Biomedical subjects

G Beckers

Publications and source records attributed to G Beckers.

12 recordsLinked to original sources

PubMed2003

[Bladder exstrophy-epispadias complex: management and preliminary results].

PURPOSE: Retrospective evaluation of operative techniques and perioperative management as related to the primary anatomical and functional situation as well as analysis of the preliminary postoperative results regarding kidney function, continence and complications. MATERIALS AND METHODS: From October 1992 to April 2003, 21 patients with bladder exstrophy-epispadias complex were treated, consisting of 12 children with untreated exstrophy and 9 who had undergone unsuccessful previous operations. Single-stage complete repair using the Erlangen concept was done during the first weeks of life in 8 infants and before school age in 3 children. One 13 year old girl had received a primary Mainz pouch II. The 9 unsuccessfully operated patients required a variety of different operations. The mean follow-up of 17 regularly controlled children was 62 months (range 3 to 129 months). RESULTS: In all children global kidney function remained stable, while reflux or obstruction was responsible for impaired unilateral split function ranging between 31 % and 45 % in 5. Four children were continent day and night after complete single-stage repair, 4 after ureterosigmoidostomy or Mainz pouch II and 5 after augmentation. CONCLUSIONS: In the newborn with previously untreated exstrophy-epispadias, we recommend single-stage complete functional reconstruction within the first weeks of life. Continence without loss of kidney function can be achieved in 50 % of these children. If adequate bladder capacity and continence cannot be achieved, an augmentation procedure or Mainz pouch II is our method of choice.

Adolescent↗

PubMed2001

Glutamate synthase of Corynebacterium glutamicum is not essential for glutamate synthesis and is regulated by the nitrogen status.

The Corynebacterium glutamicum gltB and gltD genes, encoding the large (alpha) and small (beta) subunit of glutamate synthase (GOGAT), were investigated in this study. Using RT-PCR, a common transcript of gltB and gltD was shown. Reporter gene assays and Northern hybridization experiments revealed that transcription of this operon depends on nitrogen starvation. The expression of gltBD is under control of the global repressor protein AmtR as demonstrated by gel shift experiments and analysis of gltB transcription in an amtR deletion strain. In contrast to other bacteria, in C. glutamicum GOGAT plays no pivotal role; e.g. gltB and gltD inactivation did not result in growth defects when cells were grown in standard minimal medium and only a slight increase in the doubling time of the corresponding mutant strains was observed in the presence of limiting amounts of ammonia or urea. Additionally, mutant analyses revealed that GOGAT has no essential function in glutamate production by C. glutamicum.

Bacterial Proteins↗

PubMed2000

Urease of Corynebacterium glutamicum: organization of corresponding genes and investigation of activity.

The Corynebacterium glutamicum genes encoding urease were isolated and sequenced. While ureA, ureB and ureC are encoding structural subunits of urease, ureE, ureF, ureG and ureD are encoding accessory proteins. As deduced from DNA sequence analyses, the ure genes are transcriptionally coupled, this was proven by RT-PCR at least for ureABC. Gene disruption experiments revealed that both structural (UreC) and accessory proteins (UreD) are indispensable for urease activity and growth on urea. Urease activity was determined in different Corynebacterium species after growth in various media. While the regulation patterns observed revealed species-specific differences, in general urease activity is induced upon nitrogen starvation. As in mycobacteria, in corynebacteria urease activity was highest in a pathogenic species and might also play a role in host-pathogen interaction.

Bacterial Proteins↗

PubMed1998

The immunoreactivity of glial fibrillary acidic protein in mesangial cells and podocytes of the glomeruli of rat kidney in vivo and in culture.

In this study the presence of glial fibrillary acidic protein (GFAP) in kidney is for the first time demonstrated in cryostat sections and cultures of isolated glomerular explants derived from rat kidneys. In double immunolabelling analysis of adult rat kidney sections using antiserum against GFAP and monoclonal antibody (mAb) against vimentin or desmin, the presence of immunoreactivity for GFAP could be observed in the glomerulus of the kidney and vascular cells situated in the peritubular space which expressed vimentin and desmin. Labelling of the sections with absorbed antiserum against GFAP completely abolished the staining in all these cells. The mAb against GFAP, clone GF12.24 which is known to label GFAP both in neural and non-neural cells, recognised its antigen only in the cells located in glomeruli. The investigations performed on early 2- or 3-day-old cultures from glomerular explants revealed different patterns of staining for GFAP in mesangial cells and podocytes: weak filamentous in mesangial cells and a strong non-filamentous perinuclear pattern in podocytes. Due to prominent perinuclear expression in podocytes GFAP may be considered as a marker of these cells. A different pattern of distribution of immunoreactivity for GFAP in podocytes and mesangial cells might be due to function-related posttranslational modifications of GFAP resulting in assembly or disassembly of GFAP filaments. The different pattern of staining for GFAP in the podocytes and mesangial cells, cells which exert a different influence on the capillaries of the glomeruli, suggests a role for GFAP in regulation of the tension and permeability of vascular walls. Previous investigations and present studies hint at GFAP as being a general marker of perivascular cells.

