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Objective. We introduce a robust image reconstruction algorithm named residual-guided Golub-Kahan iterative reconstruction technique (RGIRT) designed for sparse-view computed tomography (CT), which aims at high-fidelity image reconstruction from a limited number of projection views.Approach. RGIRT utilizes an inner-outer dual iteration framework, with a flexible least square QR (FLSQR) algorithm implemented in the inner iteration and a restarted iterative scheme applied in the outer iteration. The inner FLSQR employs a flexible Golub-Kahan bidiagonalization method to reduce the size of the inverse problem, and a weighted generalized cross-validation method to adaptively estimate the regularization hyper-parameter. The inner iteration efficiently yields the intermediate reconstruction result, while the outer iteration minimizes the residual and refines the solution by using the result obtained from the inner iteration.Main results. The reconstruction performance of RGIRT is evaluated and compared to other reference methods (FBPConvNet, SART-TV, and FLSQR) using projection data from both numerical phantoms and real experimental Micro-CT data. The experimental findings, from testing various numbers of projection views and different noise levels, underscore the robustness of RGIRT. Meanwhile, theoretical analysis confirms the convergence of residual for our approach.Significance. We propose a robust iterative reconstruction algorithm for x-ray CT scans with sparse views, thereby shortening scanning time and mitigating excessive ionizing radiation exposure to small animals.
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Algoritmos , Procesamiento de Imagen Asistido por Computador , Fantasmas de Imagen , Tomografía Computarizada por Rayos X , Procesamiento de Imagen Asistido por Computador/métodos , Animales , Tomografía Computarizada por Rayos X/métodos , RatonesRESUMEN
OBJECTIVE: Macroscopic optical tomography is a non-invasive method that can visualize the 3D distribution of intrinsic optical properties or exogenous fluorophores, making it highly attractive for small animal imaging. However, reconstructing the images requires prior knowledge of surface information. To address this, existing systems often use additional hardware components or integrate multimodal information, which is expensive and introduces new issues such as image registration. Our goal is to develop a multifunctional optical tomography system that can extract surface information using a concise hardware design. METHODS: Our proposed system uses a single programmable scanner to implement both surface extraction and optical tomography functions. A unified pinhole model is used to describe both the illumination and detection procedures for capturing 3D point cloud. Line-shaped scanning is adopted to improve both spatial resolution and speed of surface extraction. Finally, we integrate the extracted surface information into the optical tomographic reconstruction to more accurately map the fluorescence distribution. RESULT: Comprehensive phantom experiments with different levels of complexity were designed to evaluate the performance of surface extraction and fluorescence tomography. We also imaged the axillary lymph nodes in living mice after injection of fluorophore, demonstrating the proposed system facilitates more reliable fluorescence tomography. CONCLUSION: We have successfully developed a versatile optical tomography system by leveraging concise hardware design and unified pinhole modeling. Phantom validation demonstrates that our system provides high-precision surface information with a maximum error of 0.1 mm, while the surface-guided FMT reconstruction is more reliable than the blind reconstruction using simplified surface geometry, elevating several quantitative metrics including RMSE, CNR, and Dice. SIGNIFICANCE: Our work explores the feasibility of obtaining additional surface information using existing components of standalone optical tomography. This makes the optical tomographic technique more accurate and more accessible to biomedical researchers.
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Dispositivos Ópticos , Tomografía Óptica , Ratones , Animales , Fantasmas de ImagenRESUMEN
As businesses have had to change how they operate due to the coronavirus pandemic, the need for remote work has risen. With the continuous advancements in technology and increases in typical job demands, employees need to increase their work productivity beyond regular work hours in the office. This type of work environment creates even more opportunities for security breaches due to employees intentionally violating information security policy violations. Although explicitly prohibited by information security policies (ISP), organizations have observed that employees bring critical data out of the office to complete their work responsibilities remotely. Consequently, developing a deeper understanding of how work pressure may influence employees to violate ISPs intentionally is crucial for organizations to protect their critical information better. Based upon the fraud triangle theory, this study proposes the opportunity to copy critical data, work pressure, and work completion justification as the primary motivational factors behind why employees copy critical company data to unsecured storage devices to work at home. A survey was conducted of 207 employees from a marketing research firm. The results suggest that opportunity, work pressure, and work completion justification are positively related to nonmalicious ISP violation intentions. Furthermore, the interaction effect between work completion justification and work pressure on the ISP violation intention is significant and positive. This study provides new insights into our understanding of the roles of work pressure and work completion justification on intentional nonmalicious ISP violation behaviors.
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Abnormal cerebral accumulation of amyloid-beta peptide (Aß) is a major hallmark of Alzheimer's disease. Non-invasive monitoring of Aß deposits enables assessing the disease burden in patients and animal models mimicking aspects of the human disease as well as evaluating the efficacy of Aß-modulating therapies. Previous in vivo assessments of plaque load have been predominantly based on macroscopic fluorescence reflectance imaging (FRI) and confocal or two-photon microscopy using Aß-specific imaging agents. However, the former method lacks depth resolution, whereas the latter is restricted by the limited field of view preventing a full coverage of the large brain region. Here, we utilized a fluorescence molecular tomography (FMT)-magnetic resonance imaging (MRI) pipeline with the curcumin derivative fluorescent probe CRANAD-2 to achieve full 3D brain coverage for detecting Aß accumulation in the arcAß mouse model of cerebral amyloidosis. A homebuilt FMT system was used for data acquisition, whereas a customized software platform enabled the integration of MRI-derived anatomical information as prior information for FMT image reconstruction. The results obtained from the FMT-MRI study were compared to those from conventional planar FRI recorded under similar physiological conditions, yielding comparable time courses of the fluorescence intensity following intravenous injection of CRANAD-2 in a region-of-interest comprising the brain. In conclusion, we have demonstrated the feasibility of visualizing Aß deposition in 3D using a multimodal FMT-MRI strategy. This hybrid imaging method provides complementary anatomical, physiological and molecular information, thereby enabling the detailed characterization of the disease status in arcAß mouse models, which can also facilitate monitoring the efficacy of putative treatments targeting Aß.
