RÉSUMÉ
With the advancement in living standards, there has been a significant surge in the quantity and diversity of household waste. To safeguard the environment and optimize resource utilization, there is an urgent demand for effective and cost-efficient intelligent waste classification methodologies. This study presents MRS-YOLO (Multi-Resolution Strategy-YOLO), a waste detection and classification model. The paper introduces the SlideLoss_IOU technique for detecting small objects, integrates RepViT of the Transformer mechanism, and devises a novel feature extraction strategy by amalgamating multi-dimensional and dynamic convolution mechanisms. These enhancements not only elevate the detection accuracy and speed but also bolster the robustness of the current YOLO model. Validation conducted on a dataset comprising 12,072 samples across 10 categories, including recyclable metal and paper, reveals a 3.6% enhancement in mAP50% accuracy compared to YOLOv8, coupled with a 15.09% reduction in volume. Furthermore, the model demonstrates improved accuracy in detecting small targets and exhibits comprehensive detection capabilities across diverse scenarios. For transparency and to facilitate further research, the source code and related datasets used in this study have been made publicly available at GitHub.
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We previously demonstrated that the C-E-cad protein encoded by circ-E-cadherin promotes the self-renewal of glioma stem cells. The expression pattern of C-E-cad in breast cancer and its potential function in the tumor microenvironment are unclear. The expression of circ-E-cadherin and C-E-cad was detected in breast cancer specimens. The influence of C-E-cad expression on MDSCs was assessed using FACS and in vivo tumorigenesis experiments. The synergistic effect of anti-C-E-cad and anti-PD-1 antibodies was validated in vivo. circ-E-cadherin and the encoded protein C-E-cad were found to be upregulated in breast cancer vs. normal samples. C-E-cad promotes the recruitment of MDSCs, especially PMN-MDSCs. C-E-cad activates EGFR signaling in tumor cells and promotes the transcription of CXCL8; moreover, C-E-cad binds to MDSCs and maintains glycolysis in PMN-MDSCs. Targeting C-E-cad enhanced anti-PD-1 efficiency. Our data suggested that C-E-cad is markedly overexpressed in breast cancer and promotes MDSC recruitment and survival. Targeting C-E-cad increases the efficacy of immune checkpoint inhibitor therapy.
Sujet(s)
Tumeurs du sein , Cadhérines , Cellules myéloïdes suppressives , Cellules myéloïdes suppressives/métabolisme , Cellules myéloïdes suppressives/immunologie , Cellules myéloïdes suppressives/effets des médicaments et des substances chimiques , Tumeurs du sein/métabolisme , Tumeurs du sein/traitement médicamenteux , Tumeurs du sein/génétique , Tumeurs du sein/immunologie , Tumeurs du sein/anatomopathologie , Humains , Femelle , Cadhérines/métabolisme , Cadhérines/génétique , Animaux , Microenvironnement tumoral/effets des médicaments et des substances chimiques , Lignée cellulaire tumorale , Souris de lignée BALB C , Souris , Récepteurs ErbB/métabolisme , Récepteur-1 de mort cellulaire programmée/métabolisme , Récepteur-1 de mort cellulaire programmée/immunologie , Récepteur-1 de mort cellulaire programmée/génétique , Antigènes CD/métabolisme , Antigènes CD/génétique , Inhibiteurs de points de contrôle immunitaires/pharmacologie , Inhibiteurs de points de contrôle immunitaires/usage thérapeutiqueRÉSUMÉ
Decreased hippocampal tropomyosin receptor kinase B (TrkB) level is implicated in the pathophysiology of stress-induced mood disorder and cognitive decline. However, how TrkB is modified and mediates behavioral responses to chronic stress remains largely unknown. Here the effects and mechanisms of TrkB cleavage by asparagine endopeptidase (AEP) were examined on a preclinical murine model of chronic restraint stress (CRS)-induced depression. CRS activated IL-1ß-C/EBPß-AEP pathway in mice hippocampus, accompanied by elevated TrkB 1-486 fragment generated by AEP. Specifi.c overexpression or suppression of AEP-TrkB axis in hippocampal CaMKIIα-positive cells aggravated or relieved depressive-like behaviors, respectively. Mechanistically, in addition to facilitating AMPARs internalization, TrkB 1-486 interacted with peroxisome proliferator-activated receptor-δ (PPAR-δ) and sequestered it in cytoplasm, repressing PPAR-δ-mediated transactivation and mitochondrial function. Moreover, co-administration of 7,8-dihydroxyflavone and a peptide disrupting the binding of TrkB 1-486 with PPAR-δ attenuated depression-like symptoms not only in CRS animals, but also in Alzheimer's disease and aged mice. These findings reveal a novel role for TrkB cleavage in promoting depressive-like phenotype.
