Spiking Neural Networks (SNNs) have recently attracted enormous research interest since their event-driven and brain-inspired structure enables low-power computation. In image recognition tasks, the best results are achieved by SNN so far utilizing ANN-SNN conversion methods that replace activation functions in artificial neural networks~(ANNs) with integrate-and-fire neurons. Compared to source ANNs, converted SNNs usually suffer from accuracy loss and require a considerable number of time steps to achieve competitive accuracy. We find that the performance degradation of converted SNN stems from the fact that the information capacity of spike trains in transferred networks is smaller than that of activation values in source ANN, resulting in less information being passed during SNN inference. To better correlate ANN and SNN for better performance, we propose a conversion framework to mitigate the gap between the activation value of source ANN and the generated spike train of target SNN. The conversion framework originates from exploring an identical relation in the conversion and exploits temporal separation scheme and novel neuron model for the relation to hold. We demonstrate almost lossless ANN-SNN conversion using SpikeConverter for VGG-16, ResNet-20/34, and MobileNet-v2 SNNs on challenging datasets including CIFAR-10, CIFAR-100, and ImageNet. Our results also show that SpikeConverter achieves the abovementioned accuracy across different network architectures and datasets using 32X - 512X fewer inference time-steps than state-of-the-art ANN-SNN conversion methods.

Mammary analog secretory carcinoma (MASC) of salivary gland is a recently described neoplasm that morphologically and immunohistochemically resembles secretory carcinoma of the breast. Genetically, both of them harbor ETV-6-NTRK-3 fusion rearrangement. One case of primary MASCs arising from the eyelid is reported. The patient was a 52-year-old man. Microscopically, the tumor exhibited nodular aggregation of solid, tubular, and microcystic/macrocystic structures. Characteristic "colloid-like" eosinophilic secretory material was present within intraluminal spaces. Immunohistochemically, the tumor cells were positive for mammaglobin, S-100, STAT5a, vimentin, GCDFP-15, AE1/AE3, EMA, and CK7 and were negative for DOG-1, CK5/6, and SMA. A dual color break-apart fluorescence in situ hybridization probe identified rearrangement of the ETV6 gene locus on chromosome 12. The patient had no history of breast or salivary gland tumor. The tumor was completely excised, and the patient has no evidence of recurrent disease or metastasis after 1-year follow-up. A diagnosis of primary MASC was rendered. MASC has never been reported occurring in ocular region. This type of secretory carcinoma probably originates from sweat glands or accessory lacrimal glands, Wolfring and Krause. This unique case expands the clinicopathologic landscape of MASCs for better characterization of this rare entity.

The design of efficient materials for intracellular protein delivery has attracted great interest in recent years, however, most current materials for this purpose are limited by poor serum stability due...

Metabolic alteration influences cancer immunity. However, the role and mechanism of metabolic adaption on immune checkpoint blockade (ICB) responses remains ill-defined. Here, to identify metabolites that modulate ICB sensitivity, metabolomic profiling in mouse tumor models and cancer patients treated with ICB was performed. We identified that metabolite inosine was associated with ICB sensitivity in mice and humans, and overcame ICB resistance in several mouse tumor models. Notably, inosine sensitized tumor cells to T cell-mediated cytotoxicity by amplifying tumor-intrinsic immunogenicity. Chemical proteomics further identified that inosine directly bound and inhibited ubiquitin-activating enzyme UBA6. Tumor UBA6 loss augmented tumor immunogenicity and substituted the synergistic effect of inosine in combination with ICB. Clinically, tumor UBA6 expression negatively correlated with ICB response in cancer patients. Thus, we reveal an unappreciated function of inosine on tumor-intrinsic immunogenicity and provide UBA6 as a candidate target for immunotherapy.