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Knowledge distillation is the process of transferring knowledge from a more powerful large model (teacher) to a simpler counterpart (student). Numerous current approaches involve the student imitating the knowledge of the teacher directly, which tend to learn each spatial location's features indiscriminately. Real-world datasets frequently exhibit noise, motivating models to acquire compact and representative features instead of memorizing every details in the training data. To derive a more compact representation (concept feature) from the teacher, we propose an innovative method, termed Generative Denoise Distillation (GDD), where stochastic noises are added to the concept feature of the student to embed them into the generated instance feature from a shallow network. Then, the generated instance feature is aligned with the knowledge of the instance from the teacher. This process diminishes model redundancy while concurrently augmenting its capacity for generalization. We extensively experiment with object detection, instance segmentation, and semantic segmentation to demonstrate the versatility and effectiveness of our method. Notably, GDD achieves new state-of-the-art performance in the tasks mentioned above. We have achieved substantial improvements in semantic segmentation by enhancing PspNet and DeepLabV3, both of which are based on ResNet-18, resulting in mIoU scores of 74.67 and 77.69, respectively, surpassing their previous scores of 69.85 and 73.20 on the Cityscapes dataset of 20 categories. The code is available at https://github.com/ZhgLiu/GDD. [ABSTRACT FROM AUTHOR]

Point cloud anomaly detection is steadily emerging as a promising research area. Recognizing the importance of feature descriptiveness in this task, this study introduces the Complementary Pseudo Multimodal Feature (CPMF), which combines local geometrical information extracted by 3D handcrafted descriptors with global semantic information extracted from 2D pre-trained neural networks. Specifically, to leverage 2D pre-trained neural networks for point-wise feature extraction, this study projects original point clouds into multi-view images. These images are then fed into a pre-trained 2D neural network for informative 2D modality feature extraction. Following the 2D–3D correspondence, the multi-view 2D modality features are projected back to 3D space and aggregated to obtain point-wise 2D modality features. Finally, the point-wise 3D and 2D modality features are fused to derive the CPMF for point cloud anomaly detection. Extensive experiments conducted on MVTec 3D and Real3D datasets demonstrate the complementary capacity between 2D and 3D modality features and the effectiveness of CPMF. Notably, CPMF achieves a significantly higher object-level AUROC of 95.15% compared to other methods on the MVTec 3D benchmark. Code is available at https://github.com/caoyunkang/CPMF. • Collaboratively unifying local geometric and global semantic cues in point clouds. • Obtaining point-wise semantic point cloud features with pre-trained 2D networks. • Proven the complementation capacity between 3D and 2D modality features. [ABSTRACT FROM AUTHOR]

Prolonged skin exposure to ultraviolet radiation can lead to development of several acute and chronic diseases, with UVA exposure considered a primary cause of dermal photodamage. We prepared a wild ginseng adventitious root extract (ARE) that could alleviate UVA irradiation‐induced NIH‐3T3 cell viability decline. After employing a series of purification methods to isolate main active components of ARE, adventitious root protein mixture (ARP) was identified then tested for protective effects against UVA irradiation‐induced NIH‐3T3 cell damage. The results showed that ARP treatment significantly reduced UVA‐induced cell viability decline and confirmed that the active constituent of ARP was the protein, since proteolytic hydrolysis and heat treatment each eliminated ARP protective activity. Moreover, ARP treatment markedly inhibited UVA‐induced apoptosis, cell cycle arrest and DNA fragmentation, while also significantly reversing UVA effects (elevated Bax levels, reduced Bcl‐2 expression) by reducing Bax levels and increasing Bcl‐2 expression. Mechanistically, ARP promoted Akt phosphorylation regardless of UVA exposure, thus confirming ARP resistance to inactivation by UVA light. Notably, in the presence of Akt inhibitor SC0227, ARP could no longer counteract UVA‐induced cell viability decline and DNA fragmentation. Additionally, our results demonstrated that ARP treatment protected UVA‐irradiated NIH‐3T3 cells by preventing UVA‐induced reduction of collagen‐I expression. Taken together, these results suggest that ARP treatment of NIH‐3T3 cells effectively mitigated UVA‐induced cell viability decline by activating intracellular Akt to reduce UVA‐induced DNA damage, leading to reduced rates of apoptosis and cell cycle arrest after UVA exposure and restoring collagen expression to normal levels. [ABSTRACT FROM AUTHOR]

The visual perception of a moving target is not always true. Wheels turning rapidly, for instance, may look like rotating inversely. This phenomenon is known as the wagon‐wheel effect (WWE) and it is caused by the undersampling of visual information. Here, an analogous manifestation of the WWE concept is described in the scenario of light–matter interactions, by showing that the dynamic response of a particle, to an optical trap scanned at different rates, can be diametrically opposed. Further, such behaviors are modulated by the particle dimensions, which can be exploited for particle size selection. The results uncover a distinct paradigm of nontrivial optical manipulation and expand the bidirectional optical sorting range of dielectric particles to the sub‐200 nm scale. [ABSTRACT FROM AUTHOR]

The intensity gradient of light represents the most important property for optical tweezers to manipulate small particles, which is known to produce a conservative optical force that is either attractive or repulsive. Here, it is shown that Kerker interference, the interplay between electric and magnetic dipoles induced in nanoparticles, permits the intensity gradient to exert a nonconservative optical force, in the case of a standard optical trap created with linearly or elliptically polarized Gaussian beams. The Kerker‐type intensity‐gradient force has an "anisotropic" directionality, and it tends to repel particles away from the beam axis. Such repulsive effects can greatly sensitize the particle trapping behavior of optical tweezers to the particle size. Utilizing these peculiar properties, all‐optical sorting of Si nanoparticles is theoretically demonstrated, with tunable size‐selection criterion and accuracy. [ABSTRACT FROM AUTHOR]

