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Biomedical subjects

C Förster

Publications and source records attributed to C Förster.

At least 19 recordsLinked to original sources
PubMed1992

Mitochondrial angiopathy in a family with MELAS.

A family with mitochondrial myopathy, encephalopathy, lactic acidosis and strokelike epidoses (MELAS) affecting mother, son and daughter is described. Biochemical studies on muscle biopsy specimen in one patient revealed NADH dehydrogenase (complex I) deficiency. A mitochondrial angiopathy could be demonstrated by brain and muscle biopsy. It is suggested that the mitochondrial angiopathy is the basic pathogenic mechanism of impaired cerebral circulation in MELAS.

Acidosis, Lactic↗
PubMed1991

A specific point mutation in the mitochondrial genome of Caucasians with MELAS.

The mitochondrial DNA (mtDNA) of Japanese patients suffering from the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) exhibits a specific heteroplasmic A----G transition in the tRNA(Leu) at position 3243. In this study, we investigated mtDNA from skeletal muscle, cardiac muscle, brain, liver, diaphragm, fibroblasts and blood cells of four Caucasians with MELAS, one younger healthy sister of two MELAS patients, and eleven controls. We found that 1) the mutation was present in all investigated tissues of Caucasians with MELAS but not in controls, 2) within a single patient, the tissue-specific variation of the copy number of mutated mtDNA covered the same range as in the skeletal muscle of different patients, 3) the mutation was also present in the blood cells of the healthy sister of two MELAS siblings.

Acidosis, Lactic↗
PubMed1990

Ternary complexes of Escherichia coli aminoacyl-tRNAs with the elongation factor Tu and GTP: thermodynamic and structural studies.

The interaction of 18 different Escherichia coli aminoacyl-tRNA species with elongation factor Tu and GTP has been measured by a fluorescence titration assay under equilibrium conditions. The dissociation constants range from 1.9 +/- 0.2.10(-10) M up to 1020 +/- 250.10(-10) M depending on the nucleotide sequence, secondary structure and the chemical composition of the aminoacyl residue of the particular aminoacyl-tRNA. The 'aminoacyl domain' of tRNA consisting of the single stranded, four-nucleotide-long 3'-terminus, aminoacyl stem of seven base-pairs, T-stem and T-loop contains all elements necessary for binding EF-Tu.GTP. The efficiency of aminoacyl-tRNA interaction with EF-Tu.GTP is modulated by the sequence of this 'aminoacyl domain' and by natural modification of its nucleotide residues. An oligoribonucleotide resembling the aminoacyl stem of E.coli tRNA(Ala) and consisting of a four-membered 3'-end, a stem of seven base-pairs and a loop of six nucleotides was prepared by total chemical synthesis on a polymer support. It can be enzymatically aminoacylated by alanine but does not bind in its aminoacylated form to EF-Tu.GTP.

Anticodon↗
PubMed1990

Interaction of a selenocysteine-incorporating tRNA with elongation factor Tu from E.coli.

Selenocysteine-incorporating tRNA(Sec)(UCA), the product of selC, was isolated from E.coli and aminoacylated with serine. The equilibrium dissociation constant for the interaction of Ser-tRNA(Sec)(UCA) with elongation factor Tu.GTP was determined to be 5.0 +/- 2.5 x 10(-8) M. Compared with the dissociation constants of the two elongator Ser-tRNA(Ser) species (Kd = 7 x 10(-10) M), the selenocysteine-incorporating UGA suppressor tRNA has an almost hundred fold weaker affinity for EF-Tu.GTP. This suggests a mechanism by which the Ser-tRNA(Sec) is prevented in recognition of UGA codons. This tRNA is not bound to EF-Tu.GTP and is converted to selenocysteinyl-tRNA(Sec). We also demonstrate the lack of an efficient interaction of Sec-tRNA(Sec)(UCA) with EF-Tu.GTP. The results of this work are in support of a mechanism by which the selenocysteine incorporation at UGA nonsense codons is mediated by an elongation factor other than EF-Tu.GTP.

Chromatography, Affinity↗
PubMed1990

Comparison of plain and Gd-DTPA-enhanced MR-imaging in children.