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Dépression , Hippocampe , Stress psychologique , Animaux , Hippocampe/métabolisme , Souris , Dépression/métabolisme , Mâle , Stress psychologique/métabolisme , Récepteur trkB/métabolisme , Modèles animaux de maladie humaine , Souris de lignée C57BL , Comportement animal/physiologie , Transduction du signal/physiologie , Maladie d'Alzheimer/métabolisme , Glycoprotéines membranaires/métabolismeRÉSUMÉ
Introduction: Alzheimer's disease (AD) is the most prevalent neurodegenerative disease characterized by extracellular senile plaques including amyloid-ß peptides and intracellular neurofibrillary tangles consisting of abnormal Tau. Depression is one of the most common neuropsychiatric symptoms in AD, and clinical evidence demonstrates that depressive symptoms accelerate the cognitive deficit of AD patients. However, the underlying molecular mechanisms of depressive symptoms present in the process of AD remain unclear. Methods: Depressive-like behaviors and cognitive decline in hTau mice were induced by chronic restraint stress (CRS). Computational prediction and molecular experiments supported that an asparagine endopeptidase (AEP)-derived Tau fragment, Tau N368 interacts with peroxisome proliferator-activated receptor delta (PPAR-δ). Further behavioral studies investigated the role of Tau N368-PPAR-δ interaction in depressive-like behaviors and cognitive declines of AD models exposed to CRS. Results: We found that mitochondrial dysfunction was positively associated with depressive-like behaviors and cognitive deficits in hTau mice. Chronic stress increased Tau N368 and promoted the interaction of Tau N368 with PPAR-δ, repressing PPAR-δ-mediated transactivation in the hippocampus of mice. Then we predicted and identified the binding sites of PPAR-δ. Finally, inhibition of AEP, clearance of Tau N368 and pharmacological activation of PPAR-δ effectively alleviated CRS-induced depressive-like behaviors and cognitive decline in mice. Conclusion: These results demonstrate that Tau N368 in the hippocampus impairs mitochondrial function by suppressing PPAR-δ, facilitating the occurrence of depressive-like behaviors and cognitive decline. Therefore, our findings may provide new mechanistic insight in the pathophysiology of depression-like phenotype in mouse models of Alzheimer's disease.
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BACKGROUND: Glioblastoma (GBM) preferred to infiltrate into white matter (WM) beyond the recognizable tumor margin. OBJECTIVE: To investigate whether fiber density (FD) and structural brain connectome can provide meaningful information about WM destruction and glioma cell infiltration. METHODS: GBM cases were collected based on inclusion criteria, and baseline information and preoperative MRI results were obtained. GBM lesions were automatically segmented into necrosis, contrast-enhanced tumor, and edema areas. We obtained the FD map to compute the FD and lnFD values in each subarea and reconstructed the structural brain connectome to obtain the topological metrics in each subarea. We also divided the edema area into a nonenhanced tumor (NET) area and a normal WM area based on the contralesional lnFD value in the edema area, and computed the NET ratio. RESULTS: Twenty-five GBM cases were included in this retrospective study. The FD/lnFD value and topological metrics (aCp, aLp, aEg, aEloc, and ar) were significantly correlated with GBM subareas, which represented the extent of WM destruction and glioma cell infiltration. The FD/lnFD values and topological parameters were correlated with the NET ratio. In particular, the lnFD value in the edema area was correlated with the NET ratio (coefficient, 0.92). Therefore, a larger lnFD value indicates more severe glioma infiltration in the edema area and suggests an extended resection for better clinical outcomes. CONCLUSION: The FD and structural brain connectome in this study provide a new insight into glioma infiltration and a different consideration of their clinical application in neuro-oncology.
