Background Depressive symptoms are a common comorbidity in patients with peripheral arterial disease (PAD) and have been associated with adverse cardiovascular outcomes. However, their relationship with inflammatory and neuroendocrine biomarkers and their prognostic significance following lower extremity revascularization remains incompletely defined. This study aimed to evaluate whether baseline clinically significant depressive symptoms are associated with clinical characteristics, biomarker profiles, and 24-month clinical outcomes in patients with PAD undergoing revascularization. Methods This prospective, dual-center cohort study included 150 consecutive patients with symptomatic PAD undergoing lower limb revascularization (January 2022-December 2023). Depressive symptoms were assessed using the Patient Health Questionnaire-9 (PHQ-9), with a score ≥10 indicating clinically significant depressive symptoms. Baseline levels of C-reactive protein (CRP), interleukin-6 (IL-6), and cortisol were measured. The primary endpoint was major adverse limb events (MALE) at 24 months. Kaplan-Meier and Cox regression analyses were performed, with adjustment for clinically relevant covariates, including disease severity. Results Of 150 patients, 80 (53.3%) had clinically significant depressive symptoms. Smoking (65.0% vs 37.1%; p = 0.001) and prior cardiovascular events (46.3% vs 25.7%; p = 0.01) were more frequent in this group, which also had a higher prevalence of advanced PAD (Rutherford 4-6). CRP, IL-6, and cortisol levels were higher in patients with depressive symptoms (all p < 0.001). MALE occurred in 37.5% vs 11.4% (p < 0.001). Event-free survival was lower in patients with depressive symptoms (log-rank p < 0.001). In multivariable analysis, depressive symptoms remained associated with MALE (HR: 4.03, 95% CI: 1.84-8.83; p < 0.001). However, given the baseline imbalance in disease severity and the observational design, these findings should be interpreted with caution. Conclusions Clinically significant depressive symptoms are associated with a distinct clinical and biological profile and with worse clinical outcomes in patients undergoing lower extremity revascularization for PAD. These findings suggest a potential prognostic relationship; however, the observed associations may be influenced by disease severity and other confounding factors, and further studies are required to clarify underlying mechanisms and causality.

Early childhood development depends on stable routines, social interaction and responsive caregiving. The 2019 coronavirus disease pandemic disrupted these supports through lockdowns, reduced early-education access and elevated caregiver stress. The present review synthesized empirical studies (2020-2025) of children aged 0-5 years and found consistent evidence of modest increases in emotional and behavioral difficulties, particularly where caregiver stress or socioeconomic adversity was elevated. Cognitive, language and executive-function (EF) outcomes were found to be more heterogeneous and appeared most affected in the contexts of reduced stimulation or limited access to early learning, with EF processes showing particular sensitivity to stress-related and environmental disruptions. Biological findings (cortisol, DNA methylation and infant brain measures) showed a number of converging signals, particularly in higher-risk contexts, but remained preliminary given modest sample sizes, methodological heterogeneity and limited replication. Overall, this suggested that pandemic-related disruptions disproportionately affected children in vulnerable family contexts. Therefore, the present study suggested targeted caregiver mental-health support, preservation of early-education access during emergencies and longitudinal follow-up of high-risk cohorts.

Forensic psychiatric patients often present with severe psychopathology, functional impairment, and poor quality of life. Longitudinal follow-up studies in forensic psychiatric outpatient populations remain limited. The objective is to assess psychopathology, quality of life, global functioning, and general health in forensic psychiatric outpatients compared with psychiatric patients without a forensic history over 24 months. A prospective longitudinal study was conducted with 120 participants (63 forensic and 57 psychiatric outpatients). Assessments were conducted at baseline, 6, 12, and 24 months using validate psychometric tools, PANSS, GHQ-28, WHOQOL-BREF, and GAF. Longitudinal changes within and between groups were analyzed. Most participants were male (82.5%), single (64.2%), unemployed (72.3%), and living in urban areas (93.3%). Forensic psychiatric outpatients reported less social support than psychiatric patients (68.3% vs. 89.5%). Most had a history of incarceration (93.8%). Schizophrenia was the predominant diagnosis (98.3%). Psychopathology, functioning, quality of life, and general health improved significantly over time in both groups (p < 0.001). Positive symptoms improved more in psychiatric patients (mean change -8.96). Psychiatric patients scored significantly higher in the WHOQOL-BREF "environment" domain at baseline and at 6 months. Greater improvement in anxiety/insomnia symptoms was observed in psychiatric patients (mean change -6.44). Long-term outpatient psychiatric follow-up was associated with significant improvements in symptom severity, functioning, quality of life, and general health in both groups. However, forensic psychiatric outpatients continued to experience greater disadvantages, highlighting the need for tailored, long-term, community-based interventions in forensic mental health care.

