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Contrast materials are often injected into body to contrast specific tissues in Computed Tomography (CT) images. Contrast Enhanced CT (CECT) images obtained in this way are more useful than Non-Enhanced CT (NECT) images for medical diagnosis, but not available for everyone due to side effects of the contrast materials. Motivated by this, we develop a neural network that takes NECT images and generates their CECT counterparts. Learning such a network is extremely challenging since NECT and CECT images for training are not aligned even at the same location of the same patient due to movements of internal organs. We propose a two-stage framework to address this issue. The first stage trains an auxiliary network that removes the effect of contrast enhancement in CECT images to synthesize their NECT counterparts well-aligned with them. In the second stage, the target model is trained to predict the real CECT images given a synthetic NECT image as input. Experimental results and analysis by physicians on abdomen CT images suggest that our method outperforms existing models for neural image synthesis.

In this study, we investigated the process of X-ray-induced apoptosis of skin keratinocyte, and the functional role of protein kinase C delta (PKCdelta) and downstream signalling cascade. High-dose X-ray irradiation (10 Gy) led to the apoptosis of HaCaT keratinocyte, accompanied by PKCdelta cleavage. Treatment with PKCdelta inhibitor and adenoviral transduction of dominant-negative PKCdelta clearly inhibited the X-ray-induced apoptosis of keratinocyte. In addition, X-ray induced the phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2) and inhibition by ERK1/2 inhibitor abrogated the X-ray-induced apoptosis. Interestingly, overexpression of dominant-negative PKCdelta markedly blocked the X-ray-induced phosphorylation of ERK1/2, suggesting that ERK1/2 is the functional downstream effector of PKCdelta. Next, we investigated the difference between UVB and X-ray response. UVB induced the apoptosis of keratinocyte in a PKCdelta-dependent manner, similar to X-ray response. However, UVB irradiation induced the phosphorylation of c-jun N-terminal kinases (JNK) and inhibition of JNK significantly protected the UVB-induced apoptosis. These results demonstrate that PKCdelta is a key regulator in X-ray-induced apoptosis of keratinocyte and suggest that there is subtle difference in downstream signalling cascade between UVB and X-ray response of keratinocyte.

Summary Background Ultraviolet (UV) B irradiation causes many important biological changes in skin, which lead to pathophysiological alterations of the homeostatic environment. Objectives To gain more insight into the molecular events provoked by UVB irradiation, we performed cDNA microarray analysis. Methods Immortalized HaCaT keratinocytes were irradiated with a high cytotoxic dose of UVB (50 mJ cm−2), and total RNA was isolated. Fluorescently labelled probes were prepared by reverse transcription and were hybridized with cDNA microarray slides made using 840 cDNA clones. Results Time-course cDNA microarray analysis revealed the global gene expression profile after UVB exposure. Of 840 genes tested, 192 genes showed changes in their expression levels at one or more of four time points. The genes were clustered into four groups according to their expression patterns in a self-organizing maps analysis. Classification of these genes into nine functional categories revealed that UVB irradiation affected several biological processes. The genes that were first upregulated and then returned to normal levels included several genes related to the inhibition of cell growth and the proteasome pathway. Conversely, the expressions of many genes involved in the cytoskeleton, signal transduction, metabolism and transcription were first downregulated or unchanged and then upregulated later, reflecting the recovery of UVB-damaged cellular activities. Conclusions These results demonstrate the complexity of the transcriptional profile of the UVB response, and provide a basis for the global characterization of UV-regulated gene expression.