Search

Electrocardiograph signals reflect the current state of the heart and have great significance to the clinical diagnosis of the heart. Convolutional neural networks perform excellently in electrocardiograph pattern recognition. However, CNNs processing ECG signals need to convert them from 1D to 2D, leading to additional circuit and time costs in hardware. Here, a convolution organic transistor (COT) is proposed for monitoring the ECG with CNNs. Based on the surface electric field effect and trap effect, COT can directly process 1D ECG data without complex preprocessing. It can complete the convolution calculation of ECG signals ≈20 000 times per second in theory and reduce the number of devices by 83% compared to conventional arrays. Further, actual ECG signals are measured and input into the COT, which can initially recognize the type of ECG abnormality. Finally, a point calculation detection system is established with 96.2% recognition accuracy in the five‐heartbeat classification task by combining the 1D CNN. [ABSTRACT FROM AUTHOR]

Empowering displays with intelligent functions enables their application in intelligent image processing and intelligent interactive displays, which is the combination of future display and artificial intelligence technologies. However, existing display technologies face significant processing and transmission burdens due to their conventional hardware separation architecture, which separates memory from the processor and display module from the processing module. To address these challenges, a highly integrated memory‐ processing‐display intelligent light‐emitting hardware (MPDIH) capable of information generation, memory, processing, and visualization is proposed. The MPDIH, based on an organic light‐sensitive layer and activated by ultraviolet light irradiation, exhibits unique photoinhibition behavior attributed to the reverse light‐induced electric field formed by the directional arrangement of photo‐generated excitons. This behavior enables dynamic regulation and autonomous learning during the device training process. Leveraging this phenomenon, intelligent image processing is successfully demonstrated, achieving a significant contrast improvement with a maximum enhancement of 261% compared to unprocessed raw signals. Furthermore, the memory‐processing‐display intelligent image processing scheme enables fashion MNIST image recognition using an artificial neural network, and achieves noticeably higher recognition accuracy (>89%) compared to the original fuzzy images (<59%). Consequently, the proposed memory‐processing‐display intelligent light‐emitting hardware holds promise for future applications in integrated photonic systems and interactive artificial intelligence displays. [ABSTRACT FROM AUTHOR]

Bone is one of the most frequent sites for metastasis in breast cancer patients. Bone metastasis significantly reduces the survival time and the life quality of breast cancer patients. Germacrone (GM) can serve humans as an anti‐cancer and anti‐inflammation agent, but its effect on breast cancer‐induced osteolysis remains unclear. This study aims to investigate the functions and mechanisms of GM in alleviating breast cancer‐induced osteolysis. The effects of GM on osteoclast differentiation, bone resorption, F‐actin ring formation, and gene expression were examined in vitro. RNA‐sequencing and Western Blot were conducted to explore the regulatory mechanisms of GM on osteoclastogenesis. The effects of GM on breast cancer‐induced osteoclastogenesis, and breast cancer cell malignant behaviors were also evaluated. The in vivo efficacy of GM in the ovariectomy model and breast cancer bone metastasis model with micro‐CT and histomorphometry. GM inhibited osteoclastogenesis, bone resorption and F‐actin ring formation in vitro. Meanwhile, GM inhibited the expression of osteoclast‐related genes. RNA‐seq analysis and Western Blot confirmed that GM inhibited osteoclastogenesis via inhibition of MAPK/NF‐κB signaling pathways. The in vivo mouse osteoporosis model further confirmed that GM inhibited osteolysis. In addition, GM suppressed the capability of proliferation, migration, and invasion and promoted the apoptosis of MDA‐MB‐231 cells. Furthermore, GM could inhibit MDA‐MB‐231 cell‐induced osteoclastogenesis in vitro and alleviate breast cancer‐associated osteolysis in vivo human MDA‐MB‐231 breast cancer bone metastasis‐bearing mouse models. Our findings identify that GM can be a promising therapeutic agent for patients with breast cancer osteolytic bone metastasis. [ABSTRACT FROM AUTHOR]

Organic photoelectric neuromorphic devices that mimic the brain are widely explored for advanced perceptual computing. However, current individual neuromorphic synaptic devices mainly focus on utilizing linear models to process optoelectronic signals, which means that there is a lack of effective response to nonlinear structural information from the real world, severely limiting the computational efficiency and adaptability of networks to static and dynamic information. Here, a feedforward photoadaptive organic neuromorphic transistor with mixed‐weight plasticity is reported. By introducing the potential of the space charge to couple gate potential, photoexcitation, and photoinhibition occur successively in the channel under the interference of constant light intensity, which enables the device to transform from a linear model to a nonlinear model. As a result, the device exhibits a dynamic range of over 100 dB, exceeding the currently reported similar neuromorphic synaptic devices. Further, the device achieves adaptive tone mapping within 5 s for static information and achieves over 90% robustness recognition accuracy for dynamic information. Therefore, this work provides a new strategy for developing advanced neuromorphic devices and has great potential in the fields of intelligent driving and brain‐like computing. [ABSTRACT FROM AUTHOR]

