The study included that 35 clinically infected cattle were subjected for the clinical therapeutic trail. The age of these animals ranged from one day to above five years old. In the clinical therapeutically trail we used BUPAQUONE® as a new drug for treatment of tropical theileriosis it gave 91.4 % as an accuracy rate in general but if the diseased animals detected and treated as early as possible the accuracy rate reached 100%, in cases that complicated with respiratory signs the accuracy rate depended on the type of antibiotic that used as a treatment for control of the respiratory affection. Cases that received BUPAQUONE with Oxyteteracycline hydrochlorid as antibiotic therapy for diseased animals the accuracy rate was 81.8% but in cattle that received BUPAQUONE with Marbofloxacine as antibiotic therapy the accuracy rate was 93.3%. So we can conclude that Marbofloxacine is more preferred as antibiotic treatment in cases of tropical theileriosis that suffered from respiratory signs. We concluded that, Bupaquone® is recommended as a treatment for tropical theileriosis but in some cases that are complicated with respiratory signs using of antibiotics are recommended such as Marbofloxacine 10% which recorded higher rate of recovery than Oxyteteracycline 20% long acting in control of respiratory complication of the tropical theileriosis

Perfluorooctanic acid (PFOA) has similar characteristics to perfluorooctane sulfonate (PFOS) in reproduction toxicity featured by neonatal death. We found that PFOS exposure to mice during pregnancy led to intracranial blood vessel dilatation of fetuses accompanied by severe lung collapse which caused neonatal mortality. Thus, we adopted the corresponding experimental design to PFOS in order to characterize the neonatal death by PFOA. Pregnant ICR mice were given 1, 5 and 10 mg/kg PFOA daily by gavage from gestational day (GD) 0 to 17 and 18 for prenatal and postnatal evaluations,respectively. Five to nine dams per group were sacrificed on GD 18 for prenatal evaluation; other 10 dams were left to give birth. No maternal death was observed. The liver weight increased dosedependently,with hepatocellular hypertrophy, necrosis, increased mitosis and mild calcification at 10 mg/kg. PFOA at 10 mg/kg increased serum enzyme activities (GGT, ALT, AST and ALP) with hypoproteinemia and hypolipidemia. PFOA treatment reduced the fetal body weight at 5 and 10 mg/kg. Teratological evaluation showed delayed ossification of the sternum and phalanges and delayed eruption of incisors at 10 mg/kg, but did not show intracranial blood vessel dilatation. Postnatal evaluation revealed that PFOA reduced the neonatal survival rate at 5 and 10 mg/kg. At 5 mg/kg pups were born alive and active and 16% died within 4 days observation, while all died within 6 hours after birth at 10 mg/kg without showing intracranial blood vessel dilatation. The cause of neonatal death by PFOA may be different from PFOS.

Perfluorooctanic acid (PFOA) has similar characteristics to perfluorooctane sulfonate (PFOS) in reproduction toxicity featured by neonatal death. We found that PFOS exposure to mice during pregnancy led to intracranial blood vessel dilatation of fetuses accompanied by severe lung collapse which caused neonatal mortality. Thus, we adopted the corresponding experimental design to PFOS in order to characterize the neonatal death by PFOA. Pregnant ICR mice were given 1, 5 and 10 mg/kg PFOA daily by gavage from gestational day (GD) 0 to 17 and 18 for prenatal and postnatal evaluations,respectively. Five to nine dams per group were sacrificed on GD 18 for prenatal evaluation; other 10 dams were left to give birth. No maternal death was observed. The liver weight increased dosedependently,with hepatocellular hypertrophy, necrosis, increased mitosis and mild calcification at 10 mg/kg. PFOA at 10 mg/kg increased serum enzyme activities (GGT, ALT, AST and ALP) with hypoproteinemia and hypolipidemia. PFOA treatment reduced the fetal body weight at 5 and 10 mg/kg. Teratological evaluation showed delayed ossification of the sternum and phalanges and delayed eruption of incisors at 10 mg/kg, but did not show intracranial blood vessel dilatation. Postnatal evaluation revealed that PFOA reduced the neonatal survival rate at 5 and 10 mg/kg. At 5 mg/kg pups were born alive and active and 16% died within 4 days observation, while all died within 6 hours after birth at 10 mg/kg without showing intracranial blood vessel dilatation. The cause of neonatal death by PFOA may be different from PFOS.