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Tumeurs du cerveau , Connectome , Glioblastome , Gliome , Humains , Glioblastome/imagerie diagnostique , Glioblastome/anatomopathologie , Études rétrospectives , Tumeurs du cerveau/imagerie diagnostique , Tumeurs du cerveau/anatomopathologie , Gliome/imagerie diagnostique , Gliome/anatomopathologie , Encéphale/imagerie diagnostique , Encéphale/anatomopathologie , Oedème/anatomopathologieRÉSUMÉ
Accumulating studies indicate that circular RNAs (circRNAs) play critical roles in cancer progression. Most of them have been reported to act as microRNA sponges or interact with RNA-binding proteins; however, their full range of functions remains largely unclear. Recently, an increasing number of circRNAs have been found to encode proteins. C-E-Cad, a protein encoded by circular E-cadherin (circ-E-Cad), has been shown to have a great influence in the progression of glioblastoma, but its specific role in gastric cancer (GC) is unclear. Here, we found that both circ-E-Cad and C-E-Cad were upregulated in GC cell lines and GC tissues compared with a human gastric epithelial cell line (GES-1) and normal tissues. Knockdown of circ-E-Cad suppressed GC cell line proliferation and metastasis in vitro and in vivo, whereas overexpression of C-E-Cad had the opposite effects. Immunoblotting revealed that C-E-Cad exerted tumor-promoting functions by regulating the PI3K/AKT pathway. A rescue experiment showed that C-E-Cad but not circ-E-Cad was the executor of protumor biological functions. In addition, we demonstrated that the C-E-Cad expression level could have been increased by the TGF-ß/Smad pathway. In summary, our results indicated that the TGF-ß/Smad pathway could increase the expression of C-E-Cad to regulate GC cell proliferation, migration, and epithelial-mesenchymal transition by affecting PI3K/AKT signaling.
Sujet(s)
microARN , Tumeurs de l'estomac , Humains , Protéines proto-oncogènes c-akt/génétique , Protéines proto-oncogènes c-akt/métabolisme , Tumeurs de l'estomac/anatomopathologie , ARN circulaire/génétique , Phosphatidylinositol 3-kinases/génétique , Phosphatidylinositol 3-kinases/métabolisme , Facteur de croissance transformant bêta/génétique , Facteur de croissance transformant bêta/métabolisme , Lignée cellulaire tumorale , microARN/génétique , microARN/métabolisme , Prolifération cellulaire/génétique , Mouvement cellulaire/génétique , Régulation de l'expression des gènes tumorauxRÉSUMÉ
Mutations of the RAS oncogene are found in around 30% of all human cancers yet direct targeting of RAS is still considered clinically impractical except for the KRASG12C mutant. Here we report that RAS-ON (RASON), a novel protein encoded by the long intergenic non-protein coding RNA 00673 (LINC00673), is a positive regulator of oncogenic RAS signaling. RASON is aberrantly overexpressed in pancreatic ductal adenocarcinoma (PDAC) patients, and it promotes proliferation of human PDAC cell lines in vitro and tumor growth in vivo. CRISPR/Cas9-mediated knockout of Rason in mouse embryonic fibroblasts inhibits KRAS-mediated tumor transformation. Genetic deletion of Rason abolishes oncogenic KRAS-driven pancreatic and lung cancer tumorigenesis in LSL-KrasG12D; Trp53R172H/+ mice. Mechanistically, RASON directly binds to KRASG12D/V and inhibits both intrinsic and GTPase activating protein (GAP)-mediated GTP hydrolysis, thus sustaining KRASG12D/V in the GTP-bound hyperactive state. Therapeutically, deprivation of RASON sensitizes KRAS mutant pancreatic cancer cells and patient-derived organoids to EGFR inhibitors. Our findings identify RASON as a critical regulator of oncogenic KRAS signaling and a promising therapeutic target for KRAS mutant cancers.
