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Background Systemic lupus erythematosus (SLE) is a typical chronic immune disorder with clinical heterogeneity. The systemic abnormal immune response not only challenges the diagnosis and treatment of the disease itself but also the secondary antiphospholipid syndrome (APS), characterized by recurrent arterial or venous thrombosis, recurrent spontaneous abortion, or stillbirth. Clinical interest has primarily focused on primary APS’s pathological and clinical features. However, differences in clinical features and laboratory indicators between SLE with or without APS are still lacking, especially differences between circulating lymphocytes, which are critical in the pathogenesis of SLE and its complications. Methods In this retrospective study, we collected and analyzed clinical characteristics, general laboratory indicators, immunological indicators, and circulating lymphocyte subsets of SLE with or without APS. Results Systemic lupus erythematosus with APS (SLE-APS) had elevated SLEDAI scores, hospitalization costs and time, and frequencies of central nervous system symptoms and spontaneous abortion compared with those without APS. SLE-APS had higher positive anti-Cardiolipin antibodies, anti-β2 Glycoprotein 1 antibodies, and perinuclear antineutrophil cytoplasmic antibody (pANCA) than none-APS patients. Compared with healthy controls (HCs), the circulating lymphocyte subsets were altered to some extent in all patients, especially in patients with SLE-APS. Reduced Tregs and positive pANCA were independent risk factors for SLE secondary APS. Conclusion The present study revealed a robust association between APS secondary to SLE and reduced Tregs and positive pANCA, which provides essential information regarding the diagnosis and therapeutic possibilities of APS secondary to SLE.

In order to solve the problem of fast identification of the noise source of rotating machinery, the time-space complex envelope model of monopole sound source is studied, and a modulation method of the complex envelope is proposed. A method combining near-field acoustic holography technology and complex envelope information is proposed to reconstruct the sound field and realize the identification of rotating machinery noise sources. Using the overall fluctuation of the signal to identify the noise source of the rotating machinery greatly reduces the amount of calculation, and speeds up the positioning speed while ensuring the positioning accuracy. According to the sound field radiation characteristics of rotating machinery noise, different measurement distances, different sampling points numbers and different reconstruction distances are selected to reconstruct the sound field. The simulation data analysis results show that the near-field acoustic holography technology can still obtain high sound field reconstruction accuracy under the condition of large reconstruction distance, and does not require high sampling points numbers. Using the envelope information extracted by envelope modulation technology to reconstruct the sound field can accurately identify the number and geometric distribution of sound sources. This technology not only speeds up data processing, but also ensures the accuracy of sound field reconstruction. &nbsp

A polymer acceptor PY-DF was developed by incorporating difluorothiophenes as linking units. The resulting all-PSCs obtained the best PCE (15.7%) with both enhanced VOC (0.97 V) and JSC (23.1 mA cm−2) simultaneously.

Myocardial ischemia/reperfusion (I/R) injury is associated with the poor outcome and higher mortality after myocardial infarction. Recent studies have revealed that miR-199a-5p participates in the process of myocardial I/R injury, but the precise roles and molecular mechanisms of miR-199a-5p in myocardial I/R injury remain not well-studied. Ferroptosis has been proposed to promote cardiomyocyte death, closely associated with myocardial I/R injury. Herein, the present study aimed to explore the function and mechanisms by which miR-199a-5p regulates whether miR-199a-5p contributes to ferroptosis-induced cardiomyocyte death responding to oxygen-glucose deprivation/reoxygenation (OGD/R) injury, an in vitro model of myocardial I/R injury focusing on Akt/eNOS signaling pathway. The results found that ferroptosis-induced cardiomyocyte death occurs and is accompanied by an increase in miR-199a-5p level in OGD/R-treated H9c2 cells. MiR-199a-5p inhibitor ameliorated ferroptosis-induced cardiomyocyte death as evidenced by the increased cell viability, the reduced reactive oxygen species (ROS) generation, lactate dehydrogenase (LDH) activity, malondialdehyde (MDA) and Fe

