Body Stress Research Articles

Dendrobii Officinalis Flower improved learning and memory impairment by mediating antioxidant effect in Senescent Rats

Aging is a necessary process, with the main feature of structural and functional decline, adaptability and resistance weakened, accompanied with obvious feature of memory dysfunction. At present, the aging of population has become the basic situation in China. Elderly people aged over 60 had reached 130 million in the year of 2007, accounting for 10% of the total population. It is expected that to 2020 year, the aging population will reach 2.24 to 3 million. To the year of 2050, 60 years of age will be more than 400 million. Therefore, it is important to study methods to delay senility to improve the quality of life of elderly and prevent and control the incidence of senile diseases.Dendrobii Officinalis Flower (DOF), which is belong to Dendrobium officinale, is very popular to people for the effect of anti‐aging in China, but lack of corresponding pharmacological experiments. The aim of was to evaluate whether DOF has effect on antioxidant enzymes and improving the brain function in aging rats. DOF was administrated at a dosage of 1.38, or 0.46 g · kg−1 once a day, as well as with a normal control group and senescent control group for 8 weeks. The results showed that DOF could improving the learning function of the escape latency, total distance and target quadrant time at 1.38 g · kg−1 and 0.46 g · kg−1 in Morris water maze experiment, as well as increasing level of γ‐GABA. In addition, DOF (1.38 g · kg−1) could decrease the levels of MDA, Glu and MAO‐B, improving locomotors, SOD and GSH‐P x. Histopathological study showed DOF also could significantly reduce structural lesions and neurodegeneration in the hippocampus. In conclusion, DOF could alleviate brain aging and ameliorate the bodily functions, which may be due to attenuating body's oxidative stress, improving hippocampus damage, and balance the release of neurotransmitters.Support or Funding InformationThis study was supported by the National Key Research and Development Program (No. 2017YFC1702200), the National Science Foundation of China (No. 81673638, No. 81874352, No. 81703772 and No.81803760), the China Postdoctoral Science Foundation (No. 2018M632506)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Clinical study of electroacupuncture on perioperative analgesia in patients with thyroid surgery under cervical plexus block

To investigate the change trend and correlation between the perioperative pain degree and neuroendocrine hormone levels in the perioperative period on patients with thyroid surgery by electroacupuncture combined with cervical plexus block. Forty patients with elective thyroidectomy were enrolled and divided into a control group and an observation group according to the random number table method, 20 cases in each group. In the control group, cervical plexus block was performed. In the observation group, the cervical plexus block combined with electroacupuncture (EA) were given. After the cervical plexus block was completed, the EA was applied at the bilateral Hegu (LI 4) and Neiguan (PC 6) for 30 min. The visual analog scale (VAS) was used to assess the pain level before anesthesia (T0), 2 h after operation (T1), 12 h after operation (T2), 24 h after operation (T3) and 48 h after operation (T4). Blood samples such as adrenocorticotropic hormone (ACTH), C-reactive protein (CRP) and β-endorphin (β-EP) were collected to measure the level of neuroendocrine hormones, and to analyze the correlation between ACTH, CRP, β-EP and VAS scores. The VAS scores at T1, T2, T3 were higher than those at T0 in the two groups (all P<0.05). The VAS scores T1, T2 and T3 in the observation group were lower than those in the control group (all P<0.05). The ACTH and CRP in the control group at T1, T2 and T3 were significantly higher than those at T0 (all P<0.05). The β-EP in the observation group at T1, T2 and T3 was significantly higher than that at T0 (all P<0.05). The ACTH and CRP in the observation group at T1, T2 and T3 were lower than those in the control group,and the β-EP level was higher than that in the control group (all P<0.05).The VAS score was significantly positively correlated with ACTH and CRP levels, and negatively correlated with β-EP. EA stimulation can inhibit the secretion of ACTH and CRP, promote the release of β-EP, reduce the perioperative pain score, and inhibit the body's stress response.