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Carcinome du canal pancréatique , Tumeurs du pancréas , ARN long non codant , Humains , Animaux , Souris , ARN long non codant/génétique , Protéines proto-oncogènes p21(ras)/génétique , Protéines proto-oncogènes p21(ras)/métabolisme , Gènes ras , Fibroblastes/métabolisme , Tumeurs du pancréas/métabolisme , Carcinome du canal pancréatique/métabolisme , Guanosine triphosphate , Mutation/génétique , Tumeurs du pancréasRÉSUMÉ
Glioblastoma (GBM) is a highly aggressive primary brain tumour and is resistant to nearly all available treatments, including natural killer (NK) cell immunotherapy. However, the factors mediating NK cell evasion in GBM remain largely unclear. Here, we report that EZH2-92aa, a protein encoded by circular EZH2, is overexpressed in GBM and induces the immune evasion of GBM stem cells (GSCs) from NK cells. Positively regulated by DEAD-box helicase 3 (DDX3), EZH2-92aa directly binds the major histocompatibility complex class I polypeptide-related sequence A/B (MICA/B) promoters and represses their transcription; it also indirectly represses UL16-binding protein (ULBP) transcription by stabilizing EZH2. The downregulation of NK group 2D ligands (NKG2DLs, including MICA/B and ULBPs) in GSCs mediates NK cell resistance. Moreover, stable EZH2-92aa knockdown enhances NK cell-mediated GSC eradication in vitro and in vivo and synergizes with anti-PD1 therapy. Our results highlight the immunosuppressive function of EZH2-92aa in inhibiting the NK cell response in GBM and the clinical potential of targeting EZH2-92aa for NK-cell-directed immune therapy.
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Protéine-2 homologue de l'activateur de Zeste , Glioblastome , Sous-famille K des récepteurs de cellules NK de type lectine , Échappement de la tumeur à la surveillance immunitaire , Protéine-2 homologue de l'activateur de Zeste/génétique , Protéines liées au GPI/génétique , Glioblastome/génétique , Antigènes d'histocompatibilité de classe I/métabolisme , Humains , Ligands , Sous-famille K des récepteurs de cellules NK de type lectine/génétique , Sous-famille K des récepteurs de cellules NK de type lectine/métabolisme , Récepteurs de cellules tueuses naturellesRÉSUMÉ
Zero waste multistage utilization of biomass from Ginkgo biloba branches (GBBs) was achieved through extraction of bioactive components, analysis of antioxidant and antibacterial activities, preparation and composition of pyrolyzate, adsorption and reuse of modified biochar. The results showed that GBBs had abundant bioactive components for potential application in the industry of food, chemical raw materials and biomedicine. Especially, the bioactive compounds in acetone extract (10 mg/mL) of GBBs identified by DPPH and ABTS had free radical scavenging abilities of 92.28% and 98.18%, respectively, which are equivalent to Vitamin C used as an antioxidant in food additives. Fourier Transform Infrared and X-Ray Diffraction analysis showed that carboxymethyl cellulose (CMC) and magnetic Fe3O4 were successfully incorporated into raw biochar (RB) to form CMC-Fe3O4-RB nanomaterial. Scanning electron microscopy and X-Ray Diffraction spectroscopy displayed Fe, C, and O existed on the surface of CMC-Fe3O4-RB. Compared with RB, CMC-Fe3O4-RB had a larger specific surface area, pore volume and pore size. Meanwhile, nanomagnetic CMC-Fe3O4-RB solved the problem of agglomeration in traditional magnetized biochar production, and improved the adsorption capacity of Pb2+, which was 29.90% higher than that of RB by ICP-OES. Further, the Pb2+ (10 mg/L) adsorption capacity of CMC-Fe3O4-RB reached the highest level in 2 h at the dosage of 0.01 g/L, and remained stable at 52.987 mg/g after five cycles of adsorption and desorption. This research aided in the creation of a strategy for GBBs zero waste multistage usage and a circular economic model for GBBs industry development, which can be promoted and applied to the fields of food industry and environment improvement.
