Neurobiology of Depression and Irritable Bowel Syndrome Comorbidity

Irritable bowel syndrome is a disabling functional disorder with a frequent comorbidity of depression though underlying mechanisms remain yet little understood. Various signs and symptoms have been determined as diagnostic criteria in recent years and standardized as Rome-III criteria. Irritable bowel syndrome can have constipation-dominant, diarrhea-dominant or mixed clinical presentations. Main features can be summarized as continuous and recurrent abdominal pain or discomfort associated with a change of stool frequency or consistency and usually relief of symptoms with defe-cation in the absence of physical or laboratory abnormalities indicative of an organic etiology. The frequency of major depressive disorder diagnosis reaches up to two thirds of irritable bowel syndrome patients. Moreover, the comorbidity of irritable bowel syndrome among patients with major depression is highly frequent (30%). The mechanism underlying irritable bowel syndrome which have been considered as a kind of a somatization disorder for a long time and now as a functional bowel disease is in the brain-gut axis. Low grade mucosal inflammation and cytokines originating from mucosal inflammation have important functions in the pathophysiology of irritable bowel syndrome and its comorbidity with major depression. Besides the inflammatory factors lumbosacral visceral hyperexcitability which is an individual variation is proposed as the main underlying cause of irritable bowel syndrome. Visceral hyper-excitability is mediated by cytokines and neuro-mediators and stress is known to increase the effect of this mechanism. Furthermore, molecules participating in this mechanism (e.g. cytokines, corticotrophin releasing factor, neurokinins and monoamines) play important roles in the pathophysiology of depression. Increased activation in the pain matrix (thalamus – insula – prefrontal cortex) and insufficiency of endogenous pain inhibitory system are regarded as possible casuses of excessive feeling of irritable bowel syndrome symptoms leading to the dysfunction in the cortical representation of bodily states and negative emotional experiences. Individual variations in the interaction of cytokines, corticotrophin releasing factor, neurokinins (substance P, neurokinin A and neurokinin B) and monoamines (serotonin and norepinephrine), and neuroanatomic functions may answer the question of “why do some irritable bowel syndrome patients experience depression and some do not?”. Moreover, irritable bowel syndrome patients with comorbid depression and anxiety disorders are reported to be complaining more about their irritable bowel syndrome symptoms. Although several treatment strategies are considered by clinicians in the management of irritable bowel syndrome, it is suggested that antidepressant medications to have the priority in the treatment of irritable bowel syndrome with the comorbidity of depression. Selective serotonin re-uptake inhibitors are the drug of choice regarding their safety and side effects profile. Nevertheless, tricyclic antidepressants may also have beneficial effects in lower doses than needed to treat clinical depression. Hypnosis, supportive or cognitive behavioral therapies, dietary and defecation habits management are also suggested as beneficial. The recognition of irritable bowel syndrome by psychiatrists may enhance the success of treatment of depression with the comorbidity of irritable bowel syndrome, which disables the patient and frequently accompanies to major depression. In this review, evidence for depression and irritable bowel syndrome comorbidity, the possible underlying mechanisms of this comorbidity and current treatment approaches regarding proposed mechanisms will be discussed

The Role of Hippocampus in the Pathophysiology of Depression

Hippocampus, as a part of the limbic cortex, has a variety of functions ranging from mating behavior to memory besides its role in the regulation of emotions. The hippocampus has reciprocal interactions of with other brain regions which act in the pathophysiology of major depressive disorder (MDD). Moreover, since the hippocampus is a scene for the neurogenesis, which can be seen as a response to antidepressant treatment, the hippocampus became a focus of attention in neuroimaging studies of MDD. It has been shown that brain derived neurotrophic factor (BDNF), that is responsible from the neurogenesis, is associated with the response to the antidepressants and antidepressant drugs are ineffective if neurogenesis is hindered.Hippocampal atrophy is expected with the decrease of neurogenesis as a result of the lower BDNF levels with the deleterious effects of glucocorticoids in depression. Recurrent and severe depression seems to cause such a volume reduction though first episode MDD subjects do not differ from healthy individuals in respect to their hippocampal volumes (HCVs) measured by magnetic resonance imaging methods. One may argue regarding these findings that the atrophy in the hippocampus may be observed in the long term and the decrease in BDNF levels may predispose the volume reduction. Although it has been postulated that smaller HCV as a result of genetic and environmental factors and prior to the illness, may cause a vulnerability to MDD, sufficient evidence has not been accumulated yet and the view that HCV loss develops as depression progresses is widely accepted. Findings that serum BDNF (sBDNF) is lower in MDD patients though HCVs of patients do not differ from healthy individuals and the positive correlation of sBDNF with HCV seen only in the patient group support this view. It can be assumed that depressed patients have sensitivity for the fluctuations in BDNF levels. Follow-up studies which consider effects of hipotalamo-pituiter-adrenal axis dysregulation and monoamine systems are needed to further elucidate the role of BDNF in the pathogenesis of MDD. Results of these studies may lead the way for the treatment of resistant or recurrent depressive disorder

Public Perception of Tax Avoidance

Many conversations about business ethics involve the question of if something is legal, is it ethical? This research study examines participants’ personal ethical beliefs about tax havens, tax avoidance, tax evasion. It also compares how participants react to media biases and if the factors presented affect the participant’s ethical views of tax decisions. Participants believe that tax avoidance, while legal, is slightly unethical. Biases in media sources can also affect a participant’s viewpoint of a company or person. Companies and individuals should use this evidence in determining the harm of their reputation if there were to be a scandal involving tax avoidance strategies

Maude: specification and programming in rewriting logic

Maude is a high-level language and a high-performance system supporting executable specification and declarative programming in rewriting logic. Since rewriting logic contains equational logic, Maude also supports equational specification and programming in its sublanguage of functional modules and theories. The underlying equational logic chosen for Maude is membership equational logic, that has sorts, subsorts, operator overloading, and partiality definable by membership and equality conditions. Rewriting logic is reflective, in the sense of being able to express its own metalevel at the object level. Reflection is systematically exploited in Maude endowing the language with powerful metaprogramming capabilities, including both user-definable module operations and declarative strategies to guide the deduction process. This paper explains and illustrates with examples the main concepts of Maude's language design, including its underlying logic, functional, system and object-oriented modules, as well as parameterized modules, theories, and views. We also explain how Maude supports reflection, metaprogramming and internal strategies. The paper outlines the principles underlying the Maude system implementation, including its semicompilation techniques. We conclude with some remarks about applications, work on a formal environment for Maude, and a mobile language extension of Maude

Participatory system dynamics modelling for housing, energy and wellbeing interactions

The built environment is a key target of decarbonization policies. However, such policies often have a narrow objective and narrow focus, resulting in ‘policy-resistance’ and unintended consequences. The literature attributes these unintended consequences to a narrow financial focus, adverse incentives, and inadequate handling of knowledge, skills, communication and feedback gaps, but it provides little advice on how these complex interactions can be captured. This paper illustrates the development and application of an integrated approach to address these complex interactions with regard to housing performance, energy, communal spaces and wellbeing. In particular, it explores the dynamics created by these relationships with simulation modelling in participatory settings, and with a diverse group of stakeholders. The simulation results suggest that monitoring is key to improve the performance of the housing stock besides energy efficiency; and investments in communal spaces positively affect the adoption of energy-efficiency measures and the wellbeing of residents. The evaluation results for participatory workshops show this approach was found useful by the stakeholders for supporting more integrated decision-making about housing. In future research, this approach can be implemented for policy problems in specific contexts