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Intelligent Internet of Vehicles is the hot spot of current traffic industry, Video information as a very important part of multidimensional perception, is widely used in vehicle-vehicle interconnection, vehicle-road interconnection and vehicle-management platform interconnection. Because there are obvious differences in the efficiency level between different methods and devices in specific operation, relevant video exchange testing and verification become necessary. This paper presents a test platform and method for video information exchange in Intelligent Internet of Vehicles.Through this platform, a combination of subjective evaluation of video streams and objective testing of transmission network is used to test the availability of the test platform for video exchange on the Internet of Vehicles.

This article through the design which has the function of transcoding, distribution and authentication exchange unit, achieve a face made car video information exchange method. REST method is used to realize the interface call of video information exchange, which includes control flow, media flow and structured data flow of video content analysis results. It can be used in video exchange scenarios of vehicle and vehicle, vehicle and infrastructure, vehicle and remote management platform.

Some natural remedies in traditional Chinese medicine (TCM) inhibit tumor progression and increase sensitivity in the treatment of patients who have received radiation therapy. However, the specific synergistic effect of the active ingredients in the traditional Chinese therapeutic Rongbei Maimendong decoction (RBMD) on sensitivity to radiation therapy for non‐cell lung cancer (NSCLC) is still unclear. RBMD inhibited transplanted tumor cell growth in mice, showing a dose‐dependent effect in tumor growth inhibition following radiotherapy. Our study utilized bioinformatics analysis and liquid chromatography with tandem mass spectrometry to identify the presence of β‐thymidine (β‐thy) in Phellodendron bark, the primary component of RBMD. This compound modulated mRNA and protein levels of SOD1 by interacting with SOD1, inhibiting the malignant characteristics (proliferation, apoptosis, migration, and invasion) of NSCLC cells. Furthermore, apoptosis assays demonstrated that β‐thy attenuated tumor growth in mice following radiotherapy. Single‐cell gel electrophoresis assays demonstrated the ability of SOD1 to mitigate DNA damage in irradiated (IR) NSCLC cells, suppressing apoptosis, and that β‐thy attenuated this SOD1 protective effect, mitigating NSCLC cells resistance to radiation. We propose that the consumption of RBMD, which is rich in β‐thy, may enhance NSCLC radiosensitivity by hindering DNA repair mechanisms and facilitating apoptosis through DNA damage augmentation.

Ageing is associated with a decline in the number and fitness of adult stem cells 1 , 2 . Ageing-associated loss of stemness is posited to suppress tumorigenesis 3 , 4 , but this hypothesis has not been tested in vivo. Here we use physiologically aged autochthonous genetically engineered 5 , 6 mouse models and primary cells 5 , 6 to demonstrate that ageing suppresses lung cancer initiation and progression by degrading the stemness of the alveolar cell of origin. This phenotype is underpinned by the ageing-associated induction of the transcription factor NUPR1 and its downstream target lipocalin-2 in the cell of origin in mice and humans, which leads to functional iron insufficiency in the aged cells. Genetic inactivation of the NUPR1–lipocalin-2 axis or iron supplementation rescues stemness and promotes the tumorigenic potential of aged alveolar cells. Conversely, targeting the NUPR1–lipocalin-2 axis is detrimental to young alveolar cells through ferroptosis induction. Ageing-associated DNA hypomethylation at specific enhancer sites is associated with increased NUPR1 expression, which is recapitulated in young alveolar cells through DNA methylation inhibition. We uncover that ageing drives functional iron insufficiency that leads to loss of stemness and tumorigenesis but promotes resistance to ferroptosis. These findings have implications for the therapeutic modulation of cellular iron homeostasis in regenerative medicine and in cancer prevention. Furthermore, our findings are consistent with a model whereby most human cancers initiate at a young age, thereby highlighting the importance of directing cancer prevention efforts towards young individuals. Studies using mouse models of lung adenocarcinoma identify an association between age, iron homeostasis and tumour initiation potential that involves NUPR1 and lipocalin-2.

Transposable elements (TEs) are abundant in the human genome, and they provide the sources for genetic and functional diversity. The regulation of TEs expression and their functional consequences in physiological conditions and cancer development remain to be fully elucidated. Previous studies suggested TEs are repressed by DNA methylation and chromatin modifications. The effect of 3D chromatin topology on TE regulation remains elusive. Here, by integrating transcriptome and 3D genome architecture studies, we showed that haploinsufficient loss of selectively activates alternative promoters at the long terminal repeats (LTRs) of the TE subclasses. This activation occurs through the reorganization of topologically associating domain (TAD) hierarchical structures and recruitment of proximal enhancers. These observations indicate that TAD hierarchy restricts transcriptional activation of LTRs that already possess open chromatin features. In cancer, perturbation of the hierarchical chromatin topology can lead to co-option of LTRs as functional alternative promoters in a context-dependent manner and drive aberrant transcriptional activation of novel oncogenes and other divergent transcripts. These data uncovered a new layer of regulatory mechanism of TE expression beyond DNA and chromatin modification in human genome. They also posit the TAD hierarchy dysregulation as a novel mechanism for alternative promoter-mediated oncogene activation and transcriptional diversity in cancer, which may be exploited therapeutically.

Aging is associated with a decline in the number and fitness of adult stem cells . Aging-associated loss of stemness is posited to suppress tumorigenesis , but this hypothesis has not been tested . Here, using physiologically aged autochthonous genetically engineered mouse models and primary cells , we demonstrate aging suppresses lung cancer initiation and progression by degrading stemness of the alveolar cell of origin. This phenotype is underpinned by aging-associated induction of the transcription factor NUPR1 and its downstream target lipocalin-2 in the cell of origin in mice and humans, leading to a functional iron insufficiency in the aged cells. Genetic inactivation of the NUPR1-lipocalin-2 axis or iron supplementation rescue stemness and promote tumorigenic potential of aged alveolar cells. Conversely, targeting the NUPR1- lipocalin-2 axis is detrimental to young alveolar cells via induction of ferroptosis. We find that aging-associated DNA hypomethylation at specific enhancer sites associates with elevated NUPR1 expression, which is recapitulated in young alveolar cells by inhibition of DNA methylation. We uncover that aging drives a functional iron insufficiency, which leads to loss of stemness and tumorigenesis, but promotes resistance to ferroptosis. These findings have significant implications for the therapeutic modulation of cellular iron homeostasis in regenerative medicine and in cancer prevention. Furthermore, our findings are consistent with a model whereby most human cancers initiate in young individuals, revealing a critical window for such cancer prevention efforts.