The effects of experimentally induced Escherichia coli mastitis and flunixin meglumine administration on activity measures, feed intake, and milk parameters.

The use of flunixin meglumine (FM), a nonsteroidal antiinflammatory drug, during experimentally induced Escherichia coli mastitis was evaluated. Twenty-four primiparous and multiparous lactating dairy cows were challenged with 1×10(2) cfu of E. coli 727 in 1 uninfected quarter.

Neurotrophin signaling through the p75 receptor is deficient in traf6-/- mice.

Activation of the neurotrophin receptor p75 has been shown to elicit opposing cellular signals. Depending on the context of the cell, p75 will either promote survival or induce apoptosis after neurotrophin stimulation. p75-induced apoptosis occurs through activation of c-Jun N-terminal kinase (JNK), whereas the survival signal is mediated by nuclear factor kappaB (NFkappaB).

Moderate zinc deficiency increases cell death after brain injury in the rat.

Zinc supplementation has been used clinically to reduce Zn losses and protein turnover in patients suffering from traumatic brain injury. Despite the known role of zinc in cell survival and integrity, the influence of zinc status on central nervous system wound healing in the weeks and months after brain injury has not been addressed. In this investigation, we examined cell death after unilateral cortical stab wounds in adult rats (n = 5 per group) that were provided diets containing adequate zinc (30 mg Zn/kg diet), supplemental zinc (180 mg/kg), or moderately deficient zinc (5 mg/kg).

Free zinc increases at the site of injury after cortical stab wounds in mature but not immature rat brain.

The accumulation of free zinc (Zn2+) appears to play a role in the neuronal degeneration that occurs after brain injury. Given that neonates respond to brain injury with increased plasticity compared to adults, this study compared the effect of age on free Zn2+ and the Zn2+-binding protein metallothionein-3 (MT-3) after injury. Unilateral cortical stab wounds were produced in 3-day-old and adult rats.

Regulation of mitochondrial cytochrome b mRNA by copper in cultured human hepatoma cells and rat liver.

Copper overload and deficiency are known to cause morphological and functional mitochondrial abnormalities. The reverse transcriptase-polymerase chain reaction (RT-PCR)-based method of differential display of mRNA was used to identify genes with altered expression in cultured human hepatoma cells (Hep G2) exposed to increasing concentrations of copper (0-100 microM, 24 h). Copper regulation of a cloned PCR product, identified as the gene for the mitochondrially encoded cytochrome b, was confirmed by Northern analysis and in situ hybridization.