The report presents a case of epithelioid hemangioendothelioma in parotid gland misdiagnosed as parotid gland cyst with hemor-rhage.Based on the literature review,clinical characteristics,diagnosis and treatment of the disease are discussed.

Objective To evaluate the clinical effects of autogenous coronoid process reengineering condylar arthroplasty with simultaneous genioplasty for the correction of temporomandibular joint(TMJ)ankylosis accompanying micrognathia.Methods 21 cases of TMJ ankylosis with micrognathia from July 2003 to January 2012 were treated by autogenous coronoid process re-engineering condylar arthroplasty with simultaneous genioplasty.The follow-up period was 24 months to 8 years.TMJ function, mouth opening,occlusion,facial contour and the imaging manifestations were evaluated.Results After observation of follow-up,19 cases were improved obviously in the mandibular movement and mouth opening.Two cases had the recurrence of TMJ ankylosis. The facial appearance in all cases was significantly improved compared with before operation and the occlusal relationship had no large change compared with before operation.The coracoid process and mandibular ramus reached bone union with good reconstruc-tion by the panoramic radiographs.Compared with preoperation;the cephalometric results showed that the facial contour and process had statistical differences between postoperation and preoperation(P <0.05).Conclusion Autogenous coronoid process re-engineering condylar arthroplasty with simultaneous genioplasty can treat TMJ ankylosis accompanying micrognathia.

Golgi protein-73 (GP73) is a type-lⅡ Golgi glycoprotein localized on the membrane of the Golgi complex.Recently,a growing number of studies have demonstrated that the expression of GP73 is closely correlated with primary hepatocarcinoma (PHC).GP73 has a higher sensitivity and specificity than alpha-fetoprotein (AFP) and it may be a novel serum marker for the detection of PHC,especially for early PHC.This article reviews the relationship between GP73 and PHC.

ObjectiveTo investigate the effect of the Yap1 gene and tanshinone ⅡA on the proliferation, migration, and invasion abilities of Huh-7 hepatoma cells. MethodsA total of 10 pairs of human hepatocellular carcinoma (HCC) samples and adjacent tissue samples were collected in Zhongnan Hospital of Wuhan University from June 1 to December 1, 2019. Quantitative real-time PCR and Western blotting were used to measure the expression of the Yap1 gene and phenotype-related molecules. MTT cell proliferation detection reagent was used to measure the inhibition rate of cell proliferation after the treatment with different concentrations of tanshinone ⅡA. Western blotting was used to measure the changes in the expression of apoptosis-and migration-related markers after different interventions. Flow cytometry and Transwell assay were used to measure apoptosis and cell migration and invasion abilities. The data of 375 cases of liver cancer and 50 cases of relatively normal liver tissue samples were downloaded from The Cancer Genome Atlas, including clinicopathological information. The t-test was used for comparison of continuous data between two groups, and the chi-square test was used for comparison of categorical data between two groups. ResultsIn 8 of the 10 pairs of HCC samples and adjacent tissue samples, HCC samples had significantly higher expression of Yap1 than the adjacent tissue samples. Compared with the normal human liver epithelial cells L02, the Huh-7 and HCCL-M3 hepatoma cells had a significant increase in the expression of Yap1. The silencing efficiency of si-Yap1-3 transfection reached 87.004% at the protein level. MTT results showed that tanshinone ⅡA effectively inhibited the proliferation of Huh-7 cells, with a half inhibitory concentration of 8.683 μmol/L. After the cells were treated with si-Yap1-3 and tanshinone ⅡA, there was an increase in the expression of the downstream marker for proliferation and migration E-cadherin and a reduction in the expression of vimentin, and the results of Transwell assay showed that compared with the si-NC group, the tanshinone ⅡA+si-Yap1-3 group had significant reductions in the migration and invasion abilities of Huh-7 cells (migration: 43.19±2.88 vs 132.20±10.03, t=8.527, P=0.001; invasion: 53.95±4.20 vs 179.10±11.11, t=4.484, P=0.011). The group treated with si-Yap1-3 and tanshinone ⅡA had an increase in the expression of the apoptosis-related marker Bax and a reduction in the expression of Bcl-2, as well as a significantly higher early apoptosis rate than the si-NC group (2598% vs 9.21%, χ2=4.078, P＜0.05). ConclusionOncogene Yap1 silencing combined with tanshinone ⅡA can promote the apoptosis of Huh-7 hepatoma cells and inhibit their migration and invasion, which can provide certain guiding significance for clinical medication.

Long-term spaceflight affects numerous organ systems in the body, including metabolic dysfunction. Recently, ample evidence has demonstrated that the liver is a vulnerable organ during spaceflight. However, the changes in hepatocyte proliferation and cell cycle control under microgravity remain largely unexplored. In the present study, we first confirmed that the serum levels of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase, biochemical markers of liver function, were altered in rats under tail suspension (TS) conditions to simulate microgravity, as shown in previous reports. Next, we demonstrated that the cell proliferation activity, determined by Ki67, PCNA and PH3, was significantly decreased at the different TS time points (TS for 14, 28 and 42 days) compared with that in the control group. Consistently, the positive cell cycle regulators Ccna2, Ccnd1, Cdk1, Cdk2 and cyclin D3 were also significantly decreased in the TS groups as shown by quantitative real-time PCR and western blotting analysis. Subsequent analysis revealed that the aberrant hepatocyte proliferation inhibition under simulated microgravity was associated with the upregulation of miR-223 in the liver. We further found that miR-223 inhibited the proliferation of Hepa1-6 cells and identified CDK2 and CUL1 as its direct targets. In addition, the decreased expression of CDK2 and CUL1 was negatively correlated with the level of p27 in vitro and in vivo, which may have been responsible for retarding hepatocyte proliferation. Collectively, these data indicate that upregulation of miR-223 was associated with the inhibition of liver cell growth and reveal the role of miR-223 in rat hepatocyte proliferation disorders and the pathophysiological process under simulated microgravity.
Alanine Transaminase ; Alkaline Phosphatase ; Animals ; Aspartate Aminotransferases ; Biomarkers ; Blotting, Western ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Proliferation ; Cyclin D3 ; Hepatocytes* ; Hindlimb Suspension ; In Vitro Techniques ; Liver* ; Proliferating Cell Nuclear Antigen ; Rats* ; Real-Time Polymerase Chain Reaction ; Space Flight ; Up-Regulation* ; Weightlessness*