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Among the various remote sensing technologies that have been applied to monitor oil spills on the sea surface, passive ultraviolet (UV) imaging is a controversial one that has raised some disputes in the community of oil spill remote sensing. As a result, the research and applications of oil spill detection using passive UV imaging have not been as developed as other methods. In order to clarify some existing questions on oil spill detection using passive UV remote sensing technology, this paper discusses the needs of thin oil film detection, examines the feasibility of thin oil film detection using passive UV imaging through field experiments under controlled conditions and validates it with the UV imagery derived from the airborne visible/infrared imaging spectrometer (AVIRIS) observation of the Deepwater Horizon oil spill. Two types of fully automatic models are designed to extract the thin oil films on the water surface: (1) a binary classification model based on an adaptive threshold; (2) an unsupervised image segmentation model based on image clustering and greyscale histogram analysis. The two models are tested on the UV imagery obtained through both field experiments and AVIRIS observations. The results indicate that the binary classification model can extract the thin oil films with reasonable accuracy under stable imaging conditions, while the unsupervised image clustering model can robustly detect the thin oil films at the cost of higher computational complexity. These results infer that passive UV imaging is an effective way to detect thin oil films and could be applied to provide early warning at the beginning stage of oil spills and reduce further damage. It may also be applied as a supplementary method for oil spill detection to achieve comprehensive oil spill monitoring. [ABSTRACT FROM AUTHOR]

Objective: To examine efficacy and safety of tramadol for knee or hip osteoarthritis (OA). Methods: PubMed, Embase, Cochrane Library, and Web of Science were searched up to May 2020 for randomized controlled trials (RCTs) comparing any of the following interventions: tramadol 100 mg/day, 200 mg/day, and 300 mg/day, and placebo for knee or hip OA. Pain and function were measured at or near 12 weeks for efficacy. Gastrointestinal, cardiovascular, and central nervous system (CNS) adverse events (AEs), and withdrawals were measured for safety. Bayesian network meta‐analysis was conducted. Results: Six RCTs (3,611 participants) were included. Tramadol 100 mg/day (standardized mean difference [SMD] –0.16 [95% confidence interval (95% CI) –0.34, 0.00]), 200 mg/day (SMD –0.21 [95% CI –0.37, –0.06]), and 300 mg/day (SMD –0.30 [95% CI –0.48, –0.14]) were statistically more effective than placebo in pain relief, but only tramadol 300 mg/day was better than placebo in functional improvement (SMD –0.24 [95% CI –0.47, –0.03]). Tramadol 100 mg/day (relative risk [RR] 2.29 [95% credible interval (CrI) 1.22, 4.25]), 200 mg/day (RR 4.35 [95% CrI 2.31, 8.01]), and 300 mg/day (RR 6.02 [95% CrI 3.22, 11.1]) involved a higher risk of gastrointestinal AEs. Similarly, tramadol 100–300 mg/day showed a higher risk of CNS AEs and withdrawals. However, the risk of cardiovascular AEs remained unclear. Conclusion: Only tramadol 300 mg/day showed minimal improvement in pain and function but with increasing AEs compared with placebo. Tramadol may not be sufficiently recommended for knee or hip OA based on the presented evidence, especially in patients with the risk of gastrointestinal and CNS AEs. [ABSTRACT FROM AUTHOR]