Micro-/nanorobots (MNRs) can be autonomously propelled on demand in complex biological environments and thus may bring revolutionary changes to biomedicines. Fluorescence has been widely used in real-time imaging, chemo-/biosensing, and photo-(chemo-) therapy. The integration of MNRs with fluorescence generates fluorescent MNRs with unique advantages of optical trackability, on-the-fly environmental sensitivity, and targeting chemo-/photon-induced cytotoxicity. This review provides an up-to-date overview of fluorescent MNRs. After the highlighted elucidation about MNRs of various propulsion mechanisms and the introductory information on fluorescence with emphasis on the fluorescent mechanisms and materials, we systematically illustrate the design and preparation strategies to integrate MNRs with fluorescent substances and their biomedical applications in imaging-guided drug delivery, intelligent on-the-fly sensing and photo-(chemo-) therapy. In the end, we summarize the main challenges and provide an outlook on the future directions of fluorescent MNRs. This work is expected to attract and inspire researchers from different communities to advance the creation and practical application of fluorescent MNRs on a broad horizon.

Idiopathic pulmonary fibrosis (IPF) is the most common chronic interstitial lung disease and is characterized by progressive scarring of the lung. Transforming growth factor-β (TGF-β) signaling plays an essential role in IPF and drives fibroblast to myofibroblast transition (FMT). Dedicator of cytokinesis 2 (DOCK2) is known to regulate diverse immune functions by activating Rac and has been recently implicated in pleural fibrosis. We now report a novel role of DOCK2 in pulmonary fibrosis development by mediating FMT. In primary normal and IPF human lung fibroblasts (HLFs), TGF-β induced DOCK2 expression concurrent with FMT markers, smooth muscle α-actin (α-SMA), collagen-1, and fibronectin. Knockdown of DOCK2 significantly attenuated TGF-β-induced expression of these FMT markers. In addition, we found that the upregulation of DOCK2 by TGF-β is dependent on both Smad3 and ERK pathways as their respective inhibitors blocked TGF-β-mediated induction. TGF-β also stabilized DOCK2 protein, which contributes to increased DOCK2 expression. In addition, DOCK2 was also dramatically induced in the lungs of patients with IPF and in bleomycin, and TGF-β induced pulmonary fibrosis in C57BL/6 mice. Furthermore, increased lung DOCK2 expression colocalized with the FMT marker α-SMA in the bleomycin-induced pulmonary fibrosis model, implicating DOCK2 in the regulation of lung fibroblast phenotypic changes. Importantly, DOCK2 deficiency also attenuated bleomycin-induced pulmonary fibrosis and α-SMA expression. Taken together, our study demonstrates a novel role of DOCK2 in pulmonary fibrosis by modulating FMT and suggests that targeting DOCK2 may present a potential therapeutic strategy for the prevention or treatment of IPF.

Background: Abdominal aortic aneurysm (AAA) is a potentially lethal disease that lacks pharmacological treatment. Degradation of extracellular matrix proteins, especially elastin laminae, is the hallmark for AAA development. DOCK2 (dedicator of cytokinesis 2) has shown proinflammatory effects in several inflammatory diseases and acts as a novel mediator for vascular remodeling. However, the role of DOCK2 in AAA formation remains unknown. Methods: Ang II (angiotensin II) infusion of ApoE −/− (apolipoprotein E deficient) mouse and topical elastase-induced AAA combined with DOCK2 −/− (DOCK2 knockout) mouse models were used to study DOCK2 function in AAA formation/dissection. The relevance of DOCK2 to human AAA was examined using human aneurysm specimens. Elastin fragmentation in AAA lesion was observed by elastin staining. Elastin-degrading enzyme MMP (matrix metalloproteinase) activity was measured by in situ zymography. Results: DOCK2 was robustly upregulated in AAA lesion of Ang II–infused ApoE −/− mice, elastase-treated mice, as well as human AAA lesions. DOCK2 −/− significantly attenuated the Ang II–induced AAA formation/dissection or rupture in mice along with reduction of MCP-1 (monocyte chemoattractant protein-1) and MMP expression and activity. Accordingly, the elastin fragmentation observed in ApoE −/− mouse aorta infused with Ang II and elastase-treated aorta was significantly attenuated by DOCK2 deficiency. Moreover, DOCK2 −/− decreased the prevalence and severity of aneurysm formation, as well as the elastin degradation observed in the topical elastase model. Conclusions: Our results indicate that DOCK2 is a novel regulator for AAA formation. DOCK2 regulates AAA development by promoting MCP-1 and MMP2 expression to incite vascular inflammation and elastin degradation.