Individualism, Collectivism, and Goal-Oriented Saving

This study examines how individualism (vs. collectivism) influences people's goal-oriented saving decisions. Three experimental studies show that the effect of individualism (collectivism) on people's propensity to save is contingent on the purpose of saving. People who are chronically or situationally high in individualist values (the "individualists") have a higher propensity to save for selfenhancing purposes (e.g., job transition or education) than do those who are high in collectivist values ("the collectivists"). When saving for self-enhancing purposes, the individualists also show a higher propensity to resist temptations for immediate gratifications than do the collectivists. However, the individualists and the collectivists do not differ in their propensity to save and to resist myopic temptations when saving for self-indulging purposes (e.g., saving for a vacation)

On the non-tightness of measurement-based reductions for key encapsulation mechanism in the quantum random oracle model

Key encapsulation mechanism (KEM) variants of the Fujisaki-Okamoto (FO) transformation (TCC 2017) that turn a weakly-secure public-key encryption (PKE) into an IND-CCA-secure KEM, were widely used among the KEM submissions to the NIST Post-Quantum Cryptography Standardization Project. Under the standard CPA security assumptions, i.e., OW-CPA and IND-CPA, the security of these variants in the quantum random oracle model (QROM) has been proved by black-box reductions, e.g., Jiang et al. (CRYPTO 2018), and by non-black-box reductions (EUROCRYPT 2020). The non-black-box reductions (EUROCRYPT 2020) have a liner security loss, but can only apply to specific reversible adversaries with strict reversible implementation. On the contrary, the existing black-box reductions in the literature can apply to an arbitrary adversary with an arbitrary implementation, but suffer a quadratic security loss. In this paper, for KEM variants of the FO transformation, we first show the tightness limits of the black-box reductions, and prove that a measurement-based reduction in the QROM from breaking the standard OW-CPA (or IND-CPA) security of the underlying PKE to breaking the IND-CCA security of the resulting KEM, will inevitably incur a quadratic loss of the security, where ``measurement-based means the reduction measures a hash query from the adversary and uses the measurement outcome to break the underlying security of PKE. In particular, most black-box reductions for these FO-like KEM variants are of this type, and our results suggest an explanation for the lack of progress in improving this reduction tightness in terms of the degree of security loss. Then, we further show that the quadratic loss is also unavoidable when one turns a search problem into a decision problem using the one-way to hiding technique in a black-box manner, which has been recognized as an essential technique to prove the security of cryptosystems involving quantum random oracles

Post-Quantum Security of Key Encapsulation Mechanism against CCA Attacks with a Single Decapsulation Query

Recently, in post-quantum cryptography migration, it has been shown that an IND-1-CCA-secure key encapsulation mechanism (KEM) is required for replacing an ephemeral Diffie-Hellman (DH) in widely-used protocols, e.g., TLS, Signal, and Noise. IND-1-CCA security is a notion similar to the traditional IND-CCA security except that the adversary is restricted to one single decapsulation query. At EUROCRYPT 2022, based on CPA-secure public-key encryption (PKE), Huguenin-Dumittan and Vaudenay presented two IND-1-CCA KEM constructions called $T_{CH}$ and $T_H$, which are much more efficient than the widely-used IND-CCA-secure Fujisaki-Okamoto (FO) KEMs. The security of $T_{CH}$ was proved in both random oracle model (ROM) and quantum random oracle model (QROM). However, the QROM proof of $T_{CH}$ relies on an additional ciphertext expansion. While, the security of $T_H$ was only proved in the ROM, and the QROM proof is left open. In this paper, we prove the security of $T_H$ and $T_{RH}$ (an implicit variant of $T_H$) in both ROM and QROM with much tighter reductions than Huguenin-Dumittan and Vaudenay\u27s work. In particular, our QROM proof will not lead to ciphertext expansion. Moreover, for $T_{RH}$, $T_H$ and $T_{CH}$, we also show that a $O(1/q)$ ($O(1/q^2)$, resp.) reduction loss is unavoidable in the ROM (QROM, resp.), and thus claim that our ROM proof is optimal in tightness. Finally, we make a comprehensive comparison among the relative strengths of IND-1-CCA and IND-CCA in the ROM and QROM

Transcriptomic-metabolomic reprogramming in EGFR-mutant NSCLC early adaptive drug escape linking TGFβ2-bioenergetics-mitochondrial priming.

