Risk factors of sexual dysfunctions in postmenopausal women

Objectives: Both somatic and psychosocial factors influence women’s sexual functioning. The main objective of the conducted research was to determine the risk factors of sexual dysfunctions in women during the postmenopausal period. Material and methods: The researcher studied 666 women between the ages of 45–65 (M = 54.96 } 5.42), who had their last period no later than 12 months prior. Standardised questionnaires were used to study: sexual functions (FSFI), intensity of menopausal symptoms (KI), level of depression (BDI), body esteem (BES), health behaviours (HBI). Results: Sexual dysfunctions were diagnosed in 33.03% of the studied women. The respondents with dysfunctions differed from the respondents without dysfunctions in terms of: age (p < 0.001), education (p < 0.001), material standing (p < 0.01), relationship status (p < 0.001), body weight (p < 0.001), BMI (p < 0.05), self-assessment of health state (p < 0.001), presence of chronic diseases (p < 0.05), sexual functioning (p < 0.001), intensity of menopausal symptoms (p < 0.001), level of depression (p < 0.001), body self-esteem (p < 0.001), health behaviours (p < 0.001). Regression analysis demonstrated (R2 = 0.24) that the higher the sense of sexual attractiveness, the lower the probability of sexual dysfunctions (B = –0.13; p < 0.001). In turn, the risk increases with age (B = 0.06; p < 0.001), intensity of menopausal symptoms (B = 0.04; p < 0.01) and concern about one’s own body weight (B = 0.04; p < 0.05). Living without a partner (as compared with living in an informal relationship) increases the risk of occurrence of sexual dysfunctions by as much as 129%. Conclusions: Crucial risk factors of sexual dysfunctions in women during the postmenopausal period include: age, relationship situation, intensity of menopausal symptoms, sense of sexual attractiveness and concern about body weight

Global demographic trends and effects on tourism

Purpose: The main purpose of the paper is to try to assess the impact of demographic phenomena on the development of tourism in the world. It also attempts to describe the role and significance of transformations affecting tourist trips and highlights the most interesting problems and dilemmas that may become the subject-matter of further studies and investigations. Design/Methodology/Approach: Basic dynamics and correlation indicators were used in the research. Statistical data was taken from reports of the United Nations and World Tourism Organization. Findings: The results of a correlation analysis indicate that among the demographic factors, the greatest impact on the intensity of tourist traffic is primarily the extension of the life of the population.The demographic profiles of individual tourism market segments will lead to a clear differentiation of the services offered by tourism enterprises. Some other tendencies observed currently are the growing significance of one’s own safety, the increasing ethical concerns related to environmental protection, and the growing tendency to engage in interactive communication. Practical Implications: The presented results are important for individual countries as well as for global organisations. The detailed conclusions drawn from this study can be useful in developing the optimal tourist offers for the different demographic target groups, particularly the elderly, whose share will keep growing due to the general aging of the global population. Originality/Value: The added value of the paper is an attempt to systematize knowledge about the most important aspects of the present demographic changes and their effects on the development of tourism. It also describes the role and significance of transformations affecting tourist trips and highlights the most interesting problems and dilemmas that may become the subject-matter of further studies.peer-reviewe

Finance, Sustainability and Negative Externalities: An Overview of the European Context

[Abstract]: The goal of the paper is to examine the relation between finance and sustainability, with a special emphasis on the impact of negative externalities. Sustainable development as a concept aims to mitigate negative externalities. Conventional finance offers no room for the environment and society. Therefore, three-dimensional sustainable finance has appeared. This paper is the first original attempt to examine the relationship between: financial, economic, environmental and social development indicators from the sustainability perspective, with a special focus on externalities. To study the disparities between the European Union (EU) countries belonging to the OECD in the field of sustainable development and sustainable finance, the multi-criteria taxonomy was used. The basis of the analyses was the indicators transformed according to the relative taxonomy method. The database, based on Eurostat, contains indicators describing pillars of sustainable development such as: economic (12 indicators), social (28), environmental (7) and sustainable finance (16). The study analyses the sample of 23 countries in 2007, 2013 and 2016. The results confirm a positive relationship among the analysed indicators. On the basis of 62 statistical features selected according to the statistical methods, 7 groups of countries were obtained in 2007 and 2013 and 8 groups in 2016. In the case of Scandinavian countries, one can observe a permanent separation of economic growth from its negative impact on the natural environment. Such dependencies are no longer so obvious in the case of other EU countries belonging to the Organization for Economic Cooperation and Development (OECD). Therefore, attention should be paid to the most economically developed countries in Western rankings in the case of economic, social and very often also financial results correspond to much worse results in the case of environmental development