Perfluorooctanic acid (PFOA) has similar characteristics to perfluorooctane sulfonate (PFOS) in reproduction toxicity featured by neonatal death. We found that PFOS exposure to mice during pregnancy led to intracranial blood vessel dilatation of fetuses accompanied by severe lung collapse which caused neonatal mortality. Thus, we adopted the corresponding experimental design to PFOS in order to characterize the neonatal death by PFOA. Pregnant ICR mice were given 1, 5 and 10 mg/kg PFOA daily by gavage from gestational day (GD) 0 to 17 and 18 for prenatal and postnatal evaluations,respectively. Five to nine dams per group were sacrificed on GD 18 for prenatal evaluation; other 10 dams were left to give birth. No maternal death was observed. The liver weight increased dosedependently,with hepatocellular hypertrophy, necrosis, increased mitosis and mild calcification at 10 mg/kg. PFOA at 10 mg/kg increased serum enzyme activities (GGT, ALT, AST and ALP) with hypoproteinemia and hypolipidemia. PFOA treatment reduced the fetal body weight at 5 and 10 mg/kg. Teratological evaluation showed delayed ossification of the sternum and phalanges and delayed eruption of incisors at 10 mg/kg, but did not show intracranial blood vessel dilatation. Postnatal evaluation revealed that PFOA reduced the neonatal survival rate at 5 and 10 mg/kg. At 5 mg/kg pups were born alive and active and 16% died within 4 days observation, while all died within 6 hours after birth at 10 mg/kg without showing intracranial blood vessel dilatation. The cause of neonatal death by PFOA may be different from PFOS.

Meat adulteration constitutes an important problem in Egypt especially with the low income to make meat products of lower prices. Adulteration may occur by substitution of low priced or even banned meat species for that high priced one as well as by addition of non meat protein as soybean. This adulteration causes many diseases as infection with bacteria or virus as Bovine Spongiform Encephalopathy (BSE) and scrapie especially with addition of infected parts. Moreover consumers suffer from allergy to some proteins which may be added but not labeled. It is reported that genetically modified organisms may cause allergy and antibiotic resistance. Therefore, in this study AGID and PCR techniques were applied for detection of meat and soybean adulteration. Firstly for application of AGID technique meat extract from beef, chicken, pork and donkey as well as saline extract from heated and raw soybeans were prepared. Hyper immune sera were prepared in rabbits by subcutaneous injection of meat extracts and soybean extracts. Then rabbits were bled and blood collected to get the specific antisera. Positive results indicated by appearance of clear precipitation line between the antibody and the corresponding antigen with assurance that no cross reaction occurred between species. Two hundred samples from beef meat products (50 minced meats, 50 raw kofta, 50 sausages and 50 beef burger) were subjected to analysis by AGID technique. The incidence of adulteration of minced meat with each of chicken and pork were 6%. The rate of adulteration was 34% and 26% in raw kofta, 32% and 14% in sausage and 32% and 2% in beef burger, respectively. Donkey was detected only in beef burger at rate of 2%. The adulteration rates with heated and raw soybeans were 8% and 4% in raw kofta, 28% and 2% in sausage and 18% and 2% in beef burger, respectively. Heated and raw soybean failed to be detected in minced meat. For application of PCR technique specific primers for chicken, pork, donkey meat species, native and modified soybean were prepared, there molecular weights were 420, 343, 350, 118 and 172 bp, respectively. Deoxyribonucleic acid (DNA) was extracted from tested samples for detection of the previous species in these tested samples. Out of suspected and negative adulterated samples examined by AGID technique, fifty samples were reanalyzed by PCR technique. By using PCR technique the adulteration rates with chicken were 57%, 63.7%, 66.7% and 69% in minced meat, raw kofta, sausages and beef burger, respectively. The adulteration rates with pork were 35.7%, 45.5%, 41.7% and 23% in minced meat, raw kofta, sausages and beef burger, respectively. The adulteration rates with donkey were 7%, 18%, 8% and 7.7% in minced meat, raw kofta, sausages and beef burger, respectively. The adulteration rates with native soybean were 50%, 72.7%, 75% and 100% in minced meat, raw kofta, sausages and beef burger, respectively. The adulteration rates with modified soybean were 28.6%, 45.5%, 50% and 69% in minced meat, raw kofta, sausages and beef burger, respectively. It is noticed that about 57%, 62.5%, 66.7 % and 69% from native soybean were modified in minced meat, raw kofta, sausages and beef burger, respectively. Totally it was 65% form native soybean was modified.

perfluorooctanoic acid (PFOA)has similar characteristics to perfluorooctane sulfonate (PFOS) in reproduction toxicity featured by neonatal death. We found that PFOS exposure to mice during pregnancy led to intracranial blood vessel dilatation of fetuses accompanied by severe lung collapse which caused neonatal mortality. Thus we adopted the corresponding experimental design to PFOS in order to characterize the neonatal death by PFOA. 1,5 and 10 mg/kg PFOA were given to pregnant ICR mice daily by gavage from gestation day (GD) 0 to GD 17 and 18 for prenatal and postnatal evaluation respectively. This research showed that the cause of neonatal death by PFOA may be different from PFOS.