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Simulation of electronic dynamics in realistically large molecular systems is a demanding task that has not yet achieved the same level of quantitative prediction already realized for its static counterpart. This is particularly true for processes occurring beyond the Born-Oppenheimer regime. Non-adiabatic molecular dynamics (NAMD) simulations suffer from two convoluted sources of error: numerical algorithms for dynamics and electronic structure calculations. While the former has gained increasing attention, particularly addressing the validity of ad hoc methodologies, the effect of the latter remains relatively unexplored. Indeed, the required accuracy for electronic structure calculations to reach quantitative agreement with experiment in dynamics may be even more strict than that required for static simulations. Here, we address this issue by modeling the electronic energy transfer in a donor-acceptor-donor (D-A-D) molecular light harvesting system using fewest switches surface hopping NAMD simulations. In the studied system, time-resolved experimental measurements deliver complete information on spectra and energy transfer rates. Subsequent modeling shows that the calculated electronic transition energies are "sufficiently good" to reproduce experimental spectra but produce over an order of magnitude error in simulated dynamical rates. We further perform simulations using artificially shifted energy gaps to investigate the complex relationship between transition energies and modeled dynamics to understand factors affecting non-radiative relaxation and energy transfer rates.

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Amphimerus Barker, 1911 is a liver fluke infecting several animal species and humans. Being a digenetic trematode of the Opisthorchiidae family, Amphimerus is closely related to the genera Metorchis, Clonorchis and Opisthorchis. Recently, a high prevalence of Amphimerus infection in humans, cats, and dogs had been demonstrated in a tropical Pacific region of Ecuador. Hence, we determined and characterized the entire mt genome sequences of adult liver flukes, morphologically identified as Amphimerus, collected in the endemic region of Ecuador, and examined its phylogenetic relationships with flukes in the Opisthorchiidae family using Bayesian inference (BI) based on the concatenated amino acid sequences and partial cox1 sequences. The complete mt genome sequence (15, 151 bp in length) of the Amphimerus sp. contains 35 genes, including 12 protein-coding genes (PCGs, without atp8), two rRNAs (rrnL and rrnS) and 21 tRNAs, lacking trnG. The gene content and arrangement of the Ecuadorian Amphimerus mt genome was similar to those of other trematodes in the Opisthorchiidae family. All genes in the circular mt genome of Amphimerus sp. are transcribed from the same strand in one direction, with the A + T content of 60.77%. Genetic distances between Amphimerus sp. and other genera in Opisthorchiidae were rather high, ranging from 26.86% to 28.75% at nucleotide level and 29.37%-31.12% at amino acid level. Phylogenetic analysis placed the Ecuadorian Amphimerus within the branch of Opisthorchiidae, but very distinct from Opisthorchis. Our results indicate that the liver fluke Amphimerus from Ecuador does not belong to the genus Opisthorchis, and that it should be assigned under the genus Amphimerus. The determination of the mt genome of the Ecuadorian Amphimerus provides a new genetic resource for future studies on taxonomy and molecular epidemiology of Opisthorchiidae trematodes.

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Abstract This study aimed to investigate the cardioprotection of rosuvastatin pre-conditioning (R-Pre) in a rat model of myocardial ischemia / reperfusion (I/R). Male SD rats were assigned into three groups: sham group, I/R group and R-Pre group. Rats in I/R group and R-Pre group received ischemia for 30 min and reperfusion for 2 h. In R-Pre group, rats received intragastrical administration with rosuvastatin at 5 mg/kg once daily for 1 week. After 2-h reperfusion, the cardiac function was detected by ultrasonography; the blood was collected for biochemical analysis; the heart was collected for the TUNEL staining and immunohistochemistry for Bcl-2 and Bax. Our results showed rosuvastatin pre-conditioning for 1 week could significantly reduce the infarct ratio and improve the cardiac function after myocardial I/R injury, in which attenuation of oxidative stress and cell apoptosis played an important role. Our study provides evidence on the cardioprotection of rosuvastatin pre-conditioning and highlight the use of rosuvastatin before cardiopulmonary bypass.

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ABSTRACT This study aimed to investigate the expression and mechanism of N- methyl -D- aspartate receptor 1 (NMDAR1) in the pathogenesis of Alzheimer disease (AD). Eighty adult Wistar rats were randomly divided into 4 groups (n=20 each) to receive an injection of 0, 5, 7 and 10 μl of 1 μg/μl amyloid-β 42 (Aβ1-42) in the hippocampus. Twenty rats in normal control group were injected with equal volume of saline. After 10 days, the hippocampus was isolated from 5 randomly selected rats in each group. The NMDAR1 protein and mRNA expression was determined by immunohistochemical staining and qRT-PCR. The aquaporin-1 (AQP-1) mRNA expression was also measured by qRT-PCR. We found that both NMDAR1 and AQP-1 expression in Aβ1-42 groups was increased in a dose-dependent manner. NMDAR1 and AQP-1 expression in 7 and 10 μl Aβ1-42 groups was significantly higher compared with 0 μl Aβ1-42 group (P <0.01). Further, the 10 μl Aβ1-42 group was randomly divided into 3 subgroups: AD-NMDA, AD-MK-801, and AD-Ctrl subgroup, which was given an intraperitoneal injection of NMDAR agonist NMDA, NMDAR antagonist MK-801 and saline, respectively. The relative APQ-1 expression in each subgroup was determined by qRT-PCR and Western blot analysis after 24 h. The AQP-1 expression was significantly decreased in AD-MK-801 group (P < 0.05), but was markedly increased in AD-NMDA group when compared with AD-Ctrl group (P <0.01). Our study suggested that expression abnormity of NMDAR1 is involved in the pathogenesis of AD. NMDAR1 might regulate the pathogenic process through stimulating the expression of AQP-1.