Fish oil-induced yellow fat disease in rats. II. Enzyme histochemistry of adipose tissue

Adipose tissue in various stages of fish oil-induced yellow fat disease in the rat had the same acid phosphatase and 5-nucleotidase activity pattern as similar stages of the disorder in mink and pig. A weak acid phosphatase and 5-nucleotidase activity was seen in interstitial lipofuscin-laden macrophages in "stage M" yellow fat disease without fat cell degeneration. Activity of these macrophagic enzymes increased when there was fat cell degeneration ("stage S" and "stage E" yellow fat disease). This different phosphatase activity in the same cell type may result from phagocytosis of substrates with variable digestibility. Macrophages directly surrounding affected fat cells in steatitis areas ("stage S" and "stage E") had strong acid phosphatase and 5-nucleotidase activity. As in the pig, increased 5-nucleotidase activity was found in affected fat cells, which probably indicates plasma membrane damage. Increased nonspecific esterase activity occurred around affected fat cells. Only a small part of this esterase activity originated from inflammatory cells. This indicates that an increase of esterase activity in degenerating adipose tissue may be an endogeneous process in this tissue.     

Erwinia carotovora (Jones) Bergey et al. var. atroseptica (Hellmers et Dowson) Dye. Seed Tuber Infection Versus Symptom Expression in the Field1

Based on the time that symptoms of blackleg become evident in the field and the various ways of inoculation, it is concluded that the spread of symptom expression is due to the depth at which the bacteria penetrate into the interior of the tubers. Moreover, it is demonstrated that it is not the closed lenticels which prevent penetration, but the absence of a waterfilm in the intercellular spaces of the tuber tissue.     

The effects of ultraviolet-B (UV-B: 290–320 nm) radiation on blister blight disease of tea (Camellia sinensis)

Sunlight is known to reduce the incidence of blister blight disease of tea, caused by Exobasidium vexans . The effects of the ultraviolet-B (UV-B: 290–320 nm) component of solar radiation on the disease and the development of E. vexans were studied in the field in Sri Lanka using UV-screening filter materials held over a commercial crop. Exclusion of UV-B radiation by Polyester, which reduces fluxes in the UV-B region by approximately 75–85%, increased both the number of translucent spots (immature sites of infection) and number of sporulating blisters (mature sites of infection), but it had little or no effect on the sporulation of the pathogen. When basidiospores were artificially inoculated on leaves, and were exposed to full or filtered solar radiation, their survival and germination increased when UV-B wavelengths were removed; significant differences were found 62 h after inoculation. However, UV-B did not affect the extension of germ tubes. This study indicates that the UV-B component of solar radiation plays an important role in the natural regulation of blister blight disease in the field.