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EXs (Exosomes) secreted by mesenchymal stem cells (MSCs) have the potential to treat spinal cord injury (SCI), this study aimed to further explore the therapeutic effect of EXs on SCI. Firstly, EXs were extracted from MSCs and analyzed with a transmission electron microscope. Next, MSCs with or without the miR-145-5p plasmid were injected into the SCI rat model, and then rat damage was evaluated by BBB score, HE staining and Nissl staining. And then Luciferase experiment verified the targeting relationship between miR-145-5p and TLR4. Furthermore, LPS-induced PC12 cells were established and incubated with Dil-labeled MSC-EXs to explore their effects on cell viability, apoptosis and inflammation through MTT, flow cytometry and ELISA, respectively. In addition, expressions of TLR4/NF-κB signaling pathway related factors were measured by qRT-PCR and Western blot. The results showed that after MSCs were successfully isolated, the existence of EXs in MSCs was confirmed. Moreover, MSC-EXs containing miR-145-5p improved functional recovery and reduced histopathological injury and inflammation in SCI rats. And MSC-EXs promoted miR-145-5p expression in spinal cord tissue and inhibited TLR4/NF-κB pathway activation in SCI rats. MSC-EXs inhibited LPS-induced inflammatory response and activation of the TLR4/NF-κB pathway in PC12 cells. In addition, we also found that miR-145-5p specifically targeted TLR4. TLR4 overexpression significantly reversed the effect of EX-miR-145-5p on maintaining PC12 cell viability, inhibiting apoptosis and inflammatory response, and activating TLR4/NF- κB pathway. In conclusion, mesenchymal stem cell-derived EXs containing miR-145-5p reduce inflammation in spinal cord injury by regulating the TLR4/NF-κB signaling pathway.
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Exosomas/metabolismo , Inflamación/genética , Células Madre Mesenquimatosas/metabolismo , MicroARNs/metabolismo , Transducción de Señal , Traumatismos de la Médula Espinal/genética , Receptor Toll-Like 4/metabolismo , Animales , Apoptosis/genética , Secuencia de Bases , Supervivencia Celular/genética , Inflamación/complicaciones , Inflamación/patología , Inflamación/fisiopatología , Masculino , MicroARNs/genética , FN-kappa B/metabolismo , Células PC12 , Ratas , Ratas Sprague-Dawley , Recuperación de la Función , Traumatismos de la Médula Espinal/complicaciones , Traumatismos de la Médula Espinal/patología , Traumatismos de la Médula Espinal/fisiopatologíaRESUMEN
RNA polymerase II (RNA Pol II) plays a major role in gene transcription for eukaryote. One of the major modes of regulation in eukaryotes is the phosphorylation of the carboxyl-terminal domain (CTD) of RNA Pol II. The current study found that the phosphorylation of Ser2, Ser5, Ser7, Thr4 and Tyr1 among the heptapeptide repeats of CTD plays a key role in the transcription process. We therefore review the biological functions and inhibitors of kinases that phosphorylate these amino acid residues including transcriptional cyclin-dependent protein kinases (CDKs), bromodomain-containing protein 4 (BRD4), Polo-like kinases 3 (Plk3) and Abelson murine leukemia viral oncogene 1 and 2 (c-Abl1/2).
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Inhibidores Enzimáticos/farmacología , ARN Polimerasa II/antagonistas & inhibidores , Animales , Inhibidores Enzimáticos/química , Humanos , Estructura Molecular , Fosforilación/efectos de los fármacos , ARN Polimerasa II/química , ARN Polimerasa II/metabolismoRESUMEN
This study aims to explore the role and mechanism of lncRNA SNHG5 in spinal cord injury (SCI). The interaction between SNHG5 and Krüppel-like factor 4 (KLF4) was verified by RNA pull-down and RNA immunoprecipitation (RIP) assay. Rat neural function was evaluated by BBB and BMS scores. Results showed that GFAP and Iba-1 (specific proteins for astrocytes and microglia respectively) were upregulated in spinal cord of SCI rats. Simultaneously, spinal cord also expressed substantially higher levels of SNHG5, KLF4 and eNOS (endothelial Nitric Oxide Synthase) than sham group. In traumatically injured astrocytes and microglia, SNHG5 overexpression increased cells viability, which was significantly inhibited by SNHG5 knockdown. KLF4 is a directly target for SNHG5 and is positively regulated by SNHG5. The knockdown of KLF4 effectively decreased astrocytes and microglia viability induced by SHNG5 overexpression and attenuated the pcDNA-SNHG5-mediated repression of the apoptosis. In SCI rats, the injection of Lenti-SNHG5 reduced BBB and BMS scores and also enhanced the protein expression of KLF4, eNOS, GFAP and Iba-1. In summary, our data suggested that SNHG5 promotes SCI via increasing the viability of astrocytes and microglia. The mechanism by which SNHG5 works is its directive interaction to KLF4 and contribution to eNOS upregulation.