40 research outputs found
Lee filtration structure of torus links
We determine the quantum filtration structure of the Lee homology of all
torus links. In particular, this determines the -invariant of a torus link
equipped with any orientation. In the special case , our result
confirms a conjecture of Pardon, as well as a conjecture of
Manolescu-Marengon-Sarkar-Willis which establishes an adjunction-type
inequality of the -invariant for cobordisms in .
We also give a few applications of this adjunction inequality.Comment: 22 pages, 4 figures in color; final version, to appear in Geometry
and Topolog
Toroidal Hitomezashi Patterns
We define Hitomezashi patterns and loops on a torus and provide several
structural results for such loops. For a given pattern, our main theorems give
optimal residual information regarding the Hitomezashi loop length, loop count,
as well as possible homology classes of such loops. Special attention is paid
to toroidal Hitomezashi patterns that are symmetric with respect to the
diagonal x = y.Comment: 15 pages, 9 figure
A Short Proof to Defant and Kravitz's theorem on the Length of Hitomezashi Loops
We provide a shorter proof to Defant and Kravitz's theorem (arXiv:2201.03461,
Theorem 1.2) on the length of Hitomezashi loops modulo 8.Comment: 4 pages, 2 figure
Intention-Aware Planner for Robust and Safe Aerial Tracking
The intention of the target can help us to estimate its future motion state
more accurately. This paper proposes an intention-aware planner to enhance
safety and robustness in aerial tracking applications. Firstly, we utilize the
Mediapipe framework to estimate target's pose. A risk assessment function and a
state observation function are designed to predict the target intention.
Afterwards, an intention-driven hybrid A* method is proposed for target motion
prediction, ensuring that the target's future positions align with its
intention. Finally, an intention-aware optimization approach, in conjunction
with particular penalty formulations, is designed to generate a
spatial-temporal optimal trajectory. Benchmark comparisons validate the
superior performance of our proposed methodology across diverse scenarios. This
is attributed to the integration of the target intention into the planner
through coupled formulations.Comment: 7 pages, 10 figures, submitted to 2024 IEEE International Conference
on Robotics and Automation (ICRA
Efficacy and safety of anterior transposition of the ulnar nerve for distal humerus fractures: A systematic review and meta-analysis
BackgroundThis systematic review and meta-analysis was performed to summarize available evidence of anterior transposition of the ulnar nerve for patients with distal humerus fractures.Materials and MethodsThe databases were searched from PubMed, Cochrane, Embase, Scopus, Web of Science, Chinese National Knowledge Infrastructure (CNKI), Chongqing VIP Database (VIP), and Wan Fang Database up to June 2022. The clinical outcome included operation time, fracture healing time, hospital stays, elbow joint function, and ulnar neuritis rate. Statistical analysis was performed with Review Manager 5.3 (Cochrane Collaboration).ResultsA total of 17 studies were included (8 RCTs and 9 retrospective studies), and 1280 patients were analyzed. The results of this meta-analysis showed anterior transposition group had longer operation time (MD = 20.35 min, 95%CI: 12.56–28.14, P < 0.00001). There was no significant difference in fracture healing time (SMD = −0.50, 95%CI: −1.50–0.50, P = 0.33), hospital stays (MD = −1.23 days, 95%CI: −2.72–−0.27, P = 0.11), blood loss (MD = 2.66 ml, 95%CI: −2.45–7.76, P = 0.31), and ulnar neuritis rate (OR = 1.23, 95%CI: 0.63–2.42, P = 0.54) between two groups. Finally, elbow joint motion, elbow joint function, fracture nonunion, and post-operative infection (P > 0.05) between two groups were not significantly statistic difference.ConclusionThis meta-analysis showed that anterior transposition group is not superior to non-transposition group for patients with distal humerus fractures without ulnar nerve injury. On the contrary, non-transposition group have shorter operation time than that of anterior transposition group. Non-transposition group did not increase the post-operative ulnar neuritis rate. Therefore, both anterior transposition group and non- transposition group are the treatment options for patients with distal humerus fractures without ulnar nerve injury. Besides, these findings need to be further verified by multi-center, double-blind, and large sample RCTs
原位表征技术揭示析氢电催化剂活性中心
文章简介课题组以导电碳布上生长的氢氧化镍纳米片为模板,通过与对苯二硫酚配体反应,成功合成出具有平面Ni(SR)4配位结构的镍—硫醇配位聚合物纳米片,并发现该材料在碱性析氢测试中,催化活性随测试时间逐渐加存在明显诱导期的现象。在保持20m A/cm2的电流密度条件下,析氢所需过电位逐渐降低,约10小时后该
MicroRNA-275 and its target vitellogenin-2 are crucial in ovary development and blood digestion of Haemaphysalis longicornis
Background: The hard tick Haemaphysalis longicornis is widely distributed in eastern Asia, New Zealand and Australia and is considered the major vector of Theileria and Babesia, harmful parasites to humans and animals. Female ticks need successful blood meals to complete the life-cycle. Therefore, elucidation of the underlying molecular mechanisms of H. longicornis development and reproduction is considered important for developing control strategies against the tick and tick-borne pathogens.