UVA can penetrate dermis and cause functional damage of dermal fibroblasts leading photoaging. Ginseng is a widely used traditional Chinese medicine for skin aging. However, its effects on skin photoaging induced by UVA are not clear. In this study, we isolated ginseng proteins (GP), with molecular weights of 27 kDa and 13 kDa, and found that they alleviated the inhibitory effects of UVA on cell viability and increased percentage of NIH‐3T3 fibroblasts in the S phase of cells cycle. GP also improved cell contraction ability, increased the expression and secretion of CoL‐I, similar to MAPK phosphorylation inhibitors and reduced expression and secretion of MMP‐1, MMP‐2 and MMP‐9 as well as the enzyme activities of MMP‐2 and MMP‐9. They reduced ROS content, DNA damage and 8‐OHdG content, as well as the protein expression of p53, p21 and p16. The levels of p‐ERK, p‐p38 and p‐JNK, p‐c‐Fos and p‐c‐Jun proteins were decreased by GP. Inactivated GP did not inhibit the cellular activity and expression and secretion of CoL‐I irradiated by UVA. The results showed that GP can improve cell viability and contractile function by inhibiting DNA damage and collagen degradation to inhibit the photoaging effects of skin dermal cells caused by UVA. [ABSTRACT FROM AUTHOR]

Panax ginseng C. A. Meyer has been widely used in skin care. Our previous study showed that the phenolic acids in ginseng root extract (GRE) impart inhibitory effects on melanogenesis. In this study, we found that as the most abundant component of phenolic acids in GRE, vanillic acid decreased tyrosinase activity and melanin levels with or without α-MSH stimulation and suppressed the expression of microphthalmia-associated transcription factor (MITF) and melanogenic enzymes in B16F10 cells. Furthermore, vanillic acid downregulated NOS activity, nitric oxide (NO) content, cGMP level, guanylate cyclase (GC) and protein kinase G (PKG) activity, and the phosphorylation of cAMP-response element-binding protein (CREB), whereas arbutin had no effect on the NO/PKG pathway. These findings indicate that vanillic acid in GRE suppressed melanogenesis by inhibiting the NO/PKG signaling pathways. This study provides a potential mechanism underlying the inhibitory effect of ginseng on melanogenesis. Vanillic acid in ginseng root extract inhibits melanogenesis through NO/PKG signaling pathway in B16F10 cells. [ABSTRACT FROM AUTHOR]

Resistance to standard induction therapy and relapse remain the primary challenges for improving therapeutic effects in acute myeloid leukemia (AML); thus, novel therapeutic strategies are urgently required. Ataxia telangiectasia and Rad3-related protein (ATR) is a key regulator of different types of DNA damage, which is crucial for the maintenance of genomic integrity. The ATR-selective inhibitor VE-822 has proper solubility, potency, and pharmacokinetic properties. In this study, we investigated the anti-leukemic effects of VE-822 alone or combined with Wee1-selective inhibitor AZD1775 in AML cells. Our results showed that VE-822 inhibited AML cell proliferation and induced apoptosis in a dose-dependent manner. AZD1775 significantly promoted VE-822-induced inhibition of AML cell proliferation and led to a decreased number of cells in the G2/M phase. VE-822 and AZD1775 decreased the protein levels of ribonucleotide reductase M1 (RRM1) and M2 (RRM2) subunits, key enzymes in the synthesis of deoxyribonucleoside triphosphate, which increased DNA replication stress. VE-822 combined with AZD1775 synergistically induced AML cell apoptosis and led to replication stress and DNA damage in AML cell lines. Our study demonstrated that AZD1775 synergistically promotes VE-822-induced anti-leukemic activity in AML cell lines and provides support for clinical research on VE-822 in combination with AZD1775 for the treatment of AML patients. [ABSTRACT FROM AUTHOR]

The Belinfante spin momentum (BSM) is a fundamental yet enigmatic quantity of electromagnetic fields. It vanishes from the global momentum of the field, but can be detected locally, manifesting itself as an optical force on small particles. Hitherto, however, the BSM force is a concept well established only within the dipole approximation, and there is no explicit experimental evidence for its action on multipoles. Here, a theoretical model for multipolar BSM forces, exerted on generic Mie particles supporting multipoles of arbitrary order, is developed. This multipolar mechanical action is observed experimentally from a structured light field, which suppresses the effect of spin–orbit coupling. It can also selectively enhance the multipolar BSM forces, while restraining the dipolar component on a probe particle (Au sphere). These results constitute a distinct chapter in the physics of high‐order interactions in light–matter systems and can facilitate additional progress in optomechanics, optical manipulation, and Mie‐tronics. [ABSTRACT FROM AUTHOR]

