All optical metropolitan quantum key distribution network with post-quantum cryptography authentication.

Quantum key distribution (QKD) provides information theoretically secure key exchange requiring authentication of the classic data processing channel via pre-sharing of symmetric private keys to kick-start the process. In previous studies, the lattice-based post-quantum digital signature algorithm Aigis-Sig, combined with public-key infrastructure (PKI), was used to achieve high-efficiency quantum security authentication of QKD, and we have demonstrated its advantages in simplifying the MAN network structure and new user entry. This experiment further integrates the PQC algorithm into the commercial QKD system, the Jinan field metropolitan QKD network comprised of 14 user nodes and 5 optical switching nodes, and verifies the feasibility, effectiveness and stability of the post-quantum cryptography (PQC) algorithm and advantages of replacing trusted relays with optical switching brought by PQC authentication large-scale metropolitan area QKD network. QKD with PQC authentication has potential in quantum-secure communications, specifically in metropolitan QKD networks.

Sending or Not-Sending Twin-Field Quantum Key Distribution with Flawed and Leaky Sources.

Twin-field quantum key distribution (TF-QKD) has attracted considerable attention and developed rapidly due to its ability to surpass the fundamental rate-distance limit of QKD. However, the device imperfections may compromise its practical implementations. The goal of this paper is to make it robust against the state preparation flaws (SPFs) and side channels at the light source. We adopt the sending or not-sending (SNS) TF-QKD protocol to accommodate the SPFs and multiple optical modes in the emitted states. We analyze that the flaws of the phase modulation can be overcome by regarding the deviation of the phase as phase noise and eliminating it with the post-selection of phase. To overcome the side channels, we extend the generalized loss-tolerant (GLT) method to the four-intensity decoy-state SNS protocol. Remarkably, by decomposing of the two-mode single-photon states, the phase error rate can be estimated with only four parameters. The practical security of the SNS protocol with flawed and leaky source can be guaranteed. Our results might constitute a crucial step towards guaranteeing the practical implementation of the SNS protocol.

Altered mucosal bacteria and metabolomics in patients with Peutz-Jeghers syndrome.

BACKGROUND: Peutz-Jeghers syndrome (PJS) is a rare genetic disorder characterized by the development of pigmented spots, gastrointestinal polyps and increased susceptibility to cancers. Currently, most studies have investigated intestinal microbiota through fecal microbiota, and there are few reports about mucosa-associated microbiota. It remains valuable to search for the key intestinal microbiota or abnormal metabolic pathways linked to PJS. AIM: This study aimed to assess the structure and composition of mucosa-associated microbiota in patients with PJS and to explore the potential influence of intestinal microbiota disorders and metabolite changes on PJS. METHODS: The bacterial composition was analyzed in 13 PJS patients and 12 controls using 16S rRNA gene sequencing (Illumina MiSeq) for bacteria. Differential analyses of the intestinal microbiota were performed from the phylum to species level. Liquid chromatography-tandem mass spectrometry (LC‒MS) was used to detect the differentially abundant metabolites of PJS patients and controls to identify different metabolites and metabolic biomarkers of small intestinal mucosa samples. RESULTS: High-throughput sequencing confirmed the special characteristics and biodiversity of the mucosa microflora in patients with PJS. They had lower bacterial biodiversity than controls. The abundance of intestinal mucosal microflora was significantly lower than that of fecal microflora. In addition, lipid metabolism, amino acid metabolism, carbohydrate metabolism, nucleotide metabolism and other pathways were significantly different from those of controls, which were associated with the development of the enteric nervous system, intestinal inflammation and development of tumors. CONCLUSION: This is the first report on the mucosa-associated microbiota and metabolite profile of subjects with PJS, which may be meaningful to provide a structural basis for further research on intestinal microecology in PJS.

[A genetic optimization designing method for microorganism detection genechip probe based on genetic algorithm].

A new automatic selection approach of microorganism specific fragment combination is presented in this paper. Genetic algorithm is used to search optimal solution on the basis of classification ability of SNP combination, which is evaluated by the rough set theory. Other related experimental parameters are also been incorporated. Experimental results show that the method can find the best SNP combination pattern efficiently and accurately, which implies that it is a reliable approach to the genechip probe design.

[Effects of antisense 6 gene on colon cancer cells].

