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In this paper, a novel laser spot tracking algorithm that incorporates the Kalman filter with the continuously adaptive Meanshift algorithm (Cam-Kalm) is proposed and employed in an underwater optical wireless communication (UOWC) system. Since the Kalman filter has the advantage of predicting the state information of the target spot based on its spatial motion features, the proposed algorithm can improve the accuracy and stability of the moving laser spot tracking. A 2 m optical wireless communication experimental system with auto-tracking based on a green laser diode (LD) is built to evaluate the tracking performance of different algorithms. Experimental results verify that the proposed algorithm outperforms conventional tracking algorithms in aspects of tracking accuracy, interference resistance, and response time. With the proposed Cam-Kalm algorithm, the experimental system can establish an effective communication link, while the maximum tracking speed is 20 mm/s given the forward-error-correction (FEC) threshold.
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BACKGROUND: Cigarette smoking is commonly reported among chronic pain patients in the clinic. Although chronic nicotine exposure is directly linked to nociceptive hypersensitivity in rodents, underlying neurobiological mechanisms remain unknown. METHODS: Multi-tetrode recordings in freely moving mice were used to test the activity of dopaminergic projections from the ventral tegmental area (VTA) to pyramidal neurones in the anterior cingulate cortex (ACC) in chronic nicotine-treated mice. The VTAâACC dopaminergic pathway was inhibited by optogenetic manipulation to detect chronic nicotine-induced allodynia (pain attributable to a stimulus that does not normally provoke pain) assessed by von Frey monofilaments (force units in g). RESULTS: Allodynia developed concurrently with chronic (28-day) nicotine exposure in mice (0.36 g [0.0141] vs 0.05 g [0.0018], P<0.0001). Chronic nicotine activated dopaminergic projections from the VTA to pyramidal neurones in the ACC, and optogenetic inhibition of VTA dopaminergic terminals in the ACC alleviated chronic nicotine-induced allodynia in mice (0.06 g [0.0064] vs 0.28 g [0.0428], P<0.0001). Moreover, optogenetic inhibition of Drd2 dopamine receptor signalling in the ACC attenuated nicotine-induced allodynia (0.07 g [0.0082] vs 0.27 g [0.0211], P<0.0001). CONCLUSIONS: These findings implicate a role of Drd2-mediated dopaminergic VTAâACC pathway signalling in chronic nicotine-elicited allodynia.
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Giro del Cíngulo , Nicotina , Humanos , Ratones , Animales , Nicotina/farmacología , Hiperalgesia/inducido químicamente , Dopamina/metabolismo , DolorRESUMEN
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the onset of symptoms, typically occurring later in life, and significant deficits in cognitive functions including learning, memory, speech, and behavior. Ongoing research endeavors seek to explore methods for preventing and treating AD, as well as delving into the molecular mechanisms underlying existing and novel therapeutic approaches encompassing exercise, diet, and drug regimens for individuals with AD or those at risk of developing AD. Among these interventions, dietary interventions have garnered increasing attention due to their potential in addressing the disease. Eating is among the most fundamental of human daily activities, and controlled dietary practices, such as fasting, have gained prominence as essential clinical methods for disease prevention and treatment. Research findings indicate that fasting holds promise in effectively alleviating and improving the cognitive decline associated with age or as consequence of disease. The clinical efficacy of fasting in addressing AD and related disorders might be grounded in its influence on various molecular mechanisms, including neuroinflammation, glial cell activation, insulin resistance, autophagy regulation, nerve regeneration, the gut microbiome, and accumulations of amyloid-ß and tau proteins. The present study reviews possible molecular mechanisms underpinning the therapeutic effects of fasting in patients with AD, as well as in models of the disorder, to establish a theoretical basis for using fasting as a viable approach to treat AD.
