Your Pain Pleases Others: The Influence of Social Interaction Patterns and Group Identity on Schadenfreude.

Schadenfreude is a joyful emotional response to the misfortune of others. Individuals' schadenfreude over the misfortunes of ingroup and outgroup members may vary depending on how groups interact. Accordingly, this study examines the effects of different social interaction patterns and group identity on schadenfreude and their mechanisms. The study participants were Chinese college students. Study 1 (n = 83) investigated whether there are differences in individuals' schadenfreude towards ingroup and outgroup members under two different patterns of social interaction: cooperation and competition. On the basis of this study, Study 2 (n = 73) focused on the mechanisms underlying the influence of individuals' Schadenfreude on ingroup and outgroup members in competitive situations, and the mediating role of disgust. It was found that there was an interaction between group identity and social interaction patterns, with people showing more schadenfreude over the misfortunes of outgroup members than ingroup members, and competitive situations increasing disgust and schadenfreude over outgroup members. However, no differences were found in individuals' schadenfreude towards ingroup and outgroup members in cooperative situations. This is instructive in terms of real-life intergroup relations as well as patterns of social interaction. This proves that cooperation and group contact is a way to reduce schadenfreude.

An Intelligent Rehabilitation Assessment Method for Stroke Patients Based on Lower Limb Exoskeleton Robot.

The 6-min walk distance (6MWD) and the Fugl-Meyer assessment lower-limb subscale (FMA-LE) of the stroke patients provide the critical evaluation standards for the effect of training and guidance of the training programs. However, gait assessment for stroke patients typically relies on manual observation and table scoring, which raises concerns about wasted manpower and subjective observation results. To address this issue, this paper proposes an intelligent rehabilitation assessment method (IRAM) for rehabilitation assessment of the stroke patients based on sensor data of the lower limb exoskeleton robot. Firstly, the feature parameters of the patient were collected, including age, height, and duration, etc. The sensor data of the exoskeleton robot were also collected, including joint angle, joint velocity, and joint torque, etc. Secondly, a gait feature model was constructed to deduce the walking gait parameters of the patient according to the sensor data of the exoskeleton, including the support phase to swing phase ratio, step length and leg lift height of the patient, etc. Then, the 6MWD and FMA-LE values were collected by traditional methods, feature parameters, gait parameters and human-machine interaction parameters (joint torque) of the patient were adopted to train the rehabilitation assessment model. Finally, the assessment model was trained by a machine-learning based algorithm. The new stroke patients' the 6MWD and FMA-LE values can be predicted by the trained model. The experimental results present that the prediction accuracy for the 6MWD and FMA-LE values reach to 85.19% and 92.66%, respectively.

Comparison of brain microstructure alterations on diffusion kurtosis imaging among Alzheimer's disease, mild cognitive impairment, and cognitively normal individuals.

Objective: Our study aimed to explore the differences in brain microstructure in patients with Alzheimer's disease (AD) and with mild cognitive impairment (MCI) and in individuals with normal cognition using diffusion kurtosis imaging (DKI) to identify a potential non-invasive biomarker of AD. Materials and methods: A total of 61 subjects were included in our study, including 20 subjects diagnosed with AD, 21 patients diagnosed with amnestic MCI, and 20 cognitively normal individuals. We acquired magnetic resonance imaging (MRI) scans, and DKI images were processed. Twelve regions of interest were drawn, and various parameters were measured and analyzed using SPSS version 11.0 software. Results: Comparative analysis showed that differences in brain regions in terms of mean diffusion (MD) and mean kurtosis (MK) between groups were the most marked. Precuneus MD, temporal MK, precuneus MK, and hippocampal MK were significantly correlated with neuropsychological test scores. Hippocampal MK showed the strongest correlation with the medial temporal lobe atrophy score (r = -0.510), and precuneus MD had the strongest correlation with the Koedam score (r = 0.463). The receiver operating curve analysis revealed that hippocampal MK exhibited better diagnostic efficacy than precuneus MD for comparisons between any group pair. Conclusion: DKI is capable of detecting differences in brain microstructure between patients with AD, patients with MCI, and cognitively normal individuals. Moreover, it compensates for the deficiencies of conventional MRI in detecting pathological changes in microstructure before the appearance of macroscopic atrophy. Hippocampus MK was the most sensitive single parameter map for differentiating patients with AD, patients with MCI, and cognitively normal individuals.

Altered Microstructural Changes Detected by Diffusion Kurtosis Imaging in Patients With Cognitive Impairment After Acute Cerebral Infarction.

Objective: To detect the microstructural changes in patients with cognitive impairment after acute cerebral infarction using diffusion kurtosis imaging (DKI). Materials and Methods: A total of 70 patients with acute cerebral infarction were divided into two groups: 35 patients with cognitive impairment (VCI group), and 35 patients without cognitive impairment (N-VCI group), according to mini-mental state examination (MMSE) score. Healthy individuals (n = 36) were selected as the normal control (NORM) group. DKI parameters from 28 different brain regions of interest (ROIs) were selected, measured, and compared. Results: VCI group patients had significantly higher mean diffusion (MD) and significantly lower mean kurtosis (MK) values in most ROIs than those in the N-VCI and NORM groups. DKI parameters in some ROIs correlated significantly with MMSE score. The splenium of corpus callosum MD was most correlated with MMSE score, the correlation coefficient was -0.652, and this parameter had good ability to distinguish patients with VCI from healthy controls; at the optimal cut-off MD value (0.9915), sensitivity was 91.4%, specificity 100%, and the area under the curve value 0.964. Conclusions: Pathological changes in some brain regions may underlie cognitive impairment after acute cerebral infarction, especially the splenium of corpus callosum. These preliminary results suggest that, in patients with VCI, DKI may be useful for assessing microstructural tissue damage.

