3-(4-Amino-5-thioxo-4,5-dihydro-1H-1,2,4-triazol-3-yl)pyridinium chloride

In the title compound, C7H8N5S+·Cl−, the dihedral angle formed by the pyridine ring with the triazole ring is 10.0 (1)°. There are weak inter­molecular hydrogen-bond inter­actions in the crystal structure, involving the NH and NH2 groups as donors, and the chloride anion, the S atom in the thio­ketone group and the unsubstituted ring N atom as acceptors

Storage of 1650 modes of single photons at telecom wavelength

To advance the full potential of quantum networks one should be able to distribute quantum resources over long distances at appreciable rates. As a consequence, all components in the networks need to have large multimode capacity to manipulate photonic quantum states. Towards this end, a multimode photonic quantum memory, especially one operating at telecom wavelength, remains a key challenge. Here we demonstrate a spectro-temporally multiplexed quantum memory at 1532 nm. Multimode quantum storage of telecom-band heralded single photons is realized by employing the atomic frequency comb protocol in a 10-m-long cryogenically cooled erbium doped silica fibre. The multiplexing encompasses five spectral channels - each 10 GHz wide - and in each of these up to 330 temporal modes, resulting in the simultaneous storage of 1650 modes of single photons. Our demonstrations open doors for high-rate quantum networks, which are essential for future quantum internet

CBX4 Expression and AFB1-Related Liver Cancer Prognosis

Background: Previous studies have shown that chromobox 4 (CBX4) expression may involve in the progression of liver cancer, however, it is unclear whether it affects the prognosis of hepatocellular carcinoma (HCC) related to aflatoxin B1 (AFB1)

The Serum MicroRNA Expression Modified the Genic Toxicity Caused by Aflatoxin B1

The serum microRNAs have been reported as potential biomarkers for hepatocellular carcinoma (HCC); however, their role in genic toxicity related to aflatoxin B1 (AFB1), such as TP53 mutation and DNA damage, has not yet been evaluated. Here, we conducted a hospital-based case-control study, including 558 patients with pathologically diagnosed HCC and positive AFB1 and healthy controls (n = 630) without any evidence of liver diseases. Genic toxicity related to AFB1 was evaluated using the hot-spot mutation at the codon 269 of TP53 gene (TP53M) and AFB1-DNA adducts. Through serum microRNA PCR microarray screening analysis, we observed 10 differentially expressed microRNAs (including miR-7-2-3p, miR-4651, miR-127-3p, miR-192-5p, miR-382-5p, miR-10b-5p, miR-532-3p, miR-16-5p, miR-106b-5p, and miR-4688) among HCC cases with positive AFB1 and controls with positive AFB1. The miR-4651 and miR-382-5p were further identified to be significantly higher in AFB1-positive HCC cases compared to controls. This kind of increasing serum levels was significantly and positively associated with frequency of TP53M and the levels of AFB1-DNA adduct. Furthermore, these microRNAs also modified the prognosis of HCC related to AFB1. These results suggest that the serum levels of microRNAs might be able to modify AFB1-induced genic toxicity, and microRNA-4651 and miR-382-5p, are such potential candidates

Molecular Mechanisms of Hepatocellular Carcinoma Related to Aflatoxins: An Update

Hepatocellular carcinoma (hepatocarcinoma) is a major type of primary liver cancer and one of the most frequent human malignant neoplasms. Aflatoxins are I-type chemical carcinogen for hepatocarcinoma. Increasing evidence has shown that hepatocarcinoma induced by aflatoxins is the result of interaction between aflatoxins and hereditary factor. Aflatoxins can induce DNA damage including DNA strand break, adducts formation, oxidative DNA damage, and gene mutation and determine which susceptible individuals feature cancer. Inheritance such as alterations may result in the activation of proto-oncogenes and the inactivation of tumor suppressor genes and determine individual susceptibility to cancer. Interaction between aflatoxins and genetic susceptible factors commonly involve in almost all pathologic sequence of hepatocarcinoma: chronic liver injury, cirrhosis, atypical hyperplastic nodules, and hepatocarcinoma of early stages. In this review, we discuss the biogenesis, toxification, and epidemiology of aflatoxins and signal pathways of aflatoxin-induced hepatocarcinoma. We also discuss the roles of some important genes related to cell apoptosis, DNA repair, drug metabolism, and tumor metastasis in hepatocarcinogenesis related to aflatoxins

The Diagnostic and Prognostic Potential of MicroRNAs for Hepatocellular Carcinoma

Hepatocellular carcinoma (also termed hepatocarcinoma) is the third cancer-related cause of death worldwide. To our knowledge, markers such as α-fetoprotein display poor performance in the early diagnosis and prognosis prediction of hepatocarcinoma. MicroRNAs are an evolutionarily conserved class of small noncoding single-stranded RNA typically consisting of 18–24 nucleotides. They have been reported to act as tumor suppressors or oncogenes via reversely regulating gene expression. Recent evidence has revealed that microRNAs, especially in body fluids such as the blood and urine, display important diagnostic and prognostic potential for hepatocarcinoma. Here, we reviewed currently available data on microRNAs and hepatocarcinoma, with emphasis on the biogenesis and function of microRNAs and their potential diagnostic and prognostic value for hepatocarcinoma. We also discussed the clinical utility perspectives of microRNAs in hepatocarcinoma and possible challenges