Covert Communication through Robust Fragment Hiding in a Large Number of Images.

For covert communication in lossy channels, it is necessary to consider that the carrier of the hidden watermark will undergo multiple image-processing attacks. In order to ensure that secret information can be extracted without distortion from the watermarked images that have undergone attacks, in this paper, we design a novel fragmented secure communication system. The sender will fragment the secret data to be transmitted and redundantly hide it in a large number of multimodal carriers of messenger accounts on multiple social platforms. The receiver receives enough covert carriers, extracts each fragment, and concatenates the transmitted secret data. This article uses the image carrier as an example to fragment the text file intended for transmission and embeds it into a large number of images, with each fragment being redundant and embedded into multiple images. In this way, at the receiving end, only enough stego images need to be received to extract the information in each image, and then concatenate the final secret file. In order to resist various possible attacks during image transmission, we propose a strong robust image watermarking method. This method adopts a watermark layer based on DFT, which has high embedding and detection efficiency and good invisibility. Secondly, a watermark layer based on DCT is adopted, which can resist translation attacks, JPEG attacks, and other common attacks. Experiments have shown that our watermarking method is very fast; both the embedding time and the extraction time are less than 0.15 s for images not larger than 2000×2000. Our watermarking method has very good invisibility with 41dB PSNR on average. And our watermarking method is more robust than existing schemes and robust to nearly all kinds of attacks. Based on this strong robust image watermarking method, the scheme of fragmenting and hiding redundant transmission content into a large number of images is effective and practical. Our scheme can 100% restore the secret file completely under different RST or hybrid attacks, such as rotation by 1 degree and 5 degrees, scaling by 1.25 and 0.8, and cropping by 10% and 25%. Our scheme can successfully restore the secret file completely even if 30% of received images are lost. When 80% of received images are lost, our scheme can still restore 61.1% of the secret file. If all stego images can be obtained, the original text file can be completely restored.

Diagnostic Value of Emission Computed Tomography Combined with Computed Tomography for Metastatic Malignant Tumor of Spine.

Objective: To explore the diagnostic value of emission computed tomography (ECT) combined with computed tomography (CT) for metastatic malignant tumor of spine. Methods: By means of retrospective study, a total of 102 patients with extraskeletal primary malignant tumor treated in our hospital from February 2019 to February 2021 were selected as the subjects. All patients had single lesion of the spine, of which 72 were malignant and 30 were benign according to the results of pathological examination. ECT and CT examinations were performed to all patients, and by taking the pathological findings as the gold standard, the sensitivity, specificity, positive predictive value and negative predictive value of ECT, CT, and their combination were calculated, and their efficacy in diagnosing metastatic malignant tumor of spine was analyzed. Results: A total of 68 (94.4%) metastatic malignant spinal tumors were detected by ECT combined with CT, with a detection rate of 100% in breast cancer and lung cancer, 94.1% in liver cancer, and 78.6% in prostate cancer, respectively; the combined diagnosis had a diagnostic sensitivity of 94.4%, specificity of 73.3%, positive predictive value of 89.5%, negative predictive value of 84.6%, and diagnostic accuracy rate of 88.2%, and AUC (95% CI) = 0.839 (0.739-0.939). Conclusion: Combining ECT with CT has a good diagnostic efficacy for metastatic malignant spinal tumors.

[Cytogenetic and molecular characterization of a patient with partial 6q trisomy and 1q monosomy].

OBJECTIVE: To analyze a girl with moderate mental retardation and speech and language disorders with cytogenetics technique and next-generation sequencing (NGS). METHODS: G-banding chromosome analysis was used to ascertain the karyotype of the child and her parents, and NGS was used for determining the size and origin of the abnormal chromosome fragment. Mate-pair and PCR were used to determine its parental origin. RESULTS: The karyotype of the child was determined to be 46,XX,add(1)(q44)dn, while her parents were both normal. NGS revealed that the child has harbored a partial trisomy of 6q24.3-q27, and the breakpoint was mapped to at 6q24.3q27. In addition, a 2.5 Mb microdeletion at 1q44 was found in the patient. CONCLUSION: No recognizable phenotype was associated with 1q44 deletion. The abnormal phenotypes presented by the child may be attributed to the 6q24.3-q27 triplication. Compared with conventional cytogenetic analysis, NGS has a much higher resolution and great accuracy.

[Clinical and genetic analysis of a Chinese family affected with X-linked Charcot-Marie-Tooth disease].

OBJECTIVE: To study the clinical manifestations and identify causative mutations for a Chinese family affected with X-linked Charcot-Marie-Tooth disease. METHODS: Clinical, electrophysiological and pathological features of the family were carefully analyzed by neurologists. Blood samples were obtained from the proband and other family members. Genomic DNA was extracted. Mutation analysis of GJB1 gene was analyzed with PCR and direct sequencing. RESULTS: The family has fit with X-linked inheritance, and the affected individuals have typical clinical manifestations. A c.614A>G (p.Asn205Ser) mutation was detected in the GJB1 gene in all affected individuals in the family. CONCLUSION: A c.614A>G (p.Asn205Ser) mutation of GJB1 gene is co-segregated with the disease phenotype in this family and probably underlies the disease.

[Analysis of gene mutation in a family featuring autosomal dominant May-Hegglin anomaly].

OBJECTIVE: To analyze clinical features and mutation in MYH9 gene for a family featuring autosomal dominant May-Hegglin anomaly. METHODS: Clinical and pathological features of all family members were analyzed. Blood samples were collected from the proband and other family members, and genomic DNA was extracted. Potential mutations of MYH9 gene exons 10, 25, 26, 30, 38 and 40 were screened with PCR and direct sequencing. After a mutation was identified in the proband, other affected members as well as healthy members from this family were analyzed with a pair of primers to amplify the mutant site. The PCR products were digested with Taq I enzyme and analyzed with agarose gel electrophoresis. RESULTS: All affected members had bleeding tendency and typical features including giant platelets, thrombocytopenia and characteristic Dohle body-like leukocyte inclusions. A heterozygous missense mutation c.5521G>A (p.Glu1841Lys) in exon 38 of the MYH9 gene was identified in all affected members from this family. CONCLUSION: The variant, c.5521G>A (p.Glu1841Lys) of MYH9, has co-segregated with the phenotype in the family. The mutant site is a hot spot in Chinese population.

Novel deletion of SPAST in a Chinese family with hereditary spastic paraplegia.

INTRODUCTION: Hereditary spastic paraplegia (HSP) belongs to a large, heterogeneous group of progressive neurodegenerative diseases characterised by progressive lower extremity weakness and spasticity, which is caused by developmental failure or degeneration of motor axons in the corticospinal tract. Classical genetic studies have identified at least 46 genetic loci responsible for HSP. METHODS: A genetic study was conducted on a four-generation Chinese family with autosomal dominant HSP. The SPAST gene was investigated using linkage analysis and direct sequencing. Findings were compared with unaffected family members and 50 normal, unaffected individuals who were matched for geographical ancestry. RESULTS: We identified a novel 14-bp heterozygous deletion that induced a frameshift mutation in exon 15 of SPAST (SPG4). This mutation is predicted to have functional impact and found to cosegregate with the disease phenotype. CONCLUSION: Our results have expanded the mutation spectrum of the SPAST gene. These findings could help clinicians provide prenatal diagnosis of affected foetuses in families with a known history of such neurodegenerative diseases.