Objective: To explore influence of short-term intervention of different doses rosuvastatin on plasma levels of thrombomodulin (TM) and high sensitive C reactive protein (hsCRP) in patients with acute coronary syndrome (ACS). Methods: A total of 32 ACS patients were enrolled, randomly and equally divided into rosuvastatin 10mg group and rosuvastatin 20mg group, and another 16 patients without coronary heart disease were enrolled as normal control group. Enzyme linked immunosorbent assay (ELISA) was used to measure plasma levels of TM and hsCRP in two rosuvastatin groups before and after treatment and in normal control group at admission. Adverse drug reactions and incidence rates of cardiovascular events within one month were observed in two rosuvastatin groups. Results: Plasma levels of TM and hsCRP in two groups of ACS patients were both significantly higher than those of normal control group before treatment, P<0.001 all; compared with before treatment, there were significant decrease in levels of TM [10mg group：(54.09±52.45) μg/dl vs. (15.65±2.30) μg/dl，20mg group：(70.27±62.43) μg/dl vs. (19.86±5.49) μg/dl] and hsCRP [10mg group：(126.35±76.08) ng/ml vs. (54.85±45.30) ng/ml，20mg group：(125.35±60.29) ng/ml vs. (58.14±53.54) ng/ml] in two rosuvastatin groups after treatment 7d, P<0.01 all; But there were no significant differences in influences of two doses on plasma levels of TM and hsCRP in ACS patients, P＞0.05 all. There was no significant difference in incidence rate of adverse drug reactions between two rosuvastatin groups during follow-up (P>0.05); compared with rosuvastatin 10mg group, there was significant decrease in incidence rate of major adverse cardiovascular events（MACE）: Relapse angina pectoris (62.50% vs. 18.75%, P<0.01) in rosuvastatin 20mg group. Conclusions: Early intensive statins medication （rosuvastatin 20mg）can decrease plasma levels of thrombomodulin and high sensitive C reactive protein, and rosuvastatin 20mg/d can effectively decrease incidence rate of cardiovascular events without significant increase incidence rate of adverse drug reactions in ACS patients.

Objective To investigate the effects of nuclear respiratory factor 1(NRF1)on mitochondrial and cog-nitive dysfunction in Alzheimer's disease(AD)model mice.Methods The 5 × FAD mice were utilized as a mod-el for Alzheimer's disease,and the sparsely labeled AAV virus overexpressing NRF1(AAV-NRF1)was adminis-tered via stereotaxic injection into the brain.The expression of NRF1 in hippocampus was determined by Western blot,the morphology of mitochondria in hippocampus was observed by transmission electron microscope,the den-dritic spines of sparsely labeled neurons in the CA1 region were visualized and quantified using confocal laser mi-croscopy,cognitive and memory functions of mice were evaluated using the Morris water maze test,while electro-physiological methods were employed to detect long-term potentiation(LTP)of synaptic efficacy.Results The ex-pression of NRF1 in the hippocampus was significantly upregulated following stereotactic injection of AAV-NRF1(P＜0.001).This intervention led to notable improvements in mitochondrial morphology within hippocampal neurons,as well as enhanced cognitive and memory functions in mice(P＜0.01).Moreover,there was a significant in-crease in dendritic spine density among neurons located in the CA1 region of the hippocampus(P＜0.001),ac-companied by long-lasting and stable long-term potentiation(LTP)and a substantial elevation in fEPSP slope(P＜0.01).Conclusion The overexpression of NRF1 in a 5 × FAD mouse model of Alzheimer's disease(AD)initia-ted the restoration of mitochondrial dysfunction and enhanced synaptic plasticity,indicating that these alterations may contribute to the therapeutic efficacy of NRF1 overexpression in ameliorating cognitive dysfunction associated with AD.