Methods: Luciferase assays were used to identify the targets of micro RNA miR-275 in vitro. RNAi of Vitellogenin (Vg) was used in phenotype rescue experiments of ticks with miR-275 inhibition, and these analyses were used to identify the authentic target of miR-275 in vivo. The expression of miR-275 in different tissues and developmental stages of ticks was assessed by real-time PCR. To elucidate the functions of miR-275 in female ticks, we injected a miR-275 antagomir into female ticks and observed the phenotypic changes. Statistical analyses were performed with GraphPad5 using Student’s t-test.
Results: In this study, we identified Vg-2 as an authentic target of miR-275 both in vitro and in vivo by luciferase assays and phenotype rescue experiments. miR-275 plays the regulatory role in a tissue-specific manner and differentially in developmental stages. Silencing of miR-275 resulted in blood digestion problems, substantially impaired ovary development and significantly reduced egg mass (P < 0.0001). Furthermore, RNAi silencing of Vg-2 not only impacted the blood meal uptake (P < 0.05) but also the egg mass (P < 0.05). Significant rescue was observed in miR-275 knockout ticks when RNAi was applied to Vg-2.
Conclusion: To our knowledge, this study is the first demonstration that miR-275 targets Vg-2 in H. longicornis and regulates the functions of blood digestion and ovary development. These findings improve the molecular understanding of tick development and reproduction
Structural and mechanistic insights into the biosynthesis of CDP-archaeol in membranes
The divergence of archaea, bacteria and eukaryotes was a fundamental step in evolution. One marker of this event is a major difference in membrane lipid chemistry between these kingdoms. Whereas the membranes of bacteria and eukaryotes primarily consist of straight fatty acids ester-bonded to glycerol-3-phosphate, archaeal phospholipids consist of isoprenoid chains ether-bonded to glycerol-1-phosphate. Notably, the mechanisms underlying the biosynthesis of these lipids remain elusive. Here, we report the structure of the CDP-archaeol synthase (CarS) of Aeropyrum pernix (ApCarS) in the CTP- and Mg(2+)-bound state at a resolution of 2.4 Å. The enzyme comprises a transmembrane domain with five helices and cytoplasmic loops that together form a large charged cavity providing a binding site for CTP. Identification of the binding location of CTP and Mg(2+) enabled modeling of the specific lipophilic substrate-binding site, which was supported by site-directed mutagenesis, substrate-binding affinity analyses, and enzyme assays. We propose that archaeol binds within two hydrophobic membrane-embedded grooves formed by the flexible transmembrane helix 5 (TM5), together with TM1 and TM4. Collectively, structural comparisons and analyses, combined with functional studies, not only elucidated the mechanism governing the biosynthesis of phospholipids with ether-bonded isoprenoid chains by CTP transferase, but also provided insights into the evolution of this enzyme superfamily from archaea to bacteria and eukaryotes.Cell Research advance online publication 29 September 2017; doi:10.1038/cr.2017.122
Transcriptional regulatory control of mammalian nephron progenitors revealed by multi-factor cistromic analysis and genetic studies.