Animals↗

PubMed1997

Treatment of cirrhotic rats with L-ornithine-L-aspartate enhances urea synthesis and lowers serum ammonia levels.

CCl4-induced cirrhosis of rats was used for studying the influence of L-ornithine-L-aspartate (OA) on hyperammonemia. OA given to cirrhotic rats (2 g/kg daily) for 2 wk slightly increased net body weight and led to a significant increase in plasma urea levels and a decrease in plasma ammonia levels. Serum concentrations of glutamate, glutamine and arginine decreased significantly. In the livers of the OA-treated rats the activities of carbamoylphosphate synthetase I and arginase increased by 30 and 40%, respectively, approaching normal levels. No change in the activities of the other urea cycle enzymes as well as of glutamate dehydrogenase, glutaminase and glutamine synthetase was found. The negative correlation between glutamine synthetase activity and plasma ammonia levels reported previously for cirrhotic rats (Gebhardt and Reichen, Hepatology 20:684-691, 1994) was corroborated for cirrhotic animals not treated with OA, but was no longer apparent in OA-treated cirrhotic rats. Despite this improvement, plasma ammonia levels still varied considerably reflecting the variable accessibility and activities of glutamine synthetase in cirrhotics. Cultured hepatocytes from the two groups of rats showed a similar stimulation of urea production by addition of ammoniumacetate and/or OA to Hanks' buffered salt solution. In Williams medium E, however, the hepatocytes from the OA group produced significantly more urea than those from controls. These results suggest that treatment of cirrhotic rats with OA considerably improves urea production favoring the detoxification of ammonia that, however, is still limited by the severe alterations in liver architecture that are not influenced by OA in a 2-wk period.

Amino Acids↗

PubMed1995

The consequences of inactivating areas V1 and V5 on visual motion perception.

We studied the capacity of normal humans to discriminate the direction of motion of visual stimuli when areas V1 or V5 were reversibly inactivated with transcranial magnetic stimulation. We found that (i) magnetic stimulation of V5 at intervals of -20 to +10 ms before or after the onset of visual stimulation was effective in abolishing motion perception--other delays were not; (ii) magnetic stimulation of V1 abolished motion perception only marginally and at delays which were significantly different from those obtained with V5, the stimulation now being effective only at delays of 60-70 ms after the onset of visual stimulation. We conclude (i) that stimulation of V5 is a much more potent way of inducing akinetopsia (motion imperception) than stimulation of V1; (ii) that perceptually effective visual motion signals reach V5 at or before 30 ms and reach V1 at or before 60 ms--consequently, perceptually effective motion signals reach V5 before they reach V1; (iii) that, given the time course of arrival of signals in V1 and V5, it takes about 30-50 ms for signals from V1 to reach V5. We conclude further that there are probably two components reaching V5 from the retina, a fast one which bypasses V1 and a slow one which reaches it through V1.

Brain Mapping↗

PubMed1992

Cerebral visual motion blindness: transitory akinetopsia induced by transcranial magnetic stimulation of human area V5.

The perception of visual motion can be selectively and reversibly compromised by transcranial magnetic stimulation (TMS) of a small region of cortex, roughly 1 cm in diameter and corresponding in position to human area V5. The reversible inactivation of a small and specialized visual area which receives its predominant input from area V1 and sends a powerful return (re-entrant) input back to it allowed us to study for the first time the backward influence of area V5 on area V1. In contrast to the complete and temporary visual motion blindness which occurs during stimulation of V5, a less-prominent interference with the perception of visual motion occurs at 70-80 ms after the onset of the visual stimulus when TMS is applied to V1. Because V5 is critical for the perception of coherent motion, and because an intact re-entry of signals from V5 to V1 is essential for the conscious perception of visual motion, the results obtained with stimulation of V1 must be caused by a disruption of the re-entrant signals from V5 to V1.

Blindness↗

PubMed1992

Zero-length crosslinking between subunits delta and I of the H(+)-translocating ATPase of chloroplasts.

