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Currently, a very important thread of research on COVID-19 is to determine the dimension of the psychopathological emotional reactions induced by the COVID-19 pandemic. A non-experimental online research project was designed to determine the predictors of the severity of psychopathological symptoms, such as depression and PTSD symptoms, and the nature of the feedback mechanism between them in groups of men, remaining in hospital isolation due to infection and at-home isolation during the COVID-19 epidemic. The presence of symptoms of depression, post-traumatic stress disorder (PTSD) and a sense of threat due to the pandemic were assessed using the following screening tests: IES-R by Weiss and Marmar, PHQ-9 by Spitzer et al., and a self-constructed sliding scale for assessing COVID-19 anxiety. The study was carried out on a group of 57 firefighting cadets, hospitalized in a COVID-19 isolation room (M.sub.age = 23.01), staying in isolation due to SARS-CoV-2 virus infection and a control group of 57 healthy men (M.sub.age = 41.38) staying at home during quarantine and national lockdown. COVID-19 pandemic causes many psychopathological reactions. The predictive models revealed that the predictors of symptoms of PTSD in isolated patients included depression and the experienced sense of COVID-19 threat resulting from the disease, while in the control group the symptoms of depression were the only predictor of PTSD. PTSD experiences are usually associated with depression. It may also be a form of the re-experiencing process or the effect of high affectivity, indirectly confirmed by the participation of hyperarousal in the feedback loop. Our findings highlight the importance of mental health aspects in patients treated during the COVID-19 pandemic. The COVID-19 pandemic requires social distancing, quarantine and isolation, which may cause psychopathological symptoms not only in affected people, but also in the general population. Moreover, the need for greater psychological support can be emphasized for both: the sick and the general population., Author(s): Irena Walecka [sup.1] , Piotr Ciechanowicz [sup.1] , Klaudia Dopytalska [sup.1] , Agata Mikucka-Wituszynska [sup.1] , Elzbieta Szymanska [sup.1] , Jacek Bogucki [sup.2] , Janusz Kock [sup.2] , Karolina [...]

Background: Currently, no evidence exists on the expression of apoptosis (CASP3), autophagy (BECN1), and mitophagy (BNIP3) genes in the CA3 area after ischemia with long-term survival. Objective: The goal of the paper was to study changes in above genes expression in CA3 area after ischemia in the period of 6–24 months. Methods: In this study, using quantitative RT-PCR, we present the expression of genes associated with neuronal death in a rat ischemic model of Alzheimer's disease. Results: First time, we demonstrated overexpression of the CASP3 gene in CA3 area after ischemia with survival ranging from 0.5 to 2 years. Overexpression of the CASP3 gene was accompanied by a decrease in the activity level of the BECN1 and BNIP3 genes over a period of 0.5 year. Then, during 1-2 years, BNIP3 gene expression increased significantly and coincided with an increase in CASP3 gene expression. However, BECN1 gene expression was variable, increased significantly at 1 and 2 years and was below control values 1.5 years post-ischemia. Conclusions: Our observations suggest that ischemia with long-term survival induces neuronal death in CA3 through activation of caspase 3 in cooperation with the pro-apoptotic gene BNIP3. This study also suggests that the BNIP3 gene regulates caspase-independent pyramidal neuronal death post-ischemia. Thus, caspase-dependent and -independent death of neuronal cells occur post-ischemia in the CA3 area. Our data suggest new role of the BNIP3 gene in the regulation of post-ischemic neuronal death in CA3. This suggests the involvement of the BNIP3 together with the CASP3 in the CA3 in neuronal death post-ischemia. [ABSTRACT FROM AUTHOR]

