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The score for health behaviours was average (M = 86.18). The highest score was achieved in the area of prophylactic behaviours. General indicator of health-related behaviours was higher in women who rated their health as very good (p  less then  0.05). Women whose general indicator of health-related behaviours was higher regularly performed prophylactic gynaecological examinations (p  less then  0.05). CONCLUSIONS Results showed that women after menopause treat health mainly as a feature of their body and condition specific for this period of life. The analysis of postmenopausal women’s health behaviours and their perception of health helped to identify areas that require the focus of medical personnel in regard to health promotion and prophylaxis. The average general indicator of health-related behaviours is positive for this group of women as it shows that they care about their health, especially in terms of prophylaxis.BACKGROUND Older-age individuals are at the highest risk for disability from a traumatic brain injury (TBI). Astrocytes are the most numerous glia in the brain, necessary for brain function, yet there is little known about unique responses of astrocytes in the aged-brain following TBI. METHODS Our approach examined astrocytes in young adult, 4-month-old, versus aged, 18-month-old mice, at 1, 3, and 7 days post-TBI. We selected these time points to span the critical period in the transition from acute injury to presumably irreversible tissue damage and disability. Two approaches were used to define the astrocyte contribution to TBI by age interaction (1) tissue histology and morphological phenotyping, and (2) transcriptomics on enriched astrocytes from the injured brain. RESULTS Aging was found to have a profound effect on the TBI-induced loss of astrocyte function needed for maintaining water transport and edema-namely, aquaporin-4. The aged brain also demonstrated a progressive exacerbation of astrogliosis as a function of time after injury. Moreover, clasmatodendrosis, an underrecognized astrogliopathy, was found to be significantly increased in the aged brain, but not in the young brain. As a function of TBI, we observed a transitory refraction in the number of these astrocytes, which rebounded by 7 days post-injury in the aged brain. Transcriptomic data demonstrated disproportionate changes in genes attributed to reactive astrocytes, inflammatory response, complement pathway, and synaptic support in aged mice following TBI compared to young mice. Additionally, our data highlight that TBI did not evoke a clear alignment with the previously defined “A1/A2” dichotomy of reactive astrogliosis. CONCLUSIONS Overall, our findings point toward a progressive phenotype of aged astrocytes following TBI that we hypothesize to be maladaptive, shedding new insights into potentially modifiable astrocyte-specific mechanisms that may underlie increased fragility of the aged brain to trauma.Postoperative shivering and cold hypersensitivity are major side effects of acute and chronic opioid treatments respectively. TRPM8 is a cold and menthol-sensitive channel found in a subset of dorsal root ganglion (DRG) nociceptors. Deletion or inhibition of the TRPM8 channel was found to prevent the cold hyperalgesia induced by chronic administration of morphine. Here, we examined the mechanisms by which morphine was able to promote cold hypersensitivity in DRG neurons and transfected HEK cells. Mice daily injected with morphine for 5 days developed cold hyperalgesia. Treatment with morphine did not alter the expressions of cold sensitive TREK-1, TRAAK and TRPM8 in DRGs. However, TRPM8-expressing DRG neurons isolated from morphine-treated mice exhibited hyperexcitability. Sustained morphine treatment in vitro sensitized TRPM8 responsiveness to cold or menthol and reduced activation-evoked desensitization of the channel. Blocking phospholipase C (PLC) as well as protein kinase C beta (PKCβ), but not protein kinase A (PKA) or Rho-associated protein kinase (ROCK), restored channel desensitization. Identification of two PKC phosphorylation consensus sites, S1040 and S1041, in the TRPM8 and their site-directed mutation were able to prevent the MOR-induced reduction in TRPM8 desensitization. Our results show that activation of MOR by morphine 1) promotes hyperexcitability of TRPM8-expressing neurons and 2) induces a PKCβ-mediated reduction of TRPM8 desensitization. This MOR-PKCβ dependent modulation of TRPM8 may underlie the onset of cold hyperalgesia caused by repeated administration of morphine. Our findings point to TRPM8 channel and PKCβ as important targets for opioid-induced cold hypersensitivity.Sentrin/SUMO-specific protease 2 (SENP2) is a member of SENPs family involved in maturation of SUMO precursors and deSUMOylation of specific target, and is highly expressed in the central nervous system (CNS). Although SENP2 has been shown to modulate embryonic development, fatty acid metabolism, atherosclerosis and epilepsy, the function of SENP2 in the CNS remains poorly understood. To address the role of SENP2 in the CNS and its potential involvement in neuropathology, we generated SENP2 conditional knockout mice by crossing floxed SENP2 mice with CaMKIIα-Cre transgenic mice. Behavioral tests revealed that SENP2 ablation induced hyper-locomotor activity, anxiolytic-like behaviors, spatial working memory impairment and fear-associated learning defect. In line with these observations, our RNA sequencing (RNA-seq) data identified a variety of differential expression genes that are particularly enriched in locomotion, learning and memory related biologic process. Taken together, our results indicated that SENP2 plays a critical role in emotional and cognitive regulation. This SENP2 conditional knockout mice model may help reveal novel mechanisms that underlie a variety of neuropsychiatric disorders associated with anxiety and cognition.BACKGROUND The emergence of Zika virus (ZV) in tropical and subtropical areas of the world has created an urgent need for vaccines against ZV. MLT-748 manufacturer However, approved vaccines that prevent ZV infection are not available. To develop an effective vaccine against ZV infection, a lipidated form of ZV envelope protein domain III that possesses an intrinsic adjuvant property was rationally designed. Our goal was to examine the immunogenicity of recombinant lipidated ZV envelope protein domain III (rLZE3) and evaluate its potential as a vaccine candidate against ZV. METHODS Recombinant ZV envelope protein domain III (rZE3) and rLZE3 were prepared with an Escherichia coli-based system. Dendritic cell surface marker expression and cytokine production upon stimulation were analyzed to evaluate the function of rLZE3. Neutralizing antibody capacities were evaluated using focus reduction neutralization tests after immunization. To investigate the protective immunity in immunized mice, serum samples collected from immunized mice were adoptively transferred into AG129 mice, and then viremia levels and survival times were examined after ZV challenge.