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- Beal, Jacob, et al.
(författare)
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Robust estimation of bacterial cell count from optical density
- 2020
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Ingår i: Communications Biology. - : Springer Science and Business Media LLC. - 2399-3642. ; 3:1
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Tidskriftsartikel (refereegranskat)abstract
- Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data.
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- Nie, Huizhen, et al.
(författare)
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The short isoform of PRLR suppresses the pentose phosphate pathway and nucleotide synthesis through the NEK9-Hippo axis in pancreatic cancer
- 2021
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Ingår i: Theranostics. - : Ivyspring International Publisher. - 1838-7640. ; 11:8, s. 3898-3915
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Tidskriftsartikel (refereegranskat)abstract
- Prolactin binding to the prolactin receptor exerts pleiotropic biological effects in vertebrates. The prolactin receptor (PRLR) has multiple isoforms due to alternative splicing. The biological roles and related signaling of the long isoform (PRLR-LF) have been fully elucidated. However, little is known about the short isoform (PRLR-SF), particularly in cancer development and metabolic reprogramming, a core hallmark of cancer. Here, we reveal the role and underlying mechanism of PRLR-SF in pancreatic ductal adenocarcinoma (PDAC). Methods: A human PDAC tissue array was used to investigate the clinical relevance of PRLR in PDAC. The in vivo implications of PRLR-SF in PDAC were examined in a subcutaneous xenograft model and an orthotopic xenograft model. Immunohistochemistry was performed on tumor tissue obtained from genetically engineered KPC (KrasG12D/+; Trp53R172H/+; Pdx1-Cre) mice with spontaneous tumors. 13C-labeled metabolite measures, LC-MS, EdU incorporation assays and seahorse analyses were used to identify the effects of PRLR-SF on the pentose phosphate pathway and glycolysis. We identified the molecular mechanisms by immunofluorescence, coimmunoprecipitation, proximity ligation assays, chromatin immunoprecipitation and promoter luciferase activity. Public databases (TCGA, GEO and GTEx) were used to analyze the expression and survival correlations of the related genes. Results: We demonstrated that PRLR-SF is predominantly expressed in spontaneously forming pancreatic tumors of genetically engineered KPC mice and human PDAC cell lines. PRLR-SF inhibits the proliferation of PDAC cells (AsPC-1 and BxPC-3) in vitro and tumor growth in vivo. We showed that PRLR-SF reduces the expression of genes in the pentose phosphate pathway (PPP) and nucleotide biosynthesis by activating Hippo signaling. TEAD1, a downstream transcription factor of Hippo signaling, directly regulates the expression of G6PD and TKT, which are PPP rate-limiting enzymes. Moreover, NEK9 directly interacts with PRLR-SF and is the intermediator between PRLR and the Hippo pathway. The PRLR expression level is negatively correlated with overall survival and TNM stage in PDAC patients. Additionally, pregnancy and lactation increase the ratio of PRLR-SF:PRLR-LF in the pancreas of wild-type mice and subcutaneous PDAC xenograft tumors. Conclusion: Our characterization of the relationship between PRLR-SF signaling, the NEK9-Hippo pathway, PPP and nucleotide synthesis explains a mechanism for the correlation between PRLR-SF and metabolic reprogramming in PDAC progression. Strategies to alter this pathway might be developed for the treatment or prevention of pancreatic cancer.
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- Yin, J., et al.
(författare)
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SmartDID : A Novel Privacy-preserving Identity based on Blockchain for IoT
- 2022
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Ingår i: IEEE Internet of Things Journal. - : Institute of Electrical and Electronics Engineers (IEEE). - 2327-4662. ; , s. 1-1
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Tidskriftsartikel (refereegranskat)abstract
- Internet of Things (IoT) applications have penetrated into all aspects of human life. Millions of IoT users and devices, online services and applications combine to create a complex and heterogeneous network, which complicates digital identity management. Distributed identity is a promising paradigm to solve IoT identity problems and allows users to have soverignty over their private data. However, existing state-of-the-art methods are unsuitable for IoT due to continuing issues regarding resource limitations for IoT devices, security and privacy issues, and lack of a systematic proof system. Accordingly, in this paper, we propose SmartDID, a novel blockchain-based distributed identity aimed at establishing a self-sovereign identity and providing strong privacy preservation. First, we configure IoT devices as light nodes and design a Sybil-resistant, unlinkable and supervisable distributed identity that does not rely on central identity providers. We further develop a dual-credential model based on commitment and zero-knowledge proofs to protect the privacy of sensitive attributes, on-chain identity data and linkage of credentials. Moreover, we combine the basic credential proofs to prove the knowledge of solutions to more complex problems and create a systematic proof system. We go on to provide the security analysis of SmartDID. Experimental analysis shows that our scheme achieves better performance in terms of both credential generation and proof generation when compared with CanDID.
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- Bashar, Manijeh, et al.
(författare)
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Energy Efficiency of the Cell-Free Massive MIMO Uplink with Optimal Uniform Quantization
- 2019
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Ingår i: IEEE Transactions on Green Communications and Networking. - : IEEE. - 2473-2400. ; 3:4, s. 971-987
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Tidskriftsartikel (refereegranskat)abstract
- A cell-free Massive multiple-input multiple-output (MIMO) uplink is considered, where the access points (APs) are connected to a central processing unit (CPU) through limited-capacity wireless microwave links. The quantized version of the weighted signals are available at the CPU, by exploiting the Bussgang decomposition to model the effect of quantization. A closed-form expression for spectral efficiency is derived taking into account the effects of channel estimation error and quantization distortion. The energy efficiency maximization problem is considered with per-user power, backhaul capacity and throughput requirement constraints. To solve this non-convex problem, we decouple the original problem into two sub-problems, namely, receiver filter coefficient design, and power allocation. The receiver filter coefficient design is formulated as a generalized eigenvalue problem whereas a successive convex approximation (SCA) and a heuristic sub-optimal scheme are exploited to convert the power allocation problem into a standard geometric programming (GP) problem. An iterative algorithm is proposed to alternately solve each sub-problem. Complexity analysis and convergence of the proposed schemes are investigated. Numerical results indicate the superiority of the proposed algorithms over the case of equal power allocation.
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