FaultSSL: Seismic Fault Detection via Semi-supervised learning

The prevailing methodology in data-driven fault detection leverages synthetic data for training neural networks. However, it grapples with challenges when it comes to generalization in surveys exhibiting complex structures. To enhance the generalization of models trained on limited synthetic datasets to a broader range of real-world data, we introduce FaultSSL, a semi-supervised fault detection framework. This method is based on the classical mean teacher structure, with its supervised part employs synthetic data and a few 2D labels. The unsupervised component relying on two meticulously devised proxy tasks, allowing it to incorporate vast unlabeled field data into the training process. The two proxy tasks are PaNning Consistency (PNC) and PaTching Consistency (PTC). PNC emphasizes the feature consistency of the overlapping regions between two adjacent views in predicting the model. This allows for the extension of 2D slice labels to the global seismic volume. PTC emphasizes the spatially consistent nature of faults. It ensures that the predictions for the seismic, whether made on the entire volume or on individual patches, exhibit coherence without any noticeable artifacts at the patch boundaries. While the two proxy tasks serve different objectives, they uniformly contribute to the enhancement of performance. Experiments showcase the exceptional performance of FaultSSL. In surveys where other mainstream methods fail to deliver, we present reliable, continuous, and clear detection results. FaultSSL breaks the shackles of synthetic data, unveiling a promising route for incorporating copious amounts of field data into training and fostering model generalization across a broader spectrum of surveys.Comment: This work has been submitted to journal for possible publication. Copyright may be transferred without notice, after which this version may no longer be accessibl

MDA GAN: Adversarial-Learning-based 3-D Seismic Data Interpolation and Reconstruction for Complex Missing

The interpolation and reconstruction of missing traces is a crucial step in seismic data processing, moreover it is also a highly ill-posed problem, especially for complex cases such as high-ratio random discrete missing, continuous missing and missing in fault-rich or salt body surveys. These complex cases are rarely mentioned in current sparse or low-rank priorbased and deep learning-based approaches. To cope with complex missing cases, we propose Multi-Dimensional Adversarial GAN (MDA GAN), a novel 3-D GAN framework. It employs three discriminators to ensure the consistency of the reconstructed data with the original data distribution in each dimension. The feature splicing module (FSM) is designed and embedded into the generator of this framework, which automatically splices the features of the unmissing part with those of the reconstructed part (missing part), thus fully preserving the information of the unmissing part. To prevent pixel distortion in the seismic data caused by the adversarial learning process, we propose a new reconstruction loss Tanh Cross Entropy (TCE) loss to provide smoother gradients. We experimentally verified the effectiveness of the individual components of the study and then tested the method on multiple publicly available data. The method achieves reasonable reconstructions for up to 95% of random discrete missing, 100 traces of continuous missing and more complex hybrid missing. In surveys of fault-rich and salt bodies, the method can achieve promising reconstructions with up to 75% missing in each of the three directions (98.2% in total).Comment: This work has been submitted to journal for possible publication. Copyright may be transferred without notice, after which this version may no longer be accessibl

Peptide-fluorescent bacteria complex as luminescent reagents for cancer diagnosis

Currently in clinic, people use hematoxylin and eosin stain (H&E stain) and immunohistochemistry methods to identify the generation and genre of cancers for human pathological samples. Since these methods are inaccurate and time consuming, developing a rapid and accurate method to detect cancer is urgently demanded. In our study, binding peptides for lung cancer cell line A549 were identified using bacteria surface display method. With those binding peptides for A549 cells on the surface, the fluorescent bacteria (Escherichia coli with stably expressed green fluorescent protein) were served as specific detecting reagents for the diagnosis of cancers. The binding activity of peptide-fluorescent bacteria complex was confirmed by detached cancer cells, attached cancer cells and mice tumor xenograft samples. A unique fixation method was developed for peptide-bacteria complex in order to make this complex more feasible for the clinic use. This peptide-fluorescent bacteria complex has great potential to become a new diagnostic tool for clinical application

Decadal modulation of the relationship between tropical southern Atlantic SST and subsequent ENSO by Pacific Decadal Oscillation

This study identifies the relationship between tropical southern Atlantic (TSA) sea surface temperature anomaly (SSTA) and the El Niño-Southern Oscillation (ENSO) and focuses on how the Pacific Decadal Oscillation (PDO) modulates this relationship. Results suggest a significant but non-stationary interannual TSA-ENSO relationship which undergoes a significant decadal shift. A strong TSA-ENSO relationship is observed during the positive PDO phase, while this relationship is weak during the negative PDO phase. Two processes, involving the anomalous Pacific Walker circulation (PWC) and the intensity of air-sea interactions over the Pacific, are proposed for this decadal shift. During the positive PDO phase, the weak and variable PWC and strong air-sea interaction facilitate the development of SSTA in the tropical Pacific triggered by TSA SSTA, resulting in a strong TSA-ENSO relationship and vice versa. These findings emphasize the important role of the modulation of PDO on the TSA-ENSO relationship

