Interspecific aggregations of prey may provide benefits by mitigating predation risk, but they can also create costs if they increase competition for resources or are more easily detectable by predators. Variation in predation risk and resource availability may influence the occurrence and fitness effects of aggregating in nature. Yet tests of such possibilities are lacking. Cavity-nesting birds provide an interesting test case. They compete aggressively for resources and experience low nest predation rates, which might predict dispersion, but across 19 years of study we found that they commonly aggregate by sharing nest trees. Tree sharing was more common when aspen were more abundant and was somewhat more common in years with higher nest predation risk. Nest success was higher in shared trees when nest predation risk was higher than average. Ultimately, the costs and benefits of aggregating (nest tree sharing) varied across years, and we outline hypotheses for future studies.

This study aimed to identify distinct behavioral profiles in a population-based sample of 654 4-year-old children and characterize their relationships with brain functional networks using resting-state functional magnetic resonance imaging data. Young children showed 7 behavioral profiles, including a super healthy behavioral profile with the lowest scores across all Child Behavior CheckList (CBCL) subscales (G1) and other 6 behavioral profiles, respectively with pronounced withdrawal (G2), somatic complaints (G3), anxiety and withdrawal (G4), somatic complaints and withdrawal (G5), the mixture of emotion, withdrawal, and aggression (G6), and attention (G7) problems. Compared with children in G1, children with withdrawal shared abnormal functional connectivities among the sensorimotor networks. Children in emotionally relevant problems shared the common pattern among the attentional and frontal networks. Nevertheless, children in sole withdrawal problems showed a unique pattern of connectivity alterations among the sensorimotor, cerebellar, and salience networks. Children with somatic complaints showed abnormal functional connectivities between the attentional and subcortical networks, and between the language and posterior default mode networks. This study provides novel evidence on the existence of behavioral heterogeneity in early childhood and its associations with specific functional networks that are clinically relevant phenotypes for mental illness and are apparent from early childhood.

Sexual selection theory predicts that male investment in a current female should be a function of female density and male competition. While many studies have focused on male competition, the impact of female density on male mating investment has been widely neglected. Here, we aimed to close this gap and tested effects of mate density on male mating decisions in the orb-web spider Argiope bruennichi. Males of this species mutilate their genitalia during copulation, which reduces sperm competition and limits their mating rate to a maximum of two females (bigyny). The mating rate is frequently further reduced by female aggression and cannibalization. Males can reduce the risk of cannibalism if they jump off the female in time, but will then transfer fewer sperm. An alternative solution of this trade-off is to copulate longer, commit self-sacrifice and secure higher minimal paternity. The self-sacrificial strategy may be adaptive if prospective mating chances are uncertain. In A. bruennichi, this uncertainty may arise from quick changes in population dynamics. Therefore, we expected that males would immediately respond to information about low or high mate availability and opt for self-sacrifice after a single copulation under low mate availability. If male survival depends on information about prospective mating chances, we further predicted that under high mate availability, we would find a higher rate of males that leave the first mating partner to follow a bigynous mating strategy.

Understanding neuronal mechanisms underlying aggression in patients with autism spectrum disorder (ASD) could lead to better treatments and prognosis. The Neuroligin-3 (NL3)R451C mouse model of ASD has a heightened aggressive phenotype, however the biological mechanisms underlying this behavior are unknown. It is well established that NL3R451C mice have imbalanced excitatory and inhibitory synaptic activity in the hippocampus and somatosensory cortex. The amygdala plays a role in modulating aggressive behavior, however potential changes in synaptic activity in this region have not previously been assessed in this model. We investigated whether aggressive behavior is robustly present in mice expressing the R451C mutation, following back-crossing onto a congenic background strain. Endocannabinoids influence social interaction and aggressive behavior, therefore we also studied the effects of cannabinoid receptor 1 (CB1) agonist on NL3R451C mice. We report that NL3R451C mice have increased amplitude of miniature excitatory postsynaptic currents (EPSCs) with a concomitant decrease in the amplitude of inhibitory postsynaptic currents (IPSCs) in the basolateral amygdala. Importantly, we demonstrated that NL3R451C mice bred on a C57Bl/6 background strain exhibit an aggressive phenotype. Following non-sedating doses (0.3 and 1.0 mg/kg) of the CB1 receptor agonist WIN55,212-2 (WIN), we observed a significant reduction in aggressive behavior in NL3R451C mice. These findings demonstrate altered synaptic activity in the basolateral amygdala and suggest that the NL3R451C mouse model is a useful preclinical tool to understand the role of CB1 receptor function in aggressive behavior.

More than 90% of oral cancers are histopathologically squamous cell carcinomas (SCCs). According to clinical behavior and histopathological features, we hypothesize that oral SCC can originate from either oral squamous epithelium or minor salivary glands. Here, we examined whether some oral SCCs originate from minor salivary glands, and investigated whether these tumors show particularly aggressive biological behavior. The mRNA expression profiles of samples obtained from six patients with oral floor SCC (five men, one woman; mean age, 62.7 years) were analyzed using a microarray containing 32878 probes. The six samples were divided into two groups by clustering of expression levels of 845 probes differentially expressed in normal oral squamous epithelium and normal salivary glands. The expression profile in four cases was similar to that of normal oral squamous epithelium, and in two cases was similar to that of normal salivary glands. Furthermore, we identified nine genes that reveal the origin of the oral SCC. Subsequently, we examined the expression levels of these nine marker genes by reverse transcriptase-polymerase chain reaction to determine the origin of 66 oral SCCs. Twelve of the 66 oral SCCs were considered to originate from minor salivary glands, and these tumors showed high metastatic potential (p = 0.044, Chi-square test). Furthermore, SCC derived from minor salivary glands showed a poor event-free survival rate (p = 0.017, Kaplan-Meier analysis). In conclusion, determination of the origin of oral SCC is helpful in planning treatment for patients with oral SCC. This article is protected by copyright. All rights reserved.

De novo metastatic castration sensitive prostate cancer (mCSPC) accounts for about 4% of all prostate tumors in Western Countries. This condition has a heterogeneous biological e clinical behavior, ranging from indolent to aggressive and rapidly fatal forms. Recently, the therapeutic landscape for mCSPC has been broadly enriched; indeed robust evidence supports the addiction of chemotherapy (docetaxel) or abiraterone acetate to androgen deprivation therapy (ADT), the latter considered for long the unique standard of care. However, the prognostic stratification and the definition of the ideal therapeutic approach for the subpopulation of de novo mCSPC - albeit largely represented in pivotal clinical trials enrolling mCSPC patients - have yet to be prospectively outlined. The aim of this review was to describe the current state of art about clinical presentation, prognostic classification, and different therapeutic options available for de novo mCSPC patients. Furthermore, we shed light on ongoing clinical trials and future perspectives for this disease setting.