I. The Broadening of the Resonance Lines of Rubidium Under Different Homogenous Pressures of its Own Vapor. II. The Broadening, Asymmetry and Drift of Rubidium Resonance Lines Under Homogenous Pressures of Helium and Argon up to 100 Atmospheres

I. The broadening of the resonance lines of rubidium in absorption under pressures up to 152 mm. Hg of its own homogeneous vapor was studied by means of a 21-foot grating. Under pressures below 1 mm. Hg the broadening of the lines was very symmetrical and the line contours could be described by the dispersion formula, but when the pressure was high the lines exhibited asymmetrical broadening. The 2P½ component showed red, while the 2P3/2 component showed violet asymmetry. The broadening of the shorter wavelength component is greater than that of the longer wavelength component. Both lines showed the proportionality of the width with N. The experimental half width is greater than that predicted by Prof. Houston's theory by a factor of 1½. A narrow band was observed near the shorter wavelength side of the 2P½ component and a similar one near the longer wavelength side of the 2P3/2 component II. The broadening. asymmetry and shift of rubidium resonance lines produced under different pressures of pure helium and argon up to 100 atmospheres were studied. The 6broadening is linearly proportional to the relative densities of these gases, and is different for different doublet components. The elopes of these half-width vs. relative density curves are .735 cm-1 and .594 cm-1 per unit relative density of helium for 2P1½ and 2P½ components respectively, and the corresponding values for argon are .855 cm-1 and .627 cm-1 per unit relative density. Helium produces a violet, while argon a red asymmetry. The degree of asymmetry increases as the concentration of foreign gas increases, and is comparatively much greater for argon. For argon the asymmetry of the 2P1½ component is greater than that of the 2P1½ component, while for helium the reverse is true. Argon produces a greater shift than helium. The former produces a strong red, while the latter a violet shift. For both gases the shift of the 2P½ component la greater than that of the 2P1½ oom9onent. For helium the shift appears to be proportional to the relative density. and the shift of the 2P½ component is about twice as great as that for the shorter wave-length component while for argon the shifts for the doublet components are quite close. and the relation between shifts and relative densities obeys in general the 3/2 power relationship. Optical collision diameters as calculated from the half-width data are 13.37°A and 7.753°A for Rb-A and Rb-He respectively. From the measurement of the amount of total absorption of the line contours, f-values and the transition probabilities were evaluated. The f-values turn out to be .33 and .66 for the 2P½ and 2P1½ components of the Rb resonance lines respectively.</p

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Identification of RIP1 kinase as a specific cellular target of necrostatins

Necroptosis is a cellular mechanism of necrotic cell death induced by apoptotic stimuli in the form of death domain receptor engagement by their respective ligands under conditions where apoptotic execution is prevented. Although it occurs under regulated conditions, necroptotic cell death is characterized by the same morphological features as unregulated necrotic death. Here we report that necrostatin-1, a previously identified small-molecule inhibitor of necroptosis, is a selective allosteric inhibitor of the death domain receptor–associated adaptor kinase RIP1 in vitro. We show that RIP1 is the primary cellular target responsible for the antinecroptosis activity of necrostatin-1. In addition, we show that two other necrostatins, necrostatin-3 and necrostatin-5, also target the RIP1 kinase step in the necroptosis pathway, but through mechanisms distinct from that of necrostatin-1. Overall, our data establish necrostatins as the first-in-class inhibitors of RIP1 kinase, the key upstream kinase involved in the activation of necroptosis

Ischemia reperfusion dysfunction changes model-estimated kinetics of myofilament interaction due to inotropic drugs in isolated hearts

BACKGROUND: The phase-space relationship between simultaneously measured myoplasmic [Ca(2+)] and isovolumetric left ventricular pressure (LVP) in guinea pig intact hearts is altered by ischemic and inotropic interventions. Our objective was to mathematically model this phase-space relationship between [Ca(2+)] and LVP with a focus on the changes in cross-bridge kinetics and myofilament Ca(2+ )sensitivity responsible for alterations in Ca(2+)-contraction coupling due to inotropic drugs in the presence and absence of ischemia reperfusion (IR) injury. METHODS: We used a four state computational model to predict LVP using experimentally measured, averaged myoplasmic [Ca(2+)] transients from unpaced, isolated guinea pig hearts as the model input. Values of model parameters were estimated by minimizing the error between experimentally measured LVP and model-predicted LVP. RESULTS: We found that IR injury resulted in reduced myofilament Ca(2+ )sensitivity, and decreased cross-bridge association and dissociation rates. Dopamine (8 μM) reduced myofilament Ca(2+ )sensitivity before, but enhanced it after ischemia while improving cross-bridge kinetics before and after IR injury. Dobutamine (4 μM) reduced myofilament Ca(2+ )sensitivity while improving cross-bridge kinetics before and after ischemia. Digoxin (1 μM) increased myofilament Ca(2+ )sensitivity and cross-bridge kinetics after but not before ischemia. Levosimendan (1 μM) enhanced myofilament Ca(2+ )affinity and cross-bridge kinetics only after ischemia. CONCLUSION: Estimated model parameters reveal mechanistic changes in Ca(2+)-contraction coupling due to IR injury, specifically the inefficient utilization of Ca(2+ )for contractile function with diastolic contracture (increase in resting diastolic LVP). The model parameters also reveal drug-induced improvements in Ca(2+)-contraction coupling before and after IR injury

Adiabatic following and slow optical pulse propagation in rubidium vapor

Short pulses of narrow-line low-intensity dye-laser light nearly resonant with the Zeeman-split 2P1/2 esonance line (7948 A) of rubidium were observed to propagate through dilute rubidium vapor as slowly as (1/14)c. These slow pulse velocities showed that most of the energy in the propagating wave was contained by the vapor as coherent atomic excitation. The observed pulse velocities vp are in good agreement with the equation vp=dw/dk for the group velocity obtained from linear-dispersion theory. Also, the experimental results are quantitatively explained by adiabatic following, in which the pseudomoments of the atoms remain aligned along the effective field of the laser light. The adiabatic-following model allows for a direct comparison of our results with the work on self-induced transparency. For high-intensity light, adiabatic following predicts a nonlinear pulse velocity and the possibility of observing self-steepening.Peer reviewedElectrical and Computer Engineerin