Biomedical subjects

G Momsen

Publications and source records attributed to G Momsen.

10 recordsLinked to original sources

PubMed1997

A mathematical/physiological model of parathyroid hormone secretion in response to blood-ionized calcium lowering in vivo.

The aim of the present study was to test a mathematical model of the biochemical processes in the parathyroid glands responsible for the secretion of parathyroid hormone resulting from extracellular calcium reduction. A double exponential curve described the parathyroid hormone secretion induced by rapid lowering of blood-ionized calcium in humans with normal as well as abnormal parathyroid tissue. Our data show that it was possible to establish a simple mathematical model of the parathyroid hormone response to blood-ionized calcium lowering, sufficient to fit experimental data obtained from patients with abnormal and normal parathyroid tissue. The fitted parameters showed no significant differences between patients with insulin-dependent diabetes mellitus and controls. In primary hyperparathyroidism, the parathyroid hormone production and steady-state transport across the cell membrane were increased, probably due to the larger amount of parathyroid tissue in these patients. These observations reveal a striking functional similarity between abnormal and normal parathyroid tissue. Furthermore, an apparently linear relationship between the rate of parathyroid hormone elimination from the blood plasma and the rate of cellular production/secretion was observed. This could be interpreted as an adaptation of the parathyroid gland's ability to produce parathyroid hormone depending on the average demand from the body.

Adult↗

PubMed1996

Serum neuron specific enolase (S-NSE) reference interval evaluation by time-resolved immunofluorometry compared with a radioimmunoassay.

The serum neuron specific enolase (S-NSE; EC 4.2.1.11) reference interval was evaluated by DELFIA (Wallac) in 161 healthy blood donors and the method compared with the S-NSE RIA assay (Pharmacia). The DELFIA assay total analytical variation coefficient (CV%) was between 3.7% and 6.6%., the RIA CV% 7.6% to 13.1%. Late centrifugation (after hours) increased the variation as a result of contamination with blood cells. Log transformation into a gaussian distribution was selected by Box-Cox analysis and tested by two models: the gauss-distribution and the Refval transformation. The 95% reference intervals and corresponding 90% confidence intervals were: female 2.9-9.6 micrograms/l (2.6-3.2 and 8.5-10.7) micrograms/l and male 3.4-11.7 micrograms/l (3.0-3.8 and 10.2-13.2 micrograms/l). Mean values were significantly different (P < 0.001), female 5.3 (4.9-5.6), male 6.3 (5.8-6.7) micrograms/l. The serum NSE levels were analysed with both methods in a population of 110 patients. The results were significantly correlated (coefficient, 0.9896; r, 0.99; P < 0.0001-two tailed). For high S-NSE values (> 150.0 micrograms/l) differences between the methods exceeded the mean difference + 2S.D., while low concentrations were interconvertible. Maximal diagnostic efficacy was 0.91 for both assays, in DELFIA 17.2-23.9 micrograms/l and for RIA 17.2-21.9 micrograms/l. Identical sensitivity, specificity, discriminative power score, and likelihood ratio were found. The two methods are consequently interconvertible.

Adolescent↗

PubMed1995

Differential increase in the maternal serum concentrations of the placental proteins human chorionic gonadotrophin, pregnancy-specific beta 1-glycoprotein, human placental lactogen and pregnancy-associated plasma protein-A during the first half of normal pregnancy, elucidated by means of a mathematical model.

The present study was performed to compare the increase in maternal serum concentrations of four placental proteins during the first half of 240 normal pregnancies. The proteins were pregnancy-associated plasma protein-A (PAPP-A), human chorionic gonadotrophin (HCG), human placental lactogen (HPL) hormone, and pregnancy-specific beta 1-glycoprotein (PSG), all produced by trophoblast cells. The median increases were observed to be very close to exponential growth curves. Based on simple assumptions, these growth curves could be explained as being solely dependent on the growth of the placenta. The assumptions were that the proteins were produced in the placenta at a constant rate per gram of placental cell mass and secreted into the circulation shortly after synthesis. Our investigations showed that for two of the proteins, PSG and HPL, the rate constants were, in fact, close to the reported growth rate of the placenta, whereas the PAPP-A production rate constant was significantly higher than those of the others. The production curve for HCG was very different from that of the other proteins. PAPP-A and HCG must therefore have more complicated mechanisms for regulating the production. An equation was constructed that permitted estimation of the molar production of the placental proteins per gram of placental cell mass per day during the first half of normal pregnancy. The value was highest for HPL and lowest for PAPP-A.

