Identifying electronic transitions of defects in hexagonal boron nitride for quantum memories

A quantum memory is a crucial keystone for enabling large-scale quantum networks. Applicable to the practical implementation, specific properties, i.e., long storage time, selective efficient coupling with other systems, and a high memory efficiency are desirable. Though many quantum memory systems have been developed thus far, none of them can perfectly meet all requirements. This work herein proposes a quantum memory based on color centers in hexagonal boron nitride (hBN), where its performance is evaluated based on a simple theoretical model of suitable defects in a cavity. Employing density functional theory calculations, 257 triplet and 211 singlet spin electronic transitions have been investigated. Among these defects, we found that some defects inherit the $\Lambda$ electronic structures desirable for a Raman-type quantum memory and optical transitions can couple with other quantum systems. Further, the required quality factor and bandwidth are examined for each defect to achieve a 95\% writing efficiency. Both parameters are influenced by the radiative transition rate in the defect state. In addition, inheriting triplet-singlet spin multiplicity indicates the possibility of being a quantum sensing, in particular, optically detected magnetic resonance. This work therefore demonstrates the potential usage of hBN defects as a quantum memory in future quantum networks.Comment: 12 pages, 6 figure

Roles of matrix metalloproteinases in the cornea: A special focus on macular corneal dystrophy

Matrix metalloproteinases (MMPs) are endopeptidases that are responsible for the degradation of several components of the extracellular matrix (ECM) and some non-ECM proteins. MMPs are subdivided into 6 groups according to their structure and substrate specificity: collagenases, gelatinases, membrane-type MMPs, stromelysins, and matrilizines. Collagenases are important proteolytic tools during ECM remodeling, tissue regeneration, and organ development. MMPs, especially collagenases, have important roles in ocular processes such as retinal neurogenesis and corneal wound healing. MMP studies on eye research are limited, but there is growing evidence that MMP physiology is key for the ocular system, especially for the cornea. The cornea is predominantly composed of collagen fibrils, which form uniform lamellar lattices. Collagenase-driven ECM remodeling is essential for the cornea. Macular corneal dystrophy (MCD) is a rare inherited disease and characterized by progressive, insoluble accumulation of irregular substances in the corneal ECM. MCD can cause visual acuity loss up to blindness, and there is currently no treatment available. It has been recently reported that certain collagenases are downregulated in MCD disease progression. Here, we review the roles of MMPs in eye diseases and propose possible treatment strategies for MCD

Diagnostic utility of a targeted next-generation sequencing gene panel in the clinical suspicion of systemic autoinflammatory diseases: a multi-center study

Systemic autoinflammatory diseases (sAIDs) are a heterogeneous group of disorders, having monogenic inherited forms with overlapping clinical manifestations. More than half of patients do not carry any pathogenic variant in formerly associated disease genes. Here, we report a cross-sectional study on targeted Next-Generation Sequencing (NGS) screening in patients with suspected sAIDs to determine the diagnostic utility of genetic screening. Fifteen autoinflammation/immune-related genes (ADA2-CARD14-IL10RA-LPIN2-MEFV-MVK-NLRC4-NLRP12-NLRP3-NOD2-PLCG2-PSTPIP1-SLC29A3-TMEM173-TNFRSF1A) were used to screen 196 subjects from adult/pediatric clinics, each with an initial clinical suspicion of one or more sAID diagnosis with the exclusion of typical familial Mediterranean fever (FMF) patients. Following the genetic screening, 140 patients (71.4%) were clinically followed-up and re-evaluated. Fifty rare variants in 41 patients (20.9%) were classified as pathogenic or likely pathogenic and 32 of those variants were located on the MEFV gene. We detected pathogenic or likely pathogenic variants compatible with the final diagnoses and inheritance patterns in 14/140 (10%) of patients for the following sAIDs: familial Mediterranean fever (n=7), deficiency of adenosine deaminase 2 (n=2), mevalonate kinase deficiency (n=2), Muckle-Wells syndrome (n=1), Majeed syndrome (n=1), and STING-associated vasculopathy with onset in infancy (n=1). Targeted NGS panels have impact on diagnosing rare monogenic sAIDs for a group of patients. We suggest that MEFV gene screening should be first-tier genetic testing especially in regions with high carrier rates. Clinical utility of multi-gene testing in sAIDs was as low as expected, but extensive genome-wide familial analyses in combination with exome screening would enlighten additional genetic factors causing disease