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G van Vliet

Publications and source records attributed to G van Vliet.

15 recordsLinked to original sources

1H and (31)P magnetization transfer studies of hindleg muscle in wild-type and creatine kinase-deficient mice.

The authors addressed the hypothesis that interactions with creatine kinase (CK) play a role in the off-resonance magnetization transfer (MT) effect of creatine in skeletal muscle. Toward that aim, (1)H MT studies were done on hindleg muscle in wild-type mice and in transgenic mice, lacking cytoplasmic CK and/or mitochondrial CK. The (1)H MT effect was essentially identical in wild-type muscle and the two single CK knock-out muscles, while moderately decreased in tissue lacking both CK isoforms. (31)P-NMR showed no off-resonance (31)P MT effect in skeletal muscle for PCr in any of the mice, while the enzymatic CK reaction flux was circa 0.2-0.3 sec(-1) in the wild-type muscle and in muscle deficient in mitochondrial CK. The CK enzyme flux was negligible in the other two CK knock-outs. These data suggest that CK plays a minor role in the (1)H MT effect of creatine. Irrespective of the underlying mechanism the creatine MT phenomenon probably has no significant consequences for the thermodynamic availability of total creatine to the CK reaction.

Animals↗

Magnetic coupling of creatine/phosphocreatine protons in rat skeletal muscle, as studied by (1)H-magnetization transfer MRS.

Off-resonance saturation caused a reduction of the 3.04 ppm NMR signal from the methyl protons of creatine in rat hindleg skeletal muscle. (1)H-NMR spectra were recorded over a 200 kHz range of off-resonance saturation frequencies. The span of frequencies over which the creatine signal was reduced greatly exceeded that expected for direct saturation by the off-resonance RF-field. This suggests that there is a motionally restricted proton pool which exchanges magnetization with the free creatine pool. The experimental data were fitted to characterize the immobilized proton pool and the exchange kinetics, using a two-pool exchange model. The immobile pool was estimated to amount to ca. 2.5% of the mobile pool of free creatine, while the rate of exchange between the mobile and immobile configurations is ca. 2.3 sec(-1). After depletion of phosphocreatine by termination of the animal, the MT effect on the creatine methyl protons remained unchanged. This indicates that phosphocreatine and creatine both contribute to the MT phenomenon. Selective saturation of the mobile water pool also led to a reduction in the intensity of the total creatine methyl signal, suggesting that water and creatine are magnetically coupled via a macromolecular interface. The precise mechanism responsible for and the biological significance of the pronounced creatine magnetization transfer effect in rat skeletal muscle remains to be established. Magn Reson Med 42:665-672, 1999.

Animals↗

Phosphorylation state of red and white muscle in tilapia during graded hypoxia: an in vivo (31)P-NMR study.

The aim of this study was to measure the energetic consequences of hypoxia in different types of skeletal muscle within a single tilapia species (n = 5). To that aim, 81.0 MHz (31)P-nuclear magnetic resonance (NMR) spectra were collected, alternately, from three surface coils placed adjacent to the tissues of interest (dorsal white muscle, ventral white muscle, and lateral red muscle) during a graded hypoxia load over 6 h followed by a 5-h recovery period. The fish were contained in a flow cell, enabling us full control of the oxygen content of the bathing medium. The intracellular pH and the concentrations of ATP, phosphocreatine (PCr), and P(i) were determined from the NMR spectra. For normoxia, biochemical differences for [gamma-ATP], [PCr], and [sugar phosphates] (SP) were observed between all three locations, especially between the red and white muscle. During hypoxia stress, loss of phosphorylated compounds (PCr+P(i)+SP) was observed at all locations but was the most severe in red muscle. When the aerobic (respirometry) and anaerobic ((31)P-NMR) ATP production via an energy balance are compared, flexible metabolic depression is demonstrated during anaerobioses. It is concluded that control of the aerobic and anaerobic component of metabolism during metabolic depression is independent of each other.

Adenosine Triphosphate↗

Effects of hypoxia-ischemia and inhibition of nitric oxide synthase on cerebral energy metabolism in newborn piglets.

