Indirect selection of industrial tomato genotypes that are resistant to spider mites (Tetranychus urticae).

Acyl sugars present in the tomato Solanum lycopersicum 'LA-716' accession confer good levels of resistance to arthropod pests. The objective of the present study was to select F2 plants from the interspecific cross Solanum pennellii 'LA-716' x Solanum lycopersicum 'Redenção' to assess resistance to spider mites (Tetranychus urticae) based on the leaf acyl sugar content and repellence tests. Four genotypes were selected with high leaflet acyl sugar content (RVTA-2010 pl#31, RVTA-2010 pl#75, RVTA-2010 pl#83, and RVTA-2010 pl#94), and an additional three genotypes with low acyl sugar content were also selected (RVTA-2010 pl#33, RVTA-2010 pl#39, and RVTA-2010 pl#73). The results from the in vivo tests used to confirm the selection of plants resistant to mites indicated that the genotypes with high acyl sugars content did not differ from the resistant parent LA-716. The negative correlation between acyl sugar content and the distance run by the mite along the leaflet surface confirmed the association between high and low allelochemical content and resistance. The medium degree of dominance (MDD) was estimated (MDD = -0.83), indicating that the high acyl sugar content was due to incomplete dominance of a recessive allele. A value of 81.85% was found for the broad sense heritability estimate, which suggests that most among-plant variation in the F2 generation is genetically based. Furthermore, 0.69 genes were estimated, which presumably confirms monogenic inheritance. Thus, indirect selection was an efficient method used to obtain industrial tomato plants that are resistant to spider mites.

Acquired pure megakaryocytic aplasia: a separate haematological disease entity or a syndrome with multiple causes?

We report the case of a patient with acquired pure megakaryocytic aplasia. Until today, less than 20 cases of acquired pure megakaryocytic aplasia have been reported and the disease aetiology still seems to be unclear. This report summarizes the published data concerning possible aetiologies, treatment options and outcome of patients with acquired pure megakaryocytic aplasia. Furthermore, this case report presents an example for a possible disease progression.

[Radiation protection through cytokine release by N-acetylcysteine]. / Radioprotektion durch Zytokinfreisetzung unter N-Acetylcystein.

BACKGROUND: Interleukin-1, tumornecrosisfactor-alpha and interferon-gamma endogenously provide protection of the hematopoietic system against radiation. Thiols have already been used successfully as radioprotective agents. In this study the effect von N-acetylcysteine (NAC) on the release of interleukin-1 alpha and beta (IL-1), interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and tumornecrosisfactor-alpha (TNF-alpha) was assessed in an in vitro assay. PATIENTS AND METHODS: Whole blood samples from 8 healthy volunteers were stimulated with 7.5 micrograms/ml PHA. NAC was added at concentrations of 0.6, 6, 12 and 24 mmol/l. Subsequently the samples were irradiated with a dose of 18 Gy according to preceding validation experiments. RESULTS: IL-1 alpha, IL-1 beta b and IL-2: In comparison to stimulation and radiation alone the addition of 0.6 and 6 mmol/l, with IL-2 also 12 mmol/l, NAC resulted in a significant increase of the cytokine-concentrations. The highest concentration of 24 mmol/l NAC, however, resulted in a decrease beyond control levels. IFN-gamma and TNF-alpha: Until 12 mmol/l NAC no changes were observed. 24 mmol/l NAC resulted in a significant decrease, too. CONCLUSION: N-acetylcysteine is capable to co-stimulate radioprotective cytokines like IL-1 alpha and IL-1 beta and to enhance IL-2 in vitro, whereas higher doses result in a suppression.

Is alpha-methyldopa-type autoimmune hemolytic anemia mediated by interferon-gamma?