The impact of EGFR-mutant NSCLC precision therapy is limited by acquired resistance despite initial excellent response. Classic studies of EGFR-mutant clinical resistance to precision therapy were based on tumor rebiopsies late during clinical tumor progression on therapy. Here, we characterized a novel non-mutational early adaptive drug-escape in EGFR-mutant lung tumor cells only days after therapy initiation, that is MET-independent. The drug-escape cell states were analyzed by integrated transcriptomic and metabolomics profiling uncovering a central role for autocrine TGFβ2 in mediating cellular plasticity through profound cellular adaptive Omics reprogramming, with common mechanistic link to prosurvival mitochondrial priming. Cells undergoing early adaptive drug escape are in proliferative-metabolic quiescent, with enhanced EMT-ness and stem cell signaling, exhibiting global bioenergetics suppression including reverse Warburg, and are susceptible to glutamine deprivation and TGFβ2 inhibition. Our study further supports a preemptive therapeutic targeting of bioenergetics and mitochondrial priming to impact early drug-escape emergence using EGFR precision inhibitor combined with broad BH3-mimetic to interrupt BCL-2/BCL-xL together, but not BCL-2 alone

Structure Mediation and Properties of Poly(l-lactide)/Poly(d-lactide) Blend Fibers

Poly(l-lactic acid) (PLLA) and poly(d-lactic acid) (PDLA) blend as-spun fibers (50/50, wt.%) were prepared by melt spinning. Structure mediation under temperature and stress and properties of poly(l-lactic acid)/poly(d-lactic acid)(PLLA/PDLA) as-spun fibers were investigated by wide-angle X-ray scattering (WAXS) and differential scanning calorimetry (DSC). The results show that highly oriented stereocomplex (SC) crystals can be formed in PLLA/PDLA blend fibers drawn at 60 °C and annealed at 200 °C. However, at drawn temperature of 80 °C, only lower oriented SC crystals can be formed. For PLLA/PDLA blend fibers drawn twice at 60 °C (PLLA/PDLA-60-2), the crystallinity of SC crystals increases with annealing temperature in the range of 200 to 215 °C, while the degree of orientation decreases slightly. When the annealing temperature is 210 °C, the crystallinity and orientation of SC crystals in PLLA/PDLA-60-2 fibers reach 51% and −0.39, respectively. Moreover, PLLA/PDLA-60-2-210 fibers exhibit excellent heat-resistant property even at 200 °C. The results indicate that the oriented PLLA/PDLA blend fibers with high SC crystals content can be regulated in a short time

Vascular niche IL-6 induces alternative macrophage activation in glioblastoma through HIF-2α.

Spatiotemporal regulation of tumor immunity remains largely unexplored. Here we identify a vascular niche that controls alternative macrophage activation in glioblastoma (GBM). We show that tumor-promoting macrophages are spatially proximate to GBM-associated endothelial cells (ECs), permissive for angiocrine-induced macrophage polarization. We identify ECs as one of the major sources for interleukin-6 (IL-6) expression in GBM microenvironment. Furthermore, we reveal that colony-stimulating factor-1 and angiocrine IL-6 induce robust arginase-1 expression and macrophage alternative activation, mediated through peroxisome proliferator-activated receptor-γ-dependent transcriptional activation of hypoxia-inducible factor-2α. Finally, utilizing a genetic murine GBM model, we show that EC-specific knockout of IL-6 inhibits macrophage alternative activation and improves survival in the GBM-bearing mice. These findings illustrate a vascular niche-dependent mechanism for alternative macrophage activation and cancer progression, and suggest that targeting endothelial IL-6 may offer a selective and efficient therapeutic strategy for GBM, and possibly other solid malignant tumors

