Utilizing deep learning algorithms for automated oil spill detection in medium resolution optical imagery.

This study evaluates the performance of three typical convolutional neural network based deep learning algorithms for oil spill detection using medium-resolution optical satellite imagery from Sentinel-2 MSI, Landsat-8 OLI, and Landsat-9 OLI2. Oil slick training and validation dataset were created through a semi-automatic labeling approach, based on chronic and accidental oil spill cases reported worldwide. The research enhances UNet, BiSeNetV2, and DeepLabV3+ architectures by integrating attention mechanisms including the Squeeze-and-Excitation module (SE), Convolutional Block Attention Module (CBAM), and a Simple, parameter-free Attention Module (SimAM), analyzing the optimal model for oil spill detection. Notably, UNet integrated with CBAM, especially with sun glint as a feature, significantly outperformed others, achieving a micro-average F1 score of 88.8 %. This research highlights deep learning's potential in optical remote sensing for oil spill detection, stressing its escalating relevance with the growing deployment of medium- to high-resolution optical satellites.

Drug-induced lactate confers ferroptosis resistance via p38-SGK1-NEDD4L-dependent upregulation of GPX4 in NSCLC cells.

Ferroptosis is a newly defined non-apoptotic programmed cell death resulting from the accumulation of lipid peroxides. Whether ferroptosis plays any role in chemotherapy remains to be established. Here, we reported that ferroptosis represents a part of the chemotherapeutic drug etoposide-induced cell death response in Small Cell Lung Cancer (SCLC) cells and adaptive signaling molecule lactate protects Non-Small Cell Lung Cancer (NSCLC) from etoposide-induced ferroptosis. Lactate derived from metabolic reprogramming increases the expression of glutathione peroxidase 4 (GPX4) to promote ferroptosis resistance in NSCLC. Furthermore, we identified E3-ubiquitin ligase NEDD4L as a major regulator of GPX4 stability. Mechanistically, Lactate increases mitochondrial ROS generation and drives activation of the p38-SGK1 pathway, which attenuates the interaction of NEDD4L with GPX4 and subsequent ubiquitination and degradation of GPX4. Our data implicated the role of ferroptosis in chemotherapeutic resistance and identified a novel post-translational regulatory mechanism for the key Ferroptosis mediator GPX4.

Optical discrimination of emulsified oil in optically complex estuarine waters.

Coastal estuaries, characterized by highly varying waters with complex optical properties, pose challenges for effective oil discrimination via optical remote sensing. In this study, an object-based spectra comparison (OBSC) approach was proposed to extract emulsified oil slicks from Balikpapan Bay, Indonesia, using optical imagery from Sentinel-2 Multispectral Instrument (MSI) and PlanetScope. The OBSC approach utilizes the spectral signatures of oil emulsion to develop emulsified oil index and normalized emulsified oil index to identify potentially emulsified oil objects from MSI and PlanetScope, respectively. Reflectance spectra of the potential objects were compared with those from dynamically-selected nearby waters to rule out false-positive detections, accounting for the varying water optical properties in the estuary. This OBSC approach performed well in extracting emulsified oil slicks from optical images. Moreover, multiple sensor capabilities for oil detection were compared, and requirements for detection and discrimination of oil spills in the coastal estuary environment were further discussed.

Clinical feature and sural biopsy study in nitrous oxide-induced peripheral neuropathy.

OBJECTIVE: The objective was to analyze the clinical characteristics and pathological characteristics of sural biopsy in nitrous oxide (N2O) -induced peripheral neuropathy. METHODS: We recruited 18 patients with N2O abuse-induced neurological disorders and reported their demographic data, clinical manifestations, laboratory examinations, and nerve conduction studies. Seven patients underwent sural nerve biopsy pathologic examination. RESULTS: All 18 patients had polyneuropathy, the nerve conduction results showed significant reductions in motor and sensory amplitudes, slowing of conduction velocities, and prolongation of latencies in most tested nerves compared to the controls. Toluidine blue staining of semi-thin sections of sural nerve biopsy showed decreased myelinated nerve fiber density, increased thin myelinated nerve fiber density, and axonal regeneration. Electron microscopy showed axonal degeneration and nerve regeneration. CONCLUSION: The main manifestations of peripheral nerve damage caused by the abuse of N2O are lower limb weakness and distal sensory disorder. The nerve conduction study results demonstrated that mixed axonal and demyelinating neuropathy was the most common type of neuropathy. Sural biopsy showed the main pathological change was chronic axonal degeneration.

snoRNA23 enhances the progression of hepatocellular carcinoma via regulation of the Wnt/?-catenin pathway.

