrops and that cellular damage and apoptotic cell death might contribute to the sensorineural hearing loss found in later stages of MD. While excess reactive oxygen species (ROS) are toxic, regulated ROS, however, play an important role in cellular signaling. The ability of a cell to counteract stressful conditions, known as cellular stress response, requires the activation of pro-survival pathways and the production of molecules with anti-oxidant, anti-apoptotic or pro-apoptotic activities. Among the cellular pathways conferring protection against oxidative stress, a key role is played by vitagenes, which include heat shock proteins (Hsps) as well as the thioredoxin/thioredoxin reductase system. In this study we tested the hypothesis that in MD patients measurable increases in markers of cellular stress response and oxidative stress in peripheral blood are present. This study also explores the hypothesis that changes in the redox status of glutathione, the major endogenous antioxidant, associated with abnormal expression and activity of carbonic anhydrase can contribute to increase oxidative stress and to disruption of systemic redox homeostasis which can be associated to possible alterations on vulnerable neurons such as spiral ganglion neurons and consequent cellular degeneration. We therefore evaluated systemic oxidative stress and cellular stress response in patients suffering from Meniere’s disease (MD) and in age-matched healthy subjects. Systemic oxidative stress was estimated by measuring protein oxidation, such as protein carbonyls (PC) and 4-hydroxynonenal (HNE) in lymphocytes of MD patients, as well as ultraweak luminescence (UCL) as end-stable products of lipid oxidation in MD plasma and lymphocytes, as compared to age-matched controls, whereas heat shock proteins Hsp70 and thioredoxin (Trx) expression were measured in lymphocytes to evaluate the systemic cellular stress response. Increased levels of PC (P < 0.01) and HNE (P < 0.05) have been found in lymphocytes from MD patients with respect to control group. This was paralleled by a significant induction of Hsp70, and a decreased expression of Trx (P < 0.01), whereas a significant decrease in both plasma and lymphocyte ratio reduced glutathione GSH) vs. oxidized glutathione (GSSG) (P < 0.05) were also observed. In conclusion, patients affected by MD are under condition of systemic oxidative stress and the induction of vitagenes Hsp70 is a maintained response in counteracting the intracellular pro-oxidant status generated by decreased content of GSH as well as expression of Trx. The search for novel and more potent inducers of vitagenes will facilitate the development of pharmacological strategies to increase the intrinsic capacity of vulnerable ganglion cells to maximize antidegenerative mechanisms, such as stress response and thus cytoprotection.     

Effects of Chronic Restraint Stress and 17-β-Estradiol Replacement on Oxidative Stress in the Spinal Cord of Ovariectomized Female Rats

Previous studies have shown sex-specific oxidative changes in spinal cord of rats submitted to chronic stress, which may be due to gonadal hormones. Here, we assessed total radical-trapping potential (TRAP), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and lipid peroxidation (evaluated by the TBARS test) in the spinal cord of ovariectomized (OVX) female rats. Female rats were subjected to OVX, and half of the animals received estradiol replacement. Animals were subdivided into controls and chronically stressed (for 40 days). Our findings demonstrate that chronic stress decreased TRAP, and increased SOD activity in spinal cord homogenates from ovariectomized female rats and had no effect on GPx activity. On the other hand, groups receiving 17β-estradiol replacement presented a decreased GPx activity, but no alteration in TRAP and in SOD activity. No differences in the TBARS test were found in any of the groups analyzed. In conclusion, our results support the idea that chronic stress induces an imbalance between SOD and GPx activities, additionally decreasing TRAP. Estradiol replacement did not reverse the effects of chronic stress, but induced a decrease in GPx activity. Therefore, estradiol replacement in ovariectomized chronically stressed rats could make the spinal cord more susceptible to oxidative injury.     

JNK3 Perpetuates Metabolic Stress Induced by Aβ Peptides

Although Aβ peptides are causative agents in Alzheimer's disease (AD), the underlying mechanisms are still elusive. We report that Aβ42 induces a translational block by activating AMPK, thereby inhibiting the mTOR pathway. This translational block leads to widespread ER stress, which activates JNK3. JNK3 in turn phosphorylates APP at T668, thereby facilitating its endocytosis and subsequent processing. In support, pharmacologically blocking translation results in a significant increase in Aβ42 in a JNK3-dependent manner. Thus, JNK3 activation, which is?increased in human AD cases and a familial AD (FAD) mouse model, is integral to perpetuating Aβ42 production. Concomitantly, deletion of JNK3 from FAD mice results in a dramatic reduction in Aβ42 levels and overall plaque loads and increased neuronal number and improved cognition. This reveals AD as a metabolic disease that is under tight control by JNK3.     

Mitochondrial Dysfunction and Oxidative Stress in Parkinson’s Disease

Environmental toxins, genetic predisposition and old age are major risk factors for Parkinson’s disease (PD). Although the mechanism(s) underlying selective dopaminergic (DA) neurodegeneration remain unclear, molecular studies in both toxin based models and genetic based models of the disease suggest a major etiologic role for mitochondrial dysfunction in the pathogenesis of PD. Further, recent studies have presented clear evidence for a high burden of mtDNA deletions within the substantia nigra neurons in individuals with PD. Ultimately, an understanding of the molecular events which precipitate DA neurodegeneration in idiopathic PD will enable the development of targeted and effective therapeutic strategies. We review recent advances and current understanding of the genetic factors, molecular mechanisms and animal models of PD.     

The Effects of Water Stress on Photosystem Ⅱ in Wheat

The fluorescence yield at room temperature, the capacity of excitation energy distribution between photosystem Ⅰ and Ⅱ by Mg2+, variable fluorescence yield, variable fluorescence quenching rate and fluorescence complementary area were decreased under water stress. These indicated that photosystem Il was impaired. The inhibited variable fluorescence yield could be partly recovered by the addition of artificial electron donor DPC. Therefore, water stress inhibited not only the oxidizing site of photosystem Ⅱ but also impaired partly the reaction center of photosystem Ⅱ.     

Stress and the developing hippocampus: a double-edged sword?

The mechanisms that regulate neuronal function are a sum of genetically determined programs and experience. The effect of experience on neuronal function is particularly important during development, because early-life positive and adverse experience (stress) may influence the still “plastic” nervous system long-term. Specifically, for hippocampal-mediated learning and memory processes, acute stress may enhance synaptic efficacy and overall learning ability, and conversely, chronic or severe stress has been shown to be detrimental. The mechanisms that enable stress to act as this “double-edged sword” are unclear. Here, we discuss the molecular mediators of the stress response in the hippocampus with an emphasis on novel findings regarding the role of the neuropeptide known as corticotropin-releasing hormone (CRH). We highlight the physiological and pathological roles of this peptide in the developing hippocampus, and their relevance to the long-term effects of early-life experience on cognitive function during adulthood.