Mindfulness trait and the potential mediating role of emotional regulation strategies in bipolar disorder / Mindfulness rasgo y el potencial papel mediador de las estrategias de regulación emocional en el trastorno bipolar

En este estudio transversal se investiga la asociación entre los principales síntomas del Trastorno bipolar (TB) y las dificultades asociadas a las estrategias de regulación emocional (ERE) adaptativas y desadaptativas. Además, este estudio examina los efectos mediadores de las ERE con el mindfulness rasgo y el TB. Método. Veinticuatro adultos con TB completaron la Escala de Conciencia de Atención Plena (MAAS), el Inventario de Depresión de Beck (BDI-II), la Escala de Autoevaluación de Manía de Altman (ARSM), el Inventario de Ansiedad Rasgo (STAI-R), y el Cuestionario de Regulación Emocional Cognitiva (CERQ). Resultados. El análisis de regresión múltiple mostró cómo la depresión se relacionaba significativa y positivamente con la autoculpabilización, mientras que la ansiedad rasgo estaba positivamente asociada con la autoculpabilización y el catastrofismo. En segundo lugar, el análisis de mediación mostró un efecto de mediación significativo para la autoculpabilidad en la relación entre mindfulness y depresión (a*b = -.15; ICB 95% [-.36, -.03]) y entre mindfulness y ansiedad rasgo (a*b = -.09; ICB 95% [-.27, -.01]). Conclusiones. Nuestros resultados informan del papel de la auto-culpabilidad y el catastrofismo en el TB y de cómo éstas podrían mediar significativamente entre el mindfulness rasgo y el TB. Estos resultados sugieren que una práctica de meditación enfocada en el catastrofismo y la autoculpabilidad puede ser especialmente útil para reducir los síntomas en los pacientes bipolares.(AU)

This cross-sectional study investigates the association between the main symptoms of Bipolar disorder (BD) and emotional regulation dif-ficulties in adaptive and maladaptive emotional regulation strategies (ERS). In addition, this study examines the possible mediating effects of ERS with dispositional mindfulnessand bipolar symptoms. Method.Twenty-four adults diagnosed with BD completed the Mindful Attention Awareness Scale (MAAS), the Beck Depression Inventory (BDI-II), the Altman Mania Self-Assessment Scale (ARSM), the Trait Anxiety Inventory (STAI-R), and the Cognitive Emotional Regulation Questionnaire (CERQ). Results. First, mul-tiple regression analysis showed how depression was significantly positively related to self-blame, whereas trait anxietywas positively associated with self-blame and catastrophizing. Second, the results of the mediation analy-sis have shown a significant mediation effect for the self-blamein the rela-tionship between mindfulnessand depression (a*b = -.15; BCI 95% [-.36, -.03]) and between mindfulnessand trait anxiety (a*b = -.09; BCI 95% [-.27, -.01]). Conclusions. Our results report the role of self-blame and catastrophiz-ing in BD and how these might significantly mediate between dispositional mindfulness and symptoms of depression and anxiety. These results suggest that a meditation practice focused on reducing catastrophizing and self-blame may be especially helpful for symptoms of depression and anxiety in bipolar patients.(AU)

Assessing wild turkey productivity before and after a 14-day delay in the start date of the spring hunting season in Tennessee.