Financial and energy markets - a sustainable approach. Perspective of European countries belonging to the OECD

Purpose: This paper sets out to explore the relationships between a sustainable energy market and a sustainable financial market and energy market. The specific research objectives were: to explore whether sustainable finance only correlates with a sustainable energy market, or perhaps this relationship also exists with the traditional energy market, to identify the groups of countries for which there are correlations between the study categories. Design/Methodology/Approach: The empirical analysis is based on data from 2008, 2014, and 2018, as related to the energy market, sustainable energy, and sustainable finance for 28 European countries belonging to the OECD. A taxonomic development measure based on the reference method in the positional approach using the Weber median was used. Findings: The results confirmed the existence of a positive correlation between the energy market and the financial market in a sustainable approach. No such relationship was demonstrated for all three categories at the same time, i.e. energy market, sustainable energy market and sustainable finance. Practical Implications: This research is important for the policies of financial institutions and financial markets from the point of view of developing products and services for sustainable financing, so as to change the structure and improve the effects related to social responsibility (ESG risk reduction). Originality/value: This study examines whether relationships exist between a sustainable energy market and sustainable finance and the energy market in the traditional approach.peer-reviewe

The secret life of IGSF1: from consternation to revelation

Immunoglobulin superfamily, member 1 (IGSF1, formerly known as InhBP/p120) is a protein of unknown function, highly expressed in the pituitary gland. In this thesis, I characterized: 1) co- and post-translational processing of IGSF1, 2) expression of IGSF1 in several tissues, and 3) the link between IGSF1 and the hypothalamic-pituitary-thyroid (HPT) axis. The IGSF1/Igsf1 gene is located on the X chromosome, and multiple mRNA isoforms have been identified in both humans and mice. The canonical full-length protein is encoded by human mRNA isoforms IGSF1-1, IGSF1-3, and IGSF1-4, and murine Igsf1-1. Along with our collaborators, I demonstrated that the canonical full-length protein is co-translationally cleaved at an internal signal peptide into N-terminal (NTD) and C-terminal domains (CTD), and that N-linked glycosylation is important for trafficking of the CTD to the cell surface. I then investigated expression of IGSF1-CTD in the pituitary gland and several other tissues. Using a combination of approaches, I demonstrated Igsf1/IGSF1-CTD expression in anterior pituitary thyrotropes, somatotropes, and lactotropes, as well as in the murine hypothalamus and fetal liver. I also characterized the relative abundance of Igsf1 isoforms in the pituitary and hypothalamus, and the glycosylation patterns of IGSF1-CTD in different tissues.Finally, I sought to determine the function of IGSF1. Igsf1-deficient mice were previously generated by ablation of non-coding exon 1 (Igsf1Δex1). The mice were reported to be overtly normal, although analyses were largely limited to reproductive function, as IGSF1 had been predicted to play a role in the regulation of follicle-stimulating hormone synthesis. Our clinical collaborators identified mutations in IGSF1 in several male patients with central hypothyroidism. I showed that the disease-associated mutations lead to intracellular retention of the IGSF1-CTD protein, consistent with