Online Retailing Channel Addition: Risk Alleviation or Risk Maker?

The retailing industry traditionally considers the optimal products selection and pricing problem, a complex and challenging one, from marketing and consumer behavior\u27s perspectives. In this study, we take a risk perspective and offer an alternative solution to tackling the problem, echoing the most recent literature that looks at non-risk aspects, such as expected consumer preference, market size and predicted profitability. Adopting a mean-variance framework, our approach explicitly takes into account the interconnectedness of retail products and their impact on risk at the portfolio (retailer) level. Extending the analysis to multiple-channel decisions, our results suggest that the introduction of a new retailing channel (e.g. online shops) can reduce the portfolio risk, whereas a lack of synergy between the new channel and the existing ones may lead to a negative impact on the overall performance. We also provide managerial implications on several conditions when retailers are more economically inclined to introduce more retail channels. Interestingly, our model indicates that larger retailers are less likely to expand their online platform

Multi-Speaker Expressive Speech Synthesis via Semi-supervised Contrastive Learning

This paper aims to build an expressive TTS system for multi-speakers, synthesizing a target speaker's speech with multiple styles and emotions. To this end, we propose a novel contrastive learning-based TTS approach to transfer style and emotion across speakers. Specifically, we construct positive-negative sample pairs at both utterance and category (such as emotion-happy or style-poet or speaker A) levels and leverage contrastive learning to better extract disentangled style, emotion, and speaker representations from speech. Furthermore, we introduce a semi-supervised training strategy to the proposed approach to effectively leverage multi-domain data, including style-labeled data, emotion-labeled data, and unlabeled data. We integrate the learned representations into an improved VITS model, enabling it to synthesize expressive speech with diverse styles and emotions for a target speaker. Experiments on multi-domain data demonstrate the good design of our model.Comment: 5 pages, 3 figure

No-compressing of quantum phase information

We raise a general question of quantum information theory whether the quantum phase information can be compressed and retrieved. A general qubit contains both amplitude and phase information, while an equatorial qubit contains only a phase information. We study whether it is possible to compress the phase information of n equatorial qubits into m general qubits with m being less than n, and still those information can be retrieved perfectly. We prove that this process is not allowed by quantum mechanics.Comment: 4 pages, 1 figur

Co-delivery of polymeric metformin and cisplatin by self-assembled core-membrane nanoparticles to treat non-small cell lung cancer

Clinically, combined therapy of cisplatin (CDDP) and metformin is an effective treatment for non-small cell lung cancer (NSCLC). The success is attributed to synergistic effects between the two drugs. Therefore, we hypothesize that co-encapsulation of CDDP and metformin will avoid the prominent toxicity of CDDP while maintaining the synergy between the regimens. CDDP was first conjugated to polyglutamic acid (PGA) to form anionic PGA-CDDP which was electrostatically complexed with the cationic polymeric metformin (polymet). The nano-sized complex was then stabilized with cationic liposomes composed of DOTAP (2, 3-Dioleoyloxy-propyl)-trimethylammonium/Cholesterol/DSPE-PEG-anisamide aminoethyl. Both in vitro and in vivo experiments confirmed the synergy between polymet and CDDP. CDDP delivered with nanoparticles (NPs) exhibited significantly increased tumor accumulation over free CDDP and suppressed tumor growth through apoptosis in NSCLC H460 tumor-bearing mice without nephrotoxicity. The synergistic effect of polymet alongside CDDP demonstrates that polymet-CDDP NPs can activate the AMP-activated protein kinase α (AMPKα) pathway and inhibit mammalian target rapamycin (mTOR) activity to enhance growth suppression. In all, this platform is the first to successfully co-load polymet, a polymeric metformin, and CDDP into the same nanoparticle for successful treatment of NSCLC

BCL9 enhances the development of cervical carcinoma by deactivating CPEB3/EGFR axis

Purpose: To investigate the differential expression of BCL9 in cervical carcinoma samples, analyze its biological functions in regulating malignant phenotypes of cervical carcinoma cells, and to explore its potential molecular mechanism.Methods: Expression levels of BCL9 in 58 pairs of cervical carcinoma tissues and paracancerous tissues were determined using quantitative real time-polymerase chain reaction (qRT-PCR). Kaplan- Meier curves were used to analyze the prognostic potential of BCL9 in cervical carcinoma. After knockdown using BCL9 by lentivirus transfection, proliferative and migratory changes in Siha and HeLa cells were determined by CCK-8, colony formation and Transwell assays. Cytoplasmic polyadenylation element binding protein 3 (CPEB3), the potential downstream target of BCL9, was confirmed via dualluciferase reporter assay. Western blot analyses were conducted to determine the protein levels of CPEB3, EGFR, AKT and p21 in Siha and HeLa cells with BCL9 knockdown. The co-regulation of BCL9 and CPEB3 on phenotypes of cervical carcinoma cell was investigated.Results: BCL9 was upregulated in cervical carcinoma tissues. The high level of BCL9 was predicted by the tumor size, advanced stage and poor prognosis. The knockdown of BCL9 significantly weakened proliferative and migratory abilities of Siha and HeLa cells (p < 0.05). CPEB3 was the downstream target of BCL9, and was lowly expressed in cervical carcinoma tissues. The knockdown of BCL9 upregulated CPEB3, and downregulated EGFR, AKT and p21 (p < 0.05). The knockdown of CPEB3 also reversed the influence of silenced BCL9 in regulating its proliferative and migratory abilities in cervical carcinoma cells (p < 0.05).Conclusion: BCL9 drives the deterioration of cervical carcinoma by inhibiting the CPEB3/EGFR axis.Thus, BCL9 may be a novel molecular target for cervical carcinoma treatment