Abstract: With the development of new generation air traffic systems, Performance Based Navigation (PBN), as a part of the new generation air traffic systems, is required by the International Civil Aviation Organization (ICAO) to implement before 2025. In PBN, lateral Flight Technical Error (FTE) estimation is to be done first for the determination of the executable navigation specification among various PBN specifications. However, the estimation of lateral FTE is challenging, as some of the factors of FTE are difficult for quantification, especially for the turbulence disturbance and perturbation. In this paper, based on our previous works on the lateral FTE estimation with turbulence disturbance, we present an extended estimation method that jointly considers the system perturbation. This proposed estimation method can estimate the lateral FTE with both the turbulence disturbance and perturbation through the determination of the maximum perturbation size. To validate the proposed method, numerical simulation is performed for a final approach scenario including turbulence disturbance and system perturbation. Based on the simulation results and the comparison with the statistical data of measured lateral FTE, we can show that the proposed method can effectively estimate the lateral FTE of the perturbed system due to the turbulence disturbance. [Copyright &y& Elsevier]

Intensity-Gradient Force: Kerker-Type Intensity-Gradient Force of Light (Laser Photonics Rev. 14(4)/2020) In article number 1900265 by Yao Zhang and co-workers, a nontrivial optical intensity-gradient force is uncovered in conventional optical tweezers set-ups. Its non-conservative and anisotropic properties are in sharp contrast to the classical widespread picture of optical intensity-gradient forces. [Extracted from the article]

• PBP treatment increased cell viability and decreased the release of LDH in PC12 cells incuded by CORT. • PBP reduced CORT-induced oxidative stress by decreasing ROS levels, increasing SOD, GSH-Px activities and GSH content. • PBP had inhibitory effect on the CORT-induced inflammatory response through inhibition of NF-κB signaling pathway. • PBP inhibited CORT-induced apoptosis by down-regulating mitochondrial apoptotic signaling pathway. Pig brain polypeptides (PBP), active polypeptides hydrolysate extracted from fresh porcine brain tissue, has been shown to have neuroprotective effects in both in vitro and in vivo studies. The present study aimed to explore the molecular mechanisms underlying the neuroprotective effects of PBP in corticosterone (CORT)-induced rat adrenal pheochromocytoma PC12 cells. Cell viability and lactate dehydrogenase (LDH) release were measured in PC12 cells induced with 200 μM CORT in the presence or absence of various concentrations of PBP for 48 h. Intracellular reactive oxygen species (ROS) generation, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and glutathione (GSH) content were examined to analyze the effect of PBP on CORT-induced oxidative stress. The levels of pro-inflammatory factors, the percentage of apoptotic cells, and apoptosis-related protein expression in PC12 cells were determined. PBP is mainly composed of protein subunits with molecular weights ranging from 1000 to 10,000 Da. PBP treatment increased cell viability and decreased the release of LDH in CORT-stimulated PC12 cells. Moreover, PBP reduced the level of CORT-induced oxidative stress by decreasing ROS levels and increasing SOD, GSH-Px activities and GSH content. PBP had an inhibitory effect on the CORT-induced inflammatory response through inhibition of the NF-κB signaling pathway. PBP also inhibited CORT-induced apoptosis by downregulating the mitochondrial apoptotic signaling pathway. These results suggest that PBP exerts a neuroprotective effect against CORT-induced cell injury by inhibiting oxidative stress, inflammation, and apoptosis. PBP could act as a neuroprotective agent against nerve injury induced by CORT. [ABSTRACT FROM AUTHOR]

Spectroscopic analysis of HPLC-purified 7.3-kD Acorus tatarinowii Schott root polysaccharide ASP2-1 (FT-IR, NMR) revealed respective monosaccharide proportions of glucose: galactose: arabinose: xylose: galacturonic acid: mannose: rhamnose: glucuronic acid:fucose of 49.1:16.0:11.6:10.2:5.3:2.9:2.2:1.7:0.8. In vitro, ASP2-1 inhibited osteoclastogenesis-associated bone resorption, RANKL-induced osteoclastogenesis and F-actin ring formation and suppressed osteoclastogenesis-associated gene expression (e.g., TRAP , OSCAR , Atp6v0d2, αV, β3, MMP9 and CtsK) as shown via RT-PCR. ASP2-1-treated RANKL-stimulated bone marrow-derived macrophages exhibited decreased levels of NFATc1 and c-Fos mRNAs and corresponding transcription factor proteins, elevated expression of negative NFATc1 regulators (Mafb , IRF8 , Bcl6) and reduced their upstream negative regulator (Blimp1) expression. ASP2-1 inhibition of NFATc1 expression involved PLCγ2-Ca2+ oscillation-calcineurin axis suppression, reflecting suppression of RANKL-induced PLCγ2 activation (and associated Ca2+ oscillation) and calcineurin catalytic subunit PP2BAα expression without inhibiting NF-κB and MAPKs activation or phosphorylation. Staining (H&E, TRAP) and micro-CT assays revealed ASP2-1 attenuated bone destruction and osteoclast over-activation and improved tibia micro-architecture in a murine LPS-induced bone loss model. Thus, ASP2-1 may alleviate inflammatory bone loss-associated diseases. • A. tatarinowii Schott polysaccharide ASP2-1 was isolated and characterised. • ASP2-1 suppressed osteoclast differentiation and bone resorption induced by RANKL. • ASP2-1 represses PLCγ2-Ca2+ oscillation-calcineurin to reduce NFATc1 expression. • ASP2-1 inhibited Blimp1 signalling. • ASP2-1 was shown to alleviate bone loss in a mouse LPS-induced bone loss model. [ABSTRACT FROM AUTHOR]

