PubMed · 6802023
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R V Acuff, J T Smith. 1981. A method for determining tissue sulfate.. https://doi.org/10.1016/0003-2697(81)90188-3
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Ethylenediaminetetraacetic acid (EDTA) solution is used to decalcify bone specimens for histological examination. Sodium hydroxide (NaOH) has been used to dissolve EDTA and to bring EDTA solutions to neutral pH. This solution, however, requires several weeks to decalcify bone specimens. We investigated a new decalcification fluid using concentrated ammonium hydroxide (NH4OH) to dissolve EDTA and to adjust the pH to neutral. Decalcification was performed using a magnetic stirrer with and without vacuum, or with a sonic cleaner. Decalcification end point was confirmed using both the weight loss and X-ray methods. After decalcification, specimens were processed through paraffin and sections were stained with hematoxylin and eosin. Decalcification employing NH4OH required an average of six days. Light microscopy indicated good retention of cellular detail.
Applications for a new polymer resin, PolyFlo, are described for both the small-scale and large-scale purification of synthetic oligodeoxyribonucleotides varying in length from 18-41 bases. The unique properties of this innovative resin provide > 95% purified full-length oligodeoxyribonucleotides with greater than 90% yield starting from either crude trityl-on or trityl-off unmodified as well as base (biotin)- or backbone (e.g., phosphorothioate)-modified products. Full biological activity of recovered nucleic acid is retained, and the resin is capable of removing contaminating endotoxins during purification. The resin performance is predictable and reliable. The resin can be regenerated easily and is particularly economic when employed directly in ammonia or with the trityl-off option. PolyFlo meets the requirements of current Good Manufacturing Practices.
PURPOSE: We investigated the effects of the gastric mucosal blood flow on the pathophysiology of ammonia-induced gastric mucosal damage. DESIGN: The study was designed to show whether the damaging effect of ammonia, a product of Helicobacter pylori urease, on the gastric mucosa is increased by the decrease in gastric mucosal blood flow in rats subjected to ischemia. RESULTS: Although ammonium chloride at concentrations of 15-60 mmol/l produced no significant macroscopical lesion in normotensive rats, it caused severe macroscopic hemorrhagic gastric lesions in the stomachs of rats subjected to ischemia. Exposure of the stomach to the combination of ischemia and ammonium chloride (60-600 mmol/l, pH adjusted to 7-9 with sodium hydroxide) produced macroscopic hemorrhagic lesions. However, exposure of the mucosa to the combination of ischemia and sodium hydroxide (60-600 mmol/l, pH was reduced to 7-9 with hydrochloric acid) produced no significant lesions. CONCLUSIONS: These results indicate that the mucosal lesions observed in patients infected with H. pylori are not caused by the alkalinity of H. pylori-produced ammonia and suggest that concomitant infection with H. pylori in the ischemic stomach may lead to the development of ulceration in these patients.