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The four-stroke spark-ignition (SI) internal combustion engine has good fuel economy and high power/weight ratio, making it very suitable for small aircraft. Normally, four-stroke aviation SI engines are fuelled with gasoline. Using kerosene can improve the system safety; However, a four-stroke SI engine fuelled with kerosene suffers from a small indicated mean effective pressure (IMEP) because of the knock limit of kerosene. In this study, water injection is investigated as a method of extending the knock limitation and improving IMEP of a four-stroke SI engine fuelled with kerosene. First, a Rotax 914 engine is retrofitted. Two port-fuel-injection systems supplied with kerosene and water are developed. Then, the combustion characteristics with water injection are studied. The effects of water injection on the in-cylinder pressure and heat-release rate are analysed. Additionally, the extent of knock suppression due to water injection under various engine speeds is evaluated. The results indicate that the knock limit of the four-stroke SI engine with kerosene is extended significantly via water injection. The measured IMEP is improved by 25–28% under different engine speeds. Thus, the requirement for ordinary cruise operation is satisfied. Furthermore, the security is enhanced with water injection.

Using kerosene for an aero piston internal combustion engine can improve system safety. Constrained by the knock limit of kerosene, the indicated mean effective pressure (IMEP) of spark ignition (SI) aero piston engine using kerosene is lower than that of gasoline. In this study, an experimental study based on a four-stroke SI aero engine was carried out. The influences of water injection on the combustion process and the improvement of IMEP were evaluated. The results indicate that the knock phenomenon can be suppressed in a certain extent with an appropriate amount of water injection.

Microphthalmia-associated transcription factor (MITF) plays a crucial role in the melanogenesis and proliferation of melanocytes that is dependent on its abundance and modification. Here, we report that epidermal growth factor (EGF) induces senescence and cyclin-dependent kinase inhibitor 1A (CDKN1A) expression that is related to MITF. We found that MITF could bind TP53 to regulate CDKN1A. Furthermore, the interaction between MITF and TP53 is dependent on AKT activity. We found that AKT phosphorylates MITF at S510. Phosphorylated MITF S510 enhances its affinity to TP53 and promotes CDKN1A expression. Meanwhile, the unphosphorylative MITF promotes TYR expression. The levels of p-MITF-S510 are low in 90% human melanoma samples. Thus the level of p-MITF-S510 could be a possible diagnostic marker for melanoma. Our findings reveal a mechanism for regulating MITF functions in response to EGF stimulation and suggest a possible implementation for preventing the over proliferation of melanoma cells.

Background RTN4R (Reticulon 4 receptor) plays an essential role in regulating axonal regeneration and plasticity in the central nervous system through the activation of rho kinase, and is located within chromosome 22q11.2, a region that is known to be a hot-spot for Schizophrenia (SCZ) and Autism Spectrum Disorder (ASD). Recently, rare variants such as Copy Number Variants (CNV) and Single Nucleotide Variants (SNV) have been a focus of research because of their large effect size associated with increased susceptibility to SCZ and ASD and the possibility of elucidating the pathophysiology of mental disorder through functional analysis of the discovered rare variants. Methods In order to discover rare variants with large effect size and to explore their role in the etiopathophysiology of SCZ and ASD, we performed mutation screening of RTN4R coding exons using a sample comprised of 370 SCZ and 192 ASD patients, and association analysis using a large number of unrelated individuals (1716 SCZ, 382 ASD and 4009 controls). Results Through this mutation screening, we discovered four rare (minor allele frequency Discussion This study strengthens the evidence for association between rare variants within RTN4R and SCZ, and may shed light on the molecular mechanisms underlying the neurodevelopmental disorder.