In/Sanity as a Means of Repoliticization for British “New Political Writing”

Within the tumultuous and pressing context of the new millennium, in Britain there has been an upsurge of “New Political Writing” and the revival of interest in writing plays with clearer political focus as regards specific ethical and socio-political issues. In other words, there is a movement towards explicit political engagement and many British playwrights demonstrate eagerness to resist the dehumanizing impositions of the current world and the British subculture of violence and immorality and to retrace ethical, social, ethnic and national values. This paper explores the striking conjunction of the new political agenda with mental illness in so many of the plays written in the significant decade of the 2000s and seeks to shed light into the ethical, and socio-political ramifications it entails both for the field of drama and for the field of psychopathology. The discussion will focus on how this body of new British writing which draws on the field of psychopathology constitutes a reflection of the pathology of contemporary British society as well as of the changed identity of political British theatre but also an effort to create room for pluralistic dialectics aiming at a change of the audience’s consciousness. The presentation will demonstrate how subversive representations of insanity on the contemporary stage become an aesthetically and theoretically rich and convenient tool for articulating political concerns and criticism and will highlight the use of the phenomenology and scientific discourse of mental illness as a means to articulate a differentiated political language, a middle ground of “repoliticization.

Health Status of Afghan Refugees in Europe: Policy and Practice Implications for an Optimised Healthcare.

Four decades of civil war, violence, and destabilisation have forced millions of Afghans to flee their homes and to move to other countries worldwide. This increasing phenomenon may challenge physicians unfamiliar with the health status of this population, which may be markedly different from that of the host country. Moreover, several factors during their migration, such as transport in closed containers, accidental injuries, malnutrition, and accommodation in detention centres and refugee camps have a major influence on the health of refugees. By taking into account the variety of the specific diseases among migrant groups, the diversity of the origins of refugees and asylum seekers, and the increasing numbers of Afghan refugees, in this review we focus on the population of Afghans and describe their health status with the aim of optimising our medical approach and management. Our literature review shows that the most prevalent reported infections are tuberculosis and other respiratory tract infections and parasitic diseases, for example leishmaniasis, malaria, and intestinal parasitic infections. Anaemia, hyperlipidaemia, arterial hypertension, diabetes, smoking, overweight, malnutrition, low socioeconomic status, and poor access to healthcare facilities are additional risk factors for non-communicable diseases among Afghan refugees. With regards mental health issues, depression and post-traumatic stress disorder (PTSD) are the most common diagnoses and culture shock and the feeling of being uprooted modulate their persistence. Further research is needed in order to provide us with extensive, high-quality data about the health status of Afghan refugees. The main objective of this review is to identify protective factors which could ensure key health concepts and good clinical practice

Gut-derived immune cells and the gut-lung axis in ARDS.

The gut serves as a vital immunological organ orchestrating immune responses and influencing distant mucosal sites, notably the respiratory mucosa. It is increasingly recognized as a central driver of critical illnesses, with intestinal hyperpermeability facilitating bacterial translocation, systemic inflammation, and organ damage. The "gut-lung" axis emerges as a pivotal pathway, where gut-derived injurious factors trigger acute lung injury (ALI) through the systemic circulation. Direct and indirect effects of gut microbiota significantly impact immune responses. Dysbiosis, particularly intestinal dysbiosis, termed as an imbalance of microbial species and a reduction in microbial diversity within certain bodily microbiomes, influences adaptive immune responses, including differentiating T regulatory cells (Tregs) and T helper 17 (Th17) cells, which are critical in various lung inflammatory conditions. Additionally, gut and bone marrow immune cells impact pulmonary immune activity, underscoring the complex gut-lung interplay. Moreover, lung microbiota alterations are implicated in diverse gut pathologies, affecting local and systemic immune landscapes. Notably, lung dysbiosis can reciprocally influence gut microbiota composition, indicating bidirectional gut-lung communication. In this review, we investigate the pathophysiology of ALI/acute respiratory distress syndrome (ARDS), elucidating the role of immune cells in the gut-lung axis based on recent experimental and clinical research. This exploration aims to enhance understanding of ALI/ARDS pathogenesis and to underscore the significance of gut-lung interactions in respiratory diseases

Pathophysiology of acute lung injury in patients with acute brain injury: the triple-hit hypothesis.

It has been convincingly demonstrated in recent years that isolated acute brain injury (ABI) may cause severe dysfunction of peripheral extracranial organs and systems. Of all potential target organs and systems, the lung appears to be the most vulnerable to damage after ABI. The pathophysiology of the bidirectional brain-lung interactions is multifactorial and involves inflammatory cascades, immune suppression, and dysfunction of the autonomic system. Indeed, the systemic effects of inflammatory mediators in patients with ABI create a systemic inflammatory environment ("first hit") that makes extracranial organs vulnerable to secondary procedures that enhance inflammation, such as mechanical ventilation (MV), surgery, and infections ("second hit"). Moreover, accumulating evidence supports the knowledge that gut microbiota constitutes a critical superorganism and an organ on its own, potentially modifying various physiological functions of the host. Furthermore, experimental and clinical data suggest the existence of a communication network among the brain, gastrointestinal tract, and its microbiome, which appears to regulate immune responses, gastrointestinal function, brain function, behavior, and stress responses, also named the "gut-microbiome-brain axis." Additionally, recent research evidence has highlighted a crucial interplay between the intestinal microbiota and the lungs, referred to as the "gut-lung axis," in which alterations during critical illness could result in bacterial translocation, sustained inflammation, lung injury, and pulmonary fibrosis. In the present work, we aimed to further elucidate the pathophysiology of acute lung injury (ALI) in patients with ABI by attempting to develop the "double-hit" theory, proposing the "triple-hit" hypothesis, focused on the influence of the gut-lung axis on the lung. Particularly, we propose, in addition to sympathetic hyperactivity, blast theory, and double-hit theory, that dysbiosis and intestinal dysfunction in the context of ABI alter the gut-lung axis, resulting in the development or further aggravation of existing ALI, which constitutes the "third hit.

