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Lubricin, secreted primarily by chondrocytes, plays a critical role in maintaining the function of the cartilage lubrication system. However, both external factors such as friction and internal factors like oxidative stress can disrupt this system, leading to osteoarthritis. Inspired by lubricin, a lubricating nanozyme, that is, Poly‐2‐acrylamide‐2‐methylpropanesulfonic acid sodium salt‐grafted aminofullerene, is developed to restore the cartilage lubrication system using an "In‐Out" strategy. The "Out" aspect involves reducing friction through a combination of hydration lubrication and ball‐bearing lubrication. Simultaneously, the "In" aspect aims to mitigate oxidative stress by reducing free radical, increasing autophagy, and improving the mitochondrial respiratory chain. This results in reduced chondrocyte senescence and increased lubricin production, enhancing the natural lubrication ability of cartilage. Transcriptome sequencing and Western blot results demonstrate that it enhances the functionality of mitochondrial respiratory chain complexes I, III, and V, thereby improving mitochondrial function in chondrocytes. In vitro and in vivo experiments show that the lubricating nanozymes reduce cartilage wear, improve chondrocyte senescence, and mitigate oxidative stress damage, thereby mitigating the progression of osteoarthritis. These findings provide novel insights into treating diseases associated with oxidative stress and frictional damage, such as osteoarthritis, and set the stage for future research and development of therapeutic interventions. [ABSTRACT FROM AUTHOR]

Existing feeder block division methods fail to consider the complementary characteristics and uncertainty between power sources and loads, which result in excessive feeder blocks, low inter-block balance, and significant disparity in net load peak-valley difference. To address these issues, a mediumvoltage feeder block division method that considers the uncertainty and complementary characteristics of sources and loads is proposed. Firstly, based on the probability density characteristics of sources and loads, an uncertainty model of DG output and load demand is established. Secondly, considering the constraints of block maximum load rate and feeder non-crossing, a feeder block division model is established. Additionally, a set of center circles is defined, and based on this, an improved K-means clustering algorithm is proposed. The initial clustering centers based on the center circles is set, and the clustering centers based on the arcs of the center circles corrected. And the weighted distances between power sources and clustering centers are calculated. An algorithm flow for improved K-means clustering feeder block division is designed accordingly. Finally, the case studies show that the result of block division is improved. [ABSTRACT FROM AUTHOR]

Background: China has seen a drastic increase in the incidence of non-tuberculous mycobacteria (NTM) infection, which is a notable public health issue. Due to a lack of reliable epidemiological surveillance information, there is a need to gather accurate epidemiological and surveillance data, which can help clinicians effectively treat NTM patients. Moreover, drug susceptibility testing for NTM is not frequently performed in China. This retrospective study, therefore, determined the prevalence and resistance characteristics of NTM to provide a reference to control the NTM epidemic. Methods: Sputum, alveolar lavage fluid, and other respiratory specimens were collected from 3025 patients with suspected pulmonary tuberculosis attending The Second Affiliated Hospital of Hainan Medical University from January 2014 to December 2021. Strain identification and species distribution of NTM were performed by DNA chip technology and gene sequencing, and the drug resistance of NTM isolates was evaluated by calculating the minimum inhibitory concentration through antimicrobial susceptibility testing for NTM. Results: From 2014 to 2021, 373 strains of NTM were isolated and identified from respiratory specimens of 3025 suspected tuberculosis patients. Except in 2014, NTM-infected patients accounted for more than 10% of suspected tuberculosis patients in other years. The median age of patients with NTM infection was 62.0 years (53.0, 71.0), and the male-to-female ratio among these patients was 0.79:1. Among culture-positive strains, 12.3% (373/3040; 95% CI 11.1– 13.4%) were identified as NTM comprising forty species of NTM. The forty species of NTM included 23 slow-growing mycobacteria (SGM) and 17 rapidly-growing mycobacteria (RGM). Among the NTM isolates, 58.7% (219/373; 95% CI 53.7– 63.7%) were SGM and 41.3% (154/373; 95% CI 36.3– 46.3%) were RGM. M.avium complex(MAC)(41.3%; 95% CI 36.3– 46.3%) and M.abscessus complex (MABC)(33.2%; 95% CI 28.4– 38.0%) were the most frequently detected species, followed by M.simiae Complex (11.8%; 95% CI 8.5– 15.1%), M.fortuitum group (5.1%; 95% CI 2.9– 7.3%), and others. Drug sensitivity test results showed that most of the NTM isolates were susceptible to amikacin and clarithromycin with a drug resistance rate of less than 10%. However, clarithromycin could induce drug resistance, followed by linezolid and moxifloxacin, and their drug resistance rate was less than 50%. Conclusion: During 2014– 2021, the number of NTM isolates detected in the respiratory specimens of the study patients in The Second Affiliated Hospital of Hainan Medical University increased year by year. M. intracellulare is the most common pathogenic NTM species, and there is a high incidence of NTM infection on Hainan Island. Our findings might be of great importance for diagnosing and treating this patient population in Hainan. [ABSTRACT FROM AUTHOR]

Diffuse large B cell lymphoma (DLBCL), a heterogeneous group of invasive disease, is the most common type of B-cell non-Hodgkin's lymphomas. The mechanism of its development is closely related to the constitutive activation of NF-κB. In this study, we investigated the function and the mechanism of β-TRCP1 in DLBCL. CCK8 and EdU assays showed that β-TRCP1 could promote the growth of DLBCL cells under the stimulation of TNFα. Furthermore, overexpression of β-TRCP1 enhanced NF-κB activation in the presence of TNFα. Moreover, ectopic expression of β-TRCP1 decreased IκB-α expression but increased phospho-p65 expression. In addition, β-TRCP1 promoted cell cycle progression by accelerating G1-S phase transition. We also found that silencing of β-TrCP1 increased mitoxantrone-induced cell growth arrest and apoptosis. Based on these, we proposed that the expression of β-TRCP1 promoted cell proliferation via TNF-dependent NF-κB activation in DLBCL cells. [ABSTRACT FROM AUTHOR]

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