Redescription of <Emphasis Type="Italic">Bacciger microacetabularis</Emphasis> (Martorelli et Suriano, 1983) nov. comb. parasitizing <Emphasis Type="Italic">Paralichthys orbignyanus</Emphasis> (Pisces,Paralichthyidae) from Argentina

In this paper Steringotrema microacetabularis (Suriano et Martorelli, 1983) is redescribed and transferred to Bacciger Nicoll, 1924 in the Faustulidae Poche, 1926 based on newly collected material from the type-host, Paralichthys orbignyanus Valenciennes, 1839 and the type-locality, Mar Chiquita coastal lagoon, Buenos Aires Province, Argentina. A careful re-examination of the new specimens shows that some anatomical characteristics were ignored or incompletely described by the previous authors and they are included herein. The species is tentatively transferred to Bacciger with which it appears to have closest affinity. Despite the anatomical differences detailed in this paper, confirmation of this proposal must await further work, including molecular studies.     

Hepatic angiomyolipoma and hepatic stellate cells share a similar gene expression profile

BACKGROUND AND AIMS: Angiomyolipomas (AMLs) of the liver are rare neoplasms composed of large epithelioid cells with intermixed fat and blood vessels. Hepatic AMLs have no clear normal-cell counterpart in the liver. However, AMLs and stellate cells both are positive for neural crest-derived markers including HMB-45 antigen. METHODS: To further explore the similarities between hepatic AMLs and stellate cells, gene expression of a hepatic AML was studied by cDNA microarray. Real-time polymerase chain reaction was used to confirm gene expression. Hepatic stellate cells can be quiescent, activated, or have a myofibroblastic phenotype depending on their state of activation. Expression of known markers of activated stellate cells was compared between the AML, activated primary mouse stellate cells, and stellate cell lines with activated and myofibroblastic phenotypes. Next, 5 novel genes from the AML were selected because they were not previously known to be markers of stellate cells and mRNA expression measured in the activated mouse stellate cells and in myofibroblastic stellate cell lines. Finally, expression levels of 10 novel genes were determined in 5 cirrhotic and 5 noncirrhotic human livers. RESULTS: Overexpression of known markers of activated stellate cells including transforming growth factor beta (TGF- beta ), smooth muscle actin, and collagen was found in the hepatic AML. Three of 5 novel markers that were identified in the AML, RRAD (Ras-related associated with diabetes), CTSK (cathepsin K), and NIBAN were also found to be overexpressed in activated stellate cells compared with quiescent or myofibroblastic stellate cells. In addition, 9 of 10 novel genes overexpressed in AML were also overexpressed in cirrhotic human livers versus noncirrhotic livers. CONCLUSIONS: Hepatic AMLs share a similar gene expression profile and may differentiate toward activated stellate cells.     

Quantification of the factors that influence discharge correlation in model motor neurons

The purpose of this study was to quantify the influence of intrinsic properties, active dendritic conductances, and background excitation and inhibition on measures of discharge correlation in the time and frequency domains with known levels and patterns of common synaptic input. The study involved a computer simulation of a population of neurons with a range of input resistances (0.54-3.7 MOmega) and surface areas (407,000-712,000 microm(2)). The neurons were simulated with no, moderate, or high levels of active dendritic conductances and were activated with either excitatory input only or excitatory and inhibitory inputs. The patterns of common input, either branched common input or common modulation, were tested with 0, 30, 60, and 90% common input. The results confirm previous findings of an exponential relation between the level of common input and indexes of synchronization; only when the common input comprised >/=60% of the total excitatory input was there a significant effect on discharge correlation. Synchronization was greatest in models that had passive dendrites. Active dendritic conductances caused the discharge rate of the neuron to saturate and decreased motor-unit synchronization. However, the addition of 10% background inhibitory input increased synchronization in these models. In contrast, common rhythmic modulation of inputs at 24 Hz usually decreased synchronization. Significant coherence at the modulated frequency occurred in the commonly modulated neurons when >/=60% of the inputs were modulated. Furthermore, active dendritic conductances decreased coherence. Branched common input caused high levels of coherence across a broad spectrum and when combined with active dendritic conductances caused significant frequency peaks in the 30- to 50-Hz band. In conclusion, the level of inhibitory input and active dendritic conductances interact with the amount of common input to determine time- and frequency-domain discharge correlation.     

A new species of <Emphasis Type="Italic">Falcaustra</Emphasis> (Nematoda,Kathlaniidae) and other nematodes from <Emphasis Type="Italic">Sphenomorphus simus</Emphasis> (Squamata,Scincidae) from Papua New Guinea

Falcaustra papuensis sp. nov. (Ascaridida, Kathlaniidae) from the large intestine of Sphenomorphus simus (Squamata, Sciencidae) is described and illustrated. Falcaustra papuensis represents the 4th Australo-Papuan species assigned to this genus and is distinguished from other Australo-Papuan species by the distribution pattern of caudal papillae (6 precloacal, 6 adcloacal, 8 postcloacal, and 1 median), length of spicules (561–714 μm) and presence of a pseudosucker. Sphenomorphus simus was found to harbor 2 additional species of nematodes, Meteterakis crombiei and Oswaldocruzia bakeri. Sphenomorphus simus represents a new host record for each of these nematode species.     

Dopamine, serotonin and noradrenaline changes in the striatum of C57BL mice following myelin oligodendrocyte glycoprotein (MOG) 35-55 and complete Freund adjuvant (CFA) administration.

