ObjectiveTo clarify the expression of TRIM28 in non-M3 acute myeloid leukemia （AML） and its correlation with clinical indicators and prognosis， and to further explore the effect of TRIM28 expression levels on the proliferation and apoptosis of AML cells using small interfering RNA. MethodsThe GSE34577 dataset was analyzed using R software to compare TRIM28 expression between healthy controls and non-M3 acute myeloid leukemia （AML） patients. Clinical samples from non-M3 AML patients were collected， with TRIM28 expression levels measured using real-time quantitative PCR （qPCR）. The analysis focused on correlations between TRIM28 expression and various clinical indicators， treatment efficacy， and patient prognosis. Furthermore， small interfering RNA （siRNA） technology was employed to downregulate TRIM28 expression in human primary AML cells （HL60 cell line）. The effects on cell proliferation and apoptosis were then assessed through CCK-8 assays and flow cytometry， respectively. ResultsThe results showed that TRIM28 was up-regulated in non-M3 AML of both online database GSE34577 and clinical samples （P<0.000 1）， TRIM28 expression of new diagnosis group and relapsed refractory group was higher than iron deficiency anemia group （P<0.01）， and there was no significance between different French-American-British classification systems subtype. TRIM28 expression was higher in non-M3 AML patients with a poor genetic prognosis stratified as moderate than in the good prognosis group， and TRIM28 expression was associated with NPM1 combined with the FLT3-ITD mutation， positively correlated with age， bone marrow blast， peripheral blood blast and white blood cell， negatively correlated with hemoglobin. In addition， interference TRIM28 greatly inhibited cell proliferation and promoted cell apoptosis. ConclusionThis study reveals that TRIM28 is highly expressed in non-M3 AML and associated with prognosis， and plays a key role in the proliferation and apoptosis of AML cells， suggesting that TRIM28 may serve as a novel therapeutic target for non-M3 AML.

ObjectiveTo explore the mechanism by which Zuoguiwan improves the pancreas development in the gestational diabetes mellitus （GDM） model by observing the effects of Zuoguiwan on the expression of key regulatory factors in different stages of pancreas development. MethodsPregnant Wistar rats were randomly assigned into blank， model， insulin detemir （20 U·kg^-1） and Zuoguiwan （1.89 g·kg^-1） groups （n=18）. GDM was induced by peritoneal injection of streptozotocin on day 6.5 （E6.5d） in the embryonic stage， and the blank group was given an equal volume of sodium citrate buffer. The modeling performance was assessed by measuring the blood glucose of pregnant rats. Except the blank group and model group， pregnant rats in other groups were administrated with corresponding drugs from E9.5d to delivery. The random blood glucose of pregnant rats was monitored， and the embryos and offspring rats were measured for the length and weighed on E12.5d， E18.5d and day 21 after birth （B21d）. The Lee's index of rats on B21d was calculated. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the fasting insulin （FINS） levels of B22d rats and the Homeostasis Model Assessment for Insulin Resistance （HOMA-IR） was calculated. The serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total bilirubin （TBIL）， total cholesterol （CHO）， triglyceride （TG）， high-density lipoprotein cholesterol （HDL）， and low-density lipoprotein cholesterol （LDL） in E18.5d pregnant rats and B22d offspring were determined. The pathological changes in the pancreas of E12.5d， E18.5d and B22d rats were observed by hematoxylin-eosin （HE） staining. Western blot was used to determine the protein levels of pancreatic duodenal homeobox 1 （Pdx1）， pancreas-specific transcription factor 1a （Ptf1a）， and sex-determining region Y-box protein 9 （Sox9） in the pancreas of E12.5d embryos， Pdx1， Nkx2 homeobox 2 （Nkx2.2）， and hairy and enhancer of split-1 （Hes1） in the pancreas of E18.5d embryos， and Pdx1， v-maf musculoaponeurotic fibrosarcoma oncogene homolog A （Mafa）， and NK transcription factor-related homeobox gene family 6 locus 1 （Nkx6.1） in the pancreas of B22d rats. ResultsCompared with the blank group， the model group showed elevated blood glucose levels in pregnant rats on B0d， E9.5d， E12.5d， E15.5d， and E18.5d （P<0.05， P<0.01）， decreased body weight and body length （P<0.01） and increased Lee's index in the offspring. In addition， the B22d offspring showed rising levels of FBG， FINS， HOMA-IR， AST， and TG （P<0.01）， a declined level of HDL （P<0.01）， and pancreatic acinous cells with edema and loose arrangement. The pregnant rats on E18.5d exhibited raised levels of ALT， AST， and TG （P<0.05， P<0.01） in the pancreas and a declined level of HDL （P<0.05）. The E12.5d embryos showed up-regulated protein levels of Pdx1， Sox9， and Ptf1a in the pancreas （P<0.01） and the E18.5d embryos exhibited down-regulated protein levels of Pdx1， Nkx2.2， and Hes1 in the pancreas （P<0.01）. The protein levels of Pdx1， Nkx6.1， and Mafa in the pancreas of B22d offspring were down-regulated （P<0.01）. Compared with the model group， the insulin group exhibited lowered blood glucose in pregnant rats on B0d， E15.5d， and E18.5d （P<0.05， P<0.01）. The offspring in all treatment groups showcased increased body weight and body length （P<0.01） and decreased Lee's index. The B22d offspring exhibited declined levels of FBG， FINS， and HOMA-IR in the insulin group （P<0.01） and lowered levels of FBG and HOMA-IR in the Zuoguiwan group （P<0.01）. The B22d offspring in all the treatment groups showed reduced levels of ALT， AST， TBIL， CHO， TG， and LDL， a raised level of HDL， and alleviated edema of pancreatic acinous cells. The pregnant rats on E18.5d demonstrated declined levels of TG and ALT （P<0.05， P<0.01） and an elevated level of HDL （P<0.05）. The pancreas of E12.5d embryos presented down-regulated protein levels of Pdx1 and Sox9 and an up-regulated protein level of Ptf1a in the insulin group （P<0.05）. The pancreas of E12.5d embryos in the Zuoguiwan group presented down-regulated protein levels of Pdx1， Sox9， and Ptf1a （P<0.01）. All the treatment groups showed up-regulated protein levels of Pdx1， Nkx2.2， and Hes1 in the pancreas of E18.5d embryos （P<0.01） and Pdx1， Nkx6.1， and Mafa in the pancreas of B22d embryos （P<0.05， P<0.01）. ConclusionZuoguiwan can promote the growth and development and ameliorate the pathological changes in the pancreas of the offspring of GDM model by regulating the expression of Pdx1 pathway-related regulatory factors in different stages of pancreas development.

Objective : To investigate the impact of SOX4 on ovarian granulosa cells，stable overexpression of SOX4 was achieved in human KGN cell line，followed by analysis of its effects on proliferation，migration and apoptosis. Methods : The recombinant lentiviral plasmid pLV-EF1a-GFP / Puro-SOX4 was generated through homologous recombination with linearized pLV-EF1a-GFP / Puro vector．Human ovarian granulosa cells ( KGN cell line ) were transduced with Lentiviral expression vectors．KGN cells infected with pLV-EF1a-GFP / Puro-NC were served as the LV-CON group，while those infected with pLV-EF1a-GFP / Puro-SOX4 were designated as the LV-SOX4 group．Following transfection，puromycin selection was employed to establish stable SOX4-expressing KGN cells．The expres- sion levels of SOX4 m RNA and protein in KGN cells from the LV-CON and LV-SOX4 groups were assessed using RT-qPCR and Western blot analysis．Cell proliferation was assessed using the CCK-8 assay in both LV-CON and LV-SOX4 groups．Cell migration ability was evaluated by means of a cell scratch test in these two groups．The proportion of apoptotic cells was determined via flow cytometry analysis in both LV-CON and LV-SOX4 groups. Results: The sequencing results of pLV-EF1a-GFP / Puro-SOX4 indicated a complete match between the inserted gene se- quence and the SOX4 mRNA sequence．