Objective To evaluate the effect of limb remote ischaemic preconditioning on pul-monary function in patients undergoing cardiac valve replacement surgery with cardiopulmonary by-pass.Methods Seventy patients,32 males and 38 females,aged 18-70 years,weighing 45-90 kg, ASA physical status Ⅱ or Ⅲ,scheduled for elective cardiac valve replacement surgery with cardiopul-monary bypass,were divided into 2 groups using a random number table,35 in each group.Patients in group R received three cycles of right upper-limb 5 min ischemia (blood-pressure cuff inflation to≥ 200 mm Hg)and 5 min reperfusion (blood-pressure cuff deflation to 0 mm Hg)at 10 min after in-tubation.In group C,the cuff was placed around the arm but not inflated.At 10 min after intubation (T0),at 1 h after aortic declamping (T1)and at 6 h (T2),12 h (T3),24 h (T4)after surgery,arte-rial blood was sampled to conduct gas analysis,PaO2/FiO2ratio and alveolar-arterial oxygen gradient (A-aDO2)were calculated,and the dynamic lung compliance (Cd)and static lung compliance (Cs) were also recorded.The occurrence of pulmonary adverse events was recorded until discharge. Results Compared with T0,PaO2/FiO2was decreased in the two groups at T1-T4,A-aDO2was de-creased at T2-T4,Cs and Cd were increased in group C at T3,and were increased in group R at T2, T3(P<0.05).Compared with group C,the Cs and Cd at T2,T3were increased in group R.There were no significant differences between the two groups in the PaO2/FiO2,A-aDO2at T0-T4.The oc-currence of the pulmonary adverse events was decreased significantly in group R than in group C (P<0.05).The occurrence of pulmonary adverse events was declined significantly in group R than in group C (P<0.05).Conclusion Limb remote ischemic preconditioning can improve the lung compli-ance and reduce the occurrence of the pulmonary adverse events in patients undergoing cardiac valve replacement surgery.

Objective:To investigate the efficacy and safety of intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) in patients with maintenance hemodialysis (MHD) and acute ischemic stroke.Methods:The clinical data of 235 patients with acute ischemic stroke receiving MHD were collected in our hospital from March 2018 to October 2021. According to the treatment methods chosen by themselves, these patients were divided into control group ( n=70, only receiving standardized secondary stroke prevention), rt-PA low-dose group ( n=85, receiving rt-PA intravenous thrombolysis, 0.6 mg/kg) and rt-PA standard-dose group ( n=80, receiving rt-PA intravenous thrombolysis, 0.9 mg/kg). The effective rate 24 h after treatment, good efficacy rate 7 d after treatment, and good prognosis rate and mortality 90 d after treatment were used to evaluate the effectiveness. The incidences of intracranial hemorrhage, symptomatic intracranial hemorrhage, and severe extracranial hemorrhage 90 d after treatment were used to evaluate the safety. Results:There was no statistical difference in the good prognosis rate 90 d after treatment among the rt-PA low-dose group, the rt-PA standard-dose group and the control group (71.8%, 68.8%, and 64.3%; P>0.05), but the effective rate 24 h after treatment and good efficacy rate 7 d after treatment in the rt-PA low-dose group and rt-PA standard-dose group (44.7%, 57.7%; 46.3%, 62.5%) were both significantly higher than those in the control group (27.1%, 38.6%; P<0.05). The mortality 90 d after treatment in the rt-PA low-dose group (7.1%) was significantly lower than that in the rt-PA standard-dose group (22.5%) and control group (21.4%, P<0.05). The incidences of intracranial hemorrhage and symptomatic intracranial hemorrhage in the rt-PA low-dose group (8.2%, 3.5%) were significantly lower than those in the rt-PA standard-dose group (22.5%, 16.3%; P<0.05), and the incidences of extracranial complications and gastrointestinal bleeding (5.9%, 1.2%) were significantly lower than those in the rt-PA standard-dose group (18.8%, 10.0%; P<0.05). Conclusion:Intravenous thrombolytic therapy with 0.6 mg/kg rt-PA is recommended for acute ischemic stroke patients receiving MHD.

Objective To explore the possible mechanism of emodin in inhibiting proliferation,migration,and invasion of AGS cells and in suppressing the expressions of YAP1 and FOXD1.Methods Normal gastric cell GES-1 and gastric cancer cell AGS were cultured with different concentrations of emodin.CCK8 test,scratch test and Transwell assay were used to verify changes in the biological phenotype of AGS cells.TCGA database was applied to analyze expressions of HK2,YAP1 and FOXD1 in gastric cancer tissues and normal gastric tissues.Western blotting method was used to detect the impacts of emodin on HK2,YAP1 and FOXD1 proteins in AGS cells.Exogenous pyruvic acid was added to verify the changes in YAP1 and FOXD1.Results The IC50 of emodin was significantly higher in GES-1 cells than in AGS cells(P<0.05).CCK8 proliferation test,scratch test,and Transwell assay showed that emodin significantly inhibited the biological abilities of AGS(P<0.05 for comparisons).Analysis on the TCGA bioinformatics database found that the expression of key enzymes HK2 in the glycolysis pathway and oncogenes YAP1 and FOXD1 was significantly higher in gastric cancer tissues than in normal gastric tissues(P<0.05 for comparisons).Emodin significantly inhibited the protein expressions of key glycolytic enzymes HK2 and oncogenes YAP1 and FOXD1(P<0.05 for comparisons).With supplement of exogenous glycolytic metabolite pyruvate,the protein expressions of oncogenes YAP1 and FOXD1 significantly increased(P<0.05 for comparisons).Conclusions Emodin has a significant pharmacological inhibitory effect on gastric cancer AGS cells,markedly suppressing their biological phenotype.Emodin not only significantly inhibits the key enzyme HK2 in glycolysis metabolism,but also the protein expressions of oncogenes YAP1 and FOXD1.With the addition of exogenous pyruvate to enhance the glycolytic metabolic pathway,the protein expressions of oncogenes YAP1 and FOXD1 significantly increased.The above results suggest a close association of YAP1 and FOXD1 with glycolytic metabolism.Emodin may inhibit oncogenes YAP1 and FOXD1 through the glycolytic metabolism of gastric cancer AGS cells.