Small nucleolar non-coding RNA(snoRA)23 is upregulated in human pancreatic ductal adenocarcinoma. However, to the best of our knowledge, the role of snoRA23 in hepatocellular carcinoma progression has not been determined. MTT and colony formation assays were used to assess the cell viability and proliferation of HCC cells with snoRA23 knocked down, respectively, and a lymphatic vessel formation assay was used to determine tube formation ability of Human dermal lymphatic endothelial cells treated with conditioned media from HCC cell cultures. The results showed that snoRA23 knockdown attenuated cell viability, colony formation,and lymphatic vessel formation in HCC cells. snoRA23 was correlated with the prolonged overall survival of patients with HCC. Additionally, snoRA23 knockdown downregulated the Wnt/?-catenin signaling pathway by decreasing Wnt3a expression and ?-catenin levels.?-methylacyl-CoA racemase (AMACR) levels were notably decreased by snoRA23 depletion. Finally, it was confirmed that AMACR overexpression partially rescued snoRA23-modulated HCC tumorigenesis. The results of the present study provide further insight into the role of non-coding RNAs in the development and progression of HCC.

Remote sensing assessment of oil spills near a damaged platform in the Gulf of Mexico.

An oil platform in the Mississippi Canyon 20 (MC-20) site was damaged by Hurricane Ivan in September 2004. In this study, we use medium- to high-resolution (10-30 m) optical remote sensing imagery to systematically assess oil spills near this site for the period between 2004 and 2016. Image analysis detects no surface oil in 2004, but ~40% of the cloud-free images in 2005 show oil slicks, and this number increases to ~70% in 2006-2011, and >80% since 2012. For all cloud-free images from 2005 through 2016 (including those without oil slicks), delineated oil slicks show an average oil coverage of 14.9 km2/image, with an estimated oil discharge rate of 48 to ~1700 barrels/day, and a cumulative oil-contaminated area of 1900 km2 around the MC-20 site. Additional analysis suggests that the detected oil slick distribution can be largely explained by surface currents, winds, and density fronts.

Oil slick morphology derived from AVIRIS measurements of the Deepwater Horizon oil spill: Implications for spatial resolution requirements of remote sensors.

Using fine spatial resolution (~7.6m) hyperspectral AVIRIS data collected over the Deepwater Horizon oil spill in the Gulf of Mexico, we statistically estimated slick lengths, widths and length/width ratios to characterize oil slick morphology for different thickness classes. For all AVIRIS-detected oil slicks (N=52,100 continuous features) binned into four thickness classes (≤50 µm but thicker than sheen, 50-200 µm, 200-1000 µm, and >1000 µm), the median lengths, widths, and length/width ratios of these classes ranged between 22 and 38 m, 7-11 m, and 2.5-3.3, respectively. The AVIRIS data were further aggregated to 30-m (Landsat resolution) and 300-m (MERIS resolution) spatial bins to determine the fractional oil coverage in each bin. Overall, if 50% fractional pixel coverage were to be required to detect oil with thickness greater than sheen for most oil containing pixels, a 30-m resolution sensor would be needed.

Surface oil footprint and trajectory of the Ixtoc-I oil spill determined from Landsat/MSS and CZCS observations.

The Ixtoc-I oil spill occurred in 1979 in shallow waters (50 m) of the Bay of Campeche, Mexico. Although it is known that a large portion of the released oil from this second largest accidental marine oil spill in history reached the surface, to date there has been no attempt to document the surface footprint and trajectory of the released oil. Our study attempts to fill this knowledge gap using remote sensing data collected by Landsat/MSS and CZCS. Both showed the same general patterns of oil trajectory to the northwest and north, nearly parallel to the coastline of the western Gulf of Mexico (GoM) with possible oil landing on Mexican and Texas beaches. Field observations at selected beaches and islands along the coast of the western and southern GoM during and after the spill confirmed these satellite-based findings, which were also used to help in planning a recent field campaign to collect sediment samples in the southern GoM.

