Multilevel cycle of anthropogenic copper.

A comprehensive contemporary cycle for stocks and flows of copper is characterized and presented, incorporating information on extraction, processing, fabrication and manufacturing, use, discard, recycling, final disposal, and dissipation. The analysis is performed on an annual basis, ca. 1994, at three discrete governmental unit levels--56 countries or country groups that together comprise essentially all global anthropogenic copper stocks and flows, nine world regions, and the planet as a whole. Cycles for all of these are presented and discussed, and a "best estimate" global copper cycle is constructed to resolve aggregation discrepancies. Among the most interesting results are (1) transformation rates and recycling rates in apparently similar national economies differ by factors of two or more (country level); (2) the discard flows that have the greatest potential for copper recycling are those with low magnitude flows but high copper concentrations--electronics, electrical equipment, and vehicles (regional level); (3) worldwide, about 53% of the copper that was discarded in various forms was recovered and reused or recycled (global level); (4) the highest rate of transfer of discarded copper to repositories is into landfills, but the annual amount of copper deposited in mine tailings is nearly as high (global level); and (5) nearly 30% of copper mining occurred merely to replace copper that was discarded. The results provide a framework for similar studies of other anthropogenic resource cycles as well as a basis for supplementary studies in resource stocks, industrial resource utilization, waste management, industrial economics, and environmental impacts.

Human homocysteine catabolism: three major pathways and their relevance to development of arterial occlusive disease.

Two separate metabolic pathways that methylate homocysteine to methionine are known in humans, utilizing, respectively, 5-methyltetrahydrofolate and betaine as methyl donors. Deficiency of the folate-dependent methylation system is linked to hyperhomocysteinemia. Our data suggest that this deficiency leads to concurrent metabolic down-regulation of homocysteine transsulfuration that may contribute to hyperhomocysteinemia. By contrast, no instances have been reported of hyperhomocysteinemia resulting from deficiencies of betaine-dependent homocysteine methylation. Long-term betaine supplementation of 10 patients, who had pyridoxine-resistant homocystinuria and gross hyperhomocysteinemia due to deficiency of cystathionine beta-synthase activity, caused a substantial lowering of plasma homocysteine, which has now been maintained for periods of up to 13 years. Betaine had to be taken regularly because the effect soon disappeared when treatment was stopped. In conclusion, depressed activity of the transsulfuration pathway may contribute to hyperhomocysteinemia because of primary deficiencies of enzymes of either the transsulfuration or of the folate-dependent methylation pathways. Stimulation of betaine-dependent homocysteine remethylation causes a commensurate decrease in plasma homocysteine that can be maintained as long as betaine is taken.

Perforated colorectal neoplasms: correlation of clinical, contrast enema, and CT examinations.

Results of clinical, contrast enema (CE), and computed tomographic (CT) examinations in 39 patients with perforated colorectal neoplasms were retrospectively reviewed. Twenty patients were toxemic at initial presentation, but in only four patients was the diagnosis of perforated colorectal neoplasm initially suspected clinically. CE study was performed in 22 patients and enabled the diagnosis of perforated neoplasm in 11 cases, neoplasm alone in eight, and neither neoplasm nor perforation in three. CT was performed in 38 patients and enabled the diagnosis of perforated neoplasm in 36; pericolic phlegmon but no mass lesion was evident in two. In 16 patients, CT also demonstrated metastatic disease. Because of its reliability in establishing the diagnosis and staging the extent of the inflammatory and neoplastic disease, CT is indicated in cases of suspected or proved perforated colorectal neoplasm and in cases in which CE study findings are indeterminate or suggestive of perforated neoplasm.

CT of appendicitis.

The CT findings of 38 consecutive patients with acute appendicitis are analyzed, described, and illustrated. CT showed intraabdominal disease in 92% of patients and made a specific diagnosis of appendicitis in 79% of cases. The most common CT findings were pericecal inflammation (68%), abscess (55%), calcified appendicolith (23%), and an abnormal appendix (18%). CT had a sensitivity similar to that of contrast enema examinations, but it correlated much better with the surgical findings in detecting the precise nature, extent, and location of the disease process. Normal CT does not exclude appendicitis, since mild forms without periappendiceal disease may escape detection.

Regulation of purine de novo synthesis in cultured human fibroblasts: the role of P-ribose-PP.

Procedures for assaying the rate of purine de novo synthesis in cultured fibroblast cells have been compared. These were (i) the incorporation of [(14)C]-glycine or [(14)C]formate in alpha-N-formylglycinamide ribonucleotide (an intermediate in the purine synthetic pathway) and (ii) the incorporation of [(14)C]-formate into newly synthesised cellular purines and purines excreted by the cell into the medium. Fibroblast cells, derived from patients with a deficiency of hypoxanthine phosphoribosyltransferase (HPRT-) (EC 2.4.2.8) and increased rates of purine de novo synthesis, were compared with fibroblasts from healthy subjects (HPRT+). Fetal calf serum, which was used to supplement the assay and cell growth medium, was found to contain sufficient quantities of the purine base hypoxanthine to inhibit purine de novo synthesis in HPRT+ cells. This inhibition was the basis of differentiation between HPRT- and HPRT+ cells. In the absence of added purine base, both cell types had similar capacities for purine de novo synthesis. This result contrasts with the increased rates of purine de novo synthesis reported for a number of human HPRT- cells in culture but conforms recent studies made on human HPRT- lymphoblast cells. The intracellular concentration and utilisation of 5-phosphoribosyl-1-pyrophosphate (P-Rib-PP), a substrate and potential controlling factor for purine de novo synthesis, were determined in HPRT- and HPRT+ cells. The rate of utilisation of P-Rib-PP in the salvage of free purine bases was far greater than that in purine de novo synthesis. Although HPRT- cells had a 3-fold increase in P-Rib-PP content, the rate of P-Rib-PP generation was similar to HPRT+ cells. Thus, in fibroblasts, the concentration of P-Rib-PP appears to be critical in the control of de novo purine synthesis and its preferential utilisation in the HPRT reaction limits its availability for purine de novo synthesis. In vivo, HPRT+ cells, in contrast to HPRT- cells, may be operating purine de novo synthesis at a reduced rate because of their ability to reutilise hypoxanthine.