Investigation and identification of let-7a related functional proteins in gastric carcinoma by proteomics

Abstract. MicroRNAs are small noncoding RNA molecules that control expression of target genes. Our previous studies show that let-7a decreased in gastric carcinoma and that up-regulation of let-7a by gene augmentation inhibited gastric carcinoma cell growth both in vitro and in vivo, whereas it remains largely unclear as to how let-7a affects tumor growth. In this study, proteins associated with the function of let-7a were detected by high throughout screening. The cell line of SGC-7901 stablely overexpressing let-7a was successfully established by gene cloning. Two-dimensional gel electrophoresis (2-DEy was used to separate the total proteins of SGC-7901/let-7a, SGC-7901/EV and SGC-7901, and PDQuest software was applied to analyze 2-DE images. Ten different protein spots were identified by MALDI-TOF-MS, and they may be the proteins associated with let-7a function. The overexpressed proteins included Antioxidant protein 2, Insulin-like growth factor binding protein 2, Protein disulfide isomerase A2, C-1-tetrahydrofolate synthase, Cyclin-dependent kinase inhibitor1 (CDKN1) and Rho-GTPase activating protein 4. The underexpressed proteins consisted of S-phase kinase-associated protein 2 (Spk2), Platelet membrane glycoprotein, Fibronectin and Cks1 protein. Furthermore, the different expression levels of the partial proteins (CDKN1, Spk2 and Fibronectin) were confirmed by western blot analysis. The data suggest that these differential proteins are involved in a novel let-7a signal pathway and these findings provide the basis to investigate the functional mechanisms of let-7a in gastric carcinoma

Na+/Ca2+ Exchanger 1 in Airway Smooth Muscle of Allergic Inflammation Mouse Model

Cytosolic free Ca2+ ([Ca2+]cyt) is essential for airway contraction, secretion and remodeling. [Ca2+]cyt homeostasis is controlled by several critical molecules, one of which is the Na+/Ca2+ exchanger 1 (NCX1) in the plasma membrane. Since little is currently known about NCX1 in the airway smooth muscle and its involvement in airway diseases, the present study was designed to investigate the expression and function of NCX1 in normal airway smooth muscle and its relevance to airway inflammation. Western blot analysis, tracheal smooth muscle contraction, and [Ca2+]cyt measurements were performed in mouse tracheal smooth muscle tissues and primary airway smooth muscle cell cultures. Additional studies were performed in a mouse model of allergic airway inflammation. Our data showed that NCX1 proteins were expressed in the human bronchial smooth muscle cells (HBSMCs), murine airway and whole lung. Carbachol raised [Ca2+]cyt in mouse tracheal smooth muscle cells and induced murine tracheal contraction, all of which were significantly attenuated by KB-R7943, a selective NCX inhibitor. Removal of extracellular Na+ increased [Ca2+]cyt in HBSMCs and mouse tracheal SMCs, which was dependent on extracellular Ca2+ and sensitive to KB-R7943. TNF-α treatment of HBSMCs significantly upregulated mRNA and protein expression of NCX1 and enhanced NCX activity. Finally, KB-R7943 abolished the airway hyperresponsiveness to methacholine in an ovalbumin-induced mouse model of allergic airway inflammation. Together, these findings indicate that NCX1 in airway smooth muscle may play an important role in the development of airway hyperresponsiveness, and downregulation or inhibition of NCX1 may serve as a potential therapeutic approach for asthma

Releasing the spindle assembly checkpoint without tension

Eukaryotic cells have evolved a spindle assembly checkpoint (SAC) that facilitates accurate genomic segregation during mitosis by delaying anaphase onset in response to errors in kinetochore microtubule attachment. In contrast to the well-studied molecular mechanism by which the SAC blocks anaphase onset, the events triggering SAC release are poorly understood. Papers in this issue by Uchida et al. (Uchida, K.S.K., K. Takagaki, K. Kumada, Y. Hirayama, T. Noda, and T. Hirota. 2009. J. Cell Biol. 184:383–390) and Maresca and Salmon (Maresca, T.J., and E.D. Salmon. 2009. J. Cell Biol. 184:373–381) make an important advance by demonstrating that SAC release depends on molecular rearrangements within the kinetochore rather than tension-produced stretch between sister kinetochores