Long-wave ultraviolet A (UVA) causes skin aging by damaging the fine structures of the skin, such as elastic fibers and collagen fibers, through oxidation. Currently, the use of plant extracts to protect skin from photoaging is a popular method. Panax ginseng C.A. Meyer exerts commendable anti-photoaging and antioxidant effects. P. ginseng Meyer cv. Silvatica, also known as forest ginseng (FG), is a type of ginseng cultivated by artificially simulating the growth environment of wild ginseng aged >15 years. However, there are only a few reports on its anti-photoaging effect on the skin caused by UVA stimulation. AIM OF THE STUDY: To investigate whether isolated and extracted FG can inhibit skin photoaging as well as to explore its action mechanism. The FG extract (FGE) was obtained from the supernatant of FG after water extraction and alcohol precipitation with the D101 resin. The composition and content of phenolic acids in FGE were determined by high-performance liquid chromatography (HPLC). The MTT assay was performed to detect cell viability. The ratio of SA-β-GAL-positive cells, CoL-I level, 8-OHdG concentration, MDA, GSH, GPx, SOD, and CAT activity were measured using relevant kits. Furthermore, cell cycle alterations and ROS accumulation were assessed by flow cytometry. The expressions of p53, p21, p16, and Keap1 protein were detected by Western blotting. The Nrf2 translocation was monitored by immunofluorescence staining. The findings revealed that FGE significantly restored UVA injury-induced cell viability, reduced the proportion of SA-β-GAL-positive cells, and increased the level of CoL-I secretion in a dose-dependent manner, where the main ingredients were chlorogenic acid, protocatechuic acid, salicylic acid, p-hydroxybenzoic acid, vanillic acid, ferulic acid, and caffeic acid. Further studies indicated that this phenolic acid mixture (PAM) could alleviate UVA-induced HFF-1 cell cycle arrest and protect the DNA from oxidative damage caused by UVA stimulation. Moreover, the expressions of cell cycle regulatory proteins p53, p21, and p16 and the accumulation of ROS were inhibited, the translocation of Nrf2 into the nucleus was promoted, the expression of Keap1 protein was inhibited, the activity of intracellular antioxidant indicators GSH, GPx, SOD, and CAT was enhanced, and the expression of malondialdehyde (MDA) was inhibited. Collectively, our results demonstrated that FG phenolic acids protect DNA from oxidative damage by activating Nrf2 to safeguard the skin from photoaging induced by UVA stimulation. [Display omitted] • FGE inhibits skin photoaging induced by UVA stimulation. • The main functional components of FGE are 7 phenolic acid compounds. • PAM inhibits photoaging of HFF-1 cells by inhibiting ROS accumulation. • PAM prevents cellular ROS accumulation by promoting the Nrf2 entry into the nucleus. [ABSTRACT FROM AUTHOR]

• A robust optical diffraction tomography that integrates the quadriwave lateral shearing interferometry with the light field modulation technique. • The complex amplitude map of the specimen can be retrieved from a single-shot wire-mesh-like interferogram with a simple structure and straightforward reconstruction process. • The quantitative three-dimensional internal structure of biological cells can be imaged without the need of staining. • Not only provides unprecedented insight into the specimen but also helpful for biomedical diagnosis. Optical diffraction tomography (ODT) is an emerging microscopy that enables quantitatively three-dimensional (3D) refractive index (RI) mapping of subcellular structure inside biological cells without staining. Due to the noninvasive, label-free, and quantitative imaging capability, ODT has become an important technique in the fields of cell biology, biophysics, hematology, and so on. It is customary to acquire a set of two-dimensional (2D) phase images of a transparent sample from different illumination angles by using the classical Mach-Zehnder interferometry (MZI), and then numerically reconstruct the 3D RI distribution of the sample via appropriate tomographic algorithms. However, due to the limited stability of MZI, the cumulative measured phase errors reduce the accuracy of the reconstructed RI. Here, we propose a common-path ODT based on quadriwave lateral shearing interferometry (QLSI), referred as Q-ODT. In QLSI, the object beam carrying the phase information of sample is divided into four copies by a specially designed 2D diffraction optical element, then the diffracted waves interfere with each other to form the interferogram at the image plane. The complex amplitude map of the object is quantitatively retrieved from the single-shot interferogram by using a Fourier analysis algorithm and a 2D phase gradient integration. A spatial light modulator is employed to ensure high-precision illumination angle scanning without mechanical motion by addressing a series of different periods and orientations blazed gratings. The average fluctuation of the measured phases of a test polystyrene bead by acquiring 300 interferograms in 12 s presents 7.6 mrad, surpassing the conventional MZI-based ODT. The 3D RI distribution of the bead reconstructed from 145 complex amplitude maps via multi-illumination angles with a maximum angle of 70° matches the manufacturer's specification well, demonstrating the high accuracy of the 3D RI imaging capability of the Q-ODT. The lateral and axial resolutions of the 3D RI reconstruction were measured to be 306 ± 21 nm and 825 ± 34 nm, respectively. The proposed Q-ODT method successfully reconstructed the intracellular structure of the biological specimens of Eudorina elegans and mouse bone mesenchymal stem cells (BMSC). The Q-ODT offers a new route towards 3D RI imaging for label-free transparent samples in biomedical research. [ABSTRACT FROM AUTHOR]