The Heart Is at Risk: Understanding Stroke-Heart-Brain Interactions with Focus on Neurogenic Stress Cardiomyopathy-A Review.

In recent years, it has been convincingly demonstrated that acute brain injury may cause severe cardiac complications-such as neurogenic stress cardiomyopathy (NSC), a specific form of takotsubo cardiomyopathy. The pathophysiology of these brain-heart interactions is complex and involves sympathetic hyperactivity, activation of the hypothalamic-pituitary-adrenal axis, as well as immune and inflammatory pathways. There have been great strides in our understanding of the axis from the brain to the heart in patients with isolated acute brain injury and more specifically in patients with stroke. On the other hand, in patients with NSC, research has mainly focused on hemodynamic dysfunction due to arrhythmias, regional wall motion abnormality, or left ventricular hypokinesia that leads to impaired cerebral perfusion pressure. Comparatively little is known about the underlying secondary and delayed cerebral complications. The aim of the present review is to describe the stroke-heart-brain axis and highlight the main pathophysiological mechanisms leading to secondary and delayed cerebral injury in patients with concurrent hemorrhagic or ischemic stroke and NSC as well as to identify further areas of research that could potentially improve outcomes in this specific patient population

ARDS associated acute brain injury: from the lung to the brain.

A complex interrelation between lung and brain in patients with acute lung injury (ALI) has been established by experimental and clinical studies during the last decades. Although, acute brain injury represents one of the most common insufficiencies in patients with ALI and acute respiratory distress syndrome (ARDS), the underlying pathophysiology of the observed crosstalk remains poorly understood due to its complexity. Specifically, it involves numerous pathophysiological parameters such as hypoxemia, neurological adverse events of lung protective ventilation, hypotension, disruption of the BBB, and neuroinflammation in such a manner that the brain of ARDS patients-especially hippocampus-becomes very vulnerable to develop secondary lung-mediated acute brain injury. A protective ventilator strategy could reduce or even minimize further systemic release of inflammatory mediators and thus maintain brain homeostasis. On the other hand, mechanical ventilation with low tidal volumes may lead to self-inflicted lung injury, hypercapnia and subsequent cerebral vasodilatation, increased cerebral blood flow, and intracranial hypertension. Therefore, by describing the pathophysiology of ARDS-associated acute brain injury we aim to highlight and discuss the possible influence of mechanical ventilation on ALI-associated acute brain injury

Angiotensin II in the treatment of distributive shock: a systematic-review and meta-analysis.

BACKGROUND While non-norepinephrine vasopressors are increasingly used as a rescue therapy in cases of norepinephrine-refractory shock, data on their efficacy are limited. This systematic review and meta-analysis aims to synthesize existing literature on the efficacy of Angiotensin II (ATII) in distributive shock. METHODS We pre-registered our meta-analysis with PROSPERO (CRD42023456136). We searched PubMed, Scopus, and gray literature for studies presenting outcomes on ATII use in distributive shock. The primary outcome of the meta-analysis was all-cause mortality. We used a random effects model to calculate pooled risk ratio (RR) and 95% confidence intervals (CI). RESULTS By incorporating data from 1555 patients included in 10 studies, we found that however all-cause mortality was similar among patients receiving ATII and controls (RR 1.02, 95% CI 0.89 to 1.16, p = 0.81), the reduction in norepinephrine or norepinephrine-equivalent dose at 3 h after treatment initiation was greater among patients receiving ATII (MD -0.06, 95% CI -0.11 to -0.02, p = 0.008), while there were no higher rates of adverse events reported among ATII patients. CONCLUSIONS While ATII did not reduce mortality among distributive shock patients, it allowed for significant adjunctive vasopressor reduction at 3 h without an increase in reported adverse events, deeming it a viable alternative for the increasingly adopted multimodal vasopressor for minimizing catecholamine exposure and its adverse events

Fuchs Syndrome with Isolated Oral Mucosa Lesions due to Severe Herpes Simplex Cheilitis in a Patient with Idiopathic Thrombocytopenic Purpura.

Stevens-Johnson syndrome (SJS) is a severe dermatological disease classically characterized by erythematous target lesions and mucosal involvement. Fuchs syndrome is an incomplete presentation of SJS which has oral, conjunctival and genital manifestations but no skin lesions. To the best of our knowledge, our case of Fuchs syndrome in an 80-year-old man is the first such case related to herpes simplex virus (HSV)-1 infection to be described. Our patient quickly recovered following IVIG therapy, although specific treatment is still a topic of discussion. Research is required on this poorly understood dermatological disease to determine optimum therapy. LEARNING POINTS We report a case of Fuchs syndrome in an elderly man after HSV-1 cheilitis.Therapy always includes discontinuation of the causative drug.Specific therapy for Stevens-Johnson syndrome and Fuchs syndrome is still a topic of discussion, although we noted marked improvement following the administration of IVIG therapy