BACKGROUND:CT perfusion technology is a common non-invasive detection method, which can be used to quantitatively determine the ischemia severity and range at early stage of cerebral infarction and then judge whether ischemic brain tissues can survive or recover. OBJECTIVE:To assess the neurological function recovery of cerebral infarction rats undergoing neural stem cel transplantation using CT perfusion imaging. METHODS:A total of 60 Sprague-Dawley rats were randomly divided into control group, cerebral infarction group, transplantation group, with 20 rats in each group. Rat model of middle cerebral artery occlusion was made in the latter two groups. After 24 hours of modeling, PBS and 8×105 neural stem cels were administratedvia the tail vein into the rats in the cerebral infarction and transplantation groups, respectively. CT perfusion-weighted imaging was performed at 1, 3, 7, 14, 28 days after transplantation. Modified neurological severity scores were recorded at 1, 2, 3, 4 weeks after transplantation. Triphenyltetrazolium chloride staining was used to calculate infarct volume at 4 weeks after transplantation. Hematoxylin- eosin staining was adopted to observe pathological changes of brain tissues at 2 weeks after transplantation. RESULTS AND CONCLUSION: There were no abnormal hemodynamic changes in the control group at different time points. The transplantation group exhibited an increasing CT value with time, and the increased cerebral blood flow could improve the survival rate of neurons in the ischemic penumbra. The modified neurological severity score and infract volume in the transplantation group were both significantly lower than those in the cerebral infarction group (P < 0.05). Cel necrosis was improved obviously in the transplantation group. These results show that CT perfusion imaging can be used to observe the neurologic function recovery of cerebral infarction rats in aspects of morphology and hemodynamics.

Objective To observe the influence of the short effect antihypertension drugs- nifedipine and medial effect antihypertension drugs- extended release nifedipine on the blood pressure variability (BPV) in essential hypertension(EH). Methods Twenty-five EH patients were underwent 24-hour noninvasive ambulatory blood pressure monitoring (ABPM) and observed their BPV respectively before taking drugs, after taking nifedipine and extended release nifedipine. Meantime,25 normotensive controls (NC) were observed. Results (1)BPV in EH group was higher than that in controlled group and the severer the rise of blood pressure, the more obvious the increase of BPV (P 0.05). Conclusions Nifedipine could increase BPV but extended release nifedipine did not change BPV while they decreased blood pressure. Effect of extended release nifedipine was better than nifedipine in decreasing blood pressure.

0.05) but there was significant difference between CARG group and control group(P

Objective:To investigate the relationship between NOD-like receptor protein 3 (NLRP3) gene promoter region-30 single nucleotide polymorphism (SNP) (rs3738448) G/T and dilated cardiomyopathy (DCM) and its related risk factors.Methods:A case-control study method was used to collect 137 patients and 140 healthy controls; polymerase chain reaction-restriction endonuclease fragment length polymorphism technology combined with sequence alignment after DNA sequencing was used for data statistics; After Hardy-Weinberg balance test, the χ 2 test was used for correlation analysis; logistic regression was used to analyze the correlation between multiple risk factors and the SNP site and the incidence of DCM; SNPinfo database was used to predict and analyze the transcription factors affected by the SNP. Results:A total of GG and GT genotypes were detected at this SNP locus, and their genotype distributions were in line with Hardy-Weinberg equilibrium ( P>0.05). At the same time, the difference between the DCM group and the control group was significant ( P<0.05). Multivariate logistic regression analysis indicated that mean arterial pressure, C-reactive protein and B-type brain natriuretic peptide were independent risk factors for the onset of DCM (all P<0.05). The incidence of DCM in -30(RS3738448)G/T genotype GT group was 2.243 times higher than that in GG group (95% CI: 1.043-4.827, P<0.05). Logistic regression analysis under dominant, recessive and additive genetic models showed that there was a correlation between the dominant inheritance of SNP and the occurrence of DCM ( OR=0.44, AIC=370.4, BIC=381.3, P<0.05). Conclusions:The -30 (rs3738448) G/T SNP in the promoter region of the NLRP3 gene is associated with the pathogenesis of DCM, and provides population genetic data for the study of polymorphisms in the promoter region of NLRP3 gene.

Objective:To screen radiosensitive lipid metabolites in rat plasma and analyze their metabolic pathways in order to provide scientific basis for radiation damage biomarker.Methods:The whole body irradiation of 60Co γ rays was performed to rats with different doses of 0, 1, 3 and 5 Gy. The changes of lipids in plasma were detected by untargeted lipidomics method based on liquid chromatography coupled mass spectrometry. Results:Twenty plasma lipids were identified as the potential radiosensitive biomarkers at 7 days after irradiation, including 13 over-expressed lipids and 7 down-expressed lipids, where 12 lipids well responded to radiation doses.Conclusions:Lipid metabolites in rat plasma are significantly changed after exposure to γ rays, and the metabolic pathways of sphingolipid, glycerophospholipid and glycosylphosphatidylinositol (GPI) are significantly enriched.

Objective:To explore the effects of ultraviolet B (UVB) on the premature senescence of human immortalized keratinocytes HaCaT cells and the possible underlying molecular mechanism.Methods:HaCaT cells were exposed with UVB of different doses (20, 50, 80 and 100 mJ/cm 2). At 72 h after exposure, cellular morphology was observed by Giemsa staining, cell proliferation was detected by clone formation assay, and the proportion of premature senescence cells was detected by β-galactosidase staining. The number change of lysosomes was detected by Lyso-Tracker Red fluorescence probe at 24, 48 and 72 h after exposure. Cell migration was measured by scratch test at 24 h and 48 h after exposure. The protein expressions of p53 and p16 related to premature senescence were detected by Western blot assay at 72 h after exposure. Results:After UVB exposure, HaCaT cells showed a premature senescence phenotype. At 72 h after exposure, the cell volume increased ( F=115.18, P<0.05), the cell proliferation ability decreased ( F=410.32, P<0.05), the activity of β-galactosidase increased ( F=16.31, P<0.05), and the expressions of P53 and P16 increased. In addition, the number of lysosomes increased at 24, 48, and 72 h after exposure ( F=17.65, 38.36, 13.66, P<0.05), and cell migration capacity was inhibited at 24 and 48 h after exposure ( F=8.21, 11.48, P<0.05). Conclusions:UVB exposure can induce premature senescence of HaCaT cells by increasing the expression of p53 and p16 proteins.