Mannosylerythritol lipids (MELs) may prevent skin barrier damage, although their protective mechanisms and active monomeric constituents remain unclear. Here, three MELs were extracted from Candida antarctica cultures containing fermented olive oil then purified using silica gel-based column chromatography and semipreparative HPLC. All three compounds (MEL-A, MEL-B, MEL-C) were well separated and stable, and reliable materials were used for NMR and HRESIMS chemical structure determinations and for assessing MELs' protective effects against skin damage. Notably, MEL-B and MEL-C effectively protected HaCaT cells from UVB-induced damage by upregulating the contents of filaggrin (FLG) and transglutaminase-1 (TGM1), as determined via ELISA. Moreover, MEL-B treatment (20 μg/mL) of UVB-irradiated HaCaT cells led to the upregulation of both the expression of mRNA genes and the key proteins FLG, LOR, and TGM1, which are known to be decreased in damaged skin cells. Additionally, histopathological analysis results revealed a markedly reduced intracellular vacuolation and cell damage, reflecting improved skin function after MEL-B treatment. Furthermore, immunofluorescence results revealed that MEL-B protected EpiKutis® three-dimensional cultured human skin cells from sodium dodecyl sulfate-induced damage by up-regulating FLG, LOR, and TGM1 expression. Accordingly, MELs' protection against skin barrier damage depended on MEL-B monomeric constituent activities, thus highlighting their promise as beneficial ingredients for use in skin-care products. [ABSTRACT FROM AUTHOR]

Here, we evaluated the in vivo skin-protective effects of topical applications of Panax ginseng C. A. Meyer extract (PG2) and its phenolic acid- (PA-) based components against UVB-induced skin photoaging. PG2 or PA applied to skin of hairless mice after UVB-irradiation alleviated UVB-induced effects observed in untreated skin, such as increased transepidermal water loss (TEWL), increased epidermal thickness, and decreased stratum corneum water content without affecting body weight. Moreover, PG2 and PA treatments countered reduced mRNA-level expression of genes encoding filaggrin (FLG), transglutaminase-1 (TGM1), and hyaluronan synthases (HAS1, HAS2, and HAS3) caused by UVB exposure and reduced UVB-induced collagen fiber degradation by inhibiting the expression of matrix metalloproteinase genes encoding MMP-1, MMP-2, and MMP-9. Meanwhile, topical treatments reduced cyclooxygenase-2 (COX-2) mRNA-level expression in photodamaged skin, leading to the inhibition of interleukin-1β (IL-1β) and interleukin-6 (IL-6) mRNA-level expression. Thus, ginseng phenolic acid-based preparations have potential value as topical treatments to protect skin against UVB-induced photoaging. [ABSTRACT FROM AUTHOR]

• Combination of compound K increases the cytotoxicity of cytarabine. • Compound K strengthens cytarabine-induced apoptosis. • Compound K enhances cytarabine-induced DNA damage. • Compound K promotes ara-C metabolism as an active molecule which can be inserted into DNA. AML is a kind of hematological malignant tumor that urgently requires different treatment options in order to increase the cure rate and survival rate. Cytarabine (ara-C) is currently the main drug used to treat AML patients and is usually combined with different chemotherapeutic agents. However, due to resistance to ara-C, a new combination is needed to reduce ara-C resistance and improve treatment outcome. As is known to all, ginseng is a traditional Chinese herb; compound K is the principal metabolic product of ginsenoside which also has anti-cancer activity in some cancer cells, while the mechanism is unclear. In our previous study, we found that compound K inhibited AML cell viability and induced apoptosis, and compound K combined with ara-C synergistically induced AML cell proliferation arrest. Thus, we sought to investigate the reason for this by focusing on the mitochondrial dysfunction and DNA damage. In this paper, our results provide a foundation for the clinical evaluation of concomitant administration of compound K and ara-C in order to reduce the resistance to ara-C and improve AML treatment. [ABSTRACT FROM AUTHOR]

Living Biosensors: Red-Blood-Cell Waveguide as a Living Biosensor and Micromotor (Adv. Funct. In article number 1905568, Yao Zhang, Baojun Li, and co-workers report a biocompatible biosensor and micromotor that are assembled with an in vivo red blood cell waveguide. The living biosensor is used for the diagnosis of pH-related disorders of the blood; the waveguide can rotate as a micromotor and transport microparticles to the target region. [Extracted from the article]

With great potential in intelligent sensing and actuating systems, biosensors and micromotors are expected to be powerful instruments for early diagnosis and drug delivery in precision medicine. However, it is difficult to ensure the synthetic biosensors and micromotors are compatible with biosystems because of their exogenous building blocks. Biocompatible biosensors and micromotors assembled are reported from living red blood cells (RBCs) optically bound into a waveguide using fiber probes. By monitoring light propagation of the RBC waveguide, the pH of blood solution is detected in real time with an accuracy of 0.05. This can be used for the diagnosis of pH‐related disorders of the blood. After diagnosis, optical torque is exerted on the RBC waveguide, allowing it to rotate as a micromotor and transport microparticles to a target region. The RBC waveguide is then constructed inside zebrafish blood vessels to validate in vivo application. The living biosensors and micromotors are expected to provide a "smart" platform for precise biosensing, medical analysis, and drug delivery. [ABSTRACT FROM AUTHOR]

