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We provide data and code to replicate the results presented in "ESG Performance and Stock Market Responses to Geopolitical Turmoil: evidence from the Russia-Ukraine War" (Boccaletti, Maranzano, Morelli & Ossola, 2025). The subfolders allow replicating the following: 1. Folder "Event Study - Synthetic" replicates the event study from Section 4 2. Folder "Regressions replication - Table 5 and Table 6" replicates the regression analysis from Section 5. For each subfolder a README file is provided. It contains information about the reproduction steps. * VERSION 4 UPDATES * Compared to Version 3, Version 4 of the folder includes more detailed descriptions of the README files and methodological steps. Additionally, it includes the event study's aggregate results.

This repository contains all the supporting data for the study titled "Energy-Aware Job Shop and Transportation Scheduling under Time-of-Use Electricity Pricing and Workforce Constraints". - "Augmented_instances.xlsx" contains the augmented benchmark instances. - "Experiment_results.xlsx" contains the results of experiments conducted with the epsilon-constraint approach. The first five sheets report the average and standard deviation (<avg (std)>) values after 50 simulation replications. - "Sensitivity_analysis_results.xlsx" contains the average values of the two sensitivity analyses. - "HRIs_results.xlsx" contains the (curated) results of the sensitivity analysis on human-robot interaction durations. - "Pareto_analysis.xlsx" contains the results of the non-dominated solutions analysis.

"Chimeric enzymes enhance treatment potential for globoid cell leukodystrophy through hematopoietic stem cell gene therapy" - PMID: 40988335 - DOI: 10.1016/j.ymthe.2025.09.030 Globoid cell leukodystrophy (GLD) is a fatal lysosomal storage disorder caused by a deficiency in the β-galactosylceramidase (GALC) enzyme, leading to severe demyelination and neurodegeneration, and often death before the age of 2 years. Hematopoietic stem/progenitor cell transplantation (HSPC-T) has limited efficacy due to inadequate GALC delivery to the central (CNS) and peripheral nervous systems (PNS) and associated risks. In vivo gene therapy (GT) using adeno-associated viral vectors shows promise, but safety concerns persist. This research presents a strategy using lentiviral (LV) vector-mediated ex vivo HSPC-GT with a chimeric GALC enzyme that incorporates peptides from α-L-iduronidase (IDUA) and apolipoprotein E II (APO) to enhance expression and blood-brain barrier penetration. The chimeric IDUAsp.GALC.APO enzyme exhibited superior production and secretion compared to native GALC and previous chimeric variants in LV-transduced HSPCs, resulting in improved cross-correction and normalization of GALC activity in GLD neural cells. Proof-of-concept studies demonstrated effective enzyme production, secretion, and cross-correction capability of macrophages from GLD patients. In vivo results showed stable gene marking, sustained enzyme production, and efficient delivery of the chimeric GALC in affected organs, including the CNS and PNS. These findings highlight the potential of HSPC-GT using chimeric GALC enzymes as an innovative therapeutic approach for treating GLD. Data related to the paper are available in the folder with the same name. "Enhancement of expression, bioavailability and cross-correction of chimeric GALC enzyme to refine gene therapy approaches for globoid cell leukodystrophy" - GR 2019-12369357 - Final Report In this project, we propose a lentiviral vector-mediated gene therapy with a chimeric GALC enzyme engineered for improved expression and blood-brain barrier penetration as therapeutic approach for GLD. Our findings demonstrate that the chimeric enzyme, when expressed in LV-transduced human HSPCs and GLD iPSC derived NPC progeny, exhibits enhanced production and secretion compared to native GALC and prior chimeric variants. This leads to significant cross-correction of GALC activity in GLD neural cells. In vivo studies in immunodeficient mice and a severe GLD mouse model confirmed stable gene marking and sustained enzyme production, emphasizing our strategy's potential for effective therapeutic delivery and cross-correction of affected tissues. The data related to the final report of GR 2019-12369357 are available in the folder with the same name.

The data for this project consists of curriculum materials developed for a vocabulary intervention. Two parallel sets of instructional products were created: one monolingual (English-only) and one bilingual (English-Spanish). Each curriculum set contains materials designed for structured delivery of explicit vocabulary instruction over six weeks. Types of materials include: * Teacher lesson cards: Step-by-step guidance for instruction, including pre-teaching of vocabulary, purpose-setting for reading, read-aloud prompts, comprehension checks, and closing activities. * Student reading passages: Thematic texts that embed target vocabulary words in context. * Vocabulary cards: Word-by-word instructional supports including (a) the focal word, (b) child-friendly definitions, (c) contextual examples, (d) visual supports (images), and (e) oral repetition prompts. * Vocabulary review cards: Summative review prompts with definitions, images, and opportunities for repetition and extension questions.

