[Treatment of nasal obstruction]. / Leczenie niedroznosci nosa.

Various methods of treatment of impaired nasal patency are presented calling attention to the fact that the most frequent cause of impairment of nasal respiration is deviation of the nasal septum associated with unilateral or bilateral hypertrophy of inferior turbinates. Impaired nasal breathing leads to frequent recurrences of respiratory infections. Restoration of normal breathing route and physiological role of the nase, among others, warming and moistening of inspired air, is an important and ever present problem in laryngology. The problem has assumed a new importance when it was found that chronic impairment of nasal patency could have an adverse effect on the circulatory system which develops in connection with sleep apnoea.

[Disturbances of upper airway patency and their sequelae]. / Zaburzenia droznosci górnych dróg oddechowych i ich nastepstwa.

The authors present their investigations of the effects of upper airway compromise from hypertrophy of lymphoid tissue, nasal polyps, deviated nasal septum and hypertrophy of the nasal conchae. All the patients were under the age of 18 years. Methods of assessing children with airway compromise include 6-hour polysomnography (PSG). Special attention was paid to the heart function, as well as to pO2 and pCO2 saturation. Computer analysis of PSG studies revealed disturbances in circulatory system function, unnoticed in routine physical examination. The results may serve as one more voice in a debate about the advisability of surgical treatment of airway compromise performed in childhood.

Glycolipids and glycopeptides of red cell membranes in congenital dyserythropoietic anaemia type II (CDA II).

The composition and structure of neutral and acidic oligoglycosylceramides, polyglycosylceramides and polyglycosylpeptides were determined in erythrocyte membranes of two patients with congenital dyserythropoietic anaemia type II. In keeping with previous studies we found an elevated accumulation in CDA II erythrocytes of LacCer, Lc3Cer and nLc4Cer. Gb4Cer was elevated in erythrocytes of only one of the two patients tested. In addition we found a significant increase of 6IVNeuAcnLc4Cer ganglioside. Polyglycosylceramides were elevated 6-fold but they resembled those of cord erythrocytes with respect to complexity and the number of side chains. Polyglycosylpeptides of CDA II erythrocytes were decreased 7-fold. These glycopeptides were, however, heterogeneous with respect to branching pattern; the minor fraction was highly branched whereas the major one was more linear in structure. Both polyglycosylceramides and polyglycosylpeptides exhibited high I and i antigenicity. We postulate that the accumulation of glycolipids and underglycosylation of glycoproteins in CDA II membranes results from the prolongation of G1 and possibly M phases of the mitotic cycle of the erythroid cells in which glycolipids are preferentially synthesized.

Structure and blood-group I activity of poly(glycosyl)-ceramides.

Nitrous acid deamination of N-deacetylated blood-group O poly(glycosyl)ceramides resulted in a complete degradation of the glycolipids to give O-beta-D-galactopyranosyl-(1 leads to 4)-2,5-anhydro-D-mannose, O-alpha-L-fucopyranosyl-(1 leads to 2)-O-beta-D-galactopyranosyl-(1 leads to 4)-2,5-anhydro-D-mannose, lactosylceramide, and small proportions of free 2,5-anhydro-D-mannose. A series of straight-chain glycolipids containing up to six glycosyl residues and comprising alternating 3-O-substituted D-galactosyl and 4-O-substituted 2-acetamido-2-deoxy-D-glucosyl residues was isolated from partial acid hydrolyzates of poly(glycosyl)ceramides. Branching points of 3,6-di-O-substituted and 6-O-substituted D-galactosyl residues were observed only in fractions containing more than six glycosyl residues. Sequential periodate oxidation of poly(glycosyl)ceramides gradually eliminated the branching points. This elimination was not complete, even after four cycles of degradation. The ability of poly(glycosyl)ceramides to precipitate with anti-I serums disappeared after two cycles of degradation. These results suggest a general structure for poly(glycosyl)ceramides. I blood-group activity of the glycolipids would depend on the periodical arrangement of branched side-chains.

Isolation and characterization of poly(glycosyl)ceramides (megaloglycolipids) with A, H and I blood-group activities.

Very complex glycosphingolipids with A, H and I blood-group activities were isolated from human erythrocyte membranes. The membranes were obtained from erythrocytes of blood group A, A2 and O respectively. A general formula for the antigens is: (Fuc)3-4(Gal)n(LlcNAc)n-2(Glc)1(Sphingosine)1(where Fus is fucose, Gal is galactose, GlcNAc is N-acetylglucosamine and Glc is glucose) with values of n ranging from 10-27. A-active preparations contain additionally 2-3 residues of N-acetylgalactosamine. In view of the unusual complexity of these compounds they were designated poly(glycosyl)ceramides (formerly megaloglycolipids). Individual poly(glycosyl)ceramide fractions were isolated from A erythrocytes and were found to differ by about 8 glycosyl residues per molecule forming a series of compounds with 22, 30, 38, 51 and 59 glycosyl residues per mole. Structural studies indicate that the main sequence of poly(glycosyl)ceramides consists of the residues of galactopyranose and 2-deoxy-2-acetamidoglucopyranose substituted at 3 and 4 position respectively. These residues are probably alternating. N-Acdtylglucosamine substituted at 3 position was not found in poly(glycosyl)ceramides. Brances of poly(glycosyl)ceramides originate from 3 and 6 position of galactopyranosyl residues. The number of branches is proportional to the degree of molecular complexity. In poly(glycosyl)ceramides isolated from A and A2 erythrocytes the branches are terminated with the following structures GalNAc alpha 1 leads to 3 [Fuc alpha 1 leads to 2] Gal; Fuc alpha 1 leads to 2 Gal and Gal (presumably Gal beta 1 leads to 4 GlcNAc). In poly(glycosyl)ceramides from A cells the total number of A and H-active structures per average molecule of 30-35 glycosyl residues amounts to 2.1 and 1.2 respectively while the number of terminal galactose structures is 1.8. For poly(glycosyl)ceramides from A2 erythrocytes the corresponding figures are 0.75, 3.5, and 2.1 respectively. Poly(glycosyl)ceramides from O cells comprise about 3.8 H-active structures and 1.8 terminal galactopyranosyl residues. In poly(glycosyl)ceramides with high "n" values the number of terminal galactose structures is increased. These fractions display high blood-group I activity. However, the removal of terminal galactose with beta-galactosidase affects I-activity only slightly.