IGSF1 loss-of-function. Further, I analyzed HPT axis function of Igsf1-deficient male mice, and found that they phenocopy several features of the human disorder, thus confirming that loss of IGSF1 leads to central hypothyroidism. In addition, the mice have decreased pituitary thyroid-stimulating hormone (TSH) content and thyrotropin-releasing hormone receptor (Trhr) expression, suggestive of impaired TRH signaling. Overall, my work contributes to our understanding of IGSF1 expression, and describes a potential function for IGSF1 in regulating the HPT axis. Delineating molecular mechanisms of how IGSF1 acts in the pituitary gland to affect endocrine axes will contribute to the ongoing search for the function of this mysterious protein.Le membre 1 de la superfamille des immunoglobulines (IGSF1, anciennement connu sous le nom InhBP/p120) est une protéine ayant une fonction inconnue, fortement exprimé dans la glande pituitaire. Dans cette thèse, j'ai caractérisé: 1) les processus co-et post-traductionnels de IGSF1, 2) l'expression de IGSF1 dans plusieurs tissus, et 3) le lien entre IGSF1 et l'axe hypothalamo-hypophyso-thyroïdien (HPT).Le gène IGSF1/Igsf1 est situé sur le chromosome X, et de multiples isoformes d'ARNm ont été identifiés chez les humains et les souris. La protéine canonique complète est codée par l'ARNm des isoformes IGSF1-1, IGSF1-3, et IGSF1-4 (homme), et Igsf1-1 (murine). Avec nos collaborateurs, j'ai démontré que la protéine canonique est clivé durant sa traduction en deux parts: le domaine N-terminal (NTD) et le domaine C-terminal (CTD) à cause d'un peptide signal interne, et que la N-glycosylation est importante pour le transport du CTD à la surface de la cellule. J'ai ensuite étudié l'expression d'IGSF1-CTD dans la glande pituitaire et de plusieurs autres tissus. En utilisant une combinaison d'approches, j'ai démontré l'expression d'Igsf1/IGSF1-CTD dans les thyrotropes, somatotropes, et lactotropes de l'hypophyse antérieure, ainsi que dans l'hypothalamus murin et le foie fœtal. J'ai également caractérisé l'abondance relative des isoformes Igsf1 dans l'hypophyse et l'hypothalamus, et les motifs de glycosylation des IGSF1-CTD dans différents tissus.Enfin, j'ai cherché à déterminer la fonction d'IGSF1. Des souris déficientes en Igsf1 ont été précédemment générées par l'ablation de l'exon 1 non-codant (Igsf1Δex1). Les souris ont été ouvertement normales, même si les analyses ont été largement limitées à la fonction de reproduction, comme cela avait été prédit IGSF1 à jouer un rôle dans la régulation de la synthèse de l'hormone folliculo-stimulante. Nos collaborateurs cliniciens ont identifiés des mutations dans IGSF1 dans plusieurs patients de sexe masculin atteints d'hypothyroïdie centrale. J'ai démontré que les mutations associées à la maladie causent la rétention intracellulaire de la protéine IGSF1-CTD, menant à une perte de fonction d'IGSF1. De plus, j'ai analysé la fonction de l'axe HPT des souris males déficientes en Igsf1, et j'ai constaté qu'ils phénocopient plusieurs traits de la maladie humaine, confirmant ainsi la perte de IGSF1 conduisant à l'hypothyroïdie centrale. En outre, les souris ont une diminution de thyrotropine (TSH) dans l'hypophyse et une diminution des récepteurs thyréolibérine (Trhr) suggérant une détérioration de la signalisation de thyréolibérine (TRH).Dans l'ensemble, mon travail contribue à notre compréhension de l'expression d'IGSF1, et décrit une fonction potentielle pour IGSF1 dans la régulation de l'axe HPT. La recherche des mécanismes moléculaires de la façon dont IGSF1 affecte les axes endocriniens dans l'hypophyse contribuera à la recherche permanente de la fonction de cette protéine mystérieuse

