Biotechnologically obtained bacterial melanin (BM) has been extensively studied as a potential pharmacological preparation with neuroprotective and anti-inflammatory effects. Anti-inflammatory action of BM was tested in animal model of induced encephalomyelitis. The goal of presented research was t o examine anti-inflammatory potential of BM in lipopolysaccharide-stimulated murine RAW 264.7 cells. The cells were treated with different concentrations of BM (from 6 mg/ml to 4, 2 and 1 mg/ml) and incubated for 20 hours. Results were compared with data obtained from vehicle control treated cells. Two tailed t-test was used to evaluate the results. The obtained data showed that BM reduces the production of nitric oxide and prostaglandin E2. The substance suppresses production of pro-inflammatory cytokines including interleukin (IL)-6 and IL-1b. The results revealed that BM has anti-inflammatory activity and has a potential to suppress neuroinflammation. Brain macrophages-are the only cells that mediate brain inflammation. Extracellular neuromelanin can activate the CNS microglia inducing neuroinflammation and neurodegeneration. The water-soluble biotechnological melanin does not activate microglia – the resident brain macrophages.

Today the term “stress” is used for diverse conditions, which causes confusion. We propose to use the term stress for beneficial stimuli, in which the genome is altered in healthy animals, and men, and thus protected from environmental and other stre

The relationship between exercise and the immune system (IS) is a subject that has had widespread attention across time. Both types of behavior, lack of exercise/exhausting exercise, are suggested to weaken immunity. On the contrary, regular moderate

Breast cancer (BC) is one of the oncological diseases most frequently diagnosed in adult women worldwide. As with other cancer types, BC is thought to emerge after genetically susceptible stem epithelial cells display uncontrolled proliferation after being chronically exposed to stressful environme ntal conditions that may include altered hormonal profiles, metabolic status and/or surrounding environmental settings. This scenario, nonetheless, fails to recognize the role that psychological factors play on BC origin, progression and outcome. Accordingly, in the preceding work, we present data that supports that some psychological traits may predispose Mexican women to develop BC. In this complementary paper, we now explore the “relative weight” that emotional suppression and repression and stress symptoms have on the likelihood of women developing BC by establishing, through network analyses, the way these psychological traits interact with well accepted BC-risk environmental, genetic and physiological factors. Since in our model nodes represent personality traits and the links among them (i.e. the “activated” psychic pathways), Pearson’s correlation analyses were used to evaluate whether healthy networks are different among health-disease states. In addition, in order to study the associations with the clinical factors, an analysis of principal components (PC) and three multivariate models were constructed in order to determine with precision the psychological predictors of BC. Results show that the psychological traits, as expected, adopt a network organization, in which BC patients had the most disconnected distribution, followed by the Benign Breast Pathology (BBP) group. Breast pathology according to the resulting network seems to disconnect emotions from the stress response. Our results also show that the variance found between groups can only be explained by psychological traits, that is, in this sample only certain psychological traits increase the susceptibility to BC but none of the most recognized clinical factors do.

OBJECTIVE:The aim of this study was to explore the associations between immunological markers and anthropometric measures with linear/nonlinear parameters corresponding to the superficial electromyographic activity of uterus, or electrohysterogram (EHG), at parturition. METHODS:Ten minutes of EHG s ignals were recorded from twenty healthy volunteers in active labor at term (40±1 weeks). These signals were normalized and analyzed to estimate relevant linear and nonlinear parameters such as the average root mean square (RMS) value, the area under the curve (AUC) and the sample entropy (SampEn). Furthermore, serum levels of several maternal molecules associated with the inflammatory response in active labor such as the interleukin (IL)-10 family, the B cell activating factor belonging to the TNF family (BAFF/TNFSF13B), and the soluble hemoglobin scavenger receptor CD163 (sCD163) were all analyzed using multiplex immunoassays. In addition, we obtained maternal anthropometric measures such as the body mass index (BMI), weight, abdominal and hip circumference. RESULTS:We found several moderate but significant positive correlations between the SampEn of the EHG signals with BMI: r = 0.54, p = 0.01; weight: r = 0.41, p = 0.03 and hip circumference: r = 0.38, p = 0.04. Also, the average RMS of EHG signals exhibited moderate positive significant correlations with IL-28A: r = 0.48, p = 0.01; sCD163: r = 0.43, p = 0.02 and BAFF/TNFSF13B: r = 0.49, p = 0.01. CONCLUSION:Our results show that larger anthropometric measures were associated with higher irregularity of uterine electrical activity, and that elevated serum concentrations of IL-28A, BAFF/TNFSF13B and sCD163 were related to increased uterine muscle activity. These findings suggest an interaction among anthropometric measures, uterine activity, and inflammatory parameters at active labor.

