Project description:Mice were obtained from in house breeding of C57BL/6J and C57BL/6J-Chr 1A/Na breeding pairs (Jackson Laboratories, USA). To produce F1 hybrids, C57BL/6J females were mated with C57BL/6J-Chr 1A/Na males. The F1 hybrids were intercrossed, producing 82 F2 progeny (41 males and 41 females). Microarray analysis was performed on six pairs of affected and non-affected male animals from the F2 progeny selected on the basis of their motor activity levels (average daily levels of distance moved over a 3 days recording: 768±74 cm/hr (affected) versus 1765±175 cm/hr (non-affected)(p<0.0001).
Project description:Febrile seizures are the most prevalent type of seizures among children up to 5 years of age (2-4% of Western-European children). Complex febrile seizures are associated with an increased risk to develop temporal lobe epilepsy. To investigate short- and long-term effects of experimental febrile seizures (eFS), we induced eFS in highly febrile convulsion-susceptible C57BL/6J mice at post-natal day 10 by exposure to hyperthermia (HT) and compared them to normotherm-exposed (NT) mice. We detected structural re-organization in the hippocampus 14 days after eFS. To identify molecular candidates, which entrain this structural re-organization, we investigated temporal changes in mRNA expression profiles eFS 1 hour to 56 days after eFS. We identified 931 regulated genes and profiled several candidates using in situ hybridization and histology at 3 and 14 days after eFS. This is the first study to report genome-wide transcriptome analysis after eFS in mice. We identify temporal regulation of multiple processes, such as stress-, immune- and inflammatory responses, glia activation, glutamate-glutamine cycle and myelination. Identification of the short- and long-term changes after eFS is important to elucidate the mechanisms contributing to epileptogenesis. Acute, short-, and long-term effects of prolonged febrile seizures on gene expression were investigated in whole hippocampal samples. Samples were taken from C57BL/6J animals one hour (HT n = 8, NT n = 8), three days (HT n = 6, NT n = 6), fourteen days (HT n = 6, NT n = 6), and fifty-six days (HT n = 6, NT n = 6) after HT. Two-channel oligonucleotide microarray analysis was performed with an NT and HT sample on the same chip, including a dye-swap (technical replicate). 3 failed hybridizations were omitted from further analysis.
Project description:HUVEC (Human Umbilical Vein Endothelial Cells) cells were exposed to heat shock (42 degrees Celcius) for different time points (1hr, 3 hrs, 6 hr and 12 hrs) and compared to non heat-shock cells. External normalization controls were added in equal amounts to equivalent amounts of total RNA.
Project description:Male Sprague-Dawley rats were given NOS inhibitor L-NNA (500 mg/l water) for 4 days, 21 days or 21 days with Vitamin E in chow (0.7 g/kg BW/day) (4d-LNNA, 21d-LNNA and 21d-LNNA+VitE, respectively).
Project description:MCF7 (human mammary gland adenocarcinoma) cells were deprived of serum for 30 hrs and were compared to non-deprived cells. External normalization controls were added in equal amounts to equivalent amounts of total RNA.
Project description:HUVECs were exposed to 250 uM DETA-NONOate for 4 hours in the presence and absence of 10 uM of the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3,2]quinoxalin-1-one (ODQ). Control cells were exposed to vehicle (methanol 0.1%).
Project description:A time-course experiment was performed: HUVECs were exposed for 2, 4, 8 and 24 hours to (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NONOate) 250 uM.