Thiabendazole insensitive strains ofHelminthosporium solani, the causal agent of silver scurf, make controlling the disease with seed treatment difficult. Potato tuber seed treatments and environmental storage management practices were investigated as means to minimize silver scurf. Fungicide seed treatments were evaluated for control ofH. solani; disease was evaluated during the growing season, at harvest, and after 5 months of storage. Silver scurf was observed on progeny tubers eleven weeks after planting. Fungicides that reduced silver scurf incidence and severity on the seed resulted in reduced incidence and severity of the disease in the progeny tubers at harvest and significantly lower disease ratings after storage. Only small increases in disease incidence (0-8%) were seen after storage. Thiophanate-methyl with mancozeb, Captan with mancozeb, and fludioxonil were among the most effective in reducing the incidence and severity of silver scurf on seed and in progeny tubers (Incidence on progeny tubers at harvest for these three treatments were 3%, 9%, and 8% respectively). Thiophanatemethyl alone was not effective for control of silver scurf (48% incidence compared to 43% incidence for the untreated control).Environmental conditions in storage affected disease development. Reduced humidity (85%) during the curing period (0–3 weeks after harvest) significantly reduced (11%) the surface area of tubers infected with silver scurf. Free moisture on the tuber surfaces during storage significantly increased (15%) tuber surface area infection.H. solani was shown to survive in soil and on some potato storage building materials for up to 9 months. The silver scurf disease of potatoes can be suppressed using effective seed treatment and storage management.

The anthracnose on red pepper is caused by Colletotrichum capsici. It was not only found in the field (leaf/branch, flower and fruit), but also during transportation as well as storage or before being consumed or processed. The purpose of this research is to know both the incubation period and disease severity of anthracnose of the red pepper in the storage. This experiment using factorial completely randomized design with 2 factors and 5 replications. The first factor was inoculation (2 ways) and the second one was variety of red peppers (3 varieties). The result of the experiment showed that the incubation period of "MT999" was longer than those both "Hot Beauty" and "Local Lampung". While the disease severity of "MT999" was lower than those ones. The inoculation ability influenced the incubation period and disease severity and also no interaction between inoculation and variety

Neutral lipid storage disease (NLSD) is an autosomal recessive disorder characterized by the presence of numerous lipid droplets in virtually all tissues examined. The increased cellular triacylglycerol content results from defective recycling of triacylglycerol-derived diacylglycerol to phospholipids (Igal, R. A. and R. A. Coleman. 1996. J. Biol. Chem. 271: 16644–16651). In order to determine whether de novo glycerolipid synthesis is also altered in NLSD, we compared the ability of normal human skin fibroblasts and fibroblasts from a patient with NLSD to incorporate phospholipid precursors into cell lipids. NLSD cells had increased rates of incorporation of [14C]oleic acid and [3H]glycerol into triacylglycerol and all phospholipid species except phosphatidylethanolamine. However, the cell content of each phospholipid species was similar in control and NLSD cells, indicating a higher turnover rate in NLSD cells for phosphatidylcholine, phosphatidylinositol, phosphatidylserine, and sphingomyelin. Labeling with [14C]choline and [14C]ethanolamine confirmed the increase in the rate of phosphatidylcholine synthesis and the decreased rate of phosphatidylethanolamine synthesis through their respective CDP pathways. The activities of the major regulatory enzymes of triacylglycerol, phosphatidylcholine, and phosphatidylethanolamine biosynthesis were similar in control and NLSD cells. Taken as a whole, this study provides strong evidence for an underlying regulatory defect in NLSD that alters the rates of synthesis and degradation of the major cellular phospholipids.—Igal, R. A., and R. A. Coleman. Neutral lipid storage disease: a genetic disorder with abnormalities in the regulation of phospholipid metabolism. J. Lipid Res. 1998. 39: 31–43.

Clinical aspect of bovin diseases having particular importance in Hungary are discussed. Special attention is paid to differential diagnosis. Following disease are discussed. Congenital diseases: hydrocephalus, cerebellar hypoplasia, Weaver syndrome, lysosomal (metabolic) storage diseases. Diseases caused by viruses, prions and chlamidia: rabies, Aujeszky disease, bovine malignant catarrh, BSE, IBR, chlamydiosis. Bacterial diseases: parahypophyseal abscess, TEME, listeriosis. Diseases caused by bacterial exotoxins and toxicoses: tetanus, botulism and lead poisoning. Metabolic diseases: cerebrocortical necrosis, fatty liver syndrome, ketosis, puerperal hypocalcaemia (milk fever), hypomagnesaemia, lactacidaemia

Deficiency of lysosomal acid lipase (LAL) leads to either Wolman disease(WD) or the more benign cholesteryl ester storage disease (CESD). To identifythe molecular basis of the different phenotypes we have characterised the LALgene mutations in three new patients with LAL deficiency. A patient with WD washomozygote for a null allele Y303X. The other two patients, with CESD, presentedeither homozygosity for T267I or compound heterozygosity consisting of Q64R andan exon 8 donor splice site substitution (G→A in position–1). The mutants T267I and Q64R and the previously reported L273S, G66V,and H274Y CESD substitutions, overexpressed in stable clones, were found to befully glycosylated and show an enzymatic activity of 3–8% of that ofnormal LAL. On the other hand, the Δ254–277 mutant proteinderived from exon 8 skipping and the Y303X protein were totally inactive. Bytransient transfection of hybrid minigene constructs, the CESD G→A(–1) substitution resulted in partial exon inclusion, thus allowing theproduction of a small amount of normal LAL mRNA and hence of a functionalenzyme. In contrast, a G→Asubstitution observed in WD at position +1 of the same exon 8 donor siteresulted in complete exon skipping and the sole production of an inactiveΔ254–277 protein.In conclusion,LAL genotypes determine the level of residual enzymatic activity, thusexplaining the severity of the phenotype.—Pagani, F., R. Pariyarath, R.Garcia, C. Stuani, A. B. Burlina, G. Ruotolo, M. Rabusin, and F. E. Baralle. Newlysosomal acid lipase gene mutants explain the phenotype of Wolman disease andcholesteryl ester storage disease. J. Lipid Res. 1998. 39:1382–1388.

