An OFF-ON red-emitting phosphorescent thiol probe is designed by using the (3)MLCT photophysics of Ru(II) complexes, i.e., with Ru(II) as the electron donor. The probe is non-luminescent because the MLCT is corrupted by electron transfer from Ru(II) to an intramolecular electron sink (2,4-dinitrobenzenesulfonyl). Thiols cleave the electron sink, and the MLCT is re-established. Phosphorescence at 598 nm was enhanced by 90-fold, with a 143 nm (5256 cm(-1)) Stokes shift and a 1.1 mus luminescent lifetime.

Two highly selective OFF-ON green emitting fluorescent thiol probes (1 and 2) with intense absorption in the visible spectrum (molar extinction coefficient ε is up to 73 800 M(-1) cm(-1) at 509 nm) based on dyads of BODIPY (as electron donor of the photo-induced electron transfer, i.e.PET) and 2,4-dinitrobenzenesulfonyl (DNBS) (as electron acceptor of the PET process) were devised. The single crystal structures of the two probes were determined. The distance between the electron donor (BODIPY fluorophore) and the electron acceptor (DNBS) of probe 2 is larger than that of probe 1, as a result the contrast ratio (or the PET efficiency) of probe 2 is smaller than that of probe 1. However, fluorescence OFF-ON switching effects were observed for both probe 1 and probe 2 in the presence of cysteine (the emission enhancement is 300-fold for probe 1 and 54-fold for probe 2). The fluorescence OFF-ON sensing mechanism is rationalized by DFT/TDDFT calculations. We demonstrated with DFT calculations that DNBS is ca. 0.76 eV more potent to accept electrons than the maleimide moiety. The probes were used for fluorescent imaging of cellular thiols.

Background Achaete scute-like 2 (Ascl2), a basic helix-loop-helix (bHLH) transcription factor, controls the fate of intestinal stem cells. However, the role of Ascl2 in colon cancer progenitor cells remains unknown. The cell line HT-29 (47.5–95% of CD133 + population) and LS174T (0.45% of CD133 + population) were chosen for functional evaluation of Ascl2 in colon cancer progenitor cells after gene knockdown by RNA interference. Methodology/Principal Findings Immunohistochemistry demonstrated that Ascl2 was significantly increased in colorectal adenocarcinomas. Downregulation of Ascl2 using RNA interference in cultured colonic adenocarcinoma HT-29 and LS174T cells reduced cellular proliferation, colony-forming ability, invasion and migration in vitro, and resulted in the growth arrest of tumor xenografts in vivo. The Ascl2 protein level in CD133 + HT-29 cells was significantly higher than in CD133 − HT-29 cells. Ascl2 blockade via shRNA interference in HT-29 cells (shRNA-Ascl2/HT-29 cells) resulted in 26.2% of cells staining CD133 + compared with 54.7% in control shRNA-Ctr/HT-29 cells. The levels of ‘stemness’ associated genes, such as CD133, Sox2, Oct4, Lgr5, Bmi1, and C-myc, were significantly decreased in shRNA-Ascl2/HT-29 and shRNA-Ascl2/LS174T cells in vitro as well as in the corresponding tumor xenograft (CD133 was not performed in shRNA-Ascl2/LS174T cells). The shRNA-Ascl2/HT-29 cells had inhibited abilities to form tumorspheres compared with control. The microRNA (miRNAs) microarrays, identified 26 up-regulated miRNAs and 58 down-regulated miRNAs in shRNA-Ascl2/HT-29 cells. Expression levels of let-7b, miRNA-124, miRNA-125b, miRNA-17, miRNA-20a and miRNA-302b, involved in the regulation of ‘stemness’, were quantified with qPCR, which confirmed their identities. Restoration of miRNA-302b, via its mimic, led to the restoration of shRNA-Ascl2/HT-29 ‘stemness’ characteristics, including tumorsphere formation and ‘stemness’ associated genes levels, and the recovery of cellular behaviors, including colony-forming ability, invasion and migration in vitro. Conclusions/Significance Ascl2 may be a potential target for the inhibition of colon cancer progenitor cells, and functions through a miR-302b-related mechanism.

