Biomedical subjects

U Dydak

Publications and source records attributed to U Dydak.

6 recordsLinked to original sources

PubMed2006

Pitfalls in lactate measurements at 3T.

In clinical MR spectroscopy at higher field strengths, lactate may show reduced or absent signal intensity at an echo time of 144 ms. Although this false-negative result may be predicted from theory, experimental verification and clinical impact have not been fully established. Using scanners from 3 major vendors, spectra from phantoms and patients demonstrate the lactate signal loss and potential error in interpretation. Strategies are discussed to overcome, or at least alleviate, this problem.

Brain Diseases↗

PubMed2006

Trading spectral separation at 3T for acquisition speed in multi spin-echo spectroscopic imaging.

Fast multiple spin-echo spectroscopic imaging, also called turbo spectroscopic imaging (TSI), may be enhanced in terms of acquisition speed by taking advantage of the higher spectral separation afforded at higher field strength and by further combining it with sensitivity encoding (SENSE). This article demonstrates the possibilities of this approach at 3T, resulting in scan-time reductions of up to a factor of 10. High-resolution, in vivo, single- and multiple-section spectroscopic imaging data are presented.

Aspartic Acid↗

PubMed2005

MR-spectroscopic imaging during visual stimulation in subgroups of migraine with aura.

Migraine pathophysiology possibly involves deficient mitochondrial energy reserve and diminished cortical habituation. Using functional magnetic resonance spectroscopic imaging (fMRSI), we studied cortical lactate changes during prolonged visual stimulation to search for different pathophysiological mechanisms in clinically distinct subgroups of migraine with aura. Eleven healthy volunteers (HV) and 10 migraine patients were investigated interictally: five with visual aura (MA) and five with visual symptoms and at least one of the following: paraesthesia, paresis or dysphasia (MAplus). Using MRSI (Philips, 1.5 T) (1)H-spectra were repeatedly obtained from a 25 mm-thick slice covering visual and non-visual cortex, with the first and fifth measurements in darkness and the second to fourth with 8-Hz checkerboard stimulation. In MAplus lactate increased only during stimulation, only in visual cortex; in MA resting lactate was high in visual cortex, without further increase during stimulation. This is compatible with an abnormal metabolic strain during stimulation in MAplus, possibly due to dishabituation, and a predominant mitochondrial dysfunction in MA.

Adult↗

PubMed2001

Sensitivity-encoded spectroscopic imaging.

Sensitivity encoding (SENSE) offers a new, highly effective approach to reducing the acquisition time in spectroscopic imaging (SI). In contrast to conventional fast SI techniques, which accelerate k-space sampling, this method permits reducing the number of phase encoding steps in each phase encoding dimension of conventional SI. Using a coil array for data acquisition, the missing encoding information is recovered exploiting knowledge of the distinct spatial sensitivities of the individual coil elements. In this work, SENSE is applied to 2D spectroscopic imaging. Fourfold reduction of scan time is achieved at preserved spectral and spatial resolution, maintaining a reasonable SNR. The basic properties of the proposed method are demonstrated by phantom experiments. The in vivo feasibility of SENSE-SI is verified by metabolic imaging of N-acetylaspartate, creatine, and choline in the human brain. These results are compared to conventional SI, with special attention to the spatial response and the SNR.

Brain↗

PubMed2000

Schizophrenia: glutathione deficit in cerebrospinal fluid and prefrontal cortex in vivo.

Schizophrenia is a major psychiatric disease, which affects the centre of the personality, with severe problems of perception, cognition as well as affective and social behaviour. In cerebrospinal fluid of drug-free schizophrenic patients, a significant decrease in the level of total glutathione (GSH) by 27% (P<0.05) was observed as compared to controls, in keeping with the reported reduced level of its metabolite gamma-glutamylglutamine. With a new non-invasive proton magnetic resonance spectroscopy methodology, GSH level in medial prefrontal cortex of schizophrenic patients was found to be 52% (P = 0.0012) lower than in controls. GSH plays a fundamental role in protecting cells from damage by reactive oxygen species generated among others by the metabolism of dopamine. A deficit in GSH would lead to degenerative processes in the surrounding of dopaminergic terminals resulting in loss of connectivity. GSH also potentiates the N-methyl-D-aspartate (NMDA) receptor response to glutamate, an effect presumably reduced by a GSH deficit, leading to a situation similar to the application of phencyclidine (PCP). Thus, a GSH hypothesis might integrate many established biological aspects of schizophrenia.

Adolescent↗

PubMed1999

Metabolic aspects of phosphate replacement therapy for hypophosphatemia after renal transplantation: impact on muscular phosphate content, mineral metabolism, and acid/base homeostasis.

Hypophosphatemia caused by renal phosphate loss occurs frequently after kidney transplantation. In assumption of systemic phosphorus depletion, the presumed deficit commonly is replaced by oral phosphate supplements. However, such treatment is debatable, because intracellular phosphorus stores have not been assessed in this setting and may not be accurately reflected by serum phosphate concentrations. Moreover, disturbances in mineral metabolism from chronic renal failure, such as hypocalcemia and hyperparathyroidism, may be prolonged with oral phosphate supplements. Conversely, a neutral phosphate salt might improve renal acid excretion and systemic acid/base homeostasis for its properties as a urinary buffer and a poorly reabsorbable anion. Twenty-eight patients with mild early posttransplantation hypophosphatemia (0.3-0.75 mmol/L) were randomly assigned to receive either neutral sodium phosphate (Na(2)HPO(4)) or sodium chloride (NaCl) for 12 weeks and examined with regard to (1) correction of serum phosphate concentration and urinary phosphate handling; (2) muscular phosphate content; (3) serum calcium and parathyroid hormone (PTH); and, (4) renal acid handling and systemic acid/base homeostasis. Mean serum phosphate concentrations were similar and normal in both groups after 12 weeks of treatment; however, more patients in the NaCl group remained hypophosphatemic (93% versus 67%). Total muscular phosphorus content did not correlate with serum phosphate concentrations and was 25% below normophosphatemic controls but was completely restored after 12 weeks with and without phosphate supplementation. However, the percentage of the energy-rich phosphorus compound adenosine triphosphate (ATP) was significantly higher in the Na(2)HPO(4) group, as was the relative content of phosphodiesters. Also, compensated metabolic acidosis (hypobicarbonatemia with respiratory stimulation) was detected in most patients, which was significantly improved by neutral phosphate supplements through increased urinary titratable acidity. These benefits of added phosphate intake were not associated with any adverse effects on serum calcium and PTH concentrations. In conclusion, oral supplementation with a neutral phosphate salt effectively corrects posttransplantation hypophosphatemia, increases muscular ATP and phosphodiester content without affecting mineral metabolism, and improves renal acid excretion and systemic acid/base status.

Acid-Base Equilibrium↗