Although the CLN3 gene for Batten disease, the most common inherited neurovisceral storage disease of childhood, was identified in 1995, the function of the corresponding protein still remains elusive. We previously cloned the Saccharomyces cerevisiae homologue to the human CLN3 gene, designated BTN1, which is not essential and whose product is 39% identical and 59% similar to Cln3p. We report that btnl1-Delta deletion yeast strains are more resistant to D-(-)-threo-2-amino-1-[p-nitrophenyl]-1,3-propanediol (denoted ANP), a phenotype that is complemented in yeast by the human CLN3 gene. Furthermore, the severity of Batten disease in humans and the degree of ANP resistance in yeast are related when the equivalent amino acid replacements in Cln3p and Btn1p are compared. These results indicate that yeast can be used as a model for the study of Batten disease.

The degradation of blood group glycolipid A-6-2 (GalNAc(α1→3)[Fucα1→2]Gal(β1→4)GlcNAc(β1→3)Gal (β1→4)Glc(β1→1′)Cer, IV2-α-fucosyl-IV3-α-N-acetylgalactosaminylneolactotetraosylceramide), tritium-labeled in its ceramide moiety, was studied in situ, in skin fibroblast cultures from normal controls, from patients with defects of lysosomal α-N-acetylgalactosaminidase, and from patients with other lysosomal storage diseases. Uptake of the glycolipid with apolipoprotein E-coated liposomes was linear with time and with the amount of glycolipid added. In normal cells, the expected array of less polar products and some lipids resulting from re-using the liberated sphingosine, mainly sphingomyelin and phosphatidylcholine, were formed. In α-N-acetylgalactosaminidase-deficient cells, the glycolipid was virtually not degraded; product formation was less than 2% of the normal control rate, suggesting that blood group A-active glycolipids contribute as storage compounds to the pathogenesis of this disease. The expected accumulation of degradation intermediates was seen in fucosidosis, and in Sandhoff, Gaucher, and Farber disease cells, whereas normal turnover rates were found in Tay-Sachs disease cells, GM2 activator-deficient (variant AB of GM2 gangliosidosis) and in sulfatide activator- (sap-B-) deficient cells. In GM1 gangliosidosis and in sap precursor-deficient cells, the lysosomal glycolipid catabolism was found to be strongly retarded; accumulation of individual products could not be seen. Skin fibroblasts from patients with α-N-acetylgalactosaminidase deficiency (Schindler disease) cannot degrade the major blood group A glycolipid.—Asfaw, B., D. Schindler, J. Ledvinová, B. Černý, F. Šmíd, and E. Conzelmann. Degradation of blood group A glycolipid A-6-2 by normal and mutant human skin fibroblasts.

Unmodified and low water activity (a(w))-tolerant cells of Candida sake CPA-1 applied before harvest were compared for ability to control blue mold of apples ('Golden Delicious') caused by Penicillium expansum under commercial storage conditions. The population dynamics of strain CPA-1 on apples were studied in the orchard and during storage following application of 3 x 10(6) CFU/ml of each treatment 2 days prior to harvest. In the field, the population size of the unmodified treatment remained relatively unchanged, while the population size of the-a(w)-modified CPA-1 cells increased. During cold storage, the populations in both treatments increased from 10(3) to 10(5) CFU/g of apple after 30 days, and then declined to about 2.5 x 10(4) CFU/g of apple. In laboratory studies, the low-a(w)-tolerant cells provided significantly better disease control as compared with the unmodified cells and reduced the number of infected wounds and lesion size by 75 and 90%, respectively, as compared with the nontreated controls. After 4 months in cold storage, both unmodified and low-a(w)-tolerant cells of C. sake were equally effective against P. expansum on apple (>50% reduction in size of infected wounds).

The involvement of the yam 'head' or primary nodal complex (PNC) in several traditional practices for yam propagation, cultivation, and storage is outlined. Alternative phylogenetic and ontogenetic manifestations of the PNC, including those of different species which produce germinating seedlings and sprouting stem cuttings, bulbils, tuber pieces, and whole tubers (with 'heads'), as well as those in bulbil development are described. Failure to recognize the similarity of this unique organ in its different manifestations may have restricted the scope of research investigations for yam improvement. Previous investigations on micro-tuber production in tissue culture for distribution of disease-free germplasm, minisett techniques for production of planting setts and mini-ware tubers, and GA3 application for extension of tuber dormancy and storage life are described. It is suggested that development of improved techniques for combination of minisett production and GA3-induced enhancement of tuber storage life could lead to recognition of mini-tubers as a new staple tropical product, comparable and competitive with Solanum tuberosum in production, quality, and international utilization as a table tuber.