Viruses are the most common causes of respiratory infection. The imaging findings of viral pneumonia are diverse and overlap with those of other nonviral infectious and inflammatory conditions. However, identification of the underlying viral pathogens may not always be easy. There are a number of indicators for identifying viral pathogens on the basis of imaging patterns, which are associated with the pathogenesis of viral infections. Viruses in the same viral family share a similar pathogenesis of pneumonia, and the imaging patterns have distinguishable characteristics. Although not all cases manifest with typical patterns, most typical imaging patterns of viral pneumonia can be classified according to viral families. Although a definite diagnosis cannot be achieved on the basis of imaging features alone, recognition of viral pneumonia patterns may aid in differentiating viral pathogens, thus reducing the use of antibiotics. Recently, new viruses associated with recent outbreaks including human metapneumovirus, severe acute respiratory syndrome coronavirus, and Middle East respiratory syndrome coronavirus have been discovered. The imaging findings of these emerging pathogens have been described in a few recent studies. This review focuses on the radiographic and computed tomographic patterns of viral pneumonia caused by different pathogens, including new pathogens. Clinical characteristics that could affect imaging, such as patient age and immune status, seasonal variation and community outbreaks, and pathogenesis, are also discussed. The first goal of this review is to indicate that there are imaging features that should raise the possibility of viral infections. Second, to help radiologists differentiate viral infections, viruses in the same viridae that have similar pathogenesis and can have similar imaging characteristics are shown. By considering both the clinical and radiologic characteristics, radiologists can suggest the diagnosis of viral pneumonia. RSNA, 2018.

Purpose In multiphase coronary CT angiography (CTA), a series of CT images are taken at different levels of radiation dose during the examination. Although this reduces the total radiation dose, the image quality during the low‐dose phases is significantly degraded. Recently, deep neural network approaches based on supervised learning technique have demonstrated impressive performance improvement over conventional model‐based iterative methods for low‐dose CT. However, matched low‐ and routine‐dose CT image pairs are difficult to obtain in multiphase CT. To address this problem, we aim at developing a new deep learning framework. Method We propose an unsupervised learning technique that can remove the noise of the CT images in the low‐dose phases by learning from the CT images in the routine dose phases. Although a supervised learning approach is not applicable due to the differences in the underlying heart structure in two phases, the images are closely related in two phases, so we propose a cycle‐consistent adversarial denoising network to learn the mapping between the low‐ and high‐dose cardiac phases. Results Experimental results showed that the proposed method effectively reduces the noise in the low‐dose CT image while preserving detailed texture and edge information. Moreover, thanks to the cyclic consistency and identity loss, the proposed network does not create any artificial features that are not present in the input images. Visual grading and quality evaluation also confirm that the proposed method provides significant improvement in diagnostic quality. Conclusions The proposed network can learn the image distributions from the routine‐dose cardiac phases, which is a big advantage over the existing supervised learning networks that need exactly matched low‐ and routine‐dose CT images. Considering the effectiveness and practicability of the proposed method, we believe that the proposed can be applied for many other CT acquisition protocols.

Some phthalates such as di(2-ethylhexyl) phthalate (DEHP) and dibutyl phthalate (DBP) and their metabolites are suspected of producing teratogenic or endocrine-disrupting effects. To predict possible human exposure to phthalates in cosmetics, the levels of DEHP, diethyl phthalate (DEP), DBP, and butylbenzyl phthalate (BBP) were determined by high-performance liquid chromatography (HPLC) in 102 branded hair sprays, perfumes, deodorants, and nail polishes. DBP was detected in 19 of the 21 nail polishes and in 11 of the 42 perfumes, and DEP was detected in 24 of the 42 perfumes and 2 of the 8 deodorants. Median exposure levels to phthalates in cosmetics by dermal absorption were estimated to be 0.0006 g/kg body weight (bw)/d for DEHP, 0.6 g/kg bw/d for DEP, and 0.103 g/kg bw/d for DBP. Furthermore, if phthalates in cosmetics were assumed to be absorbed exclusively via 100% inhalation, the median daily exposure levels to phthalates in cosmetics were estimated to be 0.026 g/kg bw/d for DEHP, 81.471 g/kg bw/d for DEP, and 22.917 g/kg bw/d for DBP, which are far lower than the regulation levels set buy the Scientific Committee on Toxicity, Ecotoxicity, and the Environment (CSTEE) (37 g/kg bw/d, DEHP), Agency for Toxic Substances and Disease Registry (ATSDR) (7000 g/kg bw/d, DEP), and International Programme on Chemical Safety (IPCS) (66 g/kg bw/d, DBP), respectively. Based on these data, hazard indices (HI, daily exposure level/regulation level) were calculated to be 0.0007 for DEHP, 0.012 for DEP, and 0.347 for DBP. These data suggest that estimated exposure to-phthalates in the cosmetics mentioned are relatively small. However, total exposure levels from several sources may be greater and require further investigation.

