Trends and Influencing Factors in Problematic Smartphone Use Prevalence (2012-2022): A Systematic Review and Meta-Analysis.

Given that problematic smartphone use (PSU) has been researched for a long time, it becomes necessary to assess how the trends of PSU prevalence have evolved over time. In total, 106 articles from 2012 to 2022 with 109 studies covering 97,748 individuals were included in this systematic review and meta-analysis. The estimation of the global pooled PSU prevalence was 37.1% (95% confidence interval, 33.5 - 40.8%) and the PSU prevalence is growing over time in total. Although the PSU prevalence exhibited wide variation between regions and measurement scales, the increasing trend remained. In addition, the regression slope of the PSU prevalence trend in males was higher than that in females. Males initially had a lower prevalence of PSU than females, but this steadily changed over time until it was greater in males than in females. Moreover, the prevalence of PSU showed an increasing trend across all age groups, with a faster growth rate in the older age group. Considering the aforementioned results, it's necessary to implement proper interventions to do with this phenomenon. In addition, considering the differences in prevalence brought by regions, and measurement scales, in practice and research, we should not only take into account the disparities of PSU between countries or cultures, but also to concern about establishing unified standard and measurement tools to confirm it.

Intact maternal buffering of stress response in infant rats despite altered responsivity towards maternal olfactory cues in the valproic acid model of autism-like behavior.

Disrupted processing of social cues and altered social behaviors are among the core symptoms of autism spectrum disorders (ASDs), and they emerge as early as the first year of life. These differences in sensory abilities may affect the ability of children with ASDs to securely attach to a caregiver and experience caregiver buffering of stress. Prenatal exposure to valproic acid (VPA) has been used to model some aspects of ASDs in rodents. Here, we asked whether prenatal VPA exposure altered infant rats' behavioral responsivity to maternal olfactory cues in an Odor Preference Test (OPT) and affected maternal buffering of infants' stress responsivity to shock. In the odor preference test, 1-week old rats treated with VPA during pregnancy appeared to have impaired social recognition and/or may be less motivated to approach social odors in early infancy. These effects were particularly prominent in female pups. In 2-week old rats, VPA-exposed pups and saline-exposed pups showed similar preferences for home cage bedding. Although VPA-exposed pups may initially have a deficit in this attachment-related behavior they do recover typical responses to home cage bedding in later infancy. Both control and VPA-exposed pups showed robust stress hormone responses to repeated shocks, an effect which was blocked when a calm mother was present during shock exposure. No sex differences in the effect of maternal presence on the stress response to shock and no interactions between sex and prenatal drug exposure were observed. Although VPA-exposed pups may show impaired responsivity to maternal cues in early infancy, maternal presence is still capable of regulating the stress response in VPA-exposed pups. In this study we demonstrate the importance of utilizing multiple batteries of tests in assessing behavior, dissecting the behavior on one test into different components. Our results inform about the underlying behavioral characteristics of some of the ASD phenotypes, including sex differences reported by clinical studies, and could shed light on potential opportunities for intervention.

The mobile phone addiction index: Cross gender measurement invariance in adolescents.

The Mobile Phone Addiction Index (MPAI) is a short instrument to assess mobile phone addiction. The Chinese version of this scale has been widely used in Chinese students and shows promising psychometric characteristics. The present study tested the construct validity and measurement invariance of the MPAI by gender in middle school adolescents. The data were collected from 1,395 high school students (females, n = 646; M age = 15.3 years). Confirmatory factor analysis (CFA) and multiple-group CFA (MG-CFA) for invariance tests were conducted on the MPAI model which consisted of 17 observed items and 4 latent factors. Findings showed that the data fit the four-factor structure model well for both males and females. Furthermore, configural, metric, scalar, and residual invariance were established by gender. The results indicated that the MPAI has acceptable psychometric properties when used in adolescents. In addition, with the strict invariance requirements being satisfied, the underlying factor scores for MPAI can be meaningfully compared across genders. To our knowledge, this study is the first attempt to test the measurement invariance of the MPAI across male and female adolescents. Our results will support future research on mobile phone addiction in adolescents.

Electroconvulsive shock increases neurotrophy and neurogenesis: Time course and treatment session effects.

Increasing evidence suggests that hippocampal neurotrophy may be related to the development of major depressive disorders. Neurogenesis, which can be regulated by neurotrophic factors, is also involved in antidepressant efficacy. This paper reviewed literature on neurotrophic signaling and cell proliferation after electroconvulsive shock (ECS) treatment. All articles were from PubMed, Web of Science, and Scopus databases between 2000 and 2020. The keywords used in the literature search are: "ECS," "ECT," "electroconvulsive seizure," "electroconvulsive shock," "electroconvulsive therapy," "neurotrophic factor," "nerve growth factor," "neurotrophins," "neurogenesis," and "cell proliferation." Eighty-two articles were included in the final analysis. It was shown that compared with acute ECS, repeated ECS increased neurotrophin expression in more brain regions at higher levels and was maintained for a longer time. Similarly, ECS increased cell proliferation in a dose- and time-dependent manner. The increase in cell proliferation was positively correlated with the amount of ECS administered and the newly born cells survived for a long time. The effects of ECS in inducing increases in neurotrophin levels and neurogenesis may contribute to brain function changes and antidepressant effects. Future research may focus on optimal sessions of ECT treatment to obtain the best therapeutic effect.

Effects of electroconvulsive shock on neuro-immune responses: Does neuro-damage occur?