40 children and adolescents (aged 1-16 years) were examined by MRI at 1.0 T. Gd-DTPA was given intravenously at a dose of 0.1 mmol/kg body weight. In all cases T1-weighted SE sequences were used to demonstrate contrast enhancement. No adverse effects were seen. 30 patients had one or more lesions; in 20 patients contrast enhancement was seen. In 4 cases lesions were not observed by plain MRI and could only be detected after Gd-DTPA. In addition, contrast enhancement provided additional information about the differentiation of lesion from edema or necrosis in 13 patients. Normal brain matter did not show any changes in signal intensity. However, an age-dependent signal increase was found in the normal vertebral bone marrow in all children. Gd-DTPA should be used as a supplementary examination whenever a tumor or an infectious disease of the CNS is suspected and plain MRI is normal, or when origin and extent of a lesion cannot be adequately defined with plain MRI.

Adolescent↗
PubMed1990

Role of calcium channels and protein kinase C for release of norepinephrine and neuropeptide Y.

The role of calcium for the release of norepinephrine (NE, determined by high-pressure liquid chromatography) and neuropeptide Y (NPY, determined by radioimmunoassay) was investigated in guinea pig perfused hearts with intact sympathetic innervation. In the presence of extracellular calcium (1.85 mM), electrical stimulation of the left stellate ganglion (12 Hz, 1 min) induced a closely related release of NE and NPY with the molar ratio of approximately 400-600 (NE) to 1 (NPY). The stimulation-evoked overflow of both transmitters was dependent from the extracellular calcium concentration and was almost completely suppressed by calcium-free perfusion. The corelease of both transmitters was not affected by the L-type calcium channel blocker felodipine (1-10 microM). However, the overflow of NE and NPY was markedly attenuated by the unselective calcium antagonist flunarizine (1-10 microM) and completely prevented by the neuronal (N-type) calcium channel blockers omega-conotoxin (1-100 nM) and cadmium chloride (10-100 microM), indicating a key role for N-type calcium channels in the exocytotic release of transmitters from cardiac sympathetic nerve fibers. Possibly due to unspecific actions, such as interference with sodium channels or uptake1-blocking properties, the phenylalkylamines verapamil (0.01-10 microM) and gallopamil (1-10 microM) reduced NPY overflow with only a minor effect on NE overflow. The stimulation-induced transmitter release was increased up to twofold by activation of protein kinase C (phorbol 12-myristate 13-acetate, 3 nM-3 microM) and completely suppressed by inhibition of protein kinase C (polymyxin B, 100 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[The value of magnetic resonance tomography during radiotherapy of childhood tumors in the posterior fossa and the pineal region].

MRT is a highly sensitive method for the diagnosis of childhood tumours in the posterior fossa. Since it demonstrates tumour extent better than does CT, MRT is the method of choice for radiotherapy planning. The result of treatment can be judged morphologically and by measuring relaxation times. Changes due to treatment can be recognised more easily than by CT. A disadvantage of MRT is lack of specificity, since various processes may lead to an equal increase in T1 and T2 times.

Brain Neoplasms↗
PubMed1989

[Measuring intracellular pH in cultivated corneal epithelial cells].

Electrolyte and fluid transport across the corneal epithelium plays an important role for the maintenance of corneal transparency. Little is known about the cellular mechanisms underlying the transepithelial transport phenomena. We have therfore started to investigate the transmembranal transport processes in cultured corneal epithelial cells. Studies were performed in an established corneal epithelial cell line from the rabbit (SIRC cells) and in primary cultured bovine corneal epithelial cells. In these cells, intracellular pH was continuously measured using the pH-sensitive absorbance of intracellularly trapped dimethylcarboxyfluorescein. In both cell types, SIRC cells and cultured bovine corneal epithelial cells, evidence was found in favor of a sodium-dependent and amiloride-sensitive Na/H exchange. In cultured bovine corneal epithelial cells, Na/H exchange was shown to play an important role in intracellular pH recovery after an acid load. Furthermore, as has been demonstrated in other epithelia, Na+/H+ exchange may also be important for transepithelial corneal transport.

Acid-Base Equilibrium↗
PubMed1988

Characterization of Na+/H+ exchange in a rabbit corneal epithelial cell line (SIRC).