Specific localization of photosensitizers (PSs) to a certain organelle could result in targeted attack to cause greater trauma to cancer cells, eventually maximizing photodynamic therapy (PDT). However, currently, efficient and precise transportation of PSs via drug delivery to tumor cells and subcellular organelles is still challenging, due to a so‐called step‐reduction delivery dilemma (SRDD) which also threatens anticancer drug delivery to exert their efficacy. Herein, a cascade targeting near infrared II (NIR II) fluorescent nanoparticles (NPER/BO‐PDT) is designed that can target bone tumor first and then target the subcellular organelle of endoplasmic reticulum (ER). It is found that NPER/BO‐PDT achieves the targeted accumulation of the bone tumor and then ER. NPER/BO‐PDT generates reactive oxygen species (ROS) in the subcellular organelles of ER under near infrared light irradiation. The continuous ER stress by ROS promotes the release of more damage‐associated molecular patterns, induces immunogenic cell death, stimulates the adaptive immune response, and further synergistically inhibits tumor growth, achieving the so‐called photodynamic‐immunotherapy. Overall, this study exemplifies a safe and efficient nano‐drug delivery system for a bone and ER cascade targeting via delivery of PSs to break the SRDD and highlights potential clinical translation. [ABSTRACT FROM AUTHOR]

Background: Our recent studies have indicated that miR‐153‐3p is downregulated in the esophageal squamous cell carcinoma (ESCC) cell lines and tissues. Upregulation of miR‐153‐3p was found to inhibit migration and invasion of ESCC cells. However, whether miR‐153‐3p regulates the cisplatin sensitivity in ESCC cells remains unclear. In this study, we explored whether and how miR‐153‐3p regulates the proliferation and confers cisplatin resistance in ESCC by targeting the Nrf‐2 protein. Methods: Eca109 cell line was transfected with microRNA‐153‐3p mimics or Nrf‐2siRNA and cell proliferation and cisplatin resistance were studied. A dual‐luciferase reporter assay was performed on Eca109 cells cotransfected with the wild‐type/mutant 3′UTR sequences of Nrf‐2 and control or microRNA‐153‐3p mimics. We determined the correlation between microRNA‐153‐3p and Nrf‐2 expression in human ESCC samples and explored the effect of Nrf‐2 in the overall survival rate of ESCC patients. Results: MiR‐153‐3p significantly suppressed cell proliferation and increased the sensitivity of Eca‐109 cells to cisplatin. MiR‐153‐3p showed a negative correlation with Nrf‐2 in human esophageal carcinoma tissues. MiR‐153‐3p suppressed the expression of Nrf‐2 via binding to its 3′‐UTR region. Furthermore, inhibition of Nrf‐2 also decreased cell proliferation and increased the sensitivity of Eca109 cells to cisplatin. High expression of Nrf‐2 in human ESCC samples was associated with poor overall survival of ESCC patients. Conclusion: MiR‐153‐3p inhibits cell proliferation and confers cisplatin resistance by downregulating Nrf‐2 expression in Eca‐109 cells. Thus, miR‐153‐3p/Nrf‐2 may play an important role in conferring cisplatin resistance in ESCC. Nrf‐2 appears to be a promising therapeutic target for ESCC. [ABSTRACT FROM AUTHOR]

Long noncoding RNAs (lncRNAs) are emerging as key regulators in cancer initiation and progression. TP53TG1 is a recently identified lncRNA and several studies have shown that TP53TG1 may play the role of tumor suppressor gene or oncogene in different tumors. Nevertheless, the involvement of TP53TG1 in carcinogenesis of pancreatic ductal adenocarcinoma (PDAC) has not been characterized. In our studies, we identified that TP53TG1 was highly expressed in PDAC and was a novel regulator of PDAC development. Knockdown of TP53TG1 inhibited proliferation, induced apoptosis, and decreased migration and invasion in PDAC cells, whereas enhanced expression of TP53TG1 had the opposite effects. Mechanistically, TP53TG1 could directly bind to microRNA (miR)‐96 and effectively function as a sponge for miR‐96, thus antagonizing the functions of miR‐96 and leading to derepression of its endogenous target KRAS, which is a core oncogene in the initiation and maintenance of PDAC. Taken together, these observations imply that TP53TG1 contributes to the growth and progression of PDAC by acting as a competing endogenous RNA (ceRNA) to competitively bind to miR‐96 and regulate KRAS expression, which highlights the importance of the complicated miRNA‐lncRNA network in modulating the progression of PDAC. [ABSTRACT FROM AUTHOR]

