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Cardiac lymphangiogenesis plays an important physiological role in the regulation of interstitial fluid homeostasis, inflammatory, and immune responses. Impaired or excessive cardiac lymphatic remodeling and insufficient lymph drainage have been implicated in several cardiovascular diseases including atherosclerosis and myocardial infarction (MI). Although the molecular mechanisms underlying the regulation of functional lymphatics are not fully understood, the interplay between lymphangiogenesis and immune regulation has recently been explored in relation to the initiation and development of these diseases. In this field, experimental therapeutic strategies targeting lymphangiogenesis have shown promise by reducing myocardial inflammation, edema and fibrosis, and improving cardiac function. On the other hand, however, whether lymphangiogenesis is beneficial or detrimental to cardiac transplant survival remains controversial. In the light of recent evidence, cardiac lymphangiogenesis, a thriving and challenging field has been summarized and discussed, which may improve our knowledge in the pathogenesis of cardiovascular diseases and transplant biology.

The lymphatic system provides important functions for tissue fluid homeostasis and immune response. Lymphangiogenesis, the formation of new lymphatics, comprises a series of complex cellular events in vitro or in vivo, e.g., proliferation, differentiation, and sprouting. Recent evidence has implied that macrophages act as a direct structural contributor to lymphatic endothelial walls or secret VEGF-C/-D and VEGF-A to initiate lymphangiogenesis in inflamed or tumor tissues. Bone marrow-derived macrophages are versatile cells that express different functional programs in response to exposure to microenvironmental signals, and can be identified by specific expression of a number of proteins, F4/80, CD11b, and CD68. Several causative factors, e.g., NF-κB, IL-1β, TNF-α, SDF-1, M-CSF, especially TonEBP/VEGF-C signaling, may be actively involved in macrophage-induced lymphangiogenesis. Alteration of macrophage phenotype and function has a profound effect on the development and progression of inflammation and malignancy, and macrophage depletion for controlling lymphangiogenesis may provide a novel approach for prevention and treatment of lymphatic-associated diseases.

Background The emergence of the novel, pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a global health emergency. SARS-CoV-2 is highly contagious and has a high mortality rate in severe patients. However, there is very limited information on the effect of SARS-CoV-2 infection on the integrity of the blood–brain barrier (BBB). Methods RNA-sequencing profiling was performed to analyze the transcriptomic changes in human brain microvascular endothelial cells (hBMECs) after SARS-CoV-2 infection. Bioinformatic tools were used for differential analysis. Immunofluorescence, real-time quantitative PCR, and Western blotting analysis were used to explore biological phenotypes. Results A total of 927 differentially expressed genes were identified, 610 of which were significantly upregulated while the remaining 317 were downregulated. We verified the significant induction of cytokines, chemokines, and adhesion molecules in hBMECs by SARS-CoV-2, suggesting an activation of the vascular endothelium in brain. Moreover, we demonstrated that SARS-CoV-2 infection could increase the BBB permeability, by downregulating as well as remodeling the intercellular tight junction proteins. Conclusions Our findings demonstrated that SARS-CoV-2 infection can cause BBB dysfunction, providing novel insights into the understanding of SARS-CoV-2 neuropathogenesis. Moreover, this finding shall constitute a new approach for future prevention and treatment of SARS-CoV-2-induced CNS infection.

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome that elevates the risk of hepatocellular carcinoma (HCC). Although alteration of lipid metabolism has been increasingly recognized as a hallmark of cancer cells, the deregulated metabolic modulation of HCC cells in the NAFLD progression remains obscure. Here, we discovers an endoplasmic reticulum-residential protein, Nogo-B, as a highly expressed metabolic modulator in both murine and human NAFLD-associated HCCs, which accelerates high-fat, high-carbohydrate diet-induced metabolic dysfunction and tumorigenicity. Mechanistically, CD36-mediated oxLDL uptake triggers CEBPβ expression to directly upregulate Nogo-B, which interacts with ATG5 to promote lipophagy leading to lysophosphatidic acid-enhanced YAP oncogenic activity. This CD36-Nogo-B-YAP pathway consequently reprograms oxLDL metabolism and induces carcinogenetic signaling for NAFLD-associated HCCs. Targeting the Nogo-B pathway may represent a therapeutic strategy for HCC arising from the metabolic syndrome. Non alcoholic fatty liver disease (NAFLD) associates with an elevated risk of developing hepatocellular carcinoma (HCC). Here, the authors find that Nogo-B, an endoplasmic reticulum resident protein, is upregulated by lipid uptake and acts as an oncogene in NAFLD-associated HCC by promoting lipid droplet breakdown by lipophagy and triggering Hippo pathway dysregulation

We systematically investigate the mass spectrum and two-body open-charm strong decays of charmonium states in a coupled-channel model where the 3 P 0 quark-antiquark pair creation mechanism is employed. The results of masses, mass shifts, proportions of the c c ¯ component, and open-charm decay widths are provided. The S - D wave mixing angles and di-electric decay widths for vector mesons are also presented. Based on our results, we find that the ψ ( 3770 ) , ψ ( 4040 ) , ψ ( 4160 ) , ψ ( 4360 ) , and ψ ( 4415 ) can be assigned as the 1 3 D 1 -, 3 3 S 1 -, 2 3 D 1 -, 4 3 S 1 -, and 3 3 D 1 -dominated charmonium states, respectively. The ψ 3 ( 3842 ) is a good candidate of the ψ 3 ( 1 D ) charmonium state. The calculated mass and strong decay width of χ c 1 ( 2 P ) with significant continuum contribution ( ∼ 57%) favor the charmonium interpretation for the mysterious χ c 1 ( 3872 ) . When considering the large uncertainty in the observed decay width, the possibility to assign the χ c 0 ( 3860 ) as the χ c 0 ( 2 P ) charmonium state cannot be ruled out. One may describe well the properties of χ c 2 ( 3930 ) with the χ c 2 ( 2 P ) charmonium. The predictions on properties of other c c ¯ states can be tested by future experiments.

