Research on Communications Encryption Technology Based on Integration of Digital Watermarking

This essay describes a new radio encryption technique among communication equipments, that is embed confidential information in normal carrier by using digital watermarking to achieve the purpose of protecting confidential information and confusing illegal interceptors. Meanwhile it also gives embed watermarking based on integration and Detection Algorithm.

Ligase chain reaction assay for human mutations: the Sickle Cell by LCR assay

We can detect the β-globin gene sickle cell mutation by using an assay based on the ligase chain reaction. The simultaneous amplification of the human growth hormone gene in the same reaction serves as a control for the amount of template DNA or amplification efficiency. Ligation products, which are biotinylated at one end and tagged with an arbitrary “tail” sequence at the other, are captured by hybridization to “tail”-complementary oligonucleotides immobilized on polystyrene microwells. The captured ligation products are detected colorimetrically by use of streptavidin–alkaline phosphatase conjugate. In a study of 24 subjects, the assay unequivocally discriminated among normal, carrier, and sickle cell genotypes.

Combined Molecular and Cytogenetic Analysis for the Rapid Diagnosis of Fragile X Syndrome

The fragile X mutation is the result of an abnormal expansion of a CGG repeat sequence in the FMR-1 gene.Molecular techniques enable the detection of the mutation and also of the exact length of this DNA sequence, allowing the classification of the tested subjects as normal, carrier or affected.We propose a protocol of analysis that combines a method of non-radioactive PCR, Southern blotting and cytogenetic testing.This protocol can be used for screening programme of selected groups of mentally retarded individuals and for prevention studies in families at risk.

Finnish-type aspartylglucosaminuria detected by oligonucleotide ligation assay

Aspartylglycosaminuria (AGU) is a recessively inherited lysosomal storage disease that occurs with much higher frequency in Finland than elsewhere. AGU is caused by a deficiency in glycosylasparaginase (GA), which results in the accumulation of glycoasparagines in lysosomes. In the Finnish population, a single nucleotide change in the gene encoding GA is responsible for the disease. We have used the oligonucleotide ligation assay (OLA) to detect the mutation in polymerase chain reaction (PCR)-amplified DNA samples from normal, carrier, and affected individuals. Screening for AGU among 415 random Finnish DNA samples with PCR/OLA revealed five carriers of the mutant allele and demonstrated the potential of the method for use in carrier screening. PCR/OLA provides a rapid, reliable, nonisotopic method to detect the mutation responsible for AGU that can readily be applied to large population screening.

Correlation of Void Formation with the Reduction of Carrier Activation and Anomalous Dopant Diffusion in Si-Implanted GaAs

We report the study of high-dose Si-implanted GaAs containing doses ranging from 1×1014 to 1×1015 cm-2 and with subsequent anneals at 850°C for 1 hour. At doses ≥ 3×1014 cm-2, a severe reduction of carrier concentration and anomalous Si diffusion are observed in the near-surface region. In the same region, small, near-spherical voids are found by transmission electron microscopy. In contrast, for samples implanted with doses ≤ 1×1014 cm-2, voids are not found, and both normal carrier activation and Si diffusion profiles are observed. The concurrent onset of these three phenomena in the same region in high-dose samples leads us to conclude that the severe reduction of carrier concentration and anomalous Si diffusion are attributable to the formation of voids.

HEMOPHILIA B IN CANINES IS DUE TO A POST-TRANSCRIPTIONAL DEFECT

Factor IX is a vitamin K dependent plasma proteinsynthesized in the liver; a deficiency of Factor IX results in hemophilia B. An animal model for hemophilia B exists in dogs; affected animals have severe disease, with activity levels of less than 1%. The purpose of the current study is to determine the molecular basis of canine hemophilia. In previous work, we had shown that the Factor IX gene in hemophilic dogs appeared to be at least partly intact; thus, genomic DNA from normal, carrier and hemophilic dogs, when probed with sequences from the 4th, 7th, and 8th exons of the human gene, gave identical patterns on Southern blot. We have now completed the mapping of the hemophilic gene, using probes from the first, second, third and sixth exons, and have shown it to beentirely intact, that is, free of any large deletions or rearrangements, as determined by Southern blotting. In addition, using the guanidinium thiocyanate technique, we h^ve prepared total RNA from normal and -hemophilic dog livers add analyzed these samples by Northern blotting. The results show that the hemophilic dog synthesizes a Factor IX transcript of approximately 3 kilobases, that is, of the same size asthe normal dog. In addition, baaed on signal intensity, the transcript appears to be produced in roughlyequivalent amounts in the normal and hemophilic dogs.We conclude that the defect responsible for canine hemophilia B interferes with the production of the normal Factor IX protein at a post-transcriptional level. Moreover, since the hemophilic dogs produce Factor IX mRNA it should be possible to elucidate the gene defect in the hemophilic animals by preparing normal and hemophilic canine liver cDNA libraries and isolating and characterizing the respective Factor IX cDNAs.