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Static Shape Adjustment and Actuator Layered Optimization for Planar Phased Array Satellite Antenna
Ji-Yang Zhou,Guang-Yu Lu,Guo-Ping CAI,Guang-Qiang Fang,Liang-Liang Lv,Jun-Wei Shi 한국항공우주학회 2019 International Journal of Aeronautical and Space Sc Vol.20 No.4
Shape accuracy is of great importance in space antennas, especially in large-scale planar phased array antenna. To maintain the performance of the planar phased array antenna, shape accuracy must be strictly controlled. This paper proposes an optimization method using diagonal cables as actuators to achieve the shape adjustment. As for shape control, actuator placement has a significant impact on the controlled shape accuracy. Misplaced actuators always lead to control problems, and the desired performance may not be achieved with any choice of control forces, so the actuator placement optimization is needed. The optimization problem is challenging because of the mixed discrete–continuous nature of design variables: the actuator placement corresponds to discrete variables and the control forces are continuous variables. A layered optimization method is proposed in this paper to solve the optimal actuator placement and the corresponding control forces. A genetic algorithm is applied in the outside layer to achieve the optimization of the actuator placement, and the quadratic programming method is used in the inside layer to get the corresponding optimal control forces. The proposed layered optimization method is successfully applied to the large-scale planar phased array antenna. Using this method, the influence of the number of actuators on the controlled shape accuracy is also studied.
Yang Zou,Shuo Ji,Hui Wen Yang,Tao Ma,Yue Kun Fang,Zhi Cheng Wang,Miao Miao Liu,Ping Hui Zhou,Zheng Qi Bao,Chang Chun Zhang,Yu Chen Ye 대한척추신경외과학회 2024 Neurospine Vol.21 No.1
Objective: This study aimed to evaluate the effects of 2 endoscopic spine surgeries on the biomechanical properties of normal and osteoporotic spines. Methods: Based on computed tomography images of a healthy adult volunteer, 6 finite element models were created. After validating the normal intact model, a concentrated force of 400 N and a moment of 7.5 Nm were exerted on the upper surface of L3 to simulate 6 physiological activities of the spine. Five types of indices were used to assess the biomechanical properties of the 6 models, range of motion (ROM), maximum displacement value, intervertebral disc stress, maximum stress value, and articular protrusion stress, and by combining them with finite element stress cloud. Results: In normal and osteoporotic spines, there was no meaningful change in ROM or disc stress in the 2 surgical models for the 6 motion states. Model N1 (osteoporotic percutaneous transforaminal endoscopic discectomy model) showed a decrease in maximum displacement value of 20.28% in right lateral bending. Model M2 (unilateral biportal endoscopic model) increased maximum displacement values of 16.88% and 17.82% during left and right lateral bending, respectively. The maximum stress value of L4–5 increased by 11.72% for model M2 during left rotation. In addition, using the same surgical approach, ROM, maximum displacement values, disc stress, and maximum stress values were more significant in the osteoporotic model than in the normal model. Conclusion: In both normal and osteoporotic spines, both surgical approaches were less disruptive to the physiologic structure of the spine. Furthermore, using the same endoscopic spine surgery, normal spine biomechanical properties are superior to osteoporotic spines.
Ji-Chang Zhou,Yu-Mei Zhu,Zheng Chen,Shan He,Shi-jie Zheng,Jun-luan Mo,Xiao-Li Liu,Chun-mei Gong,Bin Hou,Hui Yang 한국유전학회 2015 Genes & Genomics Vol.37 No.5
Two single nucleotide polymorphisms (SNPs), rs2280788 (-28C[G) and rs2107538 (-403G[A), in the promoter region of chemokine (C–C motif) ligand 5 (CCL5) was reported to be involved in the immunoglobulin E (IgE) expression and IgE-mediated allergic reactions. This study was to investigate the characteristics of total serum IgE level, specific allergen sensitivities and the two SNPs in the allergic skin disease (ASD) patients. ASD patients visiting the dermatological outpatient department of a local hospital were included with certain criteria, and the fasting venous blood was sampled for analysis. Total serum IgE was assayed with an ELISA kit, and 14 kinds of allergen-specific IgE were tested with an allergen screening system. The polymerase chain reaction–restriction fragment length polymorphism method was used to analyze the two SNPs. Among the finally included 437 patients aged from 16 to 85 years, 68.2 % was positive for the total serum IgE, 49.2 % was positive for at least one of the assayed allergen-specific IgE, and 35.0 % was sensitive to house dust mite. In the SNPs analysis, the GG/(GA?AA) ratio and G/A ratio for the -403G[A locus in the male and/or female C45 years subgroup were significantly lower in the total serum IgE positive patients than in the negative patients (P\0.05). Weak linkage disequilibrium was found between -403A and -28C alleles in male subgroups adjusted by age. Conclusively, house dust mite was the most common allergen in ASD patients, and -403A allele of CCL5 promoter was a risk factor for IgE-mediated sensitization.
Yang, Jian-Zhou,Ji, Ai-Fang,Wang, Jin-Sheng,Chen, Zhong-Yi,Wen, Shi Wu Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.9
RASSF1A has been reported to be a candidate tumor suppressor in esophageal squamous cell carcinoma (ESCC). However, the association between RASSF1A promoter methylation and ESCC remains unclear. Eligible studies were identified through searching PubMed, Medline, Web of Science, and the China National Knowledge Infrastucture database. Studies were pooled and odds ratios (ORs) with corresponding confidence intervals (CIs) were calculated. Funnel plots were also performed to evaluate publication bias. Twelve studies involving 859 cases and 675 controls were included in this meta-analysis. A significant association was observed between RASSF1A methylation and ESCC overall (OR = 11.7, 95% CI: 6.59-20.9, z=8.36, P<0.00001). Subgroup analysis showed that the OR for heterogeneous tissues was 5.35 (95% CI = 2.95-9.71) while for autologous tissues it was 16.0 (8.31-30.96). For patient sample size, the OR for the <50 subgroup was 9.92 (95% CI = 2.88-34.2) and for the 50 case group was 13.1 (95% CI = 6.59-25.91). The OR for a relationship between RASSF1A methylation and TNM stages was 0.27 (95% CI=0.10-0.77), whereas there were no significant differences in RASSF1A methylation in relation to gender and differentiation among ESCC cases. This meta-analysis suggests a significant association between RASSF1A methylation and ESCC.
