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The Fazio Laterality Inventory (FLI) is a recent measure of handedness. Although initially validated, there is still a lack of studies assessing its psychometric properties in samples outside the USA. The present study explores the validity of the Polish adaptation of the FLI. We used data gathered from a convenience sample of 727 participants. They completed the FLI and the Edinburgh Handedness Inventory to establish concurrent validity. Confirmatory factor analysis was used to investigate the factor structure of the FLI. In addition, an Item Response Theory (IRT) model for continuous item scores was also used to identify the discrimination and difficulty parameters of the FLI items. The Polish version of the FLI was characterized by good reliability indices and has high concurrent validity with the Edinburgh Handedness Inventory. We identified a bi-factorial structure for the questionnaire. The IRT analyses showed that the FLI items have good discrimination and difficulty parameters. Our study provides new insights into the properties of the Fazio Laterality Inventory.

Skeletal muscle regeneration relies on the reciprocal interaction between many types of cells. Regenerative capacity may be altered in different disorders. In our study, we investigated whether the deletion of miR-378a (miR-378) affects muscle regeneration. We subjected 6-week-old wild-type (WT) and miR-378 knockout (miR-378 –/– ) animals to the glycerol-induced muscle injury and performed analyses in various time-points. In miR-378 –/– animals, an elevated abundance of muscle satellite cells (mSCs) on day 3 was found. Furthermore, fibro-adipogenic progenitors (FAPs) isolated from the muscle of miR-378 –/– mice exhibited enhanced adipogenic potential. At the same time, lack of miR-378 did not affect inflammation, fibrosis, adipose tissue deposition, centrally nucleated fiber count, muscle fiber size, FAP abundance, and muscle contractility at any time point analyzed. To conclude, our study revealed that miR-378 deletion influences the abundance of mSCs and the adipogenic potential of FAPs, but does not affect overall regeneration upon acute, glycerol-induced muscle injury.

The cross-sex shift hypothesis predicts that gay men should perform more like heterosexual women on important neurocognitive tasks on which men score higher than women, such as mental rotation. Studies also suggest sex differences exist in the neural correlates of mental rotation. However, no studies have taken sexual orientation into account or considered within-group variation attributable to recalled gender nonconformity (a developmental trait reliably associated with human nonheterosexuality). We quantified the neural correlates of mental rotation by comparing two groups of gay men, gender conforming ( n  = 23) and gender nonconforming ( n  = 23), to gender conforming heterosexual men ( n  = 22) and women ( n  = 22). We observed a sex difference between heterosexual men and women in the premotor cortex/supplementary motor cortex and left medial superior frontal gyrus. We also observed a sex difference as well as a cross-sex shift in gay men who recalled being gender nonconforming as children in the right superior frontal gyrus, right angular gyrus, right amygdala/parahippocampal gyrus, and bilaterally in the middle temporal gyrus and precuneus. Thus, cross-sex shifts may be associated with underlying developmental factors which are associated with sexual orientation (such as gender nonconformity). The results also suggest that gay men should not be studied as a homogenous group.

Abstract Neural bases of cognitive reappraisal may depend on the direction of regulation (up- or downregulation) and stimulus valence (positive or negative). This study aimed to examine this using a cognitive reappraisal task and conjunction analysis on a relatively large sample of 83 individuals. We identified regions in which activations were common for all these types of emotion regulation. We also investigated differences in brain activation between the ‘decrease’ and ‘increase’ emotional response conditions, and between the regulation of negative and positive emotions. The common activation across conditions involved mainly the prefrontal and temporal regions. Decreasing emotions was associated with stronger involvement of the dorsolateral prefrontal cortex, while increasing with activation of the amygdala and hippocampus. Regulation of negative emotions involved stronger activation of the lateral occipital cortex, while regulation of positive emotions involved stronger activation of the anterior cingulate cortex extending to the medial prefrontal cortex. This study adds to previous findings, not only by doing a conjunction analysis on both emotional valences and regulation goals, but also doing this in a bigger sample size. Results suggest that reappraisal is not a uniform process and may have different neural bases depending on regulation goals and stimulus valence.

Stress may impact the ability to effectively regulate emotions. To study the impact of stressful experiences in early and recent life on emotion regulation, we examined the relationship between early life stress, recent stress, and brain activation during cognitive reappraisal. We investigated two regulation goals: the decrease and increase of emotional response to both negative and positive stimuli. Furthermore, two models of stress consequences were examined: the cumulative and match/mismatch models. A total of 83 participants (Mage = 21.66) took part in the study. There was an interaction between cumulative stress and stimuli valence in the cuneus, superior lateral occipital cortex, superior parietal lobule, supramarginal gyrus extending to superior temporal gyrus, and precentral gyrus extending to supplementary motor area. Interaction between mismatched stress index and stimuli valence was found in the left hippocampus, left insula extending to the orbitofrontal cortex and amygdala, and in a cluster including the anterior cingulate cortex, superior frontal gyrus, and frontal pole. Furthermore, there were differences between the effects of cumulative and mismatched stress indices on brain activation during reappraisal of positive but not negative stimuli. Results indicate that cumulative stress and match/mismatch approaches are both useful for explaining brain activation during reappraisal. This finding is important for our understanding of the multifaceted impact of stress on emotion regulation.