Ten state wildlife management agencies in the United States, including six within the Southeast, have delayed their spring wild turkey (Meleagris gallopavo) hunting seasons since 2017 by five or more days to address concerns related to the potential effects of hunting on wild turkey seasonal productivity. One hypothesis posits that if the spring hunting season is too early, there may be insufficient time for males to breed hens before being harvested, thus leading to reduced seasonal productivity. We conducted an experiment to determine whether delaying the wild turkey hunting season by 2 weeks in south-middle Tennessee would affect various reproductive rates. In 2021 and 2022, the Tennessee Fish and Wildlife Commission experimentally delayed the spring hunting season to open 14 days later than the traditional date (the Saturday closest to 1 April) in Giles, Lawrence, and Wayne counties. We monitored reproductive rates from 2017 to 2022 in these three counties as well as two adjacent counties, Bedford and Maury, that were not delayed. We used a Before-After-Control-Impact design to analyze the proportion of hens nesting, clutch size, hatchability, nest success, poult survival and hen survival with linear mixed-effect models and AIC model selection to detect relationships between the 14-day delay and reproductive parameters. We detected no relationship (p > .05) between the 14-day delay and any individual reproductive parameter. In addition, recruitment (hen poults per hen that survived until the next breeding season) was very low (<0.5) and did not increase because of the 14-day delay. The traditional Tennessee start date had been in place since 1986 while the turkey harvest increased markedly until about 2006 and more recently stabilized. Our data indicate that moving the start of the hunting season from a period just prior to peak nest initiation to 2 weeks later, to coincide with a period just prior to peak nest incubation initiation, resulted in no change to productivity or populations in wild turkey flocks in south-middle Tennessee.

How does market-incentive environmental regulation affect enterprises green growth? The mediating role of R&D investment and innovation output.

Manufacturing enterprises is a country's economic mainstay. However, their longtime extensive growth pattern of "high growth and high emission" has brought huge environment pollution and restricted sustainable development. Under the circumstance of carbon reduction and global green development, market-incentive environmental regulation (MER) has attracted the attention of scholars and become a kind of important methods of encouraging manufacturing enterprises green growth. Presently, two fairly distinct viewpoints of "Follow Cost" and "Porter Hypothesis" both have their own supportive research results, and the explanation for the role of MER is completely opposite. What's more, empirical research at the enterprise level is scarce. Therefore, this study makes a further analysis from the perspective of enterprises heterogeneous innovation ability. Guided by the classic theory of "Follow Cost" and "Porter Hypothesis", this study aims to evaluate the applicable conditions of MER's environmental improvement effect, and testing the differential impact mechanism of MER on enterprise Green Total Factor Productivity (GTFP), enterprise Green Technological Change (GTC) and enterprise Green Efficiency Change (GEC). All these give theoretical and empirical supplementation for the rationality of related theories. This study examines the hypotheses and mechanism according to 1220 Chinese manufacturing listed companies data 2011-2020. The empirical results indicate that: (1) In short term, MER has a significant positive impact on GTC, and a significant negative impact on GTFP and GEC. (2) As innovation driven factors, both enterprise R&D investment and innovation output play the mediating role. (3) Heterogeneity analysis indicates that the impact mechanism varies depending on enterprise industry-type, location and digital level. Thus, policymakers should develop appropriate MER policies, and manufacturing enterprises should strengthen technological innovation to help achieve environmental sustainability and profit performance.

Prevention or ex-post forcing? The impact of dual environmental regulation on corporate environmental behavior.

Corporate reactions to environmental regulation are the hottest topics in research on corporate environmental behavior. However, a few studies incorporate other environmental behavior into the same framework. By constructing a comprehensive indicator system of dual environmental regulation, this paper uses a comparative analysis to discuss Chinese A-listed corporations' environmental behavior from 2009 to 2017, which were influenced by dual environmental regulation. The study's results show that formal environmental regulation (FER) has a significant U-shaped effect on pre-emptive environmental behavior (PEB) but an insignificant impact on ex-post environmental behavior (NEB). After categorizing the various forms of FER, this study finds that market-incentive environmental regulation has a significant inverted U-shaped effect on NEB but an insignificant impact on PEB, voluntary-participation regulation have a significant U-shaped effect on PEB and an inverted U-shaped effect on their NEB, and command-control regulation has significant influence on neither PEB nor NEB. In addition, informal environmental regulation (IER) has a significantly positive and negative effect on PEB and NEB. This study shows that corporate perceptions of policies can have a positive impact on the interaction between the FER and PEB but a negative impact on the interaction between the IER and PEB, and no impact on the interaction between FER or IER and NEB. Moreover, the impact of FER and IER on corporate environmental behavior (CEB) varies depending on factors like ownership, industry characteristics, the market environment, and regional development. Therefore, governments should understand the choices related to corporate environmental behavior under the dual environmental regulation-formal and informal-and prioritize the synergistic impact of these dual environmental regulation, highlighting their enforceability, and take into account the heterogeneity of their targets and the market to stimulate PEB and decrease NEB to help enterprises align their short-term economic objectives with their long-term social goals.

