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Background and Aim: The Watish sheep is a strain of desert sheep of smaller size compared to other desert sheep ecotypes, and there is anecdotal evidence that it is endowed with high litter size. The present study was designed for screening for polymorphisms in the known fecundity genes (bone morphogenetic protein receptor type 1B A<G in exon 6, bone morphogenetic protein 15 (BMP15) (FecXB, FecXG, FecXH, and FecXI) in exon2, growth differentiation factor 9 (GDF9) – G1 in exon1 and G8 in exon2 and PRLG<A in intron2) and their association with litter size in Watish. Materials and Methods: The study involved 156 Watish ewes of 2-6 years of age, along with data on litter size in the first, second, and third parity from Sinnar state and contiguous Blue Nile State. Genomic DNA was isolated and genotyped using polymerase chain reaction-restriction fragment length polymorphism. Allele and genotype frequencies were calculated by direct counting. Chi-square test for goodness of fit was performed for agreement with Hardy-Weinberg expectations and association testing. Results: The results demonstrated that all individuals were non-carriers for the target mutations of FecB, BMP15 (FecXB, FecXH, and FecXI), and GDF9-G8. With regard to the GDF9-G1 gene, the genotypic frequencies were 0.07% (G+) and 0.93% (++), in FecXG gene they were 0.993% (++) and 0.006% (B+), in PRL gene 0.516(++), 0.347(B+), and 0.137(BB). The Chi-square test showed a non-significant association between ewe's type of birth and the detected mutations genotypes. Conclusion: These results preliminarily indicated that GDF9-G1, BMP15 (FecXG), and PRL genes might have had some contribution for improving litter size in Watish Sudanese sheep. However, further studies using larger samples are needed to detect the effects of those mutations on Watish sheep litter size.

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Background: Parkinson's disease is a neurodegenerative disease mainly characterized by loss of dopaminergic neurons in the substantia nigra pars compacta and their terminals in the striatum. The development of neuroprotective drugs that slow or delay neurodegeneration became of a considerable interest. In numerous animal models, exogenously administered EPO exhibits neuroprotective effects. Aim: The current research investigated the impact of administration of recombinant human EPO (rhEPO) in rotenone parkinsonian rats. Materials and Methods: Thirty two adult male albino Sprague-Dawly rats were equally and randomly divided into four groups; group 1 the vehicle-treated group, group 2 rotenone-treated group, group 3 treated with rotenone in addition to intranasal rhEPO and group 4 treated with rotenone in addition to intraperitoneal rhEPO. The motor performance of the rats was evaluated. Malondialdehyde and reduced glutathione were assayed. Blood indices were measured. Histopathology of the substantia nigra was also done. Results: Results showed that rotenone-treated rats exhibited significant impairment of motor coordination and marked degeneration of substantia nigra neurons was observed. Both intranasal and intraperitoneal rhEPO treatment improved the motor deficit and significantly increased the number of neurons in the SNpc. intraperitoneal rhEPO significantly increased lipid peroxide and significantly affected blood indices. Conclusion: Our findings suggest that, EPO may have neuroprotective effect in PD. Systemic rhEPO neuroprotective effects may be attenuated by its adverse effects such as increase of OS in the vascular system and stimulation of erythropoiesis. Small doses of intranasal EPO may be sufficient to produce neuroprotection without affecting erythropoiesis and further researches are required to address the mechanisms of neuroprotective effects of EPO.

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