Predicting underwater acoustic transmission loss in the SOFAR channel from ray trajectories via deep learning.

Predicting acoustic transmission loss in the SOFAR channel faces challenges, such as excessively complex algorithms and computationally intensive calculations in classical methods. To address these challenges, a deep learning-based underwater acoustic transmission loss prediction method is proposed. By properly training a U-net-type convolutional neural network, the method can provide an accurate mapping between ray trajectories and the transmission loss over the problem domain. Verifications are performed in a SOFAR channel with Munk's sound speed profile. The results suggest that the method has potential to be used as a fast predicting model without sacrificing accuracy.

Zinc oxide nanoparticles synthesized from Aspergillus terreus induces oxidative stress-mediated apoptosis through modulating apoptotic proteins in human cervical cancer HeLa cells.

OBJECTIVES: This study was aimed to analyze the cytotoxicity of biogenic zinc oxide nanoparticles (ZnO NPs) in human cervical epithelial cancer HeLa. METHODS: The ZnO NPs was synthesized from the culture filtrated of Aspergillus terreus, and examined by UV-spectroscopy, X-ray diffraction (XRD), transmission electron microscope (TEM), energy-dispersive X-ray (EDX) and Fourier transform infrared (FTIR) analysis. The cytotoxicity of synthesized ZnO NPs was analyzed by the MTT assay, and the expression of apoptotic proteins was examined by Western blot analyses. KEY FINDINGS: The ZnO NPs exhibited concentration-dependent cytotoxicity on HeLa cells and induced the apoptosis as evidenced by reduced superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) levels, and increased reactive oxygen species (ROS) and diminished mitochondrial membrane potential (MMP) was noticed in ZnO NPs treated HeLa cells. Western blot analyses explored that the Bcl-2 expression was significantly downregulated, whereas, the expression of p53, Bax, Caspase-3, Caspase-9 and Cytochrome-c were significantly upregulated in ZnO NPs treated cells. CONCLUSION: Consequently, the mycosynthesized ZnO NPs induces apoptosis in HeLa cells by persuading oxidative damage and modulating the apoptotic proteins. Therefore, A. terreus synthesized ZnO NPs could be used as an effective chemotherapeutic agent for cervical cancer treatment.

Polydopamine Ultrathin Film Growth on Mica via In-Situ Polymerization of Dopamine with Applications for Silver-Based Antimicrobial Coatings.

The development of polydopamine (PDA) coatings with a nanometer-scale thickness on surfaces is highly desirable for exploiting the novel features arising from the specific structure on the molecular level. Exploring the mechanisms of thin-film growth is helpful for attaining desirable control over the useful properties of materials. We present a systematic study demonstrating the growth of a PDA thin film on the surface of mica in consecutive short deposition time intervals. Film growth at each deposition time was monitored through instrumental techniques such as atomic force microscopy (AFM), water contact angle (WCA) analysis, and X-ray photoelectron spectroscopy (XPS). Film growth was initiated by adsorption of the PDA molecules on mica, with subsequent island-like aggregation, and finally, a complete molecular level PDA film was formed on the surface due to further molecular adsorption. A duration of 60-300 s was sufficient for complete formation of the PDA layer within the thickness range of 0.5-1.1 nm. An outstanding feature of PDA ultrathin films is their ability to act as a molecular adhesive, providing a foundation for constructing functional surfaces. We also explored antimicrobial applications by incorporating Ag nanoparticles into a PDA film. The Ag NPs/PDA film was formed on a surgical blade and then characterized and confirmed by SEM-EDS and XPS. The modified film inhibited bacterial growth by up to 42% on the blade after cutting through a pork meat sample.

Ferulic Acid Induces Apoptosis of HeLa and Caski Cervical Carcinoma Cells by Down-Regulating the Phosphatidylinositol 3-Kinase (PI3K)/Akt Signaling Pathway.

BACKGROUND Ferulic acid is an antioxidant phenolic compound derived from plants, which has effects on cancer cells. This study aimed to investigate the effects of ferulic acid on HeLa and Caski human cervical carcinoma cells and the molecular mechanisms involved. MATERIAL AND METHODS HeLa and Caski human cervical carcinoma cells were grown in culture and treated with increasing doses of ferulic acid. The MTT assay was used to evaluate cell viability. Flow cytometry was performed with 4',6-diamidino-2-phenylindole (DAPI) and Annexin V staining for cell apoptosis. The expression of myeloid leukemia cell differentiation-1 (Mcl-1) protein and MCL-1 mRNA were determined by Western blot and reverse transcription-polymerase chain reaction (RT-PCR). RESULTS Ferulic acid significantly reduced HeLa and Caski cell viability in the concentration range of 4-20 µM (P<0.05). Ferulic acid treatment promoted DNA condensation and significantly increased apoptosis in Caski cells (P<0.05). Ferulic acid treatment resulted in the activation of pro-caspase-3, pro-caspase-8, pro-caspase-9, and PARP. The MTT assay showed that ferulic acid did not reduce the viability of Caski cells treated with the caspase inhibitor, z-VAD-fmk. Ferulic acid reduced the levels of Bcl-2 and Mcl-1, and increased the levels of Bax and reactive oxygen species (ROS). In Caski cells, Akt and PI3K phosphorylation were reduced by ferulic acid in a concentration-dependent manner. CONCLUSIONS The effects of ferulic acid were dose-dependent and resulted in cell cytotoxicity and apoptosis of HeLa and Caski cells, and the PI3K/Akt signaling pathway was down-regulated in Caski cells.

The molecular mechanism of ovarian granulosa cell tumors.

Over these years, more and more sex cord-stromal tumors have been reported. Granulosa cell tumor (GCT) is a rare tumor in ovaries, accounts for 2% to 5% of ovarian cancers. The main different feature of GCTs from other ovarian cancers is that GCTs can lead to abnormally secreted hormones (estrogen, inhibin and Müllerian inhibiting substance). The GCT is divided into two categories according to the age of patients, namely AGCT (adult granulosa cell tumor) and JGCT (Juvenile granulosa cell tumor). AGCT patients accounts for 95%. Although the pathogenesis is not clear, FOXL2 (Forkhead box L2) mutation was considered as the most critical factor in AGCT development. The current treatment is dominated by surgery. Target therapy remains in the adjuvant therapy stage, such as hormone therapy. During these years, other pathogenic factors were also explored, such as PI3K/AKT (phosphatidylinositol-3-kinase; serine/threonine kinase), TGF-ß (Transforming growth factor beta) signaling pathway, Notch signaling pathway, GATA4 and VEGF (vascular endothelial growth factor). These factors and signaling pathway play important roles in GCT cell proliferation, apoptosis, or angiogenesis. The purpose of this review is to summarize the possible pathogenic factors and signaling pathways, which may shed lights on developing potential therapeutic targets for GCT.