Continuous intracellular pH (pHi) measurements were performed in SIRC rabbit corneal epithelial cells using the pH-sensitive absorbance of intracellularly trapped 5(and 6)-carboxy-4',5'-dimethylfluorescein. Steady-state pHi in nominally bicarbonate free Ringer's solution averaged 6.87 +/- 0.02 (mean +/- S.E., n = 53). After intracellular acidification induced by the NH4Cl-prepulse technique, there was a sodium-dependent pHi recovery towards the normal steady-state pHi. The initial pHi recovery rate was a saturable function of extracellular sodium concentration with an apparent Km for external sodium of about 25 mM and a Vmax of about 0.28 pH units/min. Virtually no pHi recovery was observed in the absence of extracellular sodium. Sodium removal during steady state acidified the cells by 0.36 +/- 0.05 pH units (mean +/- S.E., n = 13) within 5 min. There was a dose-dependent inhibition of pHi recovery after NH4Cl prepulse by amiloride with an IC50 of about 15 microM. Amiloride in a concentration of 1 mM almost completely abolished pHi recovery. Amiloride (1 mM) applied during steady state induced an intracellular acidification of 0.2 +/- 0.03 pH units (mean +/- S.E., n = 7) within 5 min. These findings suggest that a Na+/H+ exchange is present in SIRC rabbit corneal epithelial cells. Na+/H+ exchange seems to be the major process involved in pHi recovery in SIRC cells after an intracellular acid load. Na+/H+ exchange also plays a role in the maintenance of steady-state pHi.

Amiloride↗
PubMed1988

Magnetic resonance imaging of normal and pathological white matter maturation.

Fifty children between 3 months postnatal and 16 years of age were examined by means of a 1.5 T superconductive magnet, run at 0.35 and 1.0 T. The myelination was studied qualitatively and quantitatively (relaxation times, proton densities, image contrast). With increasing age, a decrease of T1 and proton density of white matter was found, which was complete at one year of age. In regions with a slow progression of myelination, gray/white matter contrast showed an increase up to the end of the first decade. Pathological white matter maturation was diagnosed either as an abnormal transformation of myelin (characterized by abnormal relaxation values), or as a deficient or delayed myelin formation (in comparison with age-matched controls).

Adolescent↗
PubMed1988

Evidence for Na+/H+ exchange and pH sensitive membrane voltage in cultured bovine corneal epithelial cells.

Two methods were used to investigate cellular ion transport processes in confluent monolayers of cultured bovine corneal epithelial cells: measurements of membrane voltage (V) using conventional microelectrodes, and intracellular pH (pHi) measurements using the pH sensitive absorbance of intracellularly trapped 5 (and 6)-carboxy-4', 5'dimethyl-fluorescein. (1) V averaged -39.2 +/- 0.9 mV (mean +/- SEM, n = 71) with a range of -30 to -59 mV. Increasing extracellular potassium depolarized the cell membrane with a K+-slope of 43.3 mV/decade [K+] (for [K+] between 20 and 80 mM). Intracellular as well as extracellular acidification reversibly depolarized the cell membrane. Depolarization induced by 40 mM K+-pulses was smaller at extracellular pH (pHo) of 6.9 as compared to pHo = 7.9. These findings are compatible with a pH-sensitive K+ conductance. (2) During steady state pHi was 6.96 +/- 0.05 (mean +/- SEM, n = 7). After intracellular acidification, induced by NH4Cl-prepulse technique, pHi was regulated back towards normal steady state pHi. Application of 1 mM amiloride reversibly inhibited pHi recovery. Furthermore, pHi backregulation was inhibited by removing sodium from the extracellular solution. The effect was reversible after readdition of sodium. These findings suggest that a Na+/H+ exchange is present in corneal epithelial cells and participates in pHi backregulation after an intracellular acid load.

Acids↗
PubMed1979

[Hunger and intellectual development].

Severe hunger in infancy and early childhood is associated with reduced head size, reduction in cell number and impaired chemical composition of the brain. Intellectual deficits correlating with malnutrition persist into later life. Because malnutrition and poor socio-economic conditions often exist together the additional unfavorable influence or lack of environmental stimuli on intellectual development has to be taken in account.

Brain↗
PubMed1977

[Hydranencephaly versus spelencephaly--a report of two cases (author's transl)].

Two cases are presented, one of hydranencephaly and one of spelencephaly. Spelencephaly represents an intermediate form between multicystic encephalopathy and hydranencephaly and is characterized by preservation of the ventricular walls. There is no clinical distinction between spelencephaly and hydranencephaly. Diagnosis can be made by pneumencephalography, as described in this paper, if the gas is applied via both lumbar and ventricular puncture. Autopsy findings of both cases are presented and the possible vascular etiology of the condition is discussed.

Anencephaly↗