Explaining changes at the gene level that occur during neurodegeneration in the CA3 area is crucial from the point of view of memory impairment and the development of post-ischemic dementia. An ischemic model of Alzheimer's disease was used to evaluate changes in the expression of genes related to amyloid transport in the CA3 region of the hippocampus after 10 min of brain ischemia with survival of 2, 7 and 30 days and 12, 18 and 24 months. The quantitative reverse transcriptase PCR assay revealed that the expression of the LRP1 and RAGE genes involved in amyloid transport was dysregulated from 2 days to 24 months post-ischemia in the CA3 area of the hippocampus. LRP1 gene expression 2 and 7 days after ischemia was below control values. However, its expression from day 30 to 24 months, survival after an ischemic episode was above control values. RAGE gene expression 2 days after ischemia was below control values, reaching a maximum increase 7 and 30 days post-ischemia. Then, after 12, 18 and 24 months, it was again below the control values. The data indicate that in the CA3 area of the hippocampus, an episode of brain ischemia causes the increased expression of the RAGE gene for 7–30 days during the acute phase and that of LRP1 from 1 to 24 months after ischemia during the chronic stage. In other words, in the early post-ischemic stage, the expression of the gene that transport amyloid to the brain increases (7–30 days). Conversely, in the late post-ischemic stage, amyloid scavenging/cleaning gene activity increases, reducing and/or preventing further neuronal damage or facilitating the healing of damaged sites. This is how the new phenomenon of pyramidal neuronal damage in the CA3 area after ischemia is defined. In summary, post-ischemic modification of the LRP1 and RAGE genes is useful in the study of the ischemic pathways and molecular factors involved in the development of Alzheimer's disease. [ABSTRACT FROM AUTHOR]

In the presented study the usefulness of eye-tracking data for classification of architectural spaces as stressful or relaxing was examined. The eye movements and pupillary response data were collected using the eye-tracker from 202 adult volunteers in the laboratory experiment in a well-controlled environment. Twenty features were extracted from the eye-tracking data and after the selection process the features were used in automated binary classification with a variety of machine learning classifiers including neural networks. The results of the classification using eye-tracking data features yielded 68% accuracy score, which can be considered satisfactory. Moreover, statistical analysis showed statistically significant differences in eye activity patterns between visualisations labelled as stressful or relaxing.

Vascular diseases are one of the most common causes of death and morbidity. Lower extremity artery disease (LEAD), abdominal aortic aneurysm (AAA) and chronic venous disease (CVD) belong to this group of conditions and exhibit various presentations and courses; thus, there is an urgent need for revealing new biomarkers for monitoring and potential treatment. Next-generation sequencing of mRNA allows rapid and detailed transcriptome analysis, allowing us to pinpoint the most pronounced differences between the mRNA expression profiles of vascular disease patients. Comparison of expression data of 519 DNA-repair-related genes obtained from mRNA next-generation sequencing revealed significant transcriptomic marks characterizing AAA, CVD and LEAD. Statistical, gene set enrichment analysis (GSEA), gene ontology (GO) and literature analyses were applied and highlighted many DNA repair and accompanying processes, such as cohesin functions, oxidative stress, homologous recombination, ubiquitin turnover, chromatin remodelling and DNA double-strand break repair. Surprisingly, obtained data suggest the contribution of genes engaged in the regulatory function of DNA repair as a key component that could be used to distinguish between analyzed conditions. DNA repair–related genes depicted in the presented study as dysregulated in AAA, CVD and LEAD could be utilized in the design of new biomarkers or therapies associated with these diseases. [ABSTRACT FROM AUTHOR]

Introduction: Scleroderma (Sc) is a connective tissue disorder associated with internal organ involvement, increased mortality, and unknown pathogenesis. It has been found that the more extensive the skin involvement the more severe internal organ manifestations and increased disability. The Rodnan skin score (RSS) is one of the established methods to examine skin thickness among patients with Sc. Due to RSS limitations, for instance, lack of detection of subclinical changes, a new tool is needed for the evaluation of Sc. In recent studies, shear wave elastography (SWE) has been examined as a potential tool to assess skin involvement through the evaluation of skin strain. Aim: To verify whether elastography is a reliable method to examine Sc progression and possibly provide one useful site to perform the examination - as an easy, cheap, and reliable examination tool. Material and methods: Forty Sc patients were examined, and 28 healthy individuals were recruited for the control group. Among the patients and control group, skin thickness was assessed using the RSS and skin strain measurements using elastography in 20 body locations. Results: SWE in the right-hand finger can be treated as an important diagnostic indicator of the severity of Sc. Conclusions: SWE is a reliable method for evaluating skin involvement among patients with systemic sclerosis (SSc). Right finger measurements correlate positively with Rodnan's results and can be a predictor of the severity of SSc. This study found SWE to be a reliable method for examining SSc progression and possibly one useful site for the examination. [ABSTRACT FROM AUTHOR]