Occupational stress among Swedish audiologists in clinical practice: Reasons for being stressed

Objective: The present study reports on the application of a Swedish translation of the audiologist occupational stress questionnaire (AOSQ) on audiologists working in Sweden. The relations between AOSQ scores and perceived effort, perceived rewards, coping strategies at work, demographic variables such as salary, education length, practise length, and practice type were tested. Design: A cross-sectional e-mail survey using the AOSQ, effort-reward imbalance questionnaire, and demographic questions. Study sample: Four-hundred and four Swedish licensed audiologists working with clients. Results: The Swedish AOSQ translation demonstrated high inter-item correlations and high internal consistency. Several stress factors were identified: time spent at work, accountability, leadership at the workplace, paperwork and practice demands, equipment and clinical protocols, own health concerns, and job control. The outcome on the complete AOSQ questionnaire was related to perceived effort, perceived rewards, coping strategies at work, and age. Conclusions: The Swedish AOSQ translation seems to provide a valid measure of occupational stress among audiologists.     

There Is Something in the Air: Testing the Efficacy of a new Olfactory Stress Relief Method (AromaStick®)

In recent years, aromatherapy has become increasingly popular for clinical treatment and therapeutic management of both acute and chronic stress. It targets distinct and unique neurobiological characteristics of the olfactory system, which is tightly linked to emotions and information processing as well as the autonomous nervous system. Yet, depending on the mode of application, aromatherapeutic interventions show varying degrees of therapeutic effectiveness. In a series of five experiments, the effects of a new mode of aromatherapeutic application (inhaler) was investigated, which is specifically designed to directly stimulate the olfactory system and to reduce the activity of the sympathetic nervous system. Overall, the application of the inhaler showed consistent and large psychological and physiological effects. It also clearly outperformed other stress management techniques, like progressive muscle relaxation, Bach flowers or passive resting periods (natural control). The effects occurred shortly after very few inhalations, drastically reduced stress related biomarkers (i.e. blood pressure, heart rate and cortisol) and considerably enhanced well‐being. Copyright © 2015 John Wiley & Sons, Ltd.     

The Relationship Between Perceived Stress and Telomere Length: A Meta‐analysis

Telomeres protect the ends of chromosomes, and short telomere length is associated with poor health and mortality. This study reports a meta‐analytic investigation of the relationship between perceived stress and telomere length, including results from eight studies with a total of 1143 participants. A meta‐analytic effect size of r = ?0.25, p < 0.001, indicated that higher levels of perceived stress were associated with shorter telomere length. Examination of the studies for moderators of effect size identified some significant moderators, such as a difference in effect sizes between samples comprised of only women and mixed‐sex samples. These results are only suggestive as they are based on a small set of studies, and funnel plot analyses indicated a publication bias. A significant relationship between more perceived stress and shorter telomere length is consistent with theoretical frameworks positing that stress induces physiological changes that result in shortened telomeres. Copyright © 2014 John Wiley & Sons, Ltd.     

Stress Mediates the Relationship Between Past Drug Addiction and Current Risky Sexual Behaviour Among Low‐income Women

This study examined the role of stress as a mediator of the relationship between prior drug addiction and current high‐risk sexual behaviour. Eight hundred twenty women aged 18 to 30 years, who received care at community‐based family planning clinics, were interviewed using the Composite International Diagnostic Interview and the Sexual Risk Behavior Assessment Schedule. They also completed the brief version of the Self‐Control Scale as a measure of problem‐solving strategies and measures of recent stressful events, daily hassles and ongoing chronic stress. Regardless of addiction history, stress exposure during the previous 12 months was associated with risky sexual behaviour during the previous 12 months. Structural equation modelling revealed that 12‐month stress levels mediated the relationship between past drug addiction and 12‐month high‐risk sexual behaviours, as well as the negative relationship between problem‐solving strategies and high‐risk sexual behaviours. Problem‐solving strategies did not moderate the relationship between drug addiction and high‐risk sexual behaviours. These findings suggest that stress management training may help reduce risky behaviour among young, low‐income women Copyright © 2014 John Wiley & Sons, Ltd.     

