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Biomedical subjects

M Griese

Publications and source records attributed to M Griese.

96 records · Page 6Linked to original sources
PubMedDate not supplied

[Leprosy - An overview from a pediatric perspective].

Worldwide tourism is an increasing industry. One result of this phenomenon is the occurrence of imported infectious diseases, as recently observed even in Germany. Leprosy ranks high among dreaded infectious diseases from tropical and subtropical countries. It remains a major health threat despite marked improvements in diagnosis and therapy. This was achieved by a better understanding of bacteriological and immunological mechanisms over the past decades, resulting in a decline of Leprosy's incidence.

Age Factors↗
PubMedDate not supplied

[The beta adrenergic system of lymphocytes in children with atopic dermatitis].

A defect in the beta-adrenergic system is considered to be one of the basal causes of atopic dermatitis (AD). The number and affinity (KD) of beta-receptors was determined in lymphocytes of 19 children with AD and of 17 controls using the radioligand 125JCYP to find out whether this hypothesis is relevant. In addition, the basal cAMP level was measured as well as the cAMP-accumulation after stimulation of the adenylcyclase (AC) via the beta-receptor with 10(-4) M isoprenaline (IPN) and after direct stimulation of AC with 10(-4) M forskolin. Receptor quality and receptor quantity were compared to the severity of AD. A statistically significant difference between AD and control children was not registered for the following parameters: receptor-density, affinity for 125ICYP, cAMP-accumulation after adenylcyclase stimulation via the beta-receptor with IPN or after direct stimulation with forskolin. The increase in cAMP after IPN or forskolin was in the same range for children suffering from AD as for controls. Only the basal cAMP was significantly lower. Three patients with very severe AD (greater than 20% body surface area) had a significantly reduced number of beta-receptors (603 +/- 123 BS/Ly) compared with the control group (1142 +/- 112 BS/Ly). A linear relation existed between age, receptor density and isoprenaline-mediated cAMP accumulation for both control children and those with AD. This age-dependent response of the beta-receptor seems to be specific as cAMP-accumulation after stimulation with forskolin was not age-related.

Adolescent↗
PubMedDate not supplied

The interaction of phosphatidylcholine with alveolar type II pneumocytes is dependent on its physical state.

Dipalmitoylphosphatidylcholine, the principal phospholipid component of surfactant, inhibits agonist stimulated surfactant secretion whereas dioleoylphosphatidylcholine does not. As knowledge of the type of interaction of phosphatidylcholines is important for the detailed analysis of surfactant homeostasis, this was examined in isolated rat type II pneumocytes in primary culture. Solid state [3H]-dipalmitoylphosphatidylcholine liposomes associated with the cells rapidly. No effect of blockade of endocytosis on the cellular association was observed, whereas that of the fluid phase marker [14C]-sucrose was reduced. No evidence for the fusion of the dipalmitoylphosphatidylcholine liposomes or for phospholipid exchange with the cells was detected, suggesting that the cells primarily bound the dipalmitoylphosphatidylcholine liposomes. Although a "specific" site with a saturable binding capacity (20 nmol dipalmitoylphosphatidylcholine/mg protein, KD 25 microM) was demonstrated, the interaction did not exhibit all the characteristics of a typical pharmacological receptor. The preincubation with nonlabeled dipalmitoylphosphatidylcholine almost completely inhibited binding to the cells. In accordance with their effects on stimulated surfactant secretion, various other phosphatidylcholine liposomes inhibited binding that was very much dependent on their physical state, as only those in a solid state were inhibitory by more than 50%. These results support the view that the binding of dipalmitoylphosphatidylcholine may be involved in the feedback regulation of surfactant secretion in type II pneumocytes and that these processes are dependent on the physical state of the interacting liposomes.

1,2-Dipalmitoylphosphatidylcholine↗
PubMedDate not supplied

Influence of blood constituents on uptake of a lipid-extracted natural surfactant by alveolar type II cells.

During lung injury, blood constituents may leak into the alveolar space and impair surfactant function. This study investigated possible interferences with the alveolar surfactant life cycle, by assessing the effects of various blood constituents on size, state of aggregation, and uptake of a natural, lipid-extracted bovine surfactant preparation (Alveofact) into isolated rat type II cells in primary culture. The results showed that plasma, serum, albumin, immunoglobulin G, bilirubin, and galactose inhibited uptake according to concentration. Fibrinogen and transferrin enhanced uptake; hemoglobin, fibronectin, and vitronectin had no effect. Uptake was also impaired when the blood constituents were washed off and the surfactant was added afterward. For some of the blood constituents, a direct interaction with the surfactant liposomes was observed, resulting in changes of liposome size and state of aggregation. However, no correlation between these changes and effects on uptake were found. During lung injury with increased permeability edema, a direct inhibition of surfactant lipid uptake by blood constituents might lead to a reduced delivery of surfactant components into type II cells and disturb surfactant metabolism.

1,2-Dipalmitoylphosphatidylcholine↗
PubMedDate not supplied

[Clinical, biological and genetic heterogeneity of the inborn errors of pulmonary surfactant metabolism: SP-B deficiency and alveolar proteinosis].

Pulmonary surfactant is a multimolecular complex located at the air-water interface within the alveolus and to which a bulk of functions has been assigned, physical (surface-active properties) as well as immune or depurant. This complex consists of a surface active lipid layer (mainly phospholipids), and of an aqueous subphase. From discrete surfactant sub-fractions, one can isolate very hydrophobic proteins SP-B and SP-C as well as the collectins SP-A and SP-D, which were shown to have structural, metabolic, or defensive properties. Inborn or acquired abnormalities of surfactant, qualitative or quantitative in nature, account for a number human diseases. Beside hyaline membrane disease of the preterm neonate, a cluster of hereditary or acquired lung diseases have been characterized by the storage of periodic acid Schiff-positive material filling the alveoli. From this heterogeneous nosologic bulk, at least two discrete entities presently seem to emerge: 1) SP-B deficiency, in which an essentially proteinaceous material is stored within the alveoli, and which is a bona fide autosomal recessive Mendelian entity linked to the SFTPB gene (MIM 1786640), generally entailing neonatal respiratory distress with rapid fatal outcome, although partial or transient deficiencies have also been observed; 2) alveolar proteinosis, characterized by the storage of a mixed, protein and lipid material, and which constitutes a relatively heterogeneous clinical biological syndrome, with regards to age at onset (from the neonate through to adulthood) as well as the severity of associated signs. Murine models with a targeted mutation of the gene encoding GM-CSF (Csfgm) or the beta subunit of its receptor (Il3rbl) support the hypothesis of an abnormality of surfactant turnover in which the alveolar macrophage would be a key player. Beside SP-B deficiency, in which a near-consensus diagnostic chart can be designed, the ascertainment of other abnormalities of surfactant metabolism is not straightforward. The disentanglement of this disease cluster is however essential, with aim to propose differentiated therapeutic procedure : repeated bronchoalveolar lavages, GM-CSF replacement, bone marrow grafting or lung transplantation.

Amino Acid Metabolism, Inborn Errors↗