PReS-FINAL-2108: Long-term outcome of 114 adult JIA patients in a non-pediatric rheumatology institute in Japan

20th Congress of Paediatric Rheumatology European Society 2013年09月25日 Sloveni

PReS-FINAL-2108: Long-term outcome of 114 adult JIA patients in a non-pediatric rheumatology institute in Japan

20th Congress of Paediatric Rheumatology European Society 2013年09月25日 Sloveni

Overexpression of SMYD2 in gastric cancer

Background: SET and MYND domain-containing protein 2 (SMYD2) is a lysine methyltransferase for histone H3, p53 and Rb and inhibits their transactivation activities. In this study, we tested whether SMYD2 (1q42) acts as a cancer-promoting factor by being overexpressed in gastric cancer. Methods: We analysed 7 gastric cancer cell lines and 147 primary tumor samples of gastric cancer, which were curatively resected in our hospital. Results: SET and MYND domain-containing protein 2 was detected in these cell lines (five out of seven cell lines; 71.4%) and primary tumor samples (fifty-six out of one hundred and forty-seven cases; 38.1%). Knockdown of SMYD2 using specific small interfering RNA inhibited proliferation, migration and invasion of SMYD2-overexpressing cells in a TP53 mutation-independent manner. Overexpression of SMYD2 protein correlated with larger tumor size, more aggressive lymphatic invasion, deeper tumor invasion and higher rates of lymph node metastasis and recurrence. Patients with SMYD2-overexpressing tumours had a worse overall rate of survival than those with non-expressing tumours (P=0.0073, log-rank test) in an intensity and proportion score-dependent manner. Moreover, multivariate analysis demonstrated that SMYD2 was independently associated with worse outcome (P=0.0021, hazard ratio 4.25 (1.69–10.7)). Conclusions: These findings suggest that SMYD2 has a crucial role in tumor cell proliferation by its overexpression and highlight its usefulness as a prognostic factor and potential therapeutic target in gastric cancer

Overview on fingerprinting authentication technology

This paper addresses the characteristics, technology, and possible future of fingerprints authentication method. Fingerprint physiology makes it an ideal for biometrics authentication, primarily the tiny details located on its surface called minutiae. Fingerprint scanning systems are designed to detect minutiae. Images of detected minutiae are processed through matching algorithms in order to verify a query fingerprint that is identical to a stored fingerprint. However, fingerprint authentication based on minutiae can be easily bypassed and the need for a more secure method is required. With respect to the issue, this work explores the possibility of detecting the thickness of the skin layer within a fingerprint as a method of biometrics authentication. Current thickness measuring methods that are non-invasive for that task are identified as Laser Scanning Microscopy (LSM), Optical Coherence Tomography (OCT) and Near Infrared Spectroscopy (NIR). Of the three listed, only OCT and NIR methodology seems viable for simple yet reliable use and can become as promising methods for authentication based on skin layer thickness

PReS-FINAL-2125: A Japanese girl with childhood-onset anti-Ku antibody positive generalized morphea-myositis overlap syndrome

POSTER PRESENTATIONProceedings of 20th Pediatric Rheumatology European Society (PReS) Congress / 25-29 September 2013 / Ljubljana, Sloveni

5-HTR3 and 5-HTR4 located on the mitochondrial membrane and functionally regulated mitochondrial functions

5-HT has been reported to possess significant effects on cardiac activities, but activation of 5-HTR on the cell membrane failed to illustrate the controversial cardiac reaction. Because 5-HT constantly comes across the cell membrane via 5-HT transporter (5-HTT) into the cytoplasm, whether 5-HTR is functional present on the cellular organelles is unknown. Here we show 5-HTR3 and 5-HTR4 were located in cardiac mitochondria, and regulated mitochondrial activities and cellular functions. Knock down 5-HTR3 and 5-HTR4 in neonatal cardiomyocytes resulted in significant increase of cell damage in response to hypoxia, and also led to alternation in heart beating. Activation of 5-HTR4 attenuated mitochondrial Ca2+ uptake under the both normoxic and hypoxic conditions, whereas 5-HTR3 augmented Ca2+ uptake only under hypoxia. 5-HTR3 and 5-HTR4 exerted the opposite effects on the mitochondrial respiration: 5-HTR3 increased RCR (respiration control ratio), but 5-HTR4 reduced RCR. Moreover, activation of 5-HTR3 and 5-HTR4 both significantly inhibited the opening of mPTP. Our results provided the first evidence that 5-HTR as a GPCR and an ion channel, functionally expressed in mitochondria and participated in the mitochondria function and regulation to maintain homeostasis of mitochondrial [Ca2+], ROS, and ATP generation efficiency in cardiomyocytes in response to stress and O2 tension