RESIDUES OF THE BETA-AGONIST CLENBUTEROL IN TISSUES OF MEDICATED FARM-ANIMALS

Reports of the illegal use of clenbuterol as a growth promotant prompted the development of a competitive enzyme immunoassay for this drug. This procedure was utilized to study the elimination of clenbuterol from tissues in sheep medicated with both therapeutic and growth-promoting doses of the drug. The results indicated that prior to removal of medication clenbuterol was widely distributed throughout the animal tissues. However as the withdrawal periods increased fluid targets such as urine and bile became less effective at detecting clenbuterol usage. At both therapeutic and growth-enhancing concentrations of clenbuterol liver samples remained positive up to the maximum withdrawal time given in this experiment (15 days). Concentrations of clenbuterol likely to cause food poisoning (> 100 ng/g) were only detected in liver samples taken prior to the removal of medication. The highest recorded concentration of clenbuterol in muscle was 22.5 ng/g.

TISSUE RESIDUES IN PIGS FED ON MEAL CONTAMINATED WITH SULFADIMIDINE DURING MIXING

Two equal batches of pig feed were prepared sequentially in a half-ton mixer. The first was prepared to contain 100-mu-g/g sulphadimidine and the second had not added sulphadimidine. The medicated batch was shown to have 97.2-mu-g/g and the flush 2-mu-g/g. From the conditions of the experiment it was suggested that sulphadimidine was preferentially retained in the mixer.

SULFADIMIDINE IN DRINKING TROUGHS AT BACON FACTORIES

Water troughs in the lairages of three bacon factories were examined. Pigs were observed drinking from the troughs, some of which were contaminated with faeces. Some of the troughs contained detectable concentrations of sulphadimidine, and the highest concentration recorded was 17 mu-g/ml. Pigs which drank this contaminated water before slaughter could contain tissue residues of sulphadimidine above the permitted concentration.

Monitoring for clenbuterol abuse in N Ireland 1989-1994

Laboratory testing in N. Ireland for the illegal growth promoting agent, clenbuterol (CBL), is centralized at the Veterinary Sciences Division, Belfast. During the past 6 years a variety of testing schemes have evolved to determine the level of abuse of this drug in the local meat industry.

Association of the G4 rotavirus genotype with gastroenteritis in adults

Rotavirus is the most common etiological cause of acute viral gastroenteritis in infants and young children worldwide, yet its role in the adult population is less well understood. We have recently identified rotavirus as the causative agent of severe diarrhea in adults, specifically in two gastroenteritis outbreaks in separate care for the elderly homes. Strain typing has shown the continued presence of P[8]G1, the emergence of P[8]G9, and the reemergence of P[8]G4. A total of 26 community cases and 6 outbreak cases of rotavirus infection, positive via a molecular screening assay, were subsequently amplified using VP4 and VP7 specific primers (Con2/Con3 and 1A/1B primer sets, respectively). The age range of patients investigated was from

Deletion of Gremlin1 increases cell proliferation and migration responses in mouse embryonic fibroblasts

Gremlin1 (Grem1) is an antagonist of bone morphogenetic proteins (BMPs) that plays a critical role in embryonic and postnatal development. Grem1 has been implicated as both a promoter and an inhibitor of cell proliferation driven by BMP-4 and other mitogens in a diverse range of cell types. Recent data showed that Grem1 can trigger angiogenesis via vascular endothelial growth factor receptor (VEGFR2) binding, highlighting that the precise modalities of Grem1 signalling require further elucidation.

Fetal Cardiac Effects of Maternal Hyperglycemia During Pregnancy

Maternal diabetes mellitus is associated with increased teratogenesis, which can occur in pregestational type 1 and type 2 diabetes. Cardiac defects and with neural tube defects are the most common malformations observed in fetuses of pregestational diabetic mothers. The exact mechanism by which diabetes exerts its teratogenic effects and induces embryonic malformations is unclear. Whereas the sequelae of maternal pregestational diabetes, such as modulating insulin levels, altered fat levels, and increased reactive oxygen species, may play a role in fetal damage during diabetic pregnancy, hyperglycemia is thought to be the primary teratogen, causing particularly adverse effects on cardiovascular development. Fetal cardiac defects are associated with raised maternal glycosylated hemoglobin levels and are up to five times more likely in infants of mothers with pregestational diabetes compared with those without diabetes. The resulting anomalies are varied and include transposition of the great arteries, mitral and pulmonary atresia, double outlet of the right ventricle, tetralogy of Fallot, and fetal cardiomyopathy.

STIMULATION OF PHOSPHOLIPASE C-BETA(2) BY RECOMBINANT GUANINE-NUCLEOTIDE-BINDING PROTEIN BETA-GAMMA DIMERS PRODUCED IN A BACULOVIRUS/INSECT CELL EXPRESSION SYSTEM - REQUIREMENT OF GAMMA-SUBUNIT ISOPRENYLATION FOR STIMULATION OF PHOSPHOLIPASE-C

Recombinant wild-type beta(1) gamma(1) dimers of signal-transducing guanine nucleotide-binding proteins (G proteins) and beta(1) gamma 1 dimers carrying a mutation known to block gamma-subunit isoprenylation (beta(1) gamma(1)C71S) were expressed in baculovirus-infected insect cells. Both wild-type and mutant beta(1) gamma(1) dimers were found in soluble fractions of infected cells upon subcellular fractionation. Anion exchange chromatographic and metabolic-radiolabeling studies revealed that the soluble beta(1) gamma(1) preparation contained approximately equal amounts of non-isoprenylated and isoprenylated beta(1) gamma(1) dimers. Soluble wild-type and mutant beta(1) gamma(1) dimers and native beta(1) gamma(1) dimers purified from bovine retina were reconstituted with recombinant phospholipase C-beta(2). Only isoprenylated beta(1) gamma(1) dimers were capable of stimulating phospholipase C-beta(2). The results show that gamma-subunit isoprenylation and/or additional post-translational processing of the protein are required for beta gamma subunit stimulation of phospholipase C.