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The construct of school climate has received attention as a way to enhance student achievement and reduce problem behaviors. The purpose of this article is to evaluate the existing literature on school climate and to bring to light the strengths, weakness, and gaps in the ways researchers have approached the construct. The central information in this article is organized into five sections. In the first, we describe the theoretical frameworks to support the multidimensionality of school climate and how school climate impacts student outcomes. In the second, we provide a breakdown of the four domains that make up school climate, including academic, community, safety, and institutional environment. In the third, we examine research on the outcomes of school climate. In the fourth, we outline the measurement and analytic methods of the construct of school climate. Finally, we summarize the strengths and limitations of the current work on school climate and make suggestions for future research directions.

Transgenerational plasticity (TGP) occurs when the environment experienced by a parent influences the development of their offspring. In this article, we develop a framework for understanding the mechanisms and multigenerational consequences of TGP. First, we conceptualize the mechanisms of TGP in the context of communication between parents (senders) and offspring (receivers) by dissecting the steps between an environmental cue received by a parent and its resulting effects on the phenotype of one or more future generations. Breaking down the problem in this way highlights the diversity of mechanisms likely to be involved in the process. Second, we review the literature on multigenerational effects and find that the documented patterns across generations are diverse. We categorize different multigenerational patterns and explore the proximate and ultimate mechanisms that can generate them. Throughout, we highlight opportunities for future work in this dynamic and integrative area of study.

Many complex factors have been linked to the recent marked increase in honey bee colony failure, including pests and pathogens, agrochemicals, and nutritional stressors. It remains unclear, however, why colonies frequently react to stressors by losing almost their entire adult bee population in a short time, resulting in a colony population collapse. Here we examine the social dynamics underlying such dramatic colony failure. Bees respond to many stressors by foraging earlier in life. We manipulated the demography of experimental colonies to induce precocious foraging in bees and used radio tag tracking to examine the consequences of precocious foraging for their performance. Precocious foragers completed far fewer foraging trips in their life, and had a higher risk of death in their first flights. We constructed a demographic model to explore how this individual reaction of bees to stress might impact colony performance. In the model, when forager death rates were chronically elevated, an increasingly younger forager force caused a positive feedback that dramatically accelerated terminal population decline in the colony. This resulted in a breakdown in division of labor and loss of the adult population, leaving only brood, food, and few adults in the hive. This study explains the social processes that drive rapid depopulation of a colony, and we explore possible strategies to prevent colony failure. Understanding the process of colony failure helps identify the most effective strategies to improve colony resilience. Significance Honey bee colony death rates are unsustainably high. While many stressors have been identified that contribute to this problem, we do not know why colonies transition so rapidly from a state of apparent health to failure. It is well known that individual bees react to nutritional and pathogen stresses by foraging precociously: our study explains how colony failure arises from the social responses of individual bees to stress. We used radio tracking to monitor performance of bees and found that workers who begin foraging prematurely perform very poorly. This compounds the stresses on the colony and accelerates failure. We suggest how colonies at risk can be identified early, and the most effective interventions to prevent failure.

As is the case for humans, it has long been thought that nonhuman primates can be described in terms of their personality. Scientific observations that support this view include the presence of individual differences in social behavior and that they are relatively stable throughout life. Consequently, individuals are constrained in their behavioral flexibility when dealing with various environmental challenges. Still, the variation among individuals during development suggests that the environment influences how primates behave. Research in fields including psychology, behavior genetics, and behavioral ecology have tried to identify the mechanisms responsible for this interplay of behavioral stability and change. In this review, we integrate theories and findings from research on humans and nonhuman primates that highlight how and to what extent genetic and environmental contributions shape the development of social behavior. To do so, we first provide an overview and define what is meant by mean-level and rank-order change of behavior. We then review explanations of behavioral stability and change, focusing on the role of genetic effects, how environmental circumstances influence behavioral variation throughout development, and how genetic and environmental influences may interact to produce this variation. Finally, we point to future research directions that could help us to further understand the development of social behavior in primates from within a behavior genetics framework.

