Objective To study the values of apparent diffusion coefficient (ADC) changing with time and space in cerebral infarction,and to provide the evidence in defining the infarction stages.Methods 117 work-ups in 98 patients with cerebral infarction (12 hyperacute,43 acute,29 subacute,10 steady,and 23 chronic infarctions) were imaged with both conventional MRI and diffusion weighted imaging.The average ADC values,the relative ADC (rADC) values,and the ADC values or rADC values from the center to the periphery of the lesion were calculated.Results The average ADC values and the rADC values of hyperacute and acute infarction lesion depressed obviously.rADC values in hyperacute and acute stage was minimized,and progressively increased as time passed and appeared as "pseudonormal" values in approximately 8 to 14 days.Thereafter,rADC values became greater than normal in chronic stage.There was positive correlation between rADC values and time[ (174 ±3.47)% vs (58±6.75)%,t =2.03,P ＜0.05 ].The ADC values and the rADC values in hyperacute and acute lesions had gradient signs that these lesions increased from the center to the periphery.The ADC values and the rADC values in subacute lesions had adverse gradient signs that these lesions decreased from the center to the periphery.Conclusion The ADC values of infarction lesions have evolution rules with time and space.The evolution rules with time and those in space can be helpful to provide the evidence in guiding the treatment or judging the prognosis in infarction.

In the present study, we investigated anti-inflammatory effect of Cardamine komarovii flower (CKF) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). We determined the effect of CKF methanolic extracts on LPS-induced pro-inflammatory mediators NO and prostaglandin E2 (PGE2), production of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and related protein expression levels of MyD88/TRIF signaling pathways in peritoneal macrophages (PMs). Nuclear translocation of NF-κB-p65 was analyzed by immunofluorescence. For the in vivo experiments, an ALI model was established to detect the number of inflammatory cells and inflammatory factors (IL-1β, TNF-α, and IL-6) in bronchoalveolar lavage fluid (BALF) of mice. The pathological damage in lung tissues was evaluated through H&E staining. Our results showed that CKF can decrease the production of inflammatory mediators, such as NO and PGE2, by inhibiting their synthesis-related enzymes iNOS and COX-2 in LPS-induced PMs. In addition, CKF can downregulate the mRNA levels of IL-1β, TNF-α, and IL-6 to inhibit the production of inflammatory factors. Mechanism studies indicated that CKF possesses a fine anti-inflammatory effect by regulating MyD88/TRIF dependent signaling pathways. Immunocytochemistry staining showed that the CKF extract attenuates the LPS-induced translocation of NF-kB p65 subunit in the nucleus from the cytoplasm. In vivo experiments revealed that the number of inflammatory cells and IL-1β in BALF of mice decrease after CKF treatment. Histopathological observation of lung tissues showed that CKF can remarkably improve alveolar clearance and infiltration of interstitial and alveolar cells after LPS stimulation. In conclusion, our results suggest that CKF inhibits LPS-induced inflammatory response by inhibiting the MyD88/TRIF signaling pathways, thereby protecting mice from LPS-induced ALI.
Acute Lung Injury ; chemically induced ; drug therapy ; genetics ; metabolism ; Adaptor Proteins, Vesicular Transport ; genetics ; metabolism ; Animals ; Anti-Inflammatory Agents ; administration & dosage ; chemistry ; Cardamine ; chemistry ; Cyclooxygenase 2 ; genetics ; metabolism ; Female ; Flowers ; chemistry ; Humans ; Lipopolysaccharides ; adverse effects ; Male ; Mice ; Myeloid Differentiation Factor 88 ; genetics ; metabolism ; NF-kappa B ; genetics ; metabolism ; Nitric Oxide Synthase Type II ; genetics ; metabolism ; Plant Extracts ; administration & dosage ; chemistry ; Signal Transduction ; drug effects ; Tumor Necrosis Factor-alpha ; genetics ; metabolism