With the wide application of mobile healthcare systems, the total amount of healthcare data is ever increasing rapidly as users interact with healthcare service providers frequently. This leads to a challenging task to manage healthcare data. Existing work mainly pay attention to centralized and blockchain-based mechanisms. But they cannot adapt to the increasing amount of global healthcare data and suffer from complex application challenges, respectively. Decentralized and collaborative data management assisted by edge computing exhibits major advantages in improving overall system performance. We present a secure and efficient data management system named as EdgeCare for mobile healthcare systems. Local authorities are established to schedule edge servers for processing healthcare data and facilitating data trading. A hierarchical architecture with collaboration is designed for feasible implementation of EdgeCare. After that, we investigate secure data uploading and sharing in the system. We use an electronic medical record to show how healthcare data is processed with security considerations. We also conduct the Stackelberg game-based optimization algorithm to approach the optimal incentive mechanism for a data collector and users in the fair decentralized data trading. The numerical results with security analysis are provided to demonstrate that EdgeCare offers effective solutions to protect healthcare data, and support efficient data trading.INDEX TERMS Public healthcare, collaborative work, internet of things, distributed management. I. INTRODUCTIONRecently, mobile healthcare systems have been applied widely because of the advances in biotechnologies, information technologies and software engineering. Due to pervasive e-health services, billions of personal healthcare data records are generated annually [1]. Meanwhile, users interact with healthcare service providers frequently in current applications, e.g., mobile telemedicine, personalized medicine and emergency response [2]. Towards secure interaction,The associate editor coordinating the review of this manuscript and approving it for publication was Joel Rodrigues.

Broadband visible light-absorbing triplet photosensitizers with rhodamine as the energy donor and styryl Bodipy as the energy acceptor/spin converter were prepared.

ObjectiveCisplatin is a widely used chemotherapeutic agent in the treatment of cancers in clinic; but it often induces adverse effects on ovarian functions such as reduced fertility and premature menopause. Mesna could attenuate the cisplatin-induced ovarian damages; however, the underlying mechanism is still unknown. This study aimed to figure out the underlying mechanism of the protection of mesna for ovaries against cisplatin therapy in cancers.MethodsWe performed female adult Sprague-Dawley rats into normal saline control (NS), low-dose cisplatin (CL), high-dose cisplatin (CH), CL plus mesna (CL+M), and CH plus mesna (CH+M) groups and detected anti-Müllerian hormone (AMH)-positive follicle, oxidative stress status and anti-oxidative capability in ovaries.ResultsAMH-positive follicles were significantly decreased after cisplatin administration, which was significantly reversed when mesna was co-administered with cisplatin. The end product of lipid peroxidation, malondialdehyde (MDA), was significantly increased, but the anti-oxidative enzymatic activity of superoxide dismutase (SOD) and glutathione (GSH) were significantly decreased in cisplatin groups when compared with NS group. In contrast, after co-administration of cisplatin with mesna, MDA was significantly decreased whereas the activity of SOD and the concentration of GSH were increased. Moreover, mesna did not decrease the anti-tumor property of cisplatin in HePG2 cell lines.ConclusionCisplatin damages the granulosa cells by oxidative stress to deplete the ovarian reserve and mesna could protect ovarian reserve through anti-oxidation. These results might highlight the mechanism of the protection of mesna for ovarian reserve and open an avenue for the application of mesna as a protective additive in cisplatin chemotherapy in clinical practise.

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The introduction of video objects (VOs) is one of the innovations of MPEG-4. The alpha-plane of a VO defines its shape at a given instance in time and hence determines the boundary of its texture. In packet-based networks, shape, motion, and texture are subject to loss. While there has been considerable attention paid to the concealment of texture and motion errors, little has been done in the field of shape error concealment. In this paper, we propose a post-processing shape error-concealment technique that uses geometric boundary information of the received alpha-plane. Second-order Hermite splines are used to model the received boundary in the neighboring blocks, while third order Hermite splines are used to model the missing boundary. The velocities of these splines are matched at the boundary point closest to the missing block. There exists the possibility of multiple concealing splines per group of lost boundary parts. Therefore, we draw every concealment spline combination that does not self-intersect and keep all possible results until the end. At the end, we select the concealment solution that results in one closed boundary. Experimental results demonstrating the performance of the proposed method and comparisons with prior proposed methods are presented.