Objective To investigate the differences between subjective and objective sleep quality in recurrent depressive patients and the correlative factors. Methods Thirty-two cases of recurrent depressive patients(the recurrent group) and 32 cases of first episode depressive patients(the control group)who met the inclusion were recruited in this study. The subjectivesleep quality ,mood and objective sleep quality of patients were estimated by Pittsburgh sleep quality index(PSQI),Hamilton anxiety Scale(HAMA),Hamilton depression Scale(HAMD),respectively. O ne whole-night polysomnography (PSG) was recorded. Results On subjec-tivesleep quality,the total sleep time was shorter,the sleep latency was longer,and the sleep efficiency was lower in the recurrent group compared with the control group. On objectivesleep quality ,the wake times were increased , the NREM1 phase was longer,the NREM2 phase was shorter,the RME phase was longer,the proportion of REM phase was increased,and the latency of REM phase was shorter in the recurrent group compared with the control group(P<0.05,respectively). There were significant differences between the subjective and objective sleep quali-ty in both groups,while the differences in the recurrent group were more significant(P < 0.01). In the recurrent group,thedifference of the total time between the subjective and objective sleep was positively correlated with PSQI score,the duration of disease and the number of attacks(P < 0.05),while,the differences of the sleep latency and sleep efficiency between the subjective and objective sleep were both positively correlated withPSQI score and the HAMA-14 score,respectively(P<0.05). Conclusion There was a significant difference between the subjec-tive and objective sleep quality of patients with recurrent depression ,and the differences were related to the course of disease,the number of attack,PSQI score and HAMA-14 score.

Objective To observe the effect of human adipose mesenchymal stem cells (hADMSCs) on pancreatic tissue repair and inflammatory reaction of acute necrotic pancreatitis (ANP) in rat, and explore the possible mechanism.Methods Isolation and purification of hADMSCs and flow cytometry to detect the the surface markers including CD90, CD29, CD34 and CD45 were performed.Eighty SD male rats with the body weight of 170~210 g were randomly divided into 4 groups.There were 8 rats in the control group, 24 rats in other group.Control group underwent no treatment;sham operation group underwent intestinal wall stirring and then abdominal closure;ANP model group was established by open abdominal retrograde injection of sodium taurocholate into bile duct;and in hADMSCs group, DAPI labeled hADMSCs were injected by tail vein into the rat at 12 h after sodium taurocholate injection.The survival of the rats, and gross morphological and pathological changes of the pancreas was observed at 12, 24, and 48 h, and the serum TNF-α, IL-6, IL-10 and amylase were detected.The distribution of hADMSCs in the pancreas, liver and lung was examined in hADMSCs group.Results Rats in control group and sham operation group were all alive.In ANP group, 5 and 11 rats were dead at 24 and 48 h, respectively, and in hADMSCs group 12 rats were dead at 48 h.Compared with ANP group, the difference was not statistically significant (P>0.05).The pathological changes of the pancreas were significantly less severe in hADMSCs group than in ANP group.In hADMSCs group, the amylase at 12, 24 and 48 h was(999±110 )、(1 831±110)、(3 991±130 )U/L;TNF-α level was (62.40±2.35), (80.51±4.51) and (93.46±6.60)ng /L;IL-6 was (60.46±7.34), (80.61±8.40) and(100.58±9.49)ng /L;and these were all significantly lower than those in ANP model group [amylase (2 402±146), (3 292±137) and (5 632±112)U/L;TNF-α(87.13±3.39), (105.41±10.06), (114.57±3.06)ng/L;IL-6 (70.67±10.90)、(107.61±10.53)、(145.34±10.48)U/L], and the differences were all statistically significant (all P<0.05).IL-10 in hADMSCs group was (56.63±6.35), (81.32±5.96), (100.26±6.51)ng/L, which were increased compared with those in ANP model group [(45.26±8.04), (68.25±8.42), (80.38±5.71)ng/L], and the difference was statistically significant (all P<0.05).hADMSCs can migrate to the pancreas, liver, lungs and other damaged tissue, with most in pancreatic tissue, less in lung tissue, and least in liver tissue.Conclusions The mechanism of hADMSCs in repairing pancreatic tissue injury was associated with inhibiting TNF-α and IL-6 secreting and increasing IL-10, thus reducing inflammatory reaction.