Thymus is the central organ of immunity, which has a decisive role in the selection and removal of the autoreactive lymphocytes. The pineal gland influences the sustenance and function of thymus, the neonatal removal of thymus as well as pineal gland causes the total collapse of the immune system. Involution of pineal and/or thymus after adolescence permits the manifestation of autoimmune processes, causing the aging and determining the lifespan. Thymus involution is not a consequence of the general involution caused by the progressing age, but a prime mover of it. The pacemaker of aging could be in the suprachiasmatic nucleus of the brain, which is in neural and chemical contact with the the pineal body and the executor is the thymus, regulating the autoimmunity. From this aspect aging is caused by the continuous slow wearing of cells and organs by autoimmunity. A certain degree of autoimmunity is a natural process, which causes manifest disease if becomes enormously strong or directed towards a special organ or system. The velocity of the slow wearing as well, as the functional importance of the target organs determines the lifespan. Outer factors can not prolong the lifespan however, can shorten it by increasing thymic involution, consequently influencing autoimmunity.

Traditionally, neuroscience had dominantly focused on neurons, however the majority of cells in the brain are not neurons but glial cells including astrocytes, oligodendrocytes and microglia. Historically, the pathophysiology of psychiatric disorders has come to be understood within the neuronal do ctrine including the understandings of synaptic connections and neuronal networks. Recent human postmortem and imaging studies have indicated dysfunctions of neuron-glia interaction in various psychiatric disorders such as schizophrenia, depression and autism. We briefly introduce recent topics of glia-related pathophysiology of psychiatric disorders based on rodent and human postmortem and imaging studies. On the other hand, the most significant limitation in psychiatric research is that we cannot obtain living brain cells, including glial cells, from living human subjects based on ethical issues. We herein summarize a novel technique to produce directly induced neuronal and glial cells from somatic cells (not from the brain) such as skin fibroblasts and peripheral bloods by utilizing a gene-modification technique and/or chemical applications. Based on the above-technique, we propose a novel translational study combining with a multi-dimensional perspective; brain imaging analysis, psychometric assessments and molecular functional analysis of induced neuronal and glial cells in psychiatric patients.

Bereavement, the loss of someone close, is frequently followed by grief and can have serious implications for physical and mental health, from the increased symptoms of depression and anxiety, sleep disturbances and indigestion, and more serious physical health consequences such as cardiovascular and immune related illness. Another key factor associated with a deterioration of the body’s defence mechanisms, such as the immune system, is ageing. This review has as its focus the combined effects of bereavement and ageing on immune function. First, the relationship between bereavement and increased mortality is examined, followed by its link to various physical and mental health morbidities. Second, the effects of ageing per se on immune functions are considered. Finally, the joint impact of both ageing and bereavement are discussed, focussing on recent studies of immune function after bereavement in young and older adults.

Transforming growth factor 1 (TGF-1) is an anti-inflammatory cytokine that is expressed in different regions of the mammalian brain, and at all developmental ages. This cytokine can modulate neuron differentiation and survival, and also participate in the tissular response to injury. Based on clinical evidence, different approaches have been used to study the role of TGF-1 on modulating brain function and behavior. Here, we review evidence showing a role of TGF-1 in circadian rhythms, locomotion, sociability and depression-related behaviors. For these behaviors, suprachiamatic, hippocampal and cerebellar expression of TGF-1 have been manipulated. Further studies are required to extend these results to other brain regions and different behaviors, but so far evidence points to a role of TGF-1 on behavior disorders such as schizophrenia, depression and autism.