In the quiet years after the 1956 eruption of the Bezymianny volcano in central Kamchatka, it is doubtful that any volcano vented into the stratosphere until the 1963 eruptions of Agung (Bali), Trident (Alaska), and Surtsey (Iceland). From 1963 to the Hekla (Iceland) event in May 1970, two latitudinal belts of volcanoes have ejected ash and gases into the stratosphere. One belt is equatorial and the other is just below the Arctic Circle. The latter, where the tropopause is considerably lower, may have been the principal source of replenishment of volcanic dust and gases to the stratosphere. Submarine and phreatic volcanic eruptions may have been the sources of reported increase of water vapor in the stratosphere.

Abstract. We have studied the relaxation of OH(X2II, v, N) produced by the reaction O(1D) + H 2 -' OH* + H. Infrared emission measurements of the fundamental vibration-rotation band of OH were acquired at a temperature of 100 K in a large cryogenic chamber. Trace amounts of ozone were added to mixtures of H2, 02, and Ar at low (_<38 mT) pressures. The ozone was photolyzed to produce O(1D). Rapid reaction with H 2 produced OH*. Spectrally and temporally resolved emissions from levels up to the exothermic limit were observed with sufficient spectral resolution to permit kinetic analysis of individual level populations. The production rate was observed to scale as the rotational quantum number except at the highest levels populated. At early times we observed inverted rotational state distributions that subsequently relaxed to form thermal distributions in each vibrational level. Under these conditions, rotational relaxation was rapid in comparison with vibrational relaxation. Rotational relaxation within a given vibrational state could be represented by single quantum collisional exchange at near-gas-kinetic rates. The rotational level dependence of the deduced relaxation was determined.

The development and clinical testing of drug combinations for the treatment of Non-Hodgkin Lymphoma (NHL) and other cancers has recently shown great promise. However, determining the optimum combination and its associated dosages for maximum efficacy and minimum side effects is still a challenge. This paper describes a parametric analysis of the dynamics of malignant B-cells and the effects of an anti-sense oligonucleotide targeted to BCL-2 (as-bcl-2), anti-CD-20 (rituximab) and their combination, for a SCID mouse human lymphoma xenograft model of NHL. Our parametric model is straightforward. Several mechanisms of malignant B-cell birth and death in the nodal micro-environment are simulated. Cell death is accelerated by hypoxia and starvation induced by tumor scale, by modification of anti-apoptosis with as-bcl-2, and by direct kill effects of rituximab (cell kill by cytotoxic immune cells is not included, due to the absence of an immune system in the corresponding experiments). We show that the cell population dynamics in the control animals are primarily determined by K*, the ratio of rate constants for malignant cell death, Kd, and cell birth, Kb. Tumor growth with independent treatments is reproduced by the model, and is used to predict their effect when administered in combination. Malignant cell lifetimes are derived to provide a quantitative comparison of the efficacy of these treatments. Future experimental and clinical applications of the model are discussed.

A parametric model of tumor response to combination therapy in the presence of an immune system is described. Synergistic mechanisms which induce tumor regression are simulated with a coupled set of equations. The simulations are first compared to tumor history data obtained with a SCID mouse model to determine key parameters; predictions are then made for an immune-competent animal. The minimum immune cell birth rate relative to malignant B-cell birth rate necessary to induce tumor regression is determined, and optimization of drug combinations in the presence of an immune response is explored. The delayed effect of an immune response relative to drug scheduling is examined, and a mechanism for disease transformation in heterogeneous tumors is proposed.

No abstract