The present study was designed to examine the effects of inhibition of nitric oxide synthase on cerebral energy metabolism after hypoxia-ischemia in newborn piglets. Ten 1- to 3-d-old piglets received N(omega)-nitro-L-arginine (NNLA), an inhibitor of nitric oxide synthase (NNLA-hypoxia, n = 5), or normal saline (hypoxia, n = 5) 1 h before cerebral hypoxia-ischemia. After the infusion, hypoxia-ischemia was induced by bilateral occlusion of the carotid arteries and decreasing FiO2 to 0.07 and maintained for 60 min. Thereafter, animals were resuscitated and ventilated for another 3 h. Using 1H- and 31P-magnetic resonance spectroscopy, cerebral energy metabolism was measured in vivo at 15-min intervals throughout the experiment. Phosphocreatine to inorganic phosphate ratios decreased from 2.74 +/- 0.14 to 0.74 +/- 0.36 (hypoxia group) and 2.32 +/- 0.17 to 0.18 +/- 0.10 (NNLA-hypoxia group) during hypoxia-ischemia. Thereafter, phosphocreatine to inorganic phosphate ratios returned rapidly to baseline values in the hypoxia group, but remained below baseline values in the NNLA-hypoxia group. Intracellular pH decreased during hypoxia-ischemia and returned to baseline values on reperfusion in both groups. Intracellular pH values were lower in the NNLA-hypoxia group (p < 0.001, ANOVA). Lactate was not present during the baseline period. After hypoxia-ischemia, lactate to N-acetylaspartate ratios increased to 1.34 +/- 0.28 (hypoxia group) and 2.22 +/- 0.46 (NNLA-hypoxia group). Lactate had disappeared after 3 h of reperfusion in the hypoxia group, whereas lactate to N-acetylaspartate ratios were 1.37 +/- 1.37 in the NNLA-hypoxia group. ANOVA demonstrated a significant effect of NNLA on lactate to N-acetylaspartate ratios (p < 0.001). Inhibition of nitric oxide synthase by NNLA tended to compromise cerebral energy status during and after cerebral hypoxia-ischemia in newborn piglets.

Animals↗

Fluxes through cytosolic and mitochondrial creatine kinase, measured by P-31 NMR.

The kinetic properties of the cytoplasmic and the mitochondrial iso-enzymes of creatine kinase from striated muscle were studied in vitro and in vivo. The creatine kinase (CK) iso-enzyme family has a multi-faceted role in cellular energy metabolism and is characterized by a complex pattern of tissue-specific expression and subcellular distribution. In mammalian tissues, there is always co-expression of at least two different CK isoforms. As a result, previous studies into the role of CK in energy metabolism have not been able to directly differentiate between the individual CK species. Here, we describe experiments which were directed at achieving this goal. First, we studied the kinetic properties of the muscle-specific cytoplasmic and mitochondrial CK isoforms in purified form under in vitro conditions, using a combination of P-31 NMR and spectrophotometry. Secondly, P-31 NMR measurements of the flux through the CK reaction were carried out on intact skeletal and heart muscle from wild-type mice and from transgenic mice, homozygous for a complete deficiency of the muscle-type cytoplasmic CK isoform. Skeletal muscle and heart were compared because they differ strongly in the relative abundance of the CK isoforms. The present data indicate that the kinetic properties of cytoplasmic and mitochondrial CK are substantially different, both in vitro and in vivo. This finding particularly has implications for the interpretation of in vivo studies with P-31 NMR.

Animals↗

Growth hormone treatment of Turner syndrome patients with insufficient growth hormone response to pharmacological stimulation tests.

Growth before and during treatment with biosynthetic human growth hormone (hGH) was studied in 13 patients with Turner syndrome (TS) and a growth hormone (GH) response of less than 10 micrograms/l to two standard provocative tests. During 1 year of treatment with hGH (0.15 IU/kg per day) height velocity (mean +/- SD) increased significantly (P less than 0.001) from 3.7 +/- 1.8 cm/year to 7.6 +/- 1.5 cm/year. The auxological data in these girls before and during treatment with hGH were similar to those observed in TS patients with a normal response of GH to pharmacological stimuli. It is concluded that in girls with Turner syndrome GH testing should only be performed when height velocity is below the Turner norm. In TS patients with residual growth potential a clinically significant growth acceleration can be obtained with a higher-than-replacement dose of hGH, i.e. 0.15 IU/kg per day, regardless of GH testing.

Adolescent↗

Growth-promoting effect of growth hormone and low dose ethinyl estradiol in girls with Turner's syndrome.

