THE DEUTERIUM SULFIDE BAND AT 4590cm−14590 cm^{-1}

Author Institution: Department of Physics, Michigan State College; Mallinckrodt Chemical Laboratories, Harvard University; Mallinckrodt Chemical Laboratories, National Bureau of StandardsThe absorption of deuterium sulfide has been observed and measured under high resolution from 4500 to $4675 cm^{-1}$. The rotational structure has been analyzed through the use of published energy and line strength tables for the rigid asymmetric rotor. A classical centrifugal distortion was applied to the rigid energy levels. The absorption is attributed to the vibrational band having an excited state with the quantum numbers $(n_{1}, n_{2}, n_{3}) = (1, 1, 1)$. More than 100 lines with $J<8$ have been assigned with an average deviation of less than $.08 cm^{-1}$. Using the ground state inertial constants the D-S distance is calculated to be 1.345A and the DSD angle to be $92^{\circ}16^{\prime}$, in excellent agreement with similar structural parameters determined for $H_{2} S$ from infrared studies

National Bureau of Standards Reports

Reports discussing bands of common gases that have been tabulated and remeasured wherever necessary from 2 to 16 microns to obtain an accuracy of about 0.03 cm-1 throughout the region and to provide good calibrating points at frequent intervals. Some 600 rotation-vibration lines are illustrated in 20 spectrograms and wavenumbers are listed in companion tables with considerable intercomparison with worthy data obtained in other laboratories. The absorption bands were remeasured or calibrated by using either a precisely graduated grating circle or standard atomic lines with the fringe system formed by a Fabry-Perot interferometer. Characteristic features of the individual bands are discussed briefly and references to other publications are given. The substances used for calibration include H2O, CO2, CO, HCl, HBr, NH3, C2H2, CH4, N2O, and polystyrene film

Attenuation of PKR-like ER Kinase (PERK) Signaling Selectively Controls Endoplasmic Reticulum Stress-induced Inflammation Without Compromising Immunological Responses

Inflammation and endoplasmic reticulum (ER) stress are associated with many neurological diseases. ER stress is brought on by the accumulation of misfolded proteins in the ER, which leads to activation of the unfolded protein response (UPR), a conserved pathway that transmits signals to restore homeostasis or eliminate the irreparably damaged cell. We provide evidence that inhibition or genetic haploinsufficiency of protein kinase R-like endoplasmic reticulum kinase (PERK) can selectively control inflammation brought on by ER stress without impinging on UPR-dependent survival and adaptive responses or normal immune responses. Using astrocytes lacking one or both alleles of PERK or the PERK inhibitor GSK2606414, we demonstrate that PERK haploinsufficiency or partial inhibition led to reduced ER stress-induced inflammation (IL-6, CCL2, and CCL20 expression) without compromising prosurvival responses. In contrast, complete loss of PERK blocked canonical PERK-dependent UPR genes and promoted apoptosis. Reversal of eIF2α-mediated translational repression using ISRIB potently suppressed PERK-dependent inflammatory gene expression, indicating that the selective modulation of inflammatory gene expression by PERK inhibition may be linked to attenuation of eIF2α phosphorylation and reveals a previously unknown link between translational repression and transcription of inflammatory genes. Additionally, ER-stressed astrocytes can drive an inflammatory M1-like phenotype in microglia, and this can be attenuated with inhibition of PERK. Importantly, targeting PERK neither disrupted normal cytokine signaling in astrocytes or microglia nor impaired macrophage phagocytosis or T cell polarization. Collectively, this work suggests that targeting PERK may provide a means for selective immunoregulation in the context of ER stress without disrupting normal immune function