"seeing" ENF From Neuromorphic Events: Modeling and Robust Estimation.

Most artificial lights exhibit subtle fluctuations in intensity and frequency in response to the influence of the grid's alternating current, providing the potential to estimate the Electric Network Frequency (ENF) from conventional frame-based videos. Nevertheless, the performance of Video-based ENF (V-ENF) estimation largely relies on the imaging quality and thus may suffer from significant interference caused by non-ideal sampling, scene diversity, motion interference, and extreme lighting conditions. In this paper, we show that the ENF can be extracted without the above limitations from a new modality provided by the so-called event camera, a neuromorphic sensor that encodes the light intensity variations and asynchronously emits events with extremely high temporal resolution and high dynamic range. Specifically, we formulate and validate the physical mechanism for the ENF captured in events and then propose a simple yet robust Event-based ENF (E-ENF) estimation method through mode filtering and harmonic enhancement. To validate the effectiveness, we build the first Event-Video ENF Dataset (EV-ENFD) and its extension EV-ENFD+ with diverse scenarios, including static, dynamic, and extreme lighting scenes. Comprehensive experiments have been conducted on our proposed datasets, showcasing that our proposed E-ENF significantly outperforms the V-ENF in extracting accurate ENF traces, especially in challenging environments. The code and dataset are available at https://xlx-creater.github.io/Improved_E-ENF/.

Effect of Ursodeoxycholic Acid on Preventing SARS-CoV-2 Infection in Patients With Liver Transplantation: a multicenter retrospective cohort study.

BACKGROUND: Immunosuppressed recipients of liver transplantation (LT) are more likely to develop coronavirus disease 2019 (COVID-19) and may have an increased risk of developing worse outcomes. AIM: To assess the effect of ursodeoxycholic acid (UDCA) on preventing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in LT recipients. DESIGN: Adult patients (aged ≥ 18 years) who underwent LT between January 1st, 2015, and December 31st, 2022, were included and categorized into two groups according to their use of UDCA. METHODS: The prevalence and severity of COVID-19 among transplantation patients between the UDCA and non-UDCA groups were estimated and compared. RESULTS: Among the 897 LT patients who met the inclusion criteria, infection rate of SARS-CoV-2 was 78.4%, and the rate of severe illness was 5.1% from January 2022 to January 2023 in China. In the multivariate analysis, only UDCA treatment (P = 0.006) was found to be a protective factor against SARS-CoV-2 infection. After propensity score matching, the SARS-CoV-2 infection rate in the UDCA group was lower than that in the non-UDCA group (74.1% vs. 84.6%, P = 0.002). This rate was further reduced to 62.1% (P = 0.002) when the oral administration dose was greater than 15 mg/kg/d. There was no difference in the rates of severe COVID-19 illness, ICU admission, or ventilation rate or length of hospital stay with or without UDCA treatment (all P > 0.05). CONCLUSIONS: The use of UDCA in LT patients significantly reduced the SARS-CoV-2 infection rate and showed a dose-dependent protective effect.

Immunogenic necroptosis in liver diseases: mechanisms and therapeutic potential.

Necroptosis has received increasing attention and is extensively studied as a recently discovered mode of cell death distinct from necrosis and apoptosis. It is a programmed cell death with a necrotic morphology that occurs in various biological processes, including inflammation, immune response, embryonic development, and metabolic abnormalities. Necroptosis is indispensable in maintaining tissue homeostasis in vivo and closely correlates with the occurrence and development of various diseases. First, we outlined the etiology of necroptosis and how it affects the onset and development of prevalent liver diseases in this review. Additionally, we reviewed the therapeutic strategy by targeting the necroptosis pathway in related liver diseases. We conclude that the necroptosis signaling pathway is critical in the physiological control of liver diseases' onset, progression, and prognosis. It will likely be used as a therapeutic target in the future. Further research is required to determine the mechanisms governing the necroptosis signaling pathway and the effector molecules.

Systemic Mutation of Ncf1 Ameliorates Obstruction-Induced Renal Fibrosis While Macrophage-Rescued NCF1 Further Alleviates Renal Fibrosis.

Aims: NCF1, a subunit of the NADPH oxidase 2 (NOX2), first described the expression in neutrophils and macrophages and participated in the pathogenesis from various systems. However, there are controversial findings on the role of NCF1 in different kinds of kidney diseases. In this study, we aim to pinpoint the specific role of NCF1 in the progression of renal fibrosis induced by obstruction. Results: In this study, NCF1 expression was upregulated in kidney biopsies of chronic kidney disease patients. The expression level of all subunits of the NOX2 complex was also significantly increased in the unilateral ureteral obstruction (UUO) kidney. Then, we used wild-type mice and Ncf1 mutant mice (Ncf1m1j mice) to perform UUO-induced renal fibrosis. Results demonstrated that Ncf1m1j mice exhibited mild renal fibrosis but increased macrophages count and CD11b+Ly6Chi macrophage proportion. Next, we compared the renal fibrosis degree between Ncf1m1j mice and Ncf1 macrophage-rescued mice (Ncf1m1j.Ncf1Tg-CD68 mice). We found that rescuing NCF1 expression in macrophages further alleviated renal fibrosis and decreased macrophage infiltration in the UUO kidney. In addition, flow cytometry data showed fewer CD11b+Ly6Chi macrophages in the kidney of the Ncf1m1j.Ncf1Tg-CD68 group than the Ncf1m1j group. Innovation: We first used the Ncf1m1j mice and Ncf1m1j.Ncf1Tg-CD68 mice to detect the role of NCF1 in the pathological process of renal fibrosis induced by obstruction. Also, we found that NCF1 expressed in different cell types exerts opposing effects on obstructive nephropathy. Conclusion: Taken together, our findings support that systemic mutation of Ncf1 ameliorates renal fibrosis induced by obstruction, and rescuing NCF1 in macrophages further alleviates renal fibrosis.