Forty patients with Turner's syndrome, aged 5.0-16.6 yr, were randomly allocated to receive daily sc injections of recombinant human GH (hGH) at a dose of 1 IU/kg.week alone (group I) or in combination with 25 ng/kg.day ethinyl estradiol (E2; group II). The mean pretreatment height velocity was 3.8 cm/yr for both groups. During the first year of treatment height velocity increased significantly (P less than 0.001) in both groups, to 7.5 +/- 1.3 and 8.1 +/- 1.6 cm/yr, respectively. The difference between the two groups was not significant. The mean (+/- SD) height velocity expressed as the SD score for chronological age (Turner references) was 0.0 +/- 1.2 for group I and 0.2 +/- 1.4 for group II and increased significantly (P less than 0.001) during the first year of treatment to +4.3 +/- 1.1 in group I and +5.4 +/- 1.2 in group II. The difference between both groups was statistically significant (P less than 0.01). Height SD score for chronological age (Turner references) increased from -0.2 +/- 0.9 to +0.6 +/- 1.0 in group I and from -0.2 +/- 1.0 to +0.7 +/- 1.1 in group II. Mean bone age progressed similarly in both treatment groups (1.1 +/- 0.6 yr during 1 yr of treatment). However, bone age maturation accelerated more rapidly in younger patients. Twelve girls (three in group I and nine in group II) had minor breast development. No major adverse effects were reported. We conclude that daily sc therapy with hGH stimulates height velocity in Turner's syndrome. The beneficial effect on height velocity increment of E2 addition was small. Furthermore, even very low doses of E2 may induce breast development at an early age and accelerate bone maturation. For these reasons, the addition of E2 to hGH is not warranted in young patients with Turner's syndrome.

Adolescent↗

[Lungworm disease in cattle, a persistent problem?].

From the results of a number of studies it is concluded that: (1) Cattle of a large proportion (approximately 80 per cent) of the dairy farms in the Netherlands were infected with L3 larvae of Dictyocaulus viviparus during the grazing season in 1981. (2) Experiments showed a significant negative cubic effect on the level of infection with L3 larvae of D. viviparus on the growth of calves. (3) Sporangia of Pilobolus kleinii harbouring L3 larvae were shot significantly further away than sporangia not harbouring L3 larvae.

Animals↗

[The value of lungworm vaccination in calves (author's transl)].

Although the lungworm vaccine was found to be useful under field conditions, some questions remain, particularly epidemiological ones. Experiments with housed and grazing calves were carried out to elucidate a number of these problems. From these experiments in which vaccinated and unvaccinated calves were challenged, it was apparent: 1. that the immunity developed by vaccinated calves could resist a heavy challenge without clinical symptoms; 2. that vaccinated calves exposed to a heavy challenge could produce small numbers of lungworm larvae. It was shown that, despite the hard winter of 1978/1979, infectious lungworm larvae were present on the pasture in the spring of 1979.

Animals↗

Mauriac syndrome: three cases with retinal angiofluorescein study.

Three children with features of the Mauriac syndrome have been studied. Ocular complications, mainly characterized by increased capillary permeability have been demonstrated by fluorescein angiography. A decreased proximal tubular beta 2-microglobulin reabsorption has been found in one patient, and in another one, there was a slowed sensory nerve condition velocity. A liver biopsy, performed in one patient, has shown numerous fat filled cells and intralysosomal lipofuscin storage. No hormonal disturbance, which could explain the growth reardation, has been found. Bad metabolic control of diabetes could be responsible for all the anomalies of Mauriac syndrome.

Adolescent↗

Studies of haemoglobin types in barbary sheep (Ammotragus lervia).

1. Two haemoglobin types, haemoglobins Amm-C and Amm-B, were observed in five Barbary sheep (Ammotragus lervia). One animal was homozygous for haemoglobin Amm-C, a second was homozygous for haemoglobin Amm-B, and three were heterozygous for both. 2. Amino acid analyses of the globin from haemoglobin Amm-B showed that this type was related to, but not identical with, haemoglobin B of the domestic sheep. 3. The beta-chain of haemoglobin Amm-C was found to be composed of 141 amino acid residues. Its amino acid composition differed from that of the beta(C)-chain of the anaemic domestic sheep in at least 14 residues. The Amm-beta(C)-chain contained one isoleucyl residue. 4. The amino acid compositions of tryptic peptides T-1, T-2, T-13 and T-14 of the Amm-beta(C)-chain were similar to those of the sheep beta(C)-chain. Peptides T-3, T-4, T-6, T-7, T-8, T-11 and T-15 were the same as the corresponding peptides of the sheep beta(A)- and beta(C)-chains. Peptide T-5 and to a smaller extent peptide T-9 resembled the corresponding peptides of the sheep beta(A)-chain, and peptide T-10 was identical with peptide gammaT-10 of sheep haemoglobin F. Peptide T-12 was not recovered. 5. The results of these investigations were interpreted as being indicative that the structural Amm-beta(C)-gene is closely related to the beta(C)-gene of sheep, from which through domestication the present domestic sheep originated.

Journal Article↗