Electroconvulsive therapy (ECT) is one of the most effective treatments for treatment-resistant depression. However, this treatment may produce memory impairment. The mechanisms of the cognitive adverse effects are not known. Neuroimmune response is related to the cognitive deficits. By reviewing the available animal literature, we examined the glia activation, inflammatory cytokines, neuron oxidative stress responses, and neural morphological changes following electroconvulsive shock (ECS) treatment. The studies showed that ECS activates microglia, upregulates neuro-inflammatory cytokines, and increases oxidative stress responses. But these effects are rapid and may be transient. They normalize as ECS treatment continues, suggesting endogenous neuroprotection may be mobilized. The transient changes are well in line with the clinical observations that ECT usually does not cause significant long-lasting retrograde amnesia. The longitudinal studies will be particularly important to explore the dynamic changes of neuroplasticity following ECT (Jonckheere et al., 2018). Investigating the neuroplasticity changes in animals that suffered chronic stress may also be crucial to giving support to the translation of preclinical research.

Remote fear memory is sensitive to reconditioning.

Exposure of some individuals to recurring traumatic events from the same perpetrator or situation, such as during child abuse or domestic violence, is quite prevalent. Studies have shown that the number of traumatic events experienced is positively related to the severity of post-traumatic stress disorder and other mental disorders. Using a contextual fear conditioning (Cond1) and reconditioning (Cond2) paradigm, which were separated by either 1 or 35 days, we examined fear responses to immediate extinction and retrieval-extinction procedures after repeated fear conditioning stress. Based on the time interval between Cond1 and Cond2, the animals were divided into recent and remote fear memory groups. We observed that when Cond2 was performed in the original conditioning context in which Cond1 was performed, the reconditioned remote fear memory was resistant to the disruptive effect of immediate extinction and retrieval-extinction paradigms. Furthermore, the resistance to disruptive effects could be induced by very low shock intensities, which cannot even induce any fear response in naive animals. When Cond2 was performed in a novel context, animals with remote fear memory acquired a significantly higher fear response to the novel context. Our findings suggest that remote fear memory may be more sensitive to reconditioning and resistant to post-reconditioning disruption.

An Additional Prior Retrieval Alters the Effects of a Retrieval-Extinction Procedure on Recent and Remote Fear Memory.

Several studies have shown that the isolated retrieval of a consolidated fear memory can induce a labile phase, during which extinction training can prevent the reinstatement, a form of relapse in which fear response to a fear-provoking context returns when a mild shock is presented. However, fear memory retrieval may also have another opposing result: the enhancement of fear memory. This implies that the fear memory trace can be modified by a brief retrieval. Unclear is whether the fear-impairing effect of retrieval-extinction (RE) is altered by a prior brief retrieval. The present study investigated the responses of recent and remote fear memories to the RE procedure after the presentation of an additional prior retrieval (priRet). We found that a single RE procedure effectively blocked the reinstatement of 2-day recent contextual fear memory. The memory-impairing effect of the RE procedure on recent fear was not observed when priRet was presented 6 or 24 h before the RE procedure. In contrast to the 2-day recent memory, the RE procedure failed to block the reinstatement of 36-day remote fear memory but successfully disrupted the return of remote fear memory after priRet. This memory-disruptive effect on remote memory did not occur when priRet was performed in a novel context. Nimodipine administration revealed that the blockade of priRet-induced processes recovered the effects of the RE procedure on both recent and remote fear memories. Our findings suggest that the susceptibility of recent and remote fear memories to RE procedures can be altered by an additional retrieval.

Corticosterone combined with intramedial prefrontal cortex infusion of SCH 23390 impairs the strong fear response in high-fear-reactivity rats.

Accumulating evidence suggests that stress-dose corticosteroids impair fear memory in animals and humans. Corticosteroid treatment after critical illness is seen as a potential psychotropic medication by which to prevent posttraumatic stress disorder. However, individual difference in the responsiveness to stress (i.e., stress reactivity) is a factor that modulates the efficacy of corticosteroids. To understand the contribution of fear reactivity to the effect of post-stress corticosterone, male Sprague-Dawley rats were subjected to classical tone-cued fear conditioning and separated into high and low reactivity (HR and LR, respectively) responder groups based on their levels of freezing during conditioning. The HR rats showed significantly higher fear responses than the LR rats during conditioning as assessed by freezing behavior. At two intervals, 30 min and 48 hr later, the HR rats still displayed more pronounced conditioned responses to cued stimuli compared with the LR rats. Moreover, in contrast to the LR rats, the enhanced fear response in the HR rats was difficult to attenuate by post-training high-dose corticosterone. These results suggest that fear reactivity results in stronger fear memory, and that it is difficult to disrupt this strong fear memory in the HR phenotype using monotherapy. However, the strong fear memory in the HR rats was impaired by concurrent intramedial prefrontal cortex infusion of a high dose of the dopamine D1 receptor antagonist SCH 23390 and systemic administration of corticosterone. SCH 23390 and corticosterone alone did not decrease freezing levels in the HR rats. The fear impairment induced by SCH 23390 combined with corticosterone was not attributable to the effect of these drugs on locomotor activity. This effect was not found with administration of the D2 antagonist eticlopride combined with corticosterone. Our findings demonstrate that the conditioned fear memory in individuals with high stress reactivity is difficult to disrupt using monotherapy, but that combined pharmacotherapy may be useful for treating intervention-resistant fear.