Algorithm as Boss or Coworker? Randomized Field Experiment on Algorithmic Control and Collaboration in Gig Platform

Without a doubt, the heavy use of artificial intelligence (AI) will be involved in the future of work. Pertinent to the deployment of AI in organizations, algorithmic control is the managerial use of intelligent algorithms as a means to align individual worker behaviors with organizational objectives. While algorithmic control may facilitate efficient management of workers, it also leads to intrusive and unilateral exertion of controls over workers, also known as “algorithm as boss” phenomenon. In this study, we attempt to understand the outcomes and tradeoffs that different configurations between the AI and gig workers would produce, by conducting a randomized field experiment with one of the largest delivery rider labor unions in Asia. Overall, our study suggests that providing collaborative algorithmic control not only increases gig workers’ utility in terms of monetary rewards but also enhances their intrinsic rewards, which has the potential to benefit the gig platform as well

AI Divide versus Inclusion: An Empirical Evidence from an On-demand Food Delivery Platform

Despite the growing adoption of AI in business operations, the potential differential effects of AI adoption on individual workers remain ambiguous. Drawing on the unique microdata of an on-demand food delivery platform, we investigate the impact of AI adoption on the labor productivity of delivery workers at different skill levels. Our results show that AI adoption enhances the workers’ labor productivity by 3% on average. The enhancement effect was concentrated on low- and middle-skilled drivers (6.5% and 5%, respectively) without a significant effect on the high-skilled. Furthermore, the labor productivity gap involved improvements in overall system efficiency and customer service quality. Our study provides a piece of empirical evidence that introducing AI to markets with a significant labor productivity gap may bridge this gap and yield a Pareto improvement for all stakeholders

Revisiting Solvent-Dependent Roles of the Electrolyte Counteranion in Li–O2 Batteries upon CO2 Incorporation

Lithium–oxygen batteries are promising next-generation high-energy storage candidates. Replacing pure O2 with air and uncovering moisture and CO2-contamination effects on the O2 electrochemistry, however, represent necessary steps toward commercialization. Representatively, a CO2-induced shift toward Li2CO3 formation has been systematically disclosed in a number of electrolyte solvents. Here, we show that in tetraglyme only Li2CO3 is formed without Li2O2. Using explicit theoretical calculations, we reveal that discharge is governed by the strong chelation effect induced by oxygen lone electron pairs of the glyme, which emphasizes the importance of assessing direct interatomic interactions between Li+ and solvent molecules when determining preferred reaction pathways in these O2/CO2 systems. The choice of the electrolyte counteranion investigated here for the first time, however, has no apparent effect on the O2/CO2 electrochemistry, leading to Li2CO3. Galvanostatic results and product analysis nonetheless reveal that highly dissociated Li+ counteranions in tetraglyme favorably stabilize soluble peroxocarbonate reaction intermediates during discharge, whereas highly associated salts accelerate Li2CO3 precipitation, dramatically narrowing the cell capacity. Importantly, these observations are also distinct from prior conclusions from rationally designed electrolytes under pure O2 conditions and emphasize the need to revisit established correlations between uncovered counteranion···Li+···solvent interaction degrees and the balance between mechanistic pathways in practical Li–air devices

Influence of atmospheric conditions on the formation and structural properties of two-dimensional SbSI films

Two-dimensional heavy pnictogen chalcohalides, such as SbSI, SbSeI, and BiSI, are promising materials for solar energy harvesting (SEH) devices. In this paper, we report the influence of atmospheric conditions on the formation and structural properties of SbSI films fabricated under N2 and air atmospheres using a modified two-step method. Under N2 atmosphere, a preferentially (1 2 1)-oriented SbSI film without impurities formed. In contrast, under air atmosphere, a film with mixed crystalline phases of SbSI and secondary Sb2O3 formed. The Sb2O3 phase could be reduced by applying excess sulfur. These results provide a fundamental step toward optimizing the properties of chalcohalides for SEH device applications. © 2023 Elsevier B.V.FALS

Polyamine and EIF5A hypusination downstream of c-Myc confers targeted therapy resistance in BRAF mutant melanoma

