After the publication of the paper by Gledhill and Malan in which precision conductance techniques were used for the first time in the determination of the solubility of silver chloride, Dr. N.H. Perton of Christchurch College, New Zealand, wrote to Gledhill and suggested that the same methods might be rewarding if applied to the determination of the solubility of mercurous chloride. A review of the Chemical literature showed that the values for the solubility of mercurous chloride were not at all consistent. Into., p. 1

Thesis (Ph. D.)--Columbia University, 1925. / Vita. Description based on print version record. Bibliography: p. [70].

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

Thesis (Ph. D.)--Johns Hopkins University, 1927. / Biography. "References: p. 19.

[From Introduction]. In 1955, Dry and Gledhill, both formerly of this Department, published their paper on the Solubility of Mercurous Chloride in Water at 25°0, and it was originally intended that this thesis should be an extension of the study to cover the temperature range from 5 t o 55°0. A preliminary investigation at 25°0, however, failed to yield results which were consistent with their findings, even though their apparatus and experimental technique were used. In an effort to resolve these difficulties their method of saturating the calomel in the conductance cell was thoroughly investigated, and as this procedure was found to be responsible, it was necessary to evolve an entirely new approach. The technique finally adopted was to saturate the mercurous chloride solutions by mechanical stirring in siliconed vessels and to carry out the conductance, pH, and total mercury concentration measurements on the filter ed solution. This method gave good results, and was free from the many extrapolations prevalent in the original procedure.

Thesis (Ph. D.)--University of Pennsylvania, 1933.

No description available.

The effects of 1 min 4 hr exposures to mercuric chloride (HgCl2), methyl mercuric chloride (CH3HgCl), p-chloromercuribenzoate (p-CMB) and ethylmercurithiosalicylate (TMS) on cell viability and kinetics of cell death, microtubules, F-actin, CD3 receptor expression, protein tyrosine phosphorylation (PTyr-P), intracellular calcium [Ca2+]i and responses to polarized signals in YAC-1 lymphoma cells were investigated. We hypothesized that immunotoxic effects of HgCl2 (Hg2+) are initiated by global receptor triggering, accompanied by increased protein tyrosine phosphorylation (PTyr-P) and down-regulation of the T-cell receptor (TCR). As a polychloride anion with poor lipid solubility, inorganic Hg2+ may produce effects at the outer cell membrane before significant intracellular accumulation, loss of microtubule integrity (a sensitive target) and activation of cell death through apoptotic pathways. The organomercurial compound p-CMB is likewise thought to penetrate membranes slowly as a result of ionization. In contrast, the highly lipid-soluble organomercurial compounds CH3HgCl and TMS were expected to reduce responses to polarized stimuli only in conjunction with and not prior to loss of microtubule integrity and the onset of necrotic cell death. <p>Two general patterns of effects were observed. In HgCl2-treated YAC-1 cells, inhibition of responses to polarized stimuli preceded loss of microtubules and onset of cell death. Effects on polarized stimuli were preceded by a transient Ca2+ signal; however, this Ca2+ signal appeared abortive, accompanied by a paradoxic decrease in PTyr-P and partial down-regulation of CD3 receptors. Responses to polarised stimuli were inhibited prior to extensive loss of microtubule staining, indicating effects preceded cytosolic Hg2+ accumulation. HgCl2 exposure was followed rapidly by necrotic cell death. <p>Similarly, p-CMB-treated YAC-1 cells failed to respond to polarized stimuli before effects on microtubules or loss of viability, and proceeded rapidly to late apoptosis; however, a transient Ca2+ signal and progressive loss of F-actin preceded effects in all other assays and may account for loss of polarized responses. <p>In CH3HgCl- and TMS-treated YAC-1 cells, CD3 receptor expression, [Ca2+] and PTyr-P were increased immediately, along with loss of microtubules. These reductions preceded inhibition of polarized signaling responses and seemed to indicate a general loss of cellular homeostasis not seen in HgCl2- and p-CMB-treated cells; loss of homeostasis did not necessarily produce simultaneous loss of viability, as TMS-treated cells remained viable for 30 min while CH3HgCl-treated cells became apoptotic within 1 min. Nonetheless, the YAC-1 cells proceeded to cell death more slowly, remaining early apoptotic after 4 hr, when almost all HgCl2- and p-CMB-treated cells were necrotic. These findings indicate the two groups of mercury compounds may alter responses to polarized stimuli and induce cell death by distinct pathways, one involving an apparently abortive signal and the other mediated by much more profound disruption of cellular homeostasis. Within the larger patterns there are further differences between the effects produced by each Hg compound, likely reflecting the combined influence of pharmacokinetic and dynamic factors governing access to and interactions with different cellular targets leading to cell death. These distinct targets may in turn be reflected in the different immune effects produced by these compounds <i>in vivo</i>.

