BackgroundIn recent years novel human respiratory disease agents have been described for Southeast Asia and Australia. The causative pathogens were classified as pteropine orthoreoviruses with a strong phylogenetic relationship to orthoreoviruses of bat origin.ResultsIn this report, we isolated a novel Melaka-like reovirus (named “Cangyuan virus”) from intestinal content samples of one fruit bat residing in China’s Yunnan province. Phylogenetic analysis of the whole Cangyuan virus genome sequences of segments L, M and S demonstrated the genetic diversity of the Cangyuan virus. In contrast to the L and M segments, the phylogenetic trees for the S segments of Cangyuan virus demonstrated a greater degree of heterogeneity.ConclusionsPhylogenetic analysis indicated that the Cangyuan virus was a novel orthoreovirus and substantially different from currently known members of Pteropine orthoreovirus (PRV) species group.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-014-0293-4) contains supplementary material, which is available to authorized users.

Cryptotanshinone inhibits the proliferative and colony formation abilities of human non-small cell lung cancer cells (NSCLCs). The present study reported that signal transducer and activator of transcription 3 is not the only target of cryptotanshinone during the inhibition of human NSCLCs. It was identified that cryptotanshinone upregulates the expression levels of microRNA (miR)-30d-5p, miR-126-3p, miR-133a, miR-338-3p and miR-451a, and downregulates miR-21-5p, miR-96-5p, miR-182-5p and miR-205-5p. Among these, miR-133a was the most significantly upregulated. miR-133a targets and downregulates the expression of matrix metalloproteinase (MMP)14; however, MMP15, MMP16 and MMP24 were determined to be unaffected. This process was identified to be independent of tissue inhibitor of metalloproteinases 2. Cryptotanshinone also suppresses the invasion of human NSCLCs, which may be due to the inhibited expression of MMP14. In conclusion, cryptotanshinone may serve as a potential therapeutic agent in the treatment of lung cancer.

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BackgroundSolitary fibrous tumor of the pleura (SFTP) is a rare pleural neoplasm arising from mesenchymal cells, accounting for <5% of pleural neoplasms. Approximately 10% of cases of SFTP demonstrate malignant potential, leading to local recurrence after radical surgery and subsequent metastasis.MethodsA large malignant-like mass was found in the left thoracic cavity of a 61-year-old woman. Following radical resection of the mass, the patient was diagnosed with malignant SFTP by histologic and immunohistochemical analyses. In addition, a next-generation sequencing-based mutation test was used to reveal the mutational profile of the tumor. The genetic alteration panel was analyzed with reference to public data on the ClinVar and COSMIC databases, after which the public SFTP data were analyzed for frequency of altered genes. Finally, through overlay of the abovementioned two sets, the genetic alteration accounting for SFTP initiation was anticipated to be identified.ResultsIn the mutation panel of our malignant SFTP group, kinase insert domain receptor (KDR) and fms-related tyrosine kinase 1 (FLT1) scored high in pathogenesis but had only a medium frequency; the NAB2–STAT6 fusion appeared to be the dominant genetic alteration in public SFTP samples.ConclusionThe high frequency of NAB2–STAT6 fusion indicates its prominent role in SFTP, while somatic mutations such as FLT1-R593W and KDR-V297I may also contribute to the malignant angiogenic phenotype. The present study affirmed the heterogeneity of SFTP, and more sophisticated classification methods will be needed to explore its underlying mechanisms.SummaryWe believe that improvement in the prognosis of SFTP relies on early diagnosis, margin-free resection, and long-term follow-up. Through genetic analysis, it appears that both NAB2–STAT6 fusion and somatic mutations such as FLT1-R593W and KDR-V297I contribute to SFTP development.