Background: Acute kidney injury (AKI) causes rapid loss of renal function and leads to high morbidity and mortality. Our previous research has shown that neuronal nitric oxide synthase (NOS1) influences nitric oxide (NO)-mediated dilation of the afferent arteriole, thereby inhibiting tubuloglomerular feedback (TGF), which plays a critical role in glomerular filtration rate (GFR). Methods: We generated inducible macula densa–specific NOS1 knockout mice (NKCC2-Cre- NOS1 flox/flox) and introduced AKI by 18 min bilateral renal ischemia at 37 °C, followed by 48 h reperfusion. The kidney injury was assessed by measuring GFR, plasma creatinine, histology, cytokines, apoptosis, fibrotic factors, and proteomics. Results: Deletion of NOS1 was confirmed through immunofluorescence double staining of NKCC2 and NOS1. The results showed that crossing NKCC2 cre line with NOS1 flox line induces a complete deletion of NOS1 from the macula densa cells. In response to IR-AKI, compared with wild-type controls, NOS1 knockouts showed a dramatic GFR decline (236 ± 66 to 24 ± 22 µL/min) and elevated creatinine, alongside more severe tubular damages evidenced by H&E staining. Cytokine array analysis showed chemokines such as MCP-1, CXCL1 and macrophage marker CD68 were significantly increased; Western blot analysis showed cleaved caspase-3 levels were significantly increased, indicating enhanced apoptosis. Additionally, fibrosis markers TIMP1, collagen-3, and α-SMA were significantly upregulated at both mRNA and protein levels. We further observed increased hypoxia marker HIF-1α in MD-NOS1 KO mice. Global label-free proteomic profiling with targeted validation identified genotype-dependent responses involving haptoglobin, Tacstd2, and Cyp20a1, linking NOS1 deficiency to exaggerated inflammatory, fibrotic, and metabolic pathways. Conclusions: These findings highlight a novel role of NOS1 in AKI pathophysiology and suggest targeting NOS1 could be a therapeutic strategy to mitigate AKI severity, identified Hp as a downstream plasma signal of NOS1-dependent AKI responses, suggesting potential translational value pending human validation. 

The raw data of research article "ACSL3 is a promising therapeutic target for alleviating anxiety and depression in Alzheimer's disease"

The NSF 3D Wetlands project produced 2-meter spatial resolution maps of elevation and habitat cover for all states bordering the Gulf of (Mexico||America). A Digital Elevation Model (DEM) was generated from a compilation of LiDAR datasets. Habitat cover was generated using a machine learning model run on MAXA Worldview 2 and 3 multiband imagery.

This dataset contains the data that corresponds to the information included in 'Ampicillin- and Multidrug-Resistant Escherichia coli and Enterococcus spp. in Costa Rican Wastewater and Surface Water' (in review). The data include measurements of concentrations of total and ampicillin-resistant fecal indicator bacteria (E. coli and enterococci) from four sites in and near a wastewater treatment plant in Puntarenas, Costa Rica. The four sites at which samples were collected were the influent from hospital wastewater, influent from residential wastewater, treated wastewater effluent, and the estuary in which treated effluent is discharged. Frequency of ampicillin resistance is recorded, and ampicillin-resistant isolates were confirmed to species or genus before further testing. Multidrug resistance testing was conducted via the Kirby Bauer assay, and the zones of inhibition for each isolate, as well as the interpretation (resistant, intermediate, and sensitive), are provided. Samples were collected from each site during four sampling events from October to November 2019.

iSALE configuration files, collected data, and plotting means for the mesoscale models

Our real-world data from 96 patients confirms that abrocitinib induces rapid clinical improvement and broadly downregulates genes in cytokine and JAK-STAT signaling pathways. We also identified that patients achieving EASI-90 response had a distinct baseline profile characterized by lower Th2 cytokines and a specific transcriptomic signature of high WNT8B and low TTLL13p and KRT2 expression. This signature was validated as a predictive biomarker in an independent cohort, suggesting it can be used to stratify patients for a higher likelihood of achieving minimal disease activity with abrocitinib.