Objective: To compare the effect of intranasal dexmedetomidine and oral chloral hydrate in deep sedation of children. Methods: The Pubmed, EMBase, CENTRAL (Issue 4, 2018), Web of science, CBM, Wanfang Data, CNKI and VIP databases from the inception to January 2019 were searched. Randomized controlled trials (RCTs) with dexmedetomidine and chloral hydrate as interventions were included and the data were analyzed by RevMam 5.3 and Stata 12.0 software. The success rate of deep sedation, the indicator of sedation onset time, the recovery time, the incidence of vomiting and bradycardia were compared. Results: A total of 7 RCTs involving 1 007 patients were included for analysis. The results showed that the success rate of deep sedation (OR=2.55, 95%CI:1.46-4.44, P<0.01) and the incidence of bradycardia (OR=4.42, 95%CI:1.82-10.74, P<0.01) in the dexmedetomidine nasal group were significantly higher than those in the chloral hydrate oral group. The recovery time was significantly shorter (MD=-16.41, 95%CI:-21.54-11.28, P<0.01) and the incidence rate of vomiting (OR=0.04, 95%CI:0.01-0.17, P<0.01) in dexmedetomidine nasal group was significantly lower than those in the chloral hydrate oral group. There was no significant difference in the indicator of sedation onset time (MD=-0.47, 95%CI:-2.71-1.22, P=0.46). Conclusion Compared with the traditional oral chloral hydrate, intranasal dexmedetomidine has a higher sedation success rate and shorter recovery time after sedation with a lower incidence of nausea and vomiting.

Objective To investigate the effect and mechanism of miR-141-3p on pulmonary fibrosis in rats with acute respiratory distress syndrome(ARDS).Methods Rats were divided into the control group,the model group,the agomir negative control group and the miR-141-3p agomir group according to random number table,with 10 rats in each group.In addition to the control group,the ARDS rat model was established by lipopolysaccharide(LPS)infusion.Rat alveolar typeⅡepithelial cells RLE-6TN cells were divided into the NC group,the LPS group,the miR-NC group,the miR-141-3p mimics group,the miR-141-3p mimics+pcDNA group and the miR-141-3p mimics+NRF2 and Kelch-like ring associated protein 1(Keap1)group.LPS cell model was established in all groups except the NC group.The mRNA expression levels of miR-141-3p and Keap1 in lung tissue and cells were detected by qPCR.Western blot assay was used to analyze lung tissue and cell epithelial cadherin(E-cadherin),neural cadherin(N-cadherin),microtubule associated protein light chain 3B(LC3B),autophagy associated gene Beclin-1,α-smooth muscle actin(α-SMA),type I collagen(Col-Ⅰ),Keap1 and nuclear factors E2 related factor 2(NRF2)and heme oxygenase 1(HO-1).HE staining and Masson staining were used to observe pathological changes of lung tissue and to estimate the area of lung tissue injury and pulmonary fibrosis.Hydroxyproline(Hyp)in lung tissue was detected by the kit.Levels of inflammatory factor interleukin-1β,tumor necrosis factor(TNF-α)and oxidative stress index malondialdehyde(MDA)and superoxide dismutase(SOD)were detected by ELISA.Dual luciferase reporting experiment was used to verify the targeting relationship between miR-141-3p and Keap1.Results The expression of miR-141-3p was down-regulated and the expression of Keap1 was up-regulated in lung tissue and cells(P＜0.05).Overexpression of miR-141-3p can reduce the degree of pathological damage and fibrosis of lung tissue in rats,Hyp content,and up-regulate expression levels of SOD,E-cadherin,LC3B,Beclin-1,NRF2 and HO-1 in lung tissue and cells,and down-regulate the expression levels of IL-1β,TNF-α,MDA,N-cadherin,α-SMA,Col-I and Keap1(P＜0.05).Overexpression of Keap1 was able to reverse the improvement effect of overexpression of miR-141-3p on alveolar epithelial cell damage in ARDS rats(P＜0.05).Double Luciferase reporter gene experiment confirmed that miR-141-3p and Keap1 may have a targeted regulatory relationship.Conclusion Overexpression of miR-141-3p may activate the Keap1-NRF2/ARE signaling pathway,activate autophagy,inhibit inflammatory response,oxidative stress,and EMT progression,and improve pulmonary fibrosis in ARDS rats.

