To summarize the nursing experience of a patient with severe pulmonary hypertension complicated with giant heart after lung transplantation.Key nursing points:to set up volume management measures in stages to avoid hemodynamic disorders;to monitor cardiac function closely and be alert to the occurrence of low cardiac output syndrome;to closely observe heart rate and heart rhythm to correct arrhythmia as soon as possible;the sequential ventilation strategy was adopted to promote the recovery of lung function.Progressive implementation of individual rehabilitation was conducted,and the patient activity tolerance was improved.After careful treatment and nursing,the patient was successfully transferred to the general ward 29 days after surgery,recovered from the hospital 41 days after surgery,followed up for 6 months,and recovered well.

To summarize the nursing experience of a patient with severe pulmonary hypertension complicated with giant heart after lung transplantation.Key nursing points:to set up volume management measures in stages to avoid hemodynamic disorders;to monitor cardiac function closely and be alert to the occurrence of low cardiac output syndrome;to closely observe heart rate and heart rhythm to correct arrhythmia as soon as possible;the sequential ventilation strategy was adopted to promote the recovery of lung function.Progressive implementation of individual rehabilitation was conducted,and the patient activity tolerance was improved.After careful treatment and nursing,the patient was successfully transferred to the general ward 29 days after surgery,recovered from the hospital 41 days after surgery,followed up for 6 months,and recovered well.

LPS stimulation of macrophages production of IFN-beta plays a key role in innate immunity defending the microbial invasion. In this study, the effect of S632A3 promoting LPS-induced IFN-beta production and the underlying mechanism were investigated, mRNA level was measured by real-time PCR, cytokine production was determined by ELISA, GSK-3beta activity was investigated by kinase assay, protein phosphorylation and expression were evaluated by Western blotting. The results revealed that S632A3 significantly augmented IFN-beta production by LPS-stimulated macrophages. S632A3 inhibition of the activation of GSK-3beta, reduced the threonine 239 phosphorylation of transcription factor c-Jun but increased the total level of c-Jun in LPS-stimulated macrophages. Moreover, small interfering RNA-mediated knockdown of c-Jun level abrogated the ability of S632A3 to augment IFN-beta. The study thus demonstrates S632A3 being a new anti-inflammation lead compound and provides a molecular mechanism by which S632A3 promoted LPS-induced IFN-beta production in macrophages through inhibiting the activation of GSK-3beta.