A Seven-Layer Convolutional Neural Network for Chest CT-Based COVID-19 Diagnosis Using Stochastic Pooling.

(Aim) COVID-19 pandemic causes numerous death tolls till now. Chest CT is an effective imaging sensor system to make accurate diagnosis. (Method) This article proposed a novel seven layer convolutional neural network based smart diagnosis model for COVID-19 diagnosis (7L-CNN-CD). We proposed a 14-way data augmentation to enhance the training set, and introduced stochastic pooling to replace traditional pooling methods. (Results) The 10 runs of 10-fold cross validation experiment show that our 7L-CNN-CD approach achieves a sensitivity of 94.44±0.73, a specificity of 93.63±1.60, and an accuracy of 94.03±0.80. (Conclusion) Our proposed 7L-CNN-CD is effective in diagnosing COVID-19 in chest CT images. It gives better performance than several state-of-the-art algorithms. The data augmentation and stochastic pooling methods are proven to be effective.

Risk assessment of first upper gastrointestinal bleeding using computerized tomoscanning in esophageal varices patients with cirrhosis and portal hypertension.

To evaluate the risk of first upper gastrointestinal bleeding by computerized tomoscanning (CT) for esophageal varices patients with cirrhotic portal hypertension.One hundred thirty two esophageal varices patients with cirrhotic portal hypertension who are also complicated with gastrointestinal bleeding were recruited as bleeding group, while another 132 patients without bleeding as non-bleeding group. The diameter of esophageal varices, number of vascular sections, and total area of blood vessels were measured by CT scanning. The sensitivity and specificity of these indicators were calculated, and Youden index was adjusted with the critical point.The diameter of esophageal varices was 7.83 ±â€Š2.76 mm in bleeding group, and 6.57 ±â€Š3.42 mm in non-bleeding group. The Youden index was 0.32 with the critical point 5.55 mm. The area under the receiver operating characteristics (AUROC) was 0.72. The number of venous vessels was 4.5 ±â€Š2 in bleeding group, whereas being 4 ±â€Š2 in non-bleeding group. The Youden index was 0.35 with a critical point 4, and the area under the curve (AUC) was 0.68. The blood vessel area was 1.73 ±â€Š1.15 cm in bleeding group, and 1.12 ±â€Š0.89 cm in non-bleeding group. The Youden index was 0.48 with the critical point being 1.03 cm, and corresponding AUC was 0.82.Among all 3 indicators of the total area, diameter, and number of sections of the esophageal varices, the total area of esophageal varices showed more accuracy as a potential and novel indicator for bleeding prediction.

LINC01433 promotes hepatocellular carcinoma progression via modulating the miR-1301/STAT3 axis.

Long noncoding RNAs (lncRNAs) have been demonstrated to play significant roles in hepatocellular carcinoma (HCC) tumor progression. LINC01433 has been implicated in the progression of lung cancer. However, its biological role in HCC remains poorly understood. In our current study, we focused on the detailed mechanism of LINC01433 in HCC development. First, it was exhibited that LINC01433 was remarkably elevated in HCC cells, which indicated that LINC01433 was involved in HCC. Then, knockdown of LINC01433 was able to restrain HCC cell proliferation and cell colony formation and greatly induced cell apoptosis. On the contrary, overexpression of LINC01433 promoted HCC cell proliferation, increased cell colony formation, and enhanced cell invasion capacity. Subsequently, we found that miR-1301 was remarkably decreased in HCC cells, and it can serve as a target of LINC01433 according to bioinformatics analysis. In addition, the binding correlation between them was validated by performing RNA pull-down experiments and RIP assay. Moreover, STAT3 was predicted and validated as a target of miR-1301, and it was shown that miR-1301 mimics significantly suppressed STAT3 in HCC cells. Finally, in vivo models were established, and the results demonstrated that silencing of LINC01433 could repress HCC development through modulating miR-1301 and STAT3. Taken together, these results indicated in our study that LINC01433 participated in HCC progression through modulating the miR-1301/STAT3 axis and it might act as a novel biomarker in HCC diagnosis and treatment.

Study on the relationship between insulin growth factor 1 and liver fibrosis in patients with chronic hepatitis C with type 2 diabetes mellitus.

OBJECTIVE: To investigate the correlation between serum protein level of insulin growth factor 1 (IGF-1) and the degree of liver fibrosis in patients with chronic hepatitis C (CHC) combined with type 2 diabetes mellitus (T2DM). METHODS: The cases are divided into four groups. Then serum levels of IFG-1, alanine aminotransferase (ALT), aspartate aminotransferase (AST), hepatitis C virus (HCV) RNA, and HCV genotypes were detected simultaneously in patients with hepatitis C, liver stiffness measurement (LSM) was measured by transient elastography, and aspartate aminotransferase platelet ratio (APRI) score was determined. RESULTS: There was no significant difference between CHC with T2DM group and CHC group in diabetes family history (P > 0.05), but the difference between the two groups were significantly lower than that of T2DM group ( P < 0.05). The levels of fasting insulin and homeostatic model assessment of insulin resistance (HOMA-IR) in CHC group with T2DM group were significantly higher than those in the other two groups ( P < 0.05), while the IGF-1 RNA and the serum protein level in the two groups were significantly lower than those in the CHC group, and were lower than those in the control group ( P < 0.05). The level of serum IGF-1 was negatively correlated with HOMA-IR, LSM, and APRI score in CHC with T2DM group ( r = -0.71, -0.75, and -0.69; P < 0.01). CONCLUSION: The degree of hepatic fibrosis in patients with CHC combined with T2DM was higher than that in non-T2DM patients with CHC, which was mainly related to insulin resistance (IR) induced by 1b genotype HCV infection. IR can lead to impaired synthesis of IGF-1, and the degree of damage has a corresponding relationship with hepatic fibrosis.