Objective: To study the effect and mechanism of angiotensin (Ang II) on the proliferation of human hepatocellular carcinoma HepG2 cells. Methods: The effects of different concentrations of Ang II's (10^-8-10^-4 mol/L) on proliferated hepatocellular carcinoma HepG2 cells were detected by CCK-8 assay. The expression of angiotensin II type 1 receptor (AT1) protein and activation of ERK1/2 protein in hepatocellular carcinoma HepG2 cells after processing with Ang II were assayed by Western blot. The cells were pretreated with candesartan (AT1 receptor antagonist), sorafenib (Raf kinase inhibitor) and PD98059 (ERK1/2 inhibitor) for 1.5 h and then Ang II (10^-6 mol/L) was added. CCK-8 assay was used to determine whether it could reverse the proliferation of Ang II, and ERK phosphorylation levels were detected by Western blot. The changes in Bcl-2 and c-myc gene expression before and after Ang II processing were detected by Rt-PCR. According to different data, t-test, one-way analysis of variance or SNK method were used for statistical analysis. Results: HepG2 cells treated with different concentrations of Ang II promoted cell proliferation after 24h and 48h. After 24 h, cell vitality was strongest with Ang II concentration 10^-5 mol/L and the absorbance value was 0.990 8±0.097 8; and again after 48 h, the cell viability was strongest with Ang II concentration 10^-6 mol/L and the absorbance value was 1.302 7 ± 0.030 9. Moreover, the pro-proliferation effect of Ang II on HepG2 cells blocked candesartan, sorafenib and ERK1/2 isolated inhibitors. After treatment with 10^-6 mol/L Ang II, Western blot showed that Ang II significantly promoted AT1 receptor expression and phosphorylation of ERK1/2 protein confirmed that Ang II activated the AT1/RAF/ERK1/2 signaling pathway. In addition, Rt-PCR detection showed that the downstream of Bcl-2 and c-myc genes expressions rose significantly when the concentration of Ang II ranged from 10^-8 to 10^-6 mol/L. Conclusion Ang II can promote the proliferation of HepG2 cells by activating AT1/Raf /ERK1/2 signaling pathway and enhance the downstream of Bcl-2 and c-myc gene expression.

Objectives:To analyze the impact of target lesion calcification evaluated by coronary angiography on immediate procedure success rate and long-term clinical outcome in patients underwent percutaneous coronary intervention(PCI). Methods:Consecutive patients received angiographic calcification evaluation and underwent PCI in Fuwai Hospital,Chinese Academy of Medical Sciences from January 2017 to December 2018 were prospectively enrolled in this study.Patients are divided into 4 groups,including non-calcification group(n=14 387),mild calcification group(n=8 231),moderate calcification group(n=3 208)and severe calcification group(n=886).The primary endpoint was immediate post-PCI procedure success rate,which was defined as residual stenosis<50%without major operational complications(including coronary artery perforation,coronary artery dissection,intraoperative stent thrombosis)and failure to cross the lesion.The long-term clinical endpoint was the 3-year major adverse cardiovascular events(MACE),which included composite endpoint events such as all cause death,myocardial infarction(MI),and revascularization. Results:The severe calcification group had a lower success rate of interventional therapy(80.59%vs.94.23%vs.94.29%vs.91.49%),a higher incidence of residual stenosis≥50%(17.72%vs.5.03%vs.4.84%vs.7.29%),a higher incidence of coronary artery dissection(1.81%vs.0.66%vs.0.78%vs.1.25%),and a higher incidence of coronary artery perforation(2.14%vs.0.51%vs.0.38%vs.0.69%),and a higher incidence of failure to cross the lesion(0.23%vs.0.12%vs.0.04%vs.0.16%)compared to the non-calcification group,mild calcification group,and moderate calcification group(all P<0.05).Multivariate Cox regression analysis showed that patients with severe calcification had a higher risk of MACE(12.98%vs.9.35%,HR=1.21,95%CI:1.00-1.47,P=0.046),all-cause mortality(4.29%vs.1.80%,HR=1.55,95%CI:1.10-2.18,P=0.013),and MI(2.14%vs.0.97%,HR=1.97,95%CI:1.21-3.20,P=0.006)compared to patients without calcification. Conclusions:Patients with angiographic-detected severe calcification after PCI treatment face higher risk of PCI procedure failure,MACE,all-cause death,and MI compared to patients without,with mild,and moderate calcification.