Background: Human multipotent progenitor cells (hiMPCs) created from induced pluripotent stem cells (iPSCs) represent a new cell source for cartilage regeneration. In most studies, bone morphogenetic proteins (BMPs) are needed to enhance transforming growth factor‐β (TGFβ)‐induced hiMPC chondrogenesis. In contrast, TGFβ alone is sufficient to result in robust chondrogenesis of human primary mesenchymal stromal cells (hMSCs). Currently, the mechanism underlying this difference between hiMPCs and hMSCs has not been fully understood. Methods: In this study, we first tested different growth factors alone or in combination in stimulating hiMPC chondrogenesis, with a special focus on chondrocytic hypertrophy. The reparative capacity of hiMPCs‐derived cartilage was assessed in an osteochondral defect model created in rats. hMSCs isolated from bone marrow were included in all studies as the control. Lastly, a mechanistic study was conducted to understand why hiMPCs and hMSCs behave differently in responding to TGFβ. Results: Chondrogenic medium supplemented with TGFβ3 and BMP6 led to robust in vitro cartilage formation from hiMPCs with minimal hypertrophy. Cartilage tissue generated from this new method was resistant to osteogenic transition upon subcutaneous implantation and resulted in a hyaline cartilage‐like regeneration in osteochondral defects in rats. Interestingly, TGFβ3 induced phosphorylation of both Smad2/3 and Smad1/5 in hMSCs, but only activated Smad2/3 in hiMPCs. Supplementing BMP6 activated Smad1/5 and significantly enhanced TGFβ's compacity in inducing hiMPC chondrogenesis. The chondro‐promoting function of BMP6 was abolished by the treatment of a BMP pathway inhibitor. Conclusions: This study describes a robust method to generate chondrocytes from hiMPCs with low hypertrophy for hyaline cartilage repair, as well as elucidates the difference between hMSCs and hiMPCs in response to TGFβ. Our results also indicated the importance of activating both Smad2/3 and Smad1/5 in the initiation of chondrogenesis. [ABSTRACT FROM AUTHOR]

Summary: Sugar efflux from host plants is essential for pathogen survival and proliferation. Sugar transporter‐mediated redistribution of host sugar contributes to the outcomes of plant–pathogen interactions. However, few studies have focused on how sugar translocation is strategically manipulated during host colonization.To elucidate this question, the wheat sugar transport protein (STP) TaSTP3 responding to Puccinia striiformis f. sp. tritici (Pst) infection was characterized for sugar transport properties in Saccharomyces cerevisiae and its potential role during Pst infection by RNA interference and overexpression in wheat. In addition, the transcription factors regulating TaSTP3 expression were further determined.The results showed that TaSTP3 is localized to the plasma membrane and functions as a sugar transporter of hexose and sucrose. TaSTP3 confers enhanced wheat susceptibility to Pst, and overexpression of TaSTP3 resulted in increased sucrose accumulation and transcriptional suppression of defense‐related genes. Furthermore, TaWRKY19, TaWRKY61 and TaWRKY82 were identified as positive transcriptional regulators of TaSTP3 expression.Our findings reveal that the Pst‐induced sugar transporter TaSTP3 is transcriptionally activated by TaWRKY19/61/82 and facilitates wheat susceptibility to stripe rust possibly through elevated sucrose concentration, and suggest TaSTP3 as a strong target for engineering wheat resistance to stripe rust. [ABSTRACT FROM AUTHOR]

Diseases of the knee joint such as osteoarthritis (OA) affect all joint elements. An in vitro human cell‐derived microphysiological system capable of simulating intraarticular tissue crosstalk is desirable for studying etiologies/pathogenesis of joint diseases and testing potential therapeutics. Herein, a human mesenchymal stem cell‐derived miniature joint system (miniJoint) is generated, in which engineered osteochondral complex, synovial‐like fibrous tissue, and adipose tissue are integrated into a microfluidics‐enabled bioreactor. This novel design facilitates different tissues communicating while still maintaining their respective phenotypes. The miniJoint exhibits physiologically relevant changes when exposed to interleukin‐1β mediated inflammation, which are similar to observations in joint diseases in humans. The potential of the miniJoint in predicting in vivo efficacy of drug treatment is confirmed by testing the "therapeutic effect" of the nonsteroidal anti‐inflammatory drug, naproxen, as well as four other potential disease‐modifying OA drugs. The data demonstrate that the miniJoint recapitulates complex tissue interactions, thus providing a robust organ chip model for the study of joint pathology and the development of novel therapeutic interventions. [ABSTRACT FROM AUTHOR]