Criminal Law: Demise of “Status”—“Act” Distinction in Symptomatic Crimes of Narcotic Addiction

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Time Variation of Fine-Structure Constant Constrained by [O III] Emission-Lines at 1.1<z<3.7

[O III]$\lambda\lambda$4960,5008 doublet are often the strongest narrow emission lines in starburst galaxies and quasi-stellar objects (QSOs), and thus are a promising probe to possible variation of the fine-structure constant $\alpha$ over cosmic time. Previous such studies using QSOs optical spectra were limited to $z<1$. In this work, we constructed a sample of 40 spectra of Ly$\alpha$ emitting galaxies (LAEs) and a sample of 46 spectra of QSOs at $1.09<z<3.73$ using the VLT/X-Shooter near-infrared spectra publicly available. We measured the wavelength ratios of the two components of the spin-orbit doublet and accordingly calculated $\alpha(z)$ using two methods. Analysis on all of the 86 spectra yielded $\Delta\alpha/\alpha=(-3\pm6)\times10^{-5}$ with respect to the laboratory $\alpha$ measurements, consistent with no variation over the explored time interval. If assuming a uniform variation rate, we obtained $\alpha^{-1}{\rm d}\alpha/{\rm d}t = (-3\pm6)\times10^{-15}$ yr$^{-1}$ within the last 12 Gyrs. Extensive tests indicate that $\alpha$ variation could be better constrained using starburst galaxies' spectra than using QSO spectra in future studies.Comment: 24 pages, 22 figures. Accepted for publication in MNRA

Regulation of B cell fate by chronic activity of the IgE B cell receptor.

IgE can trigger potent allergic responses, yet the mechanisms regulating IgE production are poorly understood. Here we reveal that IgE+ B cells are constrained by chronic activity of the IgE B cell receptor (BCR). In the absence of cognate antigen, the IgE BCR promoted terminal differentiation of B cells into plasma cells (PCs) under cell culture conditions mimicking T cell help. This antigen-independent PC differentiation involved multiple IgE domains and Syk, CD19, BLNK, Btk, and IRF4. Disruption of BCR signaling in mice led to consistently exaggerated IgE+ germinal center (GC) B cell but variably increased PC responses. We were unable to confirm reports that the IgE BCR directly promoted intrinsic apoptosis. Instead, IgE+ GC B cells exhibited poor antigen presentation and prolonged cell cycles, suggesting reduced competition for T cell help. We propose that chronic BCR activity and access to T cell help play critical roles in regulating IgE responses