Trigger warnings and resilience in college students: A preregistered replication and extension.

Trigger warnings notify people that content they are about to engage with may result in adverse emotional consequences. An experiment by Bellet, Jones, and McNally (2018) indicated that trigger warnings increased the extent to which trauma-naïve crowd-sourced participants see themselves and others as emotionally vulnerable to potential future traumas but did not have a significant main effect on anxiety responses to distressing literature passages. However, they did increase anxiety responses for participants who strongly believed that words can harm. In this article, we present a preregistered replication of this study in a college student sample, using Bayesian statistics to estimate the success of each effect's replication. We found strong evidence that none of the previously significant effects replicated. However, we found substantial evidence that trigger warnings' previously nonsignificant main effect of increasing anxiety responses to distressing content was genuine, albeit small. Interpretation of the findings, implications, and future directions are discussed. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

The time-dependent and persistent effects of amphetamine treatment upon recovery from hemispatial neglect in rats.

Neglect is a neuropsychological disorder characterized by the failure to report or respond to stimuli presented to the side of the body opposite a brain lesion and occurs in approximately 40% of right hemisphere strokes. The need for effective therapies to treat neglect in humans has led to the development of a rodent model. Unilateral destruction of medial agranular cortex (AGm), which is part of a cortical network for directed attention, produces severe multimodal neglect with deficits similar to those seen in humans. Amphetamines have previously been investigated for inducing plasticity and recovery of function following brain damage. Amphetamine treatment has been shown to produce recovery from visual, frontal, and sensorimotor cortex damage in animals and this recovery may be the result of axonal growth originating from the opposite, unlesioned hemisphere. The purpose of this study was to investigate whether amphetamine treatment would induce recovery from neglect produced by unilateral AGm destruction, the time frame in which amphetamine must be administered in order to be effective, and the permanence of recovery following treatment. The results indicated that subjects injected with 2mg/kg of d-amphetamine on days 0, 2, and 5 recovered in significantly fewer days than saline-treated controls, even when administration was delayed by 2 and 7 days. Additionally, these studies indicated that recovery persisted for at least 60 days suggesting that recovery is likely to be long term.

Functional assessments in the rodent stroke model.

Stroke is a common cause of permanent disability accompanied by devastating impairments for which there is a pressing need for effective treatment. Motor, sensory and cognitive deficits are common following stroke, yet treatment is limited. Along with histological measures, functional outcome in animal models has provided valuable insight to the biological basis and potential rehabilitation efforts of experimental stroke. Developing and using tests that have the ability to identify behavioral deficits is essential to expanding the development of translational therapies. The present aim of this paper is to review many of the current behavioral tests that assess functional outcome after stoke in rodent models. While there is no perfect test, there are many assessments that are sensitive to detecting the array of impairments, from global to modality specific, after stroke.

Bone marrow-derived mononuclear cell populations in pediatric and adult patients.

BACKGROUND AIMS: Many clinical trials are currently evaluating the safety and efficacy of autologous bone marrow (BM) mononuclear cells (MNC) for various pathologies in younger and older non-cancer patients. Concern has been raised that autologous MNC derived from elderly patients may be less effective as a therapeutic option. METHODS: We compared the MNC yield, viability, phenotypic markers and in vitro functionality in pediatric patients compared with adult patients enrolled in clinical trials evaluating autologous BM MNC transplantation. Thirty-six patients (n=10 pediatric and n=26 adult) were included in this analysis. All patients underwent BM harvest in which 1-3 mL/kg was aspirated under local anesthesia. MNC were isolated by gradient densitometry. The average age of the older and younger patient groups was 59+/-7 years and 9+/-3 years, respectively. RESULTS: The average total MNC recovered from the BM in pediatric patients was 2.1 x 10(6)/mL and in older patients was 3.2 x 10(6)/mL. There were no differences in cell viability (>97%) or phenotypic markers identifying T cells, natural killer (NK) cells and neutrophils between the two groups. Of note, the Lin(-)CD34(+) cell population was not different between the groups. Average post-processing CFU-F, CFU-GEMM and BFU-E were not statistically different but there were significantly increased levels of CFU-GM in the older population. CONCLUSIONS: These results suggest that MNC from younger and older non-cancer patients are similar, but the data must be interpreted with caution given the small sample size and limited general understanding of MNC mechanisms of action on target cells. It is still possible that cells from older patients may produce fewer cytokines or be functionally impaired.

Nogo-A inhibition induces recovery from neglect in rats.

Neglect is a complex human cognitive spatial disorder typically induced by damage to prefrontal or posterior parietal association cortices. Behavioral treatments for neglect rarely generalize outside of the therapeutic context or across tasks within the same therapeutic context. Recovery, when it occurs, is spontaneous over the course of weeks to months, but often it is incomplete. A number of studies have indicated that anti-Nogo-A antibodies can be used to enhance plasticity and behavioral recovery following damage to motor cortex, and spinal cord. In the present studies the anti-Nogo-A antibodies IN-1, 7B12, or 11C7 were applied intraventricularly to adult rats demonstrating severe neglect produced by unilateral medial agranular cortex lesions in rats. The three separate anti-Nogo-A antibody groups were treated immediately following the medial agranular cortex lesions. Each of the three antibodies induced dramatic significant behavioral recovery from neglect relative to controls. Severing the corpus callosum to destroy inputs from the contralesional hemisphere resulted in reinstatement of severe neglect, pointing to a possible role of interhemispheric mechanisms in behavioral recovery from neglect.

Delayed treatment with monoclonal antibody IN-1 1 week after stroke results in recovery of function and corticorubral plasticity in adult rats.

Neuronal death due to ischemic stroke results in permanent deficits in sensory, language, and motor functions. The growth-restrictive environment of the adult central nervous system (CNS) is an obstacle to functional recovery after stroke and other CNS injuries. In this regard, Nogo-A is a potent neurite growth-inhibitory protein known to restrict neuronal plasticity in adults. Previously, we have found that treatment with monoclonal antibody (mAb) IN-1 to neutralize Nogo-A immediately after stroke enhanced motor cortico-efferent plasticity and recovery of skilled forelimb function in rats. However, immediate treatment for stroke is often not clinically feasible. Thus, the present study was undertaken to determine whether cortico-efferent plasticity and functional recovery would occur if treatment with mAb IN-1 was delayed 1 week after stroke. Adult rats were trained on a forelimb-reaching task, and the middle cerebral artery was occluded to induce focal cerebral ischemia to the forelimb sensorimotor cortex. After 1 week, animals received mAb IN-1 treatment, control antibody, or no treatment, and were tested for 9 more weeks. To assess cortico-efferent plasticity, the sensorimotor cortex opposite the stroke lesion was injected with an anterograde neuroanatomical tracer. Behavioral analysis demonstrated a recovery of skilled forelimb function, and anatomical studies revealed neuroplasticity at the level of the red nucleus in animals treated with mAb IN-1, thus demonstrating the efficacy of this treatment even if administered 1 week after stroke.