Aflatoxin G1 (AFG1), a member of the AF family with cytotoxic and carcinogenic properties, could cause DNA damage in alveolar type II (AT‐II) cells and induce lung adenocarcinoma. Recently, we found AFG1 could induce chronic lung inflammation associated with oxidative stress in the protumor stage. Chronic inflammation plays a critical role in cigarette smoke or benzo[a]pyrene‐induced lung tissues damage. However, it is unclear whether and how AFG1‐induced lung inflammation affects DNA damage in AT‐II cells. In this study, we found increased DNA damage and cytochrome P450 (CYP2A13) expression in AFG1‐induced inflamed lung tissues. Furthermore, we treated the mice with a soluble tumor necrosis factor (TNF)‐α receptor and AFG1 and found that TNF‐α neutralization inhibited the AFG1‐induced chronic lung inflammation in vivo, and then reversed the CYP2A13 expression and DNA damage in AT‐II cells. The results suggest that AFG1 induces TNF‐α‐dependent lung inflammation to regulate 2A13 expression and enhance DNA damage in AT‐II cells. Then, we treated the primary mice AT‐II cells and human AT‐II like cells (A549) with AFG1 and TNF‐α and found that TNF‐α enhanced the AFG1‐induced DNA damage in mice AT‐II cells as well as A549 cells in vitro. In AFG1‐exposed A549 cells, TNF‐α‐enhanced DNA damage and apoptosis were reversed by CYP2A13 small interfering RNA. Blocking NF‐κB pathway inhibited the TNF‐α‐enhanced CYP2A13 upregulation and DNA damage confirming that the CYP2A13 upregulation by TNF‐α plays an essential role in the activation of AFG1 under inflammatory conditions. Taken together, our findings suggest that AFG1 induces TNF‐α‐dependent lung inflammation, which upregulates CYP2A13 to promote the metabolic activation of AFG1 and enhance oxidative DNA damage in AT‐II cells. [ABSTRACT FROM AUTHOR]

Recently, we discovered that Aflatoxin G1 (AFG1) induces chronic lung inflammatory responses, which may contribute to lung tumorigenesis in Balb/C mice. The cancer cells originate from alveolar type II cells (AT-II cells). The activated AT-II cells express high levels of MHC-II and COX-2, may exhibit altered phenotypes, and likely inhibit antitumor immunity by triggering regulatory T cells (Tregs). However, the mechanism underlying phenotypic alterations of AT-II cells caused by AFG1-induced inflammation remains unknown. In this study, increased MHC-II expression in alveolar epithelium was observed and associated with enhanced Treg infiltration in mouse lung tissues with AFG1-induced inflammation. This provides a link between phenotypically altered AT-II cells and Treg activity in the AFG1-induced inflammatory microenvironment. AFG1-activated AT-II cells underwent phenotypic maturation since AFG1 upregulated MHC-II expression on A549 cells and primary human AT-II cells in vitro. However, mature AT-II cells may exhibit insufficient antigen presentation, which is necessary to activate effector T cells, due to the absence of CD80 and CD86. Furthermore, we treated A549 cells with AFG1 and TNF-α together to mimic an AFG1-induced inflammatory response in vitro, and we found that TNF-α and AFG1 coordinately enhanced MHC-II, CD54, COX-2, IL-10, and TGF-β expression levels in A549 cells compared to AFG1 alone. The phenotypic alterations of A549 cells in response to the combination of TNF-α and AFG1 were mainly regulated by TNF-α-mediated induction of the NF-κB pathway. Thus, enhanced phenotypic alterations of AT-II cells were induced in response to AFG1-induced inflammation. Thus, AT-II cells are likely to suppress anti-tumor immunity by triggering Treg activity. J. Cell. Physiol. 230: 1199-1211, 2015. © 2014 Wiley Periodicals, Inc., A Wiley Company [ABSTRACT FROM AUTHOR]

