Comparative proteomic analysis of hyphae and germinating cysts of Phytophthora pisi and Phytophthora sojae.

The recently described oomycete pathogen Phytophthora pisi causes root rot on pea and faba bean, while the closely related Phytophthora sojae is the causal agent of soybean root and stem rot. Differences in the pathogenicity factor repertoires that enable the two species to have distinct host specificity towards pea and soybean, were studied using tandem mass spectrometry in a global proteome study of hyphae and germinating cysts in P. pisi and P. sojae. In total 2775 proteins from P. pisi and 2891 proteins from P. sojae were identified. Fifty-eight orthologous proteins were more abundant in germinated cysts of both pathogens and thus identified as candidate proteins for the infective stage. Several of these proteins were associated with lipid transport and metabolism, and energy production. Twenty-three orthologous proteins were more abundant in hyphae of both pathogens and thus identified as candidate proteins for vegetative growth. Proteins uniquely present in germinating cysts of either P. pisi or P. sojae were considered as candidates for species-specific pathogenicity factors that may be involved in host specificity. Among these proteins were serine proteases, membrane transporters and a berberine-like protein. These results significantly expand the knowledge of the expressed proteome in P. pisi and P. sojae. BIOLOGICAL SIGNIFICANCE: P. sojae and P. pisi are closely related species that specifically cause root rot on soybean and pea, respectively. The pathogenicity factors contributing to their host specificity remained unknown. We carried out a comparative large-scale proteome analysis of vegetative (hyphae) and infective (germinating cysts) life stages in P. pisi and P. sojae. This study provides knowledge of the common factors and mechanism involved in initiation of infection and species-specific proteins that may contribute to the host specificity of these pathogens. This knowledge will lead to a better understanding of the infection biology of these pathogens, allowing new possibilities towards developing alternative and effective plant protection measures.

Root Rot of Pea and Faba Bean in Southern Sweden Caused by Phytophthora pisi sp. nov.

A root rot disease of pea and faba bean caused by a Phytophthora sp. was observed in fields and field soil samples in southern Sweden. Observations of the disease in pea root rot greenhouse assays were systematically recorded, and incidence and geographic distribution data were compared with the pea root rot caused by Aphanomyces euteiches. Following one successful isolation of the pathogen, isolation procedures and selective media were optimized to retrieve more isolates. Phylogenetic analysis showed that the isolates belong to a novel lineage, closely related to Phytophthora sojae, and proposed here as a new species, P. pisi sp. nov. In a collection of 13 isolates from separate fields, intraspecific variation was detected in both nuclear and mitochondrial loci. Pathogenicity tests on a range of crop plants and wild legumes suggest that the host range of the pathogen is restricted to a group of legumes closely related to pea which, in addition to pea, include the crop species faba bean, lentil, common vetch, and chickpea. Morphology, growth requirements, and pathogenicity traits indicate that the species may be identical to the organism previously described as P. erythroseptica var. pisi. The work characterizes a novel Phytophthora sp. causing root rot of legume crops.

Pressure-induced local venous constrictor responses in human fingers.

Particularly in humans, systemic veins are often exposed to extensive changes in transmural pressure at altered body positions, when centrally conveyed constrictor reflexes provide compensation to maintain a proper venous return. The present aim was to explore whether also purely local mechanisms, of e.g. myogenic and/or axon reflex nature and operating at the venular-small vein levels, may contribute to offset venous pooling at local pressure increases. For such purposes the capacitance vascular responses were recorded plethysmographically in human fingertips, as most of the blood content is here contained in venules and small veins. Local increases in transmural pressure, induced by graded venous outflow obstructions, first induced by a corresponding passive-venous distension which within a few seconds was followed by a venoconstrictor response that could return the local blood content to nearly control level within 25-35 s. On sudden release of venous obstruction this 'active' response was unmasked as a prompt volume 'undershoot' that subsided in another 15-30 s. These microvascular responses could be powerful enough almost to offset the venodistension caused by transmural pressures up to 90-100 mmHg, and at brisk pressure increases they could be quite rapid in onset. As general reflex influences seemed to be excluded. these results in humans suggest that also the capacitance microvessels, like the precapillary resistance ones, can display myogenic responses to offset pressure increases. As the venular-small vein compartment contains up to 40% of the total blood volume such local responses, if generalized, may importantly contribute to venous control in humans.

Lipid profile improvement following celiprolol.

Many beta-blockers adversely affect serum lipid levels. We have, therefore, monitored blood pressure and serum lipids in 22 patients (mean age: 42.5 years) with essential hypertension (WHO stages I-II) who were treated with celiprolol for 4 weeks, and in 12 patients (mean age: 39.8 years) with essential hypertension (WHO stages I-II) who received celiprolol for 12 months. Standing blood pressure was significantly reduced after 4 weeks and 12 months of treatment, and there were slight decreases in serum cholesterol. In addition, serum triglyceride levels decreased significantly after 4 weeks, and there was a smaller decrease in the patients treated for 12 months. The pathologically elevated pre-treatment lipid values were, therefore, reduced to levels within the normal range. Analysis by lipid electrophoresis showed an increase in the high density lipoprotein (HDL) fraction and a decrease in both the low density lipoprotein (LDL) fraction and the LDL/HDL ratio. During the long-term study there was also a significant reduction in serum fibrinogen. Our results show that celiprolol does not adversely alter serum lipids, and it may even have a beneficial effect on these variables.