• HE (PP) inhibits adhesion and inflammatory response in endothelial cells. • HE (PP) suppresses foam cell formation and apoptosis in macrophages. • HE (PP) inhibits lipid accumulation by regulating LOX-1/LXR-α/ABCA1 pathway. • HE (PP) is identified as a potential novel therapy for atherosclerosis prevention. Hirudo is an important Chinese medicine that has been widely used in patients with thrombosis-related diseases. We aimed to evaluate the protective effect and potential mechanism of Hirudo extract (HE) on the process of atherosclerosis (AS) as well as identify its active components in the lipopolysaccharide (LPS) - or oxidized low-density lipoprotein (ox-LDL)-induced cell models. After treatment, adhesion molecules and pro-inflammatory cytokines induced by LPS were examined by qPCR and ELISA. ROS production, cell apoptosis, and lipid accumulation in ox-LDL-induced cells were analyzed by flow cytometry, qPCR, western blotting, and immunofluorescence staining. In addition, the main active components of HE were identified and analyzed for preventing the progression of AS. In this study, we found that HE pretreatment for 48 h significantly inhibited monocyte adhesion and reduced the levels of adhesion factors (ICAM-1 and VCAM-1) and pro-inflammatory factors (IL-6 and TNF-α) in LPS-induced endothelial cells. Moreover, HE attenuated ox-LDL-induced ROS accumulation and apoptosis in macrophage cells via mitochondrial apoptotic pathways. Additionally, HE pretreatment effectively inhibited cholesterol uptake and increased cholesterol efflux by regulating the LOX-1/LXR-α/ABCA1 pathway. Importantly, the polypeptides from HE (PP) with a molecular weight < 10,000 Da accounted for about 62.9% of the total amount of polypeptides, which in turn may be active components of HE that are responsible for inhibiting inflammation, foam cell formation and apoptosis. PP from HE potently inhibits endothelial cell inflammatory injury and macrophage foam cell formation and apoptosis by regulating the LOX-1/LXR-α/ABCA1 pathway, thereby providing additional support to the beneficial effects of HE in preventing AS. [ABSTRACT FROM AUTHOR]

Background. The clinical anti-inflammatory drug dexamethasone (DEX) can cause many side effects such as muscle atrophy for long-term use. Muscle atrophy induced by DEX may be caused by decrease of glucose consumption. Panax ginseng C.A. Meyer was previously considered to be an antiatrophic agent for glucocorticoid- (GC-) treated therapies. As one of the main components, it remains unclear whether ginseng total protein (GP) facilitates recovery from muscle atrophy induced by DEX. Methods. In this study, GP was extracted and purified with Sephadex-G50. C2C12 myoblasts was induced with 2% horse serum to differentiate into C2C12 myotubes. Cell viability was analyzed by the MTT assay, and Ca2+ concentration was analyzed by a flow cytometer. The release of lactic dehydrogenase (LDH) and the glucose consumption were analyzed by spectrophotometry. The phosphorylation of AMP-activated protein kinase (AMPK), phosphoinositide 3-kinase (PI3K), and protein kinase B (Akt) and the expression of glucose transporter 4 (GLUT4) were analyzed by Western blotting. The phosphorylation of AS160 was quantified by Immunofluorescence staining. Results. We found that GP increased cell viability and increased myotube diameter in high-dose DEX-treated C2C12 myotubes for 24 h, but this activity was not found in the enzymatic hydrolyzed GP group. GP reduced muscle atrophy by decreasing the expression of key proteins such as muscle RING-finger protein-1 and muscle atrophy F-box, reducing the Ca2+ concentration, and decreasing the release of LDH in DEX-injured C2C12 myotubes. Moreover, GP improved glucose consumption and increased the phosphorylation of AMPK, PI3K, Akt, and AS160 and the expression of GLUT4 in DEX-treated C2C12 myotubes. Conclusion. The results of this study suggest that GP has effects on recovering DEX-induced muscle atrophy and cell injury, which may improve glucose consumption via the AMPK and PI3K/Akt pathways in high-dose DEX-treated C2C12 myotubes. This study provides in vitro mechanistic insights into the recovery of muscle atrophy with GP treatment. [ABSTRACT FROM AUTHOR]

As the basis of the research on reducing wake vortex separations, numerical simulation and constructing of fast-models for simulating wake vortex have become the focus of many international ATM research institutes. In the research field of wake vortex numerical simulation, the formation, evaluation and decay of wake vortex are calculated based on RANS, LES or DES methods. These data can help to reveal the regulation of wake vortex, and can provide basic foundation for constructing wake vortex models. In the field of fast simulation of wake vortex, Some organizations have done many theoretical researches on the formation and dissipation of wake vortex, attempting to deduce the behavioural characteristics of wake vortex by establishing complex mathematical models, including CROW instability, Greene model, APA model, TDAWP model, D2P model and the three-phase decay model, etc. The research status quo is analyzed and the key works in the next phase are also provided. [ABSTRACT FROM AUTHOR]

Highlights • Rb3 significantly inhibited CSE-induced inflammatory responses by inhibiting the p38 MAPK/NF-κB pathway in fibroblasts and epithelial cells. • Rb3 pretreatment led to the increase of anti-oxidant activity to reduce oxidative stress injury in CSE-induced fibroblasts and epithelial cells. • Rb3 decreased CSE-induced excessive accumulation of ECM by inhibiting TGF-β1/VEGF pathway in fibroblasts and epithelial cells. Abstract Cigarette smoke causes many adverse effects such as inflammation, oxidative stress, and excessive accumulation of the extracellular matrix (ECM). Ginsenoside Rb3 has anti-inflammatory and anti-oxidative effects, which may contribute to delaying the injury caused by cigarette smoke. In this study, we used cigarette smoke extract (CSE) to establish cell injury models in WI-38 human fetal lung fibroblasts and 16HBE human bronchial epithelial cells. Our results showed that Rb3 protected against CSE-induced cytotoxicity in both cell lines. In addition, it significantly inhibited the secretion of inflammatory factors, such as interleukin-8 and tumor necrosis factor alpha, by inhibiting the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB). Moreover, Rb3 pre-treatment led to an increase in the levels of glutathione (GSH) and activities of superoxide dismutase, glutathione peroxidase (GSH-Px), and catalase to reduce the oxidative stress induced by CSE. Additionally, Rb3 decreased the levels of ECM proteins including collagen I (Col I), Col III, and elastin after CSE treatment by inhibiting the expression of transforming growth factor beta 1 (TGF-β1)-induced vascular endothelial growth factor (VEGF). Our findings suggest that Rb3 prevented CSE-induced inflammation and oxidative stress as well as the excessive accumulation of ECM in WI-38 and 16HBE cells to protect against cell injury by inhibiting the p38 MAPK/NF-κB and TGF-β1/VEGF pathways. The results of this study may be valuable for the development of Rb3 to combat the damage caused by cigarette smoke. [ABSTRACT FROM AUTHOR]

