The rust fungi (Uredinales) on ferns in South Africa

The rust fungi (Uredinales, basidiomycota) occuring on ferns (Pteridophyta) in South Africa are described, illustrated and keyed out. All species belong to the pucciniastraceous genera Milesina (M. blechni), Uredinopsis (U. pteridis) or to the related uredinial anamorph genus Milesia (M. nervisequa, M. cf. magellanica, M. silvae-knysnae). Milesia silvae-knysnae on Polystichum pungens is new to science; it probably belongs to the teleomorph genus Milesina. Milesina blechni is reported from South Africa for the first time on the new hosts Blechnum punctulatum and Rumohra adiantoides; it has hitherto been known only from the Northern Hemisphere on Blechnum spicant. Rust specimens collected on Asplenium aethiopicum and A. rutifolium were tentatively assigned to Milesia magellanica which has been known so far only from southern Chile. Hyalopsora neocheilanthis, Milesina neoexigua and M. neovogesiaca are proposed as new names for Hyalopsora cheilanthis, Milesia exigua and M. vogesiaca. It is discussed that the pucciniastraceous fern rusts could have reached South Africa either by migration (M. blechni) or by long-distance air dispersal. In the absence of their gametophyte hosts, species of Abies (Pinaceae), the rusts have to propagate in South Africa by urediniospores infecting fern to fern. Taxonomical novelties Milesia silvae-knysnae R. Berndt Milesina neoexigua R. Berndt Milesina neovogesiaca R. Berndt Hyalopsora neocheilanthis R. Berndt     

Galectin-4 controls intestinal inflammation by selective regulation of peripheral and mucosal T cell apoptosis and cell cycle

Galectin-4 is a carbohydrate-binding protein belonging to the galectin family. Here we provide novel evidence that galectin-4 is selectively expressed and secreted by intestinal epithelial cells and binds potently to activated peripheral and mucosal lamina propria T-cells at the CD3 epitope. The carbohydrate-dependent binding of galectin-4 at the CD3 epitope is fully functional and inhibited T cell activation, cycling and expansion. Galectin-4 induced apoptosis of activated peripheral and mucosal lamina propria T cells via calpain-, but not caspase-dependent, pathways. Providing further evidence for its important role in regulating T cell function, galectin-4 blockade by antisense oligonucleotides reduced TNF-alpha inhibitor induced T cell death. Furthermore, in T cells, galectin-4 reduced pro-inflammatory cytokine secretion including IL-17. In a model of experimental colitis, galectin-4 ameliorated mucosal inflammation, induced apoptosis of mucosal T-cells and decreased the secretion of pro-inflammatory cytokines. Our results show that galectin-4 plays a unique role in the intestine and assign a novel role of this protein in controlling intestinal inflammation by a selective induction of T cell apoptosis and cell cycle restriction. Conclusively, after defining its biological role, we propose Galectin-4 is a novel anti-inflammatory agent that could be therapeutically effective in diseases with a disturbed T cell expansion and apoptosis such as inflammatory bowel disease.     

No effect of mobile phone-like RF exposure on patients with atopic dermatitis

This study investigates the effect of exposure to a mobile phone-like radiofrequency (RF) electromagnetic field on people with atopic dermatitis (AD). Fifteen subjects with AD were recruited and matched with 15 controls without AD. The subjects were exposed for 30 min to an RF field at 1 W/kg via an indoor base station antenna attached to a 900 MHz GSM mobile phone. Blood samples for ELISA analysis of the concentration of substance P (SP), tumor necrosis factor receptor 1 (TNF R1), and brain derived neurotrophic factor (BDNF) in serum were drawn before and after the provocation (exposure/sham). Baseline heart rate and heart rate variability, local blood flow, and electrodermal activity were also recorded. No significant differences between the subject groups were found for baseline neurophysiological data. The cases displayed a serum concentration of TNF R1 significantly higher than the control subjects and a significantly lower serum concentration of BDNF in the baseline condition. For SP there was no difference between groups. However, no effects related to RF exposure condition were encountered for any of the measured substances. As to symptoms, a possible correlation with exposure could not be evaluated, due to too few symptom reports. The result of the study does not support the hypothesis of an effect of mobile phone-like RF exposure on serum levels of SP, TNF R1, and BDNF in persons with AD.     