Ultrastructural hepatocytic alterations induced by silver nanoparticle toxicity

Silver nanoparticles (SNPs) are widely used in nanomedicine and consuming products with potential risk to human health. While considerable work was carried out on the molecular, biochemical, and physiological alterations induced by these particles, little is known of the ultrastructural pathological alterations that might be induced by nanosilver materials. The aim of the present work is to investigate the hepatocyte ultrastructural alterations that might be induced by SNP exposure. Male rats were subjected to a daily single dose (2 mg/kg) of SNPs (15–35 nm diameter) for 21 days. Liver biopsies from all rats under study were processed for transmission electron microscopy examination. The following hepatic ultrastructural alterations were demonstrated: mitochondria swelling and crystolysis, endoplasmic reticulum disruption, cytoplasmic vacuolization, lipid droplets accumulation, glycogen depletion, karyopyknosis, apoptosis, sinusoidal dilatation, Kupffer cells activation, and myelin figures formation. The current findings may indicate that SNPs can induce hepatocyte organelles alteration, leading to cellular damage that may affect the function of the liver. These findings might indicate that SNPs potentially trigger heptocyte ultrastructural alterations that may affect the function of the liver with potential risk on human health in relation to numerous applications of these particles. More work is needed to elucidate probable ultrastructural alterations in the vital organs that might result from nanosilver toxicity.     

Endoplasmic reticulum stress participates in uric acid - induced phenotypic transformation of renal tubular epithelial cells

Objective To explore the effect of endoplasmic reticulum stress (ER stress) in uric acid-induced phenotypic change in renal tubular epithelial cells (HK-2). Methods (1) HK-2 cells were cultured with 0, 75, 150, 225, 300 mg/L uric acid for 24 h in vitro. (2) The cells were divided into normal control group, ER stress inhibitor 4-PBA (5 μmol/L) group, uric acid (150 mg/L) group and 4-PBA+uric acid group for 24 h. Morphological changes of HK-2 cells were observed under inverted microscope. MTT assay was used to detect the proliferation of HK-2 cells treated with 150 mg/L uric acid for 24, 48 and 72 h. The protein expressions of α-smooth muscle actin (α-SMA), vimentin, snail, glucose regulated protein 78 (GRP78) and the phosphorylation of eukaryotic initiation factor 2α (p-eIF2α) in HK-2 cells were measured by Western blotting. Results Compared with the control group, HK-2 cells in uric acid groups (150, 225, 300 mg/L) showed fibroblast-like appearance. The protein expressions of α-SMA, vimentin, snail, GRP78 and p-eIF2α in 150 mg/L and 225 mg/L uric acid groups were higher than those in the control group (all P＜0.05). The proliferation of HK-2 cells in 150 mg/L uric acid group was lower than that in control group at 48 and 72 h (all P＜0.01). Compared with the uric acid group, the cell morphology in 4-PBA+uric acid group was improved, and the protein expressions of α-SMA, vimentin, snail, GRP78 and p-eIF2α were decreased (all P＜0.05). Conclusions Uric acid may induce the phenotype transformation of renal tubular epithelial cell, and ER stress is involved. 4-PBA may inhibit the uric acid-induced ER stress response and phenotypic transformation, and may be beneficial in attenuating uric acid-induced renal tubular damage.     

Indoxyl sulphate and kidney disease: Causes,consequences and interventions

In the last decade, chronic kidney disease (CKD), defined as reduced renal function (glomerular filtration rate (GFR) < 60 mL/min per 1.73 m²) and/or evidence of kidney damage (typically manifested as albuminuria) for at least 3 months, has become one of the fastest‐growing public health concerns worldwide. CKD is characterized by reduced clearance and increased serum accumulation of metabolic waste products (uremic retention solutes). At least 152 uremic retention solutes have been reported. This review focuses on indoxyl sulphate (IS), a protein‐bound, tryptophan‐derived metabolite that is generated by intestinal micro‐organisms (microbiota). Animal studies have demonstrated an association between IS accumulation and increased fibrosis, and oxidative stress. This has been mirrored by in vitro studies, many of which report cytotoxic effects in kidney proximal tubular cells following IS exposure. Clinical studies have associated IS accumulation with deleterious effects, such as kidney functional decline and adverse cardiovascular events, although causality has not been conclusively established. The aims of this review are to: (i) establish factors associated with increased serum accumulation of IS; (ii) report effects of IS accumulation in clinical studies; (iii) critique the reported effects of IS in the kidney, when administered both in vivo and in vitro; and (iv) summarize both established and hypothetical therapeutic options for reducing serum IS or antagonizing its reported downstream effects in the kidney.     

