High-temperature, high-pressure (HPHT) nanodiamond (ND) hosts nitrogen-vacancy (NV) centers, solid-state qubits that enable room-temperature quantum sensing by all-optical magnetometry, electrometry, and thermometry. However, the covalent surface functionalization of nanoscale diamond remains largely limited to carboxylate-based chemistries. Amine termination is particularly attractive because theoretical studies predict suppression of midgap states and extended electron-spin coherence times. Recently, chemical activation of alcohol-terminated NDs to alkyl bromides (ND-Br) using SOBr2 has enabled nucleophilic substitution through a carbocation intermediate, allowing formation of simple amine terminations. Here, we evaluate whether sterically demanding amines can form covalent diamond-nitrogen bonds on ND-Br surfaces. ND-Br was reacted with branched, linear, and cyclic amines, including polyethylenimine, diethylenetriamine, and melamine. X-ray spectroscopies were used to confirm successful and to probe the resulting electronic structure at the diamond-amine interface. These results expand the chemical toolbox for tuning diamond surface dipoles and electron affinity, providing new pathways for engineering nanodiamond surfaces for quantum sensing and photocatalysis applications.
We investigated 1-D and 2-D chemical depth mapping using SIMS, XPS and TEM-EDX. For strain/lattice spacing engineering effects, we used XRD and Raman analysis for Ge, Sn and C implantation into Si and SiGe wafers followed by RTA or laser melt annealing to form surface thin layers of SiGe, SiGeSn and SiGeC. Up to 1.15
On June 5, 2019, the SEC adopted the Regulation Best Interest Rule Package, consisting of (i) Regulation Best Interest: The Broker-Dealer Standard of Conduct (“Reg. BI”); (ii) Form CRS Relationship Summary and Amendments to Form ADV; (iii) the SEC Interpretation Regarding Standard of Conduct for Investment Advisers; and (iv) the SEC Interpretation Regarding the “Solely Incidental” Prong of the Broker-Dealer Exclusion from the Definition of Investment Adviser. Brokers were obligated to begin compliance with Reg. BI as of June 30, 2020. Reg. BI contains four component sections mandating duties for brokers and firms: Disclosure, Care, Conflicts of Interest, and Compliance. While it is the SEC ‘s position that Reg. BI does not create any new private right of action or right of rescission, the Rule does set forth duties to which brokers and firms must adhere. Therefore, these obligations may be used as support for a negligence claim for (i) a recommendation that is not in the investor’s best interests; or (ii) failure to supervise. This article will address how to assess the various Reg. BI obligations when pleading and advancing a potential negligence claim. It also includes a discussion of important considerations and documents to consider when assessing each duty.
Introduction: Saphenous veins (SVs) are frequently used in CABG surgery, but over 50% of the SV grafts fail in the first 10 years after surgery due to neointima formation. Long non-coding RNAs (lncRNAs) have emerged as attractive therapeutic targets and biomarkers for cardiovascular disease. However, studies on their role and mechanisms in humans are limited. This study aimed to unravel epigenetic mechanisms of neointima formation in human SVs and investigate the role of candidate lncRNAs in key vascular cell functions pertinent to neointima formation. Methods and Results: By using an ex vivo model of human SV graft disease wherein segments of human SV are incubated in tissue culture, we performed RNA-sequencing on human SV with and without neointima formation to interrogate the global transcriptomic changes, and determined 699 differentially expressed novel lncRNAs during neointimal formation. We then identified BAZ1A-antisense (AS)1 as a novel lncRNA highly upregulated during neointima formation. BAZ1A-AS1 overlaps antisense to its cis- regulatory gene, BAZ1A , which was reported to play a role in oxidative stress and DNA damage repair response. We found that one isoform of BAZ1A-AS1 primarily localizes to the nucleus of VSMCs. Interestingly, UV exposure of vascular smooth muscle cells (VSMCs) isolated from human SV induced significant upregulation of BAZ1A and BAZ1A-AS1, suggesting that BAZ1A-AS1 could be associated with chromatin repair processes activated during neointima formation. To investigate whether BAZ1A-AS1 can regulate VSMC functions pertinent to neointima formation, VSMCs were transfected with BAZ1A-AS1 antisense gapmers. Knockdown of BAZ1A-AS1 showed reduced cell proliferation and migration, and increased cell death and DNA damage in VSMCs. Furthermore, role of BAZ1A during neointima formation in vivo is currently under investigation in a carotid artery ligation model using BAZ1A knockout mice. Conclusions: We identified BAZ1A-AS1 as a novel lncRNA associated with neointima formation in human SV, and targeted inhibition of BAZ1A-AS1 or its cis-regulator gene BAZ1A could be a promising strategy for SV graft disease.