Optical Control of Insect Behavior and Receptors with Azobenzene-Bridged Fipronil and Imidacloprid.

Photopharmacology can be implemented in a way of regulating drug activities by light-controlling the molecular configuations. Three photochromic ligands (PCLs) that bind on one or two sites of GABARs and nAChRs were reported here. These multiphoton PCLs, including FIP-AB-FIP, IMI-AB-FIP, and IMI-AB-IMI, are constructed with an azobenzene (AB) bridge that covalently connects two fipronil (FIP) and imidacloprid (IMI) molecules. Interestingly, the three PCLs as well as FIP and IMI showed great insecticidal activities against Aedes albopictus larvae and Aphis craccivora. IMI-AB-FIP in both trans/cis isomers can be reversibly interconverted depending on light, accompanied by insecticidal activity decrease or increase by 1.5-2.3 folds. In addition, IMI-AB-FIP displayed synergistic effects against A. craccivora (LC50, IMI-AB-FIP = 14.84-22.10 µM, LC50, IMI-AB-IMI = 210.52-266.63 µM, LC50, and FIP-AB-FIP = 36.25-51.04 µM), mainly resulting from a conceivable reason for simultaneous targeting on both GABARs and nAChRs. Furthermore, modulations of wiggler-swimming behaviors and cockroach neuron function were conducted and the results indirectly demonstrated the ligand-receptor interactions. In other words, real-time regulations of receptors and insect behaviors can be spatiotemporally achieved by our two-photon PCLs using light.

Sema-3E/PlexinD1 axis modulates dendritic cell phenotypes and functions: Current status and future implications.

This comprehensive research review explores the complex interplay between the Sema-3E/PlexinD1 axis and dendritic cells (DCs), highlighting its critical role in immune modulation with implications for clinical application Critical regulators of immune responses Dendritic cells are central to adaptive immunity, and the Sema-3E /PlexinD1 axis emerges as a key modulator affecting their phenotypes and functions Review delineates the impact of this signaling axis on DC maturation, migration, antigen presentation, and cytokine production, unravels its multifaceted role in shaping the immune response. Recognizing the limitations and gaps in current knowledge, the study highlights the need for further studies to condition downstream signaling events and related information experienced by the Sema-3E/PlexinD1 axis emphasizes the clarity of the immune system. The review concludes by identifying opportunities for translation, focusing on therapeutic and diagnostic potential. It highlights the importance of collaborative, interdisciplinary efforts to address the challenges and harness the therapeutic and pathological potential of targeting the Sema-3E/PlexinD1 axis, thus opening the way for transformative advances in immunology and clinical medicine.

Insights into the function and regulation of the calcium-activated chloride channel TMEM16A.

The TMEM16A channel, a member of the TMEM16 protein family comprising chloride (Cl-) channels and lipid scramblases, is activated by the free intracellular Ca2+ increments produced by inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release after GqPCRs or Ca2+ entry through cationic channels. It is a ubiquitous transmembrane protein that participates in multiple physiological functions essential to mammals' lives. TMEM16A structure contains two identical 10-segment monomers joined at their transmembrane segment 10. Each monomer harbours one independent hourglass-shaped pore gated by Ca2+ ligation to an orthosteric site adjacent to the pore and controlled by two gates. The orthosteric site is created by assembling negatively charged glutamate side chains near the pore´s cytosolic end. When empty, this site generates an electrostatic barrier that controls channel rectification. In addition, an isoleucine-triad forms a hydrophobic gate at the boundary of the cytosolic vestibule and the inner side of the neck. When the cytosolic Ca2+ rises, one or two Ca2+ ions bind to the orthosteric site in a voltage (V)-dependent manner, thus neutralising the electrostatic barrier and triggering an allosteric gating mechanism propagating via transmembrane segment 6 to the hydrophobic gate. These coordinated events lead to pore opening, allowing the Cl- flux to ensure the physiological response. The Ca2+-dependent function of TMEM16A is highly regulated. Anions with higher permeability than Cl- facilitate V dependence by increasing the Ca2+ sensitivity, intracellular protons can replace Ca2+ and induce channel opening, and phosphatidylinositol 4,5-bisphosphate bound to four cytosolic sites likely maintains Ca2+ sensitivity. Additional regulation is afforded by cytosolic proteins, most likely by phosphorylation and protein-protein interaction mechanisms.