Most psychiatric disorders are heterogeneous and are attributed to the synergistic action of a multitude of factors. It is generally accepted that psychiatric disorders are the outcome of interactions between genetic predisposition and environmental perturbations, which involve psychosocial stress, or alterations in the physiological state of the organism. A number of hypotheses have been presented on such environmental influences that may include direct insults such as injury, malnutrition and hostile living conditions, or indirect sequelae following infection from viruses such as influenza, arboviruses, enteroviruses and several herpesviruses, or the differential expression of human endogenous retroviruses. It is known that the concept of viruses is far more extensive than their perception as mere agents of acute infections, or chronic debilitating diseases, such as AIDS or some forms of cancer. Notably, an apparent causal connection between viruses and the pathophysiology of diseases has been suggested; however, it remains unclear as to how to establish this causal connection. There are inherent difficulties in answering this question with certainty, which may be due to the multitude of genetic and environmental influences that can lead to psychopathology; the latent state of chronic infection exhibited by a number of neurotropic viruses; the late onset of psychiatric disorders with respect to the acute phase of viral infection at which detection tests would be successful; the complexity of the virome; and the existence of thousands of viral species. The present review aims to provide an outline of the conclusions that have thus far been reached regarding a possible association between viral infection and psychiatric disease, and the obstacles confronted during the quest for the truth behind the role of viruses.

Schizophrenia (SCZ) represents a considerable health concern, not only due to its impact on cognitive and psychiatric domains, but also because of its association with metabolic abnormalities. Individuals with SCZ face an increased risk of developing metabolic syndrome (MS), which contributes to the increased cardiovascular burden and reduced life expectancy observed in this population. Metabolic alterations are associated with both the SCZ condition itself and extrinsic factors, particularly the use of antipsychotic medications. Additionally, the link between SCZ and MS seems to be guided by distinct genetic parameters. The present narrative review summarizes the relationship between SCZ and MS and emphasizes the various therapeutic approaches for managing its components in patients with these conditions. Recommended therapeutic approaches include lifestyle modifications as the primary strategy, with a focus on behavioral lifestyle programs, addressing dietary patterns and physical activity. Pharmacological interventions include administering common antidiabetic medications and the selection of less metabolically harmful antipsychotics. Alternative interventions with limited clinical application are also discussed. Ultimately, a personalized therapeutic approach encompassing both the psychological and metabolic aspects is essential for the effective management of MS in patients with SCZ.

Schizophrenia is a complex mental disorder that affects cognition, emotions and behaviour. Among the signaling pathways that show dysregulation in schizophrenia is the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. JAK/STAT is a pleiotropic pathway that plays key roles in multiple cellular functions. A brief overview of dysregulated signaling in schizophrenia is provided in the present review, focusing on the JAK/STAT pathway. Depending on the disease stage, dysregulation of signaling pathways causes inflammation, which is a key factor in the onset and maintenance of schizophrenia. The dysregulated JAK/STAT signaling pathway is implicated in schizophrenia through numerous processes, including neuro- and gliogenesis, synaptic plasticity and microglia activation. Research on JAK/STAT pathway components can contribute to knowledge that will be translated into efficient therapeutic management strategies to improve the quality of life of patients with schizophrenia.