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Enfermedad de Alzheimer , Humanos , Animales , Enfermedad de Alzheimer/tratamiento farmacológico , Péptidos beta-Amiloides/metabolismo , Ayuno , Proteínas tau , Aprendizaje , Modelos Animales de EnfermedadRESUMEN
BACKGROUND: Genomic structural variant detection is a significant and challenging issue in genome analysis. The existing long-read based structural variant detection methods still have space for improvement in detecting multi-type structural variants. RESULTS: In this paper, we propose a method called cnnLSV to obtain detection results with higher quality by eliminating false positives in the detection results merged from the callsets of existing methods. We design an encoding strategy for four types of structural variants to represent long-read alignment information around structural variants into images, input the images into a constructed convolutional neural network to train a filter model, and load the trained model to remove the false positives to improve the detection performance. We also eliminate mislabeled training samples in the training model phase by using principal component analysis algorithm and unsupervised clustering algorithm k-means. Experimental results on both simulated and real datasets show that our proposed method outperforms existing methods overall in detecting insertions, deletions, inversions, and duplications. The program of cnnLSV is available at https://github.com/mhuidong/cnnLSV . CONCLUSIONS: The proposed cnnLSV can detect structural variants by using long-read alignment information and convolutional neural network to achieve overall higher performance, and effectively eliminate incorrectly labeled samples by using the principal component analysis and k-means algorithms in training model stage.
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Secuenciación de Nucleótidos de Alto Rendimiento , Programas Informáticos , Secuenciación de Nucleótidos de Alto Rendimiento/métodos , Algoritmos , Genoma , Redes Neurales de la ComputaciónRESUMEN
BACKGROUND: Long-term smoking is a risk factor for chronic pain, and chronic nicotine exposure induces pain-like effects in rodents. The anterior cingulate cortex (ACC) has been demonstrated to be associated with pain and substance abuse. This study aims to investigate whether ACC microglia are altered in response to chronic nicotine exposure and their interaction with ACC neurons and subsequent nicotine-induced allodynia in mice. METHODS: We utilized a mouse model that was fed nicotine water for 28 days. Brain slices of the ACC were collected for morphological analysis to evaluate the impacts of chronic nicotine on microglia. In vivo calcium imaging and whole-cell patch clamp were used to record the excitability of ACC glutamatergic neurons. RESULTS: Compared to the vehicle control, the branch endpoints and the length of ACC microglial processes decreased in nicotine-treated mice, coinciding with the hyperactivity of glutamatergic neurons in the ACC. Inhibition of ACC glutamatergic neurons alleviated nicotine-induced allodynia and reduced microglial activation. On the other hand, reactive microglia sustain ACC neuronal excitability in response to chronic nicotine, and pharmacological inhibition of microglia by minocycline or liposome-clodronate reduces nicotine-induced allodynia. The neuron-microglia interaction in chronic nicotine-induced allodynia is mediated by increased expression of neuronal CX3CL1, which activates microglia by acting on CX3CR1 receptors on microglial cells. CONCLUSION: Together, these findings underlie a critical role of ACC microglia in the maintenance of ACC neuronal hyperactivity and resulting nociceptive hypersensitivity in chronic nicotine-treated mice.
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Hiperalgesia , Neuralgia , Nicotina , Animales , Ratones , Giro del Cíngulo/metabolismo , Hiperalgesia/inducido químicamente , Microglía/metabolismo , Neuralgia/metabolismo , Neuronas/metabolismo , Nicotina/toxicidadRESUMEN
Cancerous inhibitor of protein phosphatase 2A (Cip2a) is an oncoprotein, playing important roles in tumor progression. However, the underlying mechanisms by which Cip2a promotes tumor aggressiveness in NSCLC remain to be further investigated. In this study, we found that Cip2a expression is elevated in NSCLC and correlates with poor prognosis. Knockdown of Cip2a significantly reduced the ability of cell proliferation, invasion, and metastasis of NSCLC both in vitro and in vivo. Furthermore, we found that Cip2a promotes tumor progression partly by inducing arginine biosynthesis, and knockdown of Cip2a exhibited a significantly increased sensitivity to arginine deprivation and mTOR inhibition. In addition, we found that p53 mutants in NSCLC cells increased Cip2a expression by inhibiting the activity of wild-type p53. Our findings provide new insights into the mechanisms of Cip2a in promoting tumor progression and suggest that Cip2a represents a potential therapeutic target for treating NSCLC.