Insertion sequence IS6770 modulates potassium symporter kup transcription in Enterococcus faecalis JH2-2 under low pH conditions.

Enterococcus faecalis is a phylogenetically and industrially relevant microorganism associated with Lactic Acid Bacteria. Some strains of this bacterium are employed as probiotics in commercial applications, while others serve as the principal component in starter cultures for artisanal regional cheese production. However, over the last decade, this species has emerged as an opportunistic multiresistant pathogen, raising concerns about its impact on human health. Recently, we identified multiple potassium transporter systems in E. faecalis, including the Ktr systems (KtrAB and KtrAD), Kup, KimA and Kdp complex (KdpFABC). Nevertheless, the physiological significance of these proteins remains not fully understood. In this study, we observed that the kup gene promoter region in the JH2-2 strain was modified due to the insertion of a complete copy of the IS6770 insertion sequence. Consequently, we investigated the influence of IS6770 on the expression of the kup gene. To achieve this, we conducted a mapping of the promoter region of this gene in the E. faecalis JH2-2 strain, employing fluorescence gene reporters. In addition, a transcriptional analysis of the kup gene was executed in a strain derived from E. faecalis V583 that lacks the IS30-related insertion element, facilitating the identification of the transcriptional start site. Next, the expression of the kup gene was evaluated via RT-qPCR under different pH stressful conditions. A strong upregulation of the kup gene was observed at an initial pH of 5.0 in the strain derived from E. faecalis V583. However, the activation of transcription was not observed in the E. faecalis JH2-2 strain due to the hindrance caused by the presence of IS6770. Besides that, our computational analysis of E. faecalis genomes elucidates a plausible association between transposition and the regulation of the kup gene. Remarkably, the ubiquitous presence of IS6770 throughout the phylogenetic tree implies its ancient existence within E. faecalis. Moreover, the recurrent co-occurrence of IS6770 with the kup gene, observed in 30 % of IS6770-positive strains, alludes to the potential involvement of this genomic arrangement in the adaptive strategies of E. faecalis across diverse niches.

Slow-Release Effect Assisted Crystallization for Sequential Deposition Realizes Efficient Inverted Perovskite Solar Cells.

The two-step sequential deposition strategy has been widely recognized in promoting the research and application of perovskite solar cells, but the rapid reaction of organic salts with lead iodide inevitably affects the growth of perovskite crystals, accompanied by the generation of more defects. In this study, the regulation of crystal growth was achieved in a two-step deposition method by mixing 1-naphthylmethylammonium bromide (NMABr) with organic salts. The results show that the addition of NMABr effectively delays the aggregation and crystallization behavior of organic salts; thereby, the growth of the optimal crystal (001) orientation of perovskite is promoted. Based on this phenomenon of delaying the crystallization process of perovskite, the "slow-release effect assisted crystallization" is defined. Moreover, the incorporation of the Br element expands the band gap of perovskite and mitigates material defects as nonradiative recombination centers. Consequently, the power conversion efficiency (PCE) of the enhanced perovskite solar cells (PSCs) reaches 20.20%. It is noteworthy that the hydrophobic nature of the naphthalene moiety in NMABr can enhance the humidity resistance of PSCs, and the perovskite phase does not decompose for more than 3000 h (30-40% RH), enabling it to retain 90% of its initial efficiency even after exposure to a nitrogen environment for 1200 h.

