Explore the vast range of titles available.

The tight correlations between the masses of supermassive black holes (BHs) and the properties of their host galaxies suggest that BHs co-evolve with galaxies. However, what is the link between BH mass (MBH) and the properties of the host galaxies of active galactic nuclei (AGNs) in the nearby Universe? We measure stellar masses (M*), colours and structural properties for ~11,500 redshift ≤0.35 broad-line AGNs, nearly 40 times more than that in any previous work, as far as we are aware. We find that early-type and late-type AGNs follow a similar MBH–M* relation. The position of AGNs on the MBH–M* plane is connected with the properties of star formation and BH accretion. Our results unveil the evolutionary paths of galaxies on the MBH–M* plane: objects above the relation tend to evolve more horizontally, with substantial M* growth; objects on the relation move along the local relation; and objects below the relation migrate more vertically, with substantial MBH growth. These trajectories suggest that radiative-mode feedback cannot quench the growth of BHs and their host galaxies for AGNs that lie below the relation, while kinetic-mode feedback barely suppresses long-term star formation for AGNs situated above the relation. This work provides important constraints for numerical simulations and offers a framework for studying the cosmic co-evolution of supermassive BHs and their host galaxies.This Article explores the evolutionary paths of galaxies on the black-hole mass–stellar mass plane in the nearby Universe, linking the properties of star formation and black-hole accretion and providing critical constraints for active galactic nuclei feedback.

The management of chronic wounds in diabetes remains challenging due to the complexity of impaired wound healing, delayed healing, susceptibility to infection, and elevated risk of reopening, highlighting the need for effective chronic wound management with innovative approaches such as multifunctional hydrogels. Here, we have produced HA-DA@rhCol hydrogels consisting of dopamine-modified hyaluronic acid and recombinant human collagen type-III (rhCol) by oxidative coupling of the catechol group using the H2O2/HRP catalytic system. The post-reactive hydrogel has a good porous structure, swelling rate, reasonable degradation, rheological and mechanical properties, and the catechol group and dopamine impart to the hydrogel tissue adhesiveness, antioxidant capacity, and excellent photothermal effects leading to superior in vitro antimicrobial activity. In addition, the ability of rhCol to confer hydrogels to promote angiogenesis and wound repair has also been investigated. Cytotoxicity and hemolysis tests demonstrated the good biocompatibility of the hydrogel. Wound closure, collagen deposition and immunohistochemical examination confirmed the ability of the hydrogel to promote diabetic wound healing. In summary, the adhesive hemostatic antioxidative hydrogel with rhCol to promote wound healing in diabetic rat is an excellent chronic wound dressing. [Display omitted] •This hydrogel is formulated by combining dopamine-modified hyaluronic acid and recombinant human collagen type-III (rhCol).•The hydrogel demonstrates tissue adhesiveness, antioxidant capacity, and photothermal effect coupled with antibacterial activity.•The introduction of dopamine enhances the anti-inflammatory effect of hyaluronic acid in diabetic wound.•RhCol promotes angiogenesis in diabetic wound, rendering it a kind of promising bioactive material for chronic wound dressing.

2,3,5,6-Tetramethylpyrazine (TMP) as an active ingredient extracted from a traditional Chinese herbal medicine Ligusticum chuanxiong Hort . has been proved to penetrate blood-brain barrier (BBB) and show neuroprotective effects on cerebral ischemia. However, whether TMP could regulate astrocytic reactivity to facilitate neurovascular restoration in the subacute ischemic stroke needs to be urgently verified. In this research, permanent occlusion of the middle cerebral artery (MCAO) model was conducted and TMP (10, 20, 40 mg/kg) was intraperitoneally administrated to rats once daily for 2 weeks. Neurological function was evaluated by motor deficit score (MDS). Magnetic resonance imaging (MRI) was implemented to analyze tissue injury and cerebral blood flow (CBF). Magnetic resonance angiography (MRA) was applied to exhibit vascular signals. Transmission electron microscopy (TEM) was performed to detect the neurovascular unit (NVU) ultrastructure. Haematoxylin and eosin (HE) staining was utilized to evaluate cerebral histopathological lesions. The neurogenesis, angiogenesis, A1/A2 reactivity, aquaporin 4 (AQP4) and connexin 43 (Cx43) of astrocytes were observed with immunofluorescent staining. Then FGF2/PI3K/AKT signals were measured by western blot. Findings revealed TMP ameliorated neurological functional recovery, preserved NVU integrity, and enhanced endogenous neurogenesis and angiogenesis of rats with subacute ischemia. Shifting A1 to A2 reactivity, suppressing excessive AQP4 and Cx43 expression of astrocytes, and activating FGF2/PI3K/AKT pathway might be potential mechanisms of promoting neurovascular restoration with TMP after ischemic stroke.

