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J Putters

Publications and source records attributed to J Putters.

4 recordsLinked to original sources

Reference interval for the bilirubin excess in cerebrospinal fluid by derivative spectrophotometry.

The value of the bilirubin excess can be a useful aid for recognizing blood from haemorrhage in cerebrospinal fluid. One of the parameters needed for the calculation of the bilirubin excess is the total bilirubin concentration in CSF. A method for measuring total bilirubin in cerebrospinal fluid is presented, based on diazotization of bilirubin according to Jendrassik-Gróf, combined with multiwavelength first derivative spectrophotometry. This bilirubin assay allows determination of total bilirubin concentrations as low as 0.045 +/- 0.002 mumols/l. This method also enables a correction for oxyhaemoglobin interference. The value of the bilirubin excess was calculated for patients (n = 66) not showing any neurological disorder. A reference interval of 0.07 +/- 0.06 mumols/l was calculated for the bilirubin excess.

Bilirubin↗

An improved spectrophotometric procedure for the determination of urinary metanephrines.

Spectrophotometric assays for urinary metanephrines are still widely used because of the simple equipment needed. These methods, however, have the major drawback of being very susceptible to interference. Using the original Pisano technique (Pisano, J. J. (1960) Clin. Chim. Acta 5, 406-414) we have often observed overestimation of the metanephrine concentration. By measuring absorbances at three different wavelengths we were able to considerably reduce this positive bias. With many patients this resulted in a significant downward adjustment of the values found for the total metanephrine excretion.

Benzaldehydes↗

Flow-force relationships in mitochondrial oxidative phosphorylation.

The rates of oxidation and phosphorylation in isolated rat-liver mitochondria have a steep dependence on the protonmotive force (delta mu H+) across the membrane. These experimentally observed relationships proved to be independent of the way in which delta mu H+ was varied. These results were obtained when the membrane potential (delta psi) was calculated from the distribution of K+ (in the presence of valinomycin). When triphenylmethylphosphonium (TPMP+) was used as a probe for delta psi, slightly different flow-force relationships were obtained. We conclude that unique relationships exist between delta mu H+ and the rates of oxidation and phosphorylation, and that under some conditions the behaviour of the probe TPMP+ is anomalous.

Animals↗

Activation of presynaptic alpha 2-adrenoceptors attenuates the inhibitory effect of mu-opioid receptor agonists on noradrenaline release from brain slices.

3H-noradrenaline release from rat neocortical slices induced by 15 mM K+ was concentration-dependently inhibited by morphine, [D-Ala2-D-Leu5] enkephalin (DADLE) and the calcium entry blocker Cd2+. Blockade of presynaptic alpha 2-adrenoceptors with phentolamine, almost doubling K+-induced 3H-noradrenaline release, slightly enhanced the relative inhibitory effects of morphine and DADLE, whereas that of Cd2+ remained unaffected. In contrast, activation of presynaptic alpha 2-adrenoceptors with clonidine (1 microM) or TL-99 (1 microM), inhibiting release by about 50%, completely abolished the inhibitory effects of morphine and DADLE without affecting that of Cd2+. When in the presence of 1 microM clonidine adenylate cyclase was activated with forskolin (10 microM), which restored release to the drug-free control level, the opioids still did not display their inhibitory effects. Therefore, mu-opioid receptor efficacy appears to be dependent on the degree of activation of alpha 2-adrenoceptors in central noradrenergic nerve terminals, probably through a local receptor interaction within the nerve terminal membrane.

Animals↗