Peripheral artery disease is a chronic vascular disorder associated with substantial morbidity, mortality, and functional decline. Depression frequently coexists with this condition and is consistently linked to adverse outcomes, including increased risk of limb loss, higher mortality, reduced adherence to therapy, and diminished benefits from revascularization procedures. This narrative review summarizes the current evidence on the prevalence of depression among patients with peripheral artery disease, its impact on clinical outcomes, and the biological and behavioral mechanisms that may explain this association. The findings emphasize the importance of recognizing depression as a major determinant of prognosis in peripheral artery disease and support systematic screening and integrated management as essential components of comprehensive patient care.

Zinc (Zn) may be associated with schizophrenia (SCH), since its altered homeostasis can contribute to abnormal glutamatergic neurotransmission, inflammation, neurodegeneration and autoimmune abnormalities. It has been proposed that a number of patients with SCH could benefit from the use of Zn, either on its own or along with vitamins C, E and B6, and prenatal supplementation of Zn during the gestation period can mitigate the lipopolysaccharide‑induced rat model of maternal immune activation. The aim of the present review was to summarize the various effects of Zn dyshomeostasis on patients with psychosis and to clarify in what ways they could benefit from Zn supplementation.

Background Chronic stress is believed to play a role in the pathophysiology of acute myocardial infarction (AMI). Cortisol is a biomarker associated with stress. We sought to assess stress contribution to AMI using hair cortisol concentration (HCCs) as a surrogate biomarker. Methods HCC was measured in hair segments, corresponding to distinctive periods before hair sampling, in 102 male AMI patients and 50 healthy male controls. Standard baseline variables were collected for both groups, whereas for AMI patients, laboratory and psychological tests were also carried out. Linear mixed models were applied to assess the effect of group and baseline variables on the trend of cortisol before hair sampling. Results HCC was significantly higher in AMI patients the last 30 days before hair sampling with an overall higher rate of increase (time-group interaction P < 0.001). AMI patients with BMI >= 25 kg/m2 had a slower rate of increase compared with those with BMI <25 kg/m2 (adjusted P = 0.008). Among AMI patients, there was no difference in the rate of cortisol increase between STEMI and NSTEMI patients (time-group interaction P = 0.841). Lower BMI conferred higher rates of cortisol increase irrespectively of AMI type. Conclusion HCC, a biomarker of stress, showed an increasing trend over a period of 2 months before the occurrence of AMI suggesting a potential role of stress, through cortisol secretion, in the pathophysiology of AMI.

Since the outbreak of the COVID-19 pandemic, there has been a global surge in patients presenting with prolonged or late-onset debilitating sequelae of SARS-CoV-2 infection, colloquially termed long COVID. This narrative review provides an updated synthesis of the latest evidence on the neurological manifestations of long COVID, discussing its clinical phenotypes, underlying pathophysiology, while also presenting the current state of diagnostic and therapeutic approaches. Approximately one-third of COVID-19 survivors experience prolonged neurological sequelae that persist for at least 12-months post-infection, adversely affecting patients’ quality of life. Core neurological manifestations comprise fatigue, post-exertional malaise, cognitive impairment, headache, lightheadedness ('brain fog'), sleep disturbances, taste or smell disorders, dysautonomia, anxiety, and depression. Some of these features overlap substantially with those reported in post-intensive-care syndrome, myalgic encephalomyelitis/chronic fatigue syndrome, fibromyalgia, and postural-orthostatic-tachycardia syndrome. Advances in data-driven research utilizing electronic-health-records combined with machine learning and artificial intelligence have propelled the identification of long COVID sub-phenotypes. Furthermore, the evolving definitions reflect the dynamic conceptualization of long COVID in both research and clinical contexts. Although the underlying pathophysiology remains incompletely elucidated, neuroinflammatory responses, endotheliopathy, and metabolic imbalances, rather than direct viral neuroinvasion, are implicated in neurological sequelae. Genetic susceptibility has also emerged as a potential risk factor. While major limitations remain with existing definitions, collaborative strategies to standardize diagnostic approaches are needed. Current therapeutic paradigms advocate for multimodal approaches, integrating pharmacological and non-pharmacological interventions along with comprehensive rehabilitation programs. Although preliminary evidence of therapeutic efficacy has been provided by a number of clinical trials, methodological constraints limit the generalizability of this evidence. Preventive measures, notably vaccination, have proven integral for reducing the global burden of long COVID. Considering the healthcare and socioeconomic repercussions incurred by long COVID worldwide, international collaborative initiatives are warranted to address the remaining challenges in diagnosing and managing patients presenting with neurological sequelae.

