Multi-modal Machine Learning for Vehicle Rating Predictions Using Image, Text, and Parametric Data

Accurate vehicle rating prediction can facilitate designing and configuring good vehicles. This prediction allows vehicle designers and manufacturers to optimize and improve their designs in a timely manner, enhance their product performance, and effectively attract consumers. However, most of the existing data-driven methods rely on data from a single mode, e.g., text, image, or parametric data, which results in a limited and incomplete exploration of the available information. These methods lack comprehensive analyses and exploration of data from multiple modes, which probably leads to inaccurate conclusions and hinders progress in this field. To overcome this limitation, we propose a multi-modal learning model for more comprehensive and accurate vehicle rating predictions. Specifically, the model simultaneously learns features from the parametric specifications, text descriptions, and images of vehicles to predict five vehicle rating scores, including the total score, critics score, performance score, safety score, and interior score. We compare the multi-modal learning model to the corresponding unimodal models and find that the multi-modal model's explanatory power is 4% - 12% higher than that of the unimodal models. On this basis, we conduct sensitivity analyses using SHAP to interpret our model and provide design and optimization directions to designers and manufacturers. Our study underscores the importance of the data-driven multi-modal learning approach for vehicle design, evaluation, and optimization. We have made the code publicly available at http://decode.mit.edu/projects/vehicleratings/.Comment: The paper submitted to IDETC/CIE2023, the International Design Engineering Technical Conferences & Computers and Information in Engineering Conference, has been accepte

Overexpression of M3 Muscarinic Receptor Suppressed Adverse Electrical Remodeling in Hypertrophic Myocardium Via Increasing Repolarizing K+ Currents

Background/Aims: Cardiac hypertrophy (CH) is an adaptive response to diverse cardiovascular conditions, which is accompanied by adverse electrical remodeling manifested as abnormal K+ channel activities. M3 subtype of muscarinic acetylcholine receptor (M3-mAChR) is a novel regulator of cardiac electrical activity. In this study we aim to explore if the overexpression of M3-mAChR could attenuate the adverse electrical remodeling in CH and then uncover its underlying electrophysiological mechanisms. Methods: Transgenic mice with M3-mAChR overexpression (M3-TG) and wild type (WT) mice were subjected to transverse aortic constriction (TAC) to induce CH. Myocardial hypertrophy and cardiac function were quantified by the measurement of echocardiography, electrocardiogram, heart weight and tibia length. Whole-cell and signal-cell patch-clamp were employed to record electrophysiological properties by acute isolation of acutely isolated ventricular cardiomyocytes and Western blot was carried out to evaluate the Kir2.1and Kv4.2/4.3 protein levels in left ventricular tissue. Results: Compared with WT group, the elevation of cardiac index, including heart weight/body weight index and heart weight/tibia length index confirmed the myocardial hypertrophic growth induced by TAC. Echocardiography detection revealed that the TAC-treated mice showed an obvious increase in the thickness of left ventricular posterior wall (LVPW) and ejection fraction (EF) due to compensatory hypertrophy, which attenuated by the overexpression of M3-mAChR. Pressure overload induced a prolongation of QTc interval in WT mice, an effect blunted in M3-TG mice. Furthermore, compared with WT mice, M3-mAChR overexpression in hypertrophic myocardium accelerated cardiac repolarization and shortened action potential duration, and thus correcting the prolongation of QTc interval. Moreover, M3-TG mice have the greater current density of IK1 and Ito in ventricular myocytes after TAC compared with WT mice. Finally, compared with WT mice, M3-TG mice expressed higher levels of Kir2.1 in ventricular myocytes. Conclusion: M3-mAChR overexpression protected against adverse electrical remodeling in CH by enhancing potassium currents and promoting repolarization

Choline Inhibits Ischemia-Reperfusion-Induced Cardiomyocyte Autophagy in Rat Myocardium by Activating Akt/mTOR Signaling

Backgroud/Aims: Growing evidence suggests that both cardiomyocyte apoptosis and excessive autophagy exacerbates cardiac dysfunction during myocardial ischemia-reperfusion (IR). As a precursor of acetylcholine, choline has been found to protect the heart by repressing ischemic cardiomyocyte apoptosis. However, the relationship between choline and cardiomyocyte autophagy is unclear. The present study aimed to investigate whether autophagy was involved in the cardioprotection of choline during IR. Methods: Rats were subjected to 30 min reversible ischemia by ligation of left anterior descending coronary artery followed by reperfusion for 2 h. Choline (5 mg/kg, i.v.) alone or along with rapamycin (5 mg/ kg, i.p.) were injected 30 min before ischemia. Transmission electron microscopy, hematoxylin and eosin (HE) and TUNEL staining were conducted to evaluate the effect of choline on cardiac apoptosis and autophagy. Protein levels of autophagic markers including LC3, beclin-1 and p62 as well as Akt and mammalian target of rapamycin (mTOR) were examined by Western blotting. Results: Myocardial IR-induced cardiac apoptosis and accumulation of autophagosomes was attenuated by choline. Choline treatment significantly ameliorated myocardial IR-induced autophagic activity characterized by repression of beclin-1 over-activation, the reduction of autophagosomes, the LC3-II/LC3-I ratio, and p62 protein abundance. In addition, IR-induced downregulation of p-Akt/mTOR cascade was increased by choline. However, the above functions of choline were abolished by rapamycin. Conclusion: These findings suggest that choline plays a protective role against myocardial IR injury by inhibiting excessive autophagy, which might be associated with the activation of Akt/mTOR pathway. This study provides new mechanistic understanding of cardioprotective effect of choline and suggests novel potential therapeutic targets for cardiac IR injury