Treatment of spinach thylakoids with 1-ethyl-3-(dimethylaminopropyl)-carbodiimide (EDC)/N-hydroxysulfosuccinimide (sulfo-NHS) induced formation of a zero-length crosslink of an apparent molecular mass of 38 kDa. This product was shown, by immunodetection, to consist of subunit delta of CF1 and subunit I of CF0. The crosslink was isolated by preparative SDS gel electrophoresis and subjected to cyanogen bromide cleavage. Electrophoretic and immunological analysis of the resulting peptides suggested that the crosslink was formed between a glutamyl or aspartyl residue at the C-terminal end of subunit I and a basic amino acid of subunit delta in the range between Val-1 to Met-165. Treatment of thylakoids with EDC/Sulfo-NHS resulted in inhibition of photophosphorylation and CF0CF1-catalyzed ATP hydrolysis without affecting formation of a proton gradient related to phenazine methosulfate-mediated cyclic electron transport. Inhibition of H+ transport-coupled ATP hydrolysis was more pronounced than non-coupled methanol-stimulated ATP hydrolysis. The results suggest that subunits delta and I form a connection between the partial complexes CF1 and CF0 in situ. Crosslinking of the two subunits may impede the translocation of protons through CF0CF1.

Amino Acid Sequence↗

PubMed1991

Impairment of visual perception and visual short term memory scanning by transcranial magnetic stimulation of occipital cortex.

Transcranial magnetic stimulation (TMS) of occipital cortex was performed using a magneto-electric stimulator with a maximum output of 2 Tesla in 24 normal volunteers. The identification of trigrams, presented for 14 ms in horizontal or vertical arrays was significantly impaired when the visual stimulus preceded the occipital magnetic shock by 40 to 120 ms. The extent of impairment was related to TMS intensity. The latency of perceptual impairment was shorter for more intense TMS. No perceptual impairment was obtained by "sham" stimulation when TMS shocks were applied to the upper cervical region rather than the occipital region to rule out unspecific startle reactions affecting attention possibly responsible for the observed reduction in performance. Occipital TMS did not evoke systematic eye movements except for blink responses at latencies beyond 40 ms which were too late to interfere with visual input. Depending on the required serial order of readout of the trigram perceptual impairment was more marked for the second and third part of the trigram. This demonstrates that TMS interferes with the internal serial processing of visual input. To elucidate this further, TMS was used in a Sternberg short term visual memory scanning task. TMS caused a marked decrease in memory scanning rates whereas visual stimulus encoding and storage remained unaffected when tested at various TMS delays. TMS appears to be a useful method to study processes of visual perception and short term memory handling in the occipital cortex. Advantages over classical visual masking techniques especially regarding topical localisation are discussed.

Adult↗

PubMed1990

Moclobemide versus amitriptyline in the treatment of depression: two small double-blind multicentre studies in Belgium.

Moclobemide was compared with amitriptyline for antidepressant efficacy, safety and tolerance. Two studies were conducted, both over at least 4 weeks; in the first, 8 patients were given moclobemide in doses ranging from 300 to 328 mg, and 9 patients amitriptyline in doses of 75 to 96 mg; in the second, the numbers were 13 on moclobemide and 14 on amitriptyline, and the mean doses were 294-408 mg and 95-129 mg respectively. Both studies showed the 2 treatments to be equally effective, and there were no significant differences at any point. Moclobemide appeared slightly more effective and slightly better tolerated than amitriptyline, but the numbers were too small for any valid conclusion.

Adult↗

PubMed1984

Double-blind clinical study comparing alprazolam and doxepin in primary unipolar depression.

The therapeutic effect and safety of alprazolam and doxepin were studied in 126 outpatients suffering from primary unipolar depression. The 6-week study was double-blind with a random allocation of treatment. Patients were treated with a flexible dose of 1.0-4.5 mg of alprazolam and 50-225 mg of doxepin per day. The mean final doses were 2.7 mg for alprazolam and 137.5 mg for doxepin. The results indicate that alprazolam and doxepin were equally efficacious. The incidence of side-effects was lower in the alprazolam treatment group.

Adolescent↗

PubMed1975

[The effect of potassium chloride and organic potassium salts on the acid-base equilibrium in normo and hypokalemic rats].

The effects of intravenous infusions of potassium chloride, potassium acetate, potassium aspartate and potassium malate on plasma electrolytes and acid-base balance were investigated in normokalemic or hypokalemic alkalotic rats. Animals who obtained equal volumes of isotonic sodium chloride solution served as controls. All of these potassium solutions increased the plasma potassium concentrations to the same extent. Potassium chloride shifted the acid-base balance to acidotic values in normal rats or corrected metabolic alkalosis in hypokalemic rats. The potassium salts of organic acids, however, caused an increase in alkalosis, acetate acting stronger than aspartate and malate. In potassium deficiency combined with metabolic alkalosis the administration of potassium chloride is preferable to the organic potassium salts since it corrects both the electrolyte disturbances at the same time.

Acetates↗