Propensity score matching study of 325 patients with spontaneous rupture of hepatocellular carcinoma.

Background: This study aims to find out the possible optimal therapy and assess the prognosis properly for patient with spontaneous rupture of hepatocellular carcinoma (HCC). Methods: Propensity score matching (PSM) analysis was used to study the data from 325 patients with ruptured HCC (RHCC) and 2,291 patients with non-RHCC. Results: The incidence and hospital mortality of RHCC were 5.1% and 0.8% respectively, with a median overall survival (OS) time of 17 months. There was no difference between ruptured and non-RHCC patients undergoing conservation treatment in terms of OS. Trans-arterial embolization (TAE) was carried out in 69 (21.2%) cases with RHCC, with a median OS of 7 months, which was no difference from that of non-RHCC (pre- and post-PSM). One hundred and sixty-nine (52.0%) RHCC cases underwent one-stage hepatectomy, with a median OS and disease-free survival (DFS) of 30 and 6 months respectively, which were shorter than that of non-RHCC (post-PSM). TAE plus two-stage hepatectomy was performed in 30 RHCC cases, with a median OS and DFS of 28 and 10 months respectively; these outcomes were better than that from RHCC patients undergoing TAE alone or one-stage hepatectomy (post-PSM), which were no difference from that of non-RHCC patients undergoing hepatectomy. The risk of death for RHCC patient undergoing one-stage hepatectomy is 1.545 times higher than that of one undergoing TAE + two-stage hepatectomy. Conclusions: TAE plus two-stage hepatectomy might be the optimal treatment for RHCC patient. Under the premise of the same pathological properties, there is no difference in prognosis between ruptured and non-RHCC patients if the therapy is appropriate.

Hepatic inflammatory myofibroblastic tumor: One case report.

Introduction: Hepatic inflammatory myofibroblastic tumor (HIMT) is a junctional neoplastic lesion of mesenchymal tissue origin that can sometimes become locally invasive and even metastasize or recur. Therefore, the diagnosis and treatment of HIMT is particularly important. However, hepatic inflammatory myofibroblastic tumor lacks a specific clinical presentation and typical imaging manifestations, thus posing a difficulty for us to diagnose and treat this disease. Case Presentation: We report here a very rare surgical case of hepatic inflammatory myofibroblastic tumor (HIMT) in a 41-year-old female who was admitted to the hospital for more than half a month for a liver-occupying lesion with fever found on physical examination.After discussion with the hepatobiliary and pancreatic surgery team, we decided to perform surgical treatment. The final postoperative pathology confirmed hepatitis myofibroblastoma. Conclusion: Our review of the domestic and international literature revealed no significant progress in the diagnosis and treatment of this disease, so we report here a case of surgical treatment. One of our aims in this case report is to highlight the efficacy of surgical treatment in HIMT. HIMT is extremely rare and difficult to diagnose. Due to their intermediate biological behavior, surgical resection should be performed whenever feasible and patients should be followed-up in order to detect recurrence and metastasis as early as possible.

Heart Disease Prediction Based on the Embedded Feature Selection Method and Deep Neural Network.

In recent decades, heart disease threatens people's health seriously because of its prevalence and high risk of death. Therefore, predicting heart disease through some simple physical indicators obtained from the regular physical examination at an early stage has become a valuable subject. Clinically, it is essential to be sensitive to these indicators related to heart disease to make predictions and provide a reliable basis for further diagnosis. However, the large amount of data makes manual analysis and prediction taxing and arduous. Our research aims to predict heart disease both accurately and quickly through various indicators of the body. In this paper, a novel heart disease prediction model is given. We propose a heart disease prediction algorithm that combines the embedded feature selection method and deep neural networks. This embedded feature selection method is based on the LinearSVC algorithm, using the L1 norm as a penalty item to choose a subset of features significantly associated with heart disease. These features are fed into the deep neural network we built. The weight of the network is initialized with the He initializer to prevent gradient varnishing or explosion so that the predictor can have a better performance. Our model is tested on the heart disease dataset obtained from Kaggle. Some indicators including accuracy, recall, precision, and F1-score are calculated to evaluate the predictor, and the results show that our model achieves 98.56%, 99.35%, 97.84%, and 0.983, respectively, and the average AUC score of the model reaches 0.983, confirming that the method we proposed is efficient and reliable for predicting heart disease.

Downregulated expression of IL­28RA is involved in the pathogenesis of pancreatic ductal adenocarcinoma.