Many data suggest involvement of inflammation in neurodegeneration. However, the exact mechanisms of this cooperation are poorly understood. We have previously shown that induction of inflammatory reaction, both before and after injury of the striatum, affects regeneration of dopaminergic neurons. In the present research we studied the role of inflammatory reaction in non-injured striatum. We used myelin oligodendrocyte glycoprotein (MOG) 35-55 in complete Freund's adjuvant (CFA) to elicit experimental autoimmune encephalomyelitis (EAE) mice model. As determined by HPLC, striatal dopamine (DA) and serotonin levels in mice treated with either MOG 35-55 in CFA or CFA alone were significantly higher compared to vehicle-treated controls on 13th day after induction. The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Noradrenaline (NA) concentration did not differ between groups. Moreover, the striatal mRNA IL-1beta and TNF-alpha levels were elevated during induction phase of EAE in both groups, as determined by RT-PCR. Our data indicate regulatory connection between dopaminergic and immune systems.     

P2x7 deficiency suppresses development of experimental autoimmune encephalomyelitis

Background  

The purinergic receptor P2x7 is expressed on myeloid cells as well as on CNS glial cells, and P2x7 activation has been shown to increase both glial and T-cell activation. These properties suggest a role in the development of autoimmune disease including multiple sclerosis.     

Porins from Salmonella enterica serovar Typhimurium activate the transcription factors activating protein 1 and NF-kappaB through the Raf-1-mitogen-activated protein kinase cascade.

In this study we examined the ability of Salmonella enterica serovar Typhimurium porins to activate activating protein 1 (AP-1) and nuclear factor kappaB (NF-kappaB) through the mitogen-activated protein kinase (MAPK) cascade, and we identified the AP-1-induced protein subunits. Our results demonstrate that these enzymes may participate in cell signaling pathways leading to AP-1 and NF-kappaB activation following porin stimulation of cells. Raf-1 was phosphorylated in response to the treatment of U937 cells with porins; moreover, the porin-mediated increase in Raf-1 phosphorylation is accompanied by the phosphorylation of MAPK kinase 1/2 (MEK1/2), p38, extracellular-signal-regulated kinase 1/2, and c-Jun N-terminal kinase. We used three different inhibitors of phosphorylation pathways: 2'-amino-3'-methoxyflavone (PD-098059), a selective inhibitor of MEK1 activator and the MAPK cascade; 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580), a specific inhibitor of the p38 pathway; and 7beta-acetoxy-1alpha,6beta,9alpha-trihydroxy-8,13-epoxy-labd-14-en-11-one (forskolin), an inhibitor at the level of Raf-1 kinase. PD-098059 pretreatment of cells decreases AP-1 and NF-kappaB activation by lipopolysaccharide (LPS) but not by porins, and SB203580 pretreatment of cells decreases mainly AP-1 and NF-kappaB activation by porins; in contrast, forskolin pretreatment of cells does not affect AP-1 and NF-kappaB activation following either porin or LPS stimulation. Our data suggest that the p38 signaling pathway mainly regulates AP-1 and NF-kappaB activation in cells treated with S. enterica serovar Typhimurium porins. Antibody electrophoretic mobility shift assays showed that JunD and c-Fos binding is found in cells treated with porins, in cells treated with LPS, and in unstimulated cells. However, by 30 to 60 min of stimulation, a different complex including c-Jun appears in cells treated with porins or LPS, while the Fra-2 subunit is present only after porin stimulation. These data suggest different molecular mechanisms of activation induced by porins or by LPS.     

Infestation of sand lizards (<Emphasis Type="Italic">Lacerta agilis</Emphasis>) resident in the Northeastern Poland by <Emphasis Type="Italic">Ixodes ricinus</Emphasis> (L.) ticks and their infection with <Emphasis Type="Italic">Borrelia burgdorferi</Emphasis> sensu lato

Sand lizards (Lacerta agilis) were trapped and examined for ticks from May to September in 2002 and 2003 in Northeastern Poland. A total of 233 Ixodes ricinus (L.) ticks (76 larvae and 157 nymphs) was found on 31 of 235 captured lizards (13.2%). The tick infestation is relatively low compared to that of mammals and passerine birds from the same area (Siński et al. 2006, Gryczyńska et al. 2002). Tick infestation depended on the month of capture, being the highest in spring. In autumn no ticks were recorded on any of the captured lizards. The oldest lizards carried the highest number of ticks but no differences related to sex of the host were found. All the collected ticks were analysed by PCR for the presence of Borrelia burgdorferi sensu lato, the etiological agents of Lyme disease. Spirochetes were detected in 11 out of 233 (4.7%) ticks tested. Genetic analysis confirmed that the spirochetes are members of the Borrelia afzelii, B. garinii and B. burgdorferi sensu stricto genospecies. Mixed infection were not detected. The prevalence of infection was analysed in relation to months of the capture, age and sex of the lizards, but differences were not statistically significant. The obtained results suggest that lizards are probably not B. burgdorferi reservoirs, but further studies are required to confirm this.     

Immunomodulation of murine collagen-induced arthritis by N,N-dimethylglycine and a preparation of <Emphasis Type="Italic">Perna canaliculus</Emphasis>

Background  

Rheumatoid arthritis (RA) and its accepted animal model, murine collagen-induced arthritis (CIA), are classic autoimmune inflammatory diseases which require proinflammatory cytokine production for pathogenesis. We and others have previously used N, N-dimethylglycine (DMG) and extracts from the New Zealand green-lipped mussel Perna canaliculus (Perna) as potent immunomodulators to modify ongoing immune and/or inflammatory responses.