Objective:To discuss the effect of inhibiting microRNA(miR)-193a-5p expression on pulmonary fibrosis in the rats with acute respiratory distress syndrome(ARDS),and to clarify the related mechanism.Methods:A total of 60 male SD rats were divided into sham operation group,model group,miR-193a-5p antagonist group(Antagomir group),and negative control group(Antagomir-NC group),and there were 15 rats in each group.The ARDS animal model was induced by administering 10 mg·kg-1 lipopolysaccharide(LPS)via tracheal instillation,while the rats in sham operation group received an equal volume of saline.After successful modeling,the rats in Antagomir group and Antagomir-NC group were treated with miR-193a-5p Antagomir or Antagomir-NC via tail vein injection.The arterial partial pressure of oxygen(PaO2)and oxygenation index(OI)of the rats in various groups were measured;HE staining and Masson staining were used to observe the pathology and collagen fiber deposition in lung tissue of the rats;kit was used to detect the level of hydroxyproline(Hyp)in lung tissue of the rats in various groups;enzyme-linked immunosorbent assay(ELISA)method was used to detect the levels of inflammatory factors tumor necrosis factor α(TNF-α),interleukin(IL)-1β,and IL-6 in bronchoalveolar lavage fluid(BALF)of the rats in various groups;real-time fluorescence quantitative PCR(RT-qPCR)method was used to detect the expression levels of miR-193a-5p in lung tissue of the rats in various groups;Western blotting method was used to detect the expression levels of β-catenin,Snail family transcriptional repressor 1(Snail1),and α-smooth muscle actin(α-SMA)proteins in lung tissue of the rats in various groups.Results:Compared with sham operation group,the PaO2 and OI of the rats in model group were significantly decreased(P<0.05);compared with model group,the PaO2 and OI of the rats in Antagomir group were significantly increased(P<0.05).The HE staining results showed that the lung tissue structure of the rats in sham operation group was normal,and there were no obvious inflammatory changes;compared with sham operation group,mild abnormalities in lung tissue structure,alveolar atrophy,and collapse were observed in the rats in model group and Antagomir-NC group,with a large number of lymphocytes and a small number of neutrophils infiltrating in the alveolar cavities,and widened alveolar spaces;compared with model group,the rats in Antagomir group showed a significant reduction in lymphocytes and neutrophil infiltration in the alveolar cavities and there were no obvious hyperplasia.The Masson staining results showed no obvious blue collagen fiber deposition in lung tissue of the rats in sham operation group;compared with sham operation group,significant blue collagen fiber deposition was observed in lung tissue of the rats in model group and Antagomir-NC group,with severe damage of the alveolar structure,indicating obvious pulmonary fibrosis;compared with model group,the deposition of blue-stained collagen fibers in lung tissue of the rats in Antagomir group was significantly reduced.Compared with sham operation group,the level of Hyp in lung tissue of the rats in model group was significantly increased(P<0.05);compared with model group,the level of Hyp of the rats in Antagomir group was significantly decreased(P<0.05).The ELISA results showed that compared with sham operation group,the levels of TNF-α,IL-1β,and IL-6 in BALF of the rats in model group were significantly increased(P<0.05);compared with model group,the levels of TNF-α,IL-1β,and IL-6 of the rats in Antagomir group were significantly decreased(P<0.05).The RT-qPCR results showed that compared with sham operation group,the expression level of miR-193a-5p in lung tissue of the rats in model group was significantly increased(P<0.05);compared with model group,the expression level of miR-193a-5p of the rats in Antagomir group was significantly decreased(P<0.05).The Western blotting results showed that compared with sham operation group,the expression levels of β-catenin,Snail1,and α-SMA proteins in lung tissue of the rats in model group were significantly increased(P<0.05);compared with model group,the expression levels of β-catenin,Snail1,and α-SMA proteins in lung tissue of the rats in Antagomir group were significantly decreased(P<0.05).Conclusion:Inhibition of miR-193a-5p expression can improve the lung function and alleviate the pulmonary fibrosis in the ARDS rats by reducing the inflammatory responses and downregulating the expressions of β-catenin,Snail1,and α-SMA proteins.

