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The box girder is an important structure widely used in the ship and marine engineering, but the fracture problem is not extensively investigated. The paper adopts the stress intensity factor (SIF) as the fracture parameter to perform the threedimensional (3D) mixed mode fracture assessment of the box girder structure with crack damage. The bending load, torsion load and side load are first introduced to study box girder fracture behavior. And the related influencing factors including crack lengths, crack angles and combined loads are investigated emphatically. Besides, the crack growth angle is also investigated to evaluate the crack propagation behavior. The results show that the load types have a significant effect on the crack propagation. The effect of bending load is generally greater than torsion load. The combined effect of bending and torsion loads may be considered adopting a linear superposition principle under transverse crack and larger angle crack. Additionally, the SIFs produced by torsion load only have a slight change with the increased crack angles. When the side load is added, the area near the crack upper surface will be easy to occur unstable expansion. These findings from the present study will provide a guiding significance to evaluate the crack propagation of box girder under combined loads. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The incidence of thyroid cancer is rising globally. Most patients progress slowly, but some patients develop lymph node and distant metastasis earlier, and their prognosis is poor. Therefore, early diagnosis and warning of malignancy are very meaningful for such patients. SAS1B gene is a newly discovered protein expressed on the surface of mature egg cells and has metalloendopeptidase activity. We aimed at exploring whether SAS1B is involved in the occurrence of thyroid cancer, and at providing evidence for early diagnosis and targeted therapy of thyroid cancer. PATIENTS AND METHODS: In this study, a rabbit anti-human SAS1B polyclonal antibody was prepared by gene recombination technology. The indirect ELISA method was used to detect the SAS1B protein expression in the serum of 69 patients with thyroid cancer and 55 normal controls, and the relevant pathological factors were analyzed. Immunohistochemistry and PCR technology were used to investigate the expression levels of SAS1B protein and mRNA in 30 thyroid cancer tissues and 23 control thyroid tissues. RESULTS: The titer of SAS1B recombinant antibody was 1:51200. The expression of SAS1B in the serum of patients with thyroid cancer was higher than that in the normal control group (p<0.01). The antibody had a good sensitivity in serum detection of cancer patients (p=0.008<0.01), the linear regression analysis result was that the expression of SAS1B gene was related to tumor envelope invasion and lymph node metastasis (p=0.003<0.01, p=0.003<0.01), and it was irrelevant to the patient's gender, age, tumor mass size, number of cancer foci, pathological stage, etc. (p>0.05). The results of immunohistochemistry showed that SAS1B protein was mainly located in the cytoplasm and membrane of thyroid cancer cells. The expression intensity in thyroid cancer tissues was higher than that in control tissues (p<0.05), but it was not expressed in normal thyroid tissues. Antibodies showed a good sensitivity that was used to detect thyroid cancer tissues (p=0.000<0.01). The results of ordinary PCR detection using thyroid cancer tissue and control thyroid tissue showed that the amplification products of the three domains (N-terminal, C-terminal and catalytic domain) of the SAS1B gene showed high expression in thyroid cancer tissue. q-PCR results showed that the expression of SAS1B gene in thyroid cancer and control thyroid tissue was higher than that in control group (p<0.05), and the genes of Aurora A and BARD1 related to centrosome replication and DNA replication forks protection during the proliferation were highly expressed in thyroid cancer tissue. The study results suggested that SAS1B was involved in the carcinogenesis of thyroid cancer. The Hum_mPLoc.2.0 software, PSORT II software and UniProt software were used to predict that SAS1B protein had secretory protein properties. CONCLUSIONS: The above data indicate that the SAS1B gene is closely related to the process of thyroid cancer and can serve as a good tumor marker that can be used for early diagnosis and early warning of thyroid malignancy. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We conducted this study to analyze the EEG abnormalities of cognitive impairment and epileptic seizures in patients with epilepsy, as well as to investigate the application value of EEG in the diagnosis of epilepsy with cognitive impairment. PATIENTS AND METHODS: 62 cases of patients that were admitted to our hospital for the first diagnosis as status epilepticus were selected. Of those, 20 cases were accompanied by cognitive impairment. The America Biology Graphene type 24 leads channel video EEG was applied to monitor staging, index, frequency, and distribution range of epileptic discharge. The revised Wechsler Adult Intelligence Scale-Revised in China (WAIS-RC) and Wechsler Memory Scale-Revised in China (WMS-RC) were adopted to test cognitive function. RESULTS: The epileptic discharge index, discharge frequency and discharge distribution range of the conscious period, sleep I-II period and sleep III-IV period of epilepsy with the cognitive impairment group were evidently higher than those of epilepsy without cognitive impairment group. The differences were statistically significant (p<0.05). Intelligence Quotient (IQ) and Memory Quotient (MQ) level of the cognitive impairment group were the lowest in sleep III-IV period, with the next being the sleep I-II period; the highest was the conscious period, and the differences were statistically significant (p<0.05). With an increase of the epileptic discharge index, the discharge range, IQ and MQ level of cognitive impairment group decreased; differences were statistically significant (p<0.05). Therefore, the discharge index, frequency, and distribution range of epileptic discharge of epilepsy with cognitive impairment in different periods differed from epilepsy patients without cognitive impairment. According to the extent of cognitive impairment in different stages, discharge index, frequency, and distribution range were also different. CONCLUSIONS: The 24 h video EEG, which was used to monitor epileptic discharge characteristics, has a great application value for early identification of epilepsy with cognitive impairment. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To clarify whether microRNA-646 could regulate the proliferative potential and cell cycle progression of nasopharyngeal carcinoma cells through targeting mammalian target of rapamycin (mTOR). It, therefore, could influence the occurrence and progression of nasopharyngeal carcinoma. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to detect expression of the levels of microRNA-646 and mTOR in tumor tissues and paracancerous tissues of patients with nasopharyngeal carcinoma. Besides, their expressions in nasopharyngeal carcinoma cell lines were determined by qRT-PCR. Survival analysis was conducted to evaluate the sensitivity and specificity of microRNA-646 in diagnosing nasopharyngeal carcinoma. The overall survival of patients with nasopharyngeal carcinoma was calculated based on their expression levels of microRNA-646. The regulatory effects of microRNA-646 and mTOR on proliferative potential and cell cycle progression were explored by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. Dual-luciferase reporter gene assay was conducted to verify the relationship between microRNA-646 and mTOR, which was further confirmed by Pearson correlation analysis. Finally, gain-of-function experiments were carried out to determine whether microRNA-646 could regulate the proliferative potential and cell cycle progression of nasopharyngeal carcinoma cells by targeting mTOR. RESULTS: MicroRNA-646 was lowly expressed in nasopharyngeal carcinoma tissues and cell lines. Survival analysis confirmed the diagnostic value of microRNA-646 in nasopharyngeal carcinoma. Besides, the nasopharyngeal carcinoma patients with high level of microRNA-646 were expected to have a longer 5-year survival time compared with those with low level. Overexpression of microRNA-646 inhibited the proliferative potential and cell cycle progression of HONE1 and SUNE1 nasopharyngeal carcinoma cells. Dual-luciferase reporter gene assay detected the binding of microRNA-646 to mTOR. Moreover, mTOR was highly expressed in nasopharyngeal carcinoma tissues and cell lines. A negative correlation was found between microRNA-646 and mTOR. That is, the overexpression of mTOR could reverse the inhibitory effects of microRNA-646 on the proliferative potential and cell cycle progression of HONE1 and SUNE1 cells. CONCLUSIONS: MicroRNA-646 remains a low level in nasopharyngeal carcinoma. It inhibits the proliferative potential and cell cycle progression of nasopharyngeal carcinoma cells by targeting mTOR. It can, therefore, inhibit the development of nasopharyngeal carcinoma. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study aimed to investigate the effect of microRNA-605-3p (miR-605-3p) on cell proliferation, invasion and migration in prostate cancer cells, as well as its effects on the Enhancer Zeste Homolog 2 (EZH2) expression and the potential regulatory mechanisms. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was applied to detect the miR-605-3p expression in 52 pairs of Prostate Cancer (PCa) tissues and normal tissues, and to analyze the relationship between miR-605-3p expression and PCa pathological parameters. MiR-605-3p mimics were transfected into PCa cell line PC-3 and DU145 to achieve miR-605-3p overexpression. Then, Cell Counting Kit-8 (CCK-8), cell colony formation assay and transwell invasion and migration assay were performed to analyze miR-605-3p's effect on the biological function of prostate cancer cells. Finally, the potential mechanisms of downstream genes were explored through bioinformatics analysis and recovery experiments. RESULTS: We found that miR-605-3p expression in PCa was markedly lower than that in normal tissues. Patients with low miR-605-3p expression had higher tumor stage, higher incidence of lymph node metastasis and distant metastasis. In vitro analysis showed that miR-605-3p overexpression leads to a significant decrease in cell proliferation, invasion and migration ability. Subsequently, it was verified in cell line and tissue that EZH2 expression was remarkably increased in PCa, which was negatively correlated with miR-605-3p expression. In addition, the recovery experiment found that EZH2 can counteract the role of miR-605-3p in PCa, together they affected the malignant progression of PCa. CONCLUSIONS: MiR-605-3p was significantly associated with PCa stage, lymph node metastasis and distant metastasis and the poor prognosis; besides, it can inhibit the malignant progression of PCa. In addition, the study showed that miR-605-3p may inhibit the proliferation, invasion and migration ability of PCa by regulating EZH2. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Hepatocellular carcinoma (HCC) is a hypervascularized tumor. Aberrant angiogenesis is the main cause, which results in cancer growth and progression. It has been showed that microRNA-302 cluster (miR-302) may be associated with angiogenesis. Here, we aimed to identify the role of miR-302a/b/c in the regulation of cell angiogenesis in HCC. PATIENTS AND METHODS: MRNA expression of miR-302a/b/c and MACC1 was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The protein of MACC1 was measured using Western blot. Cells proliferation, migration, and invasion abilities were investigated via Cell Counting Kit-8 (CCK-8) assay or transwell assay, respectively. Tube formatting assays were used to explore the tube formation capacity. The interaction among miR-302a/b/c was analyzed by luciferase assay. RESULTS: The expression of miR-302a/b/c was greatly reduced while MACC1 expression, whether mRNA or protein was conspicuously elevated in HCC tissues and cells. Then, functional experiment results showed miR-302a/b/c overexpression and MACC1 down-regulation inhibited the proliferation, migration, invasion ability, and tube formation capacity of HUVECs. In addition, we detected that miR-302a/b/c directly targeted MACC1 and suppressed MACC1 expression, and miR-302a/b/c could suppress tumor angiogenesis in HCC by targeting MACC1. CONCLUSIONS: MiR-302a/b/c may function as a potential suppressor of tumor angiogenesis in HCC by targeting MACC1, indicating a promising target for HCC therapy. [ABSTRACT FROM AUTHOR]