Aloe-Emodin Relieves High-Fat Diet Induced QT Prolongation via MiR-1 Inhibition and IK1 Up-Regulation in Rats

Background/Aims: High-fat diet (HFD) causes cardiac electrical remodeling and increases the risk of ventricular arrhythmias. Aloe-emodin (AE) is an anthraquinone component isolated from rhubarb and has a similar chemical structure with emodin. The protective effect of emodin against cardiac diseases has been reported in the literature. However, the cardioprotective property of AE is still unknown. The present study investigated the effect of AE on HFD-induced QT prolongation in rats. Methods: Adult male Wistar rats were randomly divided into three groups: control, HFD, and AE-treatment groups. Normal diet was given to rats in the control group, high-fat diet was given to rats in HFD and AE-treatment groups for a total of 10 weeks. First, HFD rats and AE-treatment rats were fed with high-fat diet for 4 weeks to establish the HFD model. Serum total cholesterol and triglyceride levels were measured to validate the HFD model. Afterward, AE-treatment rats were intragastrically administered with 100 mg/kg AE each day for 6 weeks. Electrocardiogram monitoring and whole-cell patch-clamp technique were applied to examine cardiac electrical activity, action potential and inward rectifier K+ current (IK1), respectively. Neonatal rat ventricular myocytes (NRVMs) were subjected to cholesterol and/or AE. Protein expression of Kir2.1 was detected by Western blot and miR-1 level was examined by real-time PCR in vivo and in vitro, respectively. Results: In vivo, AE significantly shortened the QT interval, action potential duration at 90% repolarization (APD90) and resting membrane potential (RMP), which were markedly elongated by HFD. AE increased IK1 current and Kir2.1 protein expression which were reduced in HFD rats. Furthermore, AE significantly inhibited pro-arrhythmic miR-1 in the hearts of HFD rats. In vitro, AE decreased miR-1 expression levels resulting in an increase of Kir2.1 protein levels in cholesterol-enriched NRVMs. Conclusions: AE prevents HFD-induced QT prolongation by repressing miR-1 and upregulating its target Kir2.1. These findings suggest a novel pharmacological role of AE in HFD-induced cardiac electrical remodeling

Outer membrane vesicle-associated lipase FtlA enhances cellular invasion and virulence in Francisella tularensis

Francisella tularensis is a highly infectious intracellular pathogen that infects a wide range of host species and causes fatal pneumonic tularemia in humans. ftlA was identified as a potential virulence determinant of the F. tularensis live vaccine strain (LVS) in our previous transposon screen, but its function remained undefined. Here, we show that an unmarked deletion mutant of ftlA was avirulent in a pneumonia mouse model with a severely impaired capacity to infect host cells. Consistent with its sequence homology with GDSL lipase/esterase family proteins, the FtlA protein displayed lipolytic activity in both E. coli and F. tularensis with a preference for relatively short carbon-chain substrates. FtlA thus represents the first F. tularensis lipase to promote bacterial infection of host cells and in vivo fitness. As a cytoplasmic protein, we found that FtlA was secreted into the extracellular environment as a component of outer membrane vesicles (OMVs). Further confocal microscopy analysis revealed that the FtlA-containing OMVs isolated from F. tularensis LVS attached to the host cell membrane. Finally, the OMV-associated FtlA protein complemented the genetic deficiency of the ΔftlA mutant in terms of host cell infection when OMVs purified from the parent strain were co-incubated with the mutant bacteria. These lines of evidence strongly suggest that the FtlA lipase promotes F. tularensis adhesion and internalization by modifying bacterial and/or host molecule(s) when it is secreted as a component of OMVs.Emerging Microbes & Infections (2017) 6, e66; doi:10.1038/emi.2017.53; published online 26 July 201

One-Step Synthesis of Peptide–Gold Nanoclusters with Tunable Fluorescence and Enhanced Gene Delivery Efficiency

In this study, peptide–gold nanoclusters with tunable fluorescence were prepared by a simple “one-pot” method, which were used for gene localization and delivery in vivo to achieve efficient intracellular colocalization, uptake, and transfection. The efficiency of pDNA transfection was up to 70.6%, and there was no obvious cytotoxicity. This study proves that the simple-composition and bio-friendly peptide–gold nanoclusters are promising gene delivery carriers and can provide a powerful theoretical and experimental basis for the application of peptide–metal nanocomplexes in gene delivery and other biomedicine fields

Selective Synthesis of Alkynylated Isoquinolines and Biisoquinolines via Rh^III Catalyzed C–H Activation/1,3-Diyne Strategy

Described herein is a convenient and highly selective synthesis of alkynylated isoquinolines and biisoquinolines from various aryl ketone <i>O</i>-pivaloyloxime derivatives and 1,3-diynes via rhodium-catalyzed C–H bond activation. In this transformations, alkynylated isoquinolines, 3,4′- and 3,3′-biisoquinolines could be obtained respectively through changing the reaction conditions. Mechanistic investigation revealed that the C–H activation of aryl ketone <i>O</i>-pivaloyloxime was the key step to this reaction