Chorionic Gonadotropin↗

PubMed1992

Normal pattern of parathyroid response to blood calcium lowering in primary hyperparathyroidism: a citrate clamp study.

OBJECTIVE: The objective of the present study was to elucidate the parathyroid responsiveness by measurements of blood ionized calcium and serum intact parathyroid hormone (PTH) concentrations, before and during trisodium citrate induced hypocalcaemia. PATIENTS AND CONTROLS: Sixteen patients with primary hyperparathyroidism and 32 healthy volunteers. DESIGN: Blood ionized calcium concentration was lowered by about 0.20 mmol/l and maintained at this level for 2 hours by blood ionized calcium controlled trisodium citrate infusion. MEASUREMENTS: Serum PTH(1-84) was measured by an immunoradiometric assay. RESULTS: In patients and controls, baseline measurements of blood ionized calcium were 1.39 +/- 0.07 vs 1.24 +/- 0.04 mmol/l (mean +/- SD) (P < 0.001) and of serum PTH (1-84) 9.7 +/- 5.4 vs 3.2 +/- 1.1 pmol/l (P < 0.001). During a trisodium citrate clamp, serum PTH(1-84) rose to a maximal concentration after 5-10 minutes in both groups, the patients to 2-10 times baseline, whereas controls rose to 4-7 times baseline values. In both groups the peak of serum PTH(1-84) declined to a steady state concentration around 2-4 times baseline. CONCLUSIONS: In conclusion, adenoma cells seem to react in almost the same way as normal parathyroid cells. They respond to initiation of hypocalcaemia by the release of preformed PTH(1-84), and continue to secrete increased amounts of PTH(1-84) during the maintenance of relative hypocalcaemia. The increased baseline concentrations of blood ionized calcium and serum PTH(1-84) and the serum PTH(1-84) response during blood ionized calcium lowering all suggest a shift upwards in the calcium set point.

Adenoma↗

PubMed1992

Hypocalcemia and parathyroid hormone responsiveness in diabetes mellitus: a tri-sodium-citrate clamp study.

The aim of this study was to elucidate the diabetic hypocalcemia and PTH responsiveness, investigated by measuring blood ionized calcium and serum intact parathyroid hormone (S-PTH(1-84)) concentrations, before and during an induced and maintained controlled hypocalcemia. In 15 patients with insulin-dependent diabetes mellitus and 19 healthy volunteers the blood ionized calcium concentration was lowered by about 0.20 mmol/l and maintained at this level by blood ionized calcium controlled tri-sodium-citrate infusion. In patients vs controls, baseline measurements averaged for blood ionized calcium (mmol/l) 1.18 +/- 0.08 vs 1.24 +/- 0.03 (p less than 0.01), for S-magnesium (mmol/l) 0.73 +/- 0.07 vs 0.81 +/- 0.07 (p less than 0.01) and for S-PTH (1-84) (pmol/l) 3.0 +/- 1.0 vs 3.1 +/- 1.0 (p greater than 0.75). During the clamp, S-PTH (1-84) peaked to comparable maximums after 5-10 min in both groups and then declined to constant concentrations two to three times above their control levels. In conclusion, we found a diabetic hypocalcemia and hypomagnesemia, though baseline levels of PTH and PTH responsiveness were normal. This may be taken to indicate a mild shift downwards in the set-point for PTH secretion in patients with insulin-dependent diabetes mellitus.

Adult↗

PubMed1981