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Carcinoma de Pulmón de Células no Pequeñas , Neoplasias Pulmonares , Humanos , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Neoplasias Pulmonares/metabolismo , Proteína p53 Supresora de Tumor , Proliferación Celular/genética , Autoantígenos/genética , Autoantígenos/metabolismo , Autoantígenos/uso terapéutico , Línea Celular TumoralRESUMEN
Currently, various problems are being faced in the treatment of influenza, so the development of new safe and effective drugs is crucial. Selenadiazole, an important component of selenium heterocyclic compounds, has received wide attention for its biological activity. This study aimed to verify the antiviral activity of 5-nitrobenzo[c][1,2,5]selenadiazole (SeD-3) in vivo and in vitro. The cell counting kit-8 assay and observation of cytopathic effect verified that SeD-3 could improve the survival of influenza A(H1N1)pdm09-infected Madin-Darby canine kidney cells. Polymerase chain reaction quantification and neuraminidase assay showed that SeD-3 could inhibit the proliferation of H1N1 virus. The time of addition assay demonstrated that SeD-3 may have a direct effect on virus particles and block some stages of H1N1 life cycle after virus adsorption. Cell cycle, JC-1, Annexin V, and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling-4',6-diamidino-2-phenylindole (TUNEL-DAPI) assays showed that SeD-3 inhibited H1N1 infection-induced apoptosis. Cytokine detection demonstrated SeD-3 inhibited the production of proinflammatory factors after infection, including tumor necrosis factor-α (TNF-α), TNF-ß, interferon-γ, interleukin 12 (IL-12), and IL-17F. In vivo experiments suggested that the pathological damage in the lungs was significantly alleviated after treatment with SeD-3 by hematoxylin and eosin staining. The TUNEL assay of lung tissues indicated that SeD-3 inhibited DNA damage during H1N1 infection. Immunohistochemical assays were performed to further explore the mechanism that SeD-3 inhibited H1N1-induced apoptosis via reactive oxygen species-mediated MAPK, AKT, and P53 signaling pathways. In conclusion, SeD-3 may become a new potential anti-H1N1 influenza virus drug due to its antiviral and anti-inflammatory activity.
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Gripe Humana , Animales , Perros , Humanos , Inflamación/tratamiento farmacológico , Estrés Oxidativo , Especies Reactivas de Oxígeno , Antivirales/farmacología , Antivirales/uso terapéuticoRESUMEN
BACKGROUND: Enterovirus A71 (EV-A71)is a prevalent infection in severe hand, foot and mouth disease HFMD and can induce acute central nervous system seizures. The three EV-A71 vaccines now circulating in the market are produced for a single subtype. While EV-A71 is constantly evolving and the vaccine's efficacy is gradually reducing, no specialized anti-EV-A71 medication has yet been developed. Therefore, it is crucial to consistently develop new anti-EV-A71 medications. METHOD: Ebselen, an organoselenium molecule with glutathione oxidase-like activity, is resistant to a range of viruses. In this investigation, we used the Cell counting kit-8 (CCK-8 kit) assay in a Vero cell model to confirm the effectiveness of ebselen against EV-A71 infection. Later, to examine ebselen's anti-EV-A71 mechanism, we measured the apoptosis level of cells in different treatment groups through Annexin V, JC-1, and cell cycle assays, as well as the intracellular reactive oxygen species (ROS) concentration. Ebselen may have an impact on the apoptotic signaling pathway caused by EV-A71 infection, according to the results of a caspase-3 activity experiment. RESULT: The results showed that Ebselen protected cell damage from ROS generation, decreased the frequency of EV-A71-induced apoptosis, and inhibited caspase-3-mediated apoptosis by lowering caspase-3 activity. CONCLUSION: To summarize, ebselen is a promising anti-EV-A71 medication.
