ABSTRACT
We present a novel approach for measuring the differential static scalar polarizability of a target ion utilizing a "polarizability scale" scheme with a reference ion co-trapped in a linear Paul trap. The differential static scalar polarizability of the target ion can be precisely extracted by measuring the ratio of the ac Stark shifts induced by an add-on infrared laser shed on both ions. This method circumvents the need for the calibration of the intensity of the add-on laser, which is usually the bottleneck for measurements of the polarizability of trapped ions. As a demonstration, ^{27}Al^{+} (the target ion) and ^{40}Ca^{+} (the reference ion) are used in this work, with an add-on laser at 1068 nm injected into the ion trap along the trap axis. The differential static scalar polarizability of ^{27}Al^{+} is extracted to be 0.416(14) a.u. by measuring the ratio of the ac Stark shifts of both ions. Compared to the most recent result [Phys. Rev. Lett. 123, 033201 (2019)PRLTAO0031-900710.1103/PhysRevLett.123.033201], the relative uncertainty of the differential static scalar polarizability of ^{27}Al^{+} is reduced by approximately a factor of 4, to 3.4%. This improvement is expected to be further enhanced by using an add-on laser with a longer wavelength.
ABSTRACT
Posterior cataract opacification(PCO)is the epithelial-mesenchymal transformation(EMT)of residual lens epithelial cells(LECs)after cataract surgery, resulting in opaque scar which is one of the main complications of cataract surgery. A large amount of fibronectin(FN)produced by LECs after cataract surgery binds to a variety of cell surface receptors, matrix components and growth factors to regulate cell behavior. The purpose of this article is to review the literatures on the treatment of PCO targeting fibronectin and provide references for clinical treatment of PCO. In this paper, the research status of fibronectin in PCO in recent years is reviewed.
ABSTRACT
<p><b>OBJECTIVE</b>To study the epidemiology and etiologic characteristics of a Dengue fever outbreak in Fuzhou from the beginning of September to the end of October in 2004 in order to understand the source of infection.</p><p><b>METHODS</b>Data on descriptive epidemiology was collected to study the characteristics and related factors to the epidemic. Dengue virus was isolated through the use of C6/36 cell line while viral serotypes were identified by indirect immunofluorecent assay with type-specific monoclonal antibody. The sources of infection were traced by nucleotide sequencing.</p><p><b>RESULTS</b>During the epidemic, 93 cases occured consistently with the region entomoplily growth and decay. The viruses of 6 strains isolated from 10 patients' blood specimens were identified as dengue virus type 1. Phylogenetic evidence suggested that the viral isolate had high genetic relation with the isolates from Kampuchea (DENV-1/KHM/2001; GenBank Accession No. L0904278).</p><p><b>CONCLUSION</b>The epidemic was caused by introduction of patients migrating into Fuzhou.</p>
