Transcriptional regulation of α1-adrenoceptor gene in the rat liver during different phases of sepsis

AbstractChanges in α1-adrenoceptor (α1AR) gene expression in the rat liver during different phases of sepsis were studied. Sepsis was induced by cecal ligation and puncture (CLP). Septic rats exhibit two metabolically distinct phases: an initial hyperglycemic phase (9 h after CLP, early sepsis) followed by a hypoglycemic phase (18 h after CLP; late sepsis). The [3H]prazosin binding studies show that the density of α1AR was increased by 30% during the early phase while it was decreased by 24% during the late phase of sepsis. Western blot analyses reveal that α1AR protein level was elevated by 48% during early sepsis but was decreased by 55% during late sepsis. Northern blot analyses depict that the steady-state level of α1bAR mRNA was enhanced by 21% during the early phase but was declined by 29% during the late phase of sepsis. Nuclear run-off assays show that the transcription rate of α1bAR gene transcript was increased by 76% during early sepsis while it was decreased by 29% during late sepsis. The actinomycin D pulse-chase studies indicate that the half-life of α1bAR mRNA remained unaffected during the early and the late phases of sepsis. These findings demonstrate that during the early phase of sepsis, the increase in the rate of transcription of α1bAR gene paralleled with the elevations in the α1bAR mRNA abundance and α1AR protein level, while during the late phase of sepsis, the decrease in the rate of transcription of α1bAR gene coincided with the declines in the α1bAR mRNA abundance and the α1AR protein level in the rat liver. These observations indicate that the altered expression of α1AR genes in the rat liver during the progression of sepsis was regulated transcriptionally

Memory and Electrical Properties of (100)-Oriented AlN Thin Films Prepared by Radio Frequency Magnetron Sputtering

The (100)-oriented aluminum nitride (AlN) thin films were well deposited onto p-type Si substrate by radio frequency (RF) magnetron sputtering method. The optimal deposition parameters were the RF power of 350 W, chamber pressure of 9 mTorr, and nitrogen concentration of 50%. Regarding the physical properties, the microstructure of as-deposited (002)- and (100)-oriented AlN thin films were obtained and compared by XRD patterns and TEM images. For electrical properties analysis, we found that the memory windows of (100)-oriented AlN thin films are better than those of (002)-oriented thin films. Besides, the interface and interaction between the silicon and (100)-oriented AlN thin films was serious important problem. Finally, the current transport models of the as-deposited and annealed (100)-oriented AlN thin films were also discussed. From the results, we suggested and investigated that large memory window of the annealed (100)-oriented AlN thin films was induced by many dipoles and large electric field applied

Role of Exogenous Hsp72 on Liver Dysfunction during Sepsis

This study examined the role of exogenous heat shock protein 72 (Hsp72) in reversing sepsis-induced liver dysfunction. Sepsis was induced by cecal ligation and puncture. Liver function was determined on the basis of the enzymatic activities of serum glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT). Apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling staining. B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3 and caspase-9, and cleaved poly (ADP-ribose) polymerase (PARP) protein expressions were analyzed using Western blotting. Results showed GOT and GPT levels increased during sepsis, and levels were restored following the administration of human recombinant Hsp72 (rhHsp72). Increased liver tissue apoptosis was observed during sepsis, and normal apoptosis resumed on rhHsp72 administration. The Bcl-2/Bax ratio, cleaved caspase-3, caspase-9, and PARP protein expressions in the liver tissues were upregulated during sepsis and normalized after rhHsp72 treatment. We conclude that, during sepsis, exogenous Hsp72 restored liver dysfunction by inhibiting apoptosis via the mitochondria-initiated caspase pathway