The link between gender nonconformity and psychopathology may be due in part to negative childhood experiences resulting from other people’s reactions to gender nonconformity. The aim of this study was to test whether recalled perceived levels of parental and peer acceptance of childhood gender nonconforming behaviors and play mediate the relationship of childhood gender nonconformity with depression and social anxiety in adulthood. We also tested whether this relationship was moderated by sexual orientation and, among gay men, whether internalized homophobia was an additional mediator. All variables were measured in a large sample of male participants using self-report ( n  = 449 gay men, age: M = 27.8 years, SD = 6.69; and n  = 296 heterosexual men, age: M = 27.4 years, SD = 6.57) in Poland. Gay men reported more childhood gender nonconformity than heterosexual men. The relationship between gender nonconformity and depressive symptoms as well as social anxiety symptoms was significant in both gay and heterosexual men. Among gay men, this relationship was partially mediated by peer but not parental acceptance of the measured aspects of gender nonconformity and internalized homophobia. Among heterosexual men, recalled perceived parental acceptance of gender nonconformity partially mediated the relationship between gender nonconformity and depressive and social anxiety symptoms. Our findings were partially in line with those found in Western European and North American samples. Although the two groups differed in their recalled perceived gender nonconformity, they did not differ in their depression or social anxiety scores. Nevertheless, childhood gender nonconformity may be an indirect risk associated with mental health symptoms, irrespective of sexual orientation. Its higher prevalence among nonheterosexual individuals makes it a particular risk for this group.

The aim of this study was to characterize neural activation during the processing of negative facial expressions in a non-clinical group of individuals characterized by two factors: the levels of stress experienced in early life and in adulthood. Two models of stress consequences were investigated: the match/mismatch and cumulative stress models. The match/mismatch model assumes that early adversities may promote optimal coping with similar events in the future through fostering the development of coping strategies. The cumulative stress model assumes that effects of stress are additive, regardless of the timing of the stressors. Previous studies suggested that stress can have both cumulative and match/mismatch effects on brain structure and functioning and, consequently, we hypothesized that effects on brain circuitry would be found for both models. We anticipated effects on the neural circuitry of structures engaged in face perception and emotional processing. Hence, the amygdala, fusiform face area, occipital face area, and posterior superior temporal sulcus were selected as seeds for seed-based functional connectivity analyses. The interaction between early and recent stress was related to alterations during the processing of emotional expressions mainly in to the cerebellum, middle temporal gyrus, and supramarginal gyrus. For cumulative stress levels, such alterations were observed in functional connectivity to the middle temporal gyrus, lateral occipital cortex, precuneus, precentral and postcentral gyri, anterior and posterior cingulate gyri, and Heschl’s gyrus. This study adds to the growing body of literature suggesting that both the cumulative and the match/mismatch hypotheses are useful in explaining the effects of stress.

Melanoma-initiating cells (MICs) contribute to the tumorigenicity and heterogeneity of melanoma. MICs are identified by surface and functional markers and have been shown to display cancer stem cell (CSC) properties. However, the existence of MICs that follow the hierarchical CSC model has been questioned by studies showing that single unselected melanoma cells are highly tumorigenic in xenotransplantation assays. Herein, we characterize cells expressing MIC markers (CD20, CD24, CD133, Sca-1, ABCB1, ABCB5, ALDHhigh) in the B16-F10 murine melanoma cell line. We use flow cytometric phenotyping, single-cell sorting followed by in vitro clonogenic assays, and syngeneic in vivo serial transplantation assays to demonstrate that the expression of MIC markers does not select CSC-like cells in this cell line. Previously, our group showed that heme-degrading enzyme heme oxygenase-1 (HO-1) can be upregulated in melanoma and increase its aggressiveness. Here, we show that HO-1 activity is important for non-adherent growth of melanoma and HO-1 overexpression enhances the vasculogenic mimicry potential, which can be considered protumorigenic activity. However, HO-1 overexpression decreases clone formation in vitro and serial tumor initiation in vivo. Thus, HO-1 plays a dual role in melanoma, improving the progression of growing tumors but reducing the risk of melanoma initiation.

Heme oxygenase-1 (HO1, Hmox1 ) degrades excess heme and is considered an anti-oxidative and anti-inflammatory enzyme. Our previous studies in Hmox1 knockout mice revealed the induction of interferon-stimulated genes (ISGs) in all cell types analyzed, despite unchanged interferon production. Here, we sought to determine whether this induction is driven by intrinsic cellular mechanisms or extrinsic cues at the organismal level, and to identify the pathway underlying HO1-dependent ISG regulation. To this end, we analyzed how ISG expression changes in cultured cells exposed to stressors typical of Hmox1 knockout mice. Using murine wild-type and Hmox1 -deficient (Hmox1 KO) fibroblasts, we found that under control conditions, the expression of most tested ISGs was independent of cellular HO1 status. We next examined the effects of extrinsic stressors, including hemolytic, oxidative, genotoxic, and replication stress, proinflammatory TNFα, and endogenous heme overload. TNFα, which is upregulated in Hmox1 knockout mice, was the sole and universal inducer of ISGs in both wild-type and Hmox1 KO fibroblasts. Unexpectedly, the response of Hmox1 KO cells to exogenous TNFα was weakened, likely due to impaired NF-κB activity and reduced nuclear retention of the p65 subunit. A similar decrease we observed for STAT1. Additionally, the presence of the TREX1 exonuclease in the nucleus pointed to compromised nuclear envelope integrity in HO-deficient cells. Notably, HO1 colocalizes with PARP1, a protein involved in envelope maintenance and regulation of cytoplasmic-nuclear transport. Inhibition of PARP1 with olaparib dampened TNFα-induced nuclear accumulation of p65 and STAT1 in wild-type cells, but not in Hmox1 KO counterparts. In summary, the inflammation observed in Hmox1 -deficient mice appears to be the main cell-extrinsic driver of ISG induction in vivo. Despite this, the inflammatory response to exogenous TNFα is intrinsically attenuated in Hmox1 KO cells, likely due to decreased nuclear retention of NF-κB and STAT1.