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During late swing phase before expected perturbations, persons with mild traumatic brain injury exhibited greater lateral acceleration of their perturbed foot and less lateral movement of their trunk compared with unperturbed gait. Control participants exhibited less lateral foot acceleration and no difference in mediolateral trunk acceleration compared with unperturbed gait during the same period. A significant group*segment interaction (p<0.001) during this part of the gait cycle suggests the groups adopted different anticipatory strategies for the perturbation.

Individuals with mild traumatic brain injury may be adopting cautious strategies for expected perturbations due to persistent neuromechanical deficits stemming from their injury.

Individuals with mild traumatic brain injury may be adopting cautious strategies for expected perturbations due to persistent neuromechanical deficits stemming from their injury.Calcineurin (CaN), acting downstream of intracellular calcium signals, orchestrates cellular remodeling in many cellular types. In astrocytes, major homeostatic players in the central nervous system (CNS), CaN is involved in neuroinflammation and gliosis, while its role in healthy CNS or in early neuro-pathogenesis is poorly understood. Here we report that in mice with conditional deletion of CaN in GFAP-expressing astrocytes (astroglial calcineurin KO, ACN-KO), at 1 month of age, transcription was largely unchanged, while the proteome was deranged in the hippocampus and cerebellum. Gene ontology analysis revealed overrepresentation of annotations related to myelin sheath, mitochondria, ribosome and cytoskeleton. Over-represented pathways were related to protein synthesis, oxidative phosphorylation, mTOR and neurological disorders, including Alzheimer's disease (AD) and seizure disorder. Comparison with published proteomic datasets showed significant overlap with the proteome of a familial AD mouse model and of human subjects with drug-resistant seizures. ACN-KO mice showed no alterations of motor activity, equilibrium, anxiety or depressive state. However, in Barnes maze ACN-KO mice learned the task but adopted serial search strategy. Strikingly, beginning from about 5 months of age ACN-KO mice developed spontaneous tonic-clonic seizures with an inflammatory signature of epileptic brains. Altogether, our data suggest that the deletion of astroglial CaN produces features of neurological disorders and predisposes mice to seizures. We suggest that calcineurin in astrocytes may serve as a novel Ca2+-sensitive switch which regulates protein expression and homeostasis in the central nervous system.Computational models of radioisotopes soil-to-plant transfer are an essential component of decision support systems for nuclear emergency and assessment impact of nuclear accidents on human beings and the environment. The soil water regime impact on cations behavior in the «soil-plant » system. Therefore, relationships between radioisotopes accumulation by plants and soil moisture should be included in the computational models. A kinetic model for simulation of Cs+ root uptake under alteration of soil moisture content in soil is presented in this paper. The model simulates Cs+ and K+ diffusion from bulk soil into rhizosphere under alteration of water content. The model results show a drop of Cs+ and K+ concentration in the rhizosphere with decreasing soil moisture. The magnitude of enhanced root uptake of Cs+ with soil moisture alteration depends on the exchangeable potassium content and soil texture. The Cs+ root uptake rate has a maximum at 60%-80% of field capacity under sufficient and high exchange potassium content. A similar dependence should also be seen for the RCs soil-to-plant transfer factor. The results indicate the importance of soil water content for modification of the RCs accumulation by plants and the necessity to include this factor into an appropriate semi-mechanistic model.During leaf senescence, chlorophyll a and b are degraded through several enzymatic reactions, including chlorophyll b reductase, 7-hydroxymethyl chlorophyll a reductase, and Mg-dechelatase. Considering that the intermediates of the chlorophyll breakdown pathway are highly photoreactive, cooperative and efficient reactions of chlorophyll metabolic enzymes may protect chloroplasts from potential photo-oxidative damage. Here, we investigated the sub-organellar localization and cooperative reactions of the enzymes involved in the chlorophyll breakdown pathway by the fractionation of thylakoid membranes and enzymatic assays using recombinant proteins. We found that these enzymes were enriched in the grana margin fraction. Furthermore, we found that chlorophyll b reductase and Mg-dechelatase efficiently catabolized chlorophylls bound to the chlorophyll-protein complexes when these two enzymes were mixed. These results suggest that the co-localization of chlorophyll catabolic enzymes enables efficient chlorophyll breakdown. The results from this study highlight a key step forward in the investigation of the photosystem breakdown process.

An estimated 18.1 million new cancer cases (excluding nonmelanoma skin cancers) were diagnosed worldwide in 2020. Despite a rising incidence of cancers worldwide, in developed countries with strong healthcare systems, survival rates are improving as a result of early detection, improved treatments and survivorship care (World Health Organisation (WHO), 2021). Whilst living longer, cancer survivors are often living with side effects of treatment, including chemotherapy related cognitive impairment, often termed "chemobrain".