A splice site variant in MADD affects hormone expression in pancreatic ß cells and pituitary gonadotropes.

MAPK activating death domain (MADD) is a multifunctional protein regulating small GTPases RAB3 and RAB27, MAPK signaling, and cell survival. Polymorphisms in the MADD locus are associated with glycemic traits, but patients with biallelic variants in MADD manifest a complex syndrome affecting nervous, endocrine, exocrine, and hematological systems. We identified a homozygous splice site variant in MADD in 2 siblings with developmental delay, diabetes, congenital hypogonadotropic hypogonadism, and growth hormone deficiency. This variant led to skipping of exon 30 and in-frame deletion of 36 amino acids. To elucidate how this mutation causes pleiotropic endocrine phenotypes, we generated relevant cellular models with deletion of MADD exon 30 (dex30). We observed reduced numbers of ß cells, decreased insulin content, and increased proinsulin-to-insulin ratio in dex30 human embryonic stem cell-derived pancreatic islets. Concordantly, dex30 led to decreased insulin expression in human ß cell line EndoC-ßH1. Furthermore, dex30 resulted in decreased luteinizing hormone expression in mouse pituitary gonadotrope cell line LßT2 but did not affect ontogeny of stem cell-derived GnRH neurons. Protein-protein interactions of wild-type and dex30 MADD revealed changes affecting multiple signaling pathways, while the GDP/GTP exchange activity of dex30 MADD remained intact. Our results suggest MADD-specific processes regulate hormone expression in pancreatic ß cells and pituitary gonadotropes.

eEF1A1 regulates the expression and alternative splicing of genes associated with Parkinson's disease in U251 cells.

BACKGROUND: Eukaryotic elongation factor 1A1 (eEF1A1) is an RNA-binding protein that is associated with PARK2 activity in cells, suggesting a possible role in Parkinson's disease (PD). OBJECTIVE: To clear whether eEF1A1 plays a role in PD through transcriptional or posttranscriptional regulation. METHODS: The GSE68719 dataset was downloaded from the GEO database, and the RNA-seq data of all brain tissue autopsies were obtained from 29 PD patients and 44 neurologically normal control subjects. To inhibit eEF1A1 from being expressed in U251 cells, siRNA was transfected into those cells, and RNA-seq high-throughput sequencing was used to determine the differentially expressed genes (DEGs) and differentially alternative splicing events (ASEs) resulting from eEF1A1 knockdown. RESULTS: eEF1A1 was significantly overexpressed in PD brain tissue in the BA9 area. GO and KEGG enrichment analyses revealed that eEF1A1 knockdown significantly upregulated the expression of the genes CXCL10, NGF, PTX3, IL6, ST6GALNAC3, NUPR1, TNFRSF21, and CXCL2 and upregulated the alternative splicing of the genes ACOT7, DDX10, SHMT2, MYEF2, and NDUFAF5. These genes were enriched in pathways related to PD pathogenesis, such as apoptosis, inflammatory response, and mitochondrial dysfunction. CONCLUSION: The results suggesting that eEF1A1 involved in the development of PD by regulating the differential expression and alternative splicing of genes, providing a theoretical basis for subsequent research.

Cognitive mechanisms and neurological foundations of companion animals' role in enhancing human psychological well-being.

The impact of companion animals on human psychological health has garnered widespread attention. Research demonstrates that companion animals contribute positively in various ways, including reducing depression, anxiety, stress, and fostering positive emotions in humans. Recent studies have revealed significant changes in the activity levels of human emotion-related cortical areas (such as the frontal cortex and amygdala) and neurotransmitter (e.g., oxytocin, cortisol) secretion due to interaction with companion animals. However, research in this domain is still in a nascent stage, with many unknowns in the cognitive neural mechanisms involved. This paper proposes that to understand the cognitive mechanisms through which companion animals affect human psychological health, we need to examine changes in emotional cognitive processing. It aims to uncover the neurological underpinnings of how companion animals enhance human psychological well-being from the perspective of brain connectivity. This approach is expected to provide theoretical support and direction for future research and practical applications in this field.