The rust mycobiota of southern Africa: Species richness, composition, and affinities

The rust mycobiota (Uredinales, Basidiomycota) of southern Africa (Botswana, Namibia, and South Africa) is analysed with regard to species richness, generic composition, and similarities to the rust mycobiotas of the remaining African continent and other regions of the world. Southern Africa is home to about 546 rust species: ca 522 species have been reported from South Africa, 73 from Namibia, and less than ten from Botswana. Thirty-two species were considered to be exotics. Two hundred and twenty-five of the species are restricted to southern Africa, suggesting an endemism rate of ca 44 %. At present, the rust fungus:host ratio is 1:38.5, which is much lower than expected from other regions of the world. This low ratio may partly be due to under-exploration of the area, but the results presented here indicate that a natural paucity of rust fungi on certain, especially species-rich plant taxa centred in southern Africa and possibly environmental factors are more important reasons. The predominant genera are Puccinia and Uromyces accounting for ca 59 % of the rust species. The genera Hemileia, Phakopsora and especially Ravenelia, centred in tropical regions, are well represented and sum up to 8 % of the species. Members of Melampsoraceae and Phragmidiaceae, common in temperate regions of the Northern Hemisphere, are scarce. Most of the other 28 recorded teleomorph genera are only represented by three or less species. In an African context, most species are shared with central and east Africa (almost 16 %). Only a few species are disjunct between southern and West Africa or Madagascar. Ca 10 % of the species are shared only with other parts of the paleotropics, especially the Indian subcontinent. Disjunctions of native species with the New World, Australia/New Zealand, or Europe are rare.     

Screening of patients at risk for 22q11 deletion

The aim of this study was to determine whether deletion 22q11.2 studies should become apart of a standardized diagnostic workup for selected groups of at risk patients. We prospectively investigated four cohorts of unselected patients referred because of 1) congenital heart defect (CHD), 2) palatal anomalies, 3) hypocalcaemia, 4) dysmorphic features suggestive of del 22q11.2. Fluorescence in situ hybridization analysis revealed deletion 22q11.2 in 9.4% (6/64) patients with CHD. From 18 patients referred because of the hypocalcaemia, six (33.3%) had 22q11.2 deletion. In the group of 31 children with dysmorphic traits, the diagnosis was confirmed in two (6.4%) patients. None of the 58 children with palatal anomalies showed evidence of 22q11.2 deletion. Conclusions: Testing for the 22q11.2 microdeletion can be recommended in all patients with conotruncal heart defects and in patients with hypocalcaemia. It should be also considered in patients presenting only with dysmorphic traits suggestive of del 22q11.2, while screening in patients with cleft palate is not warranted.     

Pathological shear stress stimulates the tyrosine phosphorylation of alpha-actinin associated with the glycoprotein Ib-IX complex.

Shear-induced platelet responses are triggered by VWF binding to the platelet GpIb-IX complex, and there is evidence that this ligand-receptor coupling stimulates transmembranous signaling through the cytoplasmic tail of glycoprotein (Gp) Ib alpha. To investigate the mechanism by which signaling is effected, new molecular interactions involving GpIb-IX that develop in response to pathological shearing stress were examined in intact human platelets. Exposure to shear, but not alpha-thrombin, results in the co-immunoprecipitation of the actin cross-linking protein alpha-actinin with the GpIb-IX complex. Blockers of VWF binding to GpIb alpha or actin polymerization inhibit the association of alpha-actinin with the GpIb-IX complex, but the association of alpha-actinin with the GpIb-IX complex is not affected by inhibiting VWF binding to platelet integrin alpha IIb beta 3 (GpIIb-IIIa). alpha-Actinin becomes tyrosine phosphorylated in response to pathological shear stress, and phosphorylated alpha-actinin associates with GpIb-IX. In resting platelets, class IA heterodimeric phosphatidylinositol 3-kinase (PI 3-K) and protein kinase N (PKN) associate with nonphosphorylated alpha-actinin. Shear stress causes PI 3-K to disassociate from alpha-actinin, while it stimulates PKN binding to alpha-actinin. These results demonstrate that shear-induced VWF binding to GpIb alpha causes enhanced binding of cytoskeletal alpha-actinin to GpIb-IX and suggest that alpha-actinin, perhaps through tyrosine phosphorylation, serves as an adapter for a signaling complex that could regulate VWF-induced platelet aggregation.