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Ginkgo biloba , Polluants chimiques de l'eau , Adsorption , Carboxyméthylcellulose de sodium , Charbon de bois , Extraits de plantes , Polluants chimiques de l'eau/analyseRÉSUMÉ
BACKGROUND: Emerging studies have revealed the potent functions of circRNAs in breast cancer tumorigenesis. However, the biogenesis, biofunction and mechanism of circRNAs in triple-negative breast cancer (TNBC) are largely unknown. METHODS: High-throughput RNA sequencing was applied to identify dysregulated circRNAs in TNBCs and paired normal tissues. RNA pulldown and luciferase assays were performed to investigate the interaction between circular CD44 (circCD44, also annotated as hsa_circ_0021735) and miR-502-5p. RNA pulldown and RIP assays were used to investigate the interaction between circCD44 and IGF2BP2. Cell viability, colony formation, migration/invasion assays and in vivo tumorigenesis were used to investigate circCD44 biological functions. RESULTS: CircCD44 is an uncharacterized circRNA, which is highly expressed in TNBC, and its expression is negatively correlated with the prognosis of TNBC patients. CircCD44 promotes TNBC proliferation, migration, invasion and tumorigenesis at least partially by sponging miR-502-5p and interacting with IGF2BP2. CONCLUSION: Our data suggested that overexpressed circCD44 promotes TNBC progression. CircCD44 is potentially a novel diagnostic and therapeutic marker for TNBC patients.
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Gènes myc/génétique , Antigènes CD44/génétique , microARN/génétique , Protéines proto-oncogènes p21(ras)/génétique , ARN circulaire , Protéines de liaison à l'ARN/génétique , Tumeurs du sein triple-négatives/génétique , Animaux , Apoptose/génétique , Marqueurs biologiques tumoraux/génétique , Lignée cellulaire tumorale , Transformation cellulaire néoplasique/génétique , Transformation cellulaire néoplasique/métabolisme , Évolution de la maladie , Femelle , Régulation de l'expression des gènes tumoraux , Humains , Antigènes CD44/composition chimique , Souris , Oncogènes , Pronostic , Interférence par ARN , Relation structure-activitéRÉSUMÉ
Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is caused by biallelic HTRA1 pathogenic variants. Recent studies have shown that heterozygous HTRA1 mutations are associated with autosomal dominant cerebral small vessel disease (CSVD). However, large studies evaluating heterozygous HTRA1 carriers are lacking and the genotype-phenotype correlation is unknown. This study aimed to describe these mutations to clarify factors playing a role in the clinical phenotype amongst these patients. We reported two unrelated families and performed a systematic review of all published cases of heterozygous HTRA1-related CSVD. The clinical phenotype severity was independently related to the pathogenicity score (CADD score; p < 0.05) and mutation in the loop 3/loop D domains (p = 0.05); the pathogenicity score was also associated with exon distribution. More importantly, patients with mutations in exon 4 (p = 0.0001) or vascular risk factors (p < 0.05) presented with more severe clinical symptoms. Thus, clinical phenotype severity is influenced by the mutation domain and vascular risk factors. Applying the pathogenicity score to predict clinical outcomes and adopting preventive measures against cerebral vascular risk factors is advantageous.
