A functional role for neutralizing antibodies in Borna disease: influence on virus tropism outside the central nervous system

Borna disease virus (BDV) is a negative-strand RNA virus that infects the central nervous systems (CNS) of warm-blooded animals and causes disturbances of movement and behavior. The basis for neurotropism remains poorly understood; however, the observation that the distribution of infectious virus in immunocompetent rats is different from that in immunoincompetent rats indicates a role for the immune system in BDV tropism: whereas in immunocompetent rats virus is restricted to the central, peripheral, and autonomic nervous systems, immunoincompetent rats also have virus in nonneural tissues. In an effort to examine the influence of the humoral immune response on BDV pathogenesis, we examined the effects of passive immunization with neutralizing antiserum in immunoincompetent rats. Serum transfer into immunoincompetent rats did not prevent persistent CNS infection but did result in restriction of virus to neural tissues. These results indicate that neutralizing antibodies may play a role in preventing generalized infection with BDV.     

The influence of various chemicals on the surface structure and the antigenicity of syngeneic glioma cells

Brain tumours were induced in inbred Fischer rats (F344) by methylnitrosourea. A pleomorphic glioma (78-219) was established in vitro and propagated as 78FR-G-219 permanent cell line. These cells were modified either by dimethylsulfate or by trinitrobenzene sulfonic acid. Antisera were raised against both native an chemically latered cells in syngeneic rats. The cytotoxicity of these sera was tested against the native glioma cell line as target, by means of the 14C-nicotinamide release. The methylated cells induced a complement--dependent humoral cytotoxicity in the range of that produced by native cells (20%); trinitrophenylation, however, resulted in a two-fold increased cytotoxic humoral immune response. Effects of chaotropic salts on methylated cell surface structure suggested a mode of action different from that of trinitrophenylation, which could be further substantiated by scanning electron microscopy. Furthermore, a new tool for the evaluation of cell surface structure, secondary ion mass spectrometry, was applied on our cell system. Significantly different ionized fragments were obtained from normal brain cells and glioma cells, respectively.     

A new modular design for test and application PCBs of SAW RF filters to ensure precisely predictable filter characteristics

This paper presents the design of an optimized test and application setup for surface acoustic wave (SAW) RF filters. These structures have been investigated, including the test devices, by simulation techniques based on full-wave methods and common SAW simulation methods. In this paper, the simulation technique will be explained in detail, focusing on the interfaces of the simulation models. Parasitic electromagnetic effects in the test and application setup will be analyzed by simulation and measurement. This paper demonstrates the possibility of accurate performance prediction of SAW RF filters using specially designed test setups in the measurement and an optimized application environment, e.g., in mobile phones. Modular parts for such test setups and the application environment are discussed.     

The guanylate cyclase-coupled natriuretic peptide receptor: a new target for prevention of cold ischemia-reperfusion damage of the rat liver

The aim of our studies was to investigate hormonal prevention of hepatic preservation damage by the atrial natriuretic peptide (ANP) and the mechanisms involved. Isolated perfusion of rat livers was performed in a nonrecirculating fashion. Twenty minutes of preischemic perfusion was performed with or without different concentrations of ANP, followed by 24-hour storage in cold University of Wisconsin (UW) solution. Two hundred nanomoles of ANP prevented hepatocellular damage during a 2-hour reperfusion period as indicated by a marked attenuation of the sinusoidal efflux of lactate dehydrogenase (LDH) and purine nucleoside phosphorylase (PNP), and by reduced Trypan blue uptake. Furthermore, postischemic bile flow as an indicator of liver function was significantly improved by about 60% with 200 nmol/L ANP. No protection was conveyed by 20 nmol/L ANP nor by pretreatment with 200 nmol/L ANP for only 10 minutes. The effects of ANP seemed to be mediated by the guanylate cyclase-coupled A (GC-A) receptor and cyclic guanosine monophosphate (cGMP): whereas expression of both GC-A and GC-B receptors as well as of the GC-C receptor was found, cGMP did protect from ischemia-reperfusion damage, but selective ligands of the B and C receptor did not. To begin to determine the mechanisms of ANP-mediated protection, different parameters were investigated: ANP had no effect on portal pressure as an indicator of hepatic circulation, nor on intracellular energy depletion determined by adenosine nucleotide concentration. However, the marked augmentation of nuclear factor kappaB (NF-kappaB) binding activity during reperfusion was prevented in ANP-pretreated livers. In conclusion, pretreatment with ANP protects the rat liver from cold ischemia-reperfusion damage. This effect is mediated via the GC-A receptor and cGMP, and may be linked to an influence of ANP on NF-kappaB activation. Thus, ANP signaling via the GC-A receptor should be considered as a new pharmacological target to prevent preservation injury of the liver.