Moral Threshold Model is Universal? Initial Evidence from China's Collectivist Culture.

PURPOSE: People choose actions that maintain their moral self-regard. This paper explains how one's moral actions influence moral self-regard. The moral threshold model (MTM) has been proposed by scholars and tested using a limited sample. However, whether the MTM is universally applicable among people is still unknown. PARTICIPANTS AND METHODS: Our sample comprised 1761 individuals living in China, a collectivist culture, who were recruited to test the two main hypotheses of the MTM. Participants engaged in a hypothetical investment task. RESULTS: 1) When the beneficiary was a prosocial cause, participants showed stronger preferences for smaller guaranteed positive payouts over larger uncertain ones; 2) as compared to making decisions for charities, when a participant made decisions exclusively for themselves, the maximum potential benefit was more likely to influence participant behavior. CONCLUSION: The current study provides initial evidence for the validity of using the worst outcome avoidance (WOA) hypothesis of MTM among members of China's collectivist culture, indicating that the WOA hypothesis of MTM may have universal application.

JNK/c-Jun-driven NLRP3 inflammasome activation in microglia contributed to retinal ganglion cells degeneration induced by indirect traumatic optic neuropathy.

BACKGROUND: Indirect traumatic optic neuropathy (ITON) is a major cause of permanent loss of vision after blunt head trauma. Neuroinflammation plays a crucial role in neurodegenerative diseases. The present study concentrated on JNK/c-Jun-driven NLRP3 inflammasome activation in microglia during the degeneration of retinal ganglion cells (RGCs) in ITON. METHODS: An impact acceleration (IA) model was employed to induce ITON, which could produce significant neurodegeneration in the visual system. Pharmacological approaches were employed to disrupt JNK and to explore whether JNK and the microglial response contribute to RGC death and axonal degeneration. RESULTS: Our results indicated that the ITON model induced significant RGC death and axonal degeneration and activated JNK/c-Jun signaling, which could further induce the microglial response and NLRP3 inflammasome activation. Moreover, JNK disruption is sufficient to suppress NLRP3 inflammasome activation in microglia and to prevent RGC death and axonal degeneration. CONCLUSIONS: ITON could promote JNK/c-Jun signaling, which further activates the NLRP3 inflammasome in microglia and contributes to the degeneration of axons and death of RGCs. JNK inhibition is able to suppress the inflammatory reaction and improve RGC survival. Although further work is needed to determine whether pharmacological inhibition of the NLRP3 inflammasome can prevent ITON, our findings indicated that such intervention could be promising for translational work.

Nontargeted metabolomic analysis of skeletal muscle in a dehydroepiandrosterone-induced mouse model of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy and an important metabolic disorder in women of reproductive age. Insulin resistance (IR) is one of its most important clinical features in patients with PCOS. Androgen excess-induced mitochondrial dysfunction contributes to skeletal muscle IR in dehydroepiandrosterone (DHEA)-induced PCOS mice. The effect of androgen excess on the skeletal muscle, however, is incompletely characterized. A nontargeted metabolomics approach was thus applied to analyze the metabolites in skeletal muscle of DHEA-induced PCOS mice. Data from metabolomic analysis revealed the significant changes in 32 metabolites and the marked impact of five metabolic pathways. ATP production was also found to be significantly reduced in skeletal muscle of DHEA mice. Combined with the quantification of type I and II myofibers and lipid measurement in the skeletal muscle of the mice, the results from the present study supported the role of mitochondrial impairment rather than lipid accumulation in the pathogenesis of skeletal muscle IR in DHEA-induced PCOS mice. In summary, we show here for the first time the profile of the metabolites in the skeletal muscle of DHEA-induced PCOS mice which exhibit IR. The work would help better understand the pathology of skeletal muscle IR in PCOS.

Dehydroepiandrosterone-induced activation of mTORC1 and inhibition of autophagy contribute to skeletal muscle insulin resistance in a mouse model of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age and also an important metabolic disorder associated with insulin resistance (IR). Hyperandrogenism is a key feature of PCOS. However, whether hyperandrogenism can cause IR in PCOS remains largely unknown. The mammalian target of rapamycin complex 1 (mTORC1) and its regulated autophagy are closely associated with IR. In the present study, we investigated the role of mTORC1-autophagy pathway in skeletal muscle IR in a dehydroepiandrosterone (DHEA)-induced PCOS mouse model. DHEA-treated mice exhibited whole-body and skeletal muscle IR, along with the activated mTORC1, repressed autophagy, impaired mitochondria, and reduced plasma membrane glucose transporter 4 (GLUT4) expression in skeletal muscle of the mice. In cultured C2C12 myotubes, treatment with high dose testosterone activated mTORC1, reduced autophagy, impaired mitochondria, decreased insulin-stimulated glucose uptake, and induced IR. Inhibition of mTORC1 or induction of autophagy restored mitochondrial function, up-regulated insulin-stimulated glucose uptake, and increased insulin sensitivity. On the contrary, inhibition of autophagy exacerbated testosterone-induced impairment. Our findings suggest that the mTORC1-autophagy pathway might contribute to androgen excess-induced skeletal muscle IR in prepubertal female mice by impairing mitochondrial function and reducing insulin-stimulated glucose uptake. These data would help understanding the role of hyperandrogenism and the underlying mechanism in the pathogenesis of skeletal muscle IR in PCOS.