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Alopécie , Infarctus cérébral , High-temperature requirement A serine peptidase 1 , Leucoencéphalopathies , Mutation , Phénotype , Maladies du rachis , Adulte , Humains , Mâle , Adulte d'âge moyen , Alopécie/génétique , Infarctus cérébral/génétique , Maladies des petits vaisseaux cérébraux/génétique , Maladies des petits vaisseaux cérébraux/anatomopathologie , Études d'associations génétiques/méthodes , Hétérozygote , High-temperature requirement A serine peptidase 1/génétique , Leucoencéphalopathies/génétique , Mutation/génétique , Maladies du rachis/génétiqueRÉSUMÉ
When operating within the environments rich with sodium chloride, steel bars of reinforced concrete structures are often subject to corrosion caused by surrounding erosive materials, and the associated rust expansion force due to corrosion takes a critical role in determining the durability of relevant reinforced concrete structures. By investigating the corrosion course of steel reinforcement with theory of elasticity, a numerical rust expansion model is established for the moment of concrete surface rupture based on non-uniform sin function. Cuboid reinforced concrete specimen with squared cross sections is tested to analyze the rust expansion when concrete cracks due to corrosive forces. The utility of the established expansion model is validated by numerical simulation with Abaqus through the comparison between the associated outcomes. The impacts of steel bar diameter and concrete cover thickness on the magnitude of rust expansion force are discussed.
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Activated EGFR signalling drives tumorigenicity in 50% of glioblastoma (GBM). However, EGFR-targeting therapy has proven ineffective in treating patients with GBM, indicating that there is redundant EGFR activation. Circular RNAs are covalently closed RNA transcripts that are involved in various physiological and pathological processes. Herein, we report an additional activation mechanism of EGFR signalling in GBM by an undescribed secretory E-cadherin protein variant (C-E-Cad) encoded by a circular E-cadherin (circ-E-Cad) RNA through multiple-round open reading frame translation. C-E-Cad is overexpressed in GBM and promotes glioma stem cell tumorigenicity. C-E-Cad activates EGFR independent of EGF through association with the EGFR CR2 domain using a unique 14-amino-acid carboxy terminus, thereby maintaining glioma stem cell tumorigenicity. Notably, inhibition of C-E-Cad markedly enhances the antitumour activity of therapeutic anti-EGFR strategies in GBM. Our results uncover a critical role of C-E-Cad in stimulating EGFR signalling and provide a promising approach for treating EGFR-driven GBM.
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Antigènes CD/métabolisme , Tumeurs du cerveau/enzymologie , Cadhérines/métabolisme , Glioblastome/enzymologie , ARN circulaire/métabolisme , Facteur de transcription STAT-3/métabolisme , Animaux , Antigènes CD/génétique , Antinéoplasiques/pharmacologie , Tumeurs du cerveau/traitement médicamenteux , Tumeurs du cerveau/génétique , Tumeurs du cerveau/anatomopathologie , Cadhérines/génétique , Lignée cellulaire tumorale , Mouvement cellulaire/effets des médicaments et des substances chimiques , Prolifération cellulaire/effets des médicaments et des substances chimiques , Récepteurs ErbB/antagonistes et inhibiteurs , Récepteurs ErbB/génétique , Récepteurs ErbB/métabolisme , Femelle , Régulation de l'expression des gènes tumoraux , Glioblastome/traitement médicamenteux , Glioblastome/génétique , Glioblastome/anatomopathologie , Humains , Souris nude , Invasion tumorale , ARN circulaire/génétique , Facteur de transcription STAT-3/génétique , Transduction du signal , Charge tumorale/effets des médicaments et des substances chimiques , Tests d'activité antitumorale sur modèle de xénogreffeRÉSUMÉ
Concrete cracking caused by corrosion of reinforcement could significantly shorten the durability of reinforced concrete structure. It remains critical to investigate the process and mechanism of the corrosion occurring to concrete reinforcement and establish the theoretical prediction model of concrete expansion force for the whole process of corrosion cracking of reinforcement. Under the premise of uniform corrosion of reinforcing steel bars, the elastic mechanics analysis method is adopted to analyze the entire process starting from the corrosion of steel bars to the cracking of concrete due to corrosion. A relationship model between the expansion force of corrosion of steel bars and the surface strain of concrete is established. On the cuboid reinforced concrete specimens with square cross-sections, accelerated corrosion tests are carried out to calibrate and verify the established model. The model can be able to estimate the real-time expansion force of reinforced concrete at any time of the whole process from the initiation of steel corrosion to the end of concrete cracking by measuring the surface strain of concrete. It could be useful for quantitative real-time monitoring of steel corrosion in concrete structures.
