Background. Engaging in health-related behaviours is conditioned by many factors, including psychological and social ones. The extent to which it is done is also determined by gender and age. Health-related activity has specific and, presumably, different meanings at different stages of adulthood, which is associated with implementing by people roles and tasks typical of a given period of life. The study aimed to determine the specifics of the healthrelated behaviour in middle and late adulthood. Material and methods. The research was conducted on a group of 285 people, including 154 persons in middle adulthood, i.e. 40-58 years old (M = 45.05, SD = 3.63) - 77 women and 77 men, and 130 in late adulthood, i.e. 61-88 years old (M = 71.32 SD = 5.81) - 70 women and 60 men. The Health Behaviour Inventory by Z. Juczyński (2001) was used to measure health-related behaviours. The tool enabled determining the overall level of health-related behaviours and four selected categories, i.e. healthy eating habits, preventive behaviours, health-related practices and positive mental attitudes. Results. The results indicate that women exhibit a higher level of health-related behaviours when compared to men (regardless of age), which is also evidenced in women in late adulthood when compared to those in middle adulthood. The extent of health-related behaviours in specific categories was also compared between groups. Functions of healthrelated behaviours were discussed with regard to their specifics of people’s roles performed in society as well as the implementation of the development tasks typical of particular stages of adulthood. Conclusions. It is recommended to adjust prevention and health promotion programmes to particular periods of human development and gender.
Evidence suggests that maternal immune activation (MIA) during pregnancy is a risk factor for neurodevelopmental disturbances including autism spectrum disorders (ASDs). Animal models support this linkage and demonstrate that MIA in rodents leads to behavioral alterations in offspring that are characteristic of autism. However, the mechanism by which MIA causes long‑term behavioral deficits is unknown. Investigation of the links between maternal infection during pregnancy, mitochondrial dysfunction, and behavioral alterations in offspring. To induce MIA, pregnant Wistar rats were injected with lipopolysaccharide (LPS; 0.1mg/kg, intraperitoneally) on gestational day 9.5, a time point analogous to the first trimester of human gestation. Brains from adolescent offspring were evaluated for mitochondrial outcomes. Prenatal exposure to MIA led to anxiety and repetitive behavior. Adolescent offspring of MIA dams exhibited up-regulation of pro-inflammatory cytokines, oxidative stress, and disturbances in redox homoeostasis. Moreover, substantial mitochondrial abnormalities were observed. A significant decrease in mitochondrial membrane potential and changes in ATP production could be attributed to a downregulation of complex I and IV. Deregulated bioenergetics of mitochondria were accompanied by impaired mitochondrial dynamics, altered expression of fusion/fission machinery proteins including mitofusin 1 and 2 (Mfn1, Mfn2), Opa1, dynamin related protein‑1 (Drp1), and fission protein 1 (Fis1). We also demonstrated lower expression of the genes coding for PGC1α and TFAM (PPARGC1A and TFAM, respectively) that are responsible for mitochondrial biogenesis. MIA at early gestation leads to long-lasting effects on the mitochondrial bioenergetics, dynamics, and biogenesis in the offspring which can lead to synaptic dysfunction and behavioral abnormalities similar to ASD. FINANCIAL SUPPORT: Supported by the NSC grant 2016/23/D/NZ4/03572.
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