493 research outputs found
Erratum: Towards a muon collider
No full textThe original online version of this article was revised: The additional reference [139] has been added. Tao Han’s ORICD ID has been incorrectly assigned to Chengcheng Han and Chengcheng Han’s ORCID ID to Tao Han. Yang Ma’s ORCID ID has been incorrectly assigned to Lianliang Ma, and Lianliang Ma’s ORCID ID to Yang Ma. The original article has been corrected
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Erratum: Towards a muon collider
No full textThe original online version of this article was revised: The additional reference [139] has been added. Tao Han’s ORICD ID has been incorrectly assigned to Chengcheng Han and Chengcheng Han’s ORCID ID to Tao Han. Yang Ma’s ORCID ID has been incorrectly assigned to Lianliang Ma, and Lianliang Ma’s ORCID ID to Yang Ma. The original article has been corrected
Erratum: Towards a muon collider
No full textThe original online version of this article was revised: The additional reference [139] has been added. Tao Han’s ORICD ID has been incorrectly assigned to Chengcheng Han and Chengcheng Han’s ORCID ID to Tao Han. Yang Ma’s ORCID ID has been incorrectly assigned to Lianliang Ma, and Lianliang Ma’s ORCID ID to Yang Ma. The original article has been corrected
sj-docx-1-tam-10.1177_17588359211038477 – Supplemental material for TGFBR2 mutation predicts resistance to immune checkpoint inhibitors in patients with non-small cell lung cancer
No full textSupplemental material, sj-docx-1-tam-10.1177_17588359211038477 for TGFBR2 mutation predicts resistance to immune checkpoint inhibitors in patients with non-small cell lung cancer by Teng Li, Han Wang, Jiachen Xu, Chengcheng Li, Yudong Zhang, Guoqiang Wang, Yutao Liu, Shangli Cai, Wenfeng Fang, Junling Li and Zhijie Wang in Therapeutic Advances in Medical Oncology</p
Supplementary_Material_a_clean_copy - Influence of More Than 5 Years of Continuous Exposure to Antipsychotics on Cerebral Functional Connectivity of Chronic Schizophrenia
No full textSupplementary_Material_a_clean_copy for Influence of More Than 5 Years of Continuous Exposure to Antipsychotics on Cerebral Functional Connectivity of Chronic Schizophrenia by Qi Miao, Chengcheng Pu, Zhijiang Wang, Chao-Gan Yan, Chuan Shi, Qingjiu Cao, Xijin Wang, Zhang Cheng, Xue Han, Lei Yang, Yunyao Lai, Yanbo Yuan, Hong Ma, Keqing Li, Nan Hong and Xin Yu in The Canadian Journal of Psychiatry</p
Preparation and study of polystyrene/organic montmorillonite nanocomposite as lubricant additive of drilling fluid
No full textSkeletal Class III Malocclusion Is Associated with ADAMTS2 Variants and Reduced Expression in a Familial Case
No full textSkeletal Class III malocclusion with maxillary deficiency is a severe maxillofacial disease with unclear pathogenic mechanisms. We recruited a Han Chinese family who was clinically diagnosed with skeletal Class III malocclusion and maxillary deficiency. Using whole exome sequencing, a missense variant in ADAMTS2 (NM_014244: c.3506G>T: p.G1169V) was identified and predicted as deleterious by in silico tools. We also found ADAMTS2 variants associated with deficient maxillary development in a cohort. ADAMTS2 expression in HEK293 cells showed significant decrease due to the variant, which was also consistent in dental pulp stem cells from the proband and a healthy control. In the adamts2-knockdown zebrafish model, the length and width of the ethmoid plate, as well as the length of the palatoquadrate became significantly shorter than the control group (p < 0.001), while there was no significant difference in the length and width of the mandible. The expression of Sox3, which was required in early embryonic craniofacial development, was significantly downregulated in the adamts2-knockdown zebrafish embryos. Bioinformatic and cellular studies showed that the decreased expression of ADAMTS2 may inhibit downstream ErbB signaling pathway transduction and restrain subsequent osteogenesis in human adult mesenchymal stromal cells. Collectively, these data showed that ADAMTS2 (c.3506G>T: p.G1169V) may confer susceptibility to risk of skeletal Class III malocclusion with maxillary deficiency
FGFR1 variants contributed to families with tooth agenesis
No full textAbstract Background Tooth agenesis is a common dental anomaly that can substantially affect both the ability to chew and the esthetic appearance of patients. This study aims to identify possible genetic factors that underlie various forms of tooth agenesis and to investigate the possible molecular mechanisms through which human dental pulp stem cells may play a role in this condition. Results Using whole-exome sequencing of a Han Chinese family with non-syndromic tooth agenesis, a rare mutation in FGFR1 (NM_001174063.2: c.103G > A, p.Gly35Arg) was identified as causative and confirmed by Sanger sequencing. Via GeneMatcher, another family with a known variant (NM_001174063.2: c.1859G > A, p.Arg620Gln) was identified and diagnosed with tooth agenesis and a rare genetic disorder with considerable intrafamilial variability. Fgfr1 is enriched in the ectoderm during early embryonic development of mice and showed sustained low expression during normal embryonic development of Xenopus laevis frogs. Functional studies of the highly conserved missense variant c.103G > A showed deleterious effects. FGFR1 (c.103G > A) was overexpressed compared to wildtype and promoted proliferation while inhibiting apoptosis in HEK293 and human dental pulp stem cells. Moreover, the c.103G > A variant was found to suppress the epithelial-mesenchymal transition. The variant could downregulate ID4 expression and deactivate the TGF-beta signaling pathway by promoting the expression of SMAD6 and SMAD7. Conclusion Our research broadens the mutation spectrum associated with tooth agenesis and enhances understanding of the underlying disease mechanisms of this condition
QCD axion dark matter and the cosmic dipole problem
No full textThere is increasing evidence suggesting a discrepancy between the cosmic
dipole observed in the number count of distant galaxies and the one derived
from the cosmic microwave background (CMB). In this study, we investigate the
possibility that the cosmic dipole problem can be addressed by considering the
QCD axion, a hypothetical particle that arises from the spontaneous breaking of
the Peccei-Quinn symmetry and is postulated to constitute the dark matter in
our universe.Comment: 6 pages, 3 figures, version accepted by PR
Probing light bino and higgsinos at the LHC
No full textMotivated by the naturalness, we study a simplified Minimal Supersymmetric Standard Model (MSSM) scenario where only the bino-like lightest supersymmetric particle (LSP) and higgsino-like next-lightest supersymmetric particle (NLSP) are light. We first scan the parameter space of this scenario, considering the constraints from the Higgs mass, flavor physics, electroweak precision measurements and dark matter experiments. Then in the allowed parameter space, we perform a Monte Carlo simulation for the [Formula: see text] production followed by [Formula: see text] and [Formula: see text]. By examining the presently available trilepton bounds on the wino-like chargino/neutralino, we find that only a narrow region [Formula: see text] and [Formula: see text] on the plane of [Formula: see text] can be excluded. Finally, we explore the potential of trilepton signature in probing such a scenario at 14 TeV Large Hadron Collider (LHC) and find that the region with [Formula: see text] and [Formula: see text] can be covered at [Formula: see text] level with luminosity [Formula: see text].</jats:p
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