Application of multimodal analgesia in video-assisted thoracoscopic lobectomy

Objective To investigate whether the use of flurbiprofen axe combined with B-ultrasound guided paravertebral nerve block in thoracoscopic lobectomy can improve the analgesic effect, inhibit the body's stress response, reduce the dosage and side effects of opioids. To further test whether the results of the study are related to ropivacaine hydrochloride concentration. Methods Sixty patients undergoing thoracoscopic lobectomy were randomly divided into 3 groups(n=20). Control group was given Flurbiprofen axetil 50 mg 30 min before induction and also give same dose 30 min before sewing, low concentration combined group was given 0.375% ropivacaine paravertebral block+Flurbiprofen axetil (in the same way as the control group), high-concentration combination group was given 0.5% ropivacaine paravertebral block+Flurbiprofen axetil (in the same way as the control group). All patients were given to patient-controlled intravenous analgesia(PCIA) after operative. Observing the recovery situation, Numerical Rating Scale (NRS) scores at rest time and during cough after postoperative, analgesia adverse reactions; recording remifentanil dosage and the total number of compressions PCIA after operative, the determination of cortisol (Cor) and β-endorphin (β-EP) concentrations. Results The incidence of restlessness and restlessness scores in the control group were significantly higher than other two groups (P 0.05). Compared with the low-dose group, the NRS score at rest and the time of coughing in the high-dose group were significantly lower at the 24 h after operation (P 0.05). There was no significant difference of the Cor and β-EP concentration in the preoperative and postoperative between the three groups (P>0.05). Compared with the control group, the concentration of Cor and β-EP were significantly low at 6 and 12 hours in the other two groups (P 0.05). There was no significant difference in the preoperative and postoperative Cor and β-EP levels among the three groups (P>0.05). Compared with the control group, the Cor and β-EP levels in the other two groups were significantly low at 6 h and 12 h (P 0.05). The concentration of Cor and β-EP was increased significantly at 6 h and 12 h after surgery in the control group (P<0.05). Conclusions Thoracic paravertebral block with 0.5% ropivacaine combined with flurbiprofen axetil for thoracoscopic lobectomy provides more effective analgesia, prolongs analgesia time, reduces opioid use and side effects, and inhibits body stress response. As a result, thoracic paraveterbral block achieves the purpose of accelerating post-operative rehabilitation of this type of surgery. Key words: Multimodal analgesia; Flurbiprofen Axetil; Ultrasound; Ropivacaine; Thoracoscopic lobectomy

PO-254 Progression in rehabilitation of Upper Crossed Syndrome

PO-254 Progression in rehabilitation of Upper Crossed Syndrome

Gastric corticotropin-releasing factor influences mast cell infiltration in a rat model of functional dyspepsia.

Functional gastrointestinal disorders (FGIDs) are characterized by dysregulated gut-brain interactions. Emerging evidence shows that low-grade mucosal inflammation and immune activation contribute to FGIDs, including functional dyspepsia (FD). Stress plays an important role in the onset of FD symptoms. In human subjects with FD, presence of gastric mast cells has been reported, but factors that influence mast cell infiltration remain uncharacterized. Corticotropin-releasing factor (CRF) initiates the body’s stress response and is known to degranulate mast cells. In this study, we delineated the role of the CRF system in the pathogenesis of FD in a rat model. Gastric irritation in neonate rat pups with iodoacetamide (IA) was used to induce FD-like symptoms. RNA interference (RNAi) was used to silence gastric CRF expression. Mast cell infiltrate in the stomach increased by 54% in IA-treated rats compared to controls and CRF-RNAi tended to decrease gastric mast cell infiltrate. Sucrose intake decreased in IA-treated rats and mast cell numbers showed a negative association with sucrose intake. IA treatment and transient silencing of gastric CRF increased hypothalamic CRF levels. In IA-treated rats, gastric levels of CRF receptor 2 (CRF2) decreased by ~76%, whereas hypothalamic CRF receptor 1 (CRF1) levels increased. Plasma levels of TNF-α showed a positive correlation with plasma CRF levels. Levels of phosphorylated p38 and ERK1/2 in the stomach showed a positive correlation with gastric CRF levels. Thus, CRF may contribute to low grade inflammation via modulating mast cell infiltration, cytokine levels, MAPK signaling, and the gut-brain axis.