Self-regulation training improves stress resilience in elite pre-pubescent female gymnasts.

Introduction: In the context of young female athletes, namely elite gymnasts, effective stress management strategies not only enhance performance, but also reduce the risk of injuries and promote overall well-being. This study aims to investigate the effects of biofeedback-based training on stress management in prepubescent elite female gymnasts, recognizing its pivotal role in promoting healthy growth and proper training load management. Methods: Eight elite young female athletes from a top flight French national league club participated in an experimental condition involving four-week biofeedback training program to improve self-regulation skills, during both rest and stress phases. Additionally, each subject experienced a control condition, with entailed exposure to domain-specific motivational videos. Comprehensive evaluations of physiological parameters were conducted to assess the impact of biofeedback training, both before and after the training, as well as during the stress and recovery phases. Furthermore, an interoceptive body awareness test, using the MAIA questionnaire, was performed. Results: The results highlight a significant enhancement of the self-regulatory skills of the gymnasts in managing the selected physiological parameters-peripheral temperature (p < 0.05) and blood volume pressure (p < 0.05)-after the biofeedback treatment. Moreover, psychological data from the MAIA questionnaire revealed a noteworthy increase in interoceptive awareness (p < 0.001), particularly in the subscales of Not Distracting (p < 0.001), Attention regulation (p < 0.05), Emotional awareness (p < 0.05), and Self-regulation (p < 0.05). Discussion: Thus, we conclude that biofeedback training improves self-regulatory and psychological resilience under stressful conditions, while reducing sensitivity to gymnastics-specific stress.

MicroRNA target homeobox messenger RNA in HIV induced hematopoietic inhibition.

Cytopenias are a common occurrence due to abnormal hematopoiesis persistent in patients suffering from and advancing with HIV/AIDS. In order to develop efficacious therapies against cytopenias, it is necessary to understand the mechanisms by which HIV infection affects the differentiation of hematopoietic stem-progenitor cells (HSPCs), causing hematopoietic inhibition, that leads to hematological disorders. Currently, only the antiretrovirals that are being used to treat HIV infection and indirectly lower the levels of virus replication also co-attenuate cytopenias. The evidence available suggests that this indirect efficacy may not prevail for the lifetime of the infected patients, and the acquired immunodeficiency can overtake the beneficial consequences of decreased virus replication. As cited in this article, we and our colleagues are the first to make a foray into the involvement of microRNAs and their use as potential interventional treatments for the cytopenias that occur with HIV/AIDS. Herein, we progressed further in the direction of the mechanisms of the involvement of homeobox gene regulation to cause cytopenias. We had previously shown that HIV-1 inhibits multi-lineage hematopoiesis of the CD34+ cells using SCID-hu Thy/Liv animals in vivo. Furthermore, we demonstrated that the virus-induced hematopoietic inhibition occurred despite the CD34+ cells being resistant to HIV-1 infection. We set out to search for the specific host factors secreted by CD4+ T-cells that likely participate in the inhibition of hematopoiesis of the HIV infection-resistant CD34+ cells. More recently, we reported the identification of virus-infected CD4+ thymocyte-secreted miRNA-15a and miRNA-24 and that their differential expression following HIV infection causes the indirect inhibition of hematopoiesis. We then hypothesized that the observed miRNA differential expression in the virus-infected T-cells causes the abnormal regulation of homeobox (HOX) gene-encoded transcriptomes in the CD34+ cells, affecting specific MAPK signaling and CD34+ cell fate, thereby disrupting normal hematopoiesis. We present that in HIV infection, miRNA-mediated post-transcriptional dysregulation of HOXB3 mRNA inhibits multi-lineage hematopoiesis, which translates into hematological disorders in virus-infected patients with HIV/AIDS. These observations portend specific microRNA candidates for potential efficacy against the virus-induced cytopenias that are otherwise not treatable by the existing HAART/ART regimens, which are primarily designed and applicable for the attenuation of virus replication.

