1.The short-term effects of different intakes of calcium and oxalic acid on the urinary excretion of these substances was studied in eight normal men and eight men with a history of calcium-containing renal stones.2. The effect of dietary oxalate on urine oxalate depended partly upon the calcium intake. Thus, on a normal calcium intake an increase in oxalate intake caused an increase in oxalate excretion that corresponded to 3.6% of the additional dietary oxalate; on a low calcium diet, however, the increase corresponded to 8.1%.3. A decrease in daily calcium intake from lo00 to 250 mg caused a fall in calcium excretion averaging 150 mg/day in the patients and 60 mg/day in the controls but this was accompanied by average rises of 10 and 7 mg/day respectively in oxalate excretion, with the result that the calcium oxalate activity products remained almost unchanged. 4.A decrease in oxalate as well as calcium intake resulted in a fall in calcium excretion that was not accompanied by a rise in oxalate excretion, and there was a statistically significant fall in the calcium oxalate activity product in both the patients and normal subjects.Key words: urinary calcium, urinary oxalic acid, renal stones, dietary calcium, dietary oxalic acid. & Nordin (1968, 1971) have shown that both normal and stone-forming urines are commonly supersaturated with respect to calcium oxalate but the mean level of supersaturation is significantly higher in patients with frequently-recurring calcium stones than in normal subjects. These results support the view that calcium stone formation is due primarily to oversaturation of urine with calcium oxalate. Robertson, PeacockThe higher degree of saturation of stone-forming urines is due primarily to higher concentrations of total and ionized calcium (Robertson et al.,

Adding vibrational spectroscopies to the arsenal of detection modes for microfluidics (mufluidics) offers benefits afforded by structurally descriptive identification of separated electrophoretic bands. We have previously applied surface-enhanced Raman spectroscopy (SERS) detection with nanocomposite metal-elastomer substrates as a detection mode in mufluidic channels. To create these mufluidic-SERS devices, silver-PDMS substrate regions are integrated into the architecture of a separation chip fabricated from PDMS or glass. Herein, we investigate analytical figures of merit for integrated mufluidic-SERS devices by implementing improvements in fluidic and SERS substrate fabrication as well as data collection strategies. Improvements are achieved by chemical modification of the PDMS channel, increasing effective detection efficiency by minimizing analyte partitioning into nonsensing walls rendering more analyte available to the metallized cover slide of channels and also by uniquely fabricating deep channels that have larger volume to SERS surface area ratios than conventional channels. A method is developed to exploit the inherent concentration profile of analyte material within an electrophoretic band in order to extend the linear dynamic range of detection on the SERS nanostructured surface. This is accomplished by spatially interrogating the Gaussian concentration profile of said bands. The subtleties of this technique give insight into the analytical utility of SERS detection in general. Finally, SERS substrates uniquely created via electron beam lithography with controllable morphologies are integrated into mufluidic-SERS devices to prove feasibility of such a coupling for future work. A separation of endocrine disrupting chemicals in a hybrid SERS nanocomposite-glass device is the capstone of this work.

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The role of metabolic acidosis in the genesis of renal osteomalacia was investigated by studying bone mineralisation and resorption rates with a combined isotope and balance technique in six patients, before and after the administration of alkali. Correction of blood pH was achieved in five cases and was associated with a significant rise in the bone mineralisation rates and a significant positive trend in the calcium balances. It is suggested that acidosis contributes to the pathogenesis of osteomalacia in renal failure by slowing skeletal mineralisation, possibly by inhibiting bone alkaline phosphatase.