Intravenous Local Anaesthetic Compared with Intraperitoneal Local Anaesthetic in Abdominal Surgery: A Systematic Review

Modern perioperative care strategies aim to optimise perioperative care by reducing the body's stress response to surgery. A major facet of optimising an abdominal surgery analgesia programme is using a multimodal opioid sparing approach. Local anaesthetics have shown promise and there has been considerable research into the most effective route for their administration. This review aims to determine if there is a difference in analgesic efficacy between intraperitoneal local anaesthetic (IPLA) and intravenous local anaesthetic (IVLA). In concordance with the PRISMA statement, a literature search was conducted to identify randomised control trials that compared IVLA with IPLA in abdominal surgery. The primary outcomes of interest were opioid analgesia requirements and pain score assessed by visual analogue score. Data were extracted and entered into pre-designed electronic spreadsheets. This review has identified six papers that compared intravenous lignocaine to intraperitoneal lignocaine. This review showed significantly lower morphine consumption at 4 and 24h in the intraperitoneal group. There was no significant difference in pain scores. From the analysis of these studies, intraperitoneal local anaesthetic had an analgesic benefit over intravenous lignocaine with regard to decreased opioid consumption for abdominal surgery. Further research investigating IVL combined with intraperitoneal local anaesthetic is warranted.

Neurogenesis and the sleeping fly

Neurogenesis As we have all experienced, the body's alertness, cognitive abilities, and stress threshold depend on obtaining sufficient sleep. But why? Studies suggest that sleep is needed to set up the right brain connections. Szuperak et al. looked at the earliest stages of sleep by monitoring fruitfly larvae. To test for periods of rest, or sleep, they tried to arouse larvae by exposing them to a bright light. Fly larvae were indeed aroused from periods of rest, and as a result of this sleep disruption, they slept more at a later time, like other animals. Sleep-deprived larvae also showed decreased neurogenesis. This work suggests that flies may be a model for sleep, with possible implications for brain development. eLife 10.7554/eLife.33220.001 (2018).

