فهرست مطالب mohammadhassan rastegar

Citrus yellow vein clearing virus (CYVCV), is the causal agent of a destructive disease that has been spreading in Iran and a number of countries in the region in recent years. To identify susceptible hosts of the disease, the budwoods of the important lime and lemon genotypes of Iran were collected from asymptomatic mother trees. Then the samples were confirmed to be CYVCV-free by biological indexing using the indicator plant. The buds of the genotypes were then propagated on sour orange (Citrus aurantium) rootstocks and the plants were simultaneously graft-inoculated with the Iranian LEN isolate (GenBank accession number: KX902488). The inoculated and control plants were maintained under controlled temperature conditions (24°C during the day and 18°C at night). Persian lime (C. latifolia) and nine lemon (C. limon) varieties were identified as disease-susceptible cultivars among the 21 studied genotypes. To confirm infection in symptomatic inoculated plants, total RNA was extracted from the bark and midrib of new flushes and a two-step RT-PCR was performed. No symptoms were observed in the other genotypes studied until one year after inoculation. Disease severity in susceptible genotypes was graded from 0 to 4 based on the severity of symptoms on the lateral veins and cultivars were divided into three groups according to the intensity of the response. The relationship between ancestral affinity of lemon cultivars and susceptibility to Citrus yellow vein clearing virus was discussed.

Angioedema secondary to C1 inhibitor deficiency has been rarely reported to be associated with systemic lupus erythematosus. A genetic defect of C1 inhibitor produces hereditary angioedema, which is usually presented with cutaneous painless edema, but edema of the genital area, gastrointestinal and laryngeal tracts have also been reported.In lupus patients, angioedema may be the result of an acquired type of C1 inhibitor deficiency, most probably due to antibody formation directed against the C1 inhibitor molecule. Herein we report a new case of lupus nephritis that developed angioedema and a rapid course of disease progression with acute renal failure and alveolar hemorrhage without response to high dose steroid and plasmapheresis.