Sensitive periods (SP) in behavioral development appeared in the biological sciences during the first decade of the 20th century, and research in animal models beginning in the 1950s provide terminology and evidence for SP effects. This paper proposes a rigorous program for human SP research and argues that the complexity of the human brain and variability of the human ecology necessitate that SP effects must be studied in humans, employ longitudinal designs starting at birth, test mechanism-based hypotheses based on animal studies that manipulate early environments, and utilize high-risk conditions as “natural experiments.” In light of research on the molecular basis of critical periods and their sequential cascades, it is proposed that the oxytocin (OT) system, an ancient and integrative system that cross-talks with the stress, reward, immune, and brain stem mediated homeostatic systems and supports mammalian sociality, plays a unique role in experience-dependent plasticity that buttresses SP effects due to its (a) dendritic mode of release leading to autoregulated functioning primed by early experience, (b) pulsatile pattern of activity, and (c) special role in neural plasticity at the molecular and network assembly levels. Synchrony, the coordination of biology and behavior during social contact, is suggested as a mechanism by which SP exert their effect on OT functionality, the social brain, and adult sociality. Findings from four high-risk birth cohorts, each followed repeatedly from birth to 10 years, provide unique “natural experiments” for human SP research based on specific programs in animal models. These include prematurity (maternal proximity), multiple birth (peer rearing), postpartum depression (low licking and grooming), and chronic unpredictable trauma (maternal rotation, variable foraging demands). In each cohort, hypotheses are based on the missing environmental component during SP, and findings on social synchrony, OT functionality, stress response, emotion regulation, and mental health accord with the multilevel and dynamic principles of developmental psychopathology. The results on the potential for reparation versus chronicity following early deprivation highlight a flexible conceptualization of resilience based on human SP research. Consideration of SP effects at the molecular, endocrine, brain, and behavioral levels and in relation to the neural plasticity and multifinality of human social functions may assist in fine-tuning early detection and the construction of targeted individualized interventions.

The honeybee is emerging as a model system for studying gut microbiota-host interactions. Previous studies reported gut microbiota effects on multiple worker bee phenotypes, all of which change during behavioral maturation—the transition from nursing to foraging. We tested whether the documented effects may stem from an effect of the microbiota on behavioral maturation. The gut microbiota only subtly affected maturation: it accelerated the onset of foraging without affecting the overall proportion of foragers or their average output. We also found no effect of the microbiota on host weight, cuticular hydrocarbon (CHC) profile, hypopharyngeal gland size, and the expression of behavioral maturation-related genes. These results are inconsistent with previous studies reporting effects of the gut microbiota on bee weight and CHC profile. Our experiments revealed that co-housed bees tend to converge in behavior and physiology, suggesting that spurious associations may emerge when rearing environments are not replicated sufficiently or accounted for analytically.

Promotive behavior refers to actions that facilitate individuals’ efforts to surmount obstacles and proactively pursue their goals, thereby fostering adaptive functioning and positive development. In contrast, prohibitive behavior refers to harmful or otherwise maladaptive actions that may hinder individuals’ personal growth and developmental outcomes. This study aims to explore the possible causal relationship between Internet use behavior and adolescent behavioral development, including promotive behavior and prohibitive behavior. There were 9,132 students’ data that were analyzed, and cross-lagged regression analysis was used to study causal relationships between two or more variables that change over time. Data were collected at two time points: T1 (2013–2014) and T2 (2014–2015), with an interval of approximately 1 year between the two waves. Results indicated a negative correlation between Internet use behavior and promotive behavior at points-in-time T1 and T2, while a positive relationship was observed between Internet use behavior and prohibitive behavior at both time points. Findings suggest that reducing problematic Internet use among adolescents contributes to the development of healthy behaviors, and active and healthy adolescent behaviors can in turn reduce their problematic Internet use.