An integrative review of contemporary literature answering the research question how does chemotherapy affect cognitive function? was undertaken utilising three computerised databases CINAHL, Medline and PUBMED, between 2015 and 2021. Data was thematically analysed to identify themes within published literature.

Thematic analysis identified four broad themes within the literature regarding chemotherapy induced cognitive impairment. Identified themes included; cognition as part of a complex scenario, proof of existence and searching for the cause, learning to play the game and timing of cognitive impairment.

Aggressive treatment with chemotherapy in the adjuvant setting has drastically improved the survival of cancer patients. Subsequent to aggressive treatments, side effects such as cognitive impairment have presented, which may persist in the long term. Despite the exact aetiology of chemotherapy induced cognitive impairment being largely unknown, the consequences of the condition are impacting cancer survivors and their quality of life.

Aggressive treatment with chemotherapy in the adjuvant setting has drastically improved the survival of cancer patients. Subsequent to aggressive treatments, side effects such as cognitive impairment have presented, which may persist in the long term. Despite the exact aetiology of chemotherapy induced cognitive impairment being largely unknown, the consequences of the condition are impacting cancer survivors and their quality of life.Emotional inertia refers to the extent to which emotional states are predictable over time and are resistant to change. High emotional inertia, characterized by emotional states that carry over from one moment to the next, has been linked with both psychological maladjustment and impaired emotion regulation abilities. However, little research has examined the psychobiological correlates of emotional inertia. As such, in this study, we examined the association between inertia of negative emotions with cortisol, the end product of the hypothalamic pituitary adrenal (HPA) axis, one of the body's primary stress response systems. Participants were 76 college students (24% male, Mage=18.53, SD=0.37), who completed five corresponding daily diaries and salivary samples to ascertain cortisol per day for 3 consecutive days. Hierarchical linear models indicated that greater inertia of negative emotion across the three days was associated with smaller cortisol awakening responses (CAR) and lower AUCg, even when controlling for average negative emotion and momentary stress perception. There were no associations with the diurnal cortisol slope. These findings shed light on the neurobiological mechanisms involved in emotion dynamics.Variations of sex hormones during the menstrual cycle can lead to changes in emotion processing. The ability to successfully regulate one's emotions is associated with better social abilities and mental health. While women show better performance in fear extinction learning under high estradiol (E2) compared to women under low E2 levels, little is known about the effect of E2 on emotion regulation. We explored whether E2 modulates emotion regulation in a functional magnetic resonance imaging paradigm and administered E2 valerate to 32 young naturally cycling women during their early follicular phase in a double-blind, placebo-controlled within-subject design. This standardized experimental control allowed us to explore the specific effect of E2 on emotion regulation while controlling for other hormones varying throughout the menstrual cycle. CDK phosphorylation Behaviorally, no difference between conditions appeared. However, on the neural level, E2 administration was associated with lower activation in the right lingual- and left calcarine gyrus, right orbitofrontal cortex and left hippocampus relative to placebo. With respect to the main effect of down-regulation higher activation of the right superior frontal gyrus and left dorsomedial prefrontal cortex was seen; which is in accordance to previous literature. An interaction between drug condition and emotion regulation appeared for the left inferior frontal gyrus extending into the middle frontal gyrus indicating lower activation during down-regulation in the E2 condition than the placebo condition. On the behavioral level, women reported less negative affect in the E2 condition. The results fit well to a previously described psychoneuroendocrinological model in which E2 plays an important modulatory role on emotional processes and risk factors of mental health in women.Adverse childhood experiences (ACEs) has been associated not only with an increased vulnerability for stress-related psychiatric disorders but also with distinct alterations of the hypothalamic-pituitary-adrenal (HPA) axis function and the immune system. The aim of this study is to examine differences in the HPA axis between major depressive disorder (MDD) patients with and without ACEs, and to explore differences in efficacy and HPA changes after long term antidepressant treatment between these two groups. A cohort of 803 patients with MDD were recruited. After the determination of cortisol (COR) and adrenocorticotropic hormone (ACTH), Hamilton Rating Scale for Depression (HAMD), Hamilton Rating Scale for Anxiety (HAMA), the Childhood Trauma Questionnaire (CTQ), 403 subjects were recruited for the following treatment study. Finally 330 MDD patients finished the monotherapy treatments of four antidepressants (Fluoxetine, Sertraline, Venlafaxine-extended release (XR), Duloxetine hydrochloride) for 12 weeks. Ofscore only in MDD patient without ACEs. Logistic regression analysis showed that the total scores of CTQ, level of COR and ACTH at baseline were significantly associated with the response and remission. These findings indicated that exposure to ACEs for MDD could influence the HPA function and severity of symptoms. ACEs, ACTH and COR could be used as predictors of long term antidepressant treatment, suggested that are poor prognostic signs for antidepressants monotherapy in MDD with ACEs.