In this study, paraffin was selected as the phase change material (PCM) and high-density polyethylene (HDPE) as the supporting material to prepare a flame-retardant PCM system. The system consisted of paraffin, HDPE, expanded graphite (EG), magnesium hydroxide (MH) and aluminum hydroxide (ATH). The thermal stability and flame retardancy were studied by thermo-gravimetric analysis (TGA), scanning electron microscopy (SEM) and cone calorimeter test (CONE). The SEM proved that the addition of MH and ATH can produce an oxide film on the surface of the composite material and form a “physical barrier” with the char layer, generated by the expansion of EG, preventing the transfer of heat and oxygen. The TGA test showed that, compared with other flame-retardant systems, the materials with added MH and ATH have a higher thermal stability and carbonization ability, and the amount of char residue has increased from 17.6% to 32.9%, which reduces the fire risk of the material. The flame retardant effect is obvious. In addition, the addition of MH and ATH has no significant effect on the phase transition temperature and latent heat value of PCMs. The CONE data further confirmed that MH and ATH can work with EG to prevent heat release, reduce the total heat release rate (THR) value and effectively suppress the generation of smoke, CO and CO2. The peak heat release rate (PHRR) value also decreased, from 1570.2 kW/m2 to 655.9 kW/m2.

Ischemic stroke elicits white matter injury typically signed by axonal disintegration and demyelination; thus, the development of white matter reorganization is needed. 2,3,5,6-Tetramethylpyrazine (TMP) is widely used to treat ischemic stroke. This study was aimed to investigate whether TMP could protect the white matter and promote axonal repair after cerebral ischemia. Male Sprague–Dawley rats were subjected to permanent middle cerebral artery occlusion (MCAO) and treated with TMP (10, 20, 40 mg/kg) intraperitoneally for 14 days. The motor function related to gait was evaluated by the gait analysis system. Multiparametric magnetic resonance imaging (MRI) was conducted to noninvasively identify gray-white matter structural integrity, axonal reorganization, and cerebral blood flow (CBF), followed by histological analysis. The expressions of axonal growth-associated protein 43 (GAP-43), synaptophysin (SYN), axonal growth-inhibitory signals, and guidance factors were measured by Western blot. Our results showed TMP reduced infarct volume, relieved gray-white matter damage, promoted axonal remodeling, and restored CBF along the peri-infarct cortex, external capsule, and internal capsule. These MRI findings were confirmed by histopathological data. Moreover, motor function, especially gait impairment, was improved by TMP treatment. Notably, TMP upregulated GAP-43 and SYN and enhanced axonal guidance cues such as Netrin-1/DCC and Slit-2/Robo-1 but downregulated intrinsic growth-inhibitory signals NogoA/NgR/RhoA/ROCK-2. Taken together, our data indicated that TMP facilitated poststroke axonal remodeling and motor functional recovery. Moreover, our findings suggested that TMP restored local CBF, augmented guidance cues, and restrained intrinsic growth-inhibitory signals, all of which might improve the intracerebral microenvironment of ischemic areas and then benefit white matter remodeling.

This paper is concerned with the multivariate stochastic volatility modeling of the stock market. We investigate a DGC-t-MSV model to find the historical volatility spillovers between nine markets, including S&P, Nasdaq, SSE, SZSE, HSI, FTSE, CAC, DAX, and Nikkei indices. We use the Bayesian network to analyze the spreading of herd behavior between nine markets. The main results are as follows: (1) the DGC-t-MSV model we considered is a useful way to estimate the parameter and fit the data well in the stock market; (2) our computational analysis shows that the S&P and Nasdaq have higher volatility spillovers to the Shanghai and Shenzhen stock markets; (3) the results also show that there is a strong correlation between stock markets in the same region.

