A rare case of left additional renal artery in a Nigerian goat

The report of the occurrence of additional renal arteries in domestic animals is rare in the literature. We report a case of an additional renal artery in the left kidney found in a Red Sokoto goat cadaver. The additional renal artery originated from the abdominal aorta 3.80 cm cranial to the origin of the main renal artery. The additional renal artery was relatively long, being 6.30 cm from its origin to the cranial pole region of the kidney where it supplied the kidney. This to the best of our knowledge is the first report in the literature indexed in the Medline of an additional renal artery in a goat

Regional myelin and axon damage and neuroinflammation in the adult mouse brain after long-term postnatal vanadium exposure

Environmental exposure to vanadium occurs in areas of persistent burning of fossil fuels; this metal is known to induce oxidative stress and oligodendrocyte damage. Here, we determined whether vanadium exposure (3\u2009mg/kg) in mice during the first 3 postnatal months leads to a sustained neuroinflammatory response. Body weight monitoring, and muscle strength and open field tests showed reduction of body weight gain and locomotor impairment in vanadium-exposed mice. Myelin histochemistry and immunohistochemistry for astrocytes, microglia, and nonphosphorylated neurofilaments revealed striking regional heterogeneity. Myelin damage involved the midline corpus callosum and fibers in cortical gray matter, hippocampus, and diencephalon that were associated with axonal damage. Astrocyte and microglial activation was identified in the same regions and in the internal capsule; however, no overt myelin and axon damage was observed in the latter. Double immunofluorescence revealed induction of high tumor necrosis factor (TNF) immunoreactivity in reactive astrocytes. Western blotting analysis showed significant induction of TNF and interleukin-1\u3b2 expression. Together these findings show that chronic postnatal vanadium exposure leads to functional deficit and region-dependent myelin damage that does not spare axons. This injury is associated with glial cell activation and proinflammatory cytokine induction, which may reflect both neurotoxic and neuroprotective responses