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Departmental sources A tailgut cyst is a type of benign congenital disease that mainly develops in the retro-rectal space. However, malignant transition can occur in some cases of tailgut cysts. Early and precise diagnosis, and proper treatment, are vital for patients with tailgut cysts with malignant transformation. In this review, we aim to summarize the similarities and differences in the diagnosis and treatment methods among the 3 most frequently reported types of tailgut cysts with malignant transformation. In our study, PubMed and Web of Science databases were used to search for the studies and the key words were "tailgut cysts" and "malignancy". We found 176 articles and selected 75 articles in our survey, with 9 reviews, 35 case reports, and 31 case reports and reviews.

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12 peripheral small lung cancers (< 20 mm) of rapid growth (volume doubling time < 150 days), detected by repeated low dose CT screening, were evaluated to examine their CT features and to correlate such features with histopathological findings. Each patient's CT images, including follow-up and thin section CT images, were studied retrospectively to determine tumour growth rate and CT morphological features. Nine of the tumours exhibited a solid tumour growth pattern: seven of these showed a well defined, homogeneous, soft tissue density with spicular or lobulated margin. These seven tumours included small cell lung cancer (n = 3), moderately differentiated adenocarcinoma (n = 2), poorly differentiated adenocarcinoma (n = 1) and squamous cell carcinoma (n = 1). The other two tumours, a moderately differentiated adenocarcinoma and a well differentiated adenocarcinoma, appeared as irregular, soft tissue density nodules with poorly defined margins. The latter exhibited an air bronchogram pattern and a small cavity. The remaining three tumours exhibited a lepidic tumour growth pattern. They showed ground glass opacity or ground glass opacity with a higher density central zone on CT images and were well differentiated adenocarcinomas. In conclusion, most peripheral small lung cancers of rapid growth were adenocarcinomas. They also included small cell lung cancer and squamous cell carcinoma. The majority showed solid tumour growth pattern and lacked an air bronchogram and/or small air spaces in the nodule. Some well differentiated adenocarcinomas with lepidic tumour growth pattern also showed rapid growth.

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The apoptosis of lens epithelial cells has been proposed as the common basis of cataract formation, with oxidative stress as the major cause. This study was performed to investigate the protective effect of the herbal constituent parthenolide against oxidative stress-induced apoptosis of human lens epithelial (HLE) cells and the possible molecular mechanisms involved. HLE cells (SRA01-04) were incubated with 50 µM H 2 O 2 in the absence or presence of different doses of parthenolide (10, 20 and 50 µM). To study apoptosis, the cells were assessed by morphologic examination and Annexin V-propidium iodide double staining flow cytometry; to investigate the underlying molecular mechanisms, the expression of caspase-3 and caspase-9 were assayed by Western blot and quantitative RT-PCR, and the activities of caspase-3 and caspase-9 were measured by a Chemicon caspase colorimetric activity assay kit. Stimulated with H 2 O 2 for 18 h, a high fraction of HLE cells underwent apoptosis, while in the presence of parthenolide of different concentrations, dose-dependent blocking of HLE cell apoptosis was observed. The expression of caspase-3 and caspase-9 induced by H 2 O 2 in HLE cells was significantly reduced by parthenolide both at the protein and mRNA levels, and the activation of caspase-3 and caspase-9 was also suppressed by parthenolide in a dose-dependent manner. In conclusion, parthenolide prevents HLE cells from oxidative stress-induced apoptosis through inhibition of the activation of caspase-3 and caspase-9, suggesting a potential protective effect against cataract formation.

In China, hepatitis B virus (HBV) infection is the major cause of hepatocellular carcinoma (HCC), which is called HBV-related HCC (HBV-HCC), but the pathogenesis has not been clearly elucidated. Long non-coding RNAs (lncRNAs) have been paid increasing attention to, as an important regulatory molecule involved in many biological processes, as well as a variety of diseases. This study examined lncRNA that might play an important role in HBV-HCC pathogenesis by conducting lncRNA and mRNA profile comparison between HBV-HCC and normal liver tissues. The differentially expressed lncRNA and mRNA profiles between HBV-HCC and normal liver tissues were analyzed by microarrays. The potential protein-encoding gene regulated by lncRNA, and the biological function (gene ontology, pathway analysis) of the target gene were investigated. The results showed that the expression levels of lncRNA and mRNA in HBV-HCC tissues were different from those in normal liver tissues. As compared with normal liver tissue, 837 (4.30%) lncRNAs exhibited more than two-fold change (P<0.05); 325 were up-regulated, and 512 were down-regulated; 991 (5.70%) mRNAs exhibited more than 2-fold change (P<0.05); 733 were up-regulated and 258 were down-regulated in HBV-HCC tissue. Besides, there were 7 lncRNAs with above 10-fold elevation, 6 lncRNAs with above 10-fold decrease, 18 mRNAs with above 10-fold elevation and 11 mRNAs with above 10-fold decrease. 444 (53.05%) lncRNAs had their corresponding mRNAs, some of which were adjacent to lncRNAs. The biological analysis showed that the target gene of differentially expressed lncRNAs took part in the important biological regulatory function. Target gene-related pathway analysis revealed the pathways in carcinoma and mitogen-activated protein kinase (MAPK) signaling pathways significantly changed in the HBV-HCC tissues as compared with normal liver tissues (P<0.05). It was suggested that as compared with normal liver tissues, the expression of lncRNAs in HBV-HCC tissues changed significantly, and lncRNAs played a key role in the pathogenesis of HBV-HCC probably by mainly regulating the carcinoma-related signaling pathway and MAPK signaling pathways.