The lentiviral titers were 7 × 108 TU / ml in the LV-CON group and 1 × 108 TU / ml in the LV-SOX4 group．The recombinant plasmid was successfully transfected into KGN cells with a transfection efficiency of over 90% under fluorescence inverted microscopy．The results of RT-qPCR and Western blot tests demonstrated a significant increase in the expression level of SOX4 in KGN cells of LV-SOX4 group compared to that of LV-CON group (t = 3. 10，P ＜0. 05 ; t = 14. 20，P ＜0. 05) ．The CCK-8 assay results demonstrated that the LV-SOX4 group exhibited a significant increase in cell proliferation (24 h : t = 45. 92，P＜0. 01 ; 72 h : t = 25. 60，P ＜0. 01) compared to the LV-CON group．The cell scratch assay indicated that the migratory capacity of KGN cells in the LV-SOX4 group was significantly enhanced (t = 7. 65，P ＜0. 01) compared to that in the LV-CON group. The LV-SOX4 group exhibited a significant reduction in apoptosis ratio (t = 25. 84，P＜0. 01) compared to the LV- CON group． Conclusion SOX4-overexpressing KGN cell line was successfully established，and the overexpression of SOX4 facilitated proliferation and migration while inhibiting apoptosis in human ovarian granulosa cells.

Objective:To explore the clinical characteristics and risk factors of the severe delayed encephalopathy after acute carbon monoxide poisoning (s-DEACMP).Methods:A retrospective analysis of 170 acute carbon monoxide poisoning (ACMP) patients treated in the Hyperbaric Oxygen (HBO) Department of Beijing Chao-yang Hospital, Capital Medical University from January 1st, 2017 to December 31st, 2020 was conducted. According to the occurrence of delayed encephalopathy, the ACMP patients were divided into DEACMP group and non-DEACMP (n-DEACMP) group. The DEACMP patients were stratified by the activities of daily living scale when they were most severely ill. The patients with total score≤60 were classified as s-DEACMP and the patients with total score >60 were classified as mild to moderate DEACMP (m-DEACMP). Their clinical characteristics were compared and the risk factors of s-DEACMP were analyzed.Results:There were 70 s-DEACMP patients, 49 m-DEACMP patients, and 51 n-DEACMP patients. Compared with the n-DEACMP group, the s-DEACMP group was older (average age: 59.0 vs. 49.0, P=0.005), had a higher proportion of patients over 40 years old (97.1% vs. 66.7%, P<0.001), lower Glasgow coma scale scores [(4.0±3.0) vs.(6.0±5.0), P=0.024] on admission to the hospital, longer consciousness disturbance [(32.0±31.8) h vs.(20.5±26.4) h, P=0.017], a higher proportion of patients with consciousness disturbance over 48 hours (24.3% vs. 9.8%, P=0.041), a lower proportion of patients receiving HBO therapy (70.0% vs. 86.3%, P=0.036), a higher proportion of patients with hypertension (38.6% vs. 17.6%, P=0.013), a higher proportion of patients with hyperhomocysteinemia (40.0% vs. 19.6%, P=0.017), and a higher proportion of patients with smoking index over 400 (24.3% vs. 9.8%, P=0.041). Compared with the m-DEACMP group, the s-DEACMP group had a higher proportion of patients with hyperhomocysteinemia (40.0% vs. 20.4%, P=0.024). Multivariate Logistic regression showed that age over 40 years old, consciousness disturbance over 48 hours, hypertension, and hyperhomocysteinemia were independent risk factors of s-DEACMP( P<0.05). Conclusion:The clinical characteristics of s-DEACMP patients are that the patients are older, have a deeper and longer consciousness disturbance, a lower proportion of early HBO intervention, a higher proportion of hypertension, hyperhomocysteinemia, and smoking index over 400. Among them, the age over 40 years old, disturbance consciousness over 48 hours, and hypertension were the independent risk factors of the occurrence of s-DEACMP.In additon hyperhomocysteinemia was also an idependent risk factor for s-DEAMP, which special worth attention.