Skin barrier dysfunction can lead to water and electrolyte loss, triggering homeostatic imbalances that can trigger atopic dermatitis and anaphylaxis. Panax ginseng C.A. Meyer is a traditional Chinese medicinal herb with known therapeutic benefits for the treatment of skin diseases, including photodamage repair effects and reduction of pigmentation. However, few reports exist that describe effectiveness of ginseng active components for repair of skin barrier damage. Ginseng oligosaccharide extract (GSO) was prepared from P. ginseng via water extraction followed by ethanol precipitation and resin and gel purification. GSO composition and structural characteristics were determined using LC-MS, HPLC, FT-IR, and NMR. To evaluate GSO as a skin barrier repair-promoting treatment, skin of UVB-irradiated BALB/c hairless mice was treated with or without GSO then skin samples were evaluated for epidermal thickness, transepidermal water loss (TEWL), and stratum corneum water content. In addition, UVB-exposed skin samples and HaCaT cells were analyzed to assess GSO treatment effects on levels of epidermal cornified envelope (CE) protein and other skin barrier proteins, such as filaggrin (FLG), involucrin (IVL), and aquaporin-3 (AQP3). Meanwhile, GSO treatment was also evaluated for effects on UVB-irradiated hairless mouse skin and HaCaT cells based on levels of serine protease inhibitor Kazal type-5 (SPINK5), trypsin-like kallikrein-related peptidase 5 (KLK5), chymotrypsin-like KLK7, and desmoglein 1 (DSG1). These proteins are associated with UVB-induced skin barrier damage manifesting as dryness and desquamation. GSO was shown to consist of oligosaccharides comprised of seven distinct types of monosaccharides with molecular weights of approximately 1 kDa that were covalently linked together via β-glycosidic bonds. In vivo , GSO applied to dorsal skin of BALB/c hairless mice attenuated UVB-induced epidermal thickening and moisture loss. Furthermore, GSO ameliorated UVB-induced reductions of levels of FLG, IVL, and AQP3 proteins. Additionally, GSO treatment led to increased DSG1 protein levels due to decreased expression of KLK7. In vitro , GSO treatment of UVB-irradiated HaCaT cells led to increases of FLG, IVL, and AQP3 mRNA levels and corresponding proteins, while mRNA levels of desquamation-related proteins SPINK5, KLK5, KLK7, and DSG1 and associated protein levels were restored to normal levels. A P. ginseng oligosaccharide preparation repaired UVB-induced skin barrier damage by alleviating skin dryness and desquamation symptoms, highlighting its potential as a natural cosmetic additive that can promote skin barrier repair after UVB exposure. [Display omitted] • Panax ginseng oligosaccharides (GSO) may induce repair of UVB-induced skin damage. • GSO may lessen UVB-induced skin dryness by increasing CE and AQP3 protein expression. • GSO treatment of UVB-damaged skin barrier reduced desquamation in vivo and in vitro. • GSO raised SPINK5 expression to lower KLK5 & KLK7 levels & reduce DSG1 degradation. • GSO treatment reduced desquamation of UVB-damaged skin by reducing DSG1 degradation. [ABSTRACT FROM AUTHOR]

Abnormal melanogenesis and melanosome transport can cause skin pigmentation disorders that are often treated using ginseng-based formulation. We previously found that phenolic acid compounds in ginseng root could inhibit melanin production and as a skin-whitening agents. However, mechanisms of action underlying effects of ginseng phenolic acid monomers on melanogenesis remain unclear. This study was conducted to investigate effects of salicylic acid, a main ginseng root phenolic acid component, on melanogenesis and melanosome functions in melanocytes of zebrafish and other species. Salicylic acid exhibited no cytotoxicity and reduced melanin levels and tyrosinase activity in B16F10 murine melanoma cells and normal human epidermal melanocytes regardless of prior cell stimulation with α-melanocyte stimulating hormone. Additionally, salicylic acid treatment reduced expression of melanogenic enzymes tyrosinase, tyrosinase-related protein 1 and tyrosinase-related protein 2, while reducing expression of their master transcriptional regulator, microphthalmia-associated transcription factor. Moreover, reduced phosphorylation of cAMP response-element binding protein was observed due to reduced cAMP levels resulting from salicylic acid inhibition of upstream signal regulators (adenylyl cyclase and protein kinase A). Furthermore, salicylic acid treatment suppressed expression of transport complex-associated proteins melanophilin and myosin Va in two UVB-treated melanocytic cell lines, suppressed phagocytosis of fluorescent microspheres by UVB-stimulated human keratinocytes (HaCaT), inhibited protease-activated receptor 2 activation by reducing both Ca2+ release and activation of phosphoinositide 3 kinase/AKT and mitogen-activated protein kinases and induced anti-melanogenic effects in zebrafish. Collectively, these results indicate that salicylic acid within ginseng root can inhibit melanocyte melanogenesis and melanin transport, while also suppressing keratinocyte phagocytic function. [Display omitted] [ABSTRACT FROM AUTHOR]