Nephron progenitor number determines nephron endowment; a reduced nephron count is linked to the onset of kidney disease. Several transcriptional regulators including Six2, Wt1, Osr1, Sall1, Eya1, Pax2, and Hox11 paralogues are required for specification and/or maintenance of nephron progenitors. However, little is known about the regulatory intersection of these players. Here, we have mapped nephron progenitor-specific transcriptional networks of Six2, Hoxd11, Osr1, and Wt1. We identified 373 multi-factor associated \u27regulatory hotspots\u27 around genes closely associated with progenitor programs. To examine their functional significance, we deleted \u27hotspot\u27 enhancer elements for Six2 and Wnt4. Removal of the distal enhancer for Six2 leads to a ~40% reduction in Six2 expression. When combined with a Six2 null allele, progeny display a premature depletion of nephron progenitors. Loss of the Wnt4 enhancer led to a significant reduction of Wnt4 expression in renal vesicles and a mildly hypoplastic kidney, a phenotype also enhanced in combination with a Wnt4 null mutation. To explore the regulatory landscape that supports proper target gene expression, we performed CTCF ChIP-seq to identify insulator-boundary regions. One such putative boundary lies between the Six2 and Six3 loci. Evidence for the functional significance of this boundary was obtained by deep sequencing of the radiation-induced Brachyrrhine (Br) mutant allele. We identified an inversion of the Six2/Six3 locus around the CTCF-bound boundary, removing Six2 from its distal enhancer regulation, but placed next to Six3 enhancer elements which support ectopic Six2 expression in the lens where Six3 is normally expressed. Six3 is now predicted to fall under control of the Six2 distal enhancer. Consistent with this view, we observed ectopic Six3 in nephron progenitors. 4C-seq supports the model for Six2 distal enhancer interactions in wild-type and Br/+ mouse kidneys. Together, these data expand our view of the regulatory genome and regulatory landscape underpinning mammalian nephrogenesis
Transcriptional regulatory control of mammalian nephron progenitors revealed by multi-factor cistromic analysis and genetic studies
Nephron progenitor number determines nephron endowment; a reduced nephron count is linked to the onset of kidney disease. Several transcriptional regulators including Six2, Wt1, Osr1, Sall1, Eya1, Pax2, and Hox11 paralogues are required for specification and/or maintenance of nephron progenitors. However, little is known about the regulatory intersection of these players. Here, we have mapped nephron progenitor-specific transcriptional networks of Six2, Hoxd11, Osr1, and Wt1. We identified 373 multi-factor associated ‘regulatory hotspots’ around genes closely associated with progenitor programs. To examine their functional significance, we deleted ‘hotspot’ enhancer elements for Six2 and Wnt4. Removal of the distal enhancer for Six2 leads to a ~40% reduction in Six2 expression. When combined with a Six2 null allele, progeny display a premature depletion of nephron progenitors. Loss of the Wnt4 enhancer led to a significant reduction of Wnt4 expression in renal vesicles and a mildly hypoplastic kidney, a phenotype also enhanced in combination with a Wnt4 null mutation. To explore the regulatory landscape that supports proper target gene expression, we performed CTCF ChIP-seq to identify insulator-boundary regions. One such putative boundary lies between the Six2 and Six3 loci. Evidence for the functional significance of this boundary was obtained by deep sequencing of the radiation-induced Brachyrrhine (Br) mutant allele. We identified an inversion of the Six2/Six3 locus around the CTCF-bound boundary, removing Six2 from its distal enhancer regulation, but placed next to Six3 enhancer elements which support ectopic Six2 expression in the lens where Six3 is normally expressed. Six3 is now predicted to fall under control of the Six2 distal enhancer. Consistent with this view, we observed ectopic Six3 in nephron progenitors. 4C-seq supports the model for Six2 distal enhancer interactions in wild-type and Br/+ mouse kidneys. Together, these data expand our view of the regulatory genome and regulatory landscape underpinning mammalian nephrogenesis