Background and Aim The incidence of distal gastric adenocarcinoma has significantly decreased, but gastric cardia adenocarcinoma has been on the rise. Cardia adenocarcinoma might be a specific entity distinct from the carcinoma of the rest stomach. The aim was to explore putative differences in p16 INK4a-retinoblastoma ( Rb) pathway and INK4a/ ARF methylation between gastric cardia and distal adenocarcinomas. Methods Ninety-six cardia adenocarcinomas and 79 distal samples were analyzed for comparing p16 INK4a- Rb expressions, INK4a/ ARF deletion, and methylation using immunohistochemistry, polymerase chain reaction, and methylation-specific polymerase chain reaction. Results The expression of p16 INK4a in cardia adenocarcinoma (43.2%) was significantly lower than in distal cases (75.0%, P < 0.05). As well, cardia adenocarcinoma showed lower expression of p14 ARF compared with distal cases (34.1% vs 57.5%, P < 0.05). The incidence of p16 INK4a deletion was 20.5% and 15.0%, while p14 ARF deletion was 18.2% and 10.0% in cardia and distal adenocarcinomas, respectively, showing no significant differences between two entities. However, the incidences of p14 ARF and p16 INK4a methylation in cardia adenocarcinoma were significantly higher than in distal samples (p14 ARF: 61.5% vs 43.6%; p16 INK4a: 73.1% vs 51.3%, P < 0.05). INK4a/ ARF methylations were more prevalent in poorly differentiated cardia carcinoma compared with poorly differentiated distal cases. Conclusions There were differences in p16 INK4a- Rb immunotypes and INK4a/ ARF methylation between two entities, indicating that cardia adenocarcinoma may be different in cell proliferation, differentiation, and gene biomarkers compared with distal gastric adenocarcinoma. [ABSTRACT FROM AUTHOR]

The correlation between low serum PG level and H. pylori infection with the development of gastric cancer has caused considerable concerns all over the world. Some authors exclaimed that gastric cancer developed only in patients infected with H. pylori, whereas the other had different findings. In this study, 1,501 adult local residents with determined serum PG levels and anti H. pylori IgG status were followed for 14 years for the development of gastric cancer in a rural community with high risk of gastric cancer in Hebei Province, China. The results showed the accumulated gastric cancer incidence in the subjects with abnormal PG level and those with H. pylori infection were all significantly higher than that in the corresponding normal controls (53.9‰ vs. 12.7‰, p < 0.05 and 23.1‰ vs. 5.93‰, p < 0.05). The highest gastric cancer incidence was seen in the subjects with both abnormal serum PG and positive H. pylori (56.0‰), and followed by the subjects with abnormal PG and negative H. pylori (47.6‰) and those with normal serum PG and positive H. pylori (18.4‰). The abnormal serum PG level (OR 3.029) and H. pylori infection (OR 4.345) were all risk factors for the development of gastric cancer. The results suggested that the subjects with abnormal serum PG level and/or positive H. pylori infection in the rural area of China were all high risk population for gastric carcinoma and the subjects with both abnormal serum PG and positive H. pylori infection were at especially high risk for the development of gastric carcinoma. [ABSTRACT FROM AUTHOR]

Ochratoxin A (OTA) is nephrotoxic, immunosuppressive, and teratogenic in many species and is a possible human carcinogen. In this study, we investigated the OTA pollution situations of grains in northern China and the signaling pathway that mediated OTA-induced apoptosis in human tubular kidney cells (HKCs). Samples of grains collected from three representative areas were determined by using high-performance liquid chromatography fluorescence method. The effects of OTA on cell apoptosis, caspase-3, Bax, and Bcl-2 expression, and phosphorylation of c-Jun NH2 terminal kinase (JNK) were detected in cultured HKCs via flow cytometry (FCM), Hoechst 33258 staining, and Western blot. It showed that OTA pollution of edible grains was very common in north China. OTA could affect caspase-3, Bax, and Bcl-2 expression and increased cell apoptosis in cultured HKCs. The JNK signalling pathway might play an important role during these cellular events. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:139-146, 2012; View this article online at . DOI 10.1002/jbt.20420 [ABSTRACT FROM AUTHOR]

Oxidization of diamond in the sintering process of diamond/glass composites results in uncontrolled expansion with many irregular pores and low bending strength of the tools. In this paper, Al powder was used as oxygen getter due to its excellent affinity with oxygen. Its oxidization product, Al2O3, entered into glass network. Consequently, oxidization of the grits was inhibited, and the wettability of diamond grits by the matrix improved. As a result, the expansion phenomenon was inhibited and the bending strength improved for all the composites. The minimum volume expansion rate and maximum bending strength were obtained for the composite with 4 wt% Al powder. This Al content resulted in a decrease of volume expansion rate from 175.2% to −10.9%, and an increase in bending strength from 11.3 to 75.1 MPa compared with the composite without Al powder. [ABSTRACT FROM AUTHOR]