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Enterovirus Humano A , Infecciones por Enterovirus , Enterovirus , Humanos , Especies Reactivas de Oxígeno , Caspasa 3 , Infecciones por Enterovirus/tratamiento farmacológico , Transducción de Señal , ApoptosisRESUMEN
BACKGROUND: The deer antler, a remarkable mammalian appendage, has a growth rate surpassing that of any other known osseous organ. Emerging evidence indicates that circRNA and MAPK1 play critical roles in chondrocytes. Thus, exploration of their functions in antler chondrocytes will help us to understand the mechanism regulating the rapid antler growth. METHODS: qRT-PCR, western blot, and immunohistochemistry were used to assess the expression of mRNAs and proteins. CCK-8, EdU, Cell migration, ALP activity detection, and ALP staining examined the effects of MAPK1 in antler chondrocytes. FISH, RIP, and luciferase assays were performed to evaluate the interactions among circRNA3634/MAPK1 and miR-124486-5. RIP and RAP assays proved the binding interaction between circRNA3634 and RBPs. Me-RIP was used to determine the m6A methylation modification of circRNA3634. RESULTS: This study revealed high MAPK1 expression in antler cartilage tissue. Overexpression of MAPK1 promoted the proliferation, migration, and differentiation of antler chondrocytes and increased the expression of MAPK3, RAF1, MEK1, RUNX2, and SOX9. The silencing of MAPK1 had the opposite effect. CircRNA3634 was found to act as a molecular sponge for miR-124486-5, leading to increased MAPK1 expression and enhanced proliferation and migration of antler chondrocytes through competitive miR-124486-5 binding. We discovered that METTL3 mediates m6A modification near the splicing site of circRNA3634 and is involved in the proliferation and differentiation of antler chondrocytes. The m6A reader YTHDC1 facilitated the nuclear export of circRNA3634 in an m6A-dependent manner. Our results indicate that m6A-modified circRNA3634 promotes the proliferation of antler chondrocytes by targeting MAPK1 and show that the nuclear export of circRNA3634 is related to the expression of YTHDC1, suggesting that circRNA3634 could represent a critical regeneration marker for the antler. CONCLUSIONS: Our results revealed a novel m6A-modified circRNA3634 promoted the proliferation and differentiation of antler chondrocytes by regulating MAPK1. The nuclear export of circRNA3634 was related to the expression of YTHDC1.
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Cuernos de Venado , Ciervos , MicroARNs , Animales , Condrocitos/metabolismo , Proliferación Celular/genética , Ciervos/genética , MicroARNs/genética , MicroARNs/metabolismoRESUMEN
In this work, a two-dimensional power allocation scheme combining fractional transmit power allocation (FTPA) and the sine cosine algorithm (SCA) is proposed for non-orthogonal multiple access (NOMA)-based underwater visible light communication (UVLC) systems. Considering the proposed power allocation scheme, a downlink NOMA-based UVLC system using blue-light-emitting diodes in the deep-sea environment is set up to evaluate the influence of the FTPA coefficient and SCA on system communication performance. The simulation results demonstrate that the two-dimensional power allocation scheme can effectively reduce the impact of user pairing on system performance and improve the system transmission rate compared with the conventional power allocation scheme.
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In this paper, an optimization scheme that can simultaneously transmit communication information, positioning the information and energy in a visible light communication and positioning (VLCP) system with energy harvesting is proposed. The time switching-power splitting (TS-PS) method is applied, where the power and time allocation factors are defined as optimization variables, so that the system can maximize the harvested energy under the constraints of the information rate and positioning error. The multi-verse optimization (MVO) algorithm is introduced to obtain the optimal power and time allocation. In addition, the performance of the integrated system using the TS-PS method is investigated and compared with that using other conventional methods. The results show that a maximized harvested energy solution using the TS-PS method can harvest the most energy. Moreover, the effects of main external environment conditions, namely, the room height and field of view (FoV) of a photo diode (PD) on the system performance are also analyzed. The increase of the room height and FoV of the PD reduces the harvested energy, but does not change the information rate and positioning accuracy in the optimized system adopted in this paper.
