Compliance with medications is very important in the management of many gastrointestinal disorders: in inflammatory bowel disease (IBD), controlled trials have shown the benefit of prophylactic medical treatment in lowering the risk of recurrences. Our aim was to appraise the association between current psychiatric disorders and medication adherence in an unselected consecutive group of outpatients with IBD. In 85 unselected consecutive outpatients with IBD, a professional structured diagnostic interview and a psychiatric assessment, by the Structured Clinical Interview for Diagnostic and Statistical Manual-III-Reviewed, were carried out. In a stepwise regression analysis, compliance, as dependent variable, correlated positively with disease duration and inversely with both disease severity and presence of psychiatric disorders. In patients with IBD, preventive liaison psychiatry interventions seem indicated.

Word count: 2754 2 ABSTRACT:Background -Although previous studies demonstrated an association between depressive

Interest in the psychiatric consequences of trauma and the subsequent surgical intervention has been increasing steadily; therefore, the authors assessed the prevalence of acute symptoms of stress in patients who experienced a craniomaxillofacial injury. Fifty patients between the ages of 18 and 65 years were evaluated and assigned a score using the Injury Severity Scale (ISS). Within 48 hours of surgery (T0) and at 3 months after surgery (T1), the authors administered the Davidson Trauma Scale (DTS) to assess post-traumatic symptoms, Spielberger's State-Trait Anxiety Inventory (STAI) to assess symptoms of anxiety, and Zung's Self-rating Depression Scale (SDS) to assess depressive symptoms. Of the subjects, 44% (22 patients at T0) had acute symptoms of stress, and 26% (13 patients at T1) had post-traumatic stress symptoms. The statistical association between demographic variables was significant only for gender, especially for women. There was a significant correlation between the psychopathologic variables and trauma-specific symptoms at both T0 and T1; the same was true for the ISS at T0. Eight of the 13 patients with positive DTS results at 3 months had aesthetic and functional sequelae that might have served as reminders of the traumatic event. It is not only necessary to restitutio ad integrum the anatomy and function, but also to provide psychiatric support for patients experiencing psychiatric symptoms caused by traumatic events.

The transcription factor Nfix belongs to the nuclear factor one family and has an essential role in prenatal skeletal muscle development, where it is a master regulator of the transition from embryonic to foetal myogenesis. Recently, Nfix was shown to be involved in adult muscle regeneration and in muscular dystrophies. Here, we have investigated the signalling that regulates Nfix expression, and show that JunB, a member of the AP-1 family, is an activator of Nfix, which then leads to foetal myogenesis. Moreover, we demonstrate that their expression is regulated through the RhoA/ROCK axis, which maintains embryonic myogenesis. Specifically, RhoA and ROCK repress ERK kinase activity, which promotes JunB and Nfix expression. Notably, the role of ERK in the activation of Nfix is conserved postnatally in satellite cells, which represent the canonical myogenic stem cells of adult muscle. As lack of Nfix in muscular dystrophies rescues the dystrophic phenotype, the identification of this pathway provides an opportunity to pharmacologically target Nfix in muscular dystrophies.

Muscular Dystrophies are severe genetic diseases due to mutations in structural genes, characterized by progressive muscle wasting that compromises patients' mobility and respiratory functions. Literature underlined oxidative stress and inflammation as key drivers of these pathologies. Interestingly among different myofiber classes, type I fibers display a milder dystrophic phenotype showing increased oxidative metabolism. This work shows the benefits of a cyanidin-enriched diet, that promotes muscle fiber-type switch and reduced inflammation in dystrophic alphasarcoglyan (Sgca) null mice having, as a net outcome, morphological and functional rescue. Notably, this benefit is achieved also when the diet is administered in dystrophic animals when the signs of the disease are seriously evident. Our work provides compelling evidence that a cyanidin-rich diet strongly delays the progression of muscular dystrophies, paving the way for a combinatorial approach where nutritional-based reduction of muscle inflammation and oxidative stress facilitate the successful perspectives of definitive treatments.

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Muscular dystrophies are genetic diseases characterized by chronic inflammation and fibrosis. Macrophages are immune cells that sustain muscle regeneration upon acute injury but seem deleterious in the context of chronic muscle injury such as in muscular dystrophies. Here, we observed that the number of macrophages expressing the transcription factor Nfix increases in two distinct mouse models of muscular dystrophies. We showed that the deletion of Nfix in macrophages in dystrophic mice delays the establishment of fibrosis and muscle wasting, and increases grasp force. Macrophages lacking Nfix expressed more TNFα and less TGFβ1, thus promoting apoptosis of fibro‐adipogenic progenitors. Moreover, pharmacological treatment of dystrophic mice with a ROCK inhibitor accelerated fibrosis through the increase of Nfix expression by macrophages. Thus, we have identified Nfix as a macrophage profibrotic factor in muscular dystrophies, whose inhibition could be a therapeutic route to reduce severity of the dystrophic disease. © 2022 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

graft tissue, skin, to an abnormal culture atmosphere (45 ,' CO2 in air) for various periods (7-48 h). Normally-cultured skin grafts caused no lymphoid malignancy. Immunogenicity of exposed grafts as a result of modification of cell-surface proteins and production of "altered self" structures may be a factor in the subsequent appearance of lymphoma in these autologous hosts.