Efficient extraction of oil from droplet microfluidic emulsions.

Droplet microfluidic techniques can perform large numbers of single molecule and cell reactions but often require controlled, periodic flow to merge, split, and sort droplets. Here, we describe a simple method to convert aperiodic flows into periodic ones. Using an oil extraction module, we efficiently remove oil from emulsions to readjust the droplet volume fraction, velocity, and packing, producing periodic flows. The extractor acts as a universal adaptor to connect microfluidic modules that do not operate under identical flow conditions, such as droplet generators, incubators, and merger devices.

Laboratory diagnosis of zinc phosphide poisoning.

Zinc phosphide, a readily-available rodenticide, poses a significant risk for intoxication in animals. Animals have been poisoned by ingesting treated bait or the carcasses of poisoned rodents. Toxicity is due to the liberation of phosphine gas in the stomach. Clinical signs include central nervous system excitation, depression and vomition. Similarities of clinical signs with other central nervous system toxicants make the diagnosis difficult without a specific diagnostic test. The procedure outlined in this paper detects phosphine liberated from zinc phosphide by the addition of hydrochloric acid as well as the phosphine previously generated by contact with stomach acid.

Aspergillus flavus and aflatoxins B1, B2, and M1 in corn associated with equine death.

Corn from an Arkansas farm, where three horses died and others became sick, was investigated for causative principles. Necropsy of the three horses revealed what appeared to be severe hepatic necrosis. Histopathological examination indicated a pattern of hepatic lesions that was suggestive of aflatoxin contamination of the feed. Mycological examination of the corn by dilution plating revealed 95% of the colonies as Aspergillus flavus. Chemical analysis of the corn for mycotoxins was positive for aflatoxin B1, B2, and M1 at concentrations of 114, 10, and 6 micrograms/Kg, respectively. Cyclopiazonic acid, sterigmatocystin, and the Fusarium toxins, vomitoxin (deoxynivalenol), T-2 toxin, and diacetoxyscirpenol, were not detected. The presence of aflatoxin metabolites in the moldy corn and the presence of appropriate lesions were compatible with the diagnosis, equine aflatoxicosis.

Nonprotein nitrogen-induced ammonia toxicosis and ammoniated feed toxicity syndrome.

In spite of all the reports and work done, the ammoniated feed toxicity syndrome still is quite a mystery. Given its enigmatic cause, prevention is our only current means of control. The data that is recorded from each new episode, however, may help to piece together the exact mechanism so that one day it can be understood and treated.

Toxicity of field samples and Fusarium moniliforme from feed associated with equine-leucoencephalomalacia.

Feed samples of corn, pelleted feed, and oats associated with equine leucoencephalomalacia (ELEM) were obtained from North Carolina, Illinois, Indiana, and Oklahoma. These samples contained a high colony density of Fusarium moniliforme Sheldon which ranged from 64 to 87% of the total fungi. Fifty-nine F. moniliforme strains were isolated. Isolates of F. moniliforme in feed samples from Illinois, Indiana, and Oklahoma were cultured on corn. The fermented corn, mixed with regular feed and fed to one-day-old ducklings, effected a high mortality coefficient (average 55%). Methanol extracts of corn fermented with each of 14 representative F. moniliforme isolates from North Carolina feed were toxic to mice and some caused rabbit skin necrosis. Vomitoxin (deoxynivalenol), T-2 toxin, zearalenone, and moniliformin were not detected in feed samples or fermented corn. However, 4 to 10 ng of aflatoxin B1 per gram of feed was present in the four North Carolina samples. Bikaverin (C20H14O8), a characteristic red pigment of Fusarium sp., was found in the North Carolina feed samples. This is the first report of bikaverin in feed samples associated with ELEM.

Equine leucoencephalomalacia (ELEM): a study of Fusarium moniliforme as an etiologic agent.

Signs and lesions characteristic of equine leucoencephalomalacia were produced in one of two donkeys given corn cultured with Fusarium moniliforme Sheldon. Gross and histopathologic lesions of the cerebrum included an extensive necrotic cavitation within one cerebral hemisphere, disruption and rarefication of the subcortical white matter, prominent perivascular hemorrhage, and some mononuclear cell perivascular cuffing. Another donkey and three rabbits fed the cultured corn did not develop characteristic signs or lesions of the toxicosis. Chick bioassay studies indicated that the cultured corn which produced the disease did not contain a monovalent salt of moniliformin.