OBJECTIVE: To investigate the effect of antisense integrin beta6 gene on the growth of colon cancer cells. METHODS: Expressing vector of antisense alphavbeta6 was constructed. Human colon cancer cells of the line HT29 were cultured and divided into 3 groups: Group A, remaining wild type; Group B, transfected with antisense integrin beta6 gene; and Group C, transfected with blank vector. RT-PCR was used to detect the integrin beta6 mRNA expression of in the HT29 cells. The integrinbeta6 protein expression on the surface of the cells was detected by immunohistochemistry and flow cytometry. The binding between the cells and fibronectin was examined. (3)H-labeled thymidine (T) was added into the culture fluid of the cells, and then the radiation amount was detected every 6 days so as to determine the capacity to proliferation of the cells in vitro. Thirty female nude mice were divided into 3 groups to be injected subcutaneously with suspension of HT29 cells of Groups A, B, and C as mentioned above. Six weeks later the size of tumors was measured and part of the tumor nodules were resected 5 weeks after the inoculation to undergo pathological examination. RESULTS: Compared with Groups A and C, no corresponding band at 141 bp was found in Group B by RT-PCR. Flow cytometry showed that the expression level of beta6 protein had was (0.30 +/- 0.051, 30%), significantly lower than those of Groups A and C [(0.80 +/- 0.038, 80%) and (0.85 +/- 0.045, 85%), both P < 0.01]. The binding between the HT29 cells and fibronectin of Group B was significantly degraded after the further addition of anti-beta1 and anti-alphav in comparison of Groups A and C (both P < 0.01). The accumulation values of (3)H-labeled T of Group B 2, 4, and 6 days after addition were all significantly lower than those of Groups A and C (all P < 0.01). The tumors in 9 of the 10 mice injected with the HT29 cells of Group B disappeared and the tumor in the only one mice in Group B was only less than 1 mm(3), significantly smaller then those in Groups A and C (15 mm(3) on average, all P < 0.01). CONCLUSION: Antisense beta6 gene significantly inhibits the mRNA and protein expression of the beta6 gene, and then inhibits the growth and proliferation of colon cancer cells, thus proving that integrin beta6 plays an important role in the regulation of colon cancer cells.

MicroRNA-299-3p suppresses proliferation and invasion by targeting VEGFA in human colon carcinoma.

Accumulating evidences have shown that microRNAs (miRNAs) are vital regulators and possess huge capabilities in post-transcriptional control. Although a large number of miRNAs have been identified to be dysregulated in human cancers especially in colon cancer, our understandings of the function of most miRNAs are still largely limited. In this study, we have demonstrated that miR-299-3p plays a critical role in suppressing colon carcinoma progression by targeting Vascular Endothelial Growth Factor A (VEGFA). We observed that miR-299-3p was down-regulated in colon carcinoma tissues and colon cancer cell lines. The level of miR-299-3p was significantly negatively correlated with that of VEGFA mRNA level in colon carcinoma. More importantly, the low level of miR-299-3p predicted poor prognosis of colon cancer patients. Functionally, overexpression of miR-299-3p inhibited the proliferation and invasion of colon carcinoma cells and suppressed the growth of colon cancer xenografts in nude mice. Luciferase reporter assays showed that miR-299-3p could target VEGFA 3' UTR. In addition, up-regulation of miR-299-3p decreased VEGFA expression both in vitro and in vivo, showing that miR-299-3p plays a suppressive effect on VEGFA via post-transcriptional control. However, ectopical expression of VEGFA could abrogate this effect and also abolish miR-299-3p-induced inhibition of cell proliferation and invasion. Taken together, our study provides evidences showing that miR-299-3p functions as a suppressor in colon cancer by targeting VEGFA, suggesting that miR-299-3p might serve as a novel target for colon cancer therapy.

Clinical significance of integrin ß6 as a tumor recurrence factor in follicular thyroid carcinoma.

BACKGROUND: Overexpression of integrin ß6 plays an important role in a variety of malignant tumor invasion and metastasis. METHODS: The expression levels of integrin ß6, matrix metalloproteinase (MMP)-2 and MMP-9 were analyzed by immunohistochemistry with human follicular thyroid carcinomas. Then we investigated their correlation with clinical outcomes parameters, relationship, and the survival time. RESULTS: The integrin ß6 staining was expressed in cellular membrane and cytoplasm of follicular thyroid carcinoma cells. The MMP-2 and MMP-9 expressions were mainly found in cellular cytoplasm. In correlation with the clinical outcome parameters of 60 patients, there were significant statistical differences of integrin ß6, MMP-2, and MMP-9 expression levels in different size of tumor. Integrin ß6 and MMP-9 expressions have significant statistical differences in T classifications. MMP-2 and MMP-9 expressions have significant statistical differences in different M classification. Other clinical outcome parameters had no significant statistical differences. CONCLUSION: Integrin ß6 expression correlated significantly with MMP-9 expression, and may be a valuable recurrence indicator for follicular thyroid carcinomas.

Vascular endothelial growth factor (VEGF) enhances gastric carcinoma invasiveness via integrin alpha(v)beta6.

Integrins play an important role in tumor metastasis induced by vascular endothelial growth factor (VEGF). However, in the case of gastric cancer, the precise role of VEGF in regulating integrin alphavbeta6 is unclear. In this study, we found that most of the alphavbeta6 integrin-positive gastric cancer tissues were also VEGF-positive. Furthermore, when gastric carcinoma cells were exposed to VEGF, expression of alphavbeta6 integrin was up-regulated and the extracellular signal-related kinase (ERK) pathway was activated. When integrin alphavbeta6 was blocked either with beta6 siRNA or anti-alphavbeta6 antibody, the migration of tumor cells normally induced by VEGF, as well as the activation of ERK, were markedly inhibited. Blocking the ERK signaling pathway significantly inhibited cell mobility. Taken together, the data suggest that VEGF is critical to the invasive process in human gastric cancer and that this occurs via up-regulation of integrin alphavbeta6 expression and activation of ERK.