RESUMO
Imaging through scattering media is a classical inverse issue in computational imaging. In recent years, deep learning(DL) methods have excelled in speckle reconstruction by extracting the correlation of speckle patterns. However, high-performance DL-based speckle reconstruction also costs huge hardware computation and energy consumption. Here, we develop an opto-electronic DL method with low computation complexity for imaging through scattering media. We design the "end-to-end" optronic structure for speckle reconstruction, namely optronic fully convolutional neural network (OP-FCNN). In OP-FCNN, we utilize lens groups and spatial light modulators to implement the convolution, down/up-sampling, and skip connection in optics, which significantly reduces the computational complexity by two orders of magnitude, compared with the digital CNN. Moreover, the reconfigurable and scalable structure supports the OP-FCNN to further improve imaging performance and accommodate object datasets of varying complexity. We utilize MNIST handwritten digits, EMNIST handwritten letters, fashion MNIST, and MIT-CBCL-face datasets to validate the OP-FCNN imaging performance through random diffusers. Our OP-FCNN reveals a good balance between computational complexity and imaging performance. The average imaging performance on four datasets achieves 0.84, 0.91, 0.79, and 16.3dB for JI, PCC, SSIM, and PSNR, respectively. The OP-FCNN paves the way for all-optical systems in imaging through scattering media.
RESUMO
Numb regulates cell proliferation and differentiation through endocytosis and ubiquitination of signaling molecules. Besides, Numb controls the migration of epithelial cells by regulating intercellular junctions. Studies have shown that Numb promotes or inhibits tumor progression in different tumors. However, its role and mechanism in colorectal cancer remain unclear. We found that the expression level of Numb in colon tumor tissues has a great variety in different patients. Numb expression was negatively correlated with TNM stage and lymph node metastasis but positively correlated with tumor size. Elevated expression of Numb was associated with a good prognosis. Inhibiting Numb expression promoted the migration and invasion of colon cancer cells induced by TGF-ß, up-regulated the expression of EMT-related molecule Snail, and prevented the expression of E-cadherin. We also found that Numb promoted the proliferation and clones formation while inhibiting colon cancer cells' late apoptosis. In addition, Numb inhibited the RhoA activation and ROCK inhibitor Y-27632 or interfered with ROCK expression, partially inhibiting Numb-regulated cell proliferation and migration. In vivo tumorigenesis assay in nude mice also found that Numb promoted the proliferation of colon cancer cells, inhibited the expression of E-cadherin, and strengthened the expression of Snail. In conclusion, our study found that Numb plays multiple roles in the occurrence and progression of colon cancer by regulating the RhoA/ROCK signaling pathway, which provides a new theoretical molecular basis for the pathogenesis of colon cancer.
Assuntos
Neoplasias do Colo/metabolismo , Neoplasias do Colo/patologia , Proteínas de Membrana/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Quinases Associadas a rho/metabolismo , Proteína rhoA de Ligação ao GTP/metabolismo , Animais , Apoptose , Movimento Celular , Proliferação de Células , Neoplasias do Colo/genética , Feminino , Regulação Neoplásica da Expressão Gênica , Técnicas de Silenciamento de Genes , Células HCT116 , Células HT29 , Xenoenxertos , Humanos , Proteínas de Membrana/antagonistas & inibidores , Proteínas de Membrana/genética , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Invasividade Neoplásica , Proteínas do Tecido Nervoso/antagonistas & inibidores , Proteínas do Tecido Nervoso/genética , Transdução de Sinais , Ensaio Tumoral de Célula-TroncoRESUMO
OBJECTIVES: Although oral sulfate solution (OSS) has been revealed to be not only safe and efficacious but also noninferior to polyethylene glycol with ascorbic acid (PEG + ASC), it is unclear whether OSS can ultimately increase the polyp detection rate (PDR) and adenoma detection rate (ADR). We performed this meta-analysis to estimate the effect of OSS on PDR and ADR during colonoscopy. METHODS: We searched PubMed, EMBASE, and the Cochrane Library to identify relevant randomized controlled trials (RCTs) investigating the comparative effect of OSS versus PEG + ASC on the PDR and ADR during colonoscopy. Cecal intubation time (CIT), cecal intubation rate (CIR), and bowel preparation score were also evaluated. Review Manager (RevMan) version 5.3.0 was used to perform statistical analysis. RESULTS: Eight RCTs involving 2059 patients fulfilled the selection criteria. Meta-analysis suggested that OSS significantly increased the PDR (47.34% vs. 40.14%, risk ratio [RR] 1.13, 95% confidence interval [CI] 1.03-1.24, P = 0.01) and ADR (44.60% vs. 38.14%, RR 1.17, 95% CI 1.03-1.33, P = 0.01) during colonoscopy. Subgroup analysis showed that the beneficial effects of OSS on PDR and ADR were consistent among patients with mean age >55 years and with body mass index <25 kg/m2 receiving outpatient colonoscopy, morning colonoscopy, and the 2-L bowel preparation protocol. Meanwhile, patients receiving OSS had a beneficial bowel preparation score. CONCLUSION: Compared with polyethylene glycol-based regimens, the OSS bowel preparation regimen significantly increased the PDR and ADR in patients undergoing colonoscopy.
