The gut-brain axis (GBA) represents an operant acting in a two-direction communication system between the gastrointestinal tract and the central nervous system, mediated by the enteric nervous system (ENS), vagus nerve, immune pathways, and endocrine signaling. In recent years, evidence has highlighted the pivotal role of the gut microbiota in modulating this axis, forming the microbiota-gut-brain axis (MGBA). Our review synthesizes current knowledge on the anatomical and functional substrates of gut-brain communication, focusing on interoceptive signaling, the roles of intrinsic primary afferent neurons (IPANs) and enteroendocrine cells (EECs) and the influence of microbial metabolites, including short-chain fatty acids (SCFAs), bile acids, and indoles. These agents modulate neurotransmission, epithelial barrier function, and neuroimmune interactions. The vagus nerve serves as a primary pathway for afferent sensory signaling from the gut influenced indirectly by the ENS and microbiota. Dysbiosis has been associated with altered gut-brain signaling and implicated in the pathophysiology of disorders ranging from irritable bowel syndrome to mood disorders and neurodegeneration. Microbial modulation of host gene expression via epigenetic mechanisms, including microRNAs, adds another layer of complexity. The gut has a crucial role as an active sensory and signaling organ capable of influencing higher-order brain functions. Understanding the MGBA has significant implications for new therapeutic interventions targeting the microbiome to manage neurogastroenterological and even neuropsychiatric conditions.

Spondyloarthritis refers to a broad group of conditions that include ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and enteropathic arthritis associated with Crohn’s disease or ulcerative colitis. They have been classified by the ASAS group (ASsessment in Ankylosing Spondylitis) into axial spondyloarthritis and peripheral spondyloarthritis. Common features include the absence of autoantibodies, genetic predisposition, and clinical aspects such as axial joint involvement, peripheral manifestations, and extra-articular involvement. However, the pathogenic mechanisms remain complex and incompletely elucidated, despite the fact that the specialized literature has described several pathways that act in synergy: genetic predisposition, environmental factors (infections and mechanical stress), or innate and acquired immune mechanisms. Finally, an inflammatory response is triggered by the recruitment of a large number of inflammatory cells and the release of innate cytokines in the affected areas: joints or periarticular or extraarticular tissues. The current article aims to update and systematize the knowledge accumulated so far on this topic, focusing on the mechanisms that have been involved in the onset, progression, and severity of ankylosing spondylitis.

Myocardial and vascular injury secondary to SARS-CoV-2 infection and vaccination has emerged as a clinically relevant phenomenon, with distinct but overlapping mechanisms. Myocardial injury in COVID-19 results from a complex interplay between direct viral effects and immune-mediated inflammation, supported by histopathological studies revealing macrophage-rich infiltrates, microthrombosis, and supporting fibrosis in isolated areas. In contrast, vaccine-associated myocarditis—reported predominantly following mRNA vaccines—has a self-limiting clinical course, with mechanisms likely involving molecular mimicry, aberrant immune activation, or hypersensitivity reactions, although these pathways require further validation. Although mRNA vaccines have been associated with a small increase in myocarditis, particularly in young men, the risk is significantly lower than that associated with COVID-19 infection, and the cardiovascular benefits of vaccination far outweigh these rare adverse events in most populations. After the end of the pandemic, the number of patients with severe forms of COVID-19 has decreased significantly, but we consider that cardiac involvement remains an important issue for the acute and long-term prognosis of patients with SARS-CoV-2 infection. Our paper synthesizes the latest epidemiological and mechanistic evidence on the link between COVID-19, vaccination, and myocardial and/or vascular injuries, highlighting the clinical implications and providing practical recommendations for management, as well as future perspectives on risk assessment, targeted immunotherapy, advanced diagnostic tools, and long-term monitoring.

Background: Rare diseases are defined as clinical conditions that affect only a small number of persons in a population, considered fewer than 1 per 2000 in the European Union or fewer than 1 per 1600 in the United States They are serious, often chronic and progressive conditions, characterized by a pronounced clinical polymorphism that crosses all medical specialties. Multiple areas of life beyond just physical health are affected with significant impact on patients, families, and healthcare systems. Objective: To analyze the socio-demographic, medical, and vocational characteristics that correlate with functional status and work disability as a measure of quality of life in rare diseases. Methods: An observational retrospective study of adults with rare diseases evaluated for eligibility for social insurance rights in the National Institute of Medical Assessment and Work Capacity Rehabilitation Bucharest (INEMRCM, the Romanian abbreviation) over a 5-year period was made. Descriptive analysis was used to present sample characteristics. Means and standard deviations (SD) were calculated to describe numerical variables, frequencies were used to describe categorical variables, and logistic regression analysis was conducted to evaluate potential predictors of work capacity. All statistical analyses were performed by PSPP.3 software. p < 0.05 was the cut-off for statistical significance with a 95% confidence interval. Results: 90 consecutive persons were included in the survey. The mean age of the group was 44.5 years ± SD 10.61 years, with a female/male ratio of 48/42 persons. The mean disease duration was 10.61 years ± SD 9.76 years. Men had more severe disease (73.81%); p = 0.018 and significantly younger retirement age, M/F = 39.10 ± 12.26/43.06 ± 9.32; p = 0.037. Less disabling diseases were predominant autoimmune conditions (85.71% of cases); genetic conditions had a more severe functional impact in 63.75% of cases; p = 0.037. People with multisystem diseases but with specific or targeted treatment can work more frequently (76.19%); those with visual impairment have more severe impairments (73.77%); p < 0.001. All individuals who received specific therapy had a better functional status, unlike only 37.21% of those who received symptomatic treatment or treatment for complications; p = 0.023. Logistic regression analysis indicated that the type of impairment and the availability of specific treatments could serve as predictors of a reduced likelihood of employment in rare disease cases. Education level and occupation were not correlated with functional impairment and work disability (NS). Conclusions: Several factors, including some that are modifiable, were associated with better outcomes, such as reduced disability and an increased potential for work participation. Sex, disease etiology, type of impairment, and treatment were all significantly linked to functional capacity. Among these, the type of impairment and the availability of specific treatments might be predictors of employment. Addressing these parameters requires a multidisciplinary team, involving specialized care and comprehensive support services to improve the overall quality of life of individuals affected by rare diseases.

