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Parent-child, teacher-student, and peer relationships are important for adolescents, and can be related to bullying victimization. However, limited research explores whether, how much, and how these three interpersonal relationships are related to bullying victimization based on different grade levels (junior high and high school) and victimization status (victims and bully victims) in a Chinese cultural context. The present research addressed the gap. Participants were 945 Chinese students in junior high and high school (M[subscript age] = 14.11, SD = 1.48). The results showed that the three interpersonal relationships were significantly and negatively associated with bullying victimization, except parent-child relationships in bully victims. However, the predictive power of the three interpersonal relationships on bullying victimization varied. Compared to high school students, parent-child and teacher-student relationships in junior high school students had greater predictive power for bullying victimization. Compared to pure victims, teacher-student relationships in bully victims had greater predictive power for bullying victimization. Compared to bully victims, parent-child relationships of pure victims had greater predictive power for bullying victimization. Furthermore, the three interpersonal relationships had different roles in bullying victimization among groups. For junior high school students, high school students, and pure victims, parent-child relationships were related to bullying victimization directly and indirectly through the mediating roles of teacher-student and classmate relationships. For bully victims, teacher-student relationships were related to bullying victimization indirectly through the mediating role of relationships with classmates. Thus, anti-bullying policies and interventions need to be more individually tailored. Moreover, parent-child relationships are an important protective factor against bullying among Chinese adolescents.

This study aimed to explore the relationship between alterations in plasma metabolites and treatment responses amongst antipsychotic-naïve female patients with schizophrenia. A total of 38 antipsychotic-naïve female schizophrenia patients (ANS) and 19 healthy female controls (HC) were recruited. Plasma samples were obtained from all participants, and targeted metabolomics were measured with FIA-MS/MS and LC-MS/MS. The positive and negative syndrome scale (PANSS) was used to assess the severity of psychotic symptoms before and after eight weeks of treatment. Receiver operator characteristics (ROC) curves were used to predict diagnostic and therapeutic responses. A total of 186 metabolites passed quality control procedures and were used in statistical analysis to identify potential biomarkers. Before treatment, the ANS patients had lower levels of γ -Aminobutyric Acid (GABA) and higher levels of Cholesteryl esters (CE) (20:3), Cholic Acid (CA) and Glycocholic Acid (GCA) compared to the HCs. These four differential metabonomic markers were synthesised into a combinatorial biomarker panel. This panel significantly distinguished ANS from HC. Moreover, this biomarker panel was able to effectively predict therapeutic responses. Our results suggest that plasma CE (20:3), CA, GCA, and GABA levels may be useful for diagnosing and predicting antipsychotic efficacy amongst female schizophrenia patients. [ABSTRACT FROM AUTHOR]

Summary: Tassel branch number (TBN) is a key agronomic trait for adapting to high‐density planting and grain yield in maize. However, the molecular regulatory mechanisms underlying tassel branching are still largely unknown.Here, we used molecular and genetic studies together to show that ZmELF3.1 plays a critical role in regulating TBN in maize.Previous studies showed that ZmELF3.1 forms the evening complex through interacting with ZmELF4 and ZmLUX to regulate flowering in maize and that RA2 and TSH4 (ZmSBP2) suppresses and promotes TBN in maize, respectively. In this study, we show that loss‐of‐function mutants of ZmELF3.1 exhibit a significant increase of TBN. We also show that RA2 directly binds to the promoter of TSH4 and represses its expression, thus leading to reduced TBN. We further demonstrate that ZmELF3.1 directly interacts with both RA2 and ZmELF4.2 to form tri‐protein complexes that further enhance the binding of RA2 to the promoter of TSH4, leading to suppressed TSH4 expression and consequently decreased TBN.Our combined results establish a novel functional link between the ELF3‐ELF4‐RA2 complex and miR156‐SPL regulatory module in regulating tassel branching and provide a valuable target for genetic improvement of tassel branching in maize. [ABSTRACT FROM AUTHOR]

Summary: Flowering time is a key agronomic trait determining environmental adaptation and yield potential of crops. The regulatory mechanisms of flowering in maize still remain rudimentary.In this study, we combine expressional, genetic, and molecular studies to identify two homologous SQUAMOSA PROMOTER BINDING PROTEIN‐LIKE (SPL) transcription factors ZmSPL13 and ZmSPL29 as positive regulators of juvenile‐to‐adult vegetative transition and floral transition in maize.We show that both ZmSPL13 and ZmSPL29 are preferentially expressed in leaf phloem, vegetative and reproductive meristem. We show that vegetative phase change and flowering time are moderately delayed in the Zmspl13 and Zmspl29 single knockout mutants and more significantly delayed in the Zmspl13/29 double mutants. Consistently, the ZmSPL29 overexpression plants display precocious vegetative phase transition and floral transition, thus early flowering. We demonstrate that ZmSPL13 and ZmSPL29 directly upregulate the expression of ZmMIR172C and ZCN8 in the leaf, and of ZMM3 and ZMM4 in the shoot apical meristem, to induce juvenile‐to‐adult vegetative transition and floral transition.These findings establish a consecutive signaling cascade of the maize aging pathway by linking the miR156‐SPL and the miR172‐Gl15 regulatory modules and provide new targets for genetic improvement of flowering time in maize cultivars. [ABSTRACT FROM AUTHOR]

Maize (Zea mays) originated in southern Mexico and has spread over a wide latitudinal range. Maize expansion from tropical to temperate regions has necessitated a reduction of its photoperiod sensitivity. In this study, we cloned a quantitative trait locus (QTL) regulating flowering time in maize and show that the maize ortholog of Arabidopsis thaliana EARLY FLOWERING3, ZmELF3.1, is the causal locus. We demonstrate that ZmELF3.1 and ZmELF3.2 proteins can physically interact with ZmELF4.1/4.2 and ZmLUX1/2, to form evening complex(es; ECs) in the maize circadian clock. Loss-of-function mutants for ZmELF3.1/3.2 and ZmLUX1/2 exhibited delayed flowering under long-day and short-day conditions. We show that EC directly represses the expression of several flowering suppressor genes, such as the CONSTANS, CONSTANS-LIKE, TOC1 (CCT) genes ZmCCT9 and ZmCCT10, ZmCONSTANS-LIKE 3, and the PSEUDORESPONSE REGULATOR (PRR) genes ZmPRR37a and ZmPRR73, thus alleviating their inhibition, allowing florigen gene expression and promoting flowering. Further, we identify two closely linked retrotransposons located in the ZmELF3.1 promoter that regulate the expression levels of ZmELF3.1 and may have been positively selected during postdomestication spread of maize from tropical to temperate regions during the pre-Columbian era. These findings provide insights into circadian clock-mediated regulation of photoperiodic flowering in maize and new targets of genetic improvement for breeding. ZmELF3.1/3.2 bridge ZmELF4.1/4.2 and ZmLUX1/2 to form evening complexes and promote flowering and adaptation of maize to temperate regions. [ABSTRACT FROM AUTHOR]