Über den Einfluß der elektrischen Umwelt auf das Verhalten gekäfigter Honigbienen

Zusammenfassung Die elektrische Körperladung von gekäfigten Bienen ist grundlegend abhängig von den elektrostatischen Eigenschaften des Käfigmaterials. Dies bedingt unterschiedliche motorische Aktivität, korreliert mit unterschiedlichem Rektalblasengewicht als Indikator der Stoffwechselrate.In PVC-Käfigen ist gegenüber geerdeten Stahlkäfigen die Aufladung und Aktivität der Tiere erhöht.

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Effects of electric environmental factors on the behaviour of encaged honey bees

The electric body loading of bees varies according to the electrostatic qualities of the boxes in which they are caged. This results in differences in motor activity correlated with the weight of the rectal bladder as an indicator of metabolism rate. In PVC-cages the loading and activity is greater than in grounded steel cages.

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Mit 4 Abbildungen

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Die Versuche wurden in einer Staatsexamensarbeit von FrauB. Masloh gemacht.     

Chloramphenicol 3. Clinical pharmacology of systemic use in the horse

The use of chloramphenicol in the horse is now prohibited as horses are classified as food-producing animals. However, chloramphenicol has until recently been widely available for oral, intramuscular or intravenous administration. A critical appraisal of the published literature on the use of chloramphenicol in the horse clearly demonstrates that there are sound pharmacokinetic and microbiological reasons for concluding that chloramphenicol is not an appropriate antibiotic for systemic use. The short half-life of chloramphenicol in the horse, together with the broad range of minimum inhibitory concentrations of target pathogens, preclude the use of practical dosage regimens. It can be concluded that the withdrawal of chloramphenicol will have no adverse effects on chemotherapy in the horse.     

Sirtuin 2 inhibitors rescue alpha-synuclein-mediated toxicity in models of Parkinson's disease

The sirtuins are members of the histone deacetylase family of proteins that participate in a variety of cellular functions and play a role in aging. We identified a potent inhibitor of sirtuin 2 (SIRT2) and found that inhibition of SIRT2 rescued alpha-synuclein toxicity and modified inclusion morphology in a cellular model of Parkinson's disease. Genetic inhibition of SIRT2 via small interfering RNA similarly rescued alpha-synuclein toxicity. Furthermore, the inhibitors protected against dopaminergic cell death both in vitro and in a Drosophila model of Parkinson's disease. The results suggest a link between neurodegeneration and aging.     

Upfront denileukin diftitox as in vivo regulatory T-cell depletion in order to enhance vaccination effects in a canine allogeneic hematopoietic stem cell transplantation model

Denileukin Diftitox (ONTAK^®, DAB₃₈₉ IL-2) is a recombinant DNA-derived fusion protein depleting cells that express high-affinity IL-2 receptor. Important cell targets are CD4⁺CD25⁺Foxp3⁺ regulatory T cells (T_reg). Elimination of immunosuppressive T_reg by Denileukin Diftitox may provide a way to modulate immune tolerance following stem cell transplantation. Here, we combined T_reg depletion with a vaccination approach to induce donor-specific immune reactions. To investigate this approach we chose the mixed chimerism canine stem cell transplantation model which represents a high state of tolerance between two hematopoietic systems. The aim was therefore to induce a graft versus hematopoiesis effect thereby converting mixed to full donor chimerism. Dog leukocyte antigen identical siblings that had developed a stable mixed chimerism after non-myeloablative stem cell transplantation received a single dose of Denileukin Diftitox (18 μg/kg, i.v.) followed by several cell-lysate vaccinations. Host peripheral blood mononuclear cell lysates combined with CpG-ODN, and Montanide^® ISA 51 were locally applied. In vitro studies demonstrated that canine T_reg are a target of Denileukin Diftitox. The suppression of T-cell proliferation by T_reg was abolished by addition of Denileukin Diftitox (10 nM). An increase of proliferation of median 300% (range: 200%–425%) was observed. No change in donor chimerism was observed after administration of Denileukin Diftitox and vaccination. This study highlights that application of Denileukin Diftitox resulted in a depletion of T_reg followed by an increase of immune response in vitro. This effect could not be confirmed in vivo even if the immune system was stimulated by vaccinations.     

Attempts to localize the defect in dysgammaglobulinemia of UM-B19 chickens by studying the effect of immunomodulating substances on immunoglobulin and antibody production

The extreme decreased levels of IgG in dysgammaglobulinemic UM-B19 chickens are linked with decreased antibody activity. Antibody activity to T-dependent (although diminished) and T-independent antigens is present but is restricted to IgM and IgA antibodies. Complete Freund's adjuvant enhances the existing isotype pattern of serum immunoglobulins and antibodies. The antibody response to a "T-independent" antigen (B. abortus) is greatly increased by CFA in dysgammaglobulinemic chickens. Beside the appearance of high levels of IgG in dysgammaglobulinemic chickens during the first weeks of life and in transitory dysgammaglobulinemia, remarkable IgG synthesis can be temporarily induced by the mitogenic activity of LPS and even more by the regulatory function of Levamisole. Furthermore, LPS and Levamisole induce IgG antibody synthesis to concomitantly administered antigen, the IgG antibodies appearing within the normal time. Contrary to a missing feedback inhibition from total IgG to IgM serum immunoglobulins, a feedback inhibition from IgG to IgM antibodies is found. No correlation can be found between Levamisole-induced IgG immunoglobulin concentrations, and IgG antibodies. Germfree rearing for one week or longer prevents the dysgammaglobulinemic defect. The following conclusions are drawn: Early antigenic stimulation seems to be the inducing factor for dysgammaglobulinemia in UM-B19 chickens. A BG cell pool is still present in adult dysgammaglobulinemic chickens. This BG cell pool is probably diminished to a varying extent. T cell helper functions seem to be present (albeit they may be disturbed) and can be stimulated. IgG specific T cell suppression is probable. From these conclusions the etiology of the dysgammaglobulinemia in UM-B19 chickens is hypothesized to be primarily due to delayed bursal development: Immature BG cells are eliminated by environmental antigens during the neonatal period in a process similar to tolerance induction. This event, in turn, induces suppressor mechanism(s) or disturbance in helper mechanism(s).