Pancreatic cancer ranks seventh in terms of cancer­related mortality in men and women worldwide, where the most common subtype is pancreatic ductal adenocarcinoma (PDAC). To date, the pathogenesis of PDAC remains incompletely understood and the prognosis of PDAC is poor. In the present study, the expression of interleukin­28 receptor α subunit (IL­28RA) in PDAC tissues was detected using immunofluorescence staining and western blotting. IL­28RA recombinant plasmids and control pCMV6­entrymammalian expression plasmid, short hairpin (sh)IL­28RA plasmids and control pRS scrambled shRNA vector purchased were used to produce stably transfected PANC­1 cells overexpressing IL­28RA or with IL­28RA expression knocked down. MTS assays were used to measure cell viability and wound healing assay was used to assess the cell migratory ability in vitro. Flow cytometry analysis was performed to determine the proportion of cells in each phase of the cell cycle whereas total protein and phosphorylated protein levels were assessed using western blotting. Xenograft models of subcutaneous tumors were established by injecting PANC­1 cells hypodermically into nude mice to investigate the effect of IL­28RA on tumorigenesis and tumor growth. The results showed that the expression of IL­28RA in PDAC tissues was lower compared with that in normal tissues. IL­28RA overexpression in vitro resulted in the activation of the IL­28RA pathway, which reduced cell viability and decreased the proportion of cells in the G2/M phase by reducing cyclin B1 expression. In addition, IL­28RA overexpression inhibited migration of PDAC cells. By contrast, an increased proportion of cells in G2/M phase, upregulated cyclin B1 expression and enhanced cell viability and migratory ability along with inhibition of the IL­28RA pathway were observed in PANC­1 cells following IL­28RA knockdown. The inhibitory effect of IL­28RA was observed by tumor size in a nude mouse model induced by PANC­1 cells with stable IL­28RA overexpression or knockdown. The tumor size induced by PANC­1 cells with stable IL­28RA overexpression were smaller, whilst larger tumors induced by PANC­1 cells were observed following stable IL­28RA knockdown, when compared to control. Further studies showed that the effect of IL­28RA on PDAC cells was exerted by regulating the phosphorylation levels of STAT1 and AKT. In conclusion, lower IL­28RA expression may contribute to the pathogenesis of PDAC, where results from the present may provide further insights into the progression of PDAC, in addition to highlighting potentially novel therapeutic targets for this disease.

Peptidase inhibitor 15 as a novel blood diagnostic marker for cholangiocarcinoma.

BACKGROUND: We aimed to screen a specific secretory protein that could serve as blood diagnostic marker for cholangiocarcinoma (CCA). METHODS: Starting with the analysis of gene expression profiles in tumor tissues and matched normal tissues from cases with CCA and hepatocellular carcinoma (HCC), we identified peptidase inhibitor 15 (PI15) was a potential diagnostic marker for CCA. We demonstrated PI15 expression levels in CCA, HCC, and normal liver tissues. Furthermore, quantitative enzyme-linked immunosorbent assay (ELISA) assessed plasma PI15 levels in CCA (n = 61), HCC (n = 72), benign liver disease (n = 28), chronic hepatitis B (CHB) patients (n = 45), and healthy individuals (n = 45). The diagnostic value of PI15 was estimated by the area under the receiver operating characteristic (ROC) curve (AUC). FINDINGS: The positive rate of PI15 expression was 70% in CCA and only 9.1% in HCC; PI15 was not detected in normal liver tissue. High levels of plasma PI15 were evident in CCA patients, whereas only low levels were observed in cases involving HCC, benign liver disease, CHB patients, and healthy individuals. Plasma PI15 levels in CCA patients were obviously reduced (p = .0014) after surgery. The AUC of plasma PI15 for discriminating between CCA and HCC was 0.735. Furthermore, with a specificity of 94.44%, the combination of CA19-9 (>98.5 U/ml) and PI15 (>13 ng/ml) yielded a sensitivity of 80.39% for CCA and HCC. INTERPRETATION: PI15 exhibits promise as a novel marker for predicting the diagnosis and follow-up of CCA patients. FUND: Natural Science Research Foundation of Anhui Province and Natural Science Foundation of China.

Talin-1 interaction network promotes hepatocellular carcinoma progression.

Talin-1 is a known oncogene-associated protein. In this study, we set out to determine its role and mechanisms in hepatocellular carcinoma (HCC) progression. We found Talin-1 to be highly expressed in HCC cells relative to non-cancer liver epithelial cells and to promote tumor growth and metastasis. We used Whole Human Genome Oligo Microarray analysis with HCC cells and HCC cells in which Talin-1 was knocked down using shRNA to identify transcripts regulated by Talin-1. Of the 40,000 tested genes, 3099 were differentially expressed after Talin-1 knockdown; expression of 1924 genes was increased, while expression of 2175 was decreased. Gene ontology (GO) profiling indicated that Talin-1 promotes many HCC progression-related activities, including ion transport and membrane depolarization, cell growth, and cell adhesion. We also characterized the network of gene transcripts regulated by Talin-1 and their role in promoting HCC progression. Our findings confirm the role of Talin-1 in carcinogenesis and provided a set of novel therapeutic targets for the treatment of HCC.

