profile modification
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Author(s):  
Sarah H. Megahed ◽  
Sari Rasheed ◽  
Jennifer Herrmann ◽  
Ebaa M. El-Hossary ◽  
Yahia I. El-Shabrawy ◽  
...  

2021 ◽  
Author(s):  
De Tian ◽  
Lizhuang Tao ◽  
Yue Hu ◽  
Bei Li ◽  
Xiaoxuan Wu ◽  
...  

Abstract Tooth surface wear is one of the most common faults of gearboxes which increases the fatigue load on the gearbox and endangers its stable output characteristics and service life. Gear meshing characteristics vary significantly with the wear location and severity. Thus, the wear fault model considering tooth profile deviation, friction and time varying mesh stiffness (TVMS) was established in order to quantitatively study the vibration characteristics of tooth fatigue wear (TFW). Tooth profile modification and friction coefficient coupling were applied to characterize TFW, and the maximum wear depth was introduced to characterize TFW severity. The gear-pair simulation models under multiple wear severities were established and imported to a single-stage parallel gearbox whose dynamic differential equation was established under multiple torque conditions. The dynamic simulation results showed good agreement with the experimental data, which validated the method’s effectiveness. The vibration characteristics under different wear severities and simulation conditions were then obtained and compared.


Author(s):  
Clara Apicella ◽  
Camino S. M. Ruano ◽  
Sébastien Jacques ◽  
Géraldine Gascoin ◽  
Céline Méhats ◽  
...  

A bioinformatics screen for non-coding genes was performed from microarrays analyzing on the one hand trophoblast fusion in the BeWo cell model, and on the other hand, placental diseases (preeclampsia and Intra-Uterine Growth Restriction). Intersecting the deregulated genes allowed to identify two miRNA (mir193b and miR365a) and one long non-coding RNA (UCA1) that are pivotal for trophoblast fusion, and deregulated in placental diseases. We show that miR-193b is a hub for the down-regulation of 135 cell targets mainly involved in cell cycle progression and energy usage/nutrient transport. UCA1 was explored by siRNA knock-down in the BeWo cell model. We show that its down-regulation is associated with the deregulation of important trophoblast physiology genes, involved in differentiation, proliferation, oxidative stress, vacuolization, membrane repair and endocrine production. Overall, UCA1 knockdown leads to an incomplete gene expression profile modification of trophoblast cells when they are induced to fuse into syncytiotrophoblast. Then we performed the same type of analysis in cells overexpressing one of the two major isoforms of the STOX1 transcription factor, STOX1A and STOX1B (associated previously to impaired trophoblast fusion). We could show that when STOX1B is abundant, the effects of UCA1 down-regulation on forskolin response are alleviated.


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