ABSTRACT
Objective To investigate the effect from helmet mass and deviation of mass center on neck muscle activity in military pilots. Methods Based on AnyBody software platform, a musculoskeletal model of head neck complex was established including C0, C1-C7, T1 and 136 muscles. Concentrated loads were applied to simulate the role of helmet. Strength from seven main muscle groups under different helmet mass, mass center and +Gz acceleration loads were simulated and calculated.Results When mass center of the helmet and the head coincided with each other, the muscle groups (such as semispinalis, levator scapulae, splenius capitis and cervicis) which took charge of extension were activated. Muscle strength increased with helmet mass linearly and +Gz acceleration loads would make this increase multiplied. Flexion muscle began to work when mass center of the helmet moved backward, so did the lateral bending muscles when mass center of helmet moved in the right-and-left direction. Conclusions Helmet mass and its center have an obvious influence on neck muscle activity in military pilots. The musculoskeletal model established in this paper can be used to calculate the change in muscle strength under different situations and conduct a quantitative analysis for helmet design and validation.
ABSTRACT
Objective To analyze the neck muscle activity during head flexion and explore the cause of muscle fatigue in human head and neck. Methods A musculoskeletal model of head neck complex was established based on AnyBody software platform, and the muscle strengths during head flexion were simulated according to the input data measured by Vicon motion capture system, which were validated with the literature data. Results The neck muscles played a major role during head flexion. The force assignment mode among muscles was different during 45% and 75% flexion process. The integral of muscle strengths on flexion angle WM could reflect the muscle fatigue to some extent. Since the largest WM was found in the semispinalis cervicis and multifidus muscles during head flexion, it may indicate that those muscles have the easy tendency to be fatigue. Conclusions The musculoskeletal model established in this paper can provide a technical support for the exploration of neck fatigue mechanism.
ABSTRACT
Objective of this study was to investigate the transcriptional regulation of BHLHB2 gene by the PML-RARα fusion protein in APL cells and reveal the pathogenesis of APL. RT-PCR was performed to detect the expression change of BHLHB2 before and after the induction of PML-RARα in PR9 cells, and its expression level after the treatment of ATRA in PR9 and APL patient derived NB4 cells. Chromatin immunoprecipitation (ChIP)-based PCR was used to analyze whether the BHLHB2 promoter could be bound by PML-RARα in vivo. A large-scale gene expression profile dataset was used to observe the expression pattern of BHLHB2 in AML. The results showed that the expression level of BHLHB2 was significantly reduced with the induction of PML-RARα and ATRA could reverse this inhibition in both PR9 and NB4 cells and increase the expression of BHLHB2. However, the expression of BHLHB2 could not be induced by ATRA in U937 cells which do not express PML-RARα. Mechanism study revealed that PML-RARα could bound to the promoter of BHLHB2 in vivo to regulate the the expression of BHLHB2. It was found that the expression of BHLHB2 was relatively lower in APL as compared with other subtypes of AML and normal bone marrow cells. It is concluded that BHLHB2 is the target of PML-RARα, and the expression of BHLHB2 is inhibited by PML-RARα through binding to its promoter in APL.