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Microorganisms of the genus Eperythrozoon are a zoonotic chronic infectious disease with wide distribution. We found that raccoons infected with Eperythrozoon showed obvious stunting, which seriously affected the economic benefits of raccoon dogs. To investigate the pathogenesis of the raccoon dog, we used transcriptome and proteome sequencing to analyze the changes in mRNA, miRNA, and protein expression in raccoon dogs infected with Eperythrozoon and normal raccoons. The results showed that the expression levels of genes related to immunity, metabolism, and enzyme activity were significantly changed. Among these, ERLIN1, IGF1R, CREB3L1, TNS1, TENC1, and mTOR play key roles. Additionally, the miR-1268, miR-125b, miR-10-5p, and miR-10 as central miRNAs regulate the expression of these genes. Integrated transcriptomic and proteomic analyses revealed consistent trends in mRNA and protein changes in MYH9, FKBP1A, PRKCA, and CYP11B2. These results suggest that Eperythrozoon may contribute to the slow development of raccoons by affecting the expression of mRNAs and miRNAs, reducing their immunity and causing metabolic abnormalities.
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MicroARNs , Mycoplasma , Animales , Multiómica , Proteómica , Perros Mapache/genética , Trastornos del Crecimiento , MicroARNs/genética , ARN Mensajero/genéticaRESUMEN
The antler is the unique mammalian organ found to be able to regenerate completely and periodically after loss, and the continuous proliferation and differentiation of mesenchymal cells and chondrocytes together complete the regeneration of the antler. Circular non-coding RNAs (circRNAs) are considered to be important non-coding RNAs that regulate body development and growth. However, there are no reports on circRNAs regulating the antler regeneration process. In this study, full-transcriptome high-throughput sequencing was performed on sika deer antler interstitial and cartilage tissues, and the sequencing results were verified and analyzed. The competing endogenous RNA (ceRNA) network related to antler growth and regeneration was further constructed, and the differentially expressed circRNA2829 was screened out from the network to study its effect on chondrocyte proliferation and differentiation. The results indicated that circRNA2829 promoted cell proliferation and increased the level of intracellular ALP. The analysis of RT-qPCR and Western blot demonstrated that the mRNA and protein expression levels of genes involved in differentiation rose. These data revealed that circRNAs play a crucial regulatory role in deer antler regeneration and development. CircRNA2829 might regulate the antler regeneration process through miR-4286-R+1/FOXO4.
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Cuernos de Venado , Ciervos , MicroARNs , Animales , Condrocitos , Transcriptoma , Cuernos de Venado/metabolismo , ARN Circular/genética , ARN Circular/metabolismo , Ciervos/genética , Diferenciación Celular/genética , Proliferación Celular/genética , MicroARNs/genética , MicroARNs/metabolismoRESUMEN
In this paper, an integrated visible light communication and positioning (VLCP) code division multiple access (CDMA) system is proposed for recovering original user data and obtaining positioning information simultaneously. A generalized modification method for balanced bipolar code set is presented, which can be applied to VLCP-CDMA system with intensity modulation. Both modified bipolar code sets, zero correlation zone (ZCZ) code set and Walsh code set, are employed and evaluated in VLCP-CDMA systems. When considering synchronous and quasi-synchronous (QS) systems, it is demonstrated that the modified ZCZ code set with ideal zero correlation zone properties performs better communication and positioning performance than the modified Walsh code set by system simulations and experiments. As a result, a bit error rate (BER) of 1.8×10-3 and an average positioning error of 1.50 cm are successfully obtained by adopting modified ZCZ code set in a 4-user real-time VLCP-CDMA system. It will offer a promising solution to meet both communication and positioning requirements of future intelligent systems.
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In this paper, a novel adaptive feedback threshold (AFT) based demodulation for mobile visible light communication and positioning (VLCP) integrated system is proposed. The AFT can vary with the received signal without excessive fluctuation and support communication and positioning in mobile environment. For the VLCP integrated system with single light emitting diodes (LED) and multiple photodetectors (PDs), maximal ratio combining (MRC) and received optical power ratio (ROPR) based on the AFT is further achieved for communication and positioning with high performance, respectively. It is demonstrated that high credible communication and high accuracy positioning for the mobile integrated VLCP system can be realized by using the proposed AFT based demodulation. As a result, the implemented VLCP system with a moving speed of 1 m/s is evaluated experimentally. Average positioning error of 3.43 cm with 800 mA current and the bit error ratio (BER) with different currents are also obtained.