Background and Objectives: Traumatic intracranial vascular lesions are rare but severe complications of traumatic brain injury (TBI) and include arterial and venous injuries such as arterial dissections, pseudoaneurysms, arterial occlusions, venous sinus thrombosis, arteriovenous fistulas, and carotid–cavernous fistulas. Despite their clinical significance, the available literature remains limited and heterogeneous. This systematic review and meta-analysis aimed to evaluate the diagnostic yield of vascular imaging, spectrum, and imaging modalities of traumatic intracranial vascular lesions in adults with TBI. Materials and Methods: A systematic literature search was conducted from database inception to 31 August 2026 in PubMed, Web of Science Core Collection, Scopus, and the Cochrane Library (CENTRAL) according to the PRISMA 2020 guidelines. Cohorts of patients who underwent vascular imaging after TBI were eligible. When the full text was available, the denominator was the number of patients imaged with a modality able to detect the lesion in question and the numerator was reported at patient level for intracranial lesions. The primary analyses were restricted to cohorts with an explicit adult age criterion or a separately reported adult subgroup; cohorts with a pediatric fraction that could not be separated entered a sensitivity analysis only. Data extraction and quality assessment using the Newcastle–Ottawa Scale and the Joanna Briggs Institute checklist for prevalence studies were performed independently by two reviewers. Proportions were pooled with a logit-transformed random-effects model with restricted maximum-likelihood estimation and prediction intervals, with Freeman–Tukey and generalized linear mixed models as sensitivity analyses. Results: Nineteen studies with 3542 imaged patients were included, eight of them adult cohorts with 2021 patients. In adult cohorts, the pooled diagnostic yield was 11.0% (95% CI, 2.3–39.8%; four cohorts) for dural venous sinus thrombosis, 4.8% (95% CI, 1.1–18.4%; three cohorts) for pseudoaneurysm, 1.1% (95% CI, 0.0–20.8%; two cohorts) for arteriovenous fistula, and 0.7% (95% CI, 0.2–3.1%; three cohorts) for carotid–cavernous fistula, with I² between 74.7% and 96.2% and prediction intervals spanning most of the possible range; arterial dissection (7.0%) and arterial occlusion (5.8%) were reported by a single adult cohort and were not pooled. The proportion of patients with any lesion was not pooled, because the seven cohorts that imaged every patient differed in whether and how the venous compartment was assessed; it ranged from 1.5% to 56.9% by cohort. Adding the eleven adult-dominant cohorts gave 17.5% for sinus thrombosis and 4.5% for pseudoaneurysm. In exploratory univariable meta-regressions for sinus thrombosis, trauma mechanism, imaging modality, and study design were each associated with part of the heterogeneity and were confounded with one another in these cohorts. Conclusions: Every estimate describes the yield of vascular imaging in adults selected for it, rests on two-to-four small cohorts, and carries very low certainty; the prediction intervals show that a new cohort may fall far from the pooled value, and none of the estimates can be read as the frequency of these lesions in TBI in general.

Cardiovascular involvement in SARS-CoV-2 infection and following vaccination has emerged as a clinically relevant phenomenon with distinct yet overlapping mechanisms. Myocardial injury in COVID-19 results from a complex interplay between direct viral ef-fects, immune-mediated inflammation, endothelial dysfunction, oxidative stress, and, in rare occasions, cytokine storm. The virus primarily binds to ACE2 receptors, which are highly expressed in endothelial cells and pericytes, leading to microvascular damage and a systemic prothrombotic state. Additional viral entry pathways, including CD147, Neu-ropilin-1, and CD26, further contribute to vascular and myocardial injury, which is a ra-ther immune-driven process rather than a direct cytopathic one. Histopathological studies that reveal macrophage-rich infiltrates, microthrombosis, and patchy fibrosis support the immune-driven process theory. In contrast, vaccine-associated myocarditis – predomi-nantly reported following mRNA vaccines – presents a self-limiting clinical course, with mechanisms probably involving molecular mimicry, aberrant immune activation, or hy-persensitivity reactions. Despite an increased incidence in young males after the second dose, the overall risk remains low compared to infection-related myocarditis. Under-standing the pathophysiological interplay between infection- and vaccine-related cardiac involvement is essential for accurate risk assessment, improved diagnostic strategies, and targeted therapeutic approaches. Future research should focus on elucidating immune pathways, refining biomarkers, and developing personalized management strategies in order to mitigate cardiovascular sequelae of both COVID-19 and vaccination.