ABSTRACT
Two novel porous luminescent metal-organic frameworks (MOFs, 1 and 2) have been constructed using 3,4-di(3,5-dicarboxyphenyl)phthalic acid using a hydrothermal method. Both MOFs can work as highly sensitive sensors to Fe(3+) by luminescent quenching. Analyses of the structures indicate a higher quenching efficiency of 2 because of the existence of active -COOH groups. Based on this consideration, the quenching mechanisms are studied and the processes are controlled by multiple mechanisms in which dynamic and static mechanisms of MOFs are discussed. Besides, the corresponding dynamic and static quenching constants are calculated, achieving the quantification evaluation of the quenching process. As expected, experimental data show that compound 2 possesses an overall quenching efficiency 6.9 times that of compound 1. Additionally, time-dependent intensity measurements, the shifts of the excitation spectrum and the appearance of a new emission peak all give visual proofs of the distinct mechanisms between the two MOFs.
Subject(s)
Ferrous Compounds/analysis , Ferrous Compounds/chemistry , Luminescent Agents/analysis , Luminescent Agents/chemistry , Luminescent Measurements/methods , Luminescence , Metals , Porosity , X-Ray DiffractionABSTRACT
OBJECTIVE: To investigate the effects of Recombined Human Neuregulin (NRG) on the expression of Glucose transporter (Glut1) in myocardium tissue of Rhesus Monkeys with Pacing-induced Heart Failure and the heart function. METHODS: Twenty four rhesus monkeys were randomly divided into three groups (shame operated group, heart failure group and NRG treated group), each with 8 monkeys. Heart failures were induced by rapid pacing (240 heart beats/min). Daily intravenous injection of recombined human NRG [3 microg/(kg x d)] and normal saline were given to the monkeys for 10 days for the NRG treated group and heart failure group respectively. Hemodynamic measurements including +dp/dt(max) and left ventricular systolic, end-diastolic blood pressures (LVSP and LVEDP) were conducted. The RT-PCR was applied to detect the expression level of PKB, Glut1 mRNA in the left ventricular cardiac muscle. RESULTS: The monkeys in the heart failure group had lower levels of + dp/dt(max) and LVSP and higher levels of LVEDP than those in the shame operated group (P < 0.05). The monkeys in the NRG treated group had higher levels of +dp/dt(max) than those in the heart failure group (P < 0.05). Lower expression of PKB, Glut1 mRNA in the heart failure group was observed compared with the shame operated group (P < 0.05) while the NRG treated group had a higher expression level of PKB,Glut1 mRNA by compared with the heart failure group (P < 0.05). CONCLUSION: Recombined human NRG can relieve heart failure syndroms through up-regulating the expression of PKB, Glut1 mRNA and improving energy supply of the ischemic cardiac muscle.