Osteoarthritis (OA) is a chronic, degenerative joint disease presenting a significant global health threat. While current therapeutic approaches primarily target symptom relief, their efficacy in repairing joint damage remains limited. Recent research has highlighted mesenchymal stem cells (MSCs) as potential contributors to cartilage repair, anti-inflammatory modulation, and immune regulation in OA patients. Notably, MSCs from different sources and their derivatives exhibit variations in their effectiveness in treating OA. Moreover, pretreatment and gene editing techniques of MSCs can enhance their therapeutic outcomes in OA. Additionally, the combination of novel biomaterials with MSCs has shown promise in facilitating the repair of damaged cartilage. This review summarizes recent studies on the role of MSCs in the treatment of OA, delving into their advantages and exploring potential directions for development, with the aim of providing fresh insights for future research in this critical field.

Chemical reduction of graphene oxide can be used to produce large quantities of reduced graphene oxide for potential application in electronics, optoelectronics, composite materials and energy-storage devices. Here we report a highly efficient one-pot reduction of graphene oxide using a sodium-ammonia solution as the reducing agent. The solvated electrons in sodium-ammonia solution can effectively facilitate the de-oxygenation of graphene oxide and the restoration of π-conjugation to produce reduced graphene oxide samples with an oxygen content of 5.6 wt%. Electrical characterization of single reduced graphene oxide flakes demonstrates a high hole mobility of 123 cm 2  Vs −1 . In addition, we show that the pre-formed graphene oxide thin film can be directly reduced to form reduced graphene oxide film with a combined low sheet resistance (~350 Ω per square with ~80% transmittance). Our study demonstrates a new, low-temperature solution processing approach to high-quality graphene materials with lowest sheet resistance and highest carrier mobility. The chemical reduction of graphene oxide can provide large quantities of reduced graphene oxide for potential application in electronics and composite materials. Feng et al . report a highly efficient low-temperature one-pot reduction of graphene oxide that uses sodium-ammonia solution as the reducing agent.

Growth-induced pattern formations in curved film-substrate structures have attracted extensive attention recently. In most existing literature, the growth tensor is assumed to be homogeneous or piecewise homogeneous. In this paper, we aim at clarifying the influence of a growth gradient on pattern formation and pattern evolution in bilayered tubular tissues under plane-strain deformation. In the framework of finite elasticity, a bifurcation condition is derived for a general material model and a generic growth function. Then we suppose that both layers are composed of neo-Hookean materials. In particular, the growth function is assumed to decay linearly either from the inner surface or from the outer surface. It is found that a gradient in the growth has a weak effect on the critical state, compared with the homogeneous growth type where both layers share the same growth factor. Furthermore, a finite-element model is built to validate the theoretical model and to investigate the post-buckling behaviours. It is found that the associated pattern transition is not controlled by the growth gradient but by the ratio of the shear modulus between two layers. Different morphologies can occur when the modulus ratio is varied. The current analysis could provide useful insight into the influence of a growth gradient on surface instabilities and suggests that a homogeneous growth field may provide a good approximation on interpreting complicated morphological formations in multiple systems.

Lymphatic vessels are a kind of heterogeneous and versatile component of the lymphatic system, with a unique ability to respond to environmental changes in different organs. The heterogeneity and plasticity of lymphatic endothelial cells (LECs) and defective lymphatic architecture are critical for organ-specific lymphatic function. Moreover, lymphatic vessels have a dual effect on tumor microenvironment (TME), and lymphangiogenesis, an active and dynamic player, is a hallmark of cancer progression and treatment resistance. Dysregulation of lymphatic vessels and uncontrolled lymphangiogenesis contribute to the pathogenesis of many diseases, including cancer. Increasing evidence has indicated that lymphangiogenesis provides a critical target for inhibiting lymphatic metastasis, in which immune checkpoint inhibitors, either alone or combined with chemotherapy, may have a therapeutic value. This article reviews the current status of tumor-associated lymphangiogenesis and lymphatic remodeling, as well as the crosstalk among LECs, immune cells and cancer cells, which will help to further understand the role of lymphangiogenesis in cancer progression, metastasis, and therapy.

Abstract TianQin is a planned space-based gravitational wave (GW) observatory consisting of three Earth-orbiting satellites with an orbital radius of about $10^5 \\, {\\rm km}$. The satellites will form an equilateral triangle constellation the plane of which is nearly perpendicular to the ecliptic plane. TianQin aims to detect GWs between $10^{-4} \\, {\\rm Hz}$ and $1 \\, {\\rm Hz}$ that can be generated by a wide variety of important astrophysical and cosmological sources, including the inspiral of Galactic ultra-compact binaries, the inspiral of stellar-mass black hole binaries, extreme mass ratio inspirals, the merger of massive black hole binaries, and possibly the energetic processes in the very early universe and exotic sources such as cosmic strings. In order to start science operations around 2035, a roadmap called the 0123 plan is being used to bring the key technologies of TianQin to maturity, supported by the construction of a series of research facilities on the ground. Two major projects of the 0123 plan are being carried out. In this process, the team has created a new-generation $17 \\, {\\rm cm}$ single-body hollow corner-cube retro-reflector which was launched with the QueQiao satellite on 21 May 2018; a new laser-ranging station equipped with a $1.2 \\, {\\rm m}$ telescope has been constructed and the station has successfully ranged to all five retro-reflectors on the Moon; and the TianQin-1 experimental satellite was launched on 20 December 2019—the first-round result shows that the satellite has exceeded all of its mission requirements.