The effects of 1 min 4 hr exposures to mercuric chloride (HgCl2), methyl mercuric chloride (CH3HgCl), p-chloromercuribenzoate (p-CMB) and ethylmercurithiosalicylate (TMS) on cell viability and kinetics of cell death, microtubules, F-actin, CD3 receptor expression, protein tyrosine phosphorylation (PTyr-P), intracellular calcium [Ca2+]i and responses to polarized signals in YAC-1 lymphoma cells were investigated. We hypothesized that immunotoxic effects of HgCl2 (Hg2+) are initiated by global receptor triggering, accompanied by increased protein tyrosine phosphorylation (PTyr-P) and down-regulation of the T-cell receptor (TCR). As a polychloride anion with poor lipid solubility, inorganic Hg2+ may produce effects at the outer cell membrane before significant intracellular accumulation, loss of microtubule integrity (a sensitive target) and activation of cell death through apoptotic pathways. The organomercurial compound p-CMB is likewise thought to penetrate membranes slowly as a result of ionization. In contrast, the highly lipid-soluble organomercurial compounds CH3HgCl and TMS were expected to reduce responses to polarized stimuli only in conjunction with and not prior to loss of microtubule integrity and the onset of necrotic cell death. <p>Two general patterns of effects were observed. In HgCl2-treated YAC-1 cells, inhibition of responses to polarized stimuli preceded loss of microtubules and onset of cell death. Effects on polarized stimuli were preceded by a transient Ca2+ signal; however, this Ca2+ signal appeared abortive, accompanied by a paradoxic decrease in PTyr-P and partial down-regulation of CD3 receptors. Responses to polarised stimuli were inhibited prior to extensive loss of microtubule staining, indicating effects preceded cytosolic Hg2+ accumulation. HgCl2 exposure was followed rapidly by necrotic cell death. <p>Similarly, p-CMB-treated YAC-1 cells failed to respond to polarized stimuli before effects on microtubules or loss of viability, and proceeded rapidly to late apoptosis; however, a transient Ca2+ signal and progressive loss of F-actin preceded effects in all other assays and may account for loss of polarized responses. <p>In CH3HgCl- and TMS-treated YAC-1 cells, CD3 receptor expression, [Ca2+] and PTyr-P were increased immediately, along with loss of microtubules. These reductions preceded inhibition of polarized signaling responses and seemed to indicate a general loss of cellular homeostasis not seen in HgCl2- and p-CMB-treated cells; loss of homeostasis did not necessarily produce simultaneous loss of viability, as TMS-treated cells remained viable for 30 min while CH3HgCl-treated cells became apoptotic within 1 min. Nonetheless, the YAC-1 cells proceeded to cell death more slowly, remaining early apoptotic after 4 hr, when almost all HgCl2- and p-CMB-treated cells were necrotic. These findings indicate the two groups of mercury compounds may alter responses to polarized stimuli and induce cell death by distinct pathways, one involving an apparently abortive signal and the other mediated by much more profound disruption of cellular homeostasis. Within the larger patterns there are further differences between the effects produced by each Hg compound, likely reflecting the combined influence of pharmacokinetic and dynamic factors governing access to and interactions with different cellular targets leading to cell death. These distinct targets may in turn be reflected in the different immune effects produced by these compounds <i>in vivo</i>.

Thesis (M.S.)--University of North Carolina at Wilmington, 2005. / Includes bibliographical references (leaves: 57-60)