Colorectal cancer (CRC) is one of the leading causes of death worldwide. Thus, the development of new therapeutic targets for CRC treatment is urgently needed. SGK1 is involved in various cellular activities, and its dysregulation can result in multiple cancers. However, little is known about its roles and associated molecular mechanisms in CRC. In present study, we found that SGK1 was highly expressed in tumor tissues compared with peri-tumor samples from CRC patients. In vitro experiments revealed that SGK1 overexpression promoted colonic tumor cell proliferation and migration and inhibited cell apoptosis induced by 5-fluorouracil (5-FU), while SGK1 shRNA and inhibitors showed the inverse effects. Using CRC xenograft mice models, we demonstrated that knockdown or therapeutic inhibition of SGK1 repressed tumor cell proliferation and tumor growth. Moreover, SGK1 inhibitors increased p27 expression and promoted p27 nuclear accumulation in colorectal cancer cells, and p27 siRNAs could attenuate the repression of CRC cell proliferation induced by SGK1 inhibitors. Collectively, SGK1 promotes colorectal cancer development via regulation of CRC cell proliferation, migration and survival. Inhibition of SGK1 represents a novel strategy for the treatment of CRC.
Animals ; Apoptosis ; Cause of Death ; Cell Proliferation ; Colon ; Colorectal Neoplasms* ; Fluorouracil ; Heterografts ; Humans ; In Vitro Techniques ; Mice ; Repression, Psychology ; RNA, Small Interfering

Objective To investigate the delay of door to signature time in primary percutaneous coronary intervention (PCI) and its influence in patients with ST segment elevation myocardial infarction (STEMI),therefore to provide a scientific basis for further effective shortening the time of primary PCI in patients with STEMI.Methods A total of 226 patients who diagnosed with STEMI and underwent primary PCI at Henan Provincial People's Hospital from June 2016 to December 2017 were enrolled in the study.Observation indicators include:(1) baseline data of patients;(2) time segments in primary PCI:total ischemic time (TIT),door to balloon time (DTBT),door-to-signature time (DTST),signature to balloon time (STBT);(3) the demographic characteristics of the family members who signed informed consent;and (4) the psychological factors and coping strategies of family members before signing informed consent.All data was analyzed using SPSS software (version 22.0).Multiple linear regression analysis was used to analyze the influencing factors of delay of DTST.A P＜0.05 was considered statistically significant.Results In this study,226 patients with STEMI who were first diagnosed in our hospital had a mean age of 55.23±10.80 years,and 181 (80.1％) were male.The median of TIT,DTBT,DTST,STBT were 312 min,166 min,82 min,and 80 min.The ratio of DTST in DTBT and TIT was 50％ and 28.5％,respectively.The multiple linear regression analysis showed that the number of direct family members (P＜0.001),the degree of educational in middle school and below (P=0.010),high school/technical secondary school (P=0.029),families worrying about the high cost of medical care (P=0.020),families consulted each other repeatedly (P=0.022),and consulted the other medical staff(P=0.022) are risk factors of DTST delay,and city residence (P=0.048) is the protection factor of DTST delay.Conclusions The long time of DTS is a reality of the practice of primary PCI in China.The factors that lead to longer DTST include demographic characteristics,psychological factors and coping strategies of family members.The STBT of primary PCI in China should be taken into the value while emphasizing the DTBT.

Objective To explore the effects of group guidance on the cognitive ability of empty nesters in a community.Methods Totally 179 empty nesters aged above 60 from a community in Xicheng District,Beijing between April 2014 and April 2015 were selected by convenience sampling,and divided into an intervention group (n=89) and a control group (n=90). Patients in the intervention group were treated by group guidance,once a week (60 min each time) for 12 months,while patients in the control group received no intervention. And the empty nesters' cognitive ability was evaluated with Mini-mental State Examination (MMSE) before and after the intervention.Results The differences found in comparing the orientation,memory, linguistic competence and cognitive ability of the empty nesters in the intervention group were statistically significant (P<0.05). And the differences found in comparing the memory and cognitive ability of the empty nesters in the control group were also statistically significant (P<0.05). Before the intervention,however,there was no significant difference between the empty nesters in the two groups in cognitive ability and other indicators (P>0.05). After the intervention,the empty nesters in the observation group scored higher in orientation, attention,numeracy,linguistic competence and cognitive ability than the empty nesters in the control group (P<0.05).Conclusions Empty nesters' cognitive ability comes to weaken and decline with age,and group guidance helps to improve their cognitive ability significantly.