Both Talin-1 and Talin-2 correlate with malignancy potential of the human hepatocellular carcinoma MHCC-97 L cell.

BACKGROUND: Talin-1 (TLN-1) and TLN-2 are implicated in many cellular processes, but their roles in hepatocellular carcinoma (HCC) remain unclear. This study aimed to assess cell cycle distribution, anoikis, invasion and migration in human HCC MHCC-97 L cells. METHODS: MHCC-97 L cells, which highly express TLN-1, were transduced with TLN-1 shRNA (experimental group) or scramble shRNA (negative control group); non-transduced MHCC-97 L cells were used as blank controls. TLN-1 and TLN-2 mRNA and protein levels were detected by real-time RT-PCR and western blot, respectively. Then, cell cycle distribution and anoikis were assessed by flow cytometry. In addition, migration and invasion abilities were assessed using Transwell and cell scratch assays. Finally, a xenograft nude mouse model was established to further assess cell tumorigenicity. RESULTS: Compared with the blank and negative control groups, TLN-1/2 mRNA and protein levels were significantly reduced in the experiment group. TLN-1/2 knockdown cells showed significantly more cells in the G0/G1 phase (79.24%) in comparison with both blank (65.36%) and negative (62.69%) control groups; conversely, less cells were found in G2/M and S phases in the experimental group compared with controls. Moreover, anoikis was enhanced (P < 0.05), while invasion and migration abilities were reduced (P < 0.05) in TLN-1/2 knockdown cells compared with controls. TLN-1/2 knockdown inhibited MHCC-97 L cell migration (Percentage of wound healing area: experimental group: 32.6 ± 0.7% vs. negative controls: 50.1 ± 0.6% and blank controls: 53.6 ± 0.6%, both P < 0.01). Finally, the tumors obtained with TLN-1/2 knockdown cells were smaller (P < 0.05) compared with controls. CONCLUSION: Both TLN-1 and TLN-2 levels correlate with tumorigenicity in human HCC, indicating that these molecules constitute important molecular targets for the diagnosis and/or treatment of HCC.

Morphological instability of grain boundaries in two-phase coherent solids.

We show both computationally and analytically that grain boundaries that exhibit shear-coupled motion become morphologically unstable in solid alloys that phase separate into coherent domains of distinct chemical compositions. We carry out simulations of continuum models demonstrating that this instability is mediated by long-range elastic interaction between compositional domains and grain boundaries. In addition, we perform a linear stability analysis that predicts the range of unstable wavelengths in good quantitative agreement with simulations. In nonlinear stages, this pattern-forming instability leads to the breakup of low-angle grain boundaries, thereby strongly impacting microstructural evolution in a wide range of phase-separating materials.

Unified theoretical framework for polycrystalline pattern evolution.

The rate of curvature-driven grain growth in polycrystalline materials is well known to be limited by interface dissipation. We show analytically and by simulations that, for systems forming modulated phases or nonequilibrium patterns with crystal ordering, growth is limited by bulk dissipation associated with lattice translation, which dramatically slows down grain coarsening. We also show that bulk dissipation is reduced by thermal noise and that this reduction leads to faster coarsening behavior dominated by interface dissipation for a high Peierls-Nabarro barrier to dislocation motion and high noise. Those results provide a unified theoretical framework for understanding and modeling polycrystalline pattern evolution in diverse systems over a broad range of length and time scales.

Distorted magnetic orders and electronic structures of tetragonal FeSe from first principles.

We use the state-of-the-art density-functional-theory method to study various magnetic orders and their effects on the electronic structures of FeSe. Our calculated results show that, for the spins of the single Fe layer, the striped antiferromagnetic orders with distortion are more favorable in total energy than the checkerboard antiferromagnetic orders with tetragonal symmetry, which is consistent with known experimental data, and the interlayer magnetic interaction is very weak. We investigate the electronic structures and magnetic property of the distorted phases. We also present our calculated spin coupling constants and discuss the reduction of the Fe magnetic moment by quantum many-body effects. These results are useful in understanding the structural, magnetic and electronic properties of FeSe, and may have some helpful implications for other FeAs-based materials.

Two-speed phase dynamics in the si(111) (7 x7)-(1 x 1) phase transition.

We propose a natural two-speed model for the phase dynamics of Si(111) 7 x 7 phase transition to high-temperature unreconstructed phase. We formulate the phase dynamics by using phase-field method and adaptive mesh refinement. Our simulated results show that a 7 x 7 island decays with its shape kept unchanged, and its area decay rate is shown to be a constant increasing with its initial area. Low-energy electron microscopy experiments concerned are explained, which confirms that the dimer chains and corner holes are broken first in the transition, and then the stacking fault is remedied slowly. This phase-field method is a reliable approach to phase dynamics of surface phase transitions.