Recurrent Chromosomal Copy Number Alterations in Sporadic Chordomas

The molecular events in chordoma pathogenesis have not been fully delineated, particularly with respect to copy number changes. Understanding copy number alterations in chordoma may reveal critical disease mechanisms that could be exploited for tumor classification and therapy. We report the copy number analysis of 21 sporadic chordomas using array comparative genomic hybridization (CGH). Recurrent copy changes were further evaluated with immunohistochemistry, methylation specific PCR, and quantitative real-time PCR. Similar to previous findings, large copy number losses, involving chromosomes 1p, 3, 4, 9, 10, 13, 14, and 18, were more common than copy number gains. Loss of CDKN2A with or without loss of CDKN2B on 9p21.3 was observed in 16/20 (80%) unique cases of which six (30%) showed homozygous deletions ranging from 76 kilobases to 4.7 megabases. One copy loss of the 10q23.31 region which encodes PTEN was found in 16/20 (80%) cases. Loss of CDKN2A and PTEN expression in the majority of cases was not attributed to promoter methylation. Our sporadic chordoma cases did not show hotspot point mutations in some common cancer gene targets. Moreover, most of these sporadic tumors are not associated with T (brachyury) duplication or amplification. Deficiency of CDKN2A and PTEN expression, although shared across many other different types of tumors, likely represents a key aspect of chordoma pathogenesis. Sporadic chordomas may rely on mechanisms other than copy number gain if they indeed exploit T/ brachyury for proliferation

Predicting individual choice and acceptance of threat- related communication under stress: insights from a psychoneuroendocrine approach to stress

Stress is a pervasive consumption experience that has important impact on consumer behavior. Existing marketing literature has exclusively focused on the psychological aspects of stress, whereas research into the physiological facets of stress is almost nonexistent. Drawing on theorizing and empirical evidence from various domains, the current study proposes a psychoneuroendocrine (PNE) perspective of stress, which views stress as an integrated process involving three relatively independent components including affective, autonomic and endocrine responses. It is expected that compared with the psychological approach to stress, the PNE model not only is a more valid representation of stress experience but also can better predict consumers' behavioral and attitudinal change under stress. Applying the PNE model to the context of stress responses to health threat, the current thesis seeks to examine the relationship among the PNE responses under stress, and the predictive validity of the PNE model relating to stress-induced food choice and the impact of positive health communication style on consumers facing threat. The research objectives were accomplished through two experimental studies. The primary objective of Study 1was to validate a laboratory task for inducing PNE stress responses to health threat. Correlation analysis showed that the PNE stress responses were not highly correlated. In addition, Study 1 provided initial evidence for the superior predictive validity of the PNE model relative to a psychological model of stress in the context of stress-induced food choice. In Study 2 I used the PNE model to examine the stress-buffering and persuasive impact of positive peripheral pictures on consumers facing health threat. Findings from Study 2 suggested that health communication presented in a positive and reassuring manner via the use of positive peripheral pictures alleviated PNE stress reactivity. Moreover, the positive peripheral pictures enhanced the persuLe stress est omniprésent dans l'expérience de consommation et il a un impact important sur le comportement du consommateur. La littérature de marketing existante est presque exclusivement concentrée sur les aspects psychologiques du stress, tandis que la recherche sur les réponses physiologiques est à peu près inexistante. En s'appuyant sur des théories et des données empiriques issues de différents domaines, la thèse actuelle propose une perspective psychoneuroendocrinienne (PNE) du stress, qui voit le stress comme un processus intégré impliquant trois composants relativement indépendants, c'est-à-dire les réponses affective, végétative et endocrinienne. On s'attend à ce que comparé à l'approche psychologique du stress prévalente, le modèle PNE soit non seulement une représentation plus pertinente de l'expérience du stress, mais aussi qu'il puisse mieux prédire le changement de comportement et d'attitude en état de stress. Appliquant le modèle PNE au contexte du stress induit par les menaces pour la santé, la thèse actuelle tente d'examiner la relation entre les réponses PNE en état de stress et la validité prédictive du modèle PNE concernant les choix alimentaires induits sous stress et l'impact de différents styles de communications de santé sur les consommateurs mis en face de menaces pour la santé. Les buts de la recherche sont atteints via deux études expérimentales. Dans l'Étude 1, à l'aide d'un protocole de mesure PNE, j'ai validé une tâche de stress en laboratoire pour l'induction d'une réponse de stress à une menace pour la santé. L'analyse de corrélation démontre que les composants PNE de la réponse de stress n'ont pas une haute corrélation. De plus, l'Étude 1 a fourni un premier indice de la validité prédictive supérieure du modèle PNE dans le contexte du choix alimentaire induit sous stress, comparativement à une approche psychologique du stress. Dans l'Étude 2, je me suis servi du modèle P