The gut‑microbiota‑brain axis is a complex bidirectional communication system linking the gastrointestinal tract to the brain. Changes in the balance, composition and diversity of the gut‑microbiota (gut dysbiosis) have been found to be associated with the development of psychosis. Early‑life stress, along with various stressors encountered in different developmental phases, have been shown to be associated with the abnormal composition of the gut microbiota, leading to irregular immunological and neuroendocrine functions, which are potentially responsible for the occurrence of first‑episode psychosis (FEP). The aim of the present narrative review was to summarize the significant differences of the altered microbiome composition in patients suffering from FEP vs. healthy controls, and to discuss its effects on the occurrence and intensity of symptoms in FEP.

Aims Endoscopic-ultrasound fine-needle-aspiration (EUS-FNA) has become the standard of care for the diagnosis of pancreatic and peripancreatic tumors, and several factors are associated with its diagnostic accuracy. The aim of this study is to evaluate factors that are associated with the diagnostic accuracy of EUS-FNA in our center.

Since the outbreak of the COVID-19 pandemic, there has been a global surge in patients presenting with prolonged or late-onset debilitating sequelae of SARS-CoV-2 infection, colloquially termed long COVID. This narrative review provides an updated synthesis of the latest evidence on the neurological manifestations of long COVID, discussing its clinical phenotypes, underlying pathophysiology, while also presenting the current state of diagnostic and therapeutic approaches. Approximately one-third of COVID-19 survivors experience prolonged neurological sequelae that persist for at least 12-months post-infection, adversely affecting patients' quality of life. Core neurological manifestations comprise fatigue, post-exertional malaise, cognitive impairment, headache, lightheadedness ('brain fog'), sleep disturbances, taste or smell disorders, dysautonomia, anxiety, and depression. Some of these features overlap substantially with those reported in post-intensive-care syndrome, myalgic encephalomyelitis/chronic fatigue syndrome, fibromyalgia, and postural-orthostatic-tachycardia syndrome. Advances in data-driven research utilizing electronic-health-records combined with machine learning and artificial intelligence have propelled the identification of long COVID sub-phenotypes. Furthermore, the evolving definitions reflect the dynamic conceptualization of long COVID in both research and clinical contexts. Although the underlying pathophysiology remains incompletely elucidated, neuroinflammatory responses, endotheliopathy, and metabolic imbalances, rather than direct viral neuroinvasion, are implicated in neurological sequelae. Genetic susceptibility has also emerged as a potential risk factor. While major limitations remain with existing definitions, collaborative strategies to standardize diagnostic approaches are needed. Current therapeutic paradigms advocate for multimodal approaches, integrating pharmacological and non-pharmacological interventions along with comprehensive rehabilitation programs. Although preliminary evidence of therapeutic efficacy has been provided by a number of clinical trials, methodological constraints limit the generalizability of this evidence. Preventive measures, notably vaccination, have proven integral for reducing the global burden of long COVID. Considering the healthcare and socioeconomic repercussions incurred by long COVID worldwide, international collaborative initiatives are warranted to address the remaining challenges in diagnosing and managing patients presenting with neurological sequelae. See also the graphical abstract(Fig. 1).

