[Evaluation of an immunochromatographic dipstick test for the assessment of tetanus immunity in horses].

Knowledge of tetanus immunity in equine patients is crucial in cases of injuries, elective surgeries, or when effective vaccination protocols are to be designed. The Fassisi® TetaCheck is a stall-side rapid test which was developed to address these issues. The purpose of the present study was to evaluate its performance parameters.

Visible light Laue diffraction from woodpile photonic crystals.

Bragg diffraction is often used as a tool to assess the structural quality of two-dimensional and three-dimensional (3D) photonic crystals. However, direct conclusions from the Laue diagrams to the underlying crystals structure cannot be drawn, as multiple scattering due to the high index contrast takes place. Here we systematically study the scattering of visible light by 3D woodpile photonic crystals with varying internal refractive index contrast Δn, to determine the limits of the single (kinematic) scattering approach.

The effect of butylated hydroxytoluene, with and without cortisol, on stimulated lymphocytes.

In the present work we undertook to ascertain whether butylated hydroxytoluene (BHT), which is used in food as an antioxidant, is capable of either inhibiting human lymphocyte stimulation or acting synergistically with cortisol and prednisolone to the same end. BHT cytotoxicity was observed at concentrations higher than 100 micrograms/ml. In the concentration range of 0.

The effect of HIV-1 infection on the lipid fatty acid content in the membrane of cultured lymphocytes.

Elevations in the levels of unsaturated fatty acids (FAs) in membrane lipids lead to an increase in cell membrane fluidity and may also be involved in cell fusion and death through the loss of normal membrane function and integrity. Since the infection of susceptible cells with HIV leads to cell fusion and subsequent loss of viability, the present study was undertaken to see whether HIV infection can alter the relative content of unsaturated FAs in the host cell membrane and to determine whether this change correlates with cell death. Peripheral lymphocytes (PBLs) of a healthy donor and two CD4+ cell lines were chosen: MT-4, which is killed following HIV infection, with significant cell death being observed 5 days postinfection, and H9 which is not killed.

Cortisol catabolism by lymphocytes of patients with chronic lymphocytic leukemia.

A low rate of catabolism of cortisol by lymphocytes correlates with high sensitivity of the cells to the steroid and causes them to die at a greater rate than control samples. Since lymphocytes of patients with chronic lymphocytic leukemia respond to treatment with glucocorticosteroids and are cortisol sensitive, we attempted to see whether their capability to catabolize cortisol differs from that of normal lymphocytes. No difference was found between the two groups of cells with regard to the pattern of cortisol metabolites.

Cortisol catabolism by lymphocytes of patients with systemic lupus erythematosus and rheumatoid arthritis.

We have shown that low cortisol catabolism by lymphocytes correlates with a high sensitivity of the cells to the steroid. In the present study, we aimed to assess whether high resistance to corticosteroid treatment correlates with a high rate of cortisol catabolism by lymphocytes. Since patients with systemic lupus erythematosus (SLE) usually require high doses of corticosteroids, while patients with rheumatoid arthritis (RA) respond to relatively low doses of steroids, we compared the capability of lymphocytes of patients with SLE and RA to catabolize cortisol.

The effect of fatty acids on the vulnerability of lymphocytes to cortisol.

We have shown previously that cortisol-sensitive lymphocytes (thymocytes) have a much lower capacity than cortisol-resistant cells to catabolize cortisol and that linoleic acid inhibits the catabolism of cortisol by lymphocytes and modulates the sensitivity of lymphocytes to cortisol. In the present study, we attempted to see whether other fatty acids are inhibitory and if inhibition of cortisol catabolism by lymphocytes indicates a change in resistance of the cells to cortisol. Measuring the effect of fatty acids on cortisol catabolism by lymphocytes indicated that the polyunsaturated fatty acids, linoleate, arachidonate, and eicosapentaenoic, inhibit cortisol catabolism by lymphocytes.

Albumin and the unique pattern of inhibitors of cortisol catabolism by lymphocytes in serum of cancer patients.

We have shown previously that sera of cancer patients (CPS) possess ethanol-extractable substances which can inhibit the catabolism of cortisol by lymphocytes (CCL). In the present study an attempt was made to purify the inhibitory material by gel filtration. Chromatography of normal serum and CPS on a Sephadex G-10 column showed one peak of CCL inhibition with control serum and two peaks with CPS.

Effect of ethanol extract of cancer patients' serum on the vulnerability of lymphocytes to cortisol.

We have shown previously that cortisol-sensitive lymphocytes (thymocytes) have a much lower capacity than cortisol-resistant cells to catabolize cortisol. We have also shown that sera of cancer patients (CPS) possess ethanol-extractable substance(s) which can inhibit the catabolism of cortisol by lymphocytes (CCL). Recently, we noted that unsaturated fatty acids can both inhibit CCL and modulate the sensitivity of lymphocytes to cortisol.

The effect of linoleic acid on the sensitivity of human lymphocytes to cortisol and their capacity to catabolize the steroid.

We have shown previously that cortisol-sensitive lymphocytes (thymocytes) have a much lower capacity than cortisol-resistant cells to catabolize cortisol. In the present study, we attempt to demonstrate that inhibition of cortisol catabolism may make cortisol-resistant lymphocytes vulnerable to the steroid. Linoleic acid, which has the capacity to inhibit the catabolism of cortisol by lymphocytes, was used for this purpose.

Effect of a non-viral fraction of acquired immunodeficiency syndrome plasma on the vulnerability of lymphocytes to cortisol.

We have observed previously that the rate of cortisol catabolism by lymphocytes (CCL) was indicative of the vulnerability of these cells to cortisol. We attempted to ascertain whether cortisol-sensitive lymphocytes (e.g.