Recently, proposal-free instance segmentation has received increasing attention due to its concise and efficient pipeline. Generally, proposal-free methods generate instance-agnostic semantic segmentation labels and instance-aware features to group pixels into different object instances. However, previous methods mostly employ separate modules for these two sub-tasks and require multiple passes for inference. We argue that treating these two subtasks separately is suboptimal. In fact, employing multiple separate modules significantly reduces the potential for application. The mutual benefits between the two complementary sub-tasks are also unexplored. To this end, this work proposes a single-shot proposal-free instance segmentation method that requires only one single pass for prediction. Our method is based on a pixel-pair affinity pyramid, which computes the probability that two pixels belong to the same instance in a hierarchical manner. The affinity pyramid can also be jointly learned with the semantic class labeling and achieve mutual benefits. Moreover, incorporating with the learned affinity pyramid, a novel cascaded graph partition module is presented to sequentially generate instances from coarse to fine. Unlike previous time-consuming graph partition methods, this module achieves 5× speedup and 9% relative improvement on Average-Precision (AP). Our approach achieves state-of-the-art results on the challenging Cityscapes dataset.

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Emerging evidence indicates that reprogramming of energy metabolism involving disturbances in energy production from a defect in cellular respiration with a shift to glycolysis is a core hallmark of cancer. Alterations in cancer cell energy metabolism are linked to abnormalities in mitochondrial function. Mitochondrial dysfunction of cancer cells includes increased glycolysis, decreased apoptosis, and resistance to radiotherapy. The study was designed for two main points: firstly, to investigate whether exogenous functional mitochondria can transfer into glioma cells and explore the underlying molecular mechanisms from the perspective of endocytosis; secondly, to further verify whether the mitochondrial transplantation is able to rescue aerobic respiration, attenuate the Warburg effect and enhance the radiosensitivity of gliomas. Methods: Mitochondria were isolated from normal human astrocytes (HA) and immediately co-incubated with starved human glioma cells (U87). Confocal microscopy and gene sequencing were performed to evaluate the ability of isolated mitochondria internalization into U87 cells. The interaction between endocytosis and isolated mitochondria transfer were captured by 3D tomographic microscopy and transmission electron microscopy. NAD + , CD38, cADPR and Ca 2+ release were determined by commercial kits, western blot, HLPC-MS and Fluo-3 AM respectively. PCR array expression profiling and Seahorse XF analysis were used to evaluate the effect of mitochondrial transplantation on energy phenotypes of U87 cells. U87 cells and U87 xenografts were both treated with mitochondrial transplantation, radiation, or a combination of mitochondrial transplantation and radiation. Apoptosis in vitro and in vivo were detected by cytochrome C, cleaved caspase 9 and TUNEL staining. Results: We found that mitochondria from HA could be transferred into starved U87 cells by simple co-incubation. Starvation treatment slowed the rate of glycolysis and decreased the transformation of NAD + to NADH in U87 cells. A large amount of accumulated NAD + was released into the extracellular space. CD38 is a member of the NAD + glycohydrolase family that catalyzes the cyclization of extracellular NAD + to intracellular cADPR. cADPR triggered release of Ca 2+ to promote cytoskeleton remodeling and plasma membrane invagination. Thus, endocytosis involving isolated mitochondria internalization was mediated by NAD + -CD38-cADPR-Ca 2+ signaling. Mitochondrial transfer enhanced gene and protein expression related to the tricarboxylic acid (TCA) cycle, increased aerobic respiration, attenuated glycolysis, reactivated the mitochondrial apoptotic pathway, inhibited malignant proliferation of U87 cells. Isolated mitochondria injected into U87...