The Investigation of NOx Formation and Reduction during O2/CO2 Combustion of Raw Coal and Coal Char

AbstractThis study investigated the behavior of NOx emissions during combustion of pulverized coal char and pulverized raw coal in O2/CO2 environments under nearly isothermal condition in a drop tube furnace. A representative Chinese coal Ling Nancang (LNC) and LNC CO2-char (made in CO2 condition) were studied with four different excess oxygen ratios (α=0.6, 0.8, 1.2, and 1.4). Combustion experiments were performed with an elevated concentration (850ppm) of NO. When α increased from 0.6 to 1.4, the total amount of NOx reduction was increased in both pulverized coal and char combustion. To investigate the effects of coal and char on NOx reburn reactions, LNC coal char and the raw coal combustion experiments were also performed under three high background NO concentrations (400, 850, and 1200ppm) in O2/CO2 atmosphere. During experiments with elevated NO concentrations, there was an increase in net NO reduction; however, there was also a decrease in the calculated NO reduction ratio

Distilled Visual and Robot Kinematics Embeddings for Metric Depth Estimation in Monocular Scene Reconstruction

Estimating precise metric depth and scene reconstruction from monocular endoscopy is a fundamental task for surgical navigation in robotic surgery. However, traditional stereo matching adopts binocular images to perceive the depth information, which is difficult to transfer to the soft robotics-based surgical systems due to the use of monocular endoscopy. In this paper, we present a novel framework that combines robot kinematics and monocular endoscope images with deep unsupervised learning into a single network for metric depth estimation and then achieve 3D reconstruction of complex anatomy. Specifically, we first obtain the relative depth maps of surgical scenes by leveraging a brightness-aware monocular depth estimation method. Then, the corresponding endoscope poses are computed based on non-linear optimization of geometric and photometric reprojection residuals. Afterwards, we develop a Depth-driven Sliding Optimization (DDSO) algorithm to extract the scaling coefficient from kinematics and calculated poses offline. By coupling the metric scale and relative depth data, we form a robust ensemble that represents the metric and consistent depth. Next, we treat the ensemble as supervisory labels to train a metric depth estimation network for surgeries (i.e., MetricDepthS-Net) that distills the embeddings from the robot kinematics, endoscopic videos, and poses. With accurate metric depth estimation, we utilize a dense visual reconstruction method to recover the 3D structure of the whole surgical site. We have extensively evaluated the proposed framework on public SCARED and achieved comparable performance with stereo-based depth estimation methods. Our results demonstrate the feasibility of the proposed approach to recover the metric depth and 3D structure with monocular inputs

Enhanced Delivery of Rituximab Into Brain and Lymph Nodes Using Timed-Release Nanocapsules in Non-Human Primates.

Tumor metastasis into the central nervous system (CNS) and lymph nodes (LNs) is a major obstacle for effective therapies. Therapeutic monoclonal antibodies (mAb) have revolutionized tumor treatment; however, their efficacy for treating metastatic tumors-particularly, CNS and LN metastases-is poor due to inefficient penetration into the CNS and LNs following intravenous injection. We recently reported an effective delivery of mAb to the CNS by encapsulating the anti-CD20 mAb rituximab (RTX) within a thin shell of polymer that contains the analogs of choline and acetylcholine receptors. This encapsulated RTX, denoted as n-RTX, eliminated lymphoma cells systemically in a xenografted humanized mouse model using an immunodeficient mouse as a recipient of human hematopoietic stem/progenitor cells and fetal thymus more effectively than native RTX; importantly, n-RTX showed notable anti-tumor effect on CNS metastases which is unable to show by native RTX. As an important step toward future clinical translation of this technology, we further analyzed the properties of n-RTX in immunocompetent animals, rats, and non-human primates (NHPs). Our results show that a single intravenous injection of n-RTX resulted in 10-fold greater levels in the CNS and 2-3-fold greater levels in the LNs of RTX, respectively, than the injection of native RTX in both rats and NHPs. In addition, we demonstrate the enhanced delivery and efficient B-cell depletion in lymphoid organs of NHPs with n-RTX. Moreover, detailed hematological analysis and liver enzyme activity tests indicate n-RTX treatment is safe in NHPs. As this nanocapsule platform can be universally applied to other therapeutic mAbs, it holds great promise for extending mAb therapy to poorly accessible body compartments

Measurement-device-independent quantum key distribution over untrustful metropolitan network

Quantum cryptography holds the promise to establish an information-theoretically secure global network. All field tests of metropolitan-scale quantum networks to date are based on trusted relays. The security critically relies on the accountability of the trusted relays, which will break down if the relay is dishonest or compromised. Here, we construct a measurement-device-independent quantum key distribution (MDIQKD) network in a star topology over a 200 square kilometers metropolitan area, which is secure against untrustful relays and against all detection attacks. In the field test, our system continuously runs through one week with a secure key rate ten times larger than previous result. Our results demonstrate that the MDIQKD network, combining the best of both worlds --- security and practicality, constitutes an appealing solution to secure metropolitan communications.Comment: 17 pages, 4 figure

Novel sequences of subgroup J avian leukosis viruses associated with hemangioma in Chinese layer hens