M-30 and 4HNE are sequestered in different aggresomes in the same hepatocytes

M-30 and 4HNE adducts are two markers of active liver disease. M-30 is a serologic marker and 4HNE adducts are histologic markers. M-30 is a marker for apoptosis because it is a fragment of cytokeratin-18 left over from proteolysis by caspase 3. 4HNE is a marker of oxidative stress because it results from lipid peroxidation. Both markers are commonly found in nonalcoholic steatohepatitis and in alcoholic hepatitis. Liver biopsies from patients with steatohepatitis, 11 alcoholic and 11 non-alcoholics were stained for 4HNE and M-30. Almost all of the biopsies in both groups showed 4HNE- and M-30-positive aggresomes in hepatocytes. Mallory Denk bodies (MDB) stained variably positive for M-30, whereas 4HNE was present in aggresomes independent of MDBs. However, they were sometimes located in hepatocytes which also contained MDBs as shown by confocal microscopy of double stained biopsies. The results indicate that the formation of M-30 and 4HNE aggresomes occurs through different pathways of liver cell injury in both types of steatohepatitis.     

Relaxin-3 in GABA projection neurons of nucleus incertus suggests widespread influence on forebrain circuits via G-protein-coupled receptor-135 in the rat

Relaxin-3 (RLX3) is a newly identified member of the relaxin/insulin peptide family that is highly conserved across a range of species from fish to mammals and is highly expressed in rat, mouse and human brain. Extensive pharmacological studies have demonstrated that RLX3 is a high affinity, selective ligand for G-protein-coupled receptor-135 (GPCR135, now classified as relaxin family peptide-3 receptor; RXFP3). In ongoing studies to understand the physiological functions of RLX3, the distribution of RLX3-containing neuronal elements in rat brain was determined by immunohistochemistry, using an affinity-purified polyclonal antiserum raised against a conserved segment of the RLX3 C-peptide (AS-R3(85-101)). Consistent with the distribution of RLX3 mRNA, neurons containing RLX3-like immunoreactivity (LI) were observed in the pontine nucleus incertus and the majority of these cells, which are known to express corticotropin-releasing factor receptor-1, were shown to express glutamic acid decarboxylase-65-immunoreactivity, suggesting a GABA phenotype. Nerve fibers and terminals containing RLX3-LI were observed adjacent to cells in the nucleus incertus and in various forebrain regions known to receive afferents from the nucleus incertus, including cortex, septum, hippocampus, thalamus, hypothalamus and midbrain. Regions that contained highest densities of RLX3-positive fibers included the medial septum, lateral preoptic area, lateral hypothalamus/medial forebrain bundle and ventral hippocampus; and additional fibers were observed in olfactory bulb and olfactory and frontal/cingulate cortices, bed nucleus of the stria terminalis, dorsal endopiriform, intergeniculate, and supramammillary nuclei, and the periaqueductal gray and dorsal raphe. The RLX3-positive network overlapped the regional distribution of GPCR135 mRNA and specific binding sites for an [125I]-GPCR135-selective, chimeric peptide. These anatomical findings further support the proposition that RLX3 is the endogenous ligand for GPCR135 in rat brain and provide evidence for broad modulatory activity of RLX3 in behavioral activation relating to autonomic and neuroendocrine control of metabolism and reproduction and higher-order processes such as stress and cognition.     

Role of glutathione in neuroprotective effects of mood stabilizing drugs lithium and valproate

Mood stabilizing drugs lithium and valproate are the most commonly used treatments for bipolar disorder. Previous studies in our laboratory indicate that chronic treatment with lithium and valproate inhibits oxidative damage in primary cultured rat cerebral cortical cells. Glutathione, as the major antioxidant in the brain, plays a key role in defending against oxidative damage. The purpose of this study was to determine the role of glutathione in the neuroprotective effects of lithium and valproate against oxidative damage. We found that chronic treatment with lithium and valproate inhibited reactive oxygen metabolite H(2)O(2)-induced cell death in primary cultured rat cerebral cortical cells, while buthionine sulfoximine, an inhibitor of glutathione rate-limiting synthesis enzyme glutamate-cysteine ligase, reduced the neuroprotective effect of lithium and valproate against H(2)O(2)-induced cell death. Further, we found that chronic treatment with lithium and valproate increased glutathione levels in primary cultured rat cerebral cortical cells and that the effects of lithium and valproate on glutathione levels were dose-dependent in human neuroblastoma SH-SY5Y cells. Chronic treatment with lithium and valproate also increased the expression of glutamate-cysteine ligase in both rat cerebral cortical cells and SH-SY5Y cells. In addition, chronic treatment with other mood stabilizing drugs lamotrigine and carbamazepine, but not antidepressants desipramine and fluoxetine, increased both glutathione levels and the expression of glutamate-cysteine ligase in SH-SY5Y cells. These results suggest that glutathione plays an important role in the neuroprotective effects of lithium and valproate, and that glutathione may be a common target for mood stabilizing drugs.