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Experimental studies on gasification of the Shenmu coal char with CO2 at elevated pressures
Wang Mingmin,Zhang Jiansheng,Zhang Shouyu,Wu Jinhu,Yue Guangxi 한국화학공학회 2008 Korean Journal of Chemical Engineering Vol.25 No.6
The gasification rates of Shenmu coal chars with CO2 were experimentally studied with a pressurized thermo- gravimetric analyzer (PTGA). Shenmu coal is a typical Chinese coal, and the coal char was prepared by a fixedbed reactor in nitrogen at 900 oC. The experiments were carried out in the dynamic heating segments from 750 oC to 1,000 oC, and the reaction pressure increased from 0.1MPa to 3.1MPa with pure CO2. The external diffusion resistances were minimized by increasing the flow rates and decreasing the thickness of sample layer before the test, to ensure the reactions were under kinetic control. The results show that the gasification rates increase proportionally to the 0.1 power of the CO2 partial pressure. The unreacted-core shrinking model was applied to predict the reaction rate by changing the molar fraction of CO2 at 0.6Mpa and 1.6Mpa total pressures, which showed a good match with experimental data.
Identification a novel de novo RUNX2 frameshift mutation associated with cleidocranial dysplasia
Gong Lei,Odilov Bekzod,Han Feng,Liu Fuqiang,Sun Yujing,Zhang Ningxin,Zuo Xiaolin,Yang Jiaojiao,Wang Shouyu,Hou Xinguo,Ren Jianmin 한국유전학회 2022 Genes & Genomics Vol.44 No.6
Background: Cleidocranial dysplasia (CCD) is a rare genetic disorder affecting bone and cartilage development. Clinical features of CCD comprise short stature, delayed ossification of craniofacial structures with numerous Wormian bones, underdeveloped or aplastic clavicles and multiple dental anomalies. Several studies have revealed that CCD development is strongly linked with different mutations in runt-related transcription factor 2 (RUNX2) gene. Objective: Identification and functional characterization of RUNX2 mutation associated with CCD. Methods: We performed genetic testing of a patient with CCD using whole exome sequencing and found a novel RUNX2 frameshift mutation: c.1550delT in a sporadic case. We also compared the functional activity of the mutant and wild-type RUNX2 through immunofluorescence microscopy and osteocalcin promoter luciferase assay. Results: We found a novel RUNX2 frameshift mutation, c.1550delT (p.Trp518Glyfs*60). Both mutant RUNX2 and wild-type RUNX2 protein were similarly confined in the nuclei. The novel mutation caused abrogative transactivation activity of RUNX2 on osteocalcin promoter. Conclusions: We explored a novel RUNX2 deletion/frameshift mutation in a sporadic CCD patient. This finding suggests that the VWRPY domain may play a key role in RUNX2 transactivation ability.