An efficient, economical, and easy mass production biochar supported zero-valent iron composite derived from direct-reduction natural goethite for Cu(II) and Cr(VI) remove.

In this study, a novel biochar-supported zero-valent iron (ZVI) composite was synthesised by a one-pot co-pyrolysis reduction method, and was used to remove Cu(II) and Cr(VI). The raw materials for the composite were derived from natural bagasse/straw and goethite. Scanning electron microscopy (SEM), X-ray diffraction (XRD) analysis, Fourier-transform infrared (FTIR) spectroscopy, thermogravimetry (TG), and Brunauer-Emmett-Teller (BET) analysis were used to characterise the biochar and biochar-supported ZVI composites. Batch removal experiments on the effects of the initial pH and citric acid concentrations were performed as well as kinetic studies and isotherm experiments. The composite materials showed better Cu(II) and Cr(VI) removal performance than single biochar and mineral. The removal of Cu(II) and Cr(VI) is pH-dependent, and proceeds via heterogeneous multilayer chemisorption. Electrochemical analysis revealed that straw biochar-supported ZVI composite exhibited greater electrical conductivity and electron transfer rate than pure biochar and ZVI. FTIR spectroscopy and X-ray photoelectron spectroscopy (XPS) elucidated the uptake mechanism, showing that Cu(II) and Cr(VI) were easily adsorbed onto the biochar surface and were then reduced by ZVI. These results indicate that biochar-supported ZVI composite is effective for heavy metal remediation, which is economical, environment-friendly, and suitable for mass production.

Long non-coding RNA SNHG1 functions as a competitive endogenous RNA to regulate PDCD4 expression by sponging miR-195-5p in hepatocellular carcinoma.

Long non-coding RNA (lncRNA) potentially regulates tumorigenesis. LncRNA small nucleolar RNA host gene 1 (SNHG1) expression remains high in hepatocellular carcinoma cells; however, its biological mechanism in hepatocellular carcinoma remains unknown. In this study, SNHG1 expression in hepatocellular carcinoma cells was detected by qRT-PCR. Proliferative and migratory potentials of hepatocellular carcinoma cells were determined by CCK-8 and Transwell assay, respectively. Then, the nude mice model of xenograft was employed to verify the effect of SNHG1 on tumor formation in vivo. We identified the potential target of SNHG1 through bioinformatics and dual-luciferase reporter gene. Furthermore, Western blot and RIP assay was used for clarifying their interaction and functions in regulating the development of hepatocellular carcinoma. Our results indicated a high expression of SNHG1 in hepatocellular carcinoma cells. Downregulation of SNHG1 inhibited proliferative and migratory potentials of hepatocellular carcinoma cells in vitro and in vivo. Moreover, the expression of programmed cell death 4 (PDCD4) was positively regulated by SNHG1 through competing with miR-195-5p. These results indicated that SNHG1 participated in the development of hepatocellular carcinoma as a ceRNA to competitively bind to miR-195-5p and thus mediate PDCD4 expression.

SIRT4 acts as a tumor suppressor in gastric cancer by inhibiting cell proliferation, migration, and invasion.

BACKGROUND: Previous study has proven that SIRT4 is downregulated in gastric cancer (GC), but the role of SIRT4 has not been clearly understood. The aim of our work was to explore in detail the function and mechanism of SIRT4 in GC. METHODS: A total of 86 pairs of GC tumor tissues and adjacent normal tissues were collected, and quantitative real-time polymerase chain reaction and Western blotting analyses were used to determine the expression of SIRT4. RESULTS: Our study revealed that the expression of SIRT4 was downregulated in GC tissues and cells. In addition, the low expression of SIRT4 was negatively correlated with tumor size, pathological grade, and lymph node metastasis, which predicted a poor prognosis. Multiple functional experiments, including Cell Counting Kit-8 assay as well as colony formation assay, demonstrated SIRT4 suppressed cell proliferation. Moreover, we found epithelial-mesenchymal transition was regulated by SIRT4, thereby regulating cell migration and invasion. CONCLUSION: Overall, our findings show that SIRT4 serves as a tumor suppressor in GC and might act as a novel biomarker and a therapeutic target of GC.

Early onset renal cell carcinoma in an adolescent girl with germline FLCN exon 5 deletion.

Birt-Hogg-Dube (BHD) disease is an autosomal dominant cancer syndrome characterized by benign skin tumors, renal cancer and spontaneous pneumothorax and is caused by mutations in the Folliculin (FLCN) gene. Benign skin tumors and pneumothorax occur in the majority of patients affected by BHD syndrome, but only 30-45% of them develop renal cell carcinoma (RCC) with a median age of diagnosis at 48. The earliest onset of RCC in a BHD patient has been reported at age 20. Here we report a case of a 14 year-old patient with germline FLCN mutation leading to an early-onset bulky RCC that could not be classified strictly according to existing histological types. Germline genetic testing revealed a deletion at FLCN exon 5. The father of the patient was identified as the asymptomatic carrier. We report the youngest patient with BHD-related RCC. This early onset presentation supports genetic testing of at-risk patients and initiation of imaging surveillance for RCC in early adolescence. In addition, future studies are necessary to understand the determinants of reduced penetrance in BHD disease.

MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN.

Recent studies suggested that microRNA-200 family microRNAs play critical roles in cancer initiation and metastasis. The underlying mechanism remained elusive. In this study, we show that microRNA-200c is upregulated in nasopharyngeal carcinoma cells. Manipulation of microRNA-200c levels affected cell growth, migration, and invasion in nasopharyngeal carcinoma cell lines. Furthermore, PTEN was identified as a direct target of microRNA-200c. Overexpression of PTEN resulted in similar effects to those of anti-microRNA-200c transfection. In vivo suppression of microRNA-200c level reduced tumor growth in mice. Overall, our data suggest that microRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN.

Comprehensive assessment of peripheral blood TCRß repertoire in infectious mononucleosis and chronic active EBV infection patients.

Epstein-Barr virus (EBV) primary infection is usually asymptomatic, but it sometimes progresses to infectious mononucleosis (IM). Occasionally, some people develop chronic active EBV infection (CAEBV) with underlying immunodeficiency, which belongs to a continuous spectrum of EBV-associated lymphoproliferative disorders (EBV+ LPD) with heterogeneous clinical presentations and high mortality. It has been well established that T cell-mediated immune response plays a critical role in the disease evolution of EBV infection. Recently, high-throughput sequencing of the hypervariable complementarity-determining region 3 (CDR3) segments of the T cell receptor (T cell receptor ß (TCRß)) has emerged as a sensitive approach to assess the T cell repertoire. In this study, we fully characterized the diversity of peripheral blood TCRß repertoire in IM (n = 6) and CAEBV patients (n = 5) and EBV-seropositive controls (n = 5). Compared with the healthy EBV-seropositive controls, both IM and CAEBV patients demonstrate a significant decrease in peripheral blood TCRß repertoire diversity, basically, including narrowed repertoire breadth, highly expanded clones, and skewed CDR3 length distribution. However, there is no significant difference between IM and CAEBV patients. Furthermore, we observed some disease-related preferences in TRBV/TRBJ usage and combinations, as well as lots of T cell clones shared by different groups (unique or overlapped) involved in public T cell responses, which provide more detailed insights into the divergent disease evolution.