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Accurate state-of-health (SOH) estimation is critical for reliable and safe operation of lithium-ion batteries. However, reliable and stable battery SOH estimation remains challenging due to diverse battery types and operating conditions. In this paper, we propose a physics-informed neural network (PINN) for accurate and stable estimation of battery SOH. Specifically, we model the attributes that affect the battery degradation from the perspective of empirical degradation and state space equations, and utilize neural networks to capture battery degradation dynamics. A general feature extraction method is designed to extract statistical features from a short period of data before the battery is fully charged, enabling our method applicable to different battery types and charge/discharge protocols. Additionally, we generate a comprehensive dataset consisting of 55 lithium-nickel-cobalt-manganese-oxide (NCM) batteries. Combined with three other datasets from different manufacturers, we use a total of 387 batteries with 310,705 samples to validate our method. The mean absolute percentage error (MAPE) is 0.87%. Our proposed PINN has demonstrated remarkable performance in regular experiments, small sample experiments, and transfer experiments when compared to alternative neural networks. This study highlights the promise of physics-informed machine learning for battery degradation modeling and SOH estimation. Reliable lithium-ion battery health assessment is vital for safety. Here, authors present a physics-informed neural network for accurate and stable state-of-health estimation, overcoming challenges of varied battery types and usage conditions.

Prostate-specific membrane antigen (PSMA), a transmembrane glycoprotein located on the cell membrane, is specifically and highly expressed in prostate cancer (PCa). Besides, its expression level is related to tumor invasiveness. As a molecular target of PCa, PSMA has been extensively studied in the past two decades. Currently, a great deal of evidence suggests that significant progresses have been made in the PSMA-targeted therapy of PCa. Herein, different PSMA-targeted therapies for PCa are reviewed, including radioligand therapy (177Lu-PSMA-RLT, 225Ac-PSMA-RLT), antibody-drug conjugates (MLN2704, PSMA-MMAE, MEDI3726), cellular immunotherapy (CAR-T, CAR/NK-92, PSMA-targeted BiTE), photodynamic therapy, imaging-guided surgery (radionuclide-guided surgery, fluorescence-guided surgery, multimodal imaging-guided surgery), and ultrasound-mediated nanobubble destruction.

Hepatocellular carcinoma (HCC) is the most common liver cancer and is highly malignant. Male prevalence and frequent activation of the Ras signaling pathway are distinct characteristics of HCC. However, the underlying mechanisms remain to be elucidated. By exploring Hras12V transgenic mice showing male-biased hepatocarcinogenesis, we performed a high-throughput comparative proteomic analysis based on tandem-mass-tag (TMT) labeling combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS) on the tissue samples obtained from HCC (T) and their paired adjacent precancerous (P) of Hras12V transgenic male and female mice (Ras-Tg) and normal liver (W) of wild-type male and female mice (Non-Tg). The further validation and investigation were performed using quantitative real-time PCR and western blot. Totally, 5193 proteins were quantified, originating from 5733 identified proteins. Finally, 1344 differentially expressed proteins (DEPs) (quantified in all examined samples; |ratios| ≥ 1.5, p < 0.05) were selected for further analysis. Comparison within W, P, and T of males and females indicated that the number of DEPs in males was much higher than that in females. Bioinformatics analyses showed the common and unique cluster-enriched items between sexes, indicating the common and gender-disparate pathways towards HCC. Expression change pattern analysis revealed HCC positive/negative-correlated and ras oncogene positive/negative-correlated DEPs and pathways. In addition, it showed that the ras oncogene gradually and significantly reduced the responses to sex hormones from hepatocytes to hepatoma cells and therefore shrunk the gender disparity between males and females, which may contribute to the cause of the loss of HCC clinical responses to the therapeutic approaches targeting sex hormone pathways. Additionally, gender disparity in the expression levels of key enzymes involved in retinol metabolism and terpenoid backbone/steroid biosynthesis pathways may contribute to male prevalence in hepatocarcinogenesis. Further, the biomarkers, SAA2, Orm2, and Serpina1e, may be sex differences. In conclusion, common and unique DEPs and pathways toward HCC initiated by ras oncogene from sexually dimorphic hepatocytes provide valuable and novel insights into clinical investigation and practice.

Current low‐temperature plasma (LTP) devices essentially use a rare gas source with a short working distance (8 to 20 mm), low gas flow rate (0.12 to 0.3 m3/h), and small effective treatment area (1‐5 cm2), limiting the applications for which LTP can be utilised in clinical therapy. In the present study, a novel type of LTP equipment was developed, having the advantages of a free gas source (surrounding air), long working distance (8 cm), high gas flow rate (10 m3/h), large effective treatment area (20 cm2), and producing an abundance of active substances (NOγ, OH, N2, and O), effectively addressing the shortcomings of current LTP devices. Furthermore, it has been verified that the novel LTP device displays therapeutic efficacy in terms of acceleration of wound healing in normal and Type I diabetic rats, with enhanced wound kinetics, rate of condensation of wound area, and recovery ratio. Cellular and molecular analysis indicated that LTP treatment significantly reduced inflammation and enhanced re‐epithelialization, fibroblast proliferation, deposition of collagen, neovascularization, and expression of TGF‐β, superoxide dismutase, glutathione peroxidase, and catalase in Type I diabetic rats. In conclusion, the novel LTP device provides a convenient and efficient tool for the treatment of clinical wounds.

