New Micarea records from Norway and Sweden and an identification key to the M. prasina group in Europe

Micarea czarnotae and M. pseudomicrococca are reported as new to Sweden, and M. fallax is reported as new to Norway. Micarea laeta and M. melanobola are reported from Sweden for the first time since 1927 and 1892, respectively. Micarea fallax is reported from three new localities in Sweden. An updated identification key for the M. prasina group in Central and Northern Europe is provided.Peer reviewe

Effects of pro-inflammatory cytokines on expression of kynurenine pathway enzymes in human dermal fibroblasts

<p>Abstract</p> <p>Background</p> <p>The kynurenine pathway (KP) is the main route of tryptophan degradation in the human body and generates several neuroactive and immunomodulatory metabolites. Altered levels of KP-metabolites have been observed in neuropsychiatric and neurodegenerative disorders as well as in patients with affective disorders. The purpose of the present study was to investigate if skin derived human fibroblasts are useful for studies of expression of enzymes in the KP.</p> <p>Methods</p> <p>Fibroblast cultures were established from cutaneous biopsies taken from the arm of consenting volunteers. Such cultures were subsequently treated with interferon (IFN)-γ 200 U/ml and/or tumor necrosis factor (TNF)-α, 100 U/ml for 48 hours in serum-free medium. Levels of transcripts encoding different enzymes were determined by real-time PCR and levels of kynurenic acid (KYNA) were determined by HPLC.</p> <p>Results</p> <p>At base-line all cultures harbored detectable levels of transcripts encoding KP enzymes, albeit with considerable variation across individuals. Following cytokine treatment, considerable changes in many of the transcripts investigated were observed. For example, increases in the abundance of transcripts encoding indoleamine 2,3-dioxygenase, kynureninase or 3-hydroxyanthranilic acid oxygenase and decreases in the levels of transcripts encoding tryptophan 2,3-dioxygenase, kynurenine aminotransferases or quinolinic acid phosphoribosyltransferase were observed following IFN-γ and TNF-α treatment. Finally, the fibroblast cultures released detectable levels of KYNA in the cell culture medium at base-line conditions, which were increased after IFN-γ, but not TNF-α, treatments.</p> <p>Conclusions</p> <p>All of the investigated genes encoding KP enzymes were expressed in human fibroblasts. Expression of many of these appeared to be regulated in response to cytokine treatment as previously reported for other cell types. Fibroblast cultures, thus, appear to be useful for studies of disease-related abnormalities in the kynurenine pathway of tryptophan degradation.</p

Changes in neuronal properties induced by neurotropic infections

The nervous system can be the target for various bacterial and viral infectious agents. Certain bacterial toxins have been found to impair specific proteins, such as proteins involved in transmitter release and in the regulation of the cytoskeleton. Viral infections can also cause specific disturbances in neuronal function, but less is known about their actions on the cellular level. The aim of the present study was to obtain further knowledge about the cellular actions of two types of neurotropic agents, clostridial toxins and enveloped RNA viruses, on central nervous system (CNS) neurons. As an experimental model, hippocampal neurons in primary culture were used. The neurons were subjected to toxin treatment or viral infection, and changes in cellular protein content were monitored by immunolabelling. The actions on synaptic transmission, or on ionic currents, were eximined by patch clamp whole-cell recordings, and relative changes of intracellular Ca2+ concentration with Ca2+ imaging. Certain presynaptic and viral proteins were overexpressed using the Semliki forest virus (SFV) vector. The following conclusions can be drawn from the present study: 1. Incubation of cultured neurons with tetanus toxin (TeTx), which cleaves the SNARE protein synaptobrevin, was found to block synaptic transmission completely. Botulinum neurotoxin A (BoNT/A) which cleaves the C- terminal of SNAP-25, on the other hand, caused only a partial inhibition of the synaptic response even at high doses. This type of synaptic block could be overcome by high frequency stimulation. When full-length SNAP-25 was overexpressed using the SFV vector, synaptic transmission was inhibited in a similar manner as after TeTx treatment, i.e. the inhibition could not be overcome by repetitive stimulation. Thus, it seems that the C-terminal of SNAP-25 plays a specific role in setting the level of transmitter release. 2. Incubation with large Clostridial Cytotoxins (LCTs), which inactivate GTPases of the Ras (Rap, Rai, R- Ras, Ras) and Rho families (Rho, Rac, Cdc42), inhibited synaptic transmission and modified the activity- dependent modulation. To examine the possible involvement of Rai, a dominant negative mutant of this GTPase, was overexpressed using the SFV vector. The Ral-overexpressing neurons exhibited an abnormal activitydependent facilitation of the synaptic response. These results provide evidence for an involvement of Ras- related non-Rab GTPases, including Rai, in presynaptic regulation. 3. Infections of cultures with mumps virus (RW) or a neuroadapted strain of influenza A virus (WSN/33), were found to affect the neuronal Ca2+ homeostasis. Mumps virus reduced voltage-dependent Ca2+ currents to the same degree in infected and non-infected neurons, probably due to a disturbed interaction between glial cells and neurons. Influenza A virus reduced Ca2+ currents in infected neurons at an early time-point, presumably due to a direct effect on Ca2+ channels. Later during infection Ca2+ Currents were also reduced in non- infected neurons. At this late time-point, a substantial fraction of the cells in culture had died due to infection, and the surviving neurons also showed an increased cytosolic Ca2+ concentration. 4. The influenza nucleoprotein (NP) is known to interact with actin. When NP was overexpressed with the SFV vector, it was targeted to dendritic spines, where it colocalized with actinin. This targeting to the postsynaptic element did not affect synaptic transmission. In summary, the study has provided further insight into the actions of clostridial toxins on presynaptic function, and shown that infection with enveloped RNA viruses affect somatic Ca2+ homeostasis by direct and indirect mechanisms. It has also shown that the SFV vector is a useful tool for analysis of synaptic function

Synonymizations and lectotypifications of some lecideoid lichens (Ascomycota, Lecanoromycetes) described from Finland or Sweden

Between 1850 and 1950, hundreds of lecideoid lichen-forming fungi were described from Fennoscandia, mainly in the genus Lecidea. The status of many of these species is still uncertain and some have not been revised since their description. We examined types and nomenclature of nine such lecideoid taxa, and found that they represent synonyms of earlier described species: Bacidia dolera (= Lecidea albofuscescens), Lecidea aviaria (= Rhizocarpon richardii), L. cavernarum (= Porpidia soredizodes), L. cuculi (= Schaereria fuscocinerea), L. frustulenta (= Micarea subnigrata), L. ivalensis (= Carbonea vorticosa), L. melaphanoides (= Scoliciosporum intrusum), L. mustialensis (= L. albofuscescens) and L. submilvina (= Miriquidica leucophaea). In addition, we examined types and nomenclature of three synonyms of Lecanora cadubriae: Biatora admixta, B. pinicola and Lecidea subinsequens. Lectotypes are designated for the basionyms Biatora admixta Th.Fr., Biatora pinicola Th.Fr. ex Hellb., Lecidea cuculi Vain., Lecidea fuscocinerea Nyl., Lecidea ivalensis Vain., Lecidea melaphanoides Nyl. and Lecidea subinsequens Nyl

Halecania pannarica new to Sweden

Halecania pannarica is reported for the first time in Fennoscandia from the provinces of Dalsland, Närke, Jämtland, Värmland and Västergötland in Sweden. It was found to contain pannarin rather than pannaric acid which was reported in the protologue