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Background: RP11-480I12. 5 is a newly identified long non-coding RNA (lncRNA) that has never been studied in breast cancer (BC). The biological function of RP11-480I12.5 in breast carcinoma and its underlying mechanism are still unknown. Methods: We scanned The Cancer Genome Atlas (TCGA) database and identified RP11-480I12.5 as one of the most dysregulated lncRNAs. The level of RP11-480I12.5 was assessed in BC tissue samples and BC cell lines. The prognostic value of RP11-480I12.5 expression was assessed using the Kaplan-Meier method. The biological influence of RP11-480I12.5 on BC cell lines was studied using proliferation and Transwell migration and invasion assays. Results: RP11-480I12.5 expression was upregulated in data from both the TCGA database and our own database. Moreover, Kaplan-Meier and Cox proportional hazard analyses indicated that high RP11-480I12.5 expression was related to poor overall survival. Moreover, RP11-480I12.5 promoted the proliferation, migration, and invasion of BC. RP11-480I12.5 promoted the expression of AURKA and the activation of the downstream Wnt/ß-catenin pathway by sponging the microRNA (miRNA) miR-490-3p. Conclusion: Taken together, our results indicate that RP11-480I12.5 is associated with tumor progression in BCs. Our findings indicate that the lncRNA RP11-480I12.5 promotes the proliferation, migration, and invasion of BC cells through the miR-490-3p-AURKA-Wnt/ß-catenin axis, which may serve as a therapeutic target in the future.
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The spatial phase-shift technique has been successfully applied to an out-of-plane speckle interferometry system. Its application to a pure in-plane sensitive system has not been reported yet. This paper presents a novel optical configuration that enables the application of the spatial phase-shift technique to pure in-plane sensitive dual-beam speckle interferometry. The new spatial phase-shift dual-beam speckle interferometry (SPS-DBSP) uses a dual-beam in-plane electronic speckle pattern interferometry configuration with individual aperture shears, avoiding the interference in the object plane by the use of a low-coherence source, and different optical paths. The measured object is illuminated by two incoherent beams that are generated by a delay line, which is larger than the coherence length of the laser. The two beams reflected from the object surface interfere with each other at the CCD plane because of different optical paths. A spatial phase shift is introduced by the angle between the two apertures when they are mapped to the same optical axis. The phase of the in-plane deformation can directly be extracted from the speckle patterns by the Fourier transform method. The capability of SPS-DBSI is demonstrated by theoretical discussion as well as experiments.
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Circular RNAs (circRNAs) are recognized as functional non-coding transcripts in eukaryotic cells. Recent evidence has indicated that even though circRNAs are generally expressed at low levels, they may be involved in many physiological or pathological processes, such as gene regulation, tissue development and carcinogenesis. Although the 'microRNA sponge' function is well characterized, most circRNAs do not contain perfect trapping sites for microRNAs, which suggests the possibility that circRNAs have functions that have not yet been defined. In this study, we show that a circRNA containing an open reading frame (ORF) driven by the internal ribosome entry site (IRES) can translate a functional protein. The circular form of the SNF2 histone linker PHD RING helicase (SHPRH) gene encodes a novel protein that we termed SHPRH-146aa. Circular SHPRH (circ-SHPRH) uses overlapping genetic codes to generate a 'UGA' stop codon, which results in the translation of the 17 kDa SHPRH-146aa. Both circ-SHPRH and SHPRH-146aa are abundantly expressed in normal human brains and are down-regulated in glioblastoma. The overexpression of SHPRH-146aa in U251 and U373 glioblastoma cells reduces their malignant behavior and tumorigenicity in vitro and in vivo. Mechanistically, SHPRH-146aa protects full-length SHPRH from degradation by the ubiquitin proteasome. Stabilized SHPRH sequentially ubiquitinates proliferating cell nuclear antigen (PCNA) as an E3 ligase, leading to inhibited cell proliferation and tumorigenicity. Our findings provide a novel perspective regarding circRNA function in physiological and pathological processes. Specifically, SHPRH-146aa generated from overlapping genetic codes of circ-SHPRH is a tumor suppressor in human glioblastoma.