Introduction to the Special Issue: The Neurobiology of Peer Victimization

Introduction to the Special Issue:The Neurobiology of Peer Victimization Tracy Vaillancourt (bio) Being the target of goal-directed aggression that is typically repeated and occurring in the context of a power imbalance (Olweus, 1993; Volk, Veenstra, & Espelage, 2017) happens at an alarming rate. Most population-based studies indicate that peer victimization affects about 30% of children and youth worldwide (Nansen et al., 2001; National Academies of Sciences, Engineering, and Medicine [NASEM], 2016; UNICEF, 2013), making it the most common form of aggression that youth are exposed to (Vaillancourt, 2018). Peer victimization has long been thought to be a normal part of growing up; however, recent research on the continuing effects of bullying has challenged this glib viewpoint. Indeed, this research has documented that the negative impact of peer victimization is extensive and enduring—affecting victims well into the future and long after the abuse has stopped (Lereya, Copeland, Costello, & Wolke, 2015; Takizawa, Maughan, & Arseneault, 2014). Given the severity of this issue (i.e., prevalent and destructive), researchers have focused their attention in earnest on identifying psychosocial risk and protective factors associated with peer victimization with the aim of developing appropriate interventions. This research has [End Page 1] been instrumental in providing insight into the prevalence, individual and contextual correlates, and negative consequences of peer victimization (NASEM, 2016). However, this research has also failed to provide insight into processes and mechanisms, given its descriptive nature (Swearer & Hymel, 2015). Another notable issue with this research is that it has failed to consider how individual and contextual factors interact with biology to confer risk, protection, or resiliency (Vaillancourt, 2018; Vaillancourt, Hymel, & McDougall, 2013; Vaillancourt, Sanderson, Arnold, & McDougall, 2017), which is the focus of this special issue on the neurobiology of peer victimization. Neurobiology is a broad term used to describe the study of the nervous system that includes the examination of its anatomy, biochemistry, molecular biology, and physiology. Research can include analyzing neural networks, genetics, neurotransmitters, and hormones. In this special issue, the emphasis is on inflammatory biomarkers, autonomic nervous system reactivity, the stress response system, and neural functioning in relation to peer victimization. These areas of inquiry are informed by a rich literature on the biological effects of stress in animals (Lupien, McEwen, Gunnar, & Heim, 2009; Lupien, Ouellet-Morin, Herba, Juster, & McEwen, 2016) and on new evidence in humans that documents how early life adversity such as being maltreated by a caregiver, or living in poverty, can program physiology and behavior (Bick et al., 2012; Lupien et al., 2009, 2016; Shalev & Belsky, 2016). Being victimized by peers is a toxic stressor that interferes with a person's fundamental need to belong (R. F. Baumeister & Leary, 1995). Toxic stress refers to the "strong and chronic activation of the body's stress system in the absence of a buffering protection to stop the activation" of the stress response system (Lupien et al., 2016, p. 7). Targets of peer abuse perceive the experience as highly stressful (Sharp, 1995), and recent studies on the biological effects of bullying, including those in this special issue, support this viewpoint. Peer victimization has been associated with: (a) changes to the neuroendocrine stress response system (Carney, Hazler, Oh, Hibel, & Granger, 2010; Hansen, Hogh, & Persson, 2011; Hansen et al., 2006; Kliewer, 2006, 2016; Ouellet-Morin, Danese, et al., 2011; Ouellet-Morin, Odgers, et al., 2011; Ouellet-Morin et al., 2013; Vaillancourt et al., 2008), (b) increased inflammation (Copeland et al., 2014; Takizawa, Danese, Maughan, & Arsenault, 2015), and (c) epigenetic alterations such as DNA methylation (Ouellet-Morin et al., 2013). Neuroimaging studies have also shown that the brain processes exclusion by peers as social pain (Rudolph, Miernicki, Troop-Gordon, Davis, & Telzer, 2016; for a review, see Vaillancourt et al., 2013), with similar regions activated [End Page 2] as those associated with physical pain (Eisenberger, 2012; Eisenberger & Lieberman, 2004; Eisenberger, Lieberman, & Williams, 2003). These biological changes are consistent with what is known about the negative effects of chronic and/or extreme stress on health and well-being (Selye, 1976). Psychological or physical stressors initiate a biological cascade that includes increased heart rate, blood pressure, and the increased production of stress hormones like cortisol. This physiological response helps the organism adapt to stressors...

Exercise, heat shock proteins and insulin resistance.

