Investigation of cytokine (tumor necrosis factor-alpha, interleukin-6, interleukin-10) concentrations in the cerebrospinal fluid of female patients with multiple sclerosis and systemic lupus erythematosus.

Humoral immune response seems to play a role in the pathogenesis of multiple sclerosis (MS) and in the central nervous system (CNS) complications of systemic lupus erythematosus (SLE). The aim of the present study was to compare the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and IL-10 in the cerebrospinal fluid of female patients with several forms of MS (50 patients), and in female patients with several types of CNS complications in SLE (50 patients). Samples were investigated using an enzyme-linked immunosorbent assay technique. Involvement of CNS in SLE patients seems to be characterized with elevated concentrations of all three cytokines in CNS and intrathecal synthesis of IL-6. In MS patients, an intrathecal synthesis of TNF-alpha (relapsing-remitting form) and IL-6 (primary progressive form) were observed. Clinical forms of MS seem to be immunologically heterogeneous. The activation of cytokine network was observed in SLE patients with CNS complications, independent of the pathological process. Similarities between SLE and MS patients with the primary progressive form of the disease were demonstrated concerning the intrathecal synthesis of IL-6. Only MS patients with the relapsing-remitting clinical form showed intrathecal TNF-alpha synthesis.

Increased levels of tumor necrosis alpha and soluble vascular endothelial adhesion molecule-1 in the cerebrospinal fluid of patients with connective tissue diseases and multiple sclerosis.

The aim of the present study was to investigate the serum and cerebrospinal fluid (CSF) concentrations of tumor necrosis factor alpha (TNF-alpha) and soluble vascular cell adhesion molecule-1 (sVCAM-1) in patients with primary progressive form of multiple sclerosis (MS) and in patients with connective tissue diseases (CTDs) complicated with central nervous system (CNS) involvement. Stimulation of sVCAM-1 release by TNF-alpha was demonstrated on endothelial cells of brain vessels. We intended to present the TNF-alpha stimulated elevation of sVCAM-1 in the serum and CSF in any cases of CNS lesion. Fifty patients with several CTDs complicated with neuropsychiatric symptoms and 25 MS patients with primary chronic progressive form of the disease were selected. Determinations of TNF-alpha and sVCAM-1 were performed using ELISA methods. TNF-alpha and sVCAM-1 concentrations were elevated in the CSF of all patients, intrathecal synthesis of sVCAM-1 was demonstrated in MS patients. The changes in the TNF-alpha and sVCAM-1 concentrations were independent from the clinical manifestations, immunoserological changes and quality of neuropsychiatric symptoms of the CTDs. The stimulatory effect of TNF-alpha was more pronounced in the CSF of MS patients.

Urinary beta 2-microglobulin and retinol binding protein: individual fluctuations in cadmium-exposed workers.

Urinary retinol binding protein (RBP) and beta 2-microglobulin (beta 2-m) were compared in apparently healthy population groups with and without occupational exposure to cadmium (Cd). The relationship observed in neutral urine was: RBP (micrograms/mmol creatinine) = 0.786 + 0.814 beta 2-m (micrograms/mmol creatinine). This relationship was similar to that reported for patients with various renal diseases [13]. Analysis of urine samples collected weekly from workers exposed occupationally to Cd revealed marked fluctuations, not only in the concentration of the acid-labile beta 2-m but also in the level of the pre-analytically more stable RBP. Therefore, repeated sampling and urine analyses are suggested as means to obtain more reliable data when monitoring Cd-exposed personnel.

Anion transport of the red cell under non-equilibrium conditions.

1. The exchange of sulphate for chloride across the human red cell membrane was measured in both directions, i.e. by sulphate influx and sulphate efflux. The influence of the concomitant transient pH changes was minimized by phosphate buffer and by choosing experimental conditions of moderate pH sensitivity (pH 6.4 and 7.8). Sulphate self exchange was determined in chloride-free erythrocyte suspensions. 2. The transport of external sulphate into red cells proceeded at a 15-fold greater rate if its initial concentration was raised from 5 to 95 mM. In contrast the velocity constant of sulphate efflux into sodium chloride medium increased only twofold when the intracellular sulphate concentration was increased. To explain this asymmetry it is proposed that external sulphate ions are more able to complete with chloride for the anion transport sites that those present in the cell interior. 3. The transient membrane potential due to the uneven distribution of sulphate and chloride was shown by the rapid introduction of chromate into the cells. When the erythrocytes contained chloride and the external anion was sulphate, the cells took up chromate 50 times (16.5 degrees C) faster than with equilibrium chloride distribution. 4. Chloride efflux into sodium sulphate media was measured by a chloride-sensitive electrode. Under buffered conditions in neutral and alkaline media two kinetic components were observed as the result of chloride exchange against hydroxyl and sulphate ions. At pH 6.4, chloride efflux was characterized by a single velocity constant identical to that of sulphate movement in the opposite direction. The results show that under appropriate circumstances net chloride efflux measurements can provide comparative data on the anion permeability of the red cell membrane.