Between February 2002 and May 2004, chicken anemia virus (CAV) was detected by PCR in organ samples from 14 flocks of poultry farms in Lagos, Ogun and Oyo States in Southwestern Nigeria. The farms reported low (<5%) to high mortalities (up to 100%) with various lesions at necropsy. The complete VP1 gene of 30 of these positive strains was sequenced. Strains that diverged by up to 4.4% on a nucleotide level differed only by up to 2.5% at the amino acid level (7 aa) as a result of clustered silent mutations. No amino acid substitutions specific for Nigerian strains were observed. Some birds had a CAV mixed infection. Genetic clustering of the VP1 gene did not correlate with differences in flock mortality but the co-infection of CAV with IBDV may be particularly lethal. This first molecular epidemiological study of CAV in Africa shows that the Nigerian strains cluster with viruses from very diverse geographic origins and were almost as diverse (4.4%) as all other strains combined (5.8%).
Arsenic acid is one of the abundant environmental pollutants present in soil, water and the air. Undoubtedly, it has found its way to the food chain in which humans and animals are the final targets thereby causing arrays of disease conditions including cardiovascular and renal dysfunction. Hence, the use of phytochemicals present in medicinal plants has gained global acceptance as chemotherapeutic agents that can prevent, ameliorate, reverse or treat diseases. From our study, arsenic acid intoxication led to significant increase in heart rate (HR), QRS, together with prolonged QT and QTc interval. However, Kolaviron (KV) at the dosage of 100 and 200 mg/kg body weight reversed the aforementioned electrocardiographic (ECG) changes. KV pre-treatment also ameliorated cardiorenal dysfunction via significant reduction in cardiac and renal markers of oxidative stress such as malondialdehyde, hydrogen peroxide generation, myeloperoxidase activity and nitric oxide contents. Immunohistochemistry revealed expressions of renal C-reactive proteins (CRP) and expressions of anti-apoptotic protein BCL2 in KV treated rats. Furthermore, cardiac troponin I (CTnI) expressions were lower in KV treated rats. Taken together, KV mitigated arsenic-acid induced cardiovascular dysfunction via up-regulation of antioxidant defense system and down-regulation of inflammatory and apoptotic signaling pathways.
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