The impact of anesthesia and surgery on neurocognitive and behavioral development in infants and children remains inadequately understood. To investigate the impact of early-life exposure to general anesthesia and surgery on cognitive and behavioral development. Children aged 0-3 years who underwent general anesthesia and surgical procedures between 2012 and 2015 were included. The cognitive and behavioral development of these children at ages 4-6 years was assessed. Age-, race-, and gender-matched children from the same geographic region, who did not undergo general anesthesia or surgery, served as the control group. The Wechsler Preschool Primary Scale of Intelligence, Fourth Edition (WPPSI-IV) was used to evaluate children's total intelligence quotient (FSIQ) and specific cognitive domains. The Gesell Development Schedules (GSCH) and Child Behavior Checklist (CBCL) were employed to assess behavioral and personality development. Additionally, the study analyzed the effects of various factors including anesthesia drugs, surgery duration, number of surgeries, age, weight, ethnicity, and gender on postoperative neurocognitive and behavioral outcomes. The study included 447 children with anesthesia/surgical exposure (AS) and 459 children in the control group. Analysis of cognitive and behavioral development showed a significant difference in the working memory index (WMI) between the AS and control groups (  < 0.05). Exploratory findings indicated that children administered remifentanil exhibited lower developmental quotient (DQ) values, whereas those given fentanyl showed higher (worse) Child Behavior Checklist (CBCL) total scores. Moreover, increased anesthesia/surgical exposures, younger age and lower body weight at exposure, and longer surgery durations were associated with cognitive and behavioral developmental challenges. This study examined the impact of early-life exposure to surgery and anesthesia on postoperative cognitive and behavioral development. Findings indicate that higher frequency of exposure to surgery and anesthesia, younger age, and lower body weight at exposure could negatively influence cognitive and behavioral development. Furthermore, variations in the effects of different anesthetics on behavior and cognition were observed. Caution is advised regarding the use of opioid analgesics such as remifentanil and fentanyl for more rigorous clinical applications.

Waddington coined the term \"epigenetic\" to attempt to explain the complex, dynamic interactions between the developmental environment and the genome that led to the production of phenotype. Waddington's thoughts on the importance of both adaptability and canalization of phenotypic development are worth recalling as well, as they emphasize the available range for epigenetic action and the importance of environmental feedback (or lack thereof) in the development of complex traits. We suggest that a dynamic systems view fits well with Waddington's conception of epigenetics in the developmental context, as well as shedding light on the study of the molecular epigenetic effects of the environment on brain and behavior. Further, the dynamic systems view emphasizes the importance of the multi-directional interchange between the organism, the genome and various aspects of the environment to the ultimate phenotype.

The present study aims to explore the association of maternal sleep disturbances during late pregnancy on child neuropsychological and behavioral development in preschool years. The study included 638 mother–child pairs from the prospective Rhea mother–child cohort in Crete, Greece. Information on antenatal sleep disturbances was collected through a computer-assisted interview. Children’s neuropsychological and behavioral development was assessed using the McCarthy Scales of Children’s Abilities (MSCA), the Attention-Deficit Hyperactivity Disorder Test (ADHDT), and the Strengths and Difficulties Questionnaire (SDQ). Multivariate analysis showed that maternal sleep duration less than 8 h was associated with reduced scores in the general cognitive scale (β = –2.28, 95% CI –4.54, –0.02, R2 = 0.417) and memory span (β = –3.24, 95% CI –5.72, –0.77, R2 = 0.304), while mild-severe daytime sleepiness was associated with reduced scores in the memory scale (β = –5.42, 95% CI –10.47, –0.37, R2 = 0.304), memory span (β = –5.44, 95% CI –10.68, –0.21, R2 = 0.304), nd functions of posterior cortex (β = –5.55, 95% CI –10.40, –0.70, R2 = 0.393) of MSCA. Snoring in late pregnancy was related to higher child hyperactivity scores in SDQ (β = 1.05, 95% CI 0.16, 1.95, R2 = 0.160). An interaction between child sex and maternal sleep duration in response to ADHD symptoms was also found (p for interaction < 0.05). Stratified analysis revealed increased hyperactivity, inattention, and ADHD total scores for girls of mothers with sleep duration less than 8 h. Maternal sleep disturbances during pregnancy may be associated with impaired child neuropsychological and behavioral development during the preschool years. Early detection and intervention is necessary to reduce sleep disturbances habits in pregnancy and improve child neurodevelopment.