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BACKGROUND: Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer with poor prognosis and limited treatment. As a major component of the tumor microenvironment, tumor-associated macrophages (TAMs) play an important role in facilitating the aggressive behavior of TNBC. This study aimed to explore the novel mechanism of TAMs in the regulation of epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties in TNBC. METHODS: Expression of the M2-like macrophage marker CD163 was evaluated by immunohistochemistry in human breast cancer tissues. The phenotype of M2 macrophages polarized from Tohoku-Hospital-Pediatrics-1 (THP1) cells was verified by flow cytometry. Transwell assays, wound healing assays, western blotting, flow cytometry, ELISA, quantitative polymerase chain reaction (qPCR), luciferase reporter gene assays, and immunofluorescence assays were conducted to investigate the mechanism by which TAMs regulate EMT and CSC properties in BT549 and HCC1937 cells. RESULTS: Clinically, we observed a high infiltration of M2-like tumor-associated macrophages in TNBC tissues and confirmed that TAMs were associated with unfavorable prognosis in TNBC patients. Moreover, we found that conditioned medium from M2 macrophages (M2-CM) markedly promoted EMT and CSC properties in BT549 and HCC1937 cells. Mechanistically, we demonstrated that chemokine (C-C motif) ligand 2 (CCL2) secretion by TAMs activated Akt signaling, which in turn increased the expression and nuclear localization of ß-catenin. Furthermore, ß-catenin knockdown reversed TAM-induced EMT and CSC properties. CONCLUSIONS: This study provides a novel mechanism by which TAMs promote EMT and enhance CSC properties in TNBC via activation of CCL2/AKT/ß-catenin signaling, which may offer new strategies for the diagnosis and treatment of TNBC. Video Abstract.
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Quimiocina CCL2 , Transición Epitelial-Mesenquimal , Células Madre Neoplásicas , Proteínas Proto-Oncogénicas c-akt , Neoplasias de la Mama Triple Negativas , Macrófagos Asociados a Tumores , beta Catenina , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Quimiocina CCL2/metabolismo , Humanos , Células Madre Neoplásicas/metabolismo , Células Madre Neoplásicas/patología , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal , Neoplasias de la Mama Triple Negativas/metabolismo , Neoplasias de la Mama Triple Negativas/patología , Microambiente Tumoral , Macrófagos Asociados a Tumores/metabolismo , Macrófagos Asociados a Tumores/patología , beta Catenina/metabolismoRESUMEN
BACKGROUND: The H1N1 influenza virus causes acute respiratory tract infection, and its clinical symptoms are very similar to those of ordinary influenza. The disease develops rapidly. If the flu is not treated, complications such as pneumonia, respiratory failure, and multiple organ damage can occur, resulting in a high fatality rate. Influenza virus mutates rapidly. At present, there is no specific drug for H1N1, so it is an urgent need for clinical care to find new drugs to treat H1N1. MATERIALS AND METHODS: The polysaccharide derived from Durvillaea Antarctica green algae has a certain antiviral effect. In this study, the results of CCK-8, apoptosis cycle detection, JC-1 and Western blotting proved that Duvira Antarctic polysaccharide (DAPP) has the ability to inhibit H1N1 infection. RESULTS: CCK-8 test showed that the DAPP with concentration at 32 µg/mL had no toxicity to MDCK cells. In addition, DAPP reduced cell apoptosis by inhibiting the ERK signaling pathway. Meanwhile, DAPP could increase the expression of STAT3 and significantly inhibited proinflammatory cytokines. CONCLUSIONS: In summary, these results suggested that DAPP may be potential with the ability to resist the H1N1 influenza virus.
