Diamond
membrane devices containing optically coherent nitrogen-vacancy
(NV) centers are key to enable novel cryogenic experiments such as
optical ground-state cooling of hybrid spin-mechanical systems and
efficient entanglement distribution in quantum networks. Here, we
report on the fabrication of a (3.4 ± 0.2) μm thin, smooth
(surface roughness rq < 0.4 nm over
an area of 20 μm by 30 μm) diamond membrane containing
individually resolvable, narrow linewidth (< 100 MHz) NV centers.
We fabricate this sample via a combination of high-energy electron
irradiation, high-temperature annealing, and an optimized etching
sequence found via a systematic study of the diamond surface evolution
on the microscopic level in different etch chemistries. Although our
particular device dimensions are optimized for cavity-enhanced entanglement
generation between distant NV centers in open, tunable microcavities,
our results have implications for a broad range of quantum experiments
that require the combination of narrow optical transitions and micrometer-scale
device geometry.
Breast cancer cells show overexpression of estrogen receptor (ER) α relative to ERβ compared to normal breast tissues. This observation has lead to the hypothesis that ERβ may modulate the proliferative effect of ERα. This study investigated how variable cellular expression ratios of the ERα and ERβ modulate the effects on cell proliferation induced by ERα or ERβ agonists, respectively. Using human osteosarcoma (U2OS) ERα or ERβ reporter cells, propyl-pyrazole-triol (PPT) was shown to be a selective ERα and diarylpropionitrile (DPN) a preferential ERβ modulator. The effects of these selective estrogen receptor modulators (SERMs) and of the model compound E2 on the proliferation of T47D human breast cancer cells with tetracycline-dependent expression of ERβ (T47D-ERβ) were characterized. E2-induced cell proliferation of cells in which ERβ expression was inhibited was similar to that of the T47D wild-type cells, whereas this E2-induced cell proliferation was no longer observed when ERβ expression in the T47D-ERβ cells was increased. In the T47D-ERβ cell line, DPN also appeared to be able to suppress cell proliferation when levels of ERβ expression were high. In the T47D-ERβ cell line, PPT was unable to suppress cell proliferation at all ratios of ERα/ERβ expression, reflecting its ability to activate only ERα and not ERβ. It is concluded that effects of estrogen-like compounds on cell proliferation are dependent on the actual ERα/ERβ expression levels in these cells or tissues and the potential of the estrogen agonists to activate ERα and/or ERβ.
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