The financial situation of enterprises in the clothing and footwear sector in the face of the COVID-19 pandemic

Purpose: The purpose of this article is to try to assess the impact of COVID-19 on the financial situation of enterprises in the clothing and footwear sector. Companies listed on the Warsaw Stock Exchange were used as a case study. Design/Methodology/Approach: The study used a synthetic measure based on the zero unitarization method, which allowed for the classification of the surveyed enterprises from the point of view of their financial condition. Findings: The methods used in the paper turned out to be a helpful tool in determining the financial condition of companies. They showed significant changes resulting from the spread of COVID-19. As the pandemic situation is still not stabilized, such analyses as in this article should be continued in the coming years. That will enable the observation of regularities or their absence, especially after the pandemic has ended. Practical Implications: The results of this kind of research can help managers, as well as current and potential shareholders, understand how the pandemic affects the company and its financial implications. Such information will help make decisions about future activities. Thus, the study fills the research gap in this area. Originality/Value: The article contributes to the current scientific discussion on the impact of the COVID-19 pandemic on the financial situation of companies in the world.peer-reviewe

Three Novel IGSF1 Mutations in Four Japanese Patients With X-Linked Congenital Central Hypothyroidism

Context: Congenital central hypothyroidism (C-CH) is a rare disease. We investigated the molecular basis of unexplained C-CH in 4 Japanese boys. Patients and Methods: C-CH was diagnosed by low free T-4 and/or T-3 and low basal TSH concentrations. We used whole-exome sequencing of one patient with C-CH to identify potential disease-causing mutations. Thereafter, PCR direct sequencing was performed to Identify genetic defects underlying C-CH in 3 more patients. We then assessed the effects of mutations identified in the Ig superfamily, member 1 (IGSF1), gene on protein expression and membrane trafficking. Results: All patients had congenital hypothyroidism, and 2 had definitive prolactin deficiency. Two patients were detected by neonatal screening. The other patients were diagnosed by short stature and failure to thrive. We identified a novel nonsense variant in IGSF1 by whole-exome sequencing in patient 1, which was confirmed by PCR direct sequencing (p.R1189X). PCR direct sequencing identified the identical nonsense mutation in patient 2. Patients 3 and 4 harbored distinct missense (p.V1082E) or nonsense (p.Q645X) mutations in IGSF1. The mothers of patients 1, 3, and 4 were heterozygous for these mutations. The R1189X mutant, which lacks the transmembrane domain, failed to traffic to the plasma membrane. V1082E could be observed at the cell surface, but at greatly diminished levels relative to the wild-type form of the protein. The severely truncated Q645X mutant could not be detected by Western blot. Conclusion: Our findings provide additional genetic evidence that loss-of-function mutations in IGSF1 cause an X-linked form of C-CH and variable prolactin deficiency

Liquid crystal epoxide network based on azoxy mesogen – electrical properties

In this work, electric properties of two matrices based on nematic epoxy monomers with azoxy groups are compared. The process of curing the monomers with DDM amine was monitored by means of dielectric spectroscopy at temperatures of 110 °C and 120 °C. In the next step, measurements of direct current conductivity were performed for the epoxy matrices cured at the temperature of 120 °C. The conductivity in the studied matrices was of the order of 10−9–10−7 S/m at temperatures between 150 °C and 170 °C. The conductivity of both the samples was of activation nature and their resistance grew rapidly below the temperature of 140 °C. Dielectric studies were also carried out for both the materials in a broad range of frequency and temperature. A relaxation process with similar activation energy was observed in both the cases. This process can be connected with the motion of polar azoxy groups present in the mesogen. An additional relaxation process appeared at higher temperatures in one of the cases, it was probably related to some structural change in the material

The short mRNA isoform of the immunoglobulin superfamily, member 1 gene encodes an intracellular glycoprotein

Mutations in the immunoglobulin superfamily, member 1 gene (IGSF1/Igsf1) cause an X-linked form of central hypothyroidism. The canonical form of IGSF1 is a transmembrane glycoprotein with 12 immunoglobulin (Ig) loops. The protein is co-translationally cleaved into two sub-domains. The carboxyl-terminal domain (CTD), which contains the last 7 Ig loops, is trafficked to the plasma membrane. Most pathogenic mutations in IGSF1 map to the portion of the gene encoding the CTD. IGSF1/Igsf1 encodes a variety of transcripts. A little studied, but abundant splice variant encodes a truncated form of the protein, predicted to contain the first 2 Ig loops of the full-length IGSF1. The protein (hereafter referred to as IGSF1 isoform 2 or IGSF1-2) is likely retained in most individuals with IGSF1 mutations. [...

IGSF1 Deficiency Leads to Reduced TSH Production Independent of Alterations in Thyroid Hormone Action in Male Mice

Loss of function mutations in IGSF1/Igsf1 cause central hypothyroidism. Igsf1 knockout mice have reduced pituitary thyrotropin-releasing hormone receptor, Trhr, expression, perhaps contributing to the phenotype. Because thyroid hormones negatively regulate Trhr, we hypothesized that IGSF1 might affect thyroid hormone availability in pituitary thyrotropes. Consistent with this idea, IGSF1 coimmunoprecipitated with the thyroid hormone transporter monocarboxylate transporter 8 (MCT8) in transfected cells. This association was impaired with IGSF1 bearing patient-derived mutations. Wild-type IGSF1 did not, however, alter MCT8-mediated thyroid hormone import into heterologous cells. IGSF1 and MCT8 are both expressed in the apical membrane of the choroid plexus. However, MCT8 protein levels and localization in the choroid plexus were unaltered in Igsf1 knockout mice, ruling out a necessary chaperone function for IGSF1. MCT8 expression was low in the pituitary and was similarly unaffected in Igsf1 knockouts. We next assessed whether IGSF1 affects thyroid hormone transport or action, by MCT8 or otherwise, in vivo. To this end, we treated hypothyroid wild-type and Igsf1 knockout mice with exogenous thyroid hormones. T4 and T3 inhibited TSH release and regulated pituitary and forebrain gene expression similarly in both genotypes. Interestingly, pituitary TSH beta subunit (Tshb) expression was consistently reduced in Igsf1 knockouts relative to wild-type regardless of experimental condition, whereas Trhr was more variably affected. Although IGSF1 and MCT8 can interact in heterologous cells, the physiological relevance of their association is not clear. Nevertheless, the results suggest that IGSF1 loss can impair TSH production independently of alterations in TRHR levels or thyroid hormone action