Background and Aims. Multiple studies have reported associations between inflammatory bowel disease (IBD) and the flora disequilibrium of Bacteroides. We performed a meta-analysis of the available data to provide a more precise estimate of the association between Bacteroides level in the gut and IBD. Methods. We searched PubMed/MEDLINE, EMBASE, Cochrane Library, Wiley Library, BIOSIS previews, Web of Science, CNKI, and ScienceDirect databases for published literature on IBD and gut microbiota from 1990 to 2016. Quality of all eligible studies was assessed using the Newcastle-Ottawa Quality Assessment Scale (NOS). We compared the level of Bacteroides in IBD patients with that in a control group without IBD, different types of IBD patients, and IBD patients with active phase and in remission. Results. We identified 63 articles, 9 of which contained sufficient data for evaluation. The mean level of Bacteroides was significantly lower in Crohn's disease (CD) and ulcerative colitis (UC) patients in active phase than in normal controls. The level of Bacteroides in remission CD and UC patients was much lower than patients in the control group. Bacteroides level was even lower in patients with CD and UC in active phase than in remission. Conclusions. This analysis suggests that lower levels of Bacteroides are associated with IBD, especially in active phase.

The flagelliform silk protein underlies the unique elastomeric properties displayed by the capture spiral of arachnid webs. To investigate molecular mechanism underlying the elastomeric recovery of the capture spiral, a model polypeptide based upon the elastomeric repeat sequence of Nephila clavipes flagelliform silk protein has been synthesized using recombinant DNA techniques. Polypeptide 1 contains 11 repeats of the 25 amino acid sequence [(Gly-Pro-Gly-Gly-Ser-Gly-Pro-Gly-Gly-Tyr)(2)-Gly-Pro-Gly-Gly-Lys] and was expressed in Escherichia coli strain BL21(DE3) as a C-terminal fusion to a decahistidine leader sequence. A combination of (1)H-(1)H COSY, DEPT, (1)H-(13)C HETCOR, and (1)H-(13)C HMBC NMR spectroscopy was employed on polypeptides 1 and the [1-(13)C]glycine-labeled analogue 1G to assign the (1)H and (13)C NMR resonances of the amino acid residues comprising the flagelliform silk repeat sequence. The conformational properties of 1 in aqueous solution were investigated using a combination of CD, FTIR, VT-NMR, and two-dimensional NOESY NMR. These techniques were consistent with the presence of small but detectable population of beta-turn conformers between Gly(1) and Gly(4) of the pentapeptide units of 1. FTIR and CD studies of solid films of 1 indicated an increase in beta-turn population in the solid state, which coincided with the decrease in hydration level of the polypeptide. The spectroscopic information suggests that the pentapeptide segments of the flagelliform silk protein adopt a beta-turn conformation in the fiber and that the mechanism of elasticity may resemble that proposed for other beta-turn forming polypeptides including elastin.

Abstract. Long non-coding RNAs (lncRNAs) have previously been reported to be involved in cancer invasion, proliferation and apoptosis. However, the association between the lncRNA, H19, and esophageal cancer (EC) has remained elusive. In the present study, reverse transcription quantitative-polymerase chain reaction revealed that the expression of H19 was significantly increased and associated with tumor depth and metastasis in 133 EC samples. Furthermore, MTT and Transwell assays revealed that overexpression of H19 in vitro promoted the proliferation and invasion of EC cell lines, whereas knockdown of H19 inhibited the proliferation and invasion of EC cell lines. In addition, it was identified that an upregulation of H19 induced epithelial-to-mesenchymal transition, while the opposite effect was observed following the downregulation of H19. In conclusion, H19 has a significant role in the development of EC and may serve as a potential prognostic marker and therapeutic target for EC. IntroductionEsophageal carcinoma (EC) is the eighth most aggressive and malignant type of cancer, with a high incidence that varies according to geographic location and ethnicity (1). Despite progress in the development of diagnostic and therapeutic options, the survival rates for EC patients remain poor. Therefore, the identification of novel genes involved in the tumorigenesis and development of EC is urgently required.Long non-coding RNAs (lncRNAs) are a class of RNAs that have been reported to be involved in the regulation, invasion, proliferation and apoptosis of multiple tumors (2,3). The association between H19 expression and the progression of various types of cancer has been demonstrated in previous studies. One study found that the overexpression of lncRNA H19 enhanced the carcinogenesis and metastasis of gastric cancer (4). MALAT-1, an abundant lncRNA present in many human cell types, has been suggested to regulate the alternative splicing of a subset of pre-messenger (m)RNAs by modulating serine/arginine splicing factor activity. This factor in turn regulates tissue or cell-type-specific alternative splicing in a phosphorylation-dependent manner (5). However, the role of H19 in EC is yet to be elucidated.The epithelial-to-mesenchymal transition (EMT) has an important role in the invasion of various types of cancer by transforming adherent and polarized epithelial cells into invasive and motile mesenchymal cells (6,7). A number of transcription factors involved in EMTs, including Twist and Snail, increase the expression level of mesenchymal markers, including fibronectin, collagen and Vimentin, and decrease the expression of epithelial markers, including E-cadherin. The breakdown of tight junctions results in the loss of epithelial markers and the acquisition of mesenchymal markers (8-10).In the present study, the expression levels of H19 in EC were investigated, in order to elucidate the role of H19 in EC. Materials and methods Clinical

Objective. Intrahepatic cholangiocarcinoma (iCCA) is a primary liver malignancy with a poor prognosis and limited treatment. Cisplatin with gemcitabine is used as the standard first-line chemotherapy regimen; however, there is still no robust evidence for second-line and successive treatments. Although preliminary evidence suggests a vital role of precision therapy or immunotherapy in a subset of patients, the gene alteration rate is relatively low. Herein, we explored the second-line and successive treatments using hepatic arterial infusion chemotherapy (HAIC) based on FOLFIRI after the failure of gemcitabine and platinum combined with target and immunotherapy in refractory CCAs. Methods. Advanced patients with iCCAs confirmed by diagnostic pathology, who progressed at least on a gemcitabine/platinum doublet and/or other systemic chemotherapy combined with target therapy and immune checkpoint inhibitor, were included. All patients received infusional 5-fluorouracil/leucovorin with irinotecan (FOLFIRI) via HAIC until progression or unacceptable toxicity. The primary objective was the feasibility of treatment, with secondary objectives of disease control rate (DCR) and 6-month survival rate. Results. A total of 9 iCCA patients treated between Dec 2020 and May 2021 were enrolled; 2 patients suffered from distant metastasis, while 7 had local lymph node metastasis and portal vein or hepatic vein invasion. HAIC was delivered as second-line therapy in 6/9 patients, while a third or successive therapy in 3/9 patients. The patients accepted an average of 2.90 ± 1.69 cycles of HAIC. The objective response rate was 22.2%; the disease control rate was 55.5% (5/9); median progression-free survival was 5 months; and 6-month survival rate was 66.7% (6/9). Conclusions. Our results provide preliminary evidence that HAIC based on FOLFIRI regimen is efficient and safe in some patients progressing after previous treatment. Therefore, HAIC may be a promising and valuable complementary therapy for advanced CCAs as a second-line and successive therapy. Otherwise, the combination of HAIC with precision medicine may improve clinical benefits (clinical registration number: 2021BAT4857).