Introduction There is accumulating evidence that SARS-CoV-2 infection, apart from physical complications, can cause a variety of symptoms related to mental health, either during the acute phase of the infection or following the resolution of acute COVID-19 (i.e., long-COVID). Objectives To investigate the demographic and clinical characteristics of a sample of hospitalized patients with COVID-19. Methods Data were collected from 1 January 2021 to 31 May 2022. In particular, clinical and demographic characteristics of patients hospitalized with COVID-19 at the “Attikon” University General Hospital and who were referred for assessment to the Consultation Liaison Psychiatry unit were collected and analyzed. Results During the study period, 107 patients, 66 men (62%) and 41 women (38%) with a mean age of 63 years, with COVID-19 were referred to the Consultation Liaison Psychiatry unit for evaluation. Among them, 58 (54.6%) had a previous psychiatric history, while 49 (45.4%) were assessed for the first time by a mental health professional. The most frequent psychiatric manifestations included anxiety manifestations [38 patients (36%)], delirium [37 patients (35%)] and depressive manifestations [15 patients (14%)]. Conclusions The description of demographic and clinical characteristics of hospitalized COVID-19 patients with concurrent psychiatric manifestations highlights the importance of early clinical detection of psychiatric comorbidity by physicians with a view to ensuring that patients’ needs are supported in an integrated, holistic and patient-centric manner. Disclosure of Interest None Declared

Diabetes has detrimental effects on many organs, including the kidneys, heart, and the central nervous system, with ophthalmic involvement and Diabetic Retinopathy (DR), specifically, being among the most severe and prominent consequences. Diabetic Retinopathy and especially advanced stages of the disease, have a crucial impact on patients’ quality of life and emotional status. In this context, emotional imbalance, psychological side effects and comorbidities, like anxiety disorders, could emerge, deteriorating the patients’ condition further. A number of questionnaires can be employed in the evaluation of the potential impact of Diabetic Retinopathy on patients’ quality of life, including the Beck Anxiety Inventory (BAI) and The National Eye Institute Visual Function Questionnaire-25 (NEI VFQ-25). Purpose: The purpose of this study was to evaluate the association of Diabetic Retinopathy (DR) and diabetic macular edema with vision-related quality of life, as well as the potential association between the disease’s severity, emotional status of patients and the manifestation of anxiety and psychological features. Results: Patients with fundoscopic findings had significantly lower scores in all VFQ-25 subscales, indicating worse quality of life in comparison to patients without DR. Severity of DR, greater levels of anxiety, daily sitting time, unemployment and lower education level, were all found to be significantly, negatively associated with a worse quality of life. Regarding emotional status, more years of suffering from diabetes, treatment with insulin and the hours being idle per day were associated with an increased burden of anxiety. In addition, the presence of a concomitant disease, findings in fundoscopy, diabetic macular edema and treatment with anti-VEFG injections, as well as the number of doses, were significantly associated with greater anxiety. Multivariate analysis showed that having Severe Non-Proliferative Diabetic Retinopathy or having Proliferative Diabetic Retinopathy and receiving insulin therapy (alone or in combination with another treatment), were significantly associated with higher levels of anxiety. Conclusion: The well-established impact of DR on the patients’ well-being, quality of life and emotional status render DR and CME prevention, stabilization or delaying progression as a necessity in order to protect patients from developing psychiatric symptoms. On the other hand, the speculated bi-directional association between emotional problems and DR progression highlights the importance of acknowledging and dealing with psychological issues with the aim of delaying DR progression.

GII.4 noroviruses have caused the overwhelming majority of norovirus-related gastroenteritis cases during the past two decades. However, a trend towards the emergence of new genotypes and novel GII.4 variants provided the impetus to explore further the changing patterns in norovirus epidemiology during the present study. Genotyping of 60 norovirus strains detected during a period of 33 months (January 2016-October 2018) was performed on the basis of the capsid VP1-coding ORF2 gene sequence. All norovirus strains detected were classified into seven genotypes, six of which belonged to genogroup GII. GII.2 was the dominant genotype till February 2017, whereas GII.4 prevailed thereafter. Most of the GII.4 strains were of the Sydney_2012 variant, whereas five strains could not be classified. Further recombination analysis at the ORF1/ORF2 gene junction revealed that 23 out of 24 strains were recombinant, thereby showcasing the significant role of genetic recombination in norovirus evolution and epidemiology. Continuous genomic surveillance and molecular characterization are essential for tracking norovirus evolution, which could contribute to the elucidation of new aspects of virus-host interactions that potentially affect host morbidity and epidemiology.