Zhou Dan,Jang Ji Min,Yang Goowon,Ha Hae Chan,Fu Zhicheng,Kim Dae Kyong 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.6
Cardiovascular diseases (CVDs) are the most common cardiovascular system disorders. Cellular senescence is a key mechanism associated with dysfunction of aged vascular endothelium. Hyaluronic acid and proteoglycan link protein 1 (HAPLN1) has been known to non-covalently link hyaluronic acid (HA) and proteoglycans (PGs), and forms and stabilizes HAPLN1-containing aggregates as a major component of extracellular matrix. Our previous study showed that serum levels of HAPLN1 decrease with aging. Here, we found that the HAPLN1 gene expression was reduced in senescent human umbilical vein endothelial cells (HUVECs). Moreover, a recombinant human HAPLN1 (rhHAPLN1) decreased the activity of senescence-associated β-gal and inhibited the production of senescence-associated secretory phenotypes, including IL-1β, CCL2, and IL-6. rhHAPLN1 also downregulated IL-17A levels, which is known to play a key role in vascular endothelial senescence. In addition, rhHAPLN1 protected senescent HUVECs from oxidative stress by reducing cellular reactive oxygen species levels, thus promoting the function and survival of HUVECs and leading to cellular proliferation, migration, and angiogenesis. We also found that rhHAPLN1 not only increases the sirtuin 1 (SIRT1) levels, but also reduces the cellular senescence markers levels, such as p53, p21, and p16. Taken together, our data indicate that rhHAPLN1 delays or inhibits the endothelial senescence induced by various aging factors, such as replicative, IL-17A, and oxidative stress-induced senescence, thus suggesting that rhHAPLN1 may be a promising therapeutic for CVD and atherosclerosis.
Yang, Ji-Yun,Zhang, Sizhong,Zhou, Qin,Guo, Hong,Zhang, Ke,Zheng, Rong,Xiao, Cuiying Korean Society for Biochemistry and Molecular Biol 2007 Journal of biochemistry and molecular biology Vol.40 No.4
Autosomal recessive polycystic kidney disease (ARPKD) is one of the important genetic disorders in pediatric practice. Mutation of the polycystic kidney and hepatic disease gene 1 (PKHD1) was identified as the cause of ARPKD. The gene encodes a 67-exon transcript for a large protein of 4074 amino acids termed fibrocystin, but its function remains unknown. The neoplastic-like in cystic epithelial proliferation and the epidermal growth factor/epidermal growth factor receptor (EGF/EGFR) axis overactivity are known as the most important characteristics of ARPKD. Since the misregulation of $Ca^{2+}$ signaling may lead to aberrant structure and function of the collecting ducts in kidney of rat with ARPKD, present study aimed to investigate the further mechanisms of abnormal proliferation of cystic cells by inhibition of PKHD1 expression. For this, a stable PKHD1-silenced HEK-293T cell line was established. Then cell proliferation rates, intracellular $Ca^{2+}$ concentration and extracellular signal-regulated kinase 1/2 (ERK1/2) activity were assessed after treatment with EGF, a calcium channel blocker and agonist, verapamil and Bay K8644. It was found that PKHD1-silenced HEK-293T cell lines were hyperproliferative to EGF stimulation. Also PKHD1-silencing lowered the intracellular $Ca^{2+}$ and caused EGF-induced ERK1/2 overactivation in the cells. An increase of intracellular $Ca^{2+}$ in PKHD1-silenced cells repressed the EGF-dependent ERK1/2 activation and the hyperproliferative response to EGF stimulation. Thus, inhibition of PKHD1 can cause EGF-induced excessive proliferation through decreasing intracellular $Ca^{2+}$ resulting in EGF-induced ERK1/2 activation. Our results suggest that the loss of fibrocystin may lead to abnormal proliferation in kidney epithelial cells and cyst formation in ARPKD by modulation of intracellular $Ca^{2+}$.
Molecular Analyses of the Metallothionein Gene Family in Rice (Oryza sativa L.)
Zhou, Gongke,Xu, Yufeng,Li, Ji,Yang, Lingyan,Liu, Jin-Yuan Korean Society for Biochemistry and Molecular Biol 2006 Journal of biochemistry and molecular biology Vol.39 No.5
Metallothioneins are a group of low molecular mass and cysteine-rich metal-binding proteins, ubiquitously found in most living organisms. They play an important role in maintaining intracellular metal homeostasis, eliminating metal toxification and protecting against intracellular oxidative damages. Analysis of complete rice genome sequences revealed eleven genes encoding putative metallothionein (OsMT), indicating that OsMTs constitute a small gene family in rice. Expression profiling revealed that each member of the OsMT gene family differs not only in sequence but also in their tissue expression patterns, suggesting that these isoforms may have different functions they perform in specific tissues. On the basis of OsMT structural and phylogenetic analysis, the OsMT family was classified as two classes and class I was subdivided into four types. Additionally, in this paper we also present a complete overview of this family, describing the gene structure, genome localization, upstream regulatory element, and exon/intron organization of each member in order to provide valuable insight into this OsMT gene family.