Cardiac CT can accurately demonstrate infective endocarditis in pre-operative patients with a similar diagnostic accuracy to TEE. The interobserver agreements for the CT findings of infective endocarditis were excellent.

Obesity is characterized by hypertrophy and/or by the differentiation or adipogenesis of pre-existing adipocytes. In this study, we investigated the inhibitory effects of theobromine, a type of alkaloid in cocoa, on adipocyte differentiation of 3T3-L1 preadipocytes and its mechanisms of action. Theobromine inhibited the accumulation of lipid droplets, the expression of PPARγ and C/EBPα, and the mRNA expression of aP2 and leptin. The inhibition of adipogenic differentiation by theobromine occurred primarily in the early stages of differentiation. In addition, theobromine arrested the cell cycle at the G0/G1 phase and regulated the expressions of CDK2, p27, and p21. Theobromine treatment increased AMPK phosphorylation and knockdown of AMPKα1/α2 prevented the ability of theobromine to inhibit PPARγ expression in the differentiating 3T3-L1 cells. Theobromine reduced the phosphorylation of ERK and JNK. Moreover, the secretion and the mRNA level of TNF-α and IL-6 were inhibited by theobromine treatment. These data suggest that theobromine inhibits adipocyte differentiation during the early stages of adipogenesis by regulating the expression of PPARγ and C/EBPα through the AMPK and ERK/JNK signaling pathways in 3T3-L1 preadipocytes.

No abstract

Little is known about the pathogenesis or molecular profiles of idiopathic pulmonary fibrosis-associated lung cancer (IPF-LC). This study was performed to investigate the genomic profiles of IPF-LC and to explore the possibility of defining potential therapeutic targets in IPF-LC. We assessed genomic profiles of IPF-LC by using targeted exome sequencing (OncoPanel version 2) in 35 matched tumour/normal pairs surgically resected between 2004 and 2014. Germline and somatic variant calling was performed with GATK HaplotypeCaller and MuTect with GATK SomaticIndelocator, respectively. Copy number analysis was conducted with CNVkit, with focal events determined by Genomic Identification of Significant Targets in Cancer 2.0, and pathway analysis (KEGG) with DAVID. Germline mutations in TERT (rs2736100, n = 33) and CDKN1A (rs2395655, n = 27) associated with idiopathic pulmonary fibrosis risk were detected in most samples. A total of 410 somatic mutations were identified, with an average of 11.7 per tumour, including 69 synonymous, 177 missense, 17 nonsense, 1 nonstop and 11 splice-site mutations, and 135 small coding indels. Spectra of the somatic mutations revealed predominant C > T transitions despite an extensive smoking history in most patients, suggesting a potential association between APOBEC-related mutagenesis and the development of IPF-LC. TP53 (22/35, 62.9%) and BRAF (6/35, 17.1%) were found to be significantly mutated in IPF-LC. Recurrent focal amplifications in three chromosomal loci (3q26.33, 7q31.2, and 12q14.3) and 9p21.3 deletion were identified, and genes associated with the JAK-STAT signalling pathway were significantly amplified in IPF-LC (P = 0.012). This study demonstrates that IPF-LC is genetically characterized by the presence of somatic mutations reflecting a variety of environmental exposures on the background of specific germline mutations, and is associated with potentially targetable alterations such as BRAF mutations.

Fucoidan is an l-fucose-enriched sulfated polysaccharide isolated from brown algae and marine invertebrates. In this study, we investigated the protective effect of fucoidan from Fucus vesiculosus on alcohol-induced murine liver damage. Liver injury was induced by oral administration of 25% alcohol with or without fucoidan (30 mg/kg or 60 mg/kg) for seven days. Alcohol administration increased serum aspartate aminotransferase and alanine aminotransferase levels, but these increases were suppressed by the treatment of fucoidan. Transforming growth factor beta 1 (TGF-β1), a liver fibrosis-inducing factor, was highly expressed in the alcohol-fed group and human hepatoma HepG2 cell; however, the increase in TGF-β1 expression was reduced following fucoidan administration. Treatment with fucoidan was also found to significantly reduce the production of inflammation-promoting cyclooygenase-2 and nitric oxide, while markedly increasing the expression of the hepatoprotective enzyme, hemeoxygenase-1, on murine liver and HepG2 cells. Taken together, the antifibrotic and anti-inflammatory effects of fucoidan on alcohol-induced liver damage may provide valuable insights into developing new therapeutics or interventions.