Wild oats (Avenu fatua L.) seed dormancy as influenced by sodium hypochlorite, moist storage and gibberellin A3

Incubation in gibberellin A₃ (GA₃) or a 1 h immersion pretreatment with 800 mm sodium hypochlorite (NaOCl) both promoted 20% germination of freshly harvested dormant wild oat (Avena fatua L.) seeds that had been imbibed on water for 10 days. GA₃ immediately following 1 h NaOCl immersion pretreatment induced maximum germination. Moist storage (MS) after NaOCl immersion pretreatment resulted in less germination on transference of the seeds to GA₃, indicating that GA₃ responsiveness was lost during MS. These seeds required a repeal NaOCl immersion plus a GA₃ treatment to induce maximum germination. However, GA₃ still gave maximum germination if the seeds were stored dry after initial NaOCl immersion. Seeds with water-induced dormancy responded similarly to freshly harvested dormant seeds when treated with NaOCl, MS, or GA₃. Seeds afterripened a longer time had a reduced requirement for exogenous GA₃ in the breaking of dormancy indicating that the depth of the GA₃-dependent dormancy decreased with duration of after-ripening. Dormant dehulled seeds with a brief NaOCl pretreatment germinated about 30% on water but gave maximum germination when incubated on GA₃, an effect that persisted even after 21 days of MS. This effect, coupled with the previous findings, suggested that the NaOCl treatment weakened membrane barriers of the seed coat through a scarification-like effect, similar to the effects of piercing and acid immersion, and thereby produced increased sensitivity to the presence of GA₃. The loss of responsiveness to GA₃ in NaOCl-treated seeds during MS may involve the restoration of integrity of the seed coverings, a process occurring only in the imbibed state, and, presumably, most rapidly in freshly harvested, intact seeds.     

Bilateral laryngeal paralysis in the horse

Four two-year-old Thoroughbreds suffered an acute gastrointestinal illness shortly after dosing with mineral oil which was thought to have been contaminated with an organophosphate compound. Three weeks later all four were noted to be dyspnoeic and endoscopic examination showed that they had developed bilateral laryngeal paralysis. Two of the horses died during severe bouts of dyspnoea six and eight months later and the third was killed shortly thereafter. Examination of the left and right recurrent laryngeal nerves from these horses showed a severe loss of myelinated fibres distally, especially in the left nerve. A similar but less severe lesion was seen in other long peripheral nerves, including the phrenic and digital nerves of the third horse. The spinal cord in two horses showed evidence of mild axonal degeneration which was not related to a particular tract or location. The fourth horse had bilateral laryngeal paralysis two years later. The acute clinical signs and delayed neurological sequelae seen in these horses were strongly suggestive of accidental organophosphate toxicity.     

Solubilization of group- and type-specific streptococcal antigens with a murolytic enzyme from Staphylococcus hyicus

Streptococcal group-specific antigens and B-streptococcal type antigens were solubilized with a murolytic enzyme from Staphylococcus hyicus. This facilitated the effective serogrouping and serotyping of streptococci isolated from humans and various animals.     

Densitometric analysis of aminopeptidase M activity in small intestine mucosa in piglets experimentally infected with Isospora suis

In gnotobiotical and conventional piglets infected a day post partum (DPP) with oocysts of the coccidium Isospora suis, densitometrical analysis of the activity of aminopeptidase M (EC.3.4.11.2; APM) was performed in the area of microvillous zone of the small intestine. Piglets were infected with different infection doses of oocysts (100,000 oocysts) in gnotobiotical piglets and 200,000 oocysts in conventional piglets). In infected gnotobiotical piglets, the APM activity was studied in the period from the 3rd to 11th day after infection (DAI) and in infected conventional piglets in the period of to the 2nd to 10th day after infection (DAI). Control piglets, in the group of the gnotobiotical animals at the age of 2 to 5 days in the group of the conventional animals at the age of 4 to 7 days, had different APM activity in the microvillous zone of the intestinal mucosa. It was stated that the microvillous zone of the intestinal mucosa gained higher values in control conventional piglets (+7.01 mean values of density). In infected gnotobiotical piglets the density fall of the reaction product of APM was demonstrated already on the third day with further marked reduction of APM density on the 4th day after infection in the whole small intestine with predominance of the persisting APM activity in ileum. Even despite the slight increase in the density of the reaction product of APM in the period from the 5th to 7th DAI (the highest increase in APM density on the 6th DAI), a further decrease of the activity was recorded again on the 8th and namely the 9th DAI in the whole small intestine (the lowest value of density was found in the rear jejunum), the ileum mucosa being affected, too. A slightly higher density of the reaction product of APM was found in the duodenum. On the 10th DAI the APM density started to change and on the 11th DAI in the duodenum and in the middle jejunum it even reached higher values in comparison with the control data. Some differences were proved in the infected conventional piglets in comparison with the development of the APM activity in the small intestine mucosa in the infected gnotobiotical piglets. On the 3rd and 4th DAI APM defect occurred in the whole small intestine, with APM density prevailing in the ileum mucosa (like in the group of infected gnotobiotical piglets). The second period of decrease in APM activity lasted for almost four days (6th to 9th DAI).(ABSTRACT TRUNCATED AT 400 WORDS)