RESUMO
Accurate lane detection is an essential function of dynamic traffic perception. Though deep learning (DL) based methods have been widely applied to lane detection tasks, such models rarely achieve sufficient accuracy in low-light weather conditions. To improve the model accuracy in foggy conditions, a new approach was proposed based on monocular depth prediction and an atmospheric scattering model to generate fog artificially. We applied our method to the existing CULane dataset collected in clear weather and generated 107,451 labeled foggy lane images under three different fog densities. The original and generated datasets were then used to train state-of-the-art (SOTA) lane detection networks. The experiments demonstrate that the synthetic dataset can significantly increase the lane detection accuracy of DL-based models in both artificially generated foggy lane images and real foggy scenes. Specifically, the lane detection model performance (F1-measure) was increased from 11.09 to 70.41 under the heaviest foggy conditions. Additionally, this data augmentation method was further applied to another dataset, VIL-100, to test the adaptability of this approach. Similarly, it was found that even when the camera position or level of brightness was changed from one dataset to another, the foggy data augmentation approach is still valid to improve model performance under foggy conditions without degrading accuracy on other weather conditions. Finally, this approach also sheds light on practical applications for other complex scenes such as nighttime and rainy days.
Assuntos
Condução de Veículo , Acidentes de Trânsito , Algoritmos , Coleta de Dados , Tempo (Meteorologia)RESUMO
LED lighting systems with large color gamuts, with multiple LEDs spanning the visible spectrum, offer the potential of increased lighting efficiency, improved human health and productivity, and visible light communications addressing the explosive growth in wireless communications. The control of this "smart lighting system" requires a silicon-integrated-circuit-compatible, visible, plenoptic (angle and wavelength) detector. A detector element, based on an offset-grating-coupled dielectric waveguide structure and a silicon photodetector, is demonstrated with an angular resolution of less than 1° and a wavelength resolution of less than 5 nm.
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Amyotrophic lateral sclerosis (ALS) is a disease of which the underlying etiology and pathogenesis are unknown. Numerous data indicate an important role of the immune system and mitochondrial function in the disease. Primary biliary cirrhosis (PBC) is an autoimmune liver disease resulting from a combination of genetic and environmental risk factors. Patients with PBC develop innate and adaptive immune reactions against mitochondrial antigens. Therefore, common mechanisms could exist in both diseases. We present two cases of ALS with PBC to explore the relationship between the two diseases from the immunological and mitochondrial aspects. Further attention should be given to immune-modulating therapy in ALS patients.
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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective loss of motor neurons. Statins are widely used as cholesterol-lowering drugs and significantly reduce the risk of cardiovascular and cerebrovascular diseases. Increasing evidence indicates the protective effects of statins against certain neurodegenerative diseases. However, in ALS, many studies have found that statins might accelerate disease progression and shorten survival, although the exact mechanism is unclear. In the present study, we investigated the effect of simvastatin on NSC34cells stably transfected with the G93A mutation in human SOD1 (NSC34-hSOD1G93A cells), a recognized in vitro model of ALS. Our results showed that simvastatin caused a decrease in cell viability and the accumulation of autophagic vacuoles with elevated levels of LC3 II/I and P62 in NSC34-hSOD1G93A cells. Conversely, these outcomes were completely reversed by co-incubation with mevalonate, farnesyl pyrophosphate (FPP) or geranylgeranyl pyrophosphate (GGPP) but not cholesterol. In addition, inhibition of geranylgeranyl transferase I by GGTI-286 led to similar alterations in cell viability and autophagic marker levels. These results indicated that the cytotoxic effect of simvastatin on NSC34-hSOD1G93A cells might be due to the aggravation of autophagic flux impairment through the inhibition of GGPP synthesis.
Assuntos
Autofagia/efeitos dos fármacos , Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia , Neurônios Motores/efeitos dos fármacos , Fosfatos de Poli-Isoprenil/metabolismo , Sinvastatina/farmacologia , Animais , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , L-Lactato Desidrogenase/metabolismo , Camundongos , Neurônios Motores/metabolismoRESUMO
As an adult-onset neurodegenerative disease, amyotrophic lateral sclerosis (ALS) results in progressive muscular atrophy and paralysis. However, the mechanism of ALS has not yet been elucidated, and no cure has been found. Research has revealed that a mutation of the Cu/Zn superoxide dismutase (SOD1) gene is linked to familial ALS and that potential sex discrepancies exist in ALS incidence. Here, NSC-34 cells stably expressing hSOD1-G93A (hSOD1-G93A cells) were transiently transfected with Cyp19a1 mouse open reading frame (ORF) cDNA or a short hairpin RNA (ShRNA) plasmid. Overexpression of aromatase resulting from Cyp19a1 mouse ORF cDNA plasmid transfection enhanced cell proliferation and reduced cell damage in hSOD1-G93A cells. This protective effect occurred through anti-apoptotic pathways related to estrogen receptor-alpha (ER-α) activation. Meanwhile, knockdown of aromatase with Cyp19a1 ShRNA plasmid transfection reduced cell proliferation, increased cell damage, promoted apoptosis, and decreased ER-α expression in hSOD1-G93A cells, and the induced apoptotic effects could be reversed by estradiol (E2). In brief, the results of our study suggest that aromatase plays a neuroprotective role against apoptosis in hSOD1-G93A cells by activating ER-α and may become a new intervention target for ALS treatment.