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OBJECTIVE: The purpose of this study was to explore the clinical significance and biological function of long noncoding RNA CASC9 (CASC9) in esophageal squamous cell carcinoma (ESCC). PATIENTS AND METHODS: Quantitative Real-time PCR (qRT-PCR) was used to determine the expression of CASC9 in ESCC tissues and cell lines. Receiver operating characteristic curves were used to evaluate the sensitivity and specificity of CASC9. The correlation between the CASC9 levels and the clinicopathological factors of the patients was also analyzed. Then, the survival was assessed by the Kaplan-Meier method and proportional hazards model. The effects of CASC9 on ESCC cells were evaluated by Cell Counting Kit-8 (CCK-8), migration and invasion. Finally, several EMT markers expression was detected by Western blot. RESULTS: We found that CASC9 was significantly upregulated in ESCC cell lines and clinical tissues. The CASC9 levels discriminated ESCC tissues from normal tissues with an area under the ROC curve (AUC) of 0.813. In addition, there is statistical significance between CASC9 expression level and tumor stage, lymph nodes metastasis, and clinical stage. Kaplan-Meier analysis indicated that high CASC9 expression had a significant impact on overall survival (p = 0.014) and disease-free survival (p = 0.0025). Moreover, CASC9 expression was an independent prognostic marker of overall survival and disease-free survival in a multivariate analysis. In vitro assay indicated that inhibition of CASC9 could suppress proliferation, migration, and invasion in ESCC. Further mechanistic studies found that aberrant CASC9 expression could modulate the expression levels of markers of EMT. CONCLUSIONS: Our data highlight the pivotal role of CASC9 as a novel diagnostic, prognostic biomarker and a potential therapeutic target of ESCC. [ABSTRACT FROM AUTHOR]

In recent years, with the changes in living standards and dietary structure, the incidence of non-alcoholic fatty liver disease has been increasing year by year in China, and the incidence rate in the general population is as high as 29.81%. An increasingly epidemiological evidence suggests that non-alcoholic fatty liver disease has become one of the causes of increasing liver cirrhosis and liver cancer. However, its etiology and pathogenesis are complex and have not yet been fully elucidated. Therefore, establishing an appropriate non-alcoholic fatty liver disease animal models for pre-clinical research is essential to elucidate its pathogenesis. This article summarizes the latest research progress of non-alcoholic fatty liver disease animal models, which are common at home and abroad in recent years.

Objective: To provide biomechnical basis for orthodontics of centronuclear myopathy (CNM) patients, we studied the oral and maxillofacial clinical features and MRI image manifestations to explore application of MRI to objective evaluation the affected facial muscles. Methods: The study consisted of 8 patients who were diagnosed as CNM (CNM group) and 20 healthy volunteers (control group). Their medical information were gathered and then we examined the ptosis situation and the facial index calculation of them. To measure the maximal hight of palate and the width of palate, patients and volunteers were made impressions. We also checked their maximum bite force with occlusion pressure tester. And they took lateral cephalometric radiographs to measure mandibular plane-Frankfort horizontal plane angle (MP-FH). At last, they were taken oral and maxillofacial region MRI to observe the affected situation of masseter muscle, medial pterygoid muscle and lateral pterygoid muscle. Results: Six patients were ptosis; 6 patients had inverse V-shaped mouth; 3 patients were difficulty in swallowing; 4 patients were anterior open bites; 4 patients were mouth breathing; 7 patients liked to eat soft foods. Morphological facial index ([91.3±0.5]%), MP-FH (34.9°±2.0°) of CNM group were greater than the control group, male maximal hight of palate ([19.0±0.2] mm), female maximal hight of palate ([18.0±0.6] mm) of CNM group were greater than the control group ( P< 0.05). Male width of palate ([34.5±0.8] mm), female width of palate ([33.4±1.0] mm), male maximum bite force ([464.3±78.2] N), female maximum bite force ([320.7±13.8] N), maximal opening of mouth ([3.4±0.3] cm) of CNM group were less than the control group ( P< 0.05). And these had significant difference compared with the control group ( P< 0.05). In MRI examination, there were 7 patients ' masseter muscles, 4 patients ' medial pterygoid muscles and 6 patients ' lateral pterygoid muscles to atrophy asymmetrically. These three pieces of muscular fatty infiltration were inordinately, focused on Grade 0 to 4 and the both sides were similar. Conclusions: CNM patients with long and thin face, high palatine arches and low bite force together were the biomechanical basis of the maxillofacial deformities. MRI can clearly show the affected masseter muscle, medial pterygoid muscle, lateral pterygoid muscle, and can serve as an objective examination method for the evaluation of facial muscles. It can be worth of clinical popularization and application.

