Murine typhus is a febrile disease caused by the bacterium, Rickettsia typhi (R. typhi), and transmitted via infected fleas. This study investigated midgut responses of infected versus uninfected cat fleas (Ctenocephalides felis) by constructing cDNA libraries and examining transcript levels. Select C. felis serine proteases, GTPases and defense response genes were compared to identify differences in gene expression between the two states of infection. A total of 1152 transcripts from both libraries were sequenced, generating 906 high quality sequences, 472 from the uninfected and 434 from the infected midgut library.
This dataset was generated to investigate long-lasting neurobiological adaptations to drugs of abuse. This dataset specifically supported the study of cocaine exposure impact of mitochondrial dynamics and morphology through early growth response factor 3 (Egr3) transcriptional regulation of mitochondria-related nuclear gene transcripts. Mitochondria-related nuclear genes were assayed following contingent or non-contingent cocaine exposure in rodents and were also examined in postmortem nucleus accumbens (NAc) of cocaine dependents.
Supplemental data in tabular forms include human demographics, DNA sequencing primers, mitochondrial statistical analysis, and gene regulations.
The following data elements were observed over a period of 7-10 days: Egr3 change in response to cocaine vs saline between rats and human postmortem issue; Egr3 binding changes in various genes promoting mitochondria in response to cocaine vs saline between rats and human postmortem issue; mRNA change in response to cocaine and saline between rats and human postmortem issue and between cocaine addict and control group; mRNA change in response to cocaine and saline between rats and human dead issue; Ribosome (the RNA binding proteins) associated mRNA changes in dopamine receptor-1 containing medium spiny neurons (D1 MSNs) and D2 MSNs in response to cocaine and saline between cocaine addict and control group.