Intergroup cooperation in the United States and Japan:Revisiting Yuki's (2003) theory on the cultural difference in the conceptualization of group boundaries

Social identity theory posits that individuals perceive the in-group as a homogenous entity comprised of depersonalized individuals, and this theory has provided a foundation to understand intergroup processes for many years. Cross-cultural research has suggested social identity theory may not apply to East Asians, who conceptualize their in-groups differently than those in from Western cultures. Specifically, Yuki and colleagues contend that East Asians perceive in-groups as networks wherein each individual is connected through personal ties, rather than homogenous entity comprised of depersonalized individuals. Furthermore, prior research has shown that East Asians are more likely to trust out-group members with potential personal connections, similarly to how they trust actual in-group members. This reflects their group boundary perception based on personal linkages rather than categorical membership. Conversely, individuals from Western cultures tend to trust in-group members more than out-group members, regardless of potential personal connections. Our preregistered study (N = 332 Japanese and 345 American university students) aimed to conceptually replicate key findings that support Yuki's account and expand upon the theory in the context of intergroup cooperation. Overall, we failed to find evidence for the network-based and category-based cooperation and trust among Japanese and Americans, respectively. Consequently, our results highlight the need for further experimental investigation and validation of Yuki and colleagues' theoretical framework

Alzheimer-related decrease in CYFIP2 links amyloid production to tau hyperphosphorylation and memory loss

Characteristic features of Alzheimer's disease are memory loss, plaques resulting from abnormal processing of amyloid precursor protein (APP), and presence of neurofibrillary tangles and dystrophic neurites containing hyperphosphorylated tau. Currently, it is not known what links these abnormalities together. Cytoplasmic FMR1 interacting protein 2 (CYFIP2) has been suggested to regulate mRNA translation at synapses and this may include local synthesis of APP and alpha-calcium/calmodulin-dependent kinase II, a kinase that can phosphorylate tau. Further, CYFIP2 is part of the Wiskott-Aldrich syndrome protein-family verprolin-homologous protein complex, which has been implicated in actin polymerization at synapses, a process thought to be required for memory formation. Our previous studies on p25 dysregulation put forward the hypothesis that CYFIP2 expression is reduced in Alzheimer's disease and that this contributes to memory impairment, abnormal APP processing and tau hyperphosphorylation. Here, we tested this hypothesis. First, in post-mortem tissue CYFIP2 expression was reduced by ∼50% in severe Alzheimer's hippocampus and superior temporal gyrus when normalized to expression of a neuronal or synaptic marker protein. Interestingly, there was also a trend for decreased expression in mild Alzheimer's disease hippocampus. Second, CYFIP2 expression was reduced in old but not in young Tg2576 mice, a model of familial Alzheimer's disease. Finally, we tested the direct impact of reduced CYFIP2 expression in heterozygous null mutant mice. We found that in hippocampus this reduced expression causes an increase in APP and β-site amyloid precursor protein cleaving enzyme 1 (BACE1) protein, but not mRNA expression, and elevates production of amyloid-β42 Reduced CYFIP2 expression also increases alpha-calcium/calmodulin-dependent kinase II protein expression, and this is associated with hyperphosphorylation of tau at serine-214. The reduced expression also impairs spine maturity without affecting spine density in apical dendrites of CA1 pyramidal neurons. Furthermore, the reduced expression prevents retention of spatial memory in the water maze. Taken together, our findings indicate that reduced CYFIP2 expression triggers a cascade of change towards Alzheimer's disease, including amyloid production, tau hyperphosphorylation and memory loss. We therefore suggest that CYFIP2 could be a potential hub for targeting treatment of the disease

D-dimer trends predict recurrent stroke in patients with cancer-related hypercoagulability

Abstract Introduction: In patients with cancer-associated hypercoagulability (CAH)-related stroke, D-dimer trends after anticoagulant therapy may offer a biomarker of treatment efficacy. The purpose of this study was to clarify the association between D-dimer trends and recurrent stroke after anticoagulant therapy in patients with CAH-related stroke. Methods: We performed retrospective cohort study of consecutive patients with CAH-related stroke at two stroke centers from 2011 through 2020. The ratio of post-treatment to pre-treatment D-dimer levels (post/pre ratio) was used as an indicator of D-dimer trends after anticoagulant therapy. Fine–Gray models were used to evaluate the association between post/pre ratio and recurrent stroke. Results: Among 360 acute ischemic stroke patients with active cancer, 73 patients with CAH-related stroke were included in this study. Recurrent stroke occurred in 13 patients (18%) during a median follow-up time of 28 days (interquartile range, 11–65 days). Multivariate analysis revealed that high post/pre ratio was independently associated with recurrent stroke (per 0.1 increase: hazard ratio 2.20, 95% confidence interval 1.61–3.01, p=0.012). Discussion and Conclusion: D-dimer levels after anticoagulant therapy were associated with recurrent stroke in CAH-related stroke patients. Patients with neutral trends in high D-dimer levels after anticoagulant therapy were at high risk of recurrent stroke