Drug-related autoimmune hemolytic anemia appearing with warm-reacting antibodies can be classified according to the offending substances. One of the subtypes can be induced by alpha-methyldopa. However, the pathophysiology of the underlying mechanism is not yet known. In parallel, patients with Parkinson's disease and other extrapyramidal disorders, who are under administration of dopaminergic drugs, often present with abnormal findings with respect to immune parameters. In order to reveal further mechanisms within the immune response, the capability of patients under dopaminergic medication to release cytokines after a stimulatory signal was examined. Therefore, 18 patients who were treated with the dopamine analogue lisuride were compared with an aged-matched control group of 21 healthy volunteers. After stimulation with phytohemagglutinin (PHA), mitogen-induced concentrations of interferon-gamma were significantly higher in the patients treated with lisuride than in the control group. Interferon-gamma leads to an upregulation of MHC class-I and especially class-II molecules on antigen-presenting cells and to an induction of antibody production in B cells. This condition can result in the induction of an autoimmune process. It might be supposed that alpha-methyldopa-type autoimmune hemolytic anemia is mediated by elevated levels of interferon-gamma produced in T cells after a stimulatory signal.

[Is dopaminergic therapy immunologically rejuvinating? Increased interferon-gamma production with the dopaminergic agent lisuride]. / Macht dopaminerge Therapie immunologisch jung? Erhöhte Interferon-gamma-Produktion unter dem Dopaminergikum Lisurid.

Eighteen patients with advanced Parkinson's disease (n = 13) or dopamine-sensitive dystonia (n = 5) were treated with the dopaminergic agent, lisuride, applied as a long-term subcutaneous infusion. The results were compared with those obtained in a group of younger, and a group of older, healthy volunteers. The liberation of gamma-interferon (gamma-IFN) following mitogenic stimulation of whole blood with phytohemagglutinin (PHA) was highly significantly elevated in comparison with the group of older healthy volunteers, and clearly, but not significantly, elevated in comparison with the younger group. There was no difference between patients with dystonia and those with Parkinson's disease. The effect observed is thus probably due to lisuride. This effect might explain the longer life expectancy and reduced proclivity for infection shown by patients with Parkinson's disease. It needs to be determined whether, on the basis of these initial data, a therapeutic principle for the treatment of diseases that can be directly influenced by gamma-IFN can be derived.

Improvement of impaired mitogen-induced interferon-gamma release of peripheral blood mononuclear cells derived from tumor patients by Factor AF2.

Factor AF2, a now standardized extract from liver and spleen of newborn lambs, showed myeloprotective capacity on platelet- and erythrocyte-count as well as on hemoglobinconcentration in patients undergoing aggressive chemotherapy. In addition, a possible influence on prolonged remission duration in patients with mammary carcinoma had been claimed. In this study, the effect of Factor AF2 on mitogen-induced interferon-gamma release by PBMC was tested in 23 healthy humans and in 23 tumor patients. All patients were prior to surgery and had not yet received radio- or chemotherapy at the time of examination. The interferon-gamma concentration of the supernatants was measured using an enzyme-linked immunosorbent assay (ELISA). The cells were stimulated with PHA at 7.5 micrograms/ml. In the reference group, interferon-gamma concentration rose to 26 units/ml and to 15.5 units/ml in the tumor patients. In the reference persons, an addition of Factor AF2 at concentrations from 10(1) micrograms/ml to 10(3) micrograms/ml resulted in a small non-significant decrease of interferon-gamma release. At 10(4) micrograms/ml, neither test group showed measurable interferon-gamma concentration. In the tumor patients, cocultivation with Factor AF2 until concentration of 10(2) micrograms/ml resulted in a dose-dependent increase of interferon-gamma release, where 20.5 units/ml interferon-gamma were reached. At 10(3) micrograms/ml, Factor AF2 showed no effect on interferon-gamma release compared with the stimulation with mitogen alone. Flow-cytometry analysis of CD3, CD4, CD8, CD16, CD19, CD56, and HLA-DR expression of the PBMC deriving either from reference persons or from patients revealed an almost identical distribution. A slight difference in CD16-positive and HLA-DR positive cells, respectively, was not significant.