Impacts of Dutch elm disease-causing fungi on foliage photosynthetic characteristics and volatiles in Ulmus species with different pathogen resistance.

Global warming affects the abiotic and biotic growth environment of plants, including the spread of fungal diseases such as Dutch elm disease (DED). Dutch elm disease-resistance of different Ulmus species varies, but how this is reflected in leaf-level physiological pathogen responses has not been investigated. We studied the impacts of mechanical injury alone and mechanical injury plus inoculation with the DED-causing pathogens Ophiostoma novo-ulmi subsp. novo-ulmi and O. novo-ulmi subsp. americana on Ulmus glabra, a more vulnerable species, and U. laevis, a more resistant species. Plant stress responses were evaluated for 12 days after stress application by monitoring leaf net CO2 assimilation rate (A), stomatal conductance (gs), ratio of ambient to intercellular CO2 concentration (Ca/Ci) and intrinsic water-use efficiency (A/gs), and by measuring biogenic volatile (VOC) release by plant leaves. In U. glabra and U. laevis, A was not affected by time, stressors or their interaction. Only in U. glabra, gs and Ca/Ci decreased in time, yet recovered by the end of the experiment. Although the emission compositions were affected in both species, the stress treatments enhanced VOC emission rates only in U. laevis. In this species, mechanical injury especially when combined with the pathogens increased the emission of lipoxygenase pathway volatiles and dimethylallyl diphosphate and geranyl diphosphate pathway volatiles. In conclusion, the more resistant species U. laevis had a more stable photosynthesis, but stronger pathogen-elicited volatile response, especially after inoculation by O. novo-ulmi subsp. novo-ulmi. Thus, stronger activation of defenses might underlay higher DED-resistance in this species.

CC-chemokine receptor CCR5-del32 mutation as a modifying pathogenetic factor in type I diabetes.

The purpose of this study was to determine the CCR5-del32 allele frequency in type I (insulin-dependent) and type II (noninsulin-dependent) diabetes patients, and to test whether and how this mutation is associated with both types of diabetes. Thirty-eight type I diabetes and 111 type II diabetes patients' genotyping was performed by polymerase chain reaction assaying, and amplified products were digested with restriction enzyme EcoRI. The results were analyzed using statistical methods. No statistical differences were found in CCR5-del32 allele frequencies in types I and II diabetes patients compared with the control group of native Estonians. However, an association exists between CCR5 gene polymorphism and the clinical course of type I diabetes. In the case of wild-type CCR5, the disease starts at an earlier age. In type II diabetes, there was a difference between genotypes in morbidity to concomitant diseases, being higher in the CCR5 wild-type genotype.