Purpose Customer misbehavior has a negative impact on frontline employees. However, the underlying mechanisms from customer misbehavior to employees’ negative outcomes need to be further unfolded and examined. This study aims to propose that employees’ affective rumination and problem-solving pondering could be the explanatory processes of customer misbehavior influencing employee attitudes in which coworker support could be a moderator. Design/methodology/approach A mixed-method approach was designed to test this study’s predictions. Study 1 conducted a scenario-based experiment among 215 full-time hospitality employees, and Study 2 used a two-wave, longitudinal survey of 305 participants. Findings The results demonstrate the impact of customer misbehavior on work–family conflict and withdrawal behaviors. The mediating role of affective rumination is supported and coworker support moderates the processes. Practical implications Customer misbehavior leads to negative outcomes among frontline employees both at work and family domains. Hotel managers should help frontline employees to cope with customer misbehavior by avoiding negative affective spillover and providing support properly. Originality/value The studies have unfolded the processes of affective rumination and problem-solving pondering through which customer misbehavior influences work–family conflict and withdrawal behaviors among frontline employees. The surprising findings that coworker support magnified the negative effects have also been discussed.

Prostate cancer is one of the major malignancies that threaten men’s health all over the world. Due to the lack of specific symptoms and signs in the early stage, as well as the limitations of existing detection methods, it is difficult to achieve early diagnosis for prostate cancer. As short single-stranded oligonucleotides (DNA or RNA) with specific 3D structure which can be produced using an in vitro selection process termed systematic evolution of ligands by exponential enrichment (SELEX), aptamers can specifically bind to the corresponding targets. They have become a class of novel targeting ligand for accurate diagnosis and effective treatment of cancer. Owing to distinctive physicochemical features, and some other special properties such as easy modifiability, good biocompatibility, being easily coupled with other ligands, nanomaterials are extensively used in biological medical field research. Enlighteningly, the combination of aptamers with nanomaterials, including metal nanoparticles, nanosilica, quantum dots, and carbon nanomaterials, can enhance the ability of nanomaterials to recognize tumor cells, which is beneficial to overcome the shortcomings such as low sensitivity in early detection and lack of specificity of traditional antineoplastic drugs, thus, clinically helpful to improve the early metaphase diagnosis rate, providing a technical guarantee for the “personalized treatment” strategy for prostate cancer. Herein, we mainly review the basic and applied research of aptamer functionalized nanocomposite in prostate cancer diagnosis and treatment, including biosensing, bioimaging, and cancer therapy, hoping to provide new ideas for prostate cancer diagnosis and treatment.

Magnetic nanomaterials have recently emerged, playing an increasingly essential role in life science and biomedicine fields, and they exhibited promising potentials in cancer diagnosis and therapy. Also, their use as contrast agents improved various cancer diagnostic imaging sensitivities and accuracy. Magnetic nanomaterials are also exploited as targeted drug carriers to increase the sensitivity and reduce the side effects of chemotherapeutic drugs. Herein, we reviewed the preparation, characterization, and surface modification of various magnetic nanomaterials and their cancer diagnosis and therapy applications.

Survey data from 226 service employees were used to test the hypothesized moderating role of chronic self-regulatory focus on the relationships between work–family conflict (WFC) and challenge/hindrance strain. A follow-up scenario-based experiment (N = 93 executives) confirmed the results of the hypothesized model. Results from the two studies together demonstrated the moderating role of self-regulatory processes: chronic promotion-focused individuals perceived WFC as a challenge-type strain, while chronic prevention-focused individuals viewed WFC as a hindrance-type strain. Individuals use self-regulation strategically: in work domains, they regulate themselves so that family does not interfere with work. Individuals’ stress perceptions differ depending on the two dimensions of WFC as they regard interferences from (WIF) as a personal challenge, perhaps affording them an opportunity to balance work and life and to refine their abilities, but interferences from family to work (FIW) act as a barrier preventing them from achieving career success. When two-way interactions between WIF/FIW and chronic promotion/prevention foci were taken into consideration, the WIF/FIW main effects on challenge/hindrance stress became insignificant, suggesting that chronic self-regulation fully moderated the relationship. The results extend the current work–family research by incorporating self-regulatory processes as an important moderating variable, suggesting new research directions. The findings can help human resource management establish policies and benefit programs that take individual differences into account.

Deficiency of γ-glutamyl carboxylation of coagulation factors, as evidenced by the elevated level of Des-γ-carboxyl prothrombin (DCP), is a common feature in hepatocellular carcinoma patients. Additionally, treatment of cancer patients with mTOR inhibitors significantly increases hemorrhagic events. However, the underlying mechanisms remain unknown. In the present study, Vitamin K epoxide reductase complex subunit 1 (VKORC1) was found to be significantly down-regulated in clinical hepatoma tissues and most tested hepatoma cell lines. In vitro investigations showed that VKORC1 expression was promoted by p-mTOR at the translational level and repressed by p-ERK at the transcriptional level. By exploring Hras12V transgenic mice, a hepatic tumor model, VKROC1 was significantly down-regulated in hepatic tumors and showed prolonged activated partial prothrombin time (APTT). In vivo investigations further showed that VKORC1 expression was promoted by p-mTOR and repressed by p-ERK in both hepatoma and hepatocytes. Consistently, APTT and prothrombin time were significantly prolonged under the mTOR inhibitor treatment and significantly shortened under the ERK inhibitor treatment. Conclusively, these findings indicate that mTOR and ERK play crucial roles in controlling VKORC1 expression in both hepatoma and hepatocytes, which provides a valuable molecular basis for preventing hemorrhage in clinical therapies.