Pd-SnO2/In2O3 with a Unique Structure for the Ultrasensitive Detection of Triethylamine near Room Temperature.

Triethylamine (TEA) is a serious threat to people's health, and it is still a challenge to detect TEA at ppb level near room temperature (RT). Herein, we developed a simple, low-cost, low-temperature, and ultra-sensitive TEA sensor based on Pd-SnO2/In2O3 composites. First, SnO2 nanoparticles were obtained by the pyrolysis of Sn-MOF@SnO2 precursor (MOF: metal organic framework), and Pd-SnO2/In2O3 composites were prepared by further compounding and doping. The results show that the Pd-SnO2/In2O3 sensor is highly sensitive to TEA gas at near RT (at 60 °C, the sensor response to 10 ppm TEA is 12,000, the response/recovery (res/rec) time is 51 s/493 s, and at 30 °C, the response value also reaches 1380, the res/rec time is 66 s/610 s), along with good selectivity, stability, and moisture resistance. Even at 10 °C operating temperature and 75% relative humidity (RH) in a low-temperature and high-humidity environment, it still maintains a high sensitivity of over 1000 to 10 ppm TEA, which shows great application potential in TEA detection. The reason for the enhanced performance of the 0.5%Pd-SnO2/In2O3 sensor can be attributed to a large number of adsorbed oxygens on the unique structure of the material, the good charge transfer ability of the n-n-type heterojunction between SnO2 and In2O3, the chemical sensitization and electronic sensitization of Pd nanoparticles, and the catalytic spillover effect. This work will provide a new approach for preparing sensors with good comprehensive properties, making full use of the advantages of the material structure-activity relationship.

Association of the D repeat polymorphism in the ASPN gene with developmental dysplasia of the hip: a case-control study in Han Chinese.

INTRODUCTION: Developmental dysplasia of the hip (DDH) is a common skeletal disease, which is characterized by abnormal seating of the femoral head in the acetabulum. Genetic factors play a considerable role in the etiology of DDH. Asporin (ASPN) is an ECM protein which can bind to TGF-ß1 and sequentially inhibit TGF-ß/Smad signaling. A functional aspartic acid (D) repeat polymorphism of ASPN was first described as an osteoarthritis-associated polymorphism. As TGF-ß is well known as an important regulator in the development of skeletal components, ASPN may also be involved in the etiology of DDH. Our objective is to evaluate whether the D repeat polymorphism of ASPN is associated with DDH in Han Chinese. METHODS: The D repeat polymorphism was genotyped in 370 DDH patients and 445 control subjects, and the allelic association of the D repeat was examined. RESULTS: From D11 to D18, eight alleles were identified. D13 allele is the most common allele both in control and DDH groups, the frequencies are 67.3% and 58.1% respectively. In the DDH group, a significantly higher frequency of the D14 allele and significantly lower frequency of D13 was observed. The association of D14 and D13 was found in both females and males after stratification by gender. There was no significant difference in any other alleles we examined. CONCLUSIONS: Our results show an obvious association between the D repeat polymorphism of ASPN and DDH. It indicates that ASPN is an important regulator in the etiology of DDH.

Association of a single nucleotide polymorphism in growth differentiate factor 5 with congenital dysplasia of the hip: a case-control study.

INTRODUCTION: Congenital dysplasia of the hip is an abnormal seating of the femoral head in the acetabulum, mainly caused by shallow acetabulum and lax joint capsule. Genetic factors play a considerable role in the pathogenesis of congenital dysplasia of the hip. The gene growth differentiate factor 5 (GDF5) has been implicated in skeletal development and joint morphogenesis in humans and mice. A functional single nucleotide polymorphism (SNP) in the 5'-untranslated region of GDF5 (rs143383) was reported to be associated with osteoarthritis susceptibility. As a key regulator in morphogenesis of skeletal components and soft tissues in and around the joints, GDF5 may be involved in the aetiology and pathogenesis of congenital dysplasia of the hip. Our objective is to evaluate if the GDF5 SNP is associated with congenital dysplasia of the hip in people of Han Chinese origin. METHODS: The GDF5 SNP was genotyped in 338 children with congenital dysplasia of the hip and 622 control subjects. RESULTS: The SNP was significantly associated with congenital dysplasia of the hip (p = 0.0037; odds ration (OR) = 1.40; 95% confidence interval (CI) = 1.11 to 1.75). A significant difference was detected in female samples when stratified by gender (p = 0.0053; OR = 1.46; 95% CI = 1.21 to 1.91), and in hip dislocation when stratified by severity (p = 0.0078; OR = 1.43; 95% CI = 1.11 to 1.85). CONCLUSIONS: Our results indicate that GDF5 is important in the aetiology of congenital dysplasia of the hip. To the authors' knowledge this is the first time that a definite association with the congenital dysplasia of the hip susceptibility has been detected.