Transcription of microRNAs is regulated by developmental signaling pathways and transcription factors.

In early embryonic development, the cross-regulation of transcription factors and signaling pathways are critical in mediating developmental and physiological processes. Additionally, many studies have shown the importance of post-transcriptional regulation of signaling and network components mediated by microRNAs (miRNAs); however, how miRNAs are transcriptionally regulated is poorly understood. miRNAs are critical fine-tuners of many biological processes and their dysregulation leads to a variety of diseases and developmental defects. Previously, we have shown that miRNAs are dynamically expressed throughout sea urchin development, suggesting that miRNAs are likely to be under transcriptional regulation. Here, we used pharmacological inhibitors, genetic constructs, and loss-of-function reagents to assess the impact of key signaling pathways (Wnt, Nodal, MAPK, Sonic Hedgehog, Delta/Notch, VEGF, and BMP) and transcription factors (Alx1, Ets1/2, and Tbr) on the transcript levels of the evolutionarily conserved miR-1, miR-31, miR-92 and miR-124; the invertebrate-specific miR-71; and the echinoderm-specific miR-2002, miR-2007, and miR-2012. We also used computational methods to identify potential transcription factor binding sites of these miRNAs. Lists of binding motifs for transcription factors (TFs) were acquired from the MEME-Suite Motif Database and used as inputs for the algorithm FIMO (Find Individual Motif Occurrences), which detects short nucleotide motifs within larger sequences. Based on experimental data on miRNA expression in conjunction with bioinformatic predictions, we propose that the transcription factors Tbr, Alx1, and Ets1 regulate SpmiR-1, SpmiR-31, and SpmiR-71, respectively. We additionally observed significant effects on miRNA levels as a result of perturbations to Wnt, Nodal, MAPK, and Sonic Hedgehog signaling pathways, while no significant change on miRNA levels were observed with perturbations to Delta/Notch, VEGF, or BMP signaling pathways. Overall, this study provides insights into the transcriptional regulation of miRNAs by signaling pathways and transcription factors and contribute to our overall understanding of the genetic regulation of developmental processes.

Emotion Regulation and Mentalization in Patients With Depression and Anxiety.

OBJECTIVE: Theoretical conceptualizations of emotion and affect regulation have a considerable common ground. However, mentalization theory considers the ability to regulate affects as being contingent on the ability to mentalize. The aim of the present study is to examine the association between emotion regulation and mentalization, operationalized as reflective functioning, in a sample of patients with depression and/or anxiety. METHODS: The study used data from the TRAns-diagnostic Cognitive behavioural Therapy versus standard cognitive behavioural therapy (TRACT-RCT) trial. Patients with depression and/or anxiety (N = 291; 64.4% female; Mage = 32.2; SD = 11.0) completed the Emotion Regulation Strategies Questionnaire (ERSQ) and the Reflective Functioning Questionnaire (RFQ-6). Correlation and regression analyses were performed to determine associations of the measures of ERSQ and RFQ-6 in relation to the outcome variables, global well-being (World Health Organization Well-being Index; WHO-5) and social functioning (Work and Social Adjustment Scale; WSAS). RESULTS: Overall, the patients had a reduced level of emotion regulation (MERSQ_Total = 1.77; SD = 0.59). However, only mildly impaired reflective functioning was found (MRFQ-6 = 3.57; SD = 1.26). ERSQ correlated significantly with RFQ-6 (r = -0.31), that is, more frequent use of emotion regulation strategies was associated with less hypomentalization. ERSQ was a stronger predictor of well-being and social function than RFQ-6. CONCLUSION: In patients with anxiety and/or depression, hypomentalization as measured by the RFQ-6 is not a major problem, but emotion regulation is. It seems that these two, theoretically related constructs, do not necessarily co-occur. Alternatively, the RFQ-6 scale might not capture the mentalization construct in a valid way. Emotion regulation strategies are highly related to symptomatology; therefore, they are likely to be an important target for psychotherapy.