Muscle atrophy, a side effect from administration of the anti-inflammatory medication dexamethasone (DEX), is preventable by concomitant administration of the major monomeric constituent of Panax ginseng C.A. Meyer, 20(S)-ginsenoside Rg3 (S-Rg3). Putative S-Rg3-associated prevention of DEX-induced muscle atrophy may involve S-Rg3 mitigation of DEX-induced mitochondrial dysfunction. In the present study, MTT assays revealed enhanced cell viability following S-Rg3 treatment of DEX-injured C2C12 myotubes. Subsequent PCR and western blotting results demonstrated S-Rg3-induced reduction of expression of muscle atrophy F-box protein (atrogin-1) and muscle RING-finger protein-1, proteins previously linked to muscle atrophy. Additionally, S-Rg3 treatment of DEX-injured myotubes led to aggregation of Rg3 monomers in cells and dose-dependent increases in cellular mitochondrial basal respiratory oxygen consumption rate and intracellular ATP levels compared with their levels in untreated DEX-injured myotubes. In addition, S-Rg3 treatment significantly reversed DEX-induced reductions of expression of key mitochondrial respiratory electron transport chain subunits of protein complexes II, III and V in DEX-injured myotube cells. Furthermore, S-Rg3 alleviation of mitochondrial dysfunction associated with DEX-induced injury of C2C12 myotubes was linked to S-Rg3-associated decreases in both forkhead box O3 (FoxO3) protein expression and phosphorylation of AMP-activated protein kinase (AMPK). Collectively, these results implicate S-Rg3 modulation of signaling within the AMPK-FoxO3 pathway as a putative mechanism underlying S-Rg3 alleviation of DEX-induced muscle atrophy. [ABSTRACT FROM AUTHOR]

We previously found that 20(S)-ginsenoside Rg3 (S-Rg3) promotes myoblast differentiation via an unknown mechanism. Here we measured levels of myosin heavy chain (MHC) and myogenin, markers of myoblast differentiation, using Western blot analysis and immunofluorescence staining. Notably, S-Rg3 treatment of C2C12 myoblasts led to increased muscle differentiation and protection from muscle atrophy in a dexamethasone (DEX)-treated C2C12 myotube-based muscle atrophy model. This effect was likely caused by S-Rg3 treatment-induced promotion of Akt/mTOR phosphorylation and inhibition of FoxO3 nuclear transcription. Additionally, S-Rg3 treatment also led to increased fruit fly climbing distances (Drosophila melanogaster) and prevented muscle atrophy in aged fruit flies. Our study provides a mechanistic framework for understanding how S-Rg3 enhances myoblast differentiation and inhibits myotube atrophy through activation of the Akt/mTOR/FoxO3 signaling pathway, as demonstrated in vitro in C2C12 cells and in vivo in fruit flies. [ABSTRACT FROM AUTHOR]

Higher levels of glucocorticoids (GCs), and impaired regulation of the hypothalamic-pituitary-adrenal (HPA) axis may cause or exacerbate the occurrence of metabolic and psychiatric disorders. It has been reported that ginseng saponin extract (GSE) has an inhibitory effect on the hyperactivity of the HPA axis induced by stresses and increased corticosterone level induced by intraperitoneal injection of adrenocorticotrophic hormone (ACTH) in mice. However, the molecular mechanisms by which GSE and its active ginsenosides inhibit corticosterone secretion remain elusive. Y1 mouse adrenocortical cells were treated with ACTH for up to 60 min to establish a cell model of corticosterone secretion. After treatment with different concentrations of GSE or ginsenoside monomers for 24 h prior to the addition of ACTH, analyses of cAMP content, PKA activity, and the levels of steroidogenesis regulators, melanocortin-2 receptor (MC2R), and melanocortin-2 receptor accessory protein (MRAP) in ACTH-induced Y1 cells were performed. We demonstrated that GSE inhibits ACTH-stimulated corticosterone production in Y1 cells by inhibiting factors critical for steroid synthesis. Ginsenoside Rd, an active ingredient of GSE, inhibits corticosterone secretion in the cells and impedes ACTH-induced corticosterone biosynthesis through down-regulation of proteins in the cAMP/PKA/CREB signaling pathway. In addition, Western blot and qPCR analyses showed that ginsenoside Rd attenuated the induction of MC2R and MRAP by ACTH. Our findings indicate that ginsenoside Rd inhibits ACTH-induced corticosterone production through blockading the MC2R-cAMP/PKA/CREB pathway in adrenocortical cells. Overall, this mechanism may represent an important therapeutic option for the treatment of stress-related disorders, further supporting the pharmacological benefits of ginseng. [ABSTRACT FROM AUTHOR]

Corrigendum to "Cytoprotective effect of Fufang Lurong Jiangu capsule against hydrogen peroxide-induced oxidative stress in bone marrow stromal cell-derived osteoblasts through the Nrf2/HO-1 signaling pathway" [Biomed. We made a mistake when labeling cells treated with MitoTracker Green (Fig. We added a new Fig. [Extracted from the article]