RESUMO
Leaf drop, wilt, and mortality were observed in September of 2007 on approximately 10% of 1- to 2-year-old olive (Olea europaea cv. Leccino) plants shipped from Europe and growing in a nursery in the District of Makwampur, Nepal. Roots of symptomatic and asymptomatic plants were disinfected in 1% NaOCl, cut into 1 cm long pieces, plated on 2% potato dextrose agar, and maintained at 20°C with 14 h of light per day. Colonies with white mycelium developed after 3 days. Microconidia and three-septated macroconidia averaged 11 × 3.9 µm and 38 × 5 µm, respectively. Chlamydospores were produced singly and in pairs. On the basis of culture characteristics, the fungus was identified as Fusarium solani (2). The ITS1-5.8S-ITS2 DNA sequences of 10 monoconidial cultures shared 99% identity with F. solani strains available on the NCBI databases (GenBank Accession Nos. 1115947 and 1115999). Pathogenicity tests were conducted with F. solani isolates NR1 and NR2 obtained from symptomatic plants. Twelve-month-old rooted cuttings of O. europaea cv. Leccino were transferred to pots containing a soilless mix and F. solani-infected oat grains (10:1 vol/vol). Fifteen plants of each F. solani isolate were inoculated. Noninfested sterilized oat grains were used for the control treatment. Symptoms on inoculated plants included leaf abscission followed by wilting and plant death approximately 10 days after inoculation and resembled those observed on the naturally infected plants. Noninoculated control plants remained healthy. The fungus was reisolated from roots of symptomatic tissues and was identical in appearance to the isolates used to inoculate the plants. No colonies of F. solani were isolated from noninoculated plants. F. solani has been reported as weakly pathogenic on olive in Spain (4) and highly aggressive on olive in Argentina (1) and India (3). To our knowledge, this is the first report of F. solani causing wilt and mortality of young olive plants in Nepal. References: (1) S. Babbit et al. Plant Dis. 86:326, 2002. (2) C. Booth. Fusarium Laboratory Guide to the Identification of the Major Species. CMI, Kew, England, 1977. (3) R. L. Munjal et al. Studies on diseases of olive in Himachal Pradesh. Page 437 in: Improvement of Forest Biomass. Symposium Proceedings. Indian Society of Tree Scientists. P. K. Kosla, ed. Sdan, India, 1982. (4) M. E. Sánchez Hernández et al. Eur. J. Plant Pathol. 104:347, 1998.
RESUMO
The inhibitory effect of cimetidine 200 mg, cimetidine 400 mg, cimetidine 200 mg + oxyphenonium bromide 10 mg and placebo was studied on nocturnal gastric acid secretion in 10 patients with duodenal ulcer. Each patient was studied over a period of four nights and trial medication was given in a randomized sequence. Cimetidine in both doses significantly inhibited the nocturnal gastric acid secretion. The drug reduced both the H+ concentration and gastric juice volume but the reduction of H+ concentration was more impressive. Mean percentage inhibition of nocturnal acid output with cimetidine 400 mg (89.6 +/- 2.868) was significantly higher than cimetidine 200 mg (80.3 +/- 4.085; p less than 0.01). Combination of cimetidine 200 mg and oxyphenonium bromide 10 mg was significantly better than cimetidine 200 mg alone (p less than 0.05) and this combination produced inhibition of gastric juice volume, H+ concentration and acid output comparable to cimetidine 400 mg.