Assuntos
Adenoma , Pólipos , Adenoma/diagnóstico , Catárticos , Colonoscopia/métodos , Humanos , Pessoa de Meia-Idade , Polietilenoglicóis , Ensaios Clínicos Controlados Aleatórios como Assunto , SulfatosRESUMO
Capture and storage of the long-lived 85 Kr is an efficient approach to mitigate the emission of volatile radionuclides from the spent nuclear fuel reprocessing facilities. However, it is challenging to separate krypton (Kr) from xenon (Xe) because of the chemical inertness and similar physical properties. Herein we prepared high-silica CHA zeolite membranes with ultra-high selectivity and irradiation stability for Kr/Xe separation. The suitable aperture size and rigid framework endures the membrane a strong size-exclusion effect. The ultrahigh selectivity of 51-152 together with the Kr permeance of 0.7-1.3×10-8 â mol m-2 s-1 Pa-1 of high-silica CHA zeolite membranes far surpass the state-of-the-art polymeric membranes. The membrane is among the most stable polycrystalline membranes for separation of humid Kr/Xe mixtures. Together with the excellent irradiation stability, high-silica CHA zeolite membranes pave the way to separate radioactive Kr from Xe for a notable reduction of the volatile nuclear waste storage volume.
RESUMO
Colistin is considered a last-resort antibiotic against most gram-negative bacteria. Recent discoveries of a plasmid-mediated, transferable mobilized colistin-resistance gene ( mcr-1) on all continents have heralded the imminent emergence of pan-drug-resistant superbacteria. The inner-membrane protein MCR-1 can catalyze the transfer of phosphoethanolamine (PEA) to lipid A, resulting in colistin resistance. However, little is known about the mechanism, and few drugs exist to address this issue. We present crystal structures revealing the MCR-1 catalytic domain (cMCR-1) as a monozinc metalloprotein with ethanolamine (ETA) and d-glucose, respectively, thus highlighting 2 possible substrate-binding pockets in the MCR-1-catalyzed PEA transfer reaction. Mutation of the residues involved in ETA and d-glucose binding impairs colistin resistance in recombinant Escherichia coli containing full-length MCR-1. Partial analogs of the substrate are used for cocrystallization with cMCR-1, providing valuable information about the family of PEA transferases. One of the analogs, ETA, causes clear inhibition of polymyxin B resistance, highlighting its potential for drug development. These data demonstrate the crucial role of the PEA- and lipid A-binding pockets and provide novel insights into the structure-based mechanisms, important drug-target hot spots, and a drug template for further drug development to combat the urgent, rising threat of MCR-1-mediated antibiotic resistance.-Wei, P., Song, G., Shi, M., Zhou, Y., Liu, Y., Lei, J., Chen, P., Yin, L. Substrate analog interaction with MCR-1 offers insight into the rising threat of the plasmid-mediated transferable colistin resistance.