Objective: To investigate the manifestation of facioscapulohumeral muscular dystrophy (FSHD) in oral and maxillofacial region. Methods: A total of 12 patients diagnosed as FSHD and 20 healthy volunteers were included in the study. Their medical history was collected from these patients. The decayed missing filled teeth (DMFT), calculus index-simplified (CI-S), occlusal relationship, maximal opening of mouth and maximum bite force were recorded. The impressions were taken to measure the maximal hight of palate and the width of palate. The lateral cephalometric radiographs were also taken to measure the mandibular plane-frankfurt horizontal plane angle (MP-FH). They finally received oral and maxillofacial region MRI examination to observe the masseter muscle, medial pterygoid muscle and lateral pterygoid muscle. The data were analyzed by t -test or Wilcoxon signed ranks test. Results: There was no significant gender difference in FSHD group. The average age of treatment was (27.5 ± 8.1) years and the average age of onset was (15.7±7.5) years. Nine patients liked to eat soft foods, 4 patients had difficulties of closing eyes, 8 patients had difficulties of cheek-bulging, 10 patients showed pouty lips and 9 patients had mesio-malocclusion. DMFT (4.0±2.3), CI-S (5.8±2.1), male maximal hight of palate (20.5±2.1) mm , female maximal hight of palate (17.9±1.6) mm, MP-FH (31.8°±2.2°) of FSHD group were greater than those of the control group. Male width of palate (34.8±1.4) mm, female width of palate (33.7±1.5) mm, male maximum bite force (451.7 ± 39.0) N, female maximum bite force (326.7 ± 21.6) N, maximal opening of mouth (3.5 ± 0.4) cm of FSHD group were less than those of the control group ( P <0.05). Maxillofacial MRI showed muscle asymmetr in 11 cases of masseter and 6 cases of medial pterygoid muscle, 5 cases of lateral pterygoid, and these muscle showed mild fatty infiltration mainly concentrating in the grade 0, grade 1 and grade 2. Conclusions: The FSHD patients have poor oral hygiene, low masticatory function, limited mouth opening, high palate and narrow arch and different degree of malocclusion. The patients' masseter muscle, medial pterygoid muscles and lateral pterygoid muscles exhibit asymmetrical atrophy and fatty infiltration.

CD226, a member of cell adhesion molecules, has been widely studied in the immune system; however, its expression in the CNS remains unknown. In our present study, we detected CD226 mRNA and protein in the mouse hippocampus and cerebellum by RT-PCR and Western blotting, respectively. Immunohistochemical studies found that CD226 is primarily located in the hilus of the dentate gyrus and stratum lucidum aligned along the pyramidal cells in the hippocampal CA3 area, the interspaces of granular cells and the somata of the Purkinje cells in the cerebellar cortex during adulthood. Double-staining results revealed that CD226 co-localized well with synaptic marker proteins including synaptophysin, syntaxin and PSD-95. During postnatal development, CD226 could not be detected at its adult locations until postnatal day 12; however, it was temporally expressed in the somata of neighboring or distant nuclei associated with its adult location. These results showed the diverse localization of CD226 in the mouse hippocampus and cerebellum for the first time and suggested its potential role in the CNS.

Using reverse transcriptase-polymerase chain reaction (RT-PCR) the changes of the angiotensin II receptor subtype 1-a (AT1a) and 1-b (AT1b) mRNA levels were examined in hypertrophied ventricles caused by ventral aorta-caval fistula of SD rats. The results show as follows. (1) Three days after operation, the ventricular weight increased significantly, whereas the level of AT1a and AT1b mRNA in both ventricles remained unchanged. (2) Twelve days after operation, the weight increase of both ventricles was more evident, the levels of AT1a and AT1b mRNA in the right ventricle increased (by 62.6% and 72.0%), as compared with control. In the left ventricle, on the other hand, the level of AT1a mRNA increased by 79.0%, while the level of AT1b mRNA showed no obvious increase. (3) Thirty-five days after operation, the levels of AT1a and AT1b mRNA in both ventricles increased still more significant, (i.e., 70.0% and 83.9% in the right and 96.5% and 86.9% in the left). Moreover, 12 d and 35 d after operation, the level of AT1a mRNA was higher than that of AT1b mRNA in both ventricles. (4) There was a positive correlation between the degree of ventricular hypertrophy with the level of AT1 mRNA in ventricular myocardium (r = 0.6168-0.8223). The results suggest that the increased mRNA expression of AT1 in myocardial hypertrophy caused by volume overload may be a mechanism underlying the increased responsiveness of hypertrophic myocardial cells to Ang II, and a difference in the expression between AT1a and AT1b mRNAs in myocardial hypertrophy may be related to the different physiological or pathophysiological roles of Ang II, mediated by the two subtypes of AT1.

To determine the contribution of cardiac renin-angiotensin system (RAS) to the physiological myocardial hypertrophy induced by swimming training and the relationship between locally produced and circulating RAS, both ventricular and plasma angiotensin (Ang) I and II contents, ventricular angiotensin converting enzyme (ACE) and plasma renin activity (PRA) were detected by means of radioimmunoassay and biochemical method. It was shown that after 5 weeks of swimming, the ventricular wet weight to body weight ratio (V/Bwt) and Ang II in both left and right ventricles and ACE activity increased markedly as compared with the controls (P < 0.05). Furthermore, significantly positive correlation was found between the ventricular Ang II and V/Bwt (r = 0.7721, P < 0.001), while the plasma Ang I and II and PRA remained at the control level. No correlation was found between plasma Ang II and V/Bwt. These above findings suggest that cardiac RAS may play an important role in physiological myocardial hypertrophy and to a large extent is in dependent on circulating RAS.