Abstract Background BRAF inhibitors are widely employed in the treatment of melanoma with the BRAF V600E mutation. However, the development of resistance compromises their therapeutic efficacy. Diverse genomic and transcriptomic alterations are found in BRAF inhibitor resistant melanoma, posing a pressing need for convergent, druggable target that reverse therapy resistant tumor with different resistance mechanisms. Methods CRISPR-Cas9 screens were performed to identify novel target gene whose inhibition selectively targets A375VR, a BRAF V600E mutant cell line with acquired resistance to vemurafenib. Various in vitro and in vivo assays, including cell competition assay, water soluble tetrazolium (WST) assay, live-dead assay and xenograft assay were performed to confirm synergistic cell death. Liquid Chromatography-Mass Spectrometry analyses quantified polyamine biosynthesis and changes in proteome in vemurafenib resistant melanoma. EIF5A hypusination dependent protein translation and subsequent changes in mitochondrial biogenesis and activity were assayed by O-propargyl-puromycin labeling assay, mitotracker, mitoSOX labeling and seahorse assay. Bioinformatics analyses were used to identify the association of polyamine biosynthesis with BRAF inhibitor resistance and poor prognosis in melanoma patient cohorts. Results We elucidate the role of polyamine biosynthesis and its regulatory mechanisms in promoting BRAF inhibitor resistance. Leveraging CRISPR-Cas9 screens, we identify AMD1 (S-adenosylmethionine decarboxylase 1), a critical enzyme for polyamine biosynthesis, as a druggable target whose inhibition reduces vemurafenib resistance. Metabolomic and proteomic analyses reveal that polyamine biosynthesis is upregulated in vemurafenib-resistant cancer, resulting in enhanced EIF5A hypusination, translation of mitochondrial proteins and oxidative phosphorylation. We also identify that sustained c-Myc levels in vemurafenib-resistant cancer are responsible for elevated polyamine biosynthesis. Inhibition of polyamine biosynthesis or c-Myc reversed vemurafenib resistance both in vitro cell line models and in vivo in a xenograft model. Polyamine biosynthesis signature is associated with poor prognosis and shorter progression free survival after BRAF/MAPK inhibitor treatment in melanoma cohorts, highlighting the clinical relevance of our findings. Conclusions Our findings delineate the molecular mechanisms involving polyamine-EIF5A hypusination-mitochondrial respiration pathway conferring BRAF inhibitor resistance in melanoma. These targets will serve as effective therapeutic targets that can maximize the therapeutic efficacy of existing BRAF inhibitors

Astrocytic autophagy plasticity modulates Aβ clearance and cognitive function in Alzheimer’s disease

Abstract Background Astrocytes, one of the most resilient cells in the brain, transform into reactive astrocytes in response to toxic proteins such as amyloid beta (Aβ) in Alzheimer’s disease (AD). However, reactive astrocyte-mediated non-cell autonomous neuropathological mechanism is not fully understood yet. We aimed our study to find out whether Aβ-induced proteotoxic stress affects the expression of autophagy genes and the modulation of autophagic flux in astrocytes, and if yes, how Aβ-induced autophagy-associated genes are involved Aβ clearance in astrocytes of animal model of AD. Methods Whole RNA sequencing (RNA-seq) was performed to detect gene expression patterns in Aβ-treated human astrocytes in a time-dependent manner. To verify the role of astrocytic autophagy in an AD mouse model, we developed AAVs expressing shRNAs for MAP1LC3B/LC3B (LC3B) and Sequestosome1 (SQSTM1) based on AAV-R-CREon vector, which is a Cre recombinase-dependent gene-silencing system. Also, the effect of astrocyte-specific overexpression of LC3B on the neuropathology in AD (APP/PS1) mice was determined. Neuropathological alterations of AD mice with astrocytic autophagy dysfunction were observed by confocal microscopy and transmission electron microscope (TEM). Behavioral changes of mice were examined through novel object recognition test (NOR) and novel object place recognition test (NOPR). Results Here, we show that astrocytes, unlike neurons, undergo plastic changes in autophagic processes to remove Aβ. Aβ transiently induces expression of LC3B gene and turns on a prolonged transcription of SQSTM1 gene. The Aβ-induced astrocytic autophagy accelerates urea cycle and putrescine degradation pathway. Pharmacological inhibition of autophagy exacerbates mitochondrial dysfunction and oxidative stress in astrocytes. Astrocyte-specific knockdown of LC3B and SQSTM1 significantly increases Aβ plaque formation and GFAP-positive astrocytes in APP/PS1 mice, along with a significant reduction of neuronal marker and cognitive function. In contrast, astrocyte-specific overexpression of LC3B reduced Aβ aggregates in the brain of APP/PS1 mice. An increase of LC3B and SQSTM1 protein is found in astrocytes of the hippocampus in AD patients. Conclusions Taken together, our data indicates that Aβ-induced astrocytic autophagic plasticity is an important cellular event to modulate Aβ clearance and maintain cognitive function in AD mice