Objective : To investigate the effect of miR-141-3p on LPS induced A549 cell injury by targeting high mobility group protein 1 (HMGB1) ． Methods : A549 cells derived from type Ⅱ alveolar epithelial cells were taken as the study object，miR-141-3p mimics，mimics NC，HMGB1 gene overexpression plasmid (pcDNA3. 1-HMGB1) and empty Vector were transfected into A549 cells respectively or co-transfected，then 10 μg / ml LPS was used for 24 h．Cell proliferation activity was detected by cell counting kit-8 ( CCK-8) ．The activity of lactate dehydrogenase ( LDH) in the supernatant of cell culture was detected by colorimetry．The apoptosis level of each group was detec- ted by flow cytometry．The levels of interleukin (IL) -1 β , IL-6 and tumor necrosis factor α (TNF-α) were detected by enzyme-linked immunosorbent assay (Elisa) ．Dual luciferase reporter gene assay verified the targeted regulatory relationship between miR-141-3p and HMGB1 . Results : After treatment with LPS ，the proliferative activity of A549 cells and the expression level of miR-141-3p decreased ( P ＜0. 05 ) ，the apoptosis rate increased ( P < 0. 05) ，the levels of IL-1 β , IL-6，TNF-α and the activity of LDH in supernatant increased (P＜0. 05) ．Overex- pression of miR-141-3p increased the proliferation activity of A549 cells treated with LPS (P ＜0. 05 ) ，and de- creased the apoptosis rate and the levels of IL-1 β , IL-6，TNF-α in cells and LDH activity in supernatant (P < 0. 05) ．However，overexpression of HMGB1 gene could reverse the ameliorative effect of miR-141-3p on LPS-in- duced A549 cell injury．Dual luciferase reporter gene experiment confirmed that HMGB1 was the downstream target gene of miR-141-3p． Conclusion miR-141-3p can inhibit LPS-induced apoptosis，reduce the expression level of inflammatory factors，and improve the damage of A549 cells，which may be related to the targeted regulation of HMGB1 expression.

Objective To investigate the epidemiological features and antiviral response of patients with genotype 6 chronic hepatitis C (CHC) in Guangxi, China. Methods A total of 97 patients with genotype 6 CHC who were admitted to The First Affiliated Hospital of Guangxi Medical University from December 2012 to December 2020 were enrolled, among whom 62 patients were given antiviral therapy. The 62 patients receiving antiviral therapy were divided into interferon group with 22 patients and direct-acting antiviral agent (DAA) group with 40 patients. Related data were collected, including general demographic data, HCV RNA, liver function, routine blood test results, and renal function. The chi-square test was used for comparison of categorical data between groups. Results Among the 97 patients, there were 69 male patients (71.1%) and 28 female patients (28.9%), with a mean age of 41.97±10.12 years, and the patients aged 30-40 years accounted for 47.4% (46/97). Of all 97 patients, 95 (97.9%) had genotype 6a, 1 had genotype 6e, and 1 had genotype 6xa. Among the 65 patients with a definite route of infection, 41 (63.1%) had intravenous drug use, 14 had medical-related operations, 9 had blood transfusion, and 4 had sexual contact as the route of infection. For the interferon group, the rapid virologic response (RVR) rate at week 4 was 81.8% (18/22), the rate of undetectable virus at the time of drug withdrawal (Epoint) was 86.4% (19/22), the rate of sustained virologic response at 12 weeks after drug withdrawal (SVR12) was 81.8%, and the rate of sustained virological response at 24 weeks after drug withdrawal (SVR24) was 81.8%; 1 patient in this group experienced recurrence. All 40 patients in the DAA group were previously untreated patients (33 patients without liver cirrhosis and 7 patients with compensated liver cirrhosis), with an overall RVR rate of 87.5%(35/40), an Epoint rate of 100%, and an SVR12 rate of 100%, and there was no treatment failure or recurrence. Although different DAA regimens had different RVR rates, they all had a SVR12 rate of 100%. The patients with compensated liver cirrhosis and other diseases had a SVR12 rate of 100%. Conclusion Intravenous drug addiction is the main route of infection for patients with genotype 6 CHC in Guangxi, and CHC is more common in men, with genotype 6a as the main subtype. DAA treatment has a higher virologic response rate than interferon treatment, with an SVR12 rate of 100%. There is no significant difference in SVR12 rate between the patients with compensated liver cirrhosis and those without liver cirrhosis.