Best known as chaperones, heat shock proteins (HSPs) also have roles in cell signalling and regulation of metabolism. Rodent studies demonstrate that heat treatment, transgenic overexpression and pharmacological induction of HSP72 prevent high-fat diet-induced glucose intolerance and skeletal muscle insulin resistance. Overexpression of skeletal muscle HSP72 in mice has been shown to increase endurance running capacity nearly twofold and increase mitochondrial content by 50%. A positive correlation between HSP72 mRNA expression and mitochondrial enzyme activity has been observed in human skeletal muscle, and HSP72 expression is markedly decreased in skeletal muscle of insulin resistant and type 2 diabetic patients. In addition, decreased levels of HSP72 correlate with insulin resistance and non-alcoholic fatty liver disease progression in livers from obese patients. These data suggest the targeted induction of HSPs could be a therapeutic approach for preventing metabolic disease by maintaining the body's natural stress response. Exercise elicits a number of metabolic adaptations and is a powerful tool in the prevention and treatment of insulin resistance. Exercise training is also a stimulus for increased HSP expression. Although the underlying mechanism(s) for exercise-induced HSP expression are currently unknown, the HSP response may be critical for the beneficial metabolic effects of exercise. Exercise-induced extracellular HSP release may also contribute to metabolic homeostasis by actively restoring HSP72 content in insulin resistant tissues containing low endogenous levels of HSPs.This article is part of the theme issue 'Heat shock proteins as modulators and therapeutic targets of chronic disease: an integrated perspective'.

Monitoring long-term oral corticosteroids.

Corticosteroids are synthetic analogues of human hormones normally produced by the adrenal cortex. They have both glucocorticoid and mineralocorticoid properties. The glucocortoid components are anti-inflammatory, immunosuppressive, anti-proliferative and vasoconstrictive. They influence the metabolism of carbohydrate and protein, in addition to playing a key role in the body’s stress response. Mineralocorticoid’s main significance is in the balance of salt and water concentrations. Due to the combination of these effects, corticosteroids can cause many adverse effects. Oral corticosteroids are absorbed systemically and are therefore more likely to cause adverse effects than topical or inhaled corticosteroids. Furthermore, it is assumed that greater duration of treatment will lead to a greater number of adverse effects, and therefore the most at risk group are those taking high dose, long-term oral corticosteroids (LTOC). High dose is defined as a prescription of >5 mg oral prednisolone and long term as duration of treatment >1 month (based on National Institute for Health and Care Excellence guidance for patient’s ’at risk' of systemic side effects). Parameters to be monitored in primary care include weight, blood pressure, triglycerides, glucose and urea and electrolytes. From clinical experience within the general practice setting, the authors propose that these patients do not receive adequate baseline monitoring before starting corticosteroids nor are these markers monitored consistently thereafter. This project intended to evidence this claim, evaluate the adverse effect profile and improve monitoring in this patient group. The initial audit of 22 patients, within a single general practice, detected at least one documented adverse effect in 64% of patients, while 41% reported more than one adverse effect. 45% had recorded weight gain, 18% had recorded osteoporosis, 18% had at least one recorded cataract, 14% had recorded Hypertension, 14% had recorded diabetes mellitus, 9% had recorded dyspepsia and 5% had a recorded psychiatric complaint. All of these recorded conditions were either directly attributed to steroid medication or occurred since LTOC were prescribed. The aim of this project was to increase the percentage of patients on LTOC with complete baseline monitoring to 100%. ’Baseline monitoring' was defined as a measurement taken within the previous 5 years. Although somewhat arbitrary, 5 years was felt to be the maximum timeframe in which monitoring would still be relevant for comparison following introduction of LTOC. Quality improvement methodology was used throughout this project with multiple PDSA (Plan, Study, Do and Act) cycles. Through this, a monitoring system and protocol for patients taking LTOC was developed. As a result of this project, five adverse effects were detected in five different patients. These included two cases of secondary hypertension, one case of diabetes mellitus, one cataract and one case of adrenal insufficiency. 12 out of 20 patients achieved complete baseline monitoring. While this study did not fully achieve its aim, the aim was deliberately ambitious. As not all patients in this study attended for monitoring, a figure of 100% was impossible to achieve. The remaining ’incompletely monitored patients' had some but not all parameters measured. The creation of a staff protocol and increased clinical experience will ensure that complete monitoring takes place in the future. In conclusion, this project has shown that adverse effects from LTOC are prevalent in a single general practice population. It is also shown that monitoring for LTOC adverse effects is inadequate but can be improved relatively easily as skills and competencies from other medication monitoring systems already exist within healthcare settings and are immediately transferable.

