Stress and the etiology of osteoarthritis

Although degenerative joint disease is an old and exceedingly common problem, clinical investigators have not reached a consensus regarding the etiology of this disease. Comparative osteological analysis of the knee, hip, shoulder, and elbow joints of 798 individuals from four human skeletal populations (Black and White Americans, Pueblo Indians, and Alaskan Eskimos) indicates that age of onset, frequency, and location of degenerative changes are directly related to the nature and degree of environmentally associated stress, as reflected by the variable life styles of the populations sampled. Eskimos have the earliest onset and most severe involvement for all four joints studied, the right side is usually more affected than the left, and Blacks are more frequently involved than Whites in the knee, shoulder, and elbow. Functional stress, when constant and severe in nature, becomes the primary focus of degenerative disease, but other background contributing agents such as age, sex, and hormonal influence must not be ignored.     

Stress and the thyroid gland

The review highlights the effects of acute and chronic stress on thyroid gland metabolism. Special attention is paid to the influence of stress and the direct effects of glucocorticoids on the thyroid status, the activities of thyrocytes, iodine uptake, its oxidation and organification as well as peripheral metabolism of thyroid hormones (deposition and transport of thyroid hormones, deiodinase activities in different tissues). The role of stress in the development of thyroid pathology is analyzed and characteristic features of thyroid function alterations during impaired functioning of the pituitary-adrenal system are established. Taking into consideration serious consequences of thyroid deficiency for the body, even in subclinical thyroid insufficiency, the mechanisms of the stress-induced impairments in thyroid functions are of interest for further studies.     

Exacerbated Headache-Related Pain in the Single Prolonged Stress Preclinical Model of Post-traumatic Stress Disorder

Chronic headache pain is one of the most commonly reported comorbid pain conditions with post-traumatic stress disorder (PTSD) patients and resistant to effective treatment, yet no combined preclinical model of the two disorders has been reported. Here, we used a modified chronic headache pain model to investigate the contribution of single prolonged stress (SPS) model of PTSD with sodium nitroprusside (SNP)-induced hyperalgesia. Injection of SNP (2 mg/kg, i.p.) occurred every other day from day 7 to day 15 after initiation of SPS in rats. Paw withdrawal threshold (PWT) to von Frey stimuli and tail flick latencies (TFL) dramatically decreased as early as 7 days after SPS and lasted until at least day 21. Basal PWT and TFL also significantly decreased during the SNP treatment period. The lower nociceptive thresholds recovered in 6 days following the final SNP injection in SNP group, but not in SPS?+?SNP group. Elevated nociceptin/OFQ (N/OFQ) levels observed in cerebrospinal fluid of SPS rats were even higher in SPS?+?SNP group. Glial fibrillary acidic protein (GFAP) and N/OFQ peptide (NOP) receptor mRNA expression increased in dorsal root ganglia (DRG) 21 days after SPS exposure; mRNA increases in the SPS/SNP group was more pronounced than SPS or SNP alone. GFAP protein expression was upregulated in trigeminal ganglia by SPS. Our results indicate that traumatic stress exaggerated chronic SNP-induced nociceptive hypersensitivity, and that N/OFQ and activated satellite glia cells may play an important role in the interaction between both conditions.

     

Oxidative Stress Impairs the Heat Stress Response and Delays Unfolded Protein Recovery

Background

Environmental changes, air pollution and ozone depletion are increasing oxidative stress, and global warming threatens health by heat stress. We now face a high risk of simultaneous exposure to heat and oxidative stress. However, there have been few studies investigating their combined adverse effects on cell viability.

Principal Findings

Pretreatment of hydrogen peroxide (H₂O₂) specifically and highly sensitized cells to heat stress, and enhanced loss of mitochondrial membrane potential. H₂O₂ exposure impaired the HSP40/HSP70 induction as heat shock response (HSR) and the unfolded protein recovery, and enhanced eIF2α phosphorylation and/or XBP1 splicing, land marks of ER stress. These H₂O₂-mediated effects mimicked enhanced heat sensitivity in HSF1 knockdown or knockout cells. Importantly, thermal preconditioning blocked H₂O₂–mediated inhibitory effects on refolding activity and rescued HSF1 +/+ MEFs, but neither blocked the effects nor rescued HSF1 -/- MEFs. These data strongly suggest that inhibition of HSR and refolding activity is crucial for H₂O₂–mediated enhanced heat sensitivity.

Conclusions

H₂O₂ blocks HSR and refolding activity under heat stress, thereby leading to insufficient quality control and enhancing ER stress. These uncontrolled stress responses may enhance cell death. Our data thus highlight oxidative stress as a crucial factor affecting heat tolerance.     

Initial Copper Stress Strengthens the Resistance of Soil Microorganisms to a Subsequent Copper Stress

To improve the prediction of essential ecosystem functioning under future environmental disturbances, it is of significance to identify responses of soil microorganisms to environmental stresses. In this study, we collected polluted soil samples from field plots with eight copper levels ranging from 0 to 3,200 mg Cu kg^?1 soil. Then, the soils with 0 and 3,200 mg Cu kg^?1 were selected to construct a microcosm experiment. Four treatments were set up including Cu0-C and Cu3200-C without further Cu addition, and Cu0-A and Cu3200-A with addition of 57.5 mg Cu kg^?1 soil. We measured substrate-induced respiration (SIR) and potential nitrification rate (PNR). Furthermore, the abundance of bacterial, archaeal 16S rRNA genes, ammonia-oxidizing bacteria and archaea amoA genes were determined through quantitative PCR. The soil microbial communities were investigated by terminal restriction fragment length polymorphism (T-RFLP). For the field samples, the SIR and PNR as well as the abundance of soil microorganisms varied significantly between eight copper levels. Soil microbial communities highly differed between the low and high copper stress. In the microcosm experiment, the PNR and SIR both recovered while the abundance of soil microorganisms varied irregularly during the 90-day incubation. The differences of microbial communities measured by pairwise Bray–Curtis dissimilarities between Cu0-A and Cu0-C on day 0 were significantly higher after subsequent stress than before. However, the differences of microbial communities between Cu3200-A and Cu3200-C on day 0 changed little between after subsequent stress and before. Therefore, initial copper stress could increase the resistance of soil microorganisms to subsequent copper stress.     

Stress and the evolution of condition-dependent signals

Stressful events are known to initiate a cascade of physiological mechanisms that are potentially costly for metabolic processes. Although these mechanisms are well understood, the long-term costs and the potential implications for individual condition and behaviour have been considered only recently. Combining information from physiological, ecological and behavioural studies can help us to understand the implications of stress for individual life history strategies. Furthermore, the concept of individual variation in stress tolerance has implications for the immunocompetence handicap hypothesis and the evolution of secondary sexual signals.     

Stress and the biology of inequality.

It is well established that health depends on socioeconomic circumstances, but the biology of this relation is not well described. Psychosocial factors operating throughout the life course, beginning in early life, influence a variety of biological variables. Research with non-human primates shows the effects of dominance hierarchy on biology, and similar metabolic differentials are evident in a hierarchy of white collar civil servants. The neuroendocrine "fight or flight" response produces physiological and metabolic alterations which parallel those observed with lower socioeconomic status. The biological effects of the psychosocial environment could explain health inequalities between relatively affluent groups.