[Roles of epidermal growth factor receptor signaling pathway in silicon dioxide-induced epithelial-mesenchymal transition in human pulmonary epithelial cells].

OBJECTIVE: To investigate the effect of silicon dioxide (SiO2) on the expression of E-cadherin, α-smooth muscle actin (α-SMA), and transforming growth factor ß1(TGF-ß1) in human pulmonary epithelial cells (A549) with epithelial-mesenchymal transition (EMT), and to study the roles of epidermal growth factor receptor (EGFR) signaling pathway in SiO2-induced EMT in A549 cells in vitro. METHODS: Alveolar macrophages (AMs) were stimulated with 50 µg/ml SiO2for 3, 6, 12, 18, 24, or 36 h, and the supernatants were collected to measure the expression of TGF-ß1protein by ELISA. The AM supernatant in which TGF-ß1reached the highest expression (T=18 h) was used as AM-conditioned supernatant. A549 cells were cultured in AM-conditioned supernatant and stimulated with indicated doses of SiO2(0, 50, 100, and 200 µg/ml) for 48 h. The cell morphological changes were observed using an inverted microscope. The cells were collected at different times, and the mRNA and protein expression levels of E-cadherin, α-SMA, and EGFR were measured by RT-PCR and immunocytofluorescence, respectively. RESULTS: After stimulation by SiO2, the expression level of TGF-ß1protein at each time point was significantly higher in the presence of AM supernatants than in the absence of AM supernatants (P<0.05). With the action time, the expression level of TGF-ß1protein increased at first and then decreased, and the highest level was reached at 18 h. After exposure to SiO2, A549 cells exhibited mesenchymal characteristics, such as a spindle shape, pseudopodia change, and fibroblast-like morphology, as observed by inverted microscope, especially in the 200 µg/ml group. With increased concentration of SiO2, the mRNA and protein expression of E-cadherin was down-regulated gradually, especially in the 200 µg/ml group, whereas the mRNA and protein expression of α-SMA and EGFR was up-regulated gradually, especially in the 200 µg/m1 group. There were significant differences between the SiO2-treated groups (50, 100, and 200 µg/ml SiO2) and the control group (P<0.05). CONCLUSION: After being stimulated by SiO2in vitro, AMs have significantly increased expression level of TGF-ß1protein. The AM supernatant together with SiO2can induce the transition of pulmonary epithelial cells to mesenchymal cells, and its mechanism may be related to the EGFR signaling pathway.

[Effect of tagalsin on p53 and Bcl-2 expression in hepatoma H(22) tumor-bearing mice].

OBJECTIVE: To explore the effect and mechanism of tagalsin on hepatoma cells. METHODS: The animal models were established by transplanting H(22) mouse hepatoma cells to mouse liver, and ten days later the mice were randomly divided into five groups: blank group, carmofur positive group and tagalsin groups, including low-dose, middle-dose and high-dose groups. Then medicine or oil was given to the mice by gastric gavage in consecutive 5 days with a 2-days interval as a course of treatment, two courses in all. All mice were killed at 24 hours after medication, and the survival period, ascites conditions, aggressive conditions intra- or extra-liver, weight changes, tumor volume and spleen index of the tumor-bearing mice were observed. Pathological changes of the tumors were examined. Apoptotic factors p53 and Bcl-2 protien and mRNA were detected by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR). RESULTS: tagalsin inhibited the hepatoma growth effectively without influencing spleen index to some extent. The tumor inhibition rate of tagalsin low, middle and high dose groups were 17.9%, 63.1% and 71.8%, respectively. Immunohistochemical results showed that the p53 and Bcl-2 protein positive cell counts of the positive control and experimental groups were significantly lower than those of the blank group (P < 0.01). RT-PCR results showed that the p53 mRNA expression was significantly enhanced and Bcl-2 mRNA expression was decreased in the positive control groups and tagalsin treatment groups, especially in the high dose group, compared with those of the blank group (P < 0.05). CONCLUSIONS: tagalsin can inhibit the growth of mouse hepatoma cells significantly. The mechanism of its anti-tumor effect may work via up-regulating the wild type p53 gene expression and down-regulating Bcl-2 gene expression and thus regulating tumor cell apoptosis.