No abstract

For approximately 30 years, the US Public Health Service and the US Environmental Protection Agency (USEPA) offered advisory opinions on the potential health effects of polyelectrolyte coagulant products used in drinking water treatment. In April 1990, the USEPA transferred this responsibility to a consortium of organizations led by the National Sanitation Foundation. Although more than 1,000 polyelectrolyte products were accepted for use by the USEPA, evidence suggests that probably fewer than 10 to 15 different types of polymer compounds are represented. Contaminants such as epichlorohydrin and acrylamide, which are of significant health concern, are associated with these product formulations.

Intermittent combination of an anabolic agent to promote bone formation and an antiresorptive agent that would prevent further bone loss is a theoretically attractive approach for restoring bone mass. We tested the potential of intermittently dosed calcitriol and calcitonin (CT) to restore bone properties in ovariectomized (Ovx) rats. Rats had Ovx or sham surgery at 8 weeks old and 4 weeks later were assigned to experimental groups: (1) sham vehicle, (2) Ovx vehicle, (3) Ovx + parathyroid hormone (PTH, 40 microg/kg), and (4) Ovx + calcitriol (2 microg/kg) + CT (2 microg/kg). Group 3 received PTH every week throughout the study, and group 4 received calcitriol at weeks 1, 3, 5, and 7 and CT at weeks 2, 4, 6, and 8. Dosing was carried out for 8 weeks with serum, and micro-computed tomographic analysis was done at 0, 4, and 8 weeks. Femurs and tibias were used for radiological analyses and for mechanical testing. Dosing with PTH improved bone mass and structure of cancellous bone at metaphyses of tibias and femurs as well as properties of cortical bone including geometry and strength. Intermittent dosing with calcitriol and CT was less potent in correcting loss of cancellous bone relative to treatment with PTH and had no effect on cortical bone parameters. However, intermittent dosing with calcitriol and CT was robust enough to improve cancellous bone mass and structure through bone formation without causing deleterious side effects. Our data provide additional evidence that therapies can be devised to ameliorate the skeletal defects associated with established osteoporosis.

No abstract

1-(Benzoyloxy), 1-(4-nitrobenzoyloxy), and 1-(3,5-dinitrobenzoyloxy) derivatives of 3-fluoro-, 3-chloro-, and 3-bromopropan-2-one were prepared by oxidation of the 1-benzoyloxy-3-halopropan-2-ols in turn prepared from the appropriate benzoyl chloride and 3-halo-1,2-propanediols, 1-Benzoyloxy-3-fluoropropan-2-one was allowed to react with acidic trimethyl orthoformate to yeild 1-benzoyloxy-2,2-dimethoxy-3-fluoropropane which upon basic hydrolysis afforded 2, 2-dimethoxy-3-fluoropropan-1-ol (fluorohydroxyacetone dimethyl ketal). This was deketalized with aqueous HCL to afford 3-fluoro-1-hydroxypropan-2-one (fluorohydroxyacetone), the title compound. By reacting 1-chloro-3-fluoropropan-2-one and 1, 3-dichloropropan-2-one with potassium acetate, 1-acetoxy-3-fluoropropan-2-one and 1-acetoxy-3-chloropropan-2-one (fluoro- and chlorohydroxyacetone acetate, respectively) were obtained. Similarly, sodium benzoate and 1-chloropropan-2-one produced 1-benzoyloxypropan-2-one. Stucture-activity relationships are discussed which relate chemical structure, alkylating ability, toxicity, and antitumor effects. Comparative toxicities in mice showed decreasing toxicity, on a molar basis, in the 1-benzoyloxy-3-halopropan-2-one series of bromo greater than fluoro greater than chloro. Ketones were much more toxic than the corresponding alcohols. In general the phosphate and benzoyloxy derivatives are more toxic than acetoxy compounds, with nitro-substituted benzoyloxy derivatives being much less toxic.