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Subtipo H1N1 del Virus de la Influenza A , Virus de la Influenza A , Gripe Humana , Regiones Antárticas , Antivirales/farmacología , Antivirales/uso terapéutico , Apoptosis , Humanos , Gripe Humana/diagnóstico , Gripe Humana/tratamiento farmacológico , Polisacáridos/farmacología , Especies Reactivas de Oxígeno/farmacología , Transducción de Señal , Sincalida/farmacología , Sincalida/uso terapéuticoRESUMEN
BACKGROUND: Currently, Liver cancer is the fifth most common tumor and the second most important reason for cancer-related death in the world. However, there are still many limitations of the clinical treatment of liver cancer, and new treatment options are clearly needed. Fortunately, studies have shown that L-Selenocysteine has a certain effect on cancer. This study was to investigate the effects of L-Selenocysteine on the inhibition of cell proliferation and the promotion of apoptosis of HepG-2 cells through ROS mediated fine signaling pathway. MATERIALS AND METHODS: CCK-8 assay was applied to evaluating the cytotoxic effect of L-Selenocysteine on HepG-2 cells. Electron microscopy, flow cytometry and Western Blot was utilization in further researching cells signaling pathways. RESULTS: The growth of HepG-2 cells was inhibited by L-selenocysteine ââtreatment in a dose-dependent manner. The cell viability decreased to 52.20%, 43.20% and 30.83% under the treatment of 4, 8, 16 µM L-selenocysteine, respectively. L-Selenocysteine had higher cytotoxicity towards HepG-2 cells than normal cells. L-Selenocysteine can induce the apoptosis of HepG-2 cells by increasing the DNA fragmentation, and activating the Caspase-3. In addition, it was found that the mechanism of the induction to HepG-2 cell apoptosis by L-Selenocysteine was closely related to the overproduction of ROS and promoted apoptosis through the Bcl-2 signaling pathway. CONCLUSIONS: Our data suggest that L-selenocysteine ââmay cause mitochondrial damage and subsequently stimulate ROS production. ROS can damage cellular DNA and mediate the production of Casapase-8, Bid, Bcl-2 and other proteins, affecting downstream signaling pathways, and ultimately induced apoptosis.
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Neoplasias Hepáticas , Selenocisteína , Apoptosis , Línea Celular Tumoral , Humanos , Neoplasias Hepáticas/metabolismo , Potencial de la Membrana Mitocondrial , Mitocondrias/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/genética , Especies Reactivas de Oxígeno/metabolismo , Selenocisteína/metabolismo , Selenocisteína/farmacología , Selenocisteína/uso terapéutico , Transducción de SeñalRESUMEN
A hybrid multi-user access scheme based on orthogonal frequency-division multiple access and non-orthogonal multiple access (OFDMA-NOMA) is proposed for visible light communication (VLC) systems with a bandwidth-constrained channel. In the scheme, a novel user resource allocation method is used, to the best of our knowledge, to reduce the unfairness among different users caused by the high-frequency fading characteristic of VLC systems. Furthermore, the particle swarm optimization (PSO) is introduced to satisfy the transmitting power requirements of each user and to improve system performance. Simulation results show that, under the same VLC system conditions, the OFDMA-NOMA scheme with PSO has significant improvements in terms of user capacity and transmission rates compared to the purely NOMA scheme and the OFDMA scheme.
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To reveal the biomedical effects and mechanisms of hydrogen molecules urgently needs hydrogen molecular imaging probes as an imperative tool, but the development of these probes is extremely challenging. A catalytic hydrogenation strategy is proposed to design and synthesize a ratiometric fluorescent probe by encapsulating Pd nanoparticles and conjugating azido-/coumarin-modified fluorophore into mesoporous silica nanoparticles, realizing inâ vitro and inâ vivo fluorescence imaging of hydrogen molecules. The developed hydrogen probe exhibits high sensitivity, rapid responsivity, high selectivity and low detection limit, enabling rapid and real-time detection of hydrogen molecules both in cells and in the body of animal and plant. By application of the developed fluorescent probe, we have directly observed the super-high transmembrane and ultrafast transport abilities of hydrogen molecules in cells, animals and plants, and discovered inâ vivo high diffusion of hydrogen molecules.