Hudson-St?hli's iron line in the cornea. Occurrence in 1968 and in 1988

Examination of 700 persons in 1968 showed presence of Hudson-St?hli's iron line in 29%. A similar examination by the same author 20 years later revealed a significantly lower occurrence (18%) and fewer cases of binocular occurrence (70% against 43%). The line is most often horizontal. If oblique, it generally passes from the upper nasal to the lower temporal region.     

Granulocyte-macrophage colony-stimulating factor enhances basophil histamine release induced by non-IgE-dependent stimulators

Some cytokines are known to affect IgE-mediated basophil histamine release. The effect of the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) on human basophil and masct cell histamine release was studies further. Blood leukocytes with approximately 2% basophils from 9 healthy individuals were incubated with recombinant human GM-CSF (0.3–30 U/ml) in combination with A23187 (10^–7–10^–6 M) or washedStaphylococcus aureus whole bacteria (0.3–2.5 mg/ml). Histamine release was measured spectrofluorometrically. GM-CSF in itself did not induce histamine release. The addition of GM-CSF to cells stimulated with A 23187 caused a dose-dependent enhancement amounting to mean 70% at 3 U/ml and mean 170% at 30 U/ml (P<0.05). GM-CSF enhanced the bacteria-induced histamine release by 30% at U/ml and by 65% at 3 U/ml (P<0.05). The enhancement did not depend on cell-bound IgE or LPS contamination. In preliminary mast cell experiments with lung tissue we did not find an enancing effect of GM-CSF on IgE-mediated histamine release.     

Cytokine-induced histamine release from basophils of AIDS patients

Basophil leukocytes obtained from AIDS patients, allergic patients and healthy controls were stimulated in vitro with interleukin 4, lymphotoxin, tumour necrosis factor alpha and interferon gamma to examine the histamine releasing effect. The cytokines caused histamine release from the basophils of approximately half the AIDS patients and from 8-17% of the allergic patients. No response was obtained in the control group. Removal of cell surface immunoglobulins abolished the response to cytokines, indicating an Ig-dependent mechanism. Passive sensitization with cell-derived Ig, with Ig deprived of IgE, or with IgG, indicated that cell-bound IgE was responsible for the cytokine-induced histamine release in AIDS patients. This response may be mediated by cytokine-selective IgE antibodies.     

Histamine release from basophil leukocytes induced by microbial antigen preparations in patients with AIDS

Type I allergy against some common microorganisms was investigated in 14 patients with AIDS and 11 human immunodeficiency virus (HIV) antibody-positive homosexual men, and in a control group consisting of 13 heterosexual men without HIV antibodies. Basophil histamine release technique was used as a sensitive method to detect type I allergy against Candida albicans (CA), Herpes simplex virus type I (HSV-I) and cytomegalovirus (CMV). Of the 14 AIDS patients 11 (78%) showed significant histamine release when stimulated with CA, and HSV-I caused release in 10 (71%), whereas no response was obtained by CMV. In the group of HIV antibody-positive men only one released histamine when stimulated with CA and HSV-I and this patient also had lymphadenopathia. In contrast to these results, no release of histamine was obtained in the control group consisting of 13 heterosexual men. The histamine release caused by CA and HSV-I is mediated by an immunological reaction, since the release was abolished and regained by removal from and refixation to the cell surface of the cell-bound immunoglobulins. These results suggest an involvement of type I allergy as a pathogenetic co-factor in some infections in AIDS, and allergic type I reactions to CA and HSV-I might be an indicator for the presence of manifest AIDS.     

Membrane sialic acid influences basophil histamine release by interfering with calcium dependence

The influence of the cell membrane content of sialic acid on basophil histamine release was examinedin vitro in allergic patients and normal controls. Enzymatical removal of sialic acid enhanced histamine release induced by allergen and anti-IgE, whereas an increase in membrane sialic acid content by insertion of sialic acid containing gangliosides into the membrane inhibited the mediator release.The reduction in membrane sialic acid content abolished the inhibitory capacity of the calcium channel antagonist nimodipine, whereas the inhibition produced by verapamil and lanthanum was not affected. This difference, together with the previous finding that alterations in membrane sialic acid content is reflected in the cell sensitivity to extracellular calcium, suggest an interaction between membrane sialic acid and the calcium channels involved in basophil histamine release.     

History of Acta Ophthalmologica – the first 50 years

Acta Ophthalmologica appeared as the scientific journal of the Nordic ophthalmological Societies in 1923. The intention was to expose the clinical and experimental developments among the ophthalmological communities of the four Nordic countries: Denmark, Finland, Norway and Sweden. The collaboration within the field of ophthalmology had been attempted with the publication of ‘Nordisk ophthalmologisk Tidsskrift’ in the years 1889–1892. Now, once again, the wish for a tighter Nordic cooperation was explored by enthusiastic ophthalmologists in all four countries. One person stands out as the driving force, K.K.K. Lundsgaard, who in spite of his early death in 1931 was remembered by name on the front page of Acta since 1936 by the Latin phrase ‘A K.K.K. Lundsgaard edi coepta’. The present review recalls details from the early years when the journal found its place in the ophthalmology and creates the background for some reflections on purpose and goals by publishing a scientific journal.     

A new method for detecting histamine release

Glass microfibres have been found to bind histamine with high affinity and selectivity. A new test for measuring basophil histamine release has been developed using the glass microfibres as a solid phase. Glass microfibres are crushed and fixed to the bottom of microtitre plates with a water-soluble glue. Histamine release is performed in the glass microfibre -prepared microtitre plates by challenging 100 microliter washed blood with 20 microliter antigen per well for 90 min at 37 degrees C. Released histamine is bound with high affinity to the glass microfibres , since 90% of histamine in the solution is adsorbed to the fibres. After incubation the microtitre plate is washed with H2O to remove cells and interfering substances. Fibre-bound histamine is detected by the fluorometric o-phthaldialdehyde method. The sensitivity of the assay is 0.63 ng histamine, 2 HCl and the histamine standard curve is linear up to at least 5 ng histamine, 2 HCl. Optimal conditions for the new assay are described. After challenge with anti-Ige a comparison with the conventional histamine release from Ficoll-Hypaque-isolated leukocytes showed almost identical results.     

Basophil Histamine Release and Humoral Changes during Immunotherapy

An in vitro pilot study was performed to determine whether basophil cell-bound specific IgE was correlated to serum-specific IgE and to basophil cell sensitivity during immunotherapy with a well-documented treatment. The findings showed a clear dissociation between these three parameters, which is in contrast to the situation before hyposensitization and to our previous study in a comparable group of non-hyposensitized patients, where highly significant correlations were observed. Further investigations are in progress to clarify whether the dissociation is involved in the clinical improvement.     

Corneal thickness after cataract extraction with air in the anterior chamber.

A total of 135 patients had the corneal thickness measured prior to cataract extraction. The chamber was re-established by air in 86, while the remainder acted as controls. On the second postoperative day the corneal thickness had increased by 12.7% in the air-inflated group, and by 17.6% in the control group. On the sixth postoperative day the increases in thickness were 7.2 and 11.1% respectively. On follow-up control 6 to 12 months later the corneal thickness was as before the operation. Epithelial oedema was significantly more frequent in the control group. The conclusion is drawn that an air bubble in the anterior chamber has no unfavourable effect on the corneal endothelium. On the contrary, it seems to protect the endothelium from postoperative damage.