The effects of the insulin resistance index on the virologic response to entecavir in patients with HBeAg-positive chronic hepatitis B and nonalcoholic fatty liver disease.

PURPOSE: To further observe and verify the effect of nonalcoholic fatty liver disease (NAFLD) on the response to antiviral therapy in patients with chronic hepatitis B (CHB) and investigate the relationship between the virologic response and insulin resistance. PATIENTS AND METHODS: A retrospective study was adopted and 61 NAFLD patients with HBeAg-positive CHB were included as the observation group (group A), and 64 patients with simple CHB were included as the control group (group B). RESULTS: After 12 weeks of treatment with entecavir, the total virologic response rate in group A was statistically significantly lower than that in group B (P<0.05). During weeks 24-96, the difference was not statistically significant (P>0.05). In weeks 48 and 96, there was no significant difference in the HBeAg seroconversion rates between the two groups (P>0.05). In weeks 12 and 24, there was also no significant difference in the alanine transaminase (ALT) normalization rate between the two groups (P>0.05). Then, in weeks 48 and 96, the ALT normalization rate of group A was obviously lower than that of group B (P<0.05). Group A patients were divided into group A1 (≤M) and group A2 (>M) according to the median value (M=2.79) of the baseline homeostatic model assessment method insulin resistance levels. In weeks 48 and 96, the ALT normalization rate of group A1 was significantly higher than that of group A2 (P<0.05). The correlation coefficient (r) of the baseline homeostatic model assessment method insulin resistance level and the severity of fatty liver in group A was 0.426 (P=0.001). CONCLUSION: NAFLD cannot affect the long-term total virologic response rate and HBeAg seroconversion rate in CHB patients treated with entecavir but can reduce the long-term biochemical response rate, which has a positive correlation with the severity of fatty liver and the insulin resistance index.

Systemic transcriptome analysis of hepatocellular carcinoma.

Liver cancer is one of the most common malignant tumors, and most of which is hepatocellular carcinoma (HCC). We aim to study the characteristic changes of numerous genes and their roles in HCC through systematical analysis of the characteristics of expression spectrum of HCC. Firstly, we made systematic clustering of the HCC samples according to the RNAseq data from TCGA (The Cancer Genome Atlas) and newly classified HCC. Then the characteristic genes in different molecular subtypes were found out and further analyzed combing with methylation and SNP 6.0 chip. Finally, these genes were subjected to do functional annotation and abnormal signaling pathways of HCC in various molecular subtypes and were screened out. There were 3843 differential genes screened; among which, 689 genes were enriched into 13 KEGG-related pathways, and the expression of 27 and 924 genes showed positive and negative correlation to methylation level, respectively, while the expression of 43 genes showed positive correlation to variation level of copy number. The methylation degree of ZSCAN18 may be considered as a marker for prognosis evaluation, and ABHD6 could be a potential anti-oncogene.

CRISPR-Cas9 for in vivo Gene Therapy: Promise and Hurdles.

Owing to its easy-to-use and multiplexing nature, the genome editing tool CRISPR-Cas9 (clustered regularly interspaced short palindromic repeats (CRISPR) associated nuclease 9) is revolutionizing many areas of medical research and one of the most amazing areas is its gene therapy potentials. Previous explorations into the therapeutic potentials of CRISPR-Cas9 were mainly conducted in vitro or in animal germlines, the translatability of which, however, is either limited (to tissues with adult stem cells amenable to culture and manipulation) or currently impermissible (due to ethic concerns). Recently, important progresses have been made on this regard. Several studies have demonstrated the ability of CRISPR-Cas9 for in vivo gene therapy in adult rodent models of human genetic diseases delivered by methods that are potentially translatable to human use. Although these recent advances represent a significant step forward to the eventual application of CRISPR-Cas9 to the clinic, there are still many hurdles to overcome, such as the off-target effects of CRISPR-Cas9, efficacy of homology-directed repair, fitness of edited cells, immunogenicity of therapeutic CRISPR-Cas9 components, as well as efficiency, specificity, and translatability of in vivo delivery methods. In this article, we introduce the mechanisms and merits of CRISPR-Cas9 in genome editing, briefly retrospect the applications of CRISPR-Cas9 in gene therapy explorations and highlight recent advances, later we discuss in detail the challenges lying ahead in the way of its translatability, propose possible solutions, and future research directions.