Assuntos
Colistina/química , Farmacorresistência Bacteriana , Proteínas de Escherichia coli/química , Escherichia coli/enzimologia , Plasmídeos , Catálise , Colistina/farmacologia , Proteínas de Escherichia coli/metabolismo , Etanolaminas/química , Etanolaminas/metabolismo , Lipídeo A/biossíntese , Lipídeo A/química , Domínios ProteicosRESUMO
The maternal liver undergoes dramatic enlargement to adapt to the increased metabolic demands during pregnancy. However, the cellular sources for liver growth during pregnancy remain largely elusive. Here, we employed a proliferation recording system, ProTracer, to examine the spatial-temporal proliferation of hepatocytes during pregnancy. We discovered that during early to late pregnancy, hepatocyte proliferation initiated from zone 1, to zone 2, and lastly to zone 3, with the majority of new hepatocytes being generated in zone 2. Additionally, using single-cell RNA sequencing, we observed that Ccnd1 was highly enriched in zone 2 hepatocytes. We further applied dual-recombinase-mediated genetic lineage tracing to reveal that Ccnd1+ hepatocytes expanded preferentially during pregnancy. Moreover, we demonstrated that estrogen induces liver enlargement during pregnancy, which was abolished in Ccnd1 knockout mice. Our work revealed a unique spatial-temporal hepatocyte proliferation pattern during pregnancy, with Ccnd1+ hepatocytes in zone 2 serving as the major cellular source for hepatic enlargement.
Assuntos
Hepatócitos , Regeneração Hepática , Camundongos , Animais , Feminino , Gravidez , Hepatócitos/metabolismo , Fígado/metabolismo , Proliferação de Células , Camundongos KnockoutRESUMO
Gastric cancer (GC) is the second leading cause of tumor-associated death and the fourth most commonly seen tumor across the world. Abnormal ncRNAs have been verified to be involved in potential metastasis via modulating epithelial-to-mesenchymal transition progression and are vital for the progression of cancers. Tumor-infiltrating immune cells (TICs) are a vital indicator of whether cancer patients will benefit from immunotherapy. Nonetheless, the association between ceRNAs and immune cells remained largely unclear. We used the ceRNA network combined with TICs for the prediction of the clinical outcome of GC patients based on TCGA datasets. The percentage of immunocytes in GC was speculated by the use of CIBERSORT. Via Lasso and multivariate assays, prognostic models were established applying survival-related genes and immune cells. Nomograms were developed, and the accuracy of the nomograms was determined using calibration curves. The association between ceRNAs and TICs was validated by the use of integration analysis. In this study, there were 2219 mRNAs (1308 increased and 911 decreased), 171 lncRNAs (51 decreased and 120 increased), and 123 miRNAs (55 decreased and 68 increased) differentially expressed between tumor groups and nontumor groups. Five lncRNAs, six miRNAs, and 64 mRNAs were used for ceRNA network construction. Eight genes including LOX, SPARC, MASTL, PI15, BMPR1B, ANKRD13B, PVT1, and miR-7-5p were applied for the development of the prognostic model. Survival assays suggested that tumor cases with high risk exhibited a shorter overall survival. In addition, we included T-cell CD4 memory activated, monocytes, and neutrophils for the development of a prognosis model. Eventually, our team demonstrated the possible associations between the ceRNA prognosis model and prognostic model based on immune cells. To sum up, the ceRNA network could be used for gene regulation and predict clinical outcomes of GC patients.
RESUMO
Organ homeostasis is orchestrated by time- and spatially restricted cell proliferation. Studies identifying cells with superior proliferative capacities often rely on the lineage tracing of a subset of cell populations, which introduces a potential selective bias. In this work, we developed a genetic system [proliferation tracer (ProTracer)] by incorporating dual recombinases to seamlessly record the proliferation events of entire cell populations over time in multiple organs. In the mouse liver, ProTracer revealed more hepatocyte proliferation in distinct zones during liver homeostasis, injury repair, and regrowth. Clonal analysis showed that most of the hepatocytes labeled by ProTracer had undergone cell division. By genetically recording proliferation events of entire cell populations, ProTracer enables the unbiased detection of specific cellular compartments with enhanced regenerative capacities.