Cardiopulmonary bypass (CPB) is often used in cardiothoracic surgery because its nonphysiological state causes pathophysiological changes in the body, causing multiorgan and multitissue damage to varying degrees. Postoperative cognitive dysfunction (POCD) is a common central nervous system complication after cardiac surgery. The etiology and mechanism of POCD are not clear. Neuroinflammation, brain mitochondrial dysfunction, cerebral embolism, ischemia, hypoxia, and other factors are related to the pathogenesis of POCD. There is a close relationship between CPB and POCD, as CPB can cause inflammation, hypoxia and reperfusion injury, and microemboli formation, all of which can trigger POCD. POCD increases medical costs, seriously affects patients' quality of life, and increases mortality. Currently, there is a lack of effective treatment methods for POCD. Commonly used methods include preoperative health management, reducing inflammation response during surgery, preventing microemboli formation, and implementing individualized rehabilitation programs after surgery. Strengthening preventive measures can minimize the occurrence of POCD and its adverse effects. Cardiopulmonary bypass (CPB) is used in cardiothoracic surgery and leads to pathophysiological changes in the body, causing multiorgan and multitissue damage and frequently leading to central nervous system complications. Here, we review the latest advances in CPB and postoperative cognitive dysfunction (POCD) in the last 3 years and analyze the pathogenesis, risk factors, detection indexes, and other factors to provide better ideas for healthcare workers to better understand the development of POCD and reduce postoperative cognitive dysfunction in patients undergoing cardiac surgery, ultimately enabling to benefit patients.

Polyetheretherketone (PEEK) is an important material applied in orthopedic applications, as it posses favorable properties for orthopedic implants, e.g., radiolucency and suitable elastic modulus. However, PEEK exhibits insufficient osteogenesis and osteointegration that limits its clinical applications. In this study, we aimed to enhance the osteogenisis of PEEK by using a surface coating approach. Nanocomposite coating composed of albumin/lithium containing bioactive glass nanospheres was fabricated on PEEK through dip-coating method. The presence of nanocomposite coating on PEEK was confirmed by SEM, FTIR, and XRD techniques. Nanocomposite coatings significantly enhanced hydrophilicity and roughness of PEEK. The nanocomposite coatings also enhanced adhesion, proliferation, and osteogenic differentiation of bone mesenchymal stem cells due to the presence of bioactive glass nanospheres and the BSA substrate film. The results indicate the great potential of the nanocomposite coating in enhancing osteogenesis and osteointegration of PEEK implants.

Background/Aims: Long noncoding RNAs (lncRNAs) have been a research hotspot, as they play important roles in tumor development. However, their expression pattern and biological function in osteosarcoma have not yet been clarified. Methods: Differentially expressed lncRNAs in osteosarcoma and paracarcinoma tissues were identified by screening an lncRNA microarray, and candidate lncRNAs were verified by quantitative real-time PCR (qRT-PCR). A series of bioinformatics and molecular biological methods were adopted to investigate the interaction among lncRNA, microRNA (miRNA), and miRNA target genes during the development and occurrence of osteosarcoma. Cell viability was measured using a Cell Counting Kit-8 assay. Results: Chip microarray screening combined with the validation of differentially expressed candidate lncRNAs showed that the lncRNA small nucleolar RNA host gene 16 (SNHG16) had the largest fold change. SNHG16 was highly expressed in osteosarcoma tissues and cell lines, and its downregulation led to the suppressed proliferation of osteosarcoma cells. Further investigations revealed that SNHG16 could upregulate zinc finger E-box-binding homeobox 1 (ZEB1) expression by acting as an endogenous sponge of miR-205. Moreover, rescue assays proved that the effects of SNHG16 on the proliferation of osteosarcoma cells were dependent on miR-205. Conclusion: SNHG16 can significantly enhance the proliferation of osteosarcoma cells. In addition, SNHG16, miR-205, and ZEB1 interact in a common pathway during the development and occurrence of osteosarcoma, providing novel targets for intervention in the treatment of osteosarcoma.

High glucose-regulated protein 78 (GRP78) expression contributes to the acquisition of a wide range of phenotypic cancer hallmarks and the pleiotropic oncogenic functions of GRP78 may result from its diverse subcellular distribution. Interestingly, GRP78 has been reported to be secreted from solid tumour cells, participating in cell-cell communication in the tumour microenvironment. However, the mechanism underlying this secretion remains elusive. Here, we report that GRP78 is secreted from colon cancer cells via exosomes. Histone deacetylase (HDAC) inhibitors blocked GRP78 release by inducing its aggregation in the ER. Mechanistically, HDAC inhibitor treatment suppressed HDAC6 activity and led to increased GRP78 acetylation; acetylated GRP78 then bound to VPS34, a class III phosphoinositide-3 kinase, consequently preventing the sorting of GRP78 into multivesicular bodies (MVBs). Of note, we found that mimicking GRP78 acetylation by substituting the lysine at residue 633, one of the deacetylated sites of HDAC6, with a glutamine resulted in decreased GRP78 secretion and impaired tumour cell growth in vitro . Our study thus reveals a hitherto-unknown mechanism of GRP78 secretion and may also provide implications for the therapeutic use of HDAC inhibitors.