ObjectiveThe human angiotensin converting enzyme2 （hACE2） transgenic mouse model was used to clarify the antiviral efficacy of BD-77 against a novel coronavirus SARS-CoV-2 and explore the action mechanism of BD-77 against SARS-CoV-2. MethodSARS-CoV-2 Omicron and Delta variant strains-infected VeroE6 cell models were established and administered with BD-77 to observe the antiviral effect of BD-77 in vitro. A kit was used to detect the effect of BD-77 in vitro on the binding of spike S protein of SARS-CoV-2 virus （Delta/Omicron） to angiotensin converting enzyme2 （ACE2）. Chromatography was adopted to detect the binding of BD-77 to the S protein and N protein of the novel coronavirus. hACE2 transgenic C57BL/6 mice were divided into a blank control group， SARS-CoV-2 infection group， BD-77 administration groups of 37.5 mg·kg^-1 and 75 mg·kg^-1， with eight mice in each group. The pneumonia model of SARS-CoV-2-infected hACE2 transgenic mice was built to observe the survival of the mice， detect the virus titer of the lung tissue of the mice， and observe the lesions in the lung tissue. ResultBD-77 had a certain inhibitory effect on Omicron and Delta variant strains in vitro， with median inhibitory concentration （IC₅₀） of 526.3 mg·L^-1 and 653.0 mg·L^-1， respectively. BD-77 had no significant inhibitory effect on the binding of the S protein of WT， Omicron， and Delta variant strains of SARS-CoV-2 to ACE2 and had no binding effect with the S protein and N protein of the novel coronavirus. No mice in the blank group died， while the mortality rate of SARS-CoV-2-infected mice was 75%. There was a large amount of virus replication in the lung tissue of the mice and large areas of inflammatory infiltration in the lung tissue and interstitium. Compared with the model group， BD-77 administration groups of 37.5 mg·kg^-1 and 75 mg·kg^-1 could reduce the mortality of mice， significantly lower the virus titer in the lung tissue of mice （P<0.05）， and improve lung lesions. ConclusionBD-77 demonstrated significant inhibitory effects against SARS-CoV-2 virus in vitro and in vivo. However， its mechanism of action did not involve direct inhibition of the virus itself or intervention in the virus-host binding process. This finding suggests that the mechanism of action of BD-77 needs to be thoroughly investigated and elucidated by further experiments.

ObjectiveTo observe the therapeutic effect of BD-77 by nebulized inhalation on animal models of various respiratory viral infections and investigate the mechanism of broad-spectrum antiviral action of BD-77 using proteomics. MethodThe influenza virus H1N1/FM1 experiment used ICR mice and divided them into a normal group， model group， Tamiflu group， and BD-77 groups of 75 and 37.5 g·L^-1 for inhalation of 20 min and 25 min. Human coronavirus 229E and OC43 experiment divided the BALB/c mice into a normal group， model group， chloroquine phosphate group， and BD-77 groups of 75， 37.5， 18.75， and 9.375 g·L^-1， with 10 mice in each group. Influenza virus H1N1/FM1 and human coronaviruses 229E and OC43 infection-induced pneumonia models were used to detect mouse lung index， and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the viral load in lung tissue. Enzyme-linked immunosorbent assay （ELISA） was used to detect related inflammatory factors in lung tissue， and proteomics analysis was performed on the lung tissue of OC43-infected mice. ResultCompared with that in the normal group， the lung index of mice in each infection group was significantly increased （P<0.01）， and viral nucleic acid could be detected in the lung tissue of mice infected with human coronaviruses 229E and OC43. The levels of interleukin-6 （IL-6）， IL-10， and tumor necrosis factor-α （TNF-α） in the lung tissue of mice infected with human coronavirus 229E were all significantly increased （P<0.01）. BD-77 could significantly reduce the lung index of mice infected with influenza virus H1N1/FM1 and human coronaviruses 229E and OC43 （P<0.05， P<0.01）， cut down the viral load in the lungs of mice infected with human coronaviruses 229E and OC43 （P<0.01）， and lower the contents of IL-6， IL-10， and TNF-α in the lung tissue of mice infected with human coronavirus 229E （P<0.01）. Proteomics analysis of the lung tissue of OC43-infected mice showed that BD-77 regulated the AMPK signaling pathway， TNF signaling pathway， NOD-like signaling pathway， IL-17 signaling pathway， Forkhead box protein O （FoxO） signaling pathway， transforming growth factor-β （TGF-β） signaling pathway， and other signaling pathways. ConclusionNebulized inhalation of BD-77 is effective in treating pneumonia caused by influenza virus H1N1/FM1 and human coronaviruses 229E and OC43 infection in mice and may exert its antiviral effects by regulating the balance of cellular metabolism， enhancing the immune function of the host， and attenuating inflammatory responses.