The causative viral agent was purified from diseased shrimp Penaeus japonicus with white spot syndrome (WSBV). Several hundred clones were obtained from libraries of the purified viral genomic DNA. According to the results of nucleotide sequence analysis, none of the WSBV clones showed considerable sequence homology with those of other known viruses, indicating that WSBV is a new virus causing a serious disease in shrimp. Based on the sequence data of WSBV genomic DNA, a pair of polymerase chain reaction (PCR) primers was designed. After 30 cycles of PCR amplification of viral genomic DNA extracted from WSBV, a single product of the expected size was detected. Southern blot hybridization confirmed that the amplified product was specific to the DNA of WSBV. The PCR system was able to detect 1 pg of WSBV DNA after 30 cycles, and efficiently amplify the target region of WSBV gene in the total nucleic acids extracted either from the diseased shrimp or hatchery shrimp with no signs of viral infection.
Abstract. Maspin is a tumor suppressor protein that stimulates apoptosis and inhibits motility, invasion and cancer metastasis. We report on a previously uncharacterized Pro/Ser (C to T) polymorphism at amino acid 176 of the human maspin protein. We analyzed the maspin mutation in 17 cancer cell lines and 36 cancer tissues. Association of polymorphic variants on apoptosis, colony formation and in vivo tumor formation was evaluated. Mutant maspin was found to be frequently expressed in gastric cancer (32/36, 89%). According to predicted maspin tertiary structure, the polymorphic residue is located on the surface of the protein proximal to the reactive site loop domain, and thus may significantly affect the protein interactions of maspin. Stable expression of the Pro and Ser forms of maspin in lung cancer cells revealed that cells expressing Ser176 maspin showed significantly decreased apoptosis and increased colony formation compared with those expressing Pro176 maspin. In a mouse model, cells expressing Ser176 maspin showed a higher rate of tumor formation in vivo than those harboring Pro176 maspin. Therefore, P176S (C526T) substitution of maspin may result in a partial loss of the tumor suppressor function of this protein, contributing to decreased susceptibility to apoptosis and malignant progression.
As smartphones become popular, manufacturers such as Samsung Electronics are developing smartphones with rich functionality such as a camera and photo editing quickly, which accelerates the adoption of open source applications in the smartphone platforms. However, developers often do not know the detail of open source applications, because they did not develop the applications themselves. Thus, it is a challenging problem to test open source applications effectively in short time. This paper reports our experience of applying concolic testing technique to test libexif, an open source library to manipulate EXIF information in image files. We have demonstrated that concolic testing technique is effective and efficient at detecting bugs with modest effort in industrial setting. We also compare two concolic testing tools, CREST-BV and KLEE, in this testing project. Furthermore, we compare the concolic testing results with the analysis result of the Coverity Prevent static analyzer. We detected a memory access bug, a null pointer dereference bug, and four divide-by-zero bugs in libexif through concolic testing, none of which were detected by Coverity Prevent.
Allium hookeri (AH) is widely consumed as a herbal medicine. It possesses biological activity against metabolic diseases. The objective of this study was to investigate effects of AH root water extract (AHR) on adipogenesis in 3T3-L1 cells and in high-fat diet (HFD)-induced obese mice. AHR inhibited lipid accumulation during adipocyte differentiation by downregulation of gene expression, such as hormone sensitive lipase (HSL), lipoprotein lipase (LPL) and an adipogenic gene, CCAAT/enhancer binding protein-α in 3T3-L1 preadipocytes. Oral administration of AHR significantly suppressed body weight gain, adipose tissue weight, serum leptin levels, and adipocyte cell size in HFD-induced obese mice. Moreover, AHR significantly decreased hepatic mRNA expression levels of cholesterol synthesis genes, such as 3-hydroxy-3-methylglutaryl CoA reductase, sterol regulatory element-binding transcription factor (SREBP)-2, and low-density lipoprotein receptor, as well as fatty acid synthesis genes, such as SREBP-1c and fatty acid synthase. Serum triglyceride levels were also lowered by AHR, likely as a result of the upregulating gene involved in fatty acid β-oxidation, carnitine palmitoyltransferase 1a, in the liver. AHR treatment activated gene expression of peroxisome proliferator-activated receptor-γ, which might have promoted HSL and LPL-medicated lipolysis, thereby reducing white adipose tissue weight. In conclusion, AHR treatment can improve metabolic alterations induced by HFD in mice by modifying expression levels of genes involved in adipogenesis, lipogenesis, and lipolysis in the white adipose tissue and liver.
Natural killer (NK) cells are large granular lymphocytes that mediate cytotoxic reactions which are not restricted by the major histocompatibility complex. In recent years it has become apparent that a minor proportion of malignant lymphomas expresses an NK-cell phenotype defined by its reactivity with the CD56 antibody. Primary purely cutaneous CD56 + lymphomas have rarely been reported. They share a generally aggressive course and are highly associated with Epstein-Barr virus. We describe a patient with a primary cutaneous nasal-type T/NK-cell lymphoma that presented as a haemophagocytic syndrome and showed an aggressive clinical course.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.