<p>Abstract</p> <p>Background</p> <p>Avian leukosis virus subgroup J (ALV-J) preferentially induces myeloid leukosis (ML) in meat-type birds. Since 2008, many clinical cases of hemangioma rather than ML have frequently been reported in association with ALV-J infection in Chinese layer flocks.</p> <p>Results</p> <p>Three ALV-J strains associated with hemangioma were isolated and their proviral genomic sequences were determined. The three isolates, JL093-1, SD09DP03 and HLJ09MDJ-1, were 7,670, 7,670, and 7,633 nt in length. Their gag and pol genes were well conserved, with identities of 94.5-98.6% and 97.1-99.5%, respectively, with other ALV-J strains at the amino acid level (aa), while the env genes of the three isolates shared a higher aa identity with the env genes of other hemangioma strains than with those of ML strains. Interestingly, two novel 19-bp insertions in the U3 region in the LTR and 5' UTR, most likely derived from other retroviruses, were found in all the three isolates, thereby separately introducing one E2BP binding site in the U3 region in the LTR and RNA polymerase II transcription factor IIB and core promoter motif ten elements in the 5' UTR. Meanwhile, two binding sites in the U3 LTRs of the three isolates for NFAP-1 and AIB REP1 were lost, and a 1-base deletion in the E element of the 3' UTR of JL093-1 and SD09DP03 introduced a binding site for c-Ets-1. In addition to the changes listed above, the rTM of the 3' UTR was deleted in each of the three isolates.</p> <p>Conclusion</p> <p>Our study is the first to discovery the coexistence of two novel insertions in the U3 region in the LTR and the 5' UTR of ALV-J associated with hemangioma symptoms, and the transcriptional regulatory elements introduced should be taken into consideration in the occurrence of hemangioma.</p

FAK Promotes Early Osteoprogenitor Cell Proliferation by Enhancing mTORC1 Signaling

Focal adhesion kinase (FAK) has important functions in bone homeostasis but its role in early osteoprogenitor cells is unknown. We show herein that mice lacking FAK in Dermo1- expressing cells exhibited low bone mass and decreased osteoblast number. Mechanistically, FAK- deficient early osteoprogenitor cells had decreased proliferation and significantly reduced mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling, a central regulator of cell growth and proliferation. Furthermore, our data showed that the pharmacological inhibition of FAK kinase- dependent function alone was sufficient to decrease the proliferation and compromise the mineralization of early osteoprogenitor cells. In contrast to the Fak deletion in early osteoprogenitor cells, FAK loss in Col3.6 Cre- targeted osteoblasts did not cause bone loss, and Fak deletion in osteoblasts did not affect proliferation, differentiation, and mTORC1 signaling but increased the level of active proline- rich tyrosine kinase 2 (PYK2), which belongs to the same non- receptor tyrosine kinase family as FAK. Importantly, mTORC1 signaling in bone marrow stromal cells (BMSCs) was reduced if FAK kinase was inhibited at the early osteogenic differentiation stage. In contrast, mTORC1 signaling in BMSCs was not affected if FAK kinase was inhibited at a later osteogenic differentiation stage, in which, however, the concomitant inhibition of both FAK kinase and PYK2 kinase reduced mTORC1 signaling. In summary, our data suggest that FAK promotes early osteoprogenitor cell proliferation by enhancing mTORC1 signaling via its kinase- dependent function and the loss of FAK in osteoblasts can be compensated by the upregulated active PYK2. © 2020 American Society for Bone and Mineral Research.Schematic model of the differential roles of FAK in the cells of osteoblast lineage. The model depicts the mechanisms of FAK action at three distinct stages of osteoblast lineage in which the roles of FAK have been addressed by genetic and pharmacological approaches as well as the respective Cre transgenes used to target Fak, including Dermo1- Cre (this study), Osterix- Cre,(10) Col3.6- Cre (this study), and Col2.3- Cre.(9) Red - indicates that the loss of FAK in osteoblasts can be compensated by the upregulated active PYK2.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162813/3/jbmr4029-sup-0001-Supinfo.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162813/2/jbmr4029_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162813/1/jbmr4029.pd

Ligustrazine Inhibits the Migration and Invasion of Renal Cell Carcinoma

Ligustrazine is a Chinese herb (Chuanxiong) approved for use as a medical drug in China. Recent evidence suggests that ligustrazine has promising antitumor properties. Our preliminary results showed that ligustrazine could inhibit the growth of human renal cell carcinoma (RCC) cell lines. However, the complicated molecular mechanism has not been fully revealed. Therefore, the purpose of this study to investigate the mechanism of ligustrazine resistance in human RCC cells. Cell proliferation, migration, invasion, and colony-formation ability of RCC cells A498 were detected by MTT assay, clonal formation rates, and transwell chamber assay in vitro. The expression of epithelial–mesenchymal transition (EMT)–related proteins were analyzed using western blot test. The effect of ligustrazine on the growth of A498 cells in nude mice was investigated in vivo. Our results showed that ligustrazine could significantly inhibit the proliferation, migration, and invasion of A498 both in vivo and vitro. Western blot analysis showed that the expressions of EMT-related, N-cadherin, snail, and slug proteins were significantly decreased in A498 in the ligustrazine treatment group. This study indicated that ligustrazine could significantly inhibit the malignant biological behaviors of RCC cell lines, possibly by inhibiting the EMT process