French version of the Parental Emotion Regulation Inventory (PERI 2).

The Parental Emotion Regulation Inventory 2 (PERI 2) is designed to assess parents' emotion regulation during discipline interactions with their children. The objective of this study was to examine the psychometric properties of a French translation and adaptation of the PERI 2. Two hundred and forty-six parents of children aged 1 to 3 years old participated in this study. The participants were recruited both face-to-face in a childcare centre and remotely through social networks. They were asked to fill out various questionnaires including the PERI 2 on an online platform. The adequacy indices of the confirmatory analysis were satisfying and validated a 4-factor model. The internal consistency of the overall scale and the subscales was satisfying. The convergent validity of the cognitive reappraisal and expressive suppression factors showed a strong association with the global reappraisal and suppression constructs. The escape factor was positively associated with constructs measuring negative experienced emotion during discipline encounters and physical aggression in children but negatively associated with measures of over reactivity. The capitulation factor was positively associated with constructs measuring negative experienced emotion during discipline encounters, child physical aggression, and global expressive suppression. The association with the laxity factor was negative. The French version of the PERI 2 is a reliable tool to measure cognitive reappraisal and expressive suppression in parents. The tool can be used in research with parents of young children in the context of disciplinary interactions. A short version could also be created for clinical use in order to assess difficulties in the emotion regulation of parents of young children and to assess treatment efficacy.

How does technological progress affect low carbon economic growth? Evidence from regional heterogeneity in China.

The rapid economic development leads to excessive consumption of fossil energy, resulting in a large number of carbon emissions, which makes the sustainable development of China's economy and society face great challenges. Under the background of global warming and environmental deterioration, developing low-carbon economy has become an inevitable choice for China to change its development model and improve its international competitiveness. Technological progress is the first driving force to promote economic growth. However, the influence degree and mechanism of technological progress on the development of low-carbon economy are still unclear. Based on this, the paper proposes the concept of low-carbon GDP, which is used to measure the low-carbon economic development of 30 Chinese provinces. Then, the panel fixed effect model is used to study the effect degree and mechanism of technological progress on low-carbon GDP and the moderating effect of other factors on the relationship between them. The results show that, first, economically developed provinces and regions have higher per capita low-carbon GDP and low-carbon GDP index, but the speed and quality of low-carbon economic development are not necessarily higher. Second, technological progress can promote the growth of low-carbon GDP and make greater contributions to resources-poor regions. Third, improving local education can make technological progress more effective in low-carbon economic development. China needs to upgrade technological development by developing new and high-tech technologies, promoting new urbanization and strengthening education in order to promote low-carbon economic development.

Bradyrhizobium japonicum HmuP is an RNA-binding protein that positively controls hmuR operon expression by suppression of a negative regulatory RNA element in the 5' untranslated region.

The hmuR operon encodes proteins for the uptake and utilization of heme as a nutritional iron source in Bradyrhizobium japonicum. The hmuR operon is transcriptionally activated by the Irr protein and is also positively controlled by HmuP by an unknown mechanism. An hmuP mutant does not express the hmuR operon genes nor does it grow on heme. Here, we show that hmuR expression from a heterologous promoter still requires hmuP, suggesting that HmuP does not regulate at the transcriptional level. Replacement of the 5' untranslated region (5'UTR) of an HmuP-independent gene with the hmuR 5'UTR conferred HmuP-dependent expression on that gene. Recombinant HmuP bound an HmuP-responsive RNA element (HPRE) within the hmuR 5'UTR. A 2 nt substitution predicted to destabilize the secondary structure of the HPRE abolished both HmuP binding activity in vitro and hmuR expression in cells. However, deletion of the HPRE partially restored hmuR expression in an hmuP mutant, and it rescued growth of the hmuP mutant on heme. These findings suggest that the HPRE is a negative regulatory RNA element that is suppressed when bound by HmuP to express the hmuR operon.