Objective:To explore the clinical characteristics and risk factors of the severe delayed encephalopathy after acute carbon monoxide poisoning (s-DEACMP).Methods:A retrospective analysis of 170 acute carbon monoxide poisoning (ACMP) patients treated in the Hyperbaric Oxygen (HBO) Department of Beijing Chao-yang Hospital, Capital Medical University from January 1st, 2017 to December 31st, 2020 was conducted. According to the occurrence of delayed encephalopathy, the ACMP patients were divided into DEACMP group and non-DEACMP (n-DEACMP) group. The DEACMP patients were stratified by the activities of daily living scale when they were most severely ill. The patients with total score≤60 were classified as s-DEACMP and the patients with total score >60 were classified as mild to moderate DEACMP (m-DEACMP). Their clinical characteristics were compared and the risk factors of s-DEACMP were analyzed.Results:There were 70 s-DEACMP patients, 49 m-DEACMP patients, and 51 n-DEACMP patients. Compared with the n-DEACMP group, the s-DEACMP group was older (average age: 59.0 vs. 49.0, P=0.005), had a higher proportion of patients over 40 years old (97.1% vs. 66.7%, P<0.001), lower Glasgow coma scale scores [(4.0±3.0) vs.(6.0±5.0), P=0.024] on admission to the hospital, longer consciousness disturbance [(32.0±31.8) h vs.(20.5±26.4) h, P=0.017], a higher proportion of patients with consciousness disturbance over 48 hours (24.3% vs. 9.8%, P=0.041), a lower proportion of patients receiving HBO therapy (70.0% vs. 86.3%, P=0.036), a higher proportion of patients with hypertension (38.6% vs. 17.6%, P=0.013), a higher proportion of patients with hyperhomocysteinemia (40.0% vs. 19.6%, P=0.017), and a higher proportion of patients with smoking index over 400 (24.3% vs. 9.8%, P=0.041). Compared with the m-DEACMP group, the s-DEACMP group had a higher proportion of patients with hyperhomocysteinemia (40.0% vs. 20.4%, P=0.024). Multivariate Logistic regression showed that age over 40 years old, consciousness disturbance over 48 hours, hypertension, and hyperhomocysteinemia were independent risk factors of s-DEACMP( P<0.05). Conclusion:The clinical characteristics of s-DEACMP patients are that the patients are older, have a deeper and longer consciousness disturbance, a lower proportion of early HBO intervention, a higher proportion of hypertension, hyperhomocysteinemia, and smoking index over 400. Among them, the age over 40 years old, disturbance consciousness over 48 hours, and hypertension were the independent risk factors of the occurrence of s-DEACMP.In additon hyperhomocysteinemia was also an idependent risk factor for s-DEAMP, which special worth attention.

Objective:To summarize the clinical nursing experience of oxygenation (ECMO) adjuvant therapy in children with acute respiratory distress syndrome (ARDS) caused by severe adenovirus pneumonia.Method:The clinical data of 20 children with severe adenovirus pneumonia complicated with ARDS who received ECMO in our hospital from April 2017 to May 2019, including general conditions, pre-treatment, complications and prognosis, were retrospectively analyzed.Results:The primary disease of 20 patients was severe adenovirus pneumonia, and the average duration of ECMO treatment was [247.50(152.00,296.75)] hours. After treatment, 12 (12/20) patients successfully escaped from ECMO, 11 (11/20) patients died, and 9 (9/20) died. Complications occurred in 17 (17/20) patients with ECMO treatment. After discharge from the hospital for six months to two years, 9 patients with good quality of life, social function, normal mental development, 2 patients with ischemia and hypoxia brain damage, in the hospital or family continued rehabilitation exercise.Conclusions:Children with severe adenovirus pneumonia combined with ARDS are critically ill. When other treatments are ineffective, ECMO treatment can provide cardiopulmonary support for children with reversible cardiopulmonary failure, but the complications are numerous and serious. Prevention and reduction of related complications are the key to the success of ECMO.