FKBP5 DNA methylation does not mediate the association between childhood maltreatment and depression symptom severity in the Detroit Neighborhood Health Study

Exposure to childhood maltreatment increases the risk of developing mental illness later in life. Childhood maltreatment and depression have both been associated with dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis—a key regulator of the body's stress response. Additionally, HPA axis dysregulation has been implicated in the etiology of a range of mental illnesses. A substantial body of work has shown history of childhood maltreatment alters DNA methylation levels within key HPA axis genes. We therefore investigated whether one of these key genes, FKBP5 mediates the relationship between childhood maltreatment and depression, and assessed FKBP5 DNA methylation and gene expression within 112 adults from the Detroit Neighborhood Health Study (DNHS). DNA methylation was assessed in 4 regions, including the upstream promoter, downstream promoter, and two glucocorticoid response elements (GREs) via pyrosequencing using whole blood derived DNA; Taqman assays measured relative RNA expression from leukocytes. Mediation analyses were conducted using sequential linear regression. Childhood maltreatment was significantly associated with depression symptom severity (FDR < 0.006), but was not a significant predictor of DNA methylation in any of the four loci examined. FKBP5 showed elevated expression levels in participants with vs. without a history of depression (p < 0.001); no significant difference in gene expression levels was observed in relation to childhood maltreatment (p > 0.05). Our results suggest DNA methylation does not mediate the childhood maltreatment-depression association in the DNHS.

Abnormal dendritic maturation of developing cortical neurons exposed to corticotropin releasing hormone (CRH): Insights into effects of prenatal adversity?

Corticotropin releasing hormone (CRH) produced by the hypothalamus initiates the hypothalamic-pituitary-adrenal (HPA) axis, which regulates the body’s stress response. CRH levels typically are undetectable in human plasma, but during pregnancy the primate placenta synthesizes and releases large amounts of CRH into both maternal and fetal circulations. Notably, placental CRH synthesis increases in response to maternal stress signals. There is evidence that human fetal exposure to high concentrations of placental CRH is associated with behavioral consequences during infancy and into childhood, however the direct effects on of the peptide on the human brain are unknown. In this study, we used a rodent model to test the plausibility that CRH has direct effects on the developing cortex. Because chronic exposure to CRH reduces dendritic branching in hippocampal neurons, we tested the hypothesis that exposure to CRH would provoke impoverishment of dendritic trees in cortical neurons. This might be reflected in humans as cortical thinning. We grew developing cortical neurons in primary cultures in the presence of graded concentrations of CRH. We then employed Sholl analyses to measure dendritic branching and total dendritic length of treated cells. A seven-day exposure to increasing levels of CRH led to a significant, dose-dependent impoverishment of the branching of pyramidal-like cortical neurons. These results are consistent with the hypothesis that, rather than merely being a marker of prenatal stress, CRH directly decreases dendritic branching. Because dendrites comprise a large portion of cortical volume these findings might underlie reduced cortical thickness and could contribute to the behavioral consequences observed in children exposed to high levels of CRH in utero.

In the face of danger

Bond determines what befuddles people's brains when the unthinkable happens, and can they do anything about it. Prior knowledge is crucial, because when disaster strikes, their brain is in no state for rational deliberation. It takes just seconds for adrenaline to flood into their bloodstream, pushing their heart rate up from about 70 beats per minute to over 200. Then the body's central stress system releases the hormone cortisol, boosting blood sugar levels and suppressing non-essential functions such as digestion. This evolved fight or flight mechanism prepares them for physical action, but inhibits areas of the brain that govern working memory and process new information. In other words, it primes them to act but not to think. With their cognitive faculties hobbled, if the threatening situation is one they have never been in before, there's little chance of figuring out a solution.

Positive parenting predicts cortisol functioning six years later in young adults.

Research which indicates that adverse experiences influence hypothalamic-pituitary-adrenal (HPA) axis functioning illustrates the social environment 'getting under the skin'. The present study extended this literature by examining whether positive social forces within the caregiving environment can also impact cortisol functioning. We conducted a prospective investigation of over 300 youth, half of whom were White and half were Black. Attachment, bonding and parental rewards for positive behaviors were observed or reported by the youth as an 8th grader. Twelve repeated measures of salivary cortisol were examined six years later when youth were young adults (mean age 20). Race differences were explored. Stronger attachment, bonding and teen-reported positive parenting were predictive of high waking cortisol and steeper diurnal slopes six years later. This effect was nonlinear and additive, such that youth whose social contexts were characterized by the strongest attachment, bonding and rewarding parental relationships had the highest waking cortisol. When effects were moderated by race, findings were such that links of positive parenting with HPA functioning were more consistent for White than Black youth. Findings suggest that positive aspects of the caregiving environment can also 'get under the skin' and these effects are additive across a range of caregiving indices. These findings dovetail with an emerging literature on the powerful role of social support for shaping the body's stress response system and are interpreted as consistent with the Adaptive Calibration Model which suggests that cortisol regulation can have adaptive significance. A video abstract of this article can be viewed at: https://youtu.be/8evHXpt_TXM.

Corticotrophin-Releasing-Hormone (CRH) modulates ovarian steroid biosynthesis in human primary granulosa cells

Introduction: Corticotrophin-Releasing-Hormone (CRH) is majorly involved in the body's stress response and regulates ovarian steroid biosynthesis by blocking GnRH release via a negative feedback loop. In addition, CRH has been highlighted to modulate ovarian response in a more direct way – most presumably via CRH-receptors (CRHRs) expressed in ovarian granulosa cells. We recently demonstrated CRHR1 to be present in human ovarian follicles. Since functional data are missing so far, the current study aimed to elucidate whether CRH is able to directly act on ovarian granulosa cells.

Early Life Stress: What Is the Human Chapter of the Mammalian Story?

AbstractAbout the time I started kindergarten, a researcher in a laboratory far away picked up a baby rat, handled it briefly, and returned it to the nest. The rat grew up to be resilient to stress, as did its brothers and sisters who were also handled. The effect was traced to changes in the brain's regulation of the body's stress and emotion systems. Thus was born the field of early experiences and stress. Years later, as a research assistant, I pondered why babies cried when uncontrollable toys made loud noises and stumbled into the same field of early experiences and stress. I have spent more than 35 years trying to use our vast knowledge of the neurobiology of stress and development in animals to understand how adverse care during early human development affects physical and mental health. This essay traces my own development as I have sought to understand the human chapter in this mammalian story.

Homosexuality and Anorexia Nervosa: An Explorative Study on Personality Traits

Background: The relationship between anorexia nervosa in males and homosexuality is debated. A higher rate of Eating Disorders (EDs) was found in homosexual than in heterosexual men population. Since anorexia nervosa in men relates with a specific personality profile, homosexual men may share personality features with men affected with anorexia nervosa which may represent risk factors for the ED's outburst. Nevertheless, they have never been compared with the same instrument. The Temperament and Character Inventory (TCI) was widely applied in the study of EDs. Methods: This study compares personality traits, assessed with the TCI in a group of males with anorexia nervosa (n=21) with two control groups; heterosexual (n=51) and homosexual (n=23). A discriminant analysis was performed. Results: Men with anorexia nervosa and homosexual controls display a higher harm avoidance and a lower self-directedness compared with heterosexual controls. Men with anorexia nervosa also display a lower reward dependence compared with homosexual controls and a lower cooperativeness compared with both control groups. Conclusions: A relationship between the personality traits of men with anorexia nervosa and homosexual orientation may exist. Nevertheless, the low reward dependence and the low cooperativeness, which are the most specific characteristics of men with anorexia nervosa, are not linked to the homosexual orientation. Homosexual controls share with men with anorexia nervosa nonspecific personality traits that may indicate a common susceptibility to body's dissatisfaction, depression and stress.

An empirical review on oxidative stress markers and their relevance in obsessive-compulsive disorder

Oxidative stress results from imbalance in the generation of oxidative free radicals in the body and neutralizing antioxidant mechanisms. It hampers various cellular biochemical processes causing dysfunction of the neurons. Reactive oxygen species and reactive nitrogen species are the two important systems regulating the body's oxidative stress. Oxidative stress has a role in several psychiatric disorders including obsessive-compulsive disorder (OCD) and other anxiety disorders. Various studies have found elevated levels of malondialdehyde, superoxide dismutase, glutathione peroxidase, and catalase in patients with OCD, which are considered the markers of oxidative stress. This review discusses the relevance of oxidative stress in OCD.

The Human BNST: Functional Role in Anxiety and Addiction.

The consequences of chronic stress on brain structure and function are far reaching. Whereas stress can produce short-term adaptive changes in the brain, chronic stress leads to long-term maladaptive changes that increase vulnerability to psychiatric disorders, such as anxiety and addiction. These two disorders are the most prevalent psychiatric disorders in the United States, and are typically chronic, disabling, and highly comorbid. Emerging evidence implicates a tiny brain region-the bed nucleus of the stria terminalis (BNST)-in the body's stress response and in anxiety and addiction. Rodent studies provide compelling evidence that the BNST plays a central role in sustained threat monitoring, a form of adaptive anxiety, and in the withdrawal and relapse stages of addiction; however, little is known about the role of BNST in humans. Here, we review current evidence for BNST function in humans, including evidence for a role in the production of both adaptive and maladaptive anxiety. We also review preliminary evidence of the role of BNST in addiction in humans. Together, these studies provide a foundation of knowledge about the role of BNST in adaptive anxiety and stress-related disorders. Although the field is in its infancy, future investigations of human BNST function have tremendous potential to illuminate mechanisms underlying stress-related disorders and identify novel neural targets for treatment.

Blocking stroke-induced immunodeficiency increases CNS antigen-specific autoreactivity but does not worsen functional outcome after experimental stroke.

Stroke-induced immunodepression (SIDS) is an essential cause of poststroke infections. Pharmacological inhibition of SIDS appears promising in preventing life-threatening infections in stroke patients. However, SIDS might represent an adaptive mechanism preventing autoreactive immune responses after stroke. To address this, we used myelin oligodendrocyte glycoprotein (MOG) T-cell receptor transgenic (2D2) mice where >80% of peripheral CD4(+) T cells express a functional receptor for MOG. We investigated in a murine model of middle cerebral artery occlusion the effect of blocking SIDS by inhibiting body's main stress axes, the sympathetic nervous system (SNS) with propranolol and the hypothalamic-pituitary-adrenal axis (HPA) with mifepristone. Blockade of both stress axes robustly reduced infarct volumes, decreased infection rate, and increased long-term survival of 2D2 and C57BL/6J wild-type mice. Despite these protective effects, blockade of SIDS increased CNS antigen-specific Type1 T helper cell (Th1) responses in the brains of 2D2 mice 14 d after middle cerebral artery occlusion. One month after experimental stroke, 2D2 mice developed signs of polyradiculitis, which were diminished by SIDS blockade. Adoptive transfer of CD4(+) T cells, isolated from 2D2 mice, into lymphocyte-deficient Rag-1KO mice did not reveal differences between SIDS blockade and vehicle treatment in functional long-term outcome after stroke. In conclusion, inhibiting SIDS by pharmacological blockade of body's stress axes increases autoreactive CNS antigen-specific